Quest A Key To Ug Paediatrics PDF

QUEST
A KEY TO UG PAEDIATRICS
(Solved WBUHS Papers of 2008 – 2018 and Semester questions of all
the medical colleges in WB)
Dr. Shatanik Sarkar MBBS, MD (Paediatric Medicine)

RMO-cum-Clinical Tutor, Department of Paediatric Medicine,
R. G. Kar Medical College, Kolkata
Dr. Debasree Guha MBBS, MD (Paediatric Medicine)

RMO-cum-Clinical Tutor, Department of Paediatric Medicine,
R. G. Kar Medical College, Kolkata
ACADEMIC PUBLISHERS
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© Academic Publishers
First edition 2018
ISBN : 978-93-87162-10-5
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II
Dedicated to
The future limelights of our medical fraternity
III
IV
Preface to the first edition
It gives us extreme appeasement to be able to present the first edition of the book
"Quest – A Key to UG Paediatrics".
Paediatrics including neonatology is now a separate subject for assessment in
Third Professional MBBS (Part II) Examination under revised MCI curriculum. Our
experiences in this subject in last 8-10 years have helped us to understand the
difficulties and confusions faced by undergraduate students during paediatric
examination. We have also observed that due to immense pressure of other major
subjects, students spend less time in studying paediatrics, which ultimately push them
into difficulties during examination. Moreover, sometimes they get confused to express
their knowledge concisely and in impressive manner during writing theory papers. All
of these shortcomings have prompted us to write a book which might help them to feel
comfortable on the D-day.
This is not a text book of paediatrics or a substitute for it. In this book, 3rd
Professional MBBS (Part II) Paediatric questions of WBUHS and semester-wise
questions of different medical colleges are compiled and answered to help the students
in quick revision before the final as well as semester examinations. All answers have
been structured in a comprehensive but concise point wise manner. Several schematic
diagrams, tabular descriptions and flow charts have been added for better remembrance
and reproduction during examination. A separate chapter has been added to cover
"The Approaches to manage different clinical cases" which come as a compulsory
question in each paper and these often pose difficulties for the students to answer in
a proper way. Our knowledge gathered from different text books, journals and recent
advances and our experience in dealing with wide varieties of clinical cases have
helped us to design and write this book.
We gladly welcome all types of suggestions, comments and criticisms from the
readers, both students and teachers, which will be gratefully acknowledged for making
the book more useful for students in future.
June, 2018
Kolkata.
Shatanik Sarkar & Debasree Guha
Shatanik Sarkar (Email id: [email protected])
Debasree Guha (Email id: [email protected])
V
VI
Acknowledgement
• It is a privilege for us to express our gratitude to all who have helped us in carrying
out this mammoth task of writing a book successfully.
• Any work can never be done successfully without the combined efforts of a group of
like-minded people. While some of them work actively on the stage, an even greater
number continue to play their ever important role behind the curtains.
• This book wouldn’t have been conceived without the knowledge and foresight of our
respected teacher, Prof. Sibarjun Ghosh, HOD, Dept of Paediatrics, Medical College &
Hospital. It was him who infused in us the courage to embark on this project, very little
is known about which previously.
• Without acknowledging the help of Prof. Malay Kumar Dasgupta, HOD, Dept of
Pediatrics, R. G. Kar Medical College & Hospital, this thing will remain incomplete, as
he gave us his valuable time, whenever we went to him seeking help regarding our work.
• We show our deepest gratitude to all our teachers and colleagues at the Department
of Pediatrics, R. G. Kar Medical College & Hospital for continuously encouraging us
throughout this entire period.
• We are deeply indebted to our spouses, Dr. Ritam Joarder and Dr. Chaitali Patra for
being with us through the good times and the bad times and for allowing us to carry
on in spite of all the problems they have faced on the way so far.
• Our acknowledgement goes to our parents and family members, who were constantly
beside us in the paths of hardness.
• We are deeply thankful to Dr. Simantini Sircar, who has helped us with the question
bank and also allayed our initial jitters with her experience in this field.
• This entire acknowledgement will remain incomplete, if we don't mention Academic
Publishers, especially Mr. Bimal Kumar Dhur and Mr. Dipankar Dhar, who inspired us
to write this book. We also thank the entire team of Academic Publishers, who worked
relentlessly for shaping up this book and making it presentable to the students.
• We are grateful to all the authors whose books have been used as references.
• Finally, we would like to thank Almighty God for all His blessings and being our strength
at all times.
VII
VIII
CONTENTS
WBUHS QUESTION PAPERS 2018 – 2015 XI – XIV
Chapter 1 : GROWTH AND DEVELOPMENT 1 – 9
Chapter 2 : NUTRITION AND MICRONUTRIENTS 10 – 35
Chapter 3 : FLUID AND ELECTROLYTE 36 – 42
Chapter 4 : NEONATOLOGY 43 – 105
Chapter 5 : IMMUNIZATION 106 – 112
Chapter 6 : INFECTIOUS DISEASES 113 – 142
Chapter 7 : RESPIRATORY SYSTEM 143 – 163
Chapter 8 : CARDIOVASCULAR SYSTEM 164 – 195
Chapter 9 : GASTRO-INTESTINAL SYSTEM 196 – 214
Chapter 10 : HEMATOLOGICAL DISORDERS 215 – 246
Chapter 11 : GENITO-UNINARY SYSTEM 247 – 269
Chapter 12 : CNS 270 – 292
Chapter 13 : MISCELLANEOUS 293 – 308
Chapter 14 : APPROACHES 309 – 347
Chapter 15 : ADDITIONAL ANSWERS OF 2018 (SUPPLEMENTARY) 348 – 353
IX
X
WBUHS QUESTIONS PAPERS OF 2018 – 2015
2018
Group – A
Q.1 : Discuss the process of vitamin D absorption and metabolism. Mention the clinical and radiological features of
Vitamin D deficient Rickets. – Ans. (See Page No. 12 : Q. 5)
Group – B
Q.2 : Write briefly on the following (any two) :
(a) ‘Warm chain’ in New born. – Ans. (See Page No. 45 : Q. 8)
(b) Differentiation of Jitteriness from convulsion in Neonate. – Ans. (See Page No. 99 : Q. 75)
(c) Clinical features and management of Acute Bronchiolitis in 6 months old infant.
– Ans. (See Page No. 152 : Q. 11)
Group – C
Q.3 : Write short notes on (any three) of the following :
(a) Baby of 3 days old, mother having chickenpox. – Ans. (See Page No. 100 : Q. 76)
(b) MMR vaccine. – Ans. (See Page No. 107 : Q. 3)
(c) Febrile convulsion. – Ans. (See Page No. 281 : Q. 9)
(d) Indications of renal biopsy in Nephrotic syndrome. – Ans. (See Page No. 269 : Q. 28)
Group – D
Q.4 : A two year old child presented in the emergency room with history of sudden onset of difficulty in breathing.
What is the probable diagnosis? How will you diagnose and manage such case ? – Ans. (See Page No.
332 : Q. 15)
2018 Supplementary
Group – A
Q.1 : Define severe acute malnutrition. Mention its 10 steps of management. How will you treat and prevent
Hypoglycemia and infection in this case ? – Ans. (See Page No. 20 : Q. 9)
Group – B
(a) Developmental milestones of a nine month old child. – Ans. (See Page No. 9 : Q. 10)
(b) Kangaroo mother care (KMC). – Ans. (See Page No. 48 : Q. 12)
(c) Routine delivery room care of a new born. – Ans. (See Page No. 94 : Q. 70)
Group – C
(a) Diagnosis of childhood pulmonary tuberculosis – RNTCP guideline. – Ans. (See Page No. 348 : Q. 1)
(b) Fluid management of Dengue Shock Syndrome. – Ans. (See Page No. 349 : Q. 2)
(c) Sequential OPV – IPV immunization. – Ans. (See Page No. 308 : Q. 1)
(d) Characteristics of skin rashes in different exanthematous fever in children. – Ans. (See Page No. 350 : Q. 3)
Group – D
Q.4 : A six year old child presented with severe anaemia without any Lymphadenopathy or Visceromegaly. Mention
the differential diagnosis and how will you approach to diagnose the case? – Ans. (See Page No. 351 : Q. 4)
XI
2017
Group – A
Q.1 : Describe the functions of the different parts of a nephron. Mention the laboratory diagnosis of Nephrotic
Syndrome. – Ans. (See Page No. 255 : Q. 9)
Group – B
(a) Late onset of Neonatal sepsis. – Ans. (See Page No. 53 : Q. 18)
(b) Developmental milestones of a normal child of one year. – Ans. (See Page No. 9 : Q. 11)
(c) Management of Hypothermia in Neonate. – Ans. (See Page No. 45 : Q. 4)
Group – C
(a) Management of foreign body in Respiratory tract. – Ans. (See Page No. 159 : Q. 18)
(b) Initial steps of resuscitation of a new born. – Ans. (See Page No. 95 : Q. 71)
(c) IPV. – Ans. (See Page No. 107 : Q. 2)
(d) Features of HIV in children. – Ans. (See Page No. 141 : Q. 29)
Group – D
Q.4 : A three year old boy has been brought to the emergency with convulsion persisting for more than 30 minutes.
(a) What is the probable diagnosis?
(b) Outline the management of such a patient. – Ans. (See Page No. 276 : Q. 4)
2017 Supplementary
Group – A
Q.1 : Discuss the cerebrospinal fluid (C.S.F) formation, circulation and absorption. Mention the clinical presentation
of tubercular meningitis including the Laboratory diagnosis of the condition. – Ans. (See Page No. 344 : Q. 24)
Group – B
(a) Danger signs in Newborn. – Ans. (See Page No. 91 : Q. 66)
(b) Acute bronchiolitis. – Ans. (See Page No. 152 : Q. 11)
(c) Hypoxic ‘blue’ spells. – Ans. (See Page No. 192 : Q. 34)
(d) Clinical features of Heart failure in infancy. – Ans. (See Page No. 188 : Q. 26)
Group – C
(a) Recent recommendation of Polio immunisation. – Ans. (See Page No. 308 : Q. 1)
(b) Complications of pre-term babies. – Ans. (See Page No. 84 : Q. 56)
(c) Low osmolar ORS. – Ans. (See Page No. 208 : Q. 13)
(d) Bronchial breath sound. – Ans. (See Page No. 161 : Q. 21)
Group – D
Q.4 : A five year old child presents with painless haematuria. Mention the causes and diagnosis of such case. – Ans.
(See Page No. 256 : Q. 10)
XII
2016
Group – A
Q.1 : Discuss the process of vitamin-D absorption and metabolism. Mention the clinical and radiological features of
vitamin D deficiency rickets. – Ans. (See Page No. 12 : Q. 5)
Group – B
(a) Types of breast milk with advantages. – Ans. (See Page No. 60 : Q. 27)
(b) Neonatal sepsis screening. – Ans. (See Page No. 51 : Q. 14)
(c) Motor milestones of a 2 year old child. – Ans. (See Page No. 9 : Q. 12)
Group – C
(a) Urine heat test. – Ans. (See Page No. 259 : Q. 16)
(b) Neonatal reflexes. – Ans. (See Page No. 98 : Q. 74)
(c) Clinical features of congestive cardiac failure in 10 years old boy. – Ans. (See Page No. 188 : Q. 25)
(d) Hyperkalaemia. – Ans. (See Page No. 41 : Q. 6)
Group – D
Q.4 : A 5 year old boy while playing in paddy field had a dog bite over face. How will you approach and protect the boy
from Rabies? – Ans. (See Page No. 139 : Q. 27)
2016 Supplementary
Group – A
Q.1 : Describe the pathogenesis of pulmonary primary complex of childhood tuberculosis. Narrate the fates of this
lesion. – Ans. (See Page No. 145 : Q. 4)
Group – B
(a) Management of Dengue shock syndrome. – Ans. (See Page No. 128 : Q. 18)
(b) Differential diagnosis of jaundice in a 6 days old neonate. – Ans. (See Page No. 100 : Q. 77)
(c) Management of neurotoxic (cobra) snake bite. – Ans. (See Page No. 297 : Q. 2)
Group – C
(a) Warm chain in newborn care. – Ans. (See Page No. 45 : Q. 8)
(b) Rheumatic chorea. – Ans. (See Page No. 179 : Q. 13)
(c) Use of zinc in diarrhoea. – Ans. (See Page No. 207 : Q. 12)
(d) Kerosene ingestion in a 3 year old girl. – Ans. (See Page No. 296 : Q. 1)
Group – D
Q.4 : A 6 year old male child admitted with severe respiratory distress and unilateral decreased breath sounds :
(a) Discuss the differential diagnosis. – Ans. (See Page No. 332 : Q. 16)
(b) Relevant investigations to confirm the diagnosis.
(c) Outline the treatment.
XIII
2015
Group – A
Q.1 : Name the common causes of generalised oedema in children. Describe the pathophysiology of oedema in
children. – Ans. (See Page No. 199 : Q. 4)
Group – B
(a) Phototherapy in neonates. – Ans. (See Page No. 82 : Q. 51)
(b) Write your plan of feeding of a premature very low birth weight newborn baby. – Ans. (See Page No. 86 :
Q. 62)
(c) Developmental milestones achieved at 9 months of age. – Ans. (See Page No. 9 : Q. 10)
Group – C
(a) M.M.R vaccine. – Ans. (See Page No. 107 : Q. 3)
(b) Kangaroo mother care. – Ans. (See Page No. 48 : Q. 12)
(c) Skeletal changes in Rickets. – Ans. (See Page No. 28 : Q. 11)
(d) Treatment of infected Scabies. – Ans. (See Page No. 294 : Q. 3)
Group – D
Q.4 : A 3 year old child presented in emergency room with history of fever and cough for 3 days and respiratory
distress for one day. Enumerate the common differential diagnosis for the case. How will you approach the
case to arrive at a definite diagnosis? – Ans. (See Page No. 326 : Q. 11)
XIV
2015
Group — A CHAPTER - 1
Name the common causes of generalised oedema in children Describe the - .
Siol f
children.
' - Ans. (See Page No. 199 : 0.4) ' Patho ph y ogyo oedema ‘"
GROWTH AND DEVELOPMENT
Group — B
02' Write briefly on the following (any two) : O. 1: Height Measurement In Pediatrics. {Murshidabadj
(a) Phototherapy in neonates. -— Ans. (See Page No.82 : O. 51) in pediatric age
Ans : Height is an important age dependent parameter of physical growth assessment
(b) Write your plan of feeding of a premature very low birth weight newborn baby. — Ans. (See of chronic deprivation.
Page No 86 ' group. especially deficiency in height is indicative
o. 62) ' '
(c) Developmental milestones achieved at 9 months of age. - Ans. (See Page No. 9 : O. 10) 0 Height measurement :
s Length - For children < 2 years
Group - C
Scale : b lntantometer _
0.3: Write short notes on (any three) of the following : > Fligid measuring table, in which length of the baby is measured from a scale. which Is set
(a) M.M.l-'l vaccine. - Ans. (See Page No. 107: 0.3) in the measuring table.
(b) Kangaroo mother care. - Ans. (See Page No. 48 : O. 12) Procedure : .
are to
Child is placed supine on a rigid measuring table/lnfantometer. (Hair pins. bulky diapers
(c) Skeletal changes in Flickets. - Ans. (See Page No. 28 : 0. 11) be
(d) Treatment of infected Scabies. — Ans. (See Page No. 294 : Q. 3)
removed).
Group — D J
0.4 : A 3 year old child presented in emergency room with history of fever and cough for 3 days and respiratory Head is held firmly in position against a fixed upright board.
distress for one day. Enumerate the common differential diagnosis for the case. How will you approach the l
case to arrive at a definite diagnosis? - Ans. (See Page No. 326 : O. 11) Legs are straightened. keeping feet at right angle to legs and toes pointing Upwards.
l
The free loot board is brought into firm contact with child's heel.
n.—
-IAH
- Standing Height — For child > 2 years

Scale : > Stadiometer
> Height measuring rod.
-
.'
> Measuring tape against a wall.

.——'.4
Procedure :
mum
Child should stand upright with heels are slightly separated and weight is borne evenly on both feel.
i
v—
Heels. buttocks. shoulder blades and back of the head are brought in contact with a vertical surface
(such as wall. measuring rod or Stadiometer).
l
Child looks directly forwards with Frank tort plane (The line joining floor of external auditory
meatus to lower margin of the orbit) and Biauricular planes being horizontal.
1' .
The head piece is kept firmly over the head to compress the hair.
i
Height is taken from measuring rod. stadiometer or by measuring tape.
Normal Height : At blrth —- 50 cm.
At 6 months - 65 cm.
1 year —75 cm.
2 year — 90 cm.
4 year — 100 cm.
Then 6 crn/year 12 year.
4
Scanned by CamScanner
GROWTH AND DEVELOPMENT Cl Chapter—i 3
QUEST : PAEDlATFllCS
There is marked acculeration of growth during puberty. > Somatic Growth (Body fat and muscle mass)- Body tissue is
-
divided into two components — fat and lean body mass. Somatic growth,
- Child's ultimate height is greatly influenced by parental height.
— Fat deposited in subcutaneous adipose tissue.
0 Children have physiological lumber lordosis upto 2-3 years of age therefore standing height
will underestimate the real length and results in an erroneous reading. - More in girls than boys.
0 Height is used to calculate some age independent markers of growth like — BMI (Body mass -— Lean body mass includes
index). Ponderal index. weight for Height etc. ' Muscle tissue
i i 4:
' Best way to record child's height is to plot on a suitable growth chart. ' Internal organs 2 3 12
' Skeleton Age in years
0.2: Laws of growfli- 1
- Correlates closely with stature.

that
Ans: Growth is defined as a net increase in the size or mass of tissue. which is an essential feature Somatic growth is accelerated during first fewyears of post natal life and at puberty and steady
distinguishes a child from an adult. during mid-childhood period.
This growth of human body occurs according to some laws. which are as follows —
0. 3: Head circumference (11).
1. Growth and development of children is a continuous and orderly process :
Ans : Head circumference. also known as occiputo-frontal circumference is the good parameter for
> There are specific period of child's life when growth accelerates. decelerates and steady. child's brain development.
> Growth is rapid during intrauterine fetal life especially in first few months. thereafter growthis Instrument :
mains
accelerated in postnatal life during first two years. after that growth slows down and
Non-stretchable measuring tape.
tains a steady velocity. Again at the time of puberty growth is accelerated.
Procedure :
2. Growth pattern of every individual is unique :
The measuring tape is passed over the supra-orbital ridges in front and that part of the occiput
‘2 Growth is never haphazard. order of growth is cephalocaudal and distal to proximal.
which gives the maximum diameter. Usually it is over the occipital protruberance but not always.
Therefore only maximum diameter is considered. Now head circumference is recorded nearest to
> During intrauterine life head growth occurs before that of neck
0.1 cm.
and arm growth before legs. in post natal life. growth of head 100%
slows down but limbs continue to grow rapidly. Normal growth :
3. Different tissues grow at different rates — Head circumference is reflected by growth and size of its content to. brain and ventricle. Since
brain growth is maximum during infra-uterine fetal life and first 2 years of post natal life especially
> Brain Growth — Fetal phase and first two post natal period are during infancy (1 year of post natal age). head circumference growth. velocity is maximum upto 2
crucial for brain development. years of age. slows down thereafter.
- Head reaches 90% of adult size by 2 years. l l _t_
I 1 l
' 12 Usual Head circumference at birth (term gestation) 33-35 cm.
2 8
Age in years First 3 months — Growth 2 cm/month
Next 3 months — Growth 1 cm/month
)v Gonadal growth - Next 6 months -— Growth 0.5 cm/month
s obvi-
Gonadal growth is dormant during childhood and become At 1 year of age Head circumference = 47 cm
ous during puberty. Gonadal growth
A12 years of age Head circumference = 49 cm
At 4 years of age Head circumference = 51 cm
- Head circumference reaches 90% of the adult size by 2 years.
é . é 1'2 - it‘s best practice to plot head circumference on growth charts.

Age in years - Head circumference more than 2 standard deviation (80) above the mean for given age. sex
and gestation IS called — Macrocephaly and below 3 standard deviation below the mean for
given age. sex and gestation is known as — Microcephaly.
> Lymphoid Growth —
ildhood
— Lymphoid growth is most prominent during mid-ch a. 4: Bone Age Estimation [CNMC] (8" Sam)
period (4-8 years).
Lymphoid Ans: Bone Age Estimation is an important part investigation for short stature and tells about skeletal
lpable lymph
- This is clinically seen as large tonsils andpa growth maturity which is according to chronological age Or not.
’ nodes as a frequent finding in children of this age. Assessment : Bone age estimation depends on
l 1 l__
'l I
> Number. size and shape of epiphyseal centres.
2 8 12
Age in years > Size. shape and density of the ends of bones.
\_
x
h‘
.\
NT 0 ChaCIEr -l 5
4 QUEST _ PAEDlATRlCS GROWTH AND DEVELOPME
t
wth chart BLGTGDMIE
Methods ot assessment: Childs hei htfwei hUhead circumference e measured and put _ on gro
t l5 been la lien to be noted
.x
b
which perc entile
to mea sure men
9 and9 sex. now in
for child‘s age the
Grecian pyle - Mas method.
‘I
Tanner \‘(hrtehouse - Rating method. Utility:
V' In pe dam: age group
There is great utility of these growth chart for monitoring of growth
.n
20 ossification centres are generally used tor determining the bone age. o
V
. . r
- Carpal bones
\
I Periodic plotting of child's growth parameter on a growth chart heir-t3 '9 639953“? 9'5”“ vex/31.1,
is the rate of growth over a fixed time interval.
(I
- Metammal bones
than monrtzcng the
- Patelta One time measurement of growth parameter h owever has no value rather
trend of this parameter over time. ‘
- Distal and proximal tees to both sexes ton of grow: .a..r.g
(I
Plotting growth velocity in growth charts is uselul tool lor early identifica
\f
- -. tal and middle phalanges in boys which may be the first manifestation of an infection’disease.
— Distal and proximal phalanges in girls. .
Following the growth curves also helps in assessing utility of sod al and remed ra' ‘measu' re. Fo:
rt
‘f
-
example. uptuming curve after successful treatment and nutritional rehabik'atron 5. PE. r: aten
t
Location:
> Hand and vmst - Ctfldren between 1 and 13 years. is reassuring. .
1|
> Ebm' and hip — Ctu‘idren between 12 and 14 years. > Velocity ol growth more accurately helps in predicting ultimate adult height.
' ghosts: Different Types of Growth Charts :
1|
> Bone Age = Cironoiogical age According References Standard -
Causes - Normal > WHO Growth Chart
n
l - Famihai short stature > CDC Growth Chart
> Bone Age < Chronological age. > IAP Growth Chart
Causes - Hypothyroidism. Growth hormone deficiency. According to growth parameters -
.II
l.'.ainutrition
- Weight for age
Vvvvvvv
main-1 t..,,.tt.s.l|..,._ ll-

- Constimtionai delay 0! growth and puberty. Height/length for age.
Weight for height
-...
> Bme Age > crronological age.

”-
Causes - Thrrotoxioosis BMl for age

o-
- Precocious puberty Skin told thickness [or age

' - Protonged Steroid therapy. Head circumference
Disadvantage : MAC for age
r) it is macho assessment and needs to be interpreted in clinical context. Growth charts are also available for different age group and also seperatefy tor boys e‘d gets.
ii) Often Osteoperia provides erroneous reading. O. 6: Utility of WHO Growth Charts (8M0) (8". Sam)
0. 5 : Growth Chart (Lit-(C) (8" Sam) Ans : Recording the growth measurement of a child over a period of time and plotting on a chart notices
process growth curve. Every growth chart contains growth standards which represent norms ct
Ans : Growth denotes unease in size or body mass. Growth in human beings is a continuous gmth.
{rem conception to until the epiphyses close. These standdards are obtained by either cross-sectional or longitudinal studies in large
peeriafion
The growth is measured by different parameter. WHO Growth Chart — WHO growth charts are internationally accepted.
‘dfl-Y‘Hmfl
> WHO growth
‘ charts were published
_ in 2006 based on the ‘Multicentre Growth Rate
- Weir}! [bone and muscle mass) 8'
(MGRS). MGRS was a community—based. muttioountry project conducted
- Length or height (statue) in Brar‘fimfl
India. Norway. Oman and the United States. The pooled sample lrom these
abate six cvtnes
— Head cirwmierm (brain growth). oonsistin of children ol both aftl - - .
standard? ”9'“ and baCkward polutatron makes it a truety lutefl‘atnml
Growth chart:
time and are plotted on a graph.
it the groom measuemerus are recorded in a child over a period of It also recapitulates the tact that child population
. . ro w snml
' - ~
those are case-d Growth curve or Growm charts. population when their health needs and basic care erg met. Iarly across the "OMS mater
from normal.
*- This is a satisfactory tool to diagnose deviation of growth infantWHO
The as the
standards
normative
make breast
growth leed'ing the biolo gica
model. ' I norm and thus establishes
distribution. breastfed
- it relers to the position at an irid‘rridual child on a given reference
. is conventionally taken 'as values The children included in MGRS study were nourish ed in su
- in grower curves normal ra nge of variation in observations ‘ .‘
3rd and 97th percent ile curves. that include 94% children, also represents children with constraints to growth such as intection. poor nutrition Ch enutonmoms "‘3‘ "WWW
between
mean 1 230 (standard deviation).
GROWTH AND DEVELOPMENT 0 Chapter-1 7
6 QUEST : PAEDIATRICS
3» WHO growth standards also include new growth parameters beyond the usual that height. DEVELOPMENT ASSESSMENT OH YEAR OLD CHILD :
weight and that are particularly useful for monitoring of children with childhood obesity. which is Developmental assessment should be a stepwise approach —
a growing epidemic worldwide such as skinlold thickness. . History :
uni
> Longititudinal nature of MGRS helps in development of growth velocity standards. enabling the - Detailed history to be taken.
early identification of under or over nutrition. — To determine risk factors affecting devel0pment.
0. 7: Utility of Growth Chart (13) - To differentiate between delay and regression.
- To make a gross impression about the development age of the child.
Ans : See 0. 5.
M
. Examination:
O. 8 : How to assess growth and development in a one year old child (Kalyani) (8" Sent) - Detailed physical examination for physicalgrowth.
Ans: Growth and development are the two essential features of life which make a child to adult both - Search [or any dysmorphism. stigmata of intrauterine infection. hypothyroidism.
physically and functionally. - Screening for vision and hearing.
Growth is net increased in the size or mass of tissues as a result of multiplication of cells and —- Detailed neurological examination and primitive reflexes (if required)
increase in intracellular substance.
— Detailed developmental assessment with appropriate tools (red ring. cube. spoon. cup. block,
Development specifies maturation of function. It is related to the maturation and myelination of the paper. pencil etc.)
nervous system.
Developmental assessment :
Assessment of growth and development is done by cenain parameters which are age specific that
is at a specific age a normal child will attain a certain growth (weight. height. head circumference Should be done with adequate time and patience. To ensure child's co-operation it is preferable
and some specific developmental milestones. to examine the baby with stepwise fashion with annoying maneuvers at the end of the examina-
tion as follows -
GROWTH ASSESSMENT OF 1 YEAR OLD CHILD : > Observation - Regarding baby's social responsiveness. alertness. concentration. interest.
Following growth parameters are to be measured - movement. '
1. Weight: > Vision and hearing assessment - To ensure intactness of response to sensory stimuli.
. Recorded from weighing scale (lever or electronic). > Vocal response - Nature. frequency. quality.
for
' Ideally the observed value to be plotted on age and sex appropriate growth chart (weight > Fine motor assessment - Interest. alertness and rapidity of response by appropriate develop-
age) and see the child's present status in reference to percentile curve (Normal range between mental tool.
3rd to 97th percentile). 3» Finally the annoying maneuvers to be done which may hinder child's co—operation.
. ll growth chart not available then expected weight to be calculated. - Assessment of reflexes.
weight.
- Then deficit or excess should be calculated by from expected weight and observed - Head circumference.
- Approximate weight at 1 year of age is birth weight it 3. — Ventral suspension. ' J
2. Length: — Pull to sit.
fable.
. Length should be taken by placing the baby on inlantometer or rigid measuring 3. Evaluation:
growth chart
- Ideally the observed value of length to be plotted on age and sex appropriate After completion of assessment conclusion is to be drawn whether the neurological and develop—
to percentile curve
(length for age) and child's present status is to be observed in reference . mental status is age appropriate or not by calculating develOpmental Quotient (00) as follows -
(Normal range between Std-97th percentile).
te length to be achieved at 1 year of age is 75 cm (At birth 50 cm + 25 cm in 1 year). Average age at attainment
0 Approxima x100
3. Head clrcumference : Observed age at attainment
passed on supra-orbital ridge in
- To be measured by a non-stretchable measuring tape to be A DO < 70% is taken as delay and warrants detailed evaluation.
rly.
front and maximum circumference of head posterio
A
. Interpretation:
observed value should be plotted on
- As other growth parameters (weight/length) ideally the For final interpretation following points are to kept in mind.
chart (Head circumfe rence for age).
age and sex appropriate growth
at 1 year is 46-47 cm (Average He at birth is 33-35 cm and i) in babies born preterm. corrected age rather than post natal age is used to determine develop-
0 Approxim ate head circumfe rence
mental status than post natal age till 2 years of age.
increases by 12 cm/1 year).
. . . ii) Wide variation of normality to be remembered.
4. Chest circumference :
measurin g tape at the level of nipples. Ideally at midway iii) Retardation should not be diagnosed on a slngle examination. Repeated examination is desir-
0 To be measured by non-stretchable
able.
between inspiration and expiration.
rence by 1 year of age (at birth chest iv) Finally the opportunities provided to a child to achieve that milestones should be kept in mind.
- Chest circumference becomes equal to head circumfe
is 3 cm less than head).
a GUEST : PAEDtATRlCS ta -l E"...
oeovrrH mo DEVELOPMENT C] O'iap
,4-
.
KEY MILESTONES TO BE ACHIEVED BY 1 YEAR CHILD: I“ t s
1. Gross motor: Age ' 95 one _.
' PM “95* W@- ' 4 month Bidextrous reach (Reaching Out r:rlob.'t‘=“3i “1“" both hands)- c
- 6 month Unidextrous reach (Reaching out of obpects with hand). -
' Sh“? “W SUDPON-
'- 5:3"a without swoon. Transfer objects. s...
' Waiting “”1 SW- ' 9 month Immature pincer grasp. .
2- fine Hater: . 12 month Mature pincer grasp. v...-
- Mature pincer grasp (with thumb and index linger). - 15 month tmitate scribbling. .
° Serf feeding fifth cup and spoon with spilling. Tower 012 blocks. ‘1
3- Social and Personal: . 18 month Scribbling
' Scanger anxienz Tower of 3 blocks. 2
- Waving bye bye. ' 2 year Tower ol 6 blocks.
' P‘.aymg
' smote
' ball game. V rt'cal and circular stroke. A
e ' s...
4. Language: - 3 year Tower ol 9 blocks-
- Bisyt‘nable words (mama. baba). Copies circle. ‘5
-
- 1-2 words with meaning. 3. Social and Personal development : lt denotes cognitive development.
J!
O. 9 : Developmental milestones of3 years old child. (N85) {8” sem) Age Milestones ~—
‘35 -' 093W is defned as maturation of brain functions and denoted by specific milestones to be ' 2 month 3063' 5mi'er a.
' 3 month Recognizes mother.
W by m age. "1
Developmental mflestones are divided into four segments. . 6 month Recognizes stranger. stranger anxiety.
1. Gross motor development : It is the attainment of Locomotion and complex motortasks in orderly
.i
. 9 month Waves bye bye.
L
-
seq . c 12 month ‘Plays simple ball game.
' 18 month Copies parents in task. :
A9'3 Milestones - 2 year Ask lor food, drink. toilet. 2‘
- 3 year Knows lull name and gender. ;
0 3 month Neck holding.
' 5 month Rolls over bed. 4. Language development: It is the receptive ability and expressive abilities.
' 6 month Sitting with own support. Age Milestones _.
' 8 month Sitting without support. ‘1
- 9 month Standing with support. ' 3 month Cooing. 4
0 4 month Laugh loud. 1
. 12 rrnntl'l Creeping.
Standing without support. 0 6 month Monosyllable words (he. da. pa. ma].
Walking with tall. - 9 month Bisyllable words (babe, dada). j
. 15 month Walking without support. ' 12 month 1-2 words with meaning.
. 13 month Running. ' 18 month 8-10 words vocabulary.
. 2 year Walking up 2 downstair (2 feet/step Jumping). ' 2 year 2‘3 words simple sentences, 1
Riding m_ ' 3 year Asks question and speaks lull name,
Going upstairs I" alternate feet. 0. 10 :Developmental milestones at 9 months of age. ]

0. 1 1 :Developmental milestones at one year of age. [12] [101(09. Supp Ie] (CNHC)
(8' sem)
O. 12 :Developmental milestones of 2 years old child. 13. so
2. Fine motor development: it denotes the development at line manipulation skills and co-ordination.
Sent) (2015) l PFi.1 i121 {09 SurplellCHC) (9m
Ans : For all above question's answer (Q. 10. 11. 12. 13 ) See 0. 9 and
Write answer unto the 899
mentioned in particular question.
NUTRITION AND MICRONUTFIIENTS U Chapter-2 11
diiterent target tissues include —

CHAPTER - 2
1. In the intestine:
NUTRITION AND MICRONUTRIENTS a) Marked increase in calcium absorption.
b) Increase in phosphate absorption.
2. In the kidney:
O. 1: Write down the pathway of vitamin D metabolism. Pathological changes a) Increase in calcium and phosphate reabsorption.
in bone in nutri-
tional rickets - Describe. (5 + 5) [mil-Supple] b) Inhibits own synthesis by inhibiting the action of ta-hydroxylase.
O. 2: Describe in short vitamin D metabolism. [12] [RGKMC c) Stimulates renal 24-hydroxylase activity which converts 25-0 to 24. 25—0 (inactive metabolite).
a" Sem]
Ans: VITAMIN D METABOLISM 3. In the bone : Increased mineralization. .'
Vitamin D is the generic . term for secosteroids. which have an important role in maintaining calcium . In the parathyroid : Suppresses PTH secretion directly and also by increasing serum calcium
and phosphorus homeostams. As it can be synthesized in epithelial cells 01 skin. it concentration (Calcium also suppresses PTH secretion).
is technically not a
vitamin. - FIDA : RDA or Recommended Daily Allowance oi vitamin D is 200 [U (5 pg) in inlants and 400 IU
Structure : Secosteroids have 3 intact rings and 1 open ring with conjugated (10 pg) in children.
double bonds.
Various vitamin D metabolites differ in the side chains attached to the 4th ring.
- Sources : (Ea 7-dehydrocholesterol Dietary Source .
l. Cutaneous Synthesis of vitamin D from the substrate 7-dehydrocholesterol. (Most important Sunlight (UV-B) /Absorption
source).
- ?
‘
2. Dietary Source : Constitutes 540% of the total vit. D. There are 2 parahorrnones. namely Vitamin D
vitamin D1 or Ergocalciterol (derived lrom plant source) and vitamin D1 or Cholecalcilerol
(derived from animal source. like - fish liver oil. tally fishes. egg yolk etc.) 25-hydroxylase
Cutaneous Synthesis : 7-dehydrocholesterol is converted to vitamin D3 (3-cholecalcilerol) by I
ultraviolet 8 radiation (UVB) from the sun (wavelength 290-315 nm). The dermal concentration of [ 25-hvdr0rvvitamin D ‘] 2MWm>qfl‘_m_sl&t.25-dihydrmvyviiamin o]
melanin regulates the amount of UVB rays that reach the epidermal layers containing the highest
concentration oi the substrate 7-dehydrocholesterol. So. skin pigmentation is the principal regula- G)
PTH. 1 Po. —-—— ~>
Po..FGF-23—Q———> 1a—hY dro Wlase KIDNEY
tor for cutaneous synthesis of vitamin 0,.
Other important factor for cutaneous synthesis is the amount of Sun exposure. which depends on—
a) Skin pigmentation
‘
b) Timing of the day

(1. 25-dihydroxy vitamin D
c) Clothing and
d) Season Vitamin D response elements
Absorption from dietary source : Vitamin D is absorbed in the duodenum by an active transport
system. In the enterocyte. vitamin D is incorporated into chylomicrons and transported to the liver.
where further metabolism starts.
‘
. Metabolism :
Bone Kidney
a) In the liver: The Iirst step of hydroxylation occurs at the liver tor all the tonne of vitamin D (i.e..
ergocalciterol. cholecalciferol and 3-cholecalciferol). The enzyme.e 25-hydroxylase converts T Mineralization - T Ca. P0. reabsorption T Ca. P04| absorption l PTH secretion
vitamin D into 25-hydroxyvitamin D (25-0) or calcidiol. This step is substrate-dependent and
without any negative feedback control. So. measurement ol 25-0 is the standard method for Vitamin D Metabolism
determining patient's vitamin D status.
muti- antiques-«Mmg-‘e -
b In the kidney : final step oI activation occurs in the kidney. where to-hydroxylase converts 25- PATHOLOGICAL CHANGES IN BONE IN NUTRITIONAL RICKEI'S
v
hydroxyvitamin 0 into 1. 25-dihydroxyvitamin D (1. 25-0) or calcitriol. the active form of vitamin Nutritional rickets is caused by the deficiency of vitamin D. either due to dietary
deficiency or due to
D. The lu-hydroxylase enzyme is upregulated by PTH (Parathormone) and hypophosphatemia. ' sunlight exposure. As one of the p rincipal action oi vitamin ‘D
decreased is mineraiizalion of bones by
whereas it is inhibited by phosphate. 1. 25-0 (negative feedback) and phosphaturic hormone increasrng calcium and phosphate levels in the body. deficiency of vitamin D in growing
chfldren results
FGF-23 (Fibroblast Growth Factor-23). in classical rachitic changes in the bone.
Action : 1.25-D or calcitriol (active Iorrn) acts by binding to an intracellular receptor. and this
complex affects gene expression by interacting with vitamin D - response elements. Final action in
10
CamScanncr
Chapter-2 13
*—
NUTRITION AND MICRONUTRIENTS D
(X
Sltes : Rachitic changes in bone
are characteristically seen in the rapidl
y growing bones lit
1. Metaphysrs of long bones (most promi
nent in wrists and ankles) clinical and radiological features are almost same in all the categories of vitamin D deficiency rickets. llke
I e- nutritional deficiency. vitamin 0 dependent rickets etc.
n
2. Costochondral junctions.
.
Pathological changes : D Clinical Features:
A General :
(h
1. Failure to thrive
. Listlessness
[I
. Muscle weakness (especially proximal)
0'1t
—...'..___
. Protruding abdomen
--..
2. In rickets. the cartilage cells go on mulli plying

giving rise to a broad, irregular cartila . Fractures (due to osteopenia).
zone and thickening of the growth plate. genous
8. Head :
3. Incomplete degeneration of cartilage and
calcification leads to softness of the bones 1. Cranlotabes : Softening of the cranial bones. giving rise to “Pingpong ball" — like feeling.
4. Weight
_ . bearing and stress by muscle pulls on unclac while applying pressure over the occiput or parietal bones.
' '
rlied metaphysrs
‘ ives rise to S I '
(Widening) and Cupping (concave edge of the
metaphysis) of the metagphysis of Ion pbzylng 2. Delayed closure of Ionianels.
and costochondral junction (Rachitic Rosary).
9 nos. 3. Delayed dentition.
5. Loss of normal calcification at the ends of th ' result - . - '
. e meta h 815 S m '"d'sur‘c‘ metaphyseat 4. Frontal bossing.
margin. known as Fraying. p y
C. Chest :
6. There
, _ is also defective
_ mineralization of the sub penosteal
' ' -"1 en
bone. resultrn ' ed 1. Rachltlc rosary: Widening of the costochondral junctions. which feels like the beads of the
tton In bone densrty (osteopenia). g g eralised r ”C
-
rosary.
7. In long-standing cases. bones under stress may become deformed or even have
pathological 2. Harrison groove : Horizontal depression along the lower. anterior chest due to pulling of the
fractures. The common deformities seen are —
softened ribs by the diaphragm during inspiration.
a) Bowing of the legs 3. Repeated respiratory infections.
:' due to weight bearing
b) Windswept deformity D. Extremlties :
c) Harrison groove (due to pulling of the softened ribs by diaphragm during inspiration). 1. Enlargement of the wrists and ankles.
2. Anterior bowing of the tibia and femur.
3. Varus or valgus deformities (like coxa vara).
Osteopenia 4. Windswept deformity : Combination of valgus deformity of 1 leg with varus detopmily of the
other.
.o-
E. Back : Kyphoscoliosis.
Rachitic changes at the
F. Hypocalcemic Symptoms : Occasionally seen. e.g..
end of the long bones.
Cupping 8. Splaying [ 1. Seizures
(a Fraying '2. Tetany (carpOpedal Spasm. laryngeal spasm etc.).
D Radiological Features :
Epiphysis
As rickets is a disease of the bones, radiological features are pathognomonic and diagnostic of
rickets.
O. 3 : Describe the metabolism of vitamin D. Write the clinical and radiological features of vitamin 0
A Long bones: '
dependent rickets. (6 + 2 + 2) MPG-2016}
Characteristic rachitic changes are seen at the metaphysis of the long bones. particularly at the
a. 4 : Write briefly on the pathway of vitamin D metabolism. Radiological changes in bone in nutri- weight-bearing ends (9.9. wrist. knee. ankle). Anteroposten'or view of the wrist joints is the most
tional rickets. [10135-2016] commonly ordered X-ray for diagnosis of rickets. Changes seen are —
0. 5 : Discuss the process of vitamin 0 absorption and metabolism. Mention the clinical and radio- 1. Loss of normal zone of provisional calcification adjacent to metaphysis is usually the earliest
logical features ol vitamin D deficiency rickets. (5 + 5) [2016, 2018] change.
2. Increased distance between diaphysis and epiphysis due to hypertrOphy of the growth plate
Ans : VITAMIN D METABOLISM cartilage.
See 0.1/02. 3. Fraylng : Edge of the melaphysis loses its sharp border. which is known as fraying.
CLINICAL AND HADIOLOGICAL FEATURES OF RICKEI'S . Splaylng : Widening of the distal end of metaphysis.
b
matrix at the growth

Rickets is a disease of the growing bones due to the presence of unmineralized 5. Cupping : Edge of the melaphysis changes from a flat or convex su dam to a more concave
many causes. But.
plates in children. Rickets is principally due to deficiency of vitamin D, which may have 'surface. known as cupping.
14 QUEST : PAEDIATRICS NUTRITION AND MICRONUTRIENTS D Chapter— 2 15
6. Coarse trabeculation of the diaphysis. Watery rickets]

7. Generalised rarelaction of the bones.
8. Bowing : Anterior bowing oi the long bones (e.g. tibia. femur, radius, ulna etc.) are seen.
9. Occasionally. there may be pathological fractures. [Serum Phosphorusl
B. Chest X-ray : Widening oi the costochondral junctions.
C. Skull:
1. Pronounced demineralization of skull bones.
2. lndistincl sutural margins.
i
Low/Normal
‘ i
High
3. Delayed tooth eruption.
D. Spine : May show kyphoscoliosis.
Blood PH
l
Chronic Kidney Disease
L Same picture “Rachitic changes at the end ofthe long bones” as at the end of the 0.1/0.2. I (CKD) orChronic Renal Fail-
; l ure‘ (CRF)
0. 6 : Outline the investigations and management of a case of Rickets. (6 + 6) [RGKMC - 8" Sem}
Ans: RICKETS :INVESTIGATIONS AND MANAGEMENT Low (Acidosis) Normal
Rickets is primarily a disease of the growing bones in children due to deficiency of vitamin D (e.g.
Nutritional. secondary to malabsorption. increased degradation by drugs etc.). But. there are other causes
l l
of rickets also. including vitamin D dependent rickets, familial hypophosphatemic rickets, renal tubular Renal Tubular [Serum PTH. CalcilJ
acidosis. chronic renal failure etc. Acidosis (RTA) ]
CI Investigations : Investigating a case of rickets includes the following facets -—
1. Confirmation of the diagnosis of rickets by — t PTH. l [(N) Calcium. Normal PTH. Normal Calcium
a) Radiological survey and
b) Laboratory values (for vitamin D deficiency)
Vitamin D dependent rickets Hypophosphatemic Rickels
2. Differentiating other causes of rickets from vitamin D deficiency (9.9.. calcium deficiency.
phosphorus deficiency).
3. Diagnosis of resistant rickets after initial management fails. D Treatment :
A Radiological Survey : See 0. 3 (Radiological Features). 1. Vitamin D: After confirmation of the diagnosis of rickets by radiological evidences. vitamin D is
B. Laboratory valueslBiochemical Survey : As vitamin D deficiency is the most common cause. administered to the child. There are 2 strategies available —
laboratory values of vitamin D deficiency is discussed first. a) Stoss therapy : Single dose of 6.00.000 IU either orally in 2-4 divided dQSes or as a single
intramuscular injection under observation. As the doses are observed. it is ideal in situa-
1. Vitamin D deficiency rickets :
tions. where adherence to therapy is questionable.
a) Serum Calcium : Low or normal values may be seen. Vitamin D deficiency usually causes b) 60.000 lUiday orally for 10 consecutive days. (Total dose = 6.00.00 lU).
low calcium level (hypocalcemia) but concomitant increase in serum PTH raises calcium
level close to normal. > After the initial dose. daily vitamin D supplementation (400 IU/day for infants. and 600-
800 lUiday for children > 1 year) should be continued.
b) Serum Phosphorus : Should be always low. because of 2 factors —
2. Calcium :
i) l ed intestinal absorption (vitamin D deficiency).
a) For children who present with symptomatic hypocalcemia. intravenous calcium is needed
ii) T PTH-induced renal loss. initially as bolus and maintenance. ‘
c) Alkaline phosphatase: Raised b) Oral calcium supplementation should be given to all patients of rickets @ 30-75mg/kglday
d) PTH : Raised along with vitamin D.
e) 25-D : Low (<10 ng/ml is intficative of deficiency) 3. Phosphorus : Oral phosphorus is to be supplemented along with calcium for vitamin D deli-
i) 1. 25-D : Even with low levels 01.25-0. there is presence of enough 25-D to maintain normal g ciency rickets.
level of 1. 25—0 in the presence of an upregulated 1a-hydroxylase. 1. 25—D levels are low t 4. Monitoring response to therapy :' Following adequate therapy. X-ray of wrist ioints are re-
only in the presence of severe vitamin D deficiency. , peated after 4 weeks to look for healing of bony changes {i.e. area of calcification at the
2. Differentiation from other causes : An increased plasma level of 1. 25-D indicates deficient , metaphyseal end. that is denser than diaphysis).
intake of calcium or phosphorus as a cause of rickets. . Second dose: If there is no sign of healing radiologically alterd wks. a second dose of vitamin
3. Diagnosis of resistant rickets : if radiological healing can not be demonstrated. despite 1-2 D (6 Lac lU) may be given.
large doses of vitamin 0, patients should be evaluated for refractory rickets/resistant rickets. 6. Resistant rickets : If no healing is observed even after 2nd dose of vitamin D. patient
should be
' -<-.
-. K.
‘N-
\u
16 QUEST : PAEDIATRICS TS CI Chaplet—2 17
1‘
NUTRITION AND MICRONUTHIEN
__
‘\
evaluated for refracto
like_ W or rest 5 t 3'“ "CKGlS
' -
(as shown above). Patient - then
IS .
managed accordingly . 4. Other: ‘ I the m
a) Growth hormone increases serum Ca" due to increased absorDllon 70f“ 9 -
n
a) CKD :
b) Cortisol can lower serum Ca".
i) Phosphate restrictioniPhosphate binder
s
ii) Calcium and vitamin D supplementation Intake (dietary) . _
{I
b) RTA : Bicarbonate and phosphate supplem Calcitriol PTH. Calcnnol
c) Vitamin D dependent rickets :

entation.
i]. p is
1"
- . one
i) Calcitriol or1. 25-0 Gm Absonion Reabsorption from—El
ii) Calcium i Phosphate from gut bone *
V
[I
‘l'
d) Hypophosphatemic Rickets :
Plasma
Calcium I Deposition in bone
i] Phosphate Supplements (Joulie solution) Secretion into gut
is;
II
ii) Calcitriol. t
. Calcitonin
Filtration Reabsorption
O. 7: Outline briefly the metabolic interaction
of vitamin D, calcium and parathorrnone. Write V
treatments of nutritional rickets. (6 + 4) [lPGMER - the
8" Sem] Kidney f LL PTH. Calcitriol
Ans : METABOLIC INTERACTON 0F VIT. D, CALCIU
M AND PTH — — --Calcitonin
Vitamin D (Calcitriol). PTH (Parathorrnone) and Calciton
in —) these 3 hormones are responsible for
maintaining calcium homeostasis in the body. by regulatin
g calcium and phOSphate metabolisml Stool (excretion) Urine (excretion)
Cl Calcium Metabolism : Normally. calcium balance is
always maintained by excreting the same
amount (through urine and stool). that is absorbed from the Cl Metabolic interaction of PTH and Calcitriol : '
gut. But. in growing children. there is
positive calcium balance due to continuous deposition of calcium
needed for bone growth. Factors f. PTH : Increases the formation of calcitriol in the kidneys by upregulating the enzyme lei-hy-
which influence the calcium balance are as follows —
droxylase.
f. Calcitriol : Calcitriol or 1. 25-dihydroxy cholecalciferol (1. 25-0) is 1 o-hydroxylase . _
synthesized in the liver (25-
hydroxylation) and the kidney (to hydroxylation) from the cholecalciferol 25-hydroxy cholecalciferol > 1. 25-dthydroxy cholecalCiferol
(vitamin 03). Vitamin
D: is the inactive form. which is either produced in the skin from 7-dehydrocholesterol or - T9 or Calcitriol
by UV-B
radiation or received from the diet. Calcidiol PTH [Active form oi vit. D]
- Calcitriol helps in calcium metabolism in the following ways —
a) In the intestine : It helps in calcium absorption by synthesis of intracellular Ca" binding 2. Calcitriol : Suppresses PTH secretion from parathyroid glands directly and also by increasing
proteins in the enterocytes. It also helps in pumping out Ca" on the basclateral aspects serum calcium (calcium also i es PTH secretion). “'
of the enterocytes.
b) In the kidney : It helps in reabsorption of Ca" from the distal nephron. I Calcitriol I— ... __ __ __ e I Parathyroid Gland]
c) In the bones : The net effect is mobilisation of calcium from the bones by increasing the
number and activity of the osteoclasts. It also helps in pumping out of Ca“ from the
osteoblasts. __._ —9-——-+
EB
2. PTH : PTH or parathormone is secreted from the chief cells of the parathyroid glands. The main
action of PTH is to increase the plasma calcium level. PTH acts via its membrane receptors and PTH Secretion
producing CAMP as second messenger. Action on Ca" meabolism are as follows —-
a) In the kidney : PTH increases calcium reabsorption in DCT (distal convoluted tubule) of the D Phosphate Metabolism : Plasma phosphate level is intimately related
to plasma caiciumlevel. as
kidneys. the product of calcium and phosphate concentration is consf ant. i.e..
b) In the bones : It increases calcium permeability of the osteoclasts. osteoblasts and osteo- [Ca“]x[P03‘] = Constant
cytes. In low concentration. PTH stimulates osteoblac activity. whereas it increases the
osteodastic activity as a longterm effect. The overall effect is mobilisation of calcium from the - Serum phosphate level is regulated mainly by PTH and calcitriol. as follows
_
bone. 1. Calcitriol : Increases PO‘ level b V helping in intestinal abso t'
3. Calcitonin : It is secreted by the perifollicular cells of the thyroid gland. Function of calcitonin is sorption of P0. "P '0" and renal tubular reab-
to decrease serum Ca" level. which is done by - 2. PTH : Decreases P0. level by reducing tubular
reabsorption of PO in the kidneys.
(
a) Decreased reabsorption of Ca“ in the kidney and 0 Treatment at nutritional rickets : See 0. 6. (Treatment).
b) Inhibition ot osteoclastic activity and deposition ol calcium in the bone.
CamScanncr
'.L:‘—Hw
1B QUEST : PAEDIATFIICS NUTRITION AND MICRONUTRIENTS U Chapter-2 19
O. 8 : What is balanced diet? What are the constituents of balanced diet. Describe dietary source, 1. Fish liver oils. Liver.
absorption and function of vit. A. (1 + 3 + 6) [2008 - Supple]
2. Dairy products.
‘
Ans: BALANCED DIET

3. Egg yolk etc.
Balanced diet is defined as nutritionally adequate and apprOpriate intake of food items that provide all 0 Absorption : Vitamin A and provitamin A are lat soluble. and their absorption depends on the
the nutrients in required amount and proper proportions.
presence of adequate lipid and protein within the meal-
In addition. it should be culturally and financially Ieasible to access and maintain the diet.
CONSTITUENTS 0F BALLANCED DIET:
From nutritional prespective. there are 6 main constituents of a balanced diet. which are as follows —
A) Macronutrients : Provitamin-A ' Retinol (vit. A)
1. Carbohydrate : Balanced diet contains 55-60% of calories from carbohydrates. They are the (carotenoids) Active transport with Retinal
main energy source for the body’s activities and are obtained from cereals. grains. vegetables. r Binding Protein ll.
Jr
Dioxygenase
imits. sugar etc. Vitamin A in the
(in small intestine)
2. Protein : Proteins constitute 10-15% of calories in a balanced diet. They give structure to the enterocyte
cells and are important for cell growth. repair and maintenance. Sources include meat. egg.
Vitamin-A
fish. pulses etc.
3. Fat : Fats contitute 25-30% of calories in balanced diet. Their main roles are providing the body Fietinyl palmitate
with thermal insulation. production oi hormones and absorption of vitamins in addition to being
a rich source of energy. They are available in oils and tats used for cooking (e.g. butter. ghee Fteleasedinto 4—.— tnoorporated into
etc.) lymphatics chylomicions
8) Micronutrients :
4. Vitamins : These are naturally occuring substances essential for health. like -
i
[Transported to liver]
a) Fat soluble vitamins - vitamin A, D. E and K.
b) Water soluble vitamins - vitamin B complex and C. Ci Functions : Vitamin A is required throughout the life cycle. beginning with embryogenesis. The
5. Minerals : Important minerals are - main functions are —
a) Iron 1. Maintenance of vision (especially night vision) : This is the best understood titration of W. A
b) Calcium and is mediated by the aldehyde ionn (Retinal) oi vitamin A. A! other functions are mediated
by Retinoic Acid.
c) Iodine
u...
Within the eye. tt-cis-retinal is bound to Rhodopsin [Rod cells) and lodopsin (Cone cells).
d) Copper etc.
.
was.-.“
C) Additional Constituent:
last constituent of a balanced In the dark. low-intensity light induces photo-isomerization oi 11 -cis-retinal to all-trans reti-
6. Water : Water is not truely a nutrient. but it is esseatial for life. So, I
_ ..C‘d: _--—O
by-products oi nal in the rhodopsin prosthetic group.

! diet is adequate intake of water to maintain hydration and excrete the harmful
metabolism through urine and stool.
itamin A:
the vitamin. Biologically active
l
This isomerizalion generates an
i
All-trans—retinal dissociates treat the
¥he term viamin A refers to all-trans-retinol. the alcohol form at
A are the oxidatio n produc ts of retinol. such as — electncai signal. opsin in a series oi steps (Bleaching).
'1‘ forms of vitamin
a) all-trans-retinal (the aldehyde form) and
”
b) all-trans-retinoic acid (acid derivative).
I Recycled and converted to 1 t-cis-reti-
Singal is transmitted to the brain
ient. as it cannot be generated de-novo by the
0 Dietary sources : Vii A is an essential micronutr via the optic nerve. nal ior repeat at the cycle.
It must be 0 btained from dietary _ in the form of provitamin A or carotenoids (a.
sources
human body.
fl-cryp toxan thines ), found in plants —
fl and r-carotenes and
Visual Sensation (Night vision or
1. Carrots. Toma toes low-fight vision).
2. Dark gr’een-leaty vegetables (e.g. spinach)
. . 2. Ilalntenance of epithelial tissues : This function of vitamin A is most pronounced in the intes-
3. Oranges. squash etc. tinal mucosa and the respiratory mucosa. Vitamin A maintains the normal mucus-secreting
sources of diet. like -
- Preformed vii. A or retinol can be found in animal epithelium. which acts as an eiiective barrier against the pathogens and toxins.
‘-
“u.
\a \_
x.
\
a\
20 QUEST : PAEDIATRICS D Chapter-2 21
NUTRITION AND MICROHUTFIIENTS
‘\
3. Genetic function
_ : Retinoic
_ acid help in the differentiation of v anous
' ' .
tissues. '
articul rt ' Management of SAM:
reproduction and fetal life by regulating gene expression.
p a y during I5 to decide, whetherthe child would
El Admission criteria : In any child diagnosed with SAM. first step
n
outpatient care.
be managed under inpatient care (Admission) or
All-trans-retinoic acid
l ‘
Retinoid receptor RAR is activated
1. Failed appetite test .
(I
tions. like - shock. sepsrs. convulsr on. sev 8TB
2. Presence of acute medical complica
RAR combines wtih RXR (another retinoid receptor)
anemia etc.
{I
3. Presence of bilateral pitting edema of nutritional origin.
Resultant heterodimer binds to specific nuclear transcription factor 4. Age S 6 months.
[I
Regulation of gene expression/Differentiation. i—J—i
1]
Yes ”0
O. 9 : A grossly emaciated child aged 3 years from low Socioeconomic status presented with weak-
ness, paflor, mouth ulcer, inability to take food. According to anthropometry, weight-6.5kg,
1'!
height/length-i'a cm. tic-44 cm, MUAC- < ff cm. What is your diagnosis? How can you estab- [Inpatient care] [Outpatieal fl]
lish your diagnosis? How will you manage the case and what are the complications?
[CNMC - 2016]
fillllllnfl
1. Failed appetite test at any visit
Ans : DIAGNOSIS 2. Medical complications
My diagnosis is Severe Acute Malnutrition (SAM) in a 3 years old child with complications like anemia, 3. Failure to gain weight by 3 wks.
oral ulcer and probaby infection.
) This child should be admitted, as there are medical complications along with inability to take
Establishing diagnosis : iood (Synonymous with tailed Appetite Test).
Cl Definition of SAM : According to IAP. SAM is defined as - 0 Inpatient Management:
i) Weight for height or weight for length < — 3 z score. using WHO growth charts. OR 1. Treat I Prevent hypoglycemia : (BG < 54 mg/di).
ii) Presence of visible severe wasting. 0R a) 10% Dextrose 0 Smllkg iv. in case of symptomatic hypoglycemia.
iii) Presence of bipedal edema of nutritional origin. OR b) 50ml of 10% glucose/sucrose solution orally or by nasogastric tube in case of asymptomatic
iv) MUAC (Mid Upper Arm Circumference) < 115 mm. hypoglycemia.
s Presence of any of the 4 criteria is diagnostic of SAM in children between 6 and 59 months. c) Frequent feeding (2 hourly) for prevention.
Ciriteria No. (iv) is not applicable in infants below 6 months. d) Antibiotics.
CI Positive features in this case : 2. Treat I Prevent hypothermia : (Axillary temp < 35° C or < 95° F)
ll)
a) Age = 3 years (fulfills age criteria). a) Warm clothing with covering of head
b) Low socio-economic status b) Rewarming with warmer, if needed
c) Gross emaciation [diagnostic criteria of SAM — (ii)] c) Initiate feeding and antibiotics.
pallor. month ulcer. 3. Treat I Prevent dehydration :
d) Clinical features of malnutrition along with complications. like — weakness,
inability to take food.
{l
a) [31:81“ low-osmolar ORS with K‘ supplements (ReSoMal) for rehydration (orally or by HG
f e .
..
:
e) Anthropometry :
..
. . .
....___..
b) [V Fluid only in shock.

i) Weight = 6.5 kg (expected wt. = 2 x 3 + 8 =14 kg)
n
expected . which falls in grade IV malnutrit ion accordin g to IAP 4. Correct Electrolyte Inbalance :
i.e.. weight is below 50% of
...._
classification. ' 3) Potassium supplements
fl
ii) Height : 70 cm (expected ht. = 6 x 3 + 77 = 95 cm). b) Salt restriction
of severe stunting (< 80%).
i.e.. heightilenght is below 75% of expect ed. which is suggestive 0) Magnesium (N on Day 1. thereafter orally). ‘_
0
iii) MUAC < 11 cm [Diagnostic criteria of SAM - (M) 5. Treatrevent Infection : (Hypoglycemia. Hypothemia and Infection act as a triad).
iv) HC = 44 cm (expected H0 at 3 years is about 49-50 cm) a) Treat infections with broad spectrum antibiotics like Ampicillin + GeatamicinlAmmacim
0
129.. there is presence of microcephaly. \
.
-.
C
NUTRITION AND MICRONUTRIENTS D Chapter-2 23
b) Maintain hand hygeine SHORT NOTES :

c) Measles vaccination. il unimmunised.
a. 10 : Clinical Features of of Rickets. [MMC - 8" Sam] [NBS - 8° Sent]
Correction mlcronutrient deficiencies :
-
a) Oral vitamin A on day 1 (Age > 1 yr —> 2 lakh IU. age 6-12 months -+ 1 lakh IU. age < 6 months 0. l l : Skeletal changes of Rickets. [2015]
—+ 50. 000 |U). .
0. I2 : Radiological features of active and healing Flicke ts. {2013 - Supple)
b) Supplement Iron. Folic acid. zinc. Copper.
Initiate feeding: O. 13 : Clinical and radiological features at Rickets. {Kalyani - 2016']
a) Initiation of feeding. as early as possible. Ans: CLINICAL FEATURES OF OF RICKETS

} See 03 -O. 5-
b) Give feeding orally or by NG tube every 2 hourly. RADIOLOGICAL FEATURES OF RICKETS ( AC’TWE RIC KETS )
c) Start with F-75 diet. (i.e.. 75 Kcall100 ml) with protein intake of 1-1.5 gmlkglday. RADIOLOGICAL FEATURES OF HEAUNG RICKEI‘S
. Catch-up growth : Alte adequate therapy with vitamin D is given. repeat X-ray is done after 4 wks to look for changes of
a) Once appetite relums. increase the volume of each feed with decreasing the frequency to 6 healing. The changes are as follows -
teedslday. I. Earliest change is seen as an area at calcification (white line) at the metaphyseal end of the
b) Change from F-75 to F-IOO diet (i.e. 100 KcllIOO ml). long bones. that is denser than diaphysis ol the same Done. It denotes de-novo caiciurn deposition
c) Increase proteins to 4-6 gmlkglday. due to the effect cl vitamin D.
Sensory Stimulation : 2. Fraying is gradually decreased.
a) Stimulating. cheerful environment 3. But. the cupping becomes more promineat initially. which gradually wanes off over Imger time.
b) Tender. loving care. 0. 14 : Biochmical changess oi Rickets.[2i112]
10. Prepare tor follow-up : Criteria for tfischarge includes —
Ans: See 0. 6. {Investigations : Laboratory valueslBiochemical Survey).
a) Absence of infection.
b) Child is having 120-130 kcllkglday (at least) with good appetite. 0. 15 : Vitamin D, deficiency in children. [BMC - 8" Sent]
c) Consistent weight gain @ 5 gm/kglday tor 3 consenctive days on exclusive oral leecfing. 0. 16 : Vitamin D deficiency Rickets. [KPC - 9" Sent]
d) Absence of edema. Ans: VITAMIN D DEFICIENCY (RICKETS)
e) Child completed immunisation appropriate for age. Vitamin D deficiency in growing children causes rickets. a disease of the growing bones.
I) Caretakers are trained. motivated and confident.
0 Causes : There are various causes that cause vit- D deficiency in chfldren and ultimately rickets -
Complications : t. Nutritional vit. D deficiency.
1. Infections: 2. Congenital vit. D deficiency (due to maternal vit- D deficiency). :
a) Septicemia 3. Secondary vit. D deficiency (e.g. Malabsorption. CKD).
b) Pneumonia 4. W. D dependent rickets (VDDFI) — Type 1 and 2.
c) Diarrhoea
Q Pathogenesis : Vit. deficiency
d) Pyoderrna
e) Scabies
Low calcium and phosphate
I) TB.
Dehydration. shock (inclurfing septic shock).
NPPPPN
Dyselectrolytemia Unmineralized matrix at the growth plate.

Hypothermia. Hypoglycemia
Anemia
l
Rickets.
Bleeding (DIC)
El CfinicalFeatures:See 0.3-0.5.
Sudden Infant Death Syndrome (SIDS).
El Investigations:
D Treatment: ] See 0'6'
IENTS CI Chapter— 2 25
24 QUEST : PAEDIATRICS NUTRITION AND MICHONUTR
O. 17 : Role of vitamin D in children. [BMC - 2016]

O. 19 : Radiological changes of rickets and scurvy. {2010 - Supple}
Ans : ROLE OF VITAMIN D
Ans : - Radiological changes of rickets See 0. 3. - 0. 5.
-
1. Role in calcium and phosphate metabolism : See 0. 7.
0 Radiological changes of scurvy - see O. 18.
2. Bole in genetics : Vit 0 receptor (VDR) acts as a heterodimer with Retinoid
Receptor (RXR) and
[CNMC - 8" Sem}
interacts with specufic DNA sequences—known as the vit. 0 Response Elements
(VDFIE). and cause O. 20 : Clinical manifestations of Vif. A deficiency.
actrvation or repression of the gene transcriptions. This way. role of vit. D has been suggested
in -
a) Preventing cancers. 0. 21 : Xerophthalmi'a. [KPC - 8" Sem]
b) Modulating immunity. Ans : CLINICAL MANIFESTATIONS 0F VIT. A DEFICIENCY
. epithelial integrity and various
c) Affecting endocrine system (Renin Angiotensin Aldosterone Axis. Insulin release) Vitamin A or Retinal is an essential micronutn'eatg needed I or vision,
etc. specific signs of vitamin A deficie ncy are the eye Iesuons.
other functions. But. most characteristic and
0. 18 : Radiological changes in scurvy. [CNMC - 2016] known as Xerophthalmia or dry eye.
y develop insidiously and rarely occur
Ans : RADIOLOGICAL CHANGES IN SCURVY 1. Xerophthalmia : Eye lesions due to vitamin A deficienc
2 yrs of age. Various signs are as follows — .
Dificiency of vitamin C leads to the clinical features of Scurvy. the earliest recongnized nutritional before
s to complete night bfind-
deficrency disease. One of the many actions of vit. C is the synthesis of collagen. which forms the basic a) Delayed adaptation to the dark is the earliest symptom. It progresse
In the Visual pigment
supporting structure of multiple connective tissues. including bones. In patients with scurvy. osteoid ness in more advanced stages of deficiency. due to the absence of retinal
deposrtion by the osteoblasts remain defective. which leads to the typical radiological changes. such Rhodopsin of the retina.
as - b) Photophobia is also a common symptom.
altered.
1. Radiological changes are particularly common at the distal ends of the long bones. like knees. c) As vitamin A deficiency progresses. the epithelial tissues of the eye become severely
ankles etc. giving rise to the classical signs of xerophthalmia or dry eye.
2. Shafts of the long bones (Diaphysis) have a characteristic ground-glass appearance due to d) Conjunctiva is the first one to be involved in the form of keratinization. xerosis and plaque
trabecular atrophy. development (Bitot's Spot) in triangular fashion. lateral to the cornea.
3. Cortex is thin and dense. giving rise to the appearance of pencil outlining of diaphysis (Pencil-thin e) Comea also keratinizes. becomes opeque and fonns dry. scaly layers of cells (corneal xerosis).
cortex).
I) In later stages. infection occurs. lymphocytes infiltrate and irreversible damage occurs in the
4- White line of Frenkel : This is the most typical radiological finding. found at metaphysis. It represents form of ulceration and degeneration (keratomalacia).
calcified cartilage at the zone of calcification and appears as irregular but thickened white line.
g) Ultimately. there is corneal scarring. leading to obstruction of vision.
5- Trumerfeld zone : It is the more specific but late radiological feature of scurvy. This zone of
h) Finally. pigment epithelium of retina also degenerates. resulting in blindness.
rarefaction under the white line of Frenkel appears as a linear break in the bone. that is proximal
and parallel to the white fine. L'J WHO classification of xerophthalmta :
6. Pelkan spur : It is the lateral prolongation of the white line with underlying triangular area of A Primary signs:
rarefaction. ‘
1. X1A : Conjunctival xerosis
7. Epiphysis : Epiphyseal centres of ossicication also have a ground-glass appearance and are
2. XIB : Bitot's spots
surrounded by sclerotic rings. This is known as Wimberger's Sign.
3. X2 : Corneal xerosis
8. Occassionally. there may be Subperiosteal hemorrhage which is often missed in plain radio
graphy. MRI can demonstrate acute, as well as healing subperiosteai hemorrhages. 4. X3A : Corneal ulceration (4: )4 rd of cornea)
5. X38 : Corneal ulceration (> )3 rd of oomea).
B. Secondary signs:
Pencil thin cortex 1. XN : Night Blindness
2. )(FzFundal changes
3. XS:Comeal scarring.
2. Skin changes : Epithelial changes in the skin are manifested as d
commonly seen in the arms, legs. shoulders and buttocks. ry. scat y. h ype rk eratotic
' 9333105.
3. Others:
Pelican Spur Trumerfeld zone 3) Increased susceptibility to infections (e.g. respirato infecuon . _
UL— White line of Frenkel infections etc.) or 5- d'allhaea. unnarv tract
Wimberger's Sign b) Poor growth velocity
c) Mental retardation.
Radiological Changes in Scum
NUTRITION AND MICRONUTRIENTS U Chapter-2 27
I-ru
0. 22 : Prevention of vitamin A deficiency. [Kalyani - 8" Sam} O. 28 : Complications of PEM. [BSMC-Bth Sem}
0. 23 : Vitamin A prophylaxis. {BMC - 2015] Ans: See 0- 9 (complications)

Ans : VITAMIN A PROPHYLAXIS a. 2.9 : Severe Acute Malnutrition. {CNMC—Sth Sem]
RATIONALE : Ans : SAM
1. Vitamin A deficiency is the leading cause of blindness in children in the developing countries. 0 Definition :
2. There is also increased susceptibility to intections. like measles, diarrhoea. ARI etc. in children with - Management : See 0. 9
wt. A deficiency. - Complications :
3. Early signs and symptoms at vit. A deficiency like delayed dark adaptation. night blindness and _ _ . ,
Bitot's Spots are often not detectable by children or their caregivers. 0- 30: WHO Ciassmcafion otPEM.[2011-Supple, 20’2'5UPPH
PROPHYLAXIS : Ans : WHO CLASSIFICATION OF PEM -t
t. Routine prophylaxls to all the under 5 children ; Under the National Vitamin A prophylaxis Assessment of nutritional status in PEM (Protein Energy Malnutrition) is done according to the follow-
Programme. Sponsored by the Ministry of Health and Family Welfare, all the children between 6 ing parameters :
months to 5 years are given oral vitamin A supplementations along with routine immunisation. tst 1. Weight lor height (W/H) or weight for length.
two doses are clubbed with routine vaccines to ensure maximum coverage. 2. Height (or length) for Age (WA).
- Schedule:
3. Weight lor Age (W/A).
i) tst dose : 9 months (along with measles/MMH vaccination).
4. Presence ol edema.
ii) 2nd dose : 16-18 months (along with DPT booster). D Z-Score :
iii) 3rd ‘10” 1 24 months. The WHO recommends the use of Z-scorzes or Standard Deviation Score (808) for evaluating
N) 4th dose : 30 months. anthropometric data, to accurately classily malnutrition. Z-score or $08 is calculated as below.
v) 5th dose: 36 months. Ob ed l _ f
vi) 6th dose : 42 months. 308 (or 25.30"?) : sersvD va ue—Median re erence value
of the reference population
vii) 7th dose : 48 months.
0 Use of Z-score : Calculation of the Z-score gives a numerical value that indicates how far away
viii) 8th dose: 54 months.
from the 50th percentile for age (Median) the child's measurement lalls. e.g. Z-score < —2 means
ix) so does : so moths (along with 2nd booster of DPT). the value is below (Median — 280)
- Dose: Z-score W/H HIA _.‘:
a) <6 months : 50,000 M (Not applicable for routine prophylaxis) 5.;
1- > -2 (Normal) Normal Normal ,.
b) 5 12 months - 1 00 000 lU
' I ' 2. < —2 (Decreased) Wasted Stunted 3
c) > 1 year: 2.00.000 lU.
2. Prophylaxis ln speclal situation : Children with measles and severe malnutrition should also U C|assificafion of acute a chronic malnutrition :
receive vitamin A proplyaxis (single dose) orally or intramuscularly. WIA
a) Oral dose : Same as above. 1 N l ”M W/H Interpretation
b) M dose: Half of the oral dose. ' onna Normal Normal Normal (No PEM)
2. Decreased Normal Decreased Acute Malnutrition
0. 24 : Management of severe Acute Malnutrition. [HRS - 8th Sam. Kalyant 91h $8111, 505104015. 3. Decreased Decreased Normal Chronic Malnutrition
HMO-2016']
4. Decreased Decreased Decreased Acute-onchronic
Ans: MANAGEMENT OF SAM . ‘ - malnutrition
Sec 0.9 (Steps 0‘ management 5 Inpatient management) , El Classification of moderate & Severe malnutrition :
f. 25 :sAdngagsizztfid(gig;3:312:51':21:32:31!) r Features Moderate Severe
ns: ee . tSSI . i 1. Edema.. No Yes
a. 26 .- WHO criteria {or SAM. {women-2016] 2- W/H (Wasting) : 70-79% (Z-score -2 lo —3) cross (Z-score <45)
i u
Ans : See 0.9 (Definition of SAM) 3. WA (Stunting): 85-89% (Z-score —2 to -3) <85% (Z-score «(-3)
0. 27 : Complications of SAM. (”CK-8th Sent, KPC2-2016]
eraZ 29
NUTRITION AND MICRONUTRIENTS o Chapt
0. 3f : Age Independent criteria of malnutrition. {BSMC—Bth Sem. 9th Sem SUMO-2016]

I) Flao's index a £939)?
Ans: AGE INDEPENDENT CRITERIA OF MALNUTRITION [Ht (emu
Since
. ' '
_ difficult_ to find true age of the child in th eunderprivrleged
. it is often andi norant t' f . Wt (k )
m dag:.lhe followrn g a g e-rnde pen d ent indices
socre ’ ' of nutritional
‘ ' status are devrsed
' to Interpret
.9 sec ion 0 the
anthropomet- g) Dugdale Index —+ m
s-2016]
1. Mid Upper Arm Circumference (MUAC) : grading of Kwashiorkor. [Maid
0. 32 : Clinical manifestation and
Also known as Mid Arm Circumference (MAC). it is the most widely used measurement as it .
Ans: KWASHIOFIKOR iency rather than calorie.
requires minimum equipment. MAC has been found to be relat'Ive l y stable between "‘3 399 group type of FEM . wher e there is predominantly protein defic the first
of 1-5 years at a value of 16—17 cm. Kwashiorkor is the means the disease of
from local language'of Ghana. which
The lenn 'Kwashiorkor’ is originated
a) MAC < 13-5 cm : Malnutrition.
child (after arrival of the second).
b) MAC <12.5 cm : Severe malnutrition.
0 Clinical Manifestations : features and non-essen-
c) MAC < 11.5 cm : Severe Acute malnutrition r can be divided into essential
Clinical features of a child with Kwashiorko osis.
mation of diagn
2. Shakir tape method : tial features. which also helps in confir
This special tape has coloured zones (red. yellow 8. green) based on the measurement of MAC. A) Essential features: to age.
Red zone corresponds to < 12.5 cm. (wasted), yellow zone : 12.5-13.5cm (borderline) and green by low weight and low height according
1. Growth retardation. as evidenced
zone : > 13.5 cm (normal) some amount of subcu taneo us fat.
2. Muscle wasting with retention of sness. lack of
3. Bangle Test : A bangle with internal diameter of 4 cm is passed above the elbow. If it can be passed by mental apathy in the form of listles
3. Psychomotor changes. as evidenced
easily. the child is having malnutrition.
interest in the surroundings.
over the pretibial
4. OUAC Stick method : < 2.59mldl) pitting edema. at least
4. Hypoalbuminemic (serum albumin
It has 2 set of markings. indicating height a MAC. MAC is measured first and then height. If the
.
region (not of cardiac. renal or hepatic origin)
height IS more than the expected height for the measured MAC child is considered malnourished. B Non-essential features :
u—r
bands
with easy pluckability. Som etrrnes, altemale
5. Skinfold thickness: 1. Hair changes : Depigmented. sparse hair
seen (Flag sign).
It is measured over Triceps by a standard caliper (e.g. Herpenden's caliper). of light and dark coloure d hairs are
a) > 10mm: Normal 2. Skin changes:
b) 6-10 mm: Mild to moderate malnutrition. i) Flaky paint dermatosis.
c) < 6 mm : Severe malnutrition. ii) Crazy pavement dermatosis.
6. Midarm muscle circumference : 3. GI system : Diarrhoea. vomiting, anorexia.
Calculated by the formula : (MAC — n x triceps skinfold thickness
) 4. Micronutrient deficiency :
7. Weight for height: i) Anemia due to iron deficiency.
It is partially age-independent and is calculated as follows : ii) Deficient potassium & magnesium.
WIH (96) = Acute weight iii) Vitamin A deficiency.
Expected weight for actual height X100 ‘ 5. Hepatomegaly : Soft. rounded margin.
. Pyoderma, Giardia etc.
8. Various ratios: 6. Superadded infections : TB. Measles. Bronchopneumonia. Diarrhoea
nt
ric parameters has evolved as age-independe r is based on the site & extent of edema. as mentiOned below,
Lastly, various ratios of different anthropomet [1 Grading : Grading of kwashiorko
indices of malnutrition. such as 1. Grade I —+ Pedal edema.
Chest Circumference (CC) 2. Grade II -+ l + Putfiness of face (Facial edema).
a Jellife's Ratio 4
Head Circumference (HC) 3. Grade m —) u +’ Edema of chestwall and back.
“I“
e malnutrition.
b MAC to Height ratio —9 < 029 indicates sever 4. Grade IV -+ III + Ascites.
c) Kanawati Index —i 5&9 0. 33 : Differentiate between marasmus and Kwashiorkor. [HMO-2016, Mars hidabad-2015]
B)? Ans: DIFFERENCE BETWEEN MERASMUS AND KWASHIORKOR.
d) BMI (Body Mass Index) .i EB
[Hi (Mil orkor are
.
the 2 ends of the spectrum of malnutritio n [PEM- wrth a '0! of
Marasmus and. Kwashi
. . n.
difference in clinical presentatio
s) Ouetlet index .+ M x100
[Ht (cmtlz
NUTRITION AND MICRONUTRIENTS D Chagal- 2 31
Gynaecomastia
99515:”
Features Marasmus Kwashiorkor Parotid Swelling
1. Appearance : Old man appearance with Puffy appearance with Eosinophitia
generalised wasting. dependent edema. 9. Spienomegaiy (sometimes).
2. Age Group : infants 1-5 years El Treatment : Wait and watch. continue nutritional rehabilitation-
increasing to the target level,
3. Prevalence : Common Rare. [1 Prevention : initiating treatment with low protein (fiet and gradually
4. Etiology : Predominantly calorie deficiency Predominantly protein deficiency may help prevent this entity and ensure a smooth recovery.
< 60% of expected 60-80% of expected
5. Weight: 0. 35 : Nutritional Rehabilitation Centre. [MCK-‘t’olfij
Growth retardation : G e
6.
Ans : NUTRITIONAL REHABILITATION cenrne
7. Edema : Nil 8 from Southern America.
' The concept of Nutritional Rehabilitation Centre (NRC) originally came
Some what preserved under supervision of
8. Subcutaneous fat : Almost absent
D Aim : Aim of NRC is to offer nutritional rehabilitation for mild to moderate PEM
nt.
9. Mental apathy : Nil/Mild 8 trained personnel to bridge the gap between house management and hospital manageme
10. Appetite : Good Very poor Cl Types : There are 2 types of NRCs —
11. Hair changes : Nit/Mild e i) Day care NRC 8.
12. Skin changes : Nil/Mild e ii) Residential NRC.
remains open from 8 AM
13. Fatty liver/ D Day Care NRC : it acts as daily basis without any provision for night stay. It
Hepatomegaly : Absent Present to 6 PM daily.
14. infections: e 8 3» Structure : It consists of -
15. Serum protein and a) A room for children,
Albumin Low normal Very low b) A kitchen,
16. Response to the c) An examination room &
treatment : Good Poor d) A teaching space I counselling room.
> Activity:
Murshidabad-20l6]
0. 34 : Nutritional Recovery Syndrome. [BSMC-2016, a) They cater 20 to 40 malnourished children along with their mothers.
marketing,
Ans : NUTRITIONAL RECOVERY SYNDROME
. b) The mothers are expected to actively involve themselves in various activities, like
Gomez Syndrome. it refers to an interesting se- cooking etc. ’1
Nutritional Recovery Syndrome is also known as of proteins during the
with very high quantity c) At least 1 good meal is provided to children. ' h
queiae of events seen in children who are being treated
n from gross malnu trition . is usually attached to a
course of rehabilitatio D Residential NRC : This is a larger and more organised NRC. The center
initially described with Kwashiorkor, it is seen in health center or the pediatric department oi a teaching hospital or an under 5 clinic.
D Etiopathogenesis : Although this syndrome was
both marasmus and Kwas hiorko r in india.
> Stalls:
be related to endocrinal disturbances.
a) Exact pathogenesis is still not known. But, it may a) A "housemother' as the fulitime head, who have responsmiiities. like -
ry gland and its target glands are depress . ed. . An adaptive
b) in PEM, the function of the pituita y dunng the penods of lower i) Daily work schedule of the mothers.
, metab olic rate & growth velocit
mechanism reduces body activity ii) Purchase of food.
dietary intake. ates
utilization of the hormones by the body stimul iii) Keeping stock,
c) During. nutritional rehabilitation. greater ACTH . TSH. FSH, LH etc.) iv) issuing the exact amount of food, as decided by doctors/nutritionist.
(e.g.
pituitary gland to produce its trophic hormones '
activit y of the target glands (e.g. Adrenal gland. Thyroid. Go- v) Maintenance of cleanliness etc.
d) This result in an increa se in the
hormo nes exces sively (includ ing estrogen) and causrng symptoms 5. b) Supervisory staffs (Part-time staffs) —
nads etc.). producing
rome .
signs of nutritional recovery synd i) Doctor,
CI Clinical Features: ii) NursefMedicai assistant,
1. increasing hepatomegaly. iii) Nutritionist.
Abdominal distension. iv) Home economist etc.

theses
Ascites. > Activities:

us network. _ a) Nutrition and health education,
Prominent thoraco-abdominal veno '
.
Hypertrichosis (increased body hair) "‘
m~x
a
it?)
2 33
NUTRITION AND MiCFlONUTRlENTS [3 Chapter—
b) Household budget teaching.
c) Feeding using locally available foodstuffs and local methods of cooking. 2. Severe dehydration with shock :
0 Indication I Criteria for admission in NRC : 1
RL with 5% D or "/14- 50 @15 ml/kg
1. Children at risk
over 1 hour (iv. or intra osseous)
2. Children who fail to gain weight over a period of 3 months.
3. Children who do not catch up in growth after serious illness (e-g. measles. diarrhoea etc.). Assess after 1 hour
1
4. Failure of breastfeeding. l
No improvement or worsening Improvement
5. Mothers and children who find it difficult to cope with their problems at home in spite of the
l (i.e. PR slows I Faster capillary refrll/
health teaching they receive at the under-Salinic.
Consider septic shock. increase in BP/ increased urine output)
6. Twins & triplets. (start ionotropes. like.
dopamine or dobutamine) Consider severe dehydration with shock.
0. 36 : Management of severe dehydration in a FEM child. [HMO-8th Sem] 1
Ans: MANAGEMENT OF SEVERE DEHYDRATlON IN PEM Repeat fluid bolus of 1 5111n over 1 hour
1
Dehydration tends to be over diagnosed and its severity overestimated in severely malnourished ASSESS
children (Particularly marasmus). On the other hand. in a child with kwashiorkor. presence of edema often J
underestimates the severity of hypovolemia f dehydration. l V
:1 Diagnosis: Acceptls orally Clinically better. but not accepting orally

i
1. H/O watery diarrhoea or vomiting (i.e. fluid loss). Start ORS G 5-10 ml/kg/hour Give ORS by NG tube @ S-IOmn/hour
2. Clinical Signs. (of severe dehydration) :
0. 37 : Dietary management of severe FEM. [2008]
a) Increased thirst.
b) Dry eyes at oral mucosa (absence of tears) Ans : DIETARY MANAGEMENT 9F SEVERE PEM
Dietary management with appropriate nutritious diet is the comerstone of management of severe
c) Sunken eyes , J—t may be present in children with PEM without dehydration also PEM. either in house or in the hospital. There are 2 Phases of dietary management.
d) Slower skin pinch
1. initiation of feeding with starter diet (1 st week)
e) Decreased urine output
2. Catch-up growth with catch-up cfiet (2nd week onwards)
1) Tachycardia. Tachypnea 1. Initiation of feeding : (tst 7 days)
i) Formula : F-75 starter diet (calorie content = 75 kcal per 100 ml)
g) Hypotensron. low pulse volume }—t seen in severe dehydration with shock
h) Lethargrc / unconscrous ii) initiate feeding as soon as possflale.
0 Treatment: iii) If the child is not able to take orally or takes <80% of the target amount. nasogastnc feeds
are
1. Severe dehydration without shock : started.
severe
i) IV route of rehydration is not recommended. unlike in normal children (plan C for iv} Total amount of feed : 130 mlfkg/day; reduced to 100 mlfkg/day. if there is generalized edema.
dehydration). due to the risk of overhydration and heart failure. v) Recommended total energy: 100 kcaI/kglday.
administration of
ii) If the child is unable to accept orally. NG tube (Nasogastric tube) is used for vi) Recommended protein intake: 1-1-5 gmikg/day.
OHS. vii) Breast feeding to be continued ad-libitum.
extra potassium
iii) Rehydration solution : As children with PEM are deficient intpotassium. Kt
viii) Types of diet :
olanty 0R3 (Na'- 75 mmol/L.
should be supplemented. IAP- recommends use of Iow-osm a) Milk-based diet
of potassrum as Syr. Potas-
—- 20 mmol/L, Glucose — 75 mmolfL) with additional 20 mmol/L b) Milk + cereal based diet — (low lactose diet) used in children with
K‘) persistent darrhoea
sium chloride [15 ml of potchlor syrup = 20 mmol of c) Lactose-free diet - Rarely needed; used only in those child
give 5-10 ml/kg/hour for the next 4-10 ‘ ‘ ‘ '
iv) Dose: 5 ml/kg every 30 mins for the first 2 hours, then even on low-lactose diet. ren having per8rstent diarrhoea
hours. ix) Feeding pattern : Feeds are started at 2 hour interval at the initiati
rehydration with F-75 starter for- . . . o .
v) Feeding : Should be initiated within 2-3 hours of starting of an indwrdual feed Is Increased. while decreasing the frequency. ans :12:q[2:31:32 Lid-Ume
mufa. Day Frequency Vollkgl'feed
it n' : Monito ' r PR. RR. unrne' output. oral mucosa etc. half hourly for 2 hours' a. then Total volume
ration (e.g. T in RR by D. - D2 2 hourty
Mon 0 ons
Wt) hourly. ng therap y should be stopped, if there is any sign of overhyd 11 ml 130 mlrkglday
1‘ in PR by 151mm , 1‘ ing edema etc.) Di _ Da 3 hourly 16 ml
51min. 13-0 ml’kg/day
D, .. D, 4 hourty 22 ml 130 mt’kg/day
NUTRITION AND MICRONUTRIENTS C] Chapter—2 35
Complementary teed : Give at least 1 Kalori serving at a time of mashed rotifbread/biscuit

2. Catch-up growth : (2nd week onwards) mixed in sweetened. undiluted milk or mashed rolilricefbread in thick dal with added ghee/oil or
kcal per 100ml).
i} Formula : F-100 catch-up diet (calorie content = 100 Khichri with added ghee/oil.
fre-
ii) Once the appetite returns. which usually takes 2-3 days. higher intakes with decreasedmain- . Add cooked vegetables in these servings or use dalia. halwa. kheer prepared in milk or mashed
achieved
quency ol feeds is achieved first. as shown above. When 4 hourly interval is boiled potatoes.
growth.
taining total volume. volume ollered at each lead is further increased to allow catch-up . Offer banana (after 9 months). mango. papaya etc. as snacks in between the servings.
diet with increase in energy 8. protein
iii) Diet is gradually transitioned lrom F-75 diet to F-100
. Keep the child in lap and feed with own hands. wash the hands of own and the child with soap
content and water every time belore feeding.
iv) Total volume 0! feed : 150-200 mlfkg/day. . Serve freshly cooked loods. cover Iood properly. avoid use of leading bottles.
v) Total energy : 150-200 kcaI/kg/day. _I
in) Total protein : 4-6 gmlkg/day.

vii) Types : same as F-75 diet.
vfii) Once target nutrition is achieved with adequate weight gain. complementary feed are intro-
duced.
0 Favourable response :
1. Resumption of alertness 8. appetite.
2. Initiation of weight gain @ 5-10 gmfkg/day.
3. Disappearance of edema (by 7-10 days).
CI Unfavourable responses :
l. Nutritional Recovery Syndrome (Gomez Syndrome).
2. Pseudotumour cerebri.
3. Encephalitis-like syndrome.
0. 38 : Diet of 1 year old infant. [2011, 2014-Supple]

O. 39 : Feeding ofa 7 months old baby. [HMO—8th Sent]
Ans : DIET! FEEDING CF 6-12 MONTHS OLD INFANTS
Here comes the
After 6 months ol age breastmilk alone is not enough to make an infant grow well.
that the child
importance ol Complementary Feeding. which complements breast milk and ensures
continues to have energy. protein and other nutrients to grow normally.
CI Factors considered while planning diet :
Q
our traditional bulky

1. Energy density : As the small child is unable to eat large quantities of
Energy
loods. giving small but energy dense foods at lrequenl Intervals severs the purpose.
every feed.
density can be increased by adding fats (eg. a teaspoon of oil or ghee) in
teaspoons)
Amount of feed : Complementary foods should be started with small amounts (1-2
better (is.
and quantity gradually increased as the child gets older and starts to accept food
teaspoon to tablespoon lo kalori)
By 8
Conslstency of feed : Al 6 months. pureed.mashed semisolid foods are offered to infants.
months.
. months. most infants can also eat linger foods (snacks eaten by them alone) and by 12
.
most children can eat from family pot.
Frequency of feeding : Breastled healthy infants need 2-3 complemen tary feedslday at 6-8
months and 3-4 leeds/day at 9-12 months of age. Additionally. 1-2 snacks meal can be given
after 8 months.
5. Hygiene : Good hygiene and proper food handling should be practised to prevent infection
(e.g. washing hands. utensils etc.)
6. Helping the child : Feeding the infant should be an active engaging and interactive altalr.
Cl Recommendations :
Breastfeed. as often as the child wants.
FLUID AND ELECTROLYTE CI Chapter - 3 37
CHAPTER -3 l
N. B. : When hyponatraemia
T lntracranial pressure
FLUID AND ELECTROLYTE develops slowly, cells have time to l
adapt. 80. patients may be . Cerebral Edema
relatively asymptomatic even dur- . ( Cerebral Blood Flow
O. 1 : Causes and clinical features of Hyponafraern mg very low levels of Na.
la. [2014] . Brainstem herniation (in acute severe hyponatraemia)
a. 2 .- Hyponafraemia. [HRS-8" Sem'j
0 Clinical Features : Symptoms are mostly related to CNS. like -
Ans : HYPONATRAEMIA
a) Anorexia. nausea, vomiting
Hyponatremia is defined as serum sodium
135-145 mqL). 0’ < ‘35 mEq’L ‘Nmma‘ serum Na‘ value is b) Lethargy. confusion or agitation
0 Causes : Hyponatraemia may develop either due to net c) Headache
loss of sodium or due to net gain of water
d) Seizures
Loss of Sodium e) Coma

Gain of Water
f) irregular respiration, cheyne stokes breathing
1. (Hypovolemic hyponatraemia) 2. Hypervolemlc hyponatraemla D Other symptoms, like — muscle cramps. weakness etc may accompany.
(a) Exu'arenal losses (a) Nephrotic syndrome D Diagnosis : 1. Exclusion of Pseudohyponaetramia and Factitious hyponatraemia.
(i) GI loss (Diarrhoea) (b) Cirrhosis of liver 2. Assessment of volume status I
(ii) Sweat (Cystic Fibrosis) (0) Congestive Cardiac failure 3. Clinical evaluation for a possible etiology.
(iii) Third space loss (Peritonitis, lleus) (d) Renal failure (Acute. chronic) 4. Measurement of urinary Na.
(1)) Renal losses — 3. Euvolemic hyponatraemia 0 Management:
(i) Diuretics (3) Drugs (Desmopressin) 1. Acute Cases : (a).Hypovolemic : Rapid correction with 3% NaCI needed. if Na < 120 mqL
(ii) Hypoaldosteronism (Congenital Adrenal (b) SIADH (Syndrome of Inappropriate ADH or patient is symptomatic. Otherwise corrected slowly over 48 hrs.
Hyperplasia, Adrenal Insufficiency) secretion) Na correction needed = [0.6 x Body wt. x (135 — serem Na)]mEq
(iii) Salt-losing Nephropaihy (Tubulo lnter- (c) Hypothyroidism b) HypervolemiclEuvolemic : Fluid restriction.
stitial Nephritis) (d) Water intoxication (Primary polydypsia, 2. Chronic cases : Corrected gradually by not more than 12 mqL/day. Rapid correction may
(iv) Bartter's syndrome Runner's hyponatraemia) cause central pontine myelinolysls.
O. 3 : Outline the physiology of water balance. [HMO-8'” Sem] _
There are 2 other conditions. where serum sodium is falsely decreased. namely — Pseudo
hyponatraemia, Factitious hyponatraemia. Ans : WATER BALANCE
Psudo hyponatraemia : When the serum solids are increased (as in Hyperlipidemia or Hyperpro- U TBW : Total Body Water (TBW) as a percentage of body weight varies with age
-
teinemia) and sodium is measured in total serum (is. water + solids). falsely low Na value is found. 1. Fetus has a very high TBW. which graduall y decreases to approximately
75% of birth weight
Factitious hyponatraemia : When serum osmolality is elevated due to increased amount of for a term infant.
osmotically active particles (Glucose, urea. mannitol), water is drawn from lCF to ECF. Thus, falsely Premature infants have higher TBW than their term counterparts.
low Na value is found. TBW further i es during the tst yr of life to approximately 60% of
body wt.
C] Pathophyslology: 4. Post puberty. TBW in males remains at 60%, but it ll e)s in female
s to about 50% due to 1‘ ed
l Serum Na fat content (Fat has lower water content than musc es .
1 D Fluid Compartments :
Serum (ECF) becomes hypotonic relative to ICF
TBW [60%]
Water moves from ECF to ICF l
l l
l
Extracellular fluid
Cellular edema lntracellu lar flurd
'
(ECF) E096]
l (ICF) [40%]
Most problematic in brain (as it is confined in skull) l 1
Plasma [5%]llntra- vascular fluid Interstitial fluid [15%]
36
FLUID AND ELECTROLYTE CI Chapter -3 39
38 QUEST: PAEDIATRICS
a. 4: Hypernatremia. [SUMO-Semester]
- in the fetus and newborn. ECF volume > lCF volume. -
Ans :HYPERNATREMIA _
- Postnatal diuresis causes 1 in ECF volume. sometimes Na > 150 mEq/L is
Hypernatremia is defined as serum Na 2- 145 mEq/L; but.
o By 1 year. ICF:ECF ratio reaches adult levels [i.e..2:t].
considered diagnostic of hypernalremia.
0 Balance between different compartments : Causes : Most commonly due to 1 ed free water losses.
. . .. . Cl
1. Balance between ECF and ICF : ECF and ICF are usually in an “Osmotic Equrlibrium'. 1. Water deficit > Na deficit:
because the cell membrane is permeable to water.
a) Volume depletion : l ECF volume a) GI loss (diarrhoea. lactulose)
l ' - b) “Cutaneous loss (Bum)

0) Renal loss (Osmotic diuretic Diabetes Mellitus).
TECF osmotality (OSM‘CF > 05M")
2- Water deficit I
Water moves lrorn ICF to ECF
. a) Diabetes lnsipidus (Central, Nephrogenic)
b) Fluid retention : .I, ECF osmolality
b) T Insensible loss (warmer. phototherapy)
c) l intake '
Water moves from ECF to ICF
3. Na excess :
2. Balance between lntravascular and Interstitial fluid :
a) Introgenic (NS, NaHCOa)
It depends on hydrostatic force's and oncotic forces of both the compartments.
b) Sea-water drowning
a) T Hydrostatic force at intravascular space
OR. c) Hyperaldosteronism.
_
1 Onootic force at intravascular space D Patho physiology : T Serum Na —> T Serum osmolality
l
Vessel _ ' l
Water moves from intravascular to interstitial space.
Hydrostatic Oncotio Flurd shifts lrom 'CF to ECF
b) Similarly, Jr Hydrostatic force at interstitium l
lForce Force .
0R,
T Onootic force at interstitium
i
Also dravrs fluid from intravascular to interstitial space.
—3———Q—
*
Hydafl‘c' ‘0ncot‘ic
i
Cell shrinkage
lntracranial hemorrhage <- Tear in the bridging vessels of brain

c) Opposite is also true. __"__ Force : I 2 Force: D Clinical Features:
lnterstitium a) T Thirst
d) This interplay is critical for tissue perfusion.
- Regulation of TBW : (by regulation of plasma osmoiality) b) lrritability, tremulousness
c) Excessive cry
Volume depletion —r T Osmolality of plasma
1 d) Seizures. Focal deficits, coma.
f ' l
Stimulation Secretion of ADH through hypothalamic El Diagnosis : Serum Na > 150 mEq/L
osmoreceplors I
0' thirst
l i l 1.
l
Restoration of vol ‘_ 1 Water intake ADH binds to V2 receptors in the collecting. Dehydration Overhydration
duct cells of kidney f—J—l l
'
} ulo - High We 1 ed ’ "’°' ”ma" T
Insertion of Aquaponn-Z channels Into the l 1 ° Urine Na - high
renal collecting ducts
i oucmi . Diarrhoea l
. l ed Intake Excessive 3% NaCI
I
Water reabsorptio‘nl—-——l or NaHCO, .
T ' . Restoration of
Urine osmolality and concentration volume
T‘ -- ...... -- —
4O QUEST : PAEDIATRICS
ter-3 41
FLUID AND ELECTROLYTE U Chap
Management : Fluid deficit to be corre

cted slowly over 48 hours or longer
0 Diagnosis :
Serum K' < 3.5 mEq/L
- Fluid deficit: {0.6 x Body weight x[w -1 Lt
Expected Na - l
Exclude 1 ed intake. risk factors for transcettular shift
- Usual fluid used for correction is 0.2
DNS. 1
° In cases of central DI, Vasopressin is Measure BP
used.
1
in nephrogenic Dl, DOC is thiazide l— l
diuretics (DOC = Drug of choice)
BP normal 7 BP
0. 5 : Hypokalemfa in children. {HMO
-Semester} l
l
Ans : HYPOKALEMIA Urine K' Renin, Aldosterone
1
Hypokalemia is defined as serum potass
ium < 3.5 mqL. Normal serum K‘ level l l I L l .
is 3.5 — 5 mqL. l
Relnm
D Causes : < 20 mEq > 20 mEq/L T Renlin Hm
t. Decreased intake : Anorexia Nervosa Extrarenal losses Renal losses Renovascu 3' f— l
2. Increased loss: l Aldosterone iAldo
a) Extrarenal loss : Diarrhoea. vomiting. ‘ CAH _ Primary

' CUSh'”9'5 . Hyperaldo-
b) Renal loss : steronism
i) Renal Tubular acidosis (Type I. ll) 0 Treatment :
ii) Diuretics - K' supplementation (KC!) —+ Oral/IV.
iii) Bartter’s syndrome 0 Correction is usually done slowly and daily K' should not exceed 4 mEq/Kgfday.
iv) Congenital Adrenal Hyperplasia 0 Rapid correction is needed in cases with —+ arrhythmias, bradycardia, shallow respiration
v) Cushing's syndrome etc.
vi) Primary Hyperaldosteronism 0. 6: Hyperkalemla. [2016]

vii) Renovascular Hypertension.
Ans : HYPERKALEMIA
3. Transcellular shift : (Shift of K' from ECF to lCF) Hyperkalemia is defined as serum potassium > 5 mqL.
a) Alkalemia 0 Causes :
b) Insulin 1. Increased Intake : Moral. Blood Transfusion.
c) Catecholamines 2. Decreased excretion : (via kidney)
d) Refeeding Syndrome. a) Renal Failure (AKI. CKD)
b) Addison's disease
0 Cllnlcal Features : C/Fs are limited to GI tract. musculoskeletal and cardiovascular systems —
c) i ed Mineraiocorticoid activity (CAH. Psuedohypoaldosteronism)
1. 6s
d) RTA, type W.
a) Abdominal distension
e) Hyporeninemic Hypoaldosteronism (J- ed renin due to kidney damage in obstructive
b) Paralytic ileus. umpathy, sickle cell disease).
2. Musculoskeletal : 1) Drugs (ACE Inhibiters. Aldosterone antagonists).
a) Muscle weakness 3. Transcellular shifts : (Shift from ICF to ECF).
b) Hypotonia a) Aclden'tia .
b) B-blockers
3. CVS:
c) Crush injury. bum, rhabdomyolysis. hemolysis.
a) Bradycardia
4. Spurious Lab. Value : Tissue tschaemia during blood drawing.
b) Arrhythmias
c) ECG changes (low voltage ORS. ST depression. Flat T wave. appearance of U wave). 0 Cllnlcal Features : Mild degrees of hyperkalemia are generally well-tolerated 5 very few
symptoms. But. when K' value crosses 6-6.5 mEqIL, there are risks oi life-threatening cardiac
anhythmias.
a) ECG changes : Tall. peaked T waves (earty change) that ma y p ro g ress to ST de PFBSS' Ion. T CHAPTER —4'
ex_
PR interval and widening of OHS compl
b) Ventricular eclopics, VT, VF. NEONATOLOGY
0 Diagnosis:
1) Exclusion of spurious lab. value by checking a second value.
SHORT NOTES
2) HIO drug intake. blood transfusion, iniuriesfbum.
3) Renal function (BUN, Creatinine)
0. 1. Thermoregufation of newborn. [CNMC-G“ Sem]
4) Acid-base status (ABG) " SemJ/Non-shivering thermogenesis {HMO-2016]
0. 2. Thermogenesr’s in newborn babies. [CMC-Q
5) Measurement of Ftenin and Aldosterone.
Ans : THERMOGENESISH’HERMOHEGULATION
0 Treatment : Thennoregulation invo Ives maintenance of , -
Production of heat in the body is known as thermogenesis.
1. To avoid all intake of potassium through dietary source. body tempera ture by means of thermog enesis in respons e to cold.
2. Drugs to be avoided : Cl Mechanisms of thermogenesis :
a) ACE inhibitors (Enalapril. Captoprii etc.) 1. Shivering (muscular),
b) ARE (Losartan. Olmesartan etc.) 2. Non-shivering (metabolic).
muscular activity in response to cold ambience. But
c) K‘ sparing diuretics (Spironolactone. Amiloride) D Shivering thermogenesis : Shivering occurs by
in newbor n infants, shiverin g is not a significa nt source of heat production, and it appears only when
d) NSAl below 25°C.
the environmental tempera ture falls
e) Succinylcholine (during intubation). important source of heat production in newborn
El Non-shivering thermogenesis (NST): It is the most
3. Measures to tackle Hyperkalemla : and it occurs as a result of metabo lism of the brown fat.
when K' > 6
a) Clacium Gluconate (10%) : Used for immediate cardioprotective action, Brown fat:
Dextrose. MOA
mqL Dose : 0.5-1 mlfkg over 5-10 mins, diluted E equal volume of 5% 0 Fetal brown fat is laid down mostly during the third
trimester of pregnancy. Thus, preterm and
: Membrane stabilisation. LBW babies are deficient in brown fat.
rly.
b) NaHCO:l : Cardioprotective action. Dose : 1 mEq/kg. MOA: Shifts K° intracellula ' It is located at —
gm/kg Glucose + 0.1
c) Glucose + Insulin : Slower onset of action (30 mins) Dose : (0.5-1 a) Nape of the neck.
unitfkg Insulin) as infusion. MOA : K' shift into cells. b) lnterscapular region.
+ insulin) Dose : 5-10 mg.
d) Nebulised l3z agonisl : (Salbutamol) Alternative to (glucose of Axillae.
MOA : K' shift into the cells. d) Groin and
lemia. as it excretes K' from
9) K' exchange resins (Kayexalate) : Used for chronic hyperka e) Around kidneys and adrenals
gm/kg P0 or PR. MOA : Exchang es Na' for K' across colonic
body slowly. Dose : 1
mucosa. I Mechanism of MST)— Skin becomes cold
Afferent Nv.
Heal regulating centre at hypothalamus
Elferent Nv.
' Reaches Brown fat
Noradrenaline
BROWN FAT——> Local release of
(NA)
TG GlyCerol
Distributed to different parts of the
body through circulation Fatty acids
Heat
generation ‘ I 60% re-eslerilied 10% goes in circulation ‘
30% o'xidized
43
TE
T“!
44 QUEST : PAEDIATRICS 45
NEONATOLOGY l] Chapter-4
- the
Ouanti
rotatibodfi
is di gtlfy related to the brrth
' weigh
' t of the baby and in a CNMC—B" Sem] {Hafdia-2016}
term baby. accounts for 4% of O. 4. Management of Hypothermia in neonate. [2017, MCK-fl" Sem,
- Characterized by: (In comparison to white Ans: MANAGEMENT OF HYPOTHERMIA
fat)
a) Rounded nucleus and granular cytopla is abnormal and
sm. Normal body temperature in newborn is 36-5 - 375°C. Body temperatures of < 365°C
b) Large number of mitochondria. < 36°C is known as hypothermia. According to severity, there are 3 grades—
c) Abundant tat vacuoles. 1. Cold stress — 36°C - 364°C
d) Increased vascularity.
2. Moderate hypothermia — 32°C - 359°C
- Extra 02 and glucose are needed for these metabolic 3 Severe hypothermia — < 32°C
efforts and it can be safely
' 30, effective NST demands - 0 Management of Cold Stress : Cold stress is a Iorrn of mild hypothermia
h managed at home or keeping the baby with mother. The following steps can be undertaken—
a) Integrity of CNS pathways
a) Remove all wet/cold clothes from the baby's contact.
b) Adequacy of brown fat
b)Cover the baby adequately with warm clothes/towel.
c) Availability of glucose and oxygen.
c]Decrease heat loss by covering the peripheries with cap. socks and mittens.
0. 3. Etiology of Hypothermia in a newborn. [KPC-Q'" Sem] d)Warm the environment including bed and room.
Care
Ans : ETIOLOGY 0F HYPOTHERMIA e)Ensure skin-to—skin contact with mother as far as possible, applying Kangaroo Mother
(KMC) protocols.
35 Snothermia in a newborn baby is defined as core temperature I) Immediately breast-feed the baby.
of < 36°C. [Normal temperature -—>
.1 :15 C, Cold stress ~+ (BB-364°C). Hypothermia may persue because
of any of the following —> 0 Management of Moderate Hypothermia : Additional source of heat should be provided to manage
. mecmnism
tuationss.contributing
namely— to excessive heat loss -. l n newborns. heat loss may occur’ moderate hypothermia in newborn.
by 4
a) Provide extra heat by radiant warmer. incubator or room heater. whichever is feasible.
a) Conduction, b) Take measures to reduce heat loss.
b) Convection, d) Warm environment and linen.
c) Radiation and D Management of Severe Hypothermia : These babies are always managed at hospital settings.
d) Evaporation. a) Rapid rewarming — Started immediately using a radiant warmer or incubator. done upto 34°C.
- These 4 mechanisms contribute to heat loss alone or in combination in following situations — b) Slow rewarming—As baby's temperature reaches 34°C rewarming should be done sloniytill 365°C.
a) Cold environment — Winter season, in labour room (immediately after delivery), in operation c) Take all measures to reduce heat loss.
theatre (during surgical procedures). d) iVF (LV fluid) - Started as per maintenance requirement.
b) During transport, e) Hypoglycemia - CBG to be checked and treat any hypoglycemia with bolus d oefls of 10% Dex-
trose @ 2mlikg. ..
c) Contact with cold linen

I) Moist 0: provided with head box.
d) Bathing 9) Give injection Vitamin k 1mg i.mfr.v, iI not already received recently.
e) Increased airflow currents with low humidity h) If the baby doesn't improve with all these measures or there is recurrent/pe rsistent hypothermia.
2. Poor ability to conserve heat : Preterm and LBW babies are particularly vulnerable to hypother- think of causes like sepsis and start lV antibiotics.
mia due to this handicap. Factors responsible are— D Monitoring : Temperature to be monitored in all the babies diagnosed with hypothermia (including
a) Relatively large surface area (this is true for term babies also) - Body mass of a newborn is 5% cold stress) as per followrng schedule.
of an adult, whereas surface area is 15% of an adult. 1. Every Y2 an hour till it reaches 365°C.
b) Paucity of fat 2. Hourly for next 4 hrs.
c) Poor insulation due to thin and delicate-skin. 3. 2 hourly for 12 hrs thereafter.
d) Poor muscle tone hampers the ability to reduce surface area by assuming a flexed posture. 0. 5. Causes and management of hypothermia in newborn [2068-5upple][$DMC-20161
3. Poor metabolic heat production (NST) : Ans : See 0.3 and 0.4.
a) Deficiency of Brown Fat. 9.9. in preterm and small for date babies. O. 6. Prevention of Hypothermia in newborn {2012}
integrity of neurogenic
b) CNS damage, e.g. anoxia, intracranial hemorrhage etc. interfere with the '
0. 7. Mention the steps of prevention of hypothermia in a newborn. Which b ' b''95 d0 partrcu
source? {4+ 1] [RGKar-e" Sam}
-
pathways (both afferent and efferent) Iariy need additional heat
metabolic heat production pathway. o. 8. Warm chain in newborn care. [MIG-Supple, NBS-9" Sam] [Murshidabad-2016}
z; Hypogijcemia } Oz and glucose are needed in the
46 QUEST : PAEDIATRICS NEONATOLOGY U Chapter-4 47
Ans : PREVENTION OF HYPOTHERMIN WARM CHAIN a. 9. Cold stress In newborn. [IPGMEH-Q" Semi
The warm chain is a set of ten interlinked steps carried out at birth and later. which will reduce the Ans : COLD STRESS :
chances of hypothermia in all newborns. Hypothermia can be effectively prevented. it warm chain is between
Cold stress is a form of mild hypothermia. When body temperature of a newborn baby is
properly maintained.
36°C — 364°C. it is known as cold stress.
1. Warm Delivery Room : Delivery room needs to be prepared well in advance —-
Normal temp - 365°C — 376°C
a) Room should be clean. warm (25°C - 28°C).
Hypothermia —- < 36°C.
b) Room to be free from draughts from open doors and windows or from fans.
c) it the temperature is less than optimal, heater should be available to warm the room. or at D Risk factors :
least. the baby receiving area. 1. Situations contributing to excessive heat loss
-
d) Radiant warmer. if available. should be switched on at least 20-30 mins. in advance and put a) Cold environment
into manual mode with 100% heater output. b) During transport
e) All the towels. blankets and baby's clothes are prewarmed before delivery. c) Bathing
2. Warm Resuscitation : All the resuscitation equipments should be warm and baby resuscitated d) Contact with cold linens.
In warm area.
2. Poor ability to conserve heat - Preterm and LBW babies.
3. Immediate Drying : After birth. baby should be immediately dried with a dry towel. starting with
3. Poor nonshlvering thermogenesls -
the head. After drying. baby is covered with a second dry towel.
4. Skin-to-skin contact : Skin-to-skin contact with mother should always be promoted. as it effec- a) Deficiency of Brown lat (Preterm. SFD babies)
tively prevents hypothermia. ' b) CNS damage (Asphyxia. intravenous hemorrhage)
a) Immediately after delivery. baby kept over mother's chest/abdome n, while attending mother c) Hypoxia
for placental delivery. episiotomy repair etc. d) Hypoglycemia-
b) In postnatal ward. promote Kangaroo mother care. especially for preterm and LBW babies. 0 Clinical features : Baby is uncomlortable. restless and there would be refusal to feed. Peripher-
c) Skin-to skin contact is also utilized during transport of a newborn. ies would be cold to touch.
within 1 hour.
5. Breast feeding : Initiate breast feeding. as soon as possible after birth. preferably - If unattended at this stage. baby will go to frank hypothermia with dangerous consequences.
This ensures adequate supply of glucose and calories for heat generation.
in a term baby till - Chroniclrecurrent cold stress may hamper adequate postnatal weight gain. as food would be
6. Postponement of bathing and weighing : Bathing should be postponed wasted for heat production.
24hrs at least.
[1 Diagnosis :
and making zero correc-
- Weighing should be done only after covering the baby adequately
a) Ctinica! assessment: Baby’s abdomen and soles are touched with dorsum of hand. It abdo-
tion for clothing. "
of clothes depending on men is warrn to touch. but soles are cold. ciod stress is diagnosed.
7. Appropriate clothing : Baby should be covered with one or two layers
b) Temperature measurement by thermometer: Ideally. rectal temperature should be recorded
the season. Use of cap. socks and mittens are encouraged.
preferably in the same bedlsame as core temperature by means of low-reading thermometer (30°C - 40°C). But due to techni-
8. Booming in : Mother and baby should be nursed together cal difficulty and poor availability of instruments at all the heapital settings. axillary tempera-
room for 24 hrs. tures is commonly used to diagnose cold stress (36°C - 364°C) and hypothermia (< (36°C).
ensured in case of transport — to home. to
9. Warm Transportation : Thermal protection should be D Prevention : 10 steps of warm chain :
l or to anothe r department of the same hospital.
another hospita
1. Warm delivery room
Stable babies (includin g preterm and LBW ones) to be transported well-wrapped or in skin-
3) 2. Warm resuscitations
to-skin contact with the mother/family members.
in an incubator. 3. Immediate drying
b) VLBW. ELBW and unstable babies to be transported
send the mothers before delivery for in— 4. Skin-to-skin contact
c) For high risk mothers. peripheral hospitals should ‘
.
- 5. Breast feeding
-_-
utero transport of the babies.

care personnel involved in the newborn care 6. Postponement of bathing and weighing
a..."
10. Professional alertness and training : All heath

._...
d about the principles of warm chain. 7. Appropriate clothing

should be adequately trained and informe
A—
——<—-.—
' I Th cm. I
. 8. Booming-in
Answerto O. 7 (Second Part)
“on.
and Gestationa Age. us. a r iona 9. Warm transportation

Risk of h othermia is inversely proportional to Birth Weight
Low Birth Weight (LBW) babies [More for VLBW.
heat sourceyiFsJ particularly needed lor Preterm and 10. Professional alertness and training
ELBW and gross ly prete rm babies].
El Treatment: See 0. 4. (Management of Cold stress) + (Monitoring section)
1
._
--
T’
“I
_-....
'
-_—-
48 QUEST : PAEDlATFiICS
.
NEONATOLOGY U Chapter-r. 49
O. 10. Hypothermia in newborn. {2009-Supple

. HMO-9" Sem. NBMC-B‘“ Sem} (HMO. Kaiyan [1 Benefits of KMC :
f—2016]
Ans : HYPOTHERMIA
t. It improves bonding between mother and baby.
Newborn babies are more prone to hypothermia than
ture of a newborn is 36-5°C _ 376°C. h YP ertherm‘Ia or fever. . Promotes breast feeding with better yield of milk.
camp-pore
Normal body tempera-
Stabilises vital signs with effective thermal control.
0 Grading of hypothermia : Reduces risk of apnoea.
1. Cold stress - 36°C - 36-4°C (Mild hypothermia) . Reduces risk of infections.
2. Moderate hypothermia - 32°C - 35-9°C . Babies cry less. sleep better and show satisfactory neurobehavioral development.
3. Severe hypothermia — < 32°C. 7. Better weight gain occurs with early discharge from the hospital setup.
0 tielinition of hypothermia generally excludes cold 0 Types : a) Continuous. b) Intermittent.
stress. but there are different views on that
a so. 0 Limitations (of continuous type):
Ci Causes/Risk factors : See 0. 3 for details and 0. 9 for shorter 1. Poor cultural acceptability in our society.
version.
0 Clinical features : 2. Lack of garment design for easy ambulation of mothers practising KMC.
1. Peripheral vasoconstrictlon results in acrocyanosis, cool extremitie 3. it is uncomfortable for the mother to remain constantly stuck with the baby throughout day and
s and delayed CRT.
Skin mottling may be present. night during the hot summer months.
2. Babies are initially restless and then lethargic. 0 Prerequisites for initiation of KMC :
3. Vital functions are all depressed. resulting in Bradycardia. Hypolension. slow 1. Appropriate health facility : Health facility should allow entry of the parents in the neonatal unit
breathing!
apnoea. and have separate space for giving KMC-
4. Refusal to feed may be the earliest sign. 2. Appropriate support stalls and professionals : Presence of trained. fulltime health care workers
5. Depression of immunity predisposes to septicemia. is indispensable.
3. Good quality monitoring and follow-up facility.
6. Chronic cold stress may result in inadequate weight gain.
4. Mother's criteria : Mother should be willing. should be free from serious fitness and maintain
D Biochemical consequences :
good personal hygiene.
t. Hypoxia and hypoglycemia sets in due to consumption of 02 and Glucose during metabolic 5. Supportive family members.
heat production. 6. Social and community support.
t I] Candidates for KMC:
2. Metabolic acidosis due to anaerobic metabolism
All stable LBW babies are eligible for KMC. However. sick and very small babies (< 1200 gm)
3. Rt to It. shunting of blood — aggravates hypoxia. needing special care should be cared under radiant warmer and KMC started in these babies. once
they are hemodynamically stable.
J»
4. Rise in serum K' and NPN levels due to tissue catabolism (NPN = Non-protein Nitrogen). [It Procedure : _
5. Liver damage may cause coagulopathy. 1. Counselling : Counselling is of utmost impedance before KMC is initiated. Parents and even
0 Prevention: See 0.9. family members are counselled about the benefits. procedure and monitoring of KMC.
D Treatment: See 0.4. 2. Mother’ s clothing : Mother can wear any front-open dress as per local culture.
3. Baby‘s clothing : Baby is dressed with cap. socks. mittens. nappy and front-open steam shirt.
O. 11. Outline the clinical features, complications and Prevention of hypothermia in a newborn 4. Positioning :
baby. [Haida-2016] a) Baby is placed between mother‘s breasts in an upright position,
Ans : HYPOTHERMIA b) Head is turned to one side and kept in a slightly extended position to keep the airway
open.
Ct C/F : See 0. 10. c) Hips and arms are flexed and abducted to maintain "frog-like' position,
d) Bottom of the body to be supported with a sling or binder.
D Complications : O. 10. (Biochemical consequences)
e) Back of the baby to be covered by a woolen shawl.
0 Prevention : O. 6.
5. Monitoring : Vitals (colour. respiration. temperature).
O. 12. Kangaroo Homer Care. [2013. 201 f. Kalyanf- 9 " Sent}(2015. MEMO-9'" Semjflliis Midnapore. Ct Discontinuation and weaning : KMC is continued till baby achieves wei ht of arson
CNMC - 2016] Baby is weaned. when baby shows discomfort or there is visible sweating£_I d 2500 gms.
Ans : KANGAROO MOTHER CARE . .

O. 13. Give an outline of the clinical features of Neonatal Sepsis. [2008}
Cl Kangaroo Mother Care (KMC) is a method of care of preterm or LBWinfants by placing them in
skin to skin oontactwith mother or other caregiver in order to ensure optimum growth and develop-
Ans .- CLINICAL FEATURES or NEONATAL SEPSIS \
ment of the infant. A neonate with sepsis can ‘present with a wide variety of symptoms 0n the oth
- e r hand, there may
be very subtle symptoms or baby may be asymptomatic during initia| period.
0 It was first introduced In 1978 by Edgar Fley in Colombia.
7
T l “ ‘ _
50 QUEST : PAEDIATRICS NEONATOLOGY Cl Chapter-4 51
. Generalized features : iii) Passage of blood per rectum

a) Alteration in the behaviour and established feeding pattern oi the baby are characteristic iv) IPS diminished or absent.
early Ieatures. d) Disseminated lntravascular Coagulation —
b) Baby may become suddenly lethargic. inactive and reluses to suck. i) Excessive bleeding trorn venipuncture sites
c) Hypothermia (including cold stress) - common in preterm babies. ii) Pulmonary hemorrhage
d) Fever (very rare) - may manilest in term babies. iii) CNS bleeding.
e) Prolonged jaundice
0. 14. Neonatal sepsis Screening. {2013. 2014-Supple][2011] {2016. CNMC-a’ Sem. NBMC-ii"I Sem)
t) Hepatosplenomegaly [CNMC, BMC, BSMC. KPC, SDMC, lCARE-Sem 2016}
g) Apnoea with cyanosis
Ans .' NEONATAL SEPSIS SCREENING
h) Failure to gain weight may be the only feature.
All neonates suspected to have sepsis should have a sepsis screen to corroborate the diagnosis be-
. Localized teatu res : fore blood culture report is available. (Blood culture is confirmatory ot septicemia, but it takes time and is
a) Pneumonia — Common in early onset sepsis. Presents with positive in about 60% 01 cases).
i) Tachypnoea D ComponentslParameters :
ii) Retractions 1. Total Leukocyte Count (TLC) -> < 5,000lmm’.
iii) Grunting 2. Absolute Neutrophil Count (ANC) —> Low count as per Manroe's charts (or term intents and
iv) Crepitations. led breath sounds. Mouzinho's chart for VLBW babies. (On an average ANC < 1800/mm3. is considered abnormal).
b) Meningitis — Common in late onset sepsis. Presents with - 3. Immature neutrOphit (Band cell) : Total neutrophil ratio -+ (I : T ratio) > 0.2 or > 20%.
4. MIcro—ESR —-) >15 mm in tst hour.
i) Fever
ii) Convulsions 5. C-reactive protein (CRP) ‘ > 1 mgldl (varies among ditierent laboratories for different methods
of estimation).
iii) Bulging anterior lontanelle
El Interpretation :
iv) Excessive cry
a) Considered positive. when 2 or more parameters are positive (out of the S).
v) Neck retraction (seen in ventriculitis). b) When initial screen is negative. but clinical suspicion ol sepsis is high. it should be repeated
asymptomatic. but may
c) Pyelonephritis — More common in preterm and male babies. Mostly alter 12 hours. Two consecutively negative sepsis screen excludes the diagnosis with
have — reasonable certainty.
i) Enlarged. palpable kidneys. c) Sensitivity and specificity are approximately 93% and 88% respectively.
ii) Poor weight gain inspite of adequate intake of leads. d) Negative predictive value is more than positive predictive value.
d Osteomyelitis and septic arthritis : N.B : For early onset sepsis. documentation 0! polymorphs in the neonatal gastric aspirate at birth
n...-
limitation of movements of
i) Signs of inflammation with redness. swelling. tenderness and ._
serves as a marker oi chorioamnionitis and it may be taken as one parameter of sepsis screen.
involved ioint or bone. 0. 15. Laboratory diagnosis of Neonatal Sepsis. “Pas" Sent]
arthritis. but osteomyelrtis can in—
ii) Hip. knee and wrist are commonly involved in septic
volve any bone. 0. 16. Marker of Neonatal Sepsis. [CNMC Sent]
. Features of complications : Ans : LABORATORY DIAGNOSIS OF NEONATAL SEPSIS
a) Shock - Neonatal sepsis is a clinical syndrome. characterized by signs and symptoms 01 infection with or
'
i) Cold extremities without accompanying bacteremia in the 1“ month of tile. Identification ol the pathogenic organism by
ii) Pale. grayish skin colour with mottling. culture of blood or any other body fluids is conlirmatory for sepsis. but culture takes time and even with
greatest efforts. positive report occurs in about 60%. Thus, for rapid results. lew indirect markers oi
iii) 1‘ ed CRT 2 3 sec. infection are studied collectively to guide antibiotic therapy. known as “Sepsis Screen“.
b) Sclerema — '
0 Sepsis Screen: 2 ol the following 5 parameters. if positive. is suggestive of sepsis -
l) Stretched out and shiny skin ' . l. TLC < 5.000(mm‘
. -
ii) Unpinchable skin tory 2. ANC < 1800imm‘ [Low count as per Manroe's chart forte rm babies and Mouzinho's chart tor
and legs. chest rs Involved last causrng respira
iii) Progress centripetally starting from face VLBW babies]
compromise. 3. IT ratio > 0.2 [Immature neutrophil (Band cell) :Total neutrophil]
c) Necrotlslng enterocolities - 4. Micro ESR > 15mmlt‘I hour
i) Abdominal distension 5. cap >1mgidl.
ii) Bilious vomiting
52 QUEST : PAEDlATRlCS
NEONATOLOGY E] Chapter-4 53
D General Investigations :
1. Blood
_ culture
_ - Blood
. for culture
. _ and sen srttvrty
" ' is ' the gold standard invest' t' 1. Antimicrobial therapy : Antimicrobial therapy is the mainstay of management of neonatal sepsis.
confirmation of sepsrs and for gurdrng appropriate sensitiv
e antibiotic therapy 9:331:03: for D indication -
should always be sent before starting antibiotictherapy. . ure a) For early onset sepsis -+ (EOS)
2)) gonventronal methods oi culture usually takes
7-10 days belore final result comes liquor.
ewer methods i) 3 3 risk factors for E08 (Risk lactors include LBW, preterm. Meconium stained
and greater yield. (BACTEC and BACT/ALERT ) give ‘ taster results (Within
- - 12-24 hours)
' Prolonged rupture of membranes, Prolonged labour, Birth asphyxia etc.)
2. Blood counts - E) 2 2 risk factors + Positive septic screen.
TLC < 5000.
may be - ANC < 1800 and l : T > 0.2 are included
' 'In sepsrs
' screen. Apart from that. there iii) Foul smelling liquor.
iv) Strong clinical suspicion.
a) l Hbié b) For LOS -
b) l Platelet count i) Positive sepsis screen
c) Dohle bodies and Toxic granules in neutrophils. ii) Strong clinical suspicion.
3. Acute Phase Reactants - 0 Choice — Depends on local sensitivity pattern for each hOSpiial setting, presence of meningitis
a) CFiP< — most commonly used marker and included in se sis scre en, and etiological agent. '
' '
readily available. p as It Is cheap and a) Commonly used antibiotics are
b) Micro-ESE — Can be done bedside and is also included in sepsis screen. - Ampicillin + Gentamicin (ist line)
c) Procalcr‘tonr'n — More reliable marker of sepsis compared to CRP, having a sensitivity and - Ceiotaxime + Amikacin (2nd line)
specificrty of around 100%. . - Piperacillin — TazobactamlMerOpenem/Ciprofloxacin + Amikacin (3rd line)
d) Cytokr'nes — e.g. lL-6. b) Meningitis —) Antibiotics with good CSF penetration are used in meningitisOS (eg. 3rd
generation cephaiospon'ns, cefuroxime, Mempenem)
- SpecificJLocaiized investigations :
c) For suspected Staphylococcal (MRSA) infection —> Vancomycin
1. For pneumonia — Chest X-ray detects any pneumonic consolidation and also excludes other
d) For suspected Pseudomonas infection —+ Piperacillin — Tazobactam.
DID (like - RDS).
0 Change — Antibiotics are usually changed, if -
2. For Meningitis T Lumbar Puncture (LP) and neuro imaging should be done in all cases of
a) No response seen after 48 hrs, or
Late Onset Sepsrs (LOS).
b) After receipt of sensitivity report (according to report).
a) LP : 0 CSF cytology with cell count > 30 cellslmm3
0 Duration-
- Cell type — > 60% polymorphs
a) Presumed/clinical sepsis (sereen and culture negative) -+ 5-7 days.
32%;: - Glucose - < 50% of Blood glucose b) Screen + ve. but culture — ve -+ 7-10 days
0 Protein - > 150 mg/dl (Term) or > 180 mg/dl (preterm) c) Culture + ve (No meningitis) —i 14 days
- Culture — rarely + ve. if) Meningitis -+ 21 days
b) Neuro imaging : USG of Brain is MC investigation done in LOS; MRI brain indicated in e) Ventriculitis/Arthritis ., 4-6 wks.
proved Clo meningitis later to detect any brain damage. 2. Supportive therapy :
3. For UTllelonephritis — a) Maintenance of temperature (nursed in warmer).
a) Urine culture and WE b) Moist 01 (for respiratory distress ordesaturation).
b) USG —- KUB region. c) intravenous Fluid with maintenance of nomioglycemia
4. For septic arthritis/osteornyelitis - X-ray of concerned joint or bone is done. d) Volume expansion and lnotropes for shock.
- Supportive investigations : (To detect complication/organ damage) e) Anticonvulsants (for convulsion)
1. LFT - tor jaundice 0 Respiratory Support (with CPAP or ventilator), if needed.
9) Blood products .- Transfusion oi Packed cells. FFP and Platelets. as and when required.
2. RH - urea/oreatinine
Newer therapiesllmmunothera py: Used in reiractory cases.
3. Glucose (both hypo and hyperglycemia can occur) 9°
a) Exchange Transfusion
4. PT, aP‘iT- for 010.
b) Intravenous immunoglobulin
0. 17. Management 0! Neonatal Sepsis. [BSMC-Q‘" Sam) c) G-CSFIGM-CSF.
Ans : MANAGEMENT OF NEONATAL SEPSIS 0. 18. Late onset of Neonatal Sepsis. [2017)
antibiotic therapy with optimal
Earty recognition, prompt administration of efie dive and ‘ appropriate
e therapy improve intact survival rate of neonates wrth sepsis. Ans : LATE ONSET SEPSIS
supportiv
NEONATOLOGY D Chapter-4 55
0) Hypothermia
Neonatal sepsis is a clinical syndrome. characterised by signs and symptoms of infection with or with-
72 hours of life, d) Polycythemia
out accompanying bacteremia in the 1" month of life. When onset of symptoms occur after
4. Decreased production/Miscellaneous:
it is known as Late Onset Sepsis (L05). amino 5
a) lEM : Defects in carbohydrate metabolism (Glycogen Storage Disease), Delects indetect).
U E‘iOIOQ)’ 1 Source 0' infection in L03 is either nosocomial (hospital-acquired) 0’ community acquired. acid metabolism (organic acidemias). Defects in fat metabolism (Fatty acid
oxidation
- Organisms :
b) EHdOCfiDOPaihY 1 Adrenal insufficiency, Glucagon deficiency, Congenital hYPOPitUilarism-
i) Gram negative (about 2/3“ cases) - Like Klebsiella. E.Coli. Pseudomonas. Acenatobacler c) Exchange transfusion with heparinized blood.
etc. mostly subtle and non-spa»
coagulase negative Sta- 0 Clinical Features : Symptoms of hypoglycemia in neonates are
it) Gram positive (about 113'‘1 cases) — Like Staphylococcus aureous. ciitirci. Majority of the hypoglyce mic babies may remain totally asymptom atic. Babies may present
phyioooocus etc. w: -
0 Risk factors: a) lrritability of the CNS. like jitteriness. tremors, convulsions
a) For Hospital —acquired: [1) Depression of CNS, like apathy. stupor, coma.
i) LBW, Prematurity. c) Non-specific signs, like reiusal to feed. apnoea. cyanosis. hypothermia.
ii) NlCU admission, d) Tachycardia and sweating (ieatu res of Ted sympathetic activity)
iii) Mechanical Ventilation,
[:1 Diagnosis :
iv) Invasive procedures (9.9. Exchange Transfusion) a) Bedside reagent strips (Glucose oxidase) : not reliable. useful for screening.
v) Administration of IV fluid. b) Laboratory diagnosis : all hypoglycemias diagnos
ed at bedside are to be confirmed by lab value.
For community — acquired : Screening I Prevention : The importance of screening blood glucose levels in susceptible new-
V—I’
b
0 Poor hygiene tissue
boms lies in the fact that even without producing symptoms, hypoglycemia can damage brain
'
causing longtenn morbidities. Screening is recommended in :
ii) Poor cord care.
1. LBW (< 2kg)
iii) Bottle feeding.
2, Preterm (< 35 wks)
iv) Prelacteai feeds. 3. SGA
is the most common clinical presentation).
Cl Clinical features : See :0. 13 (Meningitis 4, LGA
L'J Laboratory diagnosis: See 0. 15. 16. _
5. IBM
D Management: See 0. 17.
sin Sam, CNMC-st‘ Sem] (Mes, 6- Rh incomnatibility
a. 19 :Hypogiycemia in neonate. [2014} (MEMO, 9» Sem} [Mes- 7. Any sick neonate on WP or Total Parenteral Nutrition.
MaIda-2015] on IVFITPN are
- T me schedule of screening : 2. 6, 12, 24. 48 and 72 hrs. after birth. Sick neonates
MI _ n [as is termed as usually screened 6-8 hrly.
Ans :HYPOGLYCEMIA lN NEONATE
) '" "9° a El Treatment:
Blood glucose value of < 40 “19"" (plasma glucose <45 mg
hypoglycemia.
l 36 < 40 mgldl I < GlFl = Glucose Infusion Rate >
[J Etiology:
r y
1. Hyperlnsulinism : - .
a) lnfantof Diabetic mother, LGA infants Symptomatic without Seizures
b) Erythroblastosis fetalis. seizures . y
.
c) Beckwith —- lMedemann syndrome. Bolus of 2,“n of _ [us of 5—ml’kg oi
Ire 20.40 mgldl I [*8G < 20 mg/dll
d) insulin producing tumors (Nesidioblastoma) ' 10% Dextrose 1 0% Dextrose E
CB gene)
9) Genetic (mutation in ABC i
2. Decreased sto re/inta ke: rial of oral feeds Glucose infusion/NF with GlR of ea mglkgim_inl
_
a) Prematurity CBG after 30 Minutes (Monitor every 30 mins. I till BG >40. then 4 hrly) g.
.
b) IUGR/SGA TGIR by 2mgikglmin, if BG < 40 on subsequent
3, increased utilization = Continue feeding/Monitor BG < 40 recordings upto 12mglkglmin.
a) Birth asphyxia
' - _\
b) Sepsis
NEONATOLOGY D Chapter-4
' If B migsev
thost: < gfiomtr
' hgfiggt: gimjgstg/rnrn.
' the conditio
' ' n is known as Resistant hypog needs exclusion of other potentially severe eti-
lycemia. In D Differential diagnosis : Diagnosis of TTN usually
a) Hydroconisone ologies of respiratory distress appearing in 1’1 6 hours.
b) Glucagon 1. PneumoniaiEOS
c) Diazoxide 2. Respiratory Distress Syndrome (R08)
d) Octreotide 3. Meconium Aspiration
4. Congenital cyanotic heart disease
0. 20. Management of Hypoglycemia in newborn. [SSKM-2 5. Perinatal Asphyxia.
016]
Ans : MANAGEMENT OF HYPOGLYCEMIA D Investigations :
See Diagnosis and Treatment part of O. No. 19. 1. Sepsis Screen — to rule out E08.
engorgement of periarterial
2. CXFl -— Prominent perihilar streaking (Sunburst Pattern) due to
O. 21. Transient Tachypnoea of newborn. [201 O} lymphatics is seen in TTN.
Ans : TRANSIENT TACHYPNEA OF NEWBORN 0 Treatment : Only supportive treatment is nedded. as the disease is self-limiting.
Transient Tachypnoea of Newborn (Tl'N is a beni n ' '' -' - . 1. Moist 0: inhalation by head box usually suffices.
at late preterm or term gestation. ) 9 I mg Condition which affects Infants born
s Self-Ill“ t
to improve lung
2. More severe cases may need CPAP (Continuous Positive Airway Pressure)
0 Pathophyslology : In utero. fetal lungs are usually fluid-filled which is required for recruitment.
nonnal lung-
growth. (Secretory mode) 3. NF or Nasogastric tube feeding may be required initially.
i 4. IV antibiotics may be started in dubious cases and stopped after 48-72 hours. once symptoms
At birth. lungs must switch from secretory mode of in utero to an absorptive resolve and sepsis screen is negative.
mode. (Absorption of fluids are required for normal breathing and gas exchange).
0. 22. Hemorrhagic disease of newborn. [2014, 201 f-Suppie. MCK-8" Sem]
l
During normal labour and normal vaginal delivery. 0. 23. C/F and Wm of Heamorrhagic disease of newborn. [2008-Suppie]
1 3.: a. 24. Classical hemorrhagic disorder of newborn. [SSKM-2016]

Surge in. Glucocorticoids and cat- Fluid squeezes out from lungs Ans : HEMORRHAGIC DISEASE 0F NEWBORN
echolamtnes during passage through birth
Hemorrhagic manifestations in a newborn baby due to deficiency of Vitamin K is known as hemor-
t canal
rhagic disease of newborn (HDN).
Helps in absorption of fluids through Cl Pathogenesis : Wamin K is required for the synthesis of coagulation factors It . VII, 1% and X in liver.
capillaries and lymphatics
Minimal transplacental Limited hepatic
D Disruption or delay in clearance of lung fluids causes transient pulmonary edema that characte rises passage storage
| IN (Wet lung syndrome) Aggravating factors 3‘ l
Cl Risk factors : 9.9. Maternal drug intake. mm“ Newborns are physiologtcatly Low content in
Malabsorption. aggravates deficient in vlt. K. Breast milk
1. Birth by cesarean section l
cholestasis
2. Precipitated labour
Detective carboxylation of glutamic acid
3. Maternal diabetes. residues in Vit K dependent clotting factors
0 Clinical features : (ll. VII, IX. X)
i .
1. Affected term or late pretram infants usually present within 1‘1 6 hours of life.
impaired activation of clotting factors
2. Tachypnoea (HR of 60-120lmin) is the consistent sign.
retrac- l
3. May or may not be associated with signs of mild to moderate respiratory distress (like Bleeding manifestations.
'
tions, grunting. nasal flaring etc.).
at FiO, < 0.4.
4. Occasionally. mild cyanosls may occur. which responds to supplemental 02 ct Types :
tion. (there may also be pushed
5. Increased antero posterior diameter of chest due to hyperinfla
1. Early HDN : Risk factor is maternal intake of wartarin, anticonvulsa “t 5 - Phenobar-
(Phenvtom.
down liver and spleen).
bitone). lNH. Rifampicin etc.
6. Air entry is usually good.
cases.
7. Signs usually resolve by 12-24 hours in mild cases and within 72 hours in severe
NEONATOLOGY Cl Chapter-4 59
l", if the facility promotes breast JI

Presentation : Life-threatening hemorrhagic manifestations are seen in-utero or within 24 0 Certification : A hospital is certified as “Baby Friendly Hospita
hours of life, like — concealed hemorrhages inside cranium, thorax or abdomen.
feeding maintaining all the 10 steps well.
2. Classical HDN : task forces, if all the criteria are met
' Certification is done by the national and slate BFHI
- Most common type of HDN. properly.
- Occurs due to physiological Wt. K deficiency. 0 The Ten Steps in BFHI :
- Aggravated by exclusive breast feeding. icated to all health care staff.
I. Have a written breast feeding policy that is routinely commun
Presentation : Commonly during 2nd or 3rd day of life (upto 1-7 days), there is -
2. Train all health care staff in skills necessary to implement this policy.
Umbilical stump bleecfing, breast feeding.
3. Inform all pregnant women about the benefits and managementof
Nasal bleeding Not life threatening
4. Help mothers initiate breast feeding within an hour of birth.
GI bleeding etc.
5. Show mothers how to breast feed and how to maintain lactation even if they are separated
3. Late HDN : Risk factors include — from their infants.
a) Chronic diarrhoea, 6. Give newborn infants no food or drink other than breast milk. unless medically indicated.
b) Malabsorption,
7. Practise rooming-in and mothers and infants to remain together 24 hours a day.
c) Cholestasis.
8. Encourage breast feeding on demand.
d) Prolonged administration of broad-spectrum antibiotics etc.
9. Give no artificial teats or pacifiers to breast-feeding infants.
Presentation : Presents after 15‘ week of life (2-16 weeks) with life-threatening bleeding mani-
Ieslations (intracranial bleed). but bleeding may occur from any site (skin. GIT etc). Mortality
1 0. Foster the establishment of breast-feeding support groups and refer mothers to them on
risk is around 20%.
discharge from the hospital or clinic.
0 Contact points where mothers can be counselled :
D Diagnosis :
3) During antenatal visits
1. Infants do not appear cfinically ill or toxic.
b) Delivery room/operation theatre
2 Coagulation Profile:
c) Primary immunization sessions.
a) Bleerfing Time - Normal
b) Clotting Time — Prolonged 0. 2E. Physiological reflexes in facfogenesis. {Semester-2016]
c) Prothrombin Time — Prolonged Ans: PHYSIOLOGICAL REFLEXES IN LACTOGENESIS
d) aPTT — Prolonged (may be normal initially. as F VII has the lowest half life Lactogenesis or milk production depends on 2 physiological reflexes, mediated by 2 separate
and it is the
earliest clotting factor to decline resulting in ‘IPT and normal aPTT). hormones, namely—
3. PIVKA (Protein induced in vit. K absence) -+ Elevated. 1. Prolactin Reflex and
Prophylaxis : All newborns born in hospital settings should be given 0.5-1 2. Oxytocin Reflex.
mg of vitamin K
J"
intramuscularfy at birth or within 24 hours of life (0.5 mg for newborns < 1000
gms) 0 Anatomy of Breast : Before discussing prolactin and oxytccin reflexes. anatomy of the breast
Treatment: Vitamin K has 3 forms according to the source. K1 (plant source) tissue. including glands and ducts. should be known well.
and K2 (animal source)
are safe in newborns. but K: (synthetic) is potentially toxic.
1. Early HDN - Precfisposed infants should receive vit KI(2 mg) at birth.
Myoepithelial cells ~0xytocin
- Delivery preferably by LUCS.
2. Classical HDN - Vat Kl - 1 to 2 mg i.vfr.m. causes dramatic response. Milk-secreting cells — Prolactin
-
3. Late HON — Predisposed infants should receive vit K1 (1 mg) Lm. monthly. till underlying
disorder . Tub U les I D UCtSI
tS controlled. Milk secreting glands
4. Life-threafemhg hemorrhage — FFP transfusion along with vit. K injection. (Enlarged view) Lactiferous sinus (Milk collects here)
5. Whole Blood/P880 Transfusion - For large amount of bleeding (> 20% blood Areola
loss).
.i-
0. 25. Baby Friendly Hospital Initiative. MPG-2016] Nipple

.- .__..L..J—J.L—i‘-;.‘:
Ans : BABY FRIENDLY HOSPITAL INITIATIVE

Lactilerous ducts
Baby Friendly Hospital Initiative (BFHI) is a global programme organised by
UNICEF. It was launched
in 1992 and adepted by India in 1993. After the Introduction
of BFHI. exclusive demand feeding is
accepted as the only mode for early lnla nt feeding and exclusi
_
ve breast feeding ls recommended for 15‘

.LHJ'. ..
6 months of life. -
‘\‘\_
CamScanncr
T
GO QUEST : PAEDIATRICS Chapter—4 61
NEONATOLOGY D
Ct Prolactln Reflex : (Also known as Milk—s

ecretion reflex) Ans : TYPES OF BREAST MILK if d‘ and also
.
- Afferent pathway : Baby sucks at breast The composition of breast milk varies according to the stages of lactation, phases 0 etc "19 ossibie
l gestational age of the newborn baby (is. Tenn/Praia rm). to meet the needs of the baby as ar as p -
Sensory impulse travels to anterior pituitary Therefore. breast milk is not only species specific, it is baby specrfrc.
l A. According to the stages of lactation : _
Proiactin hormone produced. l. Colostrum : It is the golden-yellow milk secreted during the first 3 days after delivery.
.
- Efferent pathway : Prolactin passes through blood - Characters : Yellow and thick. secreted in small quantities.
l c Advantage :
a) Rich in abtibodies and W805. - - .. u .
Promotes milk secretion from milk-secreting cells.
- Enhancing factors : b) Loaded with secretory lgAs. which confers mucosa! immunity (works like 1 vaccine
shot" for the baby).
a) Sucking (early and frequent sucking acts as good
stimulus) c) Higher protein content.
b) Expression of milk
- It should never be discarded. as it is indeed the ideal 15‘ meal for the baby.
c) Complete emptying of breast
2. Transitional milk : It is secreted during the following 2 weeks. The immunoglobulin and protein
d) Night feeds (as prolactin reflex is more active at night) content decreases while the fat and sugar content increases.
- Hindering factors : 3. Mature milk : It follows transitional milk. It is thinner and watery. but contains all the nutrients
a) Incorrect positioning during feeding essential for optimal growth of the baby.
b) Painful breast B. According to the phase of feeding :
c) Prelacteal feedsop feeding. 1. Foremilk : It is the milk secreted at the start of a feed from a particular breast.
0 Oxytocin Fteflex : (Also known as Milk-election reflex). ° Character: Watery : Rich in protein. sugar. vitamins and minerals.
- Afferent pathway : Sucking of the baby ° Advantage : High water and sugar content alleviates baby's thurst and hunger quickly and
calms the baby.
i 2. Hindmilk : It is released towards the end of a feed.
Stimulation of nerve endings
l 0 Character: Rich in fat content.
Sensory impulse travels to posterior pituitary 0 Advantage :
l a) Provide more energy, as fat is the main source of energy (9 kcal/gm. whereas protein and
Oxytocin production. carbohydrate gives 4 kcal/gm energy).
0 Efferent pathway: Oxytocin released in blood b) Helps in adequate postnatal weight gain. 3.
1 c) Prevents frequent watery stools with perianal excoriation (seen in babies fed with foremilk
Contraction of myoepithelial cells around glands only).
l > For optimum growth. the baby needs both foremilk as well as hindmilk. Thus. one breast
Ejection of milk from the glands into the Iactiferous sinuses through tubules. should be completely emptied before the baby is put on opposite breast.
- Enhancing factors : C. According to Baby's GA :
a) Loving thought of the baby by mother t. Preterm milk : The milk of a mother. who delivers prematurely. contains all the nutrients in
adequate quantity needed by her preterm infant.
b) Sound of baby
- Character (Compared with term milk) :
c) Sight of baby
a) Higher calories
d) Relaxed, comfortable and confident mother.
b) Higher fat. protein and sodium
0 Hindering factors: c) Lower lactose. calcium and phosphorus.
a) Worry . Advantage: Meets the need for extra protein. fat and calorie
in preterm babies for adequate
b) Stress catch up growth. Thus. negates the need for extraneous sources of
protein and calorie (Preterm
c) Pain formula. HMF etc.) '
d) Doubt/low confidence. 2. Term milk : Milk of a mother who delivers a term baby after 37 con'pleted weeks
is known as
term milk. .
0. 27. Types of breast milk with advantages. [2016}
- DRIP MILK: Milk that drips from the opposite breast during breast-feedin ‘ - -
O. 28. Composition of colostrum, fore milk, hind milk and preterm milk. [MRS-9“ Semi It is mainly foremilk with relatively low energy and fat content. Q Is calleddnp milk.
‘-‘a
NEONATOLOGY E] Chapter-4 63
Cl. 29. Colostrum. flPGMEFl-S“ Sem] 2. Physiological :

Ans : COLOSTRUM a) Breast milk is the sweetest milk with high lactose content in milk.
Colostrum is the thick. golden-yellow milk. secreted from breast during the last few days before deliv- b) Protein in breast milk is easily digestible.
ery and upto 3 days after delivery. Then. it is gradually trasitioned to mature milk over the next 2 weeks. As c) Lipids are rich in essential fatty acids, poly unsaturated fatty acids (PUFA) and phospho
it is very much important for the baby with several benefits. it is also termed as “Liquid Gold". lipids.
0 Characters : d) It supplies various enzymes. like amylase. lipase. oxidase etc.
1. Small in quantity. but enormous in quality. c) it also contains several growth factors.
2. Thicker than mature breast milk. 3. Biochemical:
3. Colour is yellow or golden yellow. a) Protein is mostly whey protein (80%) rich in a-lactalbumin (precursor of serotonin) and
Cl Contents : Iactolerrin (helps in iron absorption). Rest is casein (20%).
1. Higher protein content compared to mature milk. b) Allergens like a-casein and Iactoglobulin are absent in breast milk.
2. Lower carbohydrate and fat content. c) Ca : P is more than 2. which helps in calcium absorption.
3. Sodium - higher d) Solute load is low due to l protein and certain minerals.
4. Potassium — lower 4. Microbiological :
5. Rich in antibodies (lgG. lgA). cytokines and W805. a) Lactolern'n is bacterioslatic and inhibits E. coli.
'3 Advantages : b) PABA (Para amino benzoic acid) protects against malaria.
1. Colos is the ideal 'first meal" for the baby due to its high protein content. 5. Immunological :
2 it is often called "white blood" because it provides large amounts of living cells (Lymphocytes a) Supplies passive immunity with WBCs. lysozymes. complements and various antibodies.
and Macrophages similar to those in blood) which will defend against infections.
(b) slgA provides mucosal protection to the GI tract and respiratory tract.
3. it is considered as baby's ‘first vaccine shot". as it is loaded with large amounts of Secretory
6. Psychological :
lgAs (slgA). which confers mucosal immunity to the GI mucosa.
(a) Promotes mother-infant bonding.
4. Colostrum has a laxative effect. which _.,
(b) Helps in brain development and improves l0.
a) Helps in bowel movement and early passage of meconium in the baby.
B. Advantages to the mother :
b) Helps in clearing bilirubin —> les enterohepatic circulation —) prevents neonatal jaundice
It helps to decrease PPH.
mmPyh’r‘
exaggeration.
5. it has an important role in protecting GI tract. Newborn's intestines are very permeable. Colos- Helps in involution of uterus by virtue of oxytocin.
trum seals the 'holes' by painting the GI tract with a barrier. which prevents most foreign pro- Bums off extra fat accumulated during pregnancy.
teins from penetrating the gut and possibly sensitizing the baby to an allergy. Decreases incidence of breast and ovarian cancer.
6. Colostrum is proving to have neuroprotecting effects which may prevent Alzhimer‘s disease in . Helps in contraception through lactational amenorrhoea.
future (under research).
. It is convenient for the mother to breast feed. as there is no need to
0 Breaking the myth : carry or sterilize various
utensils for top feeding.
There are several myths regarding feeding of colostrum which needs to be broken by health care 0. Advantages to family and society :
workers through information. education and communication —
1. Breastfeeding is economical. as it saves the cost of buying packaged
a) Many think colostrum is inadequate in quantity during the first few days of life and indulges in milk. which are rather
costy.
giving top feeding and prelacteal feeds. It needs to be emphasized that newborn needs very
2. It prevents various infections. and thus reduces health care ex penses
little fluid during early days and colostrum is sufficient to meet that need. of the family and of the
society.
b) Many discard this yellow fluid from mothers breast showing concerns about hygiene. But. colostrum
is rather preventive against all infectious agents that may attack the baby in neonatal period. O. 31. Causes of failure of breast feeding. {2009]
0. 30. Advantages of breast feeding. [Zoos-Supplemen tary} [SUMO-2016] Ans .- CAUSES OF‘FAILUHE or assist FEEDING
‘ Failure to breastfeed property and adequately may be due to
Ans : ADVANTAGES OF BREAST FEEDIN'G decreased secretion or action of prolactin
(True Lactational failure). but it occurs more c ommonly due to the
Exclusive breast feeding during the first 6 months of life have numerous advantages - psychosocial causes (which are pre-
venlable in most of the cases).
A. Advantages to the baby : A. Causes of True Lactational Failure: Decrease d
lactation.“ ed milk secretion) is most commonly
1. Physical: Breast milk is supplied at an optimum fluidity and warmth. found in hormonal imbalance (l Prolactin). but overall incrdence
of true lactational failure is very
very low. Causes are —
NEONATOLOGY D Chapter - 4
t. HypOpItuItarismlGH deficiency : Impaired secretion of Prolactin and

Growth Hormone (GH)
from anterior pituitary cause Iactational failure. 3. Colour: Bluish; may be bluish gray or blackish blue also.
always
2. Sheehan's Syndrome Postpartum hypopituitan‘sm due to ischemic necrosis from hypovolemi 4. Colour gradually fades as the child grows. lt normally disappears by 2-3 years and almost
a by puberty.
dunng and after child brrth rs known as Sheehan‘s Syndrome and causes failure of lactation.
3. Smoking/Nicotine intake : Nicotine delays the suckling induced release of prolactin Cl Pathogenesis : Mongolian spot is a congenital developmental condition seen in Asian. Black and
therefore, lactation.
and Hispanic children. There exists no relation with Mongolism or Down Syndrome.
‘
0 Metanocytes (melanin-containing cells) are usually located in the epidermis, rte. most superfl-
4. Breast hypoplasla : Inadequate glandular tissue of the breasts is another cause of true
cial layer of skin. During their migration from the neural crest to the epidermis during embryonic
lactational failure.
development. entrapment of melanocytes in the lower half to two-thirds of the dermis results In
5. Obesity : Can result in Iactational failure due to inhibition of prolactin secretion. development of Mongolian Spots.
6. Drugs : Drugs that stimulates 02 receptor suppresses prolactin release by dopaminergic 0 Differential diagnosis : They may be mistaken for bruises and may raise concerns about child
pathway: abuse.
a) 02 receptor agonist: Bromocn'ptine. Pergolide. Ct Treatment: No treatment is required. as it is a benign condition with no malignant potential.
b) Indirect 02 receptor activator: Amphetamines
0. 33. Congenital Diaphragmatic Hernia. {MEMO-8" Sent]
B. Psychosocial causes : These causes are more frequent and are easily preventable with
Ans : CONGENITAL DIAPHRAGMATIC HERNIA
adequate maternal counselling.
Congenital diaphragmatic Hernia (CDH) is associated with congenital defects in diaphragm and
1. Nipple confusion : It occurs when baby is given water. artificial milk or even expressed breast
herniation of abdominal contents into the thorax.
milk through a bottle. helshe get used to the nipple of the bottle which has a wide opening. So. _
the baby doesn't make adequate effort to suckle and empty the breast. This is known as 'nipple D Site: Left sided hernias are more common than right side and posterior part (Foramen of Bochdalek)
confusion' and is the most common cause of breast feeding failure. is usually involved.
0 Incidence: 1 in 2000—5000 live births.
2. Supplementation with formula feeds : Mothers are always concerned about the adequacy of
breast mflk production. Thus, many a times. they supplement breast feeding with formula milk. O Pathology : Defect in diaphragm (MC. Lt. sided foramen of Bochdalek).
Baby gets satisfied with those feeds and loses interest in breast feeding. i
3. Inverted nipple : If not solved quickly, mother gets frustrated and gives up breast feeding. Hemiation of abdominal contents (like stomach and intestine) into thorax.
4. Sore nipple J u
These are all results of improper positioning and attachment. Hypoplasia of the ipsilateral lung. Mediastinal shift to opposite side.
5. Breast engorgement
6. Breast abscess l El Clinical features :
Causes pain during breastfeeding. 1. Babies with CDH usually present at birth with respiratory difficulty or gasping respiration or
inadequate spontaneous respiration.
Ir
. Mrlder cases may present later. but rarely after first week -of life.
Eventually may lead to failure of breast feeding.
. There is diminished air entry to the affected lung.
0’01t
7. Sickness of mother : Minor illnesses (9.9. fever. cough, coryza, diarrhoea), that are never . Occasionally. peristaltic sounds may be heard at ipsilateral chest.
contraindications for breast feeding. make the mother wary of transmitting the infection to her . Heart is displaced to opposite side with shifting of the apex beat.
baby. So, she stops feerfing the baby and makes herself vulnerable to failure of breast feeding. . Abdomen usually appears scaphoid or flat.
8. Stress : Unnecessary stress about breast feeding adequacy. baby’s health impairs milk secre- U D gnosis :
tion and ejection reflexes in mother. which may lead to Iactational failure. a) Prenatal diagnosis : Antenatal USG after 16 weeks of gestation can pick up CDH in the fetus.
Polyhydramnios is present in about 70% of cases. .
0. 32. Mongolian Spot. [201 1-Supplementary]
b) Postnatal diagnosis : In all babies with difficult resuscitation should undergo urgent skiagram
Ans : MONGOLIAN SPOT of chest.
congenital binh
Mongolian Spot. also known as Congenital Dermal Melanocytosis. is a benign. flat > CXR shows : - Mediastinal shift,
mark seen at birth in over 80% of Asian children. 0 Finding of bowel loops in hemithorax.
(lower back). But. these
D Sites : Most common location of mongofian spot is the lumbosacral area 0 Treatment :
location includes shoulder. face
are also seen at the buttocks, back (upper back) and flanks. Flare
' a) Prenatal : Antenatally diagnosed CDH can be repaired in-utero b fetal 3
and extremities. y urge W at around 26-28
weeks of gestation.
D Character:
b) Postnatal :
1. Flat patches of varying size and shape. 1. During resuscitation ' urgent
. . . endotracheal
. inlubation should be do he to s - .
2. May be more than 1 in number. trlatron (Bag and Tube ventrlatron or Mechanical ventilation). tart assrsted ven
CamScanncr
66 QUEST : PAEDIATRICS NEONATOLOGY L'J Chapter-4 67
2. Bag and Mask Ventilation is contraindicated. as it causes gaseous distension of bowel and 0. Metabolic causes :
respiratory difficulty worsens with more compression of lung. i. Hypothermia
3. Nasogastric Aspiration done frequently to decompress the distended bowel of air and fluids. 2. Hypoglycemia
4. Enteral feeding is contraindicated and baby is put on IV fluid and total parenteral nutrition. if 3. Metabolic acidosis (9.9., shock. late metabolic acidosis).
facilities are there. E. Chest wall abnormalities :
5. Surgical Repair should be done as eady as possible after correction of pH and blood gases. t. Asphyxiating Thoracic Dystrophy (hampers lung expansion).
0 Complication : 2. Werdnig-Hoffman disease (Spinal Muscular Atrophy type f ) :Weakness of respiratory muscles
1. Pulmonary hypertension. causes RD in this condition.
2. Pneumothorax (of opposite healthy lung). 0. 35. Respiratory Distress Syndrome. [BSMC-Q'" Sem]
CI Prognosis : Prognosis and outcome depends entirely on the degree of pulmonary hypoplasia. 0. 36. Hyaline Membrane Disease. {CNMC-B” Sent] [Mama-2016]
O. 34. Causes of Respiratory Distress in Newborn. [lPGMER-B‘" Semester] Ans : RDSIHMD
Ans : CAUSES OF RESPIRATORY DISTRESS IN NEWBORN Respiratory Distress Syndrome (RDS). formerly known as Hyaline Membrane Disease (HMD), is primarily
caused by inadequate pulmonary surfactant in preterm babies. But. surfactant may be deficient in term
Respiratory distress in the neonate is defined as the presence of tachypnoea (RR > (SO/min) along with
babies also due to various risk factors.
chest retractions and/or grunting. Other less common signs of respiratory distress include nasal flaring,
cyanosis etc. The causes for respiratory distress are as follows -- 0 Risk factors :
A. ReSpiratory causes : 1. Factors that affect lung development : (and subsequent surfactant production)
1. Respiratory Distress Syndrome (RDS) : Also known as Hyaline Membrane Disease (HMD). it a) Prematurity (Most important etiologic factor)
is a disease of the preterrns due to immaturity of the lungs. There is deficiency of the surfactant, b) Gestational diabetes in mother
which leads to alveolar collapse during expiration.
c) Genetic factors
Meccnium Aspiration Syndrome (MAS) : In-utero passage of meconium causes Meconium
2. Factors that impair surfactant production :
Stained Amniotic Fluid (MSAF), aspiration of which during delivery may cause respiratory dis-
tress in term babies, known as MAS. a) Perinatal Asphyxia
Pneumonia : Pneumonia is the common presentation of early onset sepsis and can involve b) Congenital surfactant deficiency (Mutation of genes producing surfactant proteins B and
C).
both term and preterm babies. D Pathogenesis : Pulmonary
. surfactant is composed of phospholip ' id
' (Lecrthln
‘ ' and hos hand ' I
Transient Tachypnoea of Newborn (TTN) : It is a benign condition affecting mostly term and Glycerol) and proteins. It decreases surface tension inside the alveoli to maintain
statifilily.p y
late preterm babies born by cesarean section. Delayed absorption of lung fluids is thought to be
responsible for lachypnoea and respiratory distress in these babies. ROS/HMO —-—-—+ lSurfactant
. Others : (Less common) l
T Surface tension inside alveoli
3) Persistent pulmonary hypertension (PPHN)
b) Pneumothorax Alveoli tends to collapse at end-expiration
c) Chronic Lung disease or Bronchopulmonary Dysplasia (8P0).
d) Tracheo-esophageal fistula l Gas exchange
e) Congenital Diaphragmatic Hernia i
f) Congenital Lobar Emphysema ——+|i-lypoxia (lPaOz), Acidosis (lpH), Tpafl
B. Cardiologlcal causes : l l
1. Left-to-right shunts : Like VSD. PDA etc. cause respiratory distress due to pulmonary edema LPulmonary Vasoconstriction I
associated with congestive heart failure.
Cyanotic heart diseases : Like transposition of great vessels (TGV). Hypoplastic Left Heart [fit to Lt shunts]
Syndrome (HU'tS) etc.
3. Heart failure : May also occur with cardiomyopathies and cardiac rhythm disorders. 0 Clinical Features : Preterm babies present with signs of respiratory
distress immediately after birth 3}"
or within the first 6 hours of life :
C. Neurological causes : .~
1. Tachypnoea(RR>601min)
1. Birth Asphyxia
2. Chest retractions (Interoostal, subcostal) gt
2. lntracranial hemorrhage 55
3. Grunting (expiratory)
3. Cerebral edema.
4. Cyanosis
l
Chaptor~4 69
68 QUEST : PAEDIATRICS NEONATOLOGY D
' I ‘-
_ Q .
to '.
5. 1 ed air entry rm with small or absent nip pfe.

, 5 mm in term babies.
d) Breast nodule : < 5 mm in prete
- Severity of respiratory distress is assessed by these 5 parameters according to Downe's
e) Genrtalta : is less pigmented and
score (score —+ O-lO). tum
. rnal spermatic ring and scro
i) Male : Both testes are at or ab ove exte
0 Diagnosis : Diagnosis is confirmed by chest may in a preterm baby with typical history. X—ray chest Testes ar e well descended in
term.
less rugosed in case of preterm babies.
shows any one of the following : b. sed in preterm
expo
separated and labia 'minora‘ clearly
a) Reticulogranular pattern ii) Female Labia majora are widely a In term he res.
letely covers labra minor
babies. whereas labia majora comp
b) Groundglass opacity with air bronchogram anterior ll3_rd of sole or no deep (393595 3‘
f) Sole creases : There is a single deep crease over .
c) White out lungs (severs R08).
. Deep sole crease s cover the entire sole In term babies.
all in preterm babies In
reliabl e for precis e estim ate of GA
0 Treatment : Neonates with R08 need to be cared in NICU under radiant warmer. Treatment modalities ' eters are more
are I 2. Neurological criteria : Neurological param
newborns.
sed on
1. IV Fluid : as per maintenance fluid requirement. as maturity progresses. Tone is asses
2. Moist Oz : through head box. 3) Muscle tone : lt progressively increases in utero
the basis of 3 parameters.
3. Monitoring of 0: saturation : by Pulse oximetry attitude. wh ereas preterms show frog-
i) Posture or attitude : Term babies have more flexed
4. Assessment of severity of respiratory distress : by Downe’s score, which gives 02 score to
like posture with extended limbs.
5 parameters. as described above.
a) Mild RDS : Score of 0-3 ii) Passive tone : Assessed by -
b) Moderate RDS : Score of 4-6 ' Scart sign : Elbow crosses midline in preterm babies.
c) Severe RDS : Score of 7-10. - Popliteal angle : Angle is more in preterms.
5. Respiratory Support : - Heel to ear test : Heel goes more close to ear in preterm.
a) Mild RDS : doesn't need any form of respiratory support except moist 02 inhalation. iii) Active tone : Assessed by —
b) Moderate RDS : these babies can be managed with CPAP (Continuous Positive Airway ' Arm Recoil : More instantaneous recoil in term babies.
Pressure), which is a non-invasive modality of support. A continuous distending pressure of 0 Traction response : When supine baby is lifted gently by holding at the hands. term
infants
4-7 cm — H20 is applied through nostrils to keep the alveoli open. This is an excellent modal- are able to maintain his head in line with the trunk. Whereas. there is head lag in preterms.
ity which minimizes ventilator-related infection, lung injury etc.
b) Joint mobility: Degree of flexion at ankle and wrist (square window) is limited in preterm babies
c) Severe RDS : these babies need mechanical ventilation (invasive modality).
because of relative stiffness of joints in early gestation.
6. Surfactant Replacement : Exogenous surfactant replacement is the treatment of choice in
moderate and severe RDS along with respiratory support. c) Neonatal reflexes : Each of the neonatal reflexes appear at a particular gestation. 80. GA can
be assessed on the basis of presence of different reflexes in the baby.
- Bovine or Porcine surfactant is given intratracheally through endotracheal tube.
eg. : Moro reflex - appears at 28-30 weeks. but complete adduction occurs after 38 vveeks.
0 Babies with moderate R08 are given surfactant by INSURE approach (tubation. SURfactant
replacement and Extubation to CPAP). - Pupillary reflex - (Light reflex) present after 30 weeks.
D Prevention : Administration of antenatal steroids (Betamethasone or Dexamethasone) to mothers - Rooting and coordinated sucking appears at 34 weeks.
in preterm labour (GA 2 24-34 weeks) accelerates lung maturity and surfactant production, within > Different scoring systems are available for accurate estimation of GA in newborns. Most widely
24 hours.
used scoring system is Modified Ballard Score which includes 6 physical criteria (as above) and s
neurological criteria (namely, posture. arm recoil, square window, scarf Sign. popliteal angle and
0. 37. Assessment of Gestational Age in newborn. [2012-Supple, Murshidabad-ZOIG}
heel-to—ear test).
Ans : ASSESSMENT OF GESTATIONAL AGE
- _
0. 38. Give a brief outline of the clinical features, diagnosis and treatment of m eco n 1'1"" 35p"a
‘<
of the
The clinical assessment of gestational age at birth by physical and neurological examination tion syndrome. [Haida-2016]
..
should be
baby is more reliable as compared to the methods of assessment of baby in-utero. Assessment
bar-n...
done at 24-48 hrs of life. a. 39. Meconium Aspiration Syndrome. [BSMC-2016]

1. Physical criteria : Helps to divide babies between term (2 37 completed weeks of gestation) and- Ans : MECONIUM ASPIRATION SYNDROME
pretenn (< 37 weeks). - . . term now-
'
tlgiloercnrgnrum ' t'ron S yndrome (MAS) rs
A sprra '
' an rmportanlcause of respiratory distress in
a) Skin : More smooth, transparent. red in preterm babies with visible veins over skin. Term babies
show rare veins, superficial peeling or cracking over the skin.
D Pathophysiology
. : Meconium Stained Amniotic Fluid (MSAF) occur sdueto -In-utero assa e f
b) Lanugo hair : Abundant in preterm babies. less in term counterparts. _ . . .
° - p .9 0
meconrum ph srol rcall in ost-tenn babre
c) Ear cartilage : Deficient in preterm. causing poor and delayed recoil. Cartilage
is well-formed in infection y og y p S and patholecally due to fetal distress (hypoxia) or
term babies.
NEONATOLOGY U Chapter—4 71
O. ’
t'
D Complications :
1. Air leaks (like pneumothorax)
2. PPHN
3. BPD
Postpartum Aspiration ln-utero gasping
0 Delivery room management of MSAF :
N. B : MAS is clinically a Baby born with MSAF
heterogenous disease I Meconium Aspiration j—fi i
with both ateleciasis and
Assess HR, Respiration and muscle tone
:ll‘rfulslzllypzlllg alltlgrf'rlallallfi l Airway obstruction I njrrggfiés
./ \
. ' HR < too/min. (or)
Complite lbrtial - HR>1OOImIn - . . .
. , o Apnea/GaSprng reprratrons.(or)
- Spontaneous resprratrons
0 Poor muscle tone
Ball-valve effect - Good muscle tone
l Non-vigorous baby
V/Q mismatch ‘ Vigorous baby ‘l'
l Endotracheal intubation l direct laryngoscopy
Air leaks _—_————: “fligjfcggggfa Routine care Intratracheal Suctioning of meconium
Proceed for resuscitation.

El Clinical Features : Respiratory distress appears within 24 hours of life (usually within 6 hrs) in term,
post-term and IUGFi babies, and without treatment. progresses rapidly to the point of respiratory O. 40. Apnea in newborn. [BSMC—ZOIG}
failure. Ans : APNEA
a) Signs of respiratory distress. like tachypnoea (RR > 60/min). relractions, grunting. cyanosis etc. Apnea in newborns is defined as cessation of respiration for > 20 seconds or shorter duration in presence
b) Amara-posterior diameter of chest may be 1‘ ed. of cyanosis or bradycardia.
c) Percussion note is variable (due to heterogenous nature of the disease). [3 Classification :
d) Bilateral wet sounds may be heard on auscultation. 1. Central apnea : When there is absent inspiratory efforts (40%).
e) Yellowish slain in umbilical cord. nails and generalised skin surface (Meconium stain). 2. Obstructive apnea : When inspiratory efforts persist in the presence of airway obstruction (10%).
0 Diagnosis : Diagnosis of MAS needs - 3. Mixed apnea : When airway obstruction precedes or follows central apnea (50%). l
i) H/O MSAF D Etiology:
ii) Onset of RD within 24 hours. 1. Apnea of Prematurity : Around 25% of babies with GA < 34 wks and almost all babies with GA
ifi) Other CIF suggestive of MAS < 28 wks develop apnea of prematurity. Onset is within 2-7 days of life and may continue upto 37
weeks postmenstrual age. -
iv) CXR : Bilateral hyperaeration due to obstructive emphysema and coarse nodular opacities due
to areas of atelectasis and consolidation. 2. Pulmonary causes : RDS, Pneumonia. Pulmonary hemorrhage etc-
v) Exclusion of other causes like sepsis by sepsis screen. 3. Neurologicall‘causes : Perinatal asphyxia, intracranial hemorrhage. seizures, Maternal
medications (like morphine or pethidine), meningitis etc.
Cl Treatment : MAS is the commonest life-threatening respiratory emergency in term babies. In the
absence of any definitive therapy, supportive treatment is all that can be given to infants with MAS. 4. Metabolic causes : Hypoglycemia, hypocalcemia etc.
a) Thermoneutral environment to prevent hypothermia. 5. Septicemia i
b) Maintenance of normoglycemia with appropriate lV Fluids. 6. Congenital malformations : Choanal atresia, TEF (Tracheo esophageal fistula) etc.
c) Moist 01 inhalation (through head-box) a Management:
d) Respiratory support : in the town of CPAP or Mechanical ventilation, according to severity of A. Monitoring : All premature babies < 34 wks gestation should be monitored at
leastduring the 1"
respiratory distress (assessed by Downe's score). week of life. I
e) Use of exogenous surfactant may be beneficial. as meconium causes surfactant deficiency. But, B. Investigations : All the infants, whether term or - _
- should under 0 n ' -
preterm, . 9 lo owing Investrga
the routine use is still controversial. trons attend episode of apnea:
1i
72 QUEST : PAEDIATRICS NEONATOLOGY U Chapter-4
. Sepsis screen (CBC. CRP. ESR)
wearers-
El Cllnlcal Slgnlflcance:
Electrolytes (Na. K. Ca)
1. Very large AF may be seen In :
Glucose
CXR a) Hypothyroidism (Congenital)
Cranial USG b) Trisomy Syndromes
. ABG. c) IUGR
C. Treatment: d) Rickets
1. Drugs : Drugs used to treat apnoea of prematurity are — cafleine citrate and aminophylline c) Osteogenesis irriperlecta.
(Methylxanthines).
2. Sunken tontanelle: Indicates dehydration
2. Nasal CPAP : Very uselul in case at obstructive and mixed apneas. as it helps to keep the
pressure. which is seen in —
upper airway open. 3. Bulged lontanelle : Indicates raised Intracranial.
3. Mechanical ventilation : Used tor apneas not responding to above modalities of treatment. a) Meningitis
4. Treatment of the underlying cause: in do secondary causes. b) lntracranial hemorrhage
D. Prophylaxis : All newborns < 1.25 kg or < 30 wks' GA should be given prophylactic caffeine till
c) Benign lntracranial Hypertension (Pseudoturnor Cerebri).
they attain 37 wks' maturity and are apnea-free for 7 days.
4. Very small or almost closed AF may be seen In : Craniosynostosis.
(NB. : Dose of caffeine citrate is 20 mg/kg (loading dose). followed by 5-7mglkglday once daily
Cl Physiological Signlflcance (Advantage) :
(maintenance dose”. canal.
1. It allows the skull to delonn during birth to ease its passage through the birth
0. 41. Anterior Fontanelle. [201 0-Supplementary] 2. It allows expansion of the brain after birth to help in brain growtl'i.
to the presence of
Ans : ANTERIOR FONTANELLE 3. Any rise in intracranial pressure can be temporarily alleviated in intents due
Anterior lontanelle (AF) is the largest ol the fontanelles and is placed at the junction ol the sagittal AF. which protects against T lCP-induoed brain injuries.
probe.
suture. coronal suture and frontal (metopic) suture. 4. AF gives a window to see the brain parenchyma and ventricles by means of ultrasound
to
Cl Shape : AF is demand-shaped with its comers extended into the respective sutures. Thus. more costly and deleterious investigations like CT and MRI are not needed routinely
newborn and inlants.
D Oblitention : AF is an unossified. membranous area between the skull bones (Frontal and Parietal
bone). It is the last lontanelle to be obliterated. It is completely closed at around 15’: to 2 years ol o. 42. Loose stools in newborn. [zoos-Supplementary]
age.
Ans : LOOSE STOOLS IN NEWBORN
CI Measurement : Clnioel examination oi newborn includes measurement of AF and its palpation.
Measurement is done as shown below : Newborn infants are physiologically very prone to develop loose stools. So. in most "pl the intents
presenting with loose stools. no intervention is needed and counselling and reassurance suffices.
1, —-———-—+ Frontal (Metopic) Suture A. Physiological causes : Exclusively breast fed infants usually tend to pass softer and more tre-
quent stools than babies led on cow’s milk or formula milk due to —
' (a) lrontal bone i) Higher lactose content and
(L) frontal bone
ii) Lower casein.
................
AF . Co ronalSutu re 1. Transltlonal stools : During third and lourth day of Iile. neonates often pass semi-loose, green
ish yellow stools in increased frequency due to change in breast milk contents (colostrum to
D C - transitional milk). This condition is known as 'transltlonal stools'. It settles down spontane-
(L) parietal (a) parietal bone ously within next 2448 hours.
2. Gastrooollc reflex : Many babies pass loose stools while being fed or soon alter tearing due to
exaggerated gastrooolic rellex. It may persist lor 1-2 weeks.
8. Pathological causes : Change in baby's established bowel pattern towards increase hequency
and looseness should be taken seriously. Other markers for pathological causes include _
Sagitlal Suture I) Inadequate weight gain
ii) Oliguria
> A.B.CandDarethernidpointsolthe4armsolthedirnond.AFismeasuredas—ACcraD iii) Poor looting
cm(AC=DistanoebetweenAandC.BD=DistanoebetweenBendD).
10
NEONATOLOGY D Chapter-4 75
CI Treatment :
iv) Perianal excoriation
v) Blood and mucus in steel. [ Neonate with seizureJ
water in higher
s ied only on ioremilk gets only lactose and
1. Improper feeding technique: Babie may present with loose stools,
se oi protein and let oi hind milk. They . Secure airway. breathing. circulation and temperature
concentration in the expen s this pos-
t gain. Proper feeding history points toward Start 02 (it seizures continue)
perianai excoriation and inadequate weigh 0
corrects the proble m. Secure IV access and send routine investigations
sibility and correction of feeding technique -
may be poor 1
ion : Iniecti ve dianh oea is more common in babies ted by bottle. There
2. Infect They should be treated as sepsis Babies at risk of I Measure CBG| a I 8G <40 mg/dl I -—-) 10% Dextrose @
and blood/ mucus in stools as presen tation.
feeding. oliguria \
Hypocaicemia J, .a 2 5 milk
with parenteral antibiotics.
a) VLBW (< 1-5 kg) so. > 40 mg/di t g
3. Other rare causes : b) Severe birth asphyxia lseizure (4.) Seizure controlled
a) Congenital thyrotoxicosis. (Specially iorbabies l
c) Infant of diabetic mother 10% calcium gluconate @
b) Salt-losing variety of CAH.
at risk for having Start IVF with GIR
2 mn (Bolus) hypocalcemia) 6 mglkgimin
haridase and enterokinase deficiency).
c) Malabsorption Syndromes (9.9. disacc l Seizure (+)
cline, laxatives).
d) Maternal drugs (e.g. ampicillin, tetracy Seizure controlled lnj. Phenobarbitone @ 20mg/kg -+ Maintain with 3—5 mglkg/day
res. MRS, CNMC-2016, IPGMER-2015] l (loading dose)
O. 43. Management of neonatal seizu
SEIZURES Measure Calcium l Seizure (t)
Ans : MANAGEMENT OF NEONATAL J . N _ Repeat phenobarbitone 010 mglkg
ioural or autonomic
ion in neurologic function. 9.9. motor. behav
Seizure is defined as a paroxysmal alterat 50% of all seizur es). l Calcium (N) Calcrum for 2 doses. (Total —+ 40 mgfkg)
e is subtle seizur es (about
function. Commonest type oi neonatal seizur l i l Seizure (+)
seizure are —
0 Etiologies : Common causes of neonatal Bmnlday of 4mllkglday
10% Calcium of 10% Cal- lnj. Phenytoi n G 20 mg/kg '4' Maintain With 3'5 mglltglday
(loading dose)
1. Perinatal asphyxia (MC) .
gluconate x 3 cium glucon-
2. Metabolic causes: days ate it 3 days 1' Seizure M
a) Hypoglycemia Repeat Phenytoin @ 10 mgfkg
fort dose.
b) Hypocalcemia
iv Seizure (+)
c) Hypomagnesemia In]. Midazolaml In]. Lorazepam
.
3. Meningitis : as part of late onset sepsis
4. Intracraniai hemorrhag e a. 44. How will you take care of umbilical stum in a newb 9 ' '
delayed fall of umbilical cord. p om baby (3n1e;)t’[7¥n6:ijggfiis::rgjf
5. Developmental defects of brain
0 Investigations: Ans : CARE OF UMBILICAL STUMP
1. General/Routine Investigations : [Ilmflllical cord stump is an important site oi entry for infections (including tetanus)
a) Blood sugar . er- delivery , umbilical cord should be clamped and cut at about 2-3cm from a t - ' '
etc.) 2. Stenle blades should be used for cutting the cord. n 9'10? abdomnal W3“-
b) Electrolytes (calcium. sodium
after 72 hrs of tile) 3. Cut end oi the cord should be ligated with sterile ligatures, like —
c) CSF examination (for seizures appearing
a) Disposable clamps. or
d) Cranial ultrasound
b) Rubber band. or
2. 2" line Investigations : c) Thread (It is not preierred. as it loosens once '
a) Neurolmaging (CT, MRI) in bleeding from umbilical stump. the cord shrinks alter a law hours oi birth, resulting
_ _ 4. Cord should be repeatedly inspected every 15-30 minutes tor the first few hours alter birth
b) EEG
CH)
c) Screening lor congenital infections (TOR 5. Nothing
previous should
beliefs).be applied over cord a n d 'it should be kept dry to prevent intections (contrary to
(ior lnbom Errors of Metab olism)
d) Metabolic screen ‘
6. it there is bleeding from stump . check the ti h Iness of I - t. - - .
and Change '1' " found l°°5°- W- V“.
K (1 mg) — lm. to be given to prevent and trgeat HON. Iga ure
‘\
NEONATOLOGY El Chapter-4 77
7. If there is any discharge or oozing.

local antis optics can
be used (like betadine, spirit etc).
8. Parenteral antibiotics are indicated for
Cl Treatment :
umbilical sepsis (criteria for -
induration of > 2 cm around umbilicus). diagnosis -+ redness and a) It doesn't need any therapy, but the baby should be closely monitored for increasing severity of C
jaundice (> 15 mg/dl) and its persistence beyond normal period (> ‘4 days)
DELAYED FALL OF UHBILICAL CORD : b) Mother should be instructed to give frequent feeds.
The cord normally falls after 5 to 10 days. Cause c) Mother to be reassured about benign nature of the condition. l
s of delayed fall of umbilical cord include .4
1. immunodeficiency (Leukoc
a. 46. Causes or Neonataf Hyperbilirubi’nemfa. [asuc—afh sent, Miro-s"I Sam. macaw Semi ‘
.
allormmune neutropenia etc.) yte Adhesion Defect T ype 1' Neonatal
(L'ntierbit of local { 2. Excessive use of antiseptics to cleanse the Ans : NEONATAL HYPERBILIRUBINEMIA : CAUSES ‘
inecmn isneces cord.
for separa tion sa
at 'Y ---ic therapy
3. Parenteral antibiot - Jaundice or Hyperbilirubinemia is the commonest abnormal physical finding during the first week of
for sepsis. life. Commonest cause of neonatal hyperbilirubinemia is Physiological Jaundice. which affects about 60% 1
cord.) 4. Premature birth of the term and 80% of the preterm babies.
5. Urachal anomalies A. Physiological : l
6. Histiocytosis X. Unconjugated hyperbilirubinemia during the tst 7-14 days of life occurs due to physiological ‘
0. 6. Physiological Jaundr'ce. [2013-Suppie][BMC-9' Sent, immaturity of the newborn. Causes are - I
MEMO-8" Sam) Widnapae, Murshfdabad-
2016] t. Overproduction due to increased FlBC mass and reduced BBC lifespan. ~
Ans : PHYSIOLOGICAL JAUNDICE 2. Reduced uptake, conjugation and excretion by the immature liver of the baby.
_ Jauncfice due to physiological immaturity of the newborn is known as 3. increased enterohepatic circulation due to relative lack of bacteria in the gut. ‘.
physiological jaundice. It occurs
in about 60% of the term babies and nearly 80% of the pretem babies. 8. Pathological : Outside the range of physiological jaundice.
El BM : As biiimbin is a potent antioxidant. physiological jaundice may actually t. Unconiugated Hyperbilirubinemia - 1
protect the baby
against oxygen free radical induced damages in the earlier days of life. a) Exaggeration of Physiological Jaundice : occurs in the following conditions. like —
D Timelhe : i) lmmaturitnrematurity. LBW, :
ii) Birth asphyxia.
Gestational Age (GA) Appearance Maximum intensity Disappearance iii) Hypothermia. hypoglycemia. c
Term 36-72 hrs Day 4 7-10 days of life iv) Acidosis.
Preterm Earlier. but never before Day 5-Day 6 10-14 days of life v) Infections etc. c
24 hrs (24-48 hrs)
b) Hemolysis :
i) Hemolytlc disease of newborn (Rh-incompatibility. ABO incompatibility. Minor blood ,.
Cl Etiopathogenesis ' group incompatibilities). .- ‘
. Overpmducti‘on of bilirubin. due to — ii) RBC enzyme detects (9.9. GSPD deficiency).
a) Poiycythernia
iii) RBC membrane defect (e.g. Hereditary Spherocytosis). C
b) Reduced life span of fetal 8803 (around 90 days) in comparison with 120 days for adult
iv) Homozygous u-thalassemia.
HBCs.)
v) Acquired hemolysis by drugs (9.9. Vitamin K. Sullonamides etc.)
2. Reduced uptake of bilirubin by the liver due to deficiency of ligandin or Y-acceptor protein in the I
hepatocytee. c) Extravasated blood :
3. Reduced Cordugafr'm of bilimbin due to relative deficiency of the conjugating enzyme and sub- i) Petechiae, Bruising. '
strate (UDP giucuronic acid). ii) Hematomas (9.9. oephal hematoma).
4. Reduced excretion of conjugated bilinibin due to immaturity of liver. iii) Concealed hemorrhage (e.9. intiacranial bleeding). ‘
5. Cariugated bfiiribin mterhg the gut can not be converted to stercobilin due to relative lack of d) Polycythemia
bacteria in the gin. e) Increased Enterohepatic circulation : ' .
6. increased enterohepatic circulation, due to overactivity oi B-glucuronidase enzyme. which i) Intestinal obstmction (9.9. duodenal atresia. pyloric stenosis etc.).
. , ‘
deconjugates the biiirubin.
seventy and ii) Hirschprung disease.
7. These handcapa are more pronounced in preterm babies, resulting in increased
duration of physiological jaundice in them. iii) Meconium ileus. ‘
0 investigation : f) Defects In conjugation (l-iei'editary) : _
. t f UCB (Unoonjugated Bilirubin) i) Crigler-Najiar syndrome. ‘
. c3 (Coqugated Biiiribin) — Normal. i) Gibert syndrome
i
78 QUEST : PAEDIATRICS NEONATOLOGY El Chapter—4 79
4. Factors responsible for this hyperbilirubinemia In breastfed babies are as follows :

9] Breast milk laundlce.
a) Colonization of the gut is delayed in breastfed infants. resulting in greater deconjugallon of
hi Hypothyroidism.
bilirubin and enhanced enterohepatic circulation.
2. Conjugated Hyperbilirubinemia :
b) Hepatic conjugation oi bilirubin is compromised due to the presence of 3-a. 20-[lpregnanediol
a) Infections : in breast milk of 1-296 of women.
i) Sepsis c) High concentrations of unsaturated fatty acids in the human milk may also inhibit conjugation
i) Intrauterine infections (TORCH) and uptake of bilinbin.
b) Obstructive : 5. Diagnosis of breast milk jaundice should be considered in newboms with prolongation of jaun-
I) Biliary attesia dice. when -
i) Choiedocl'lal cyst. a) There is unconjugated hyperbilirubinemia, and
c) Defects in hepatic excretion (Hereditary) : b) Other common causes of prolonged unconjugated jaundice are excluded by investigation
l) Dubin Johnson syndrome (9.9. Blood group incompatibility, GBPD deficiency. extravasated blood. hypothyroidism etc.)
i) Rotor syndrome 6. Cessation of breast feeding for about 48-72 hours results in prompt fall of serum bilirubin (by 2-
d) Iletabolic diseases - hits 6 mg/dl) and breastfeeding can be reestablished withom any ask of recurrence
<
I) Galactosemia 7. But, in view of the transient and benign nature of the disease. breast feeding should not be
i) Hereditary Fructose intolerance stopped either for diagnosis or for treatment of breast milk jaundice.
ii) Tyrosinen'l'a 8. it is different from Breast feeding jaundice, which is seen in early neonatal period due to inad-
equate breast milk production and inadequate feeding and resultant dehydration.
iv) ay-antitrypsin deficiency etc.
e) Total Parenteral Nutrition O. 48. Pathological Jaundlce. [MEMO-2016}
' ' o to be pathological ? wma characteristics or

a. am will you diagnose neonatal jaundloSem] Ans : PATHOLOGICAL JAUNDICE
breast miikjaundice. (2 + 3) [HGKMC—Q‘" 0 Definition : I See 0. ‘7
‘ . Ana .- DIAGNOSIS or PATHOLOGICAL JAUNDICE D Criteria for diagnosis:

gical limit or does not conform to the time table D Causes : See 0. 46 (Causes of pathological jaundice)
When jaundice in the newborn crosses the physiolo
for physio logical jaundic e. it is design ated as 'Pathological Jaundlce' and demands investigations D Management:
deserted
(like phototherapy or exchange translusion).
for the cause and therapeutic interventions e. But.
A. Investigation :
between physiological and pathological jaundic
D Criteria : There is no deem demarcation 1. Serum Bilirubln —
raise the suspic ion of pathol ogical jaundice —
the tolowing chara cters a) Total.
24 hours.
1. Appearance of jaundice within ist b) Direct,
expected normal range according to age. 9.9.
a Total Serum Bilirubin (T88) level above the c) Indirect.
a) T58 >5 mgldl on Day 1. 2. Blood group of
b) TSB >10 mg/dl on Day 2, a) Moflter
c) TSB >15 mgldl on Day 3. b) BdJy (lfmoiheris‘O' or Fth we).
mgldi/hour.
3. Ftise of serum bilirubin >0.5 3. DirectCoornhs Test—Positive in immune hemolysis.
by -—
4, Conjugated hyperbiiirubinenfia. evidenced 4. Hunatoorit—ledinttemolysis
urine stain ing of the napp y. 5. Reticulocytecount-TedinHemolysis
a) Dark
l or 15% of T38. .
b) Conjugated Bifinrbin >2 rngld 6. GGPDievel
nd 3 weeks of life (Perststent Menace/Prolonged jaundice). 7. Others-
5, Persistence of ctinical jaundice beyo
' . . . .
HILK JAUN DICE a) Waste-n
CHARACTERISTICS OF BREAST W
MaWdM WWnWW b) Liver fu'xttim fast
1. MMWM
c) Thyroid functim (FT‘I TSH)
ks.
. but may persist upto 6-8 wee
intensity between 10-14 days d) TORCH screen'ng
2 Jaundice is maximum in ally high er. but never
the range of 10-15 mgldl or occasion
ly in e) USG abdomen (:1 do conjugated hyperbiimbinenia)
3. Total serum bilirubin level is usua
hange transfusion.
I severe enough to need exc
80 QUEST : PAEDIATRICS at
NEONATOLOGY D Chapter—4
B. Treatment :
7. Thyroid lunction : FT‘I TSH
1. Phototherapy - Mainstay of therapy during initial 7-10 days of life.
8. USG abdomen : For pyloric stenosis or other causes of intestinal obstruction.
2. Exchange transfusion — In more severe cases. 9. UDP-Glucuronyl transferase activity : For Crigler-Najjar and Gilbert syndrome.
3. Specific therapy — According to the cause, like 10. Breast milk jaundice is the diagnosis of exclusion.
a) Antibiotic tor sepsis CI Treatment :
b) Thyroxine in hypothyroidism 1. According to the cause.
c) Kasai operation in biliary atresia. 2. Reassurance, if no cause is found. as breast milk jaundice (in exclusively breastfed babies) 5 a
benign condition and resolves spontaneously within 6-8 weeks.
0. 49. Persistence of neonatal unconjugated hyperbifirubinemia. [iPGMER-J‘h Sent]
0. 50. Kemicterus. {20 12-Supple]
Ans : PERSISTENT UNCONJUGATED HYPERBILIRUBINEMIA
When clinically evident hyperbilirubinemia persists beyond 3 weeks of life, it is known as persistent Ans : KERNICTEFIUS
jaundice. Persistent hyperbilirubinen'iia may be both unconjugated and conjugated and there are separate Kemicterus or Bilirubin encephalopathy is the most dreaded complication of unconjugated hyperbiliru-
list oi causes for both the types. binemia in the newborn during the first week of life. when blood brain barrier remains Immature-
0 Causes: U Pathogenesis : Bilirubin in plasma exists as albumin bound complex, which cannot penetrate the
cell wall (1 gm Albumin binds to 8.5 mg of Bifirubin)
Prematurity.
“PNPFPP’PT‘
l
Hemolytic disease of newborn due to fetornatemal blood group incompatibility. When Bilirubin-binding capacity of albumin is exhausted
Other hemolytic jaundice: (9.9. GGPD deficiency). (9.9. low albumin, high bilirubin)
Breast mitt jamcice. 1
Free Bilirubin diffuses into interstitial
Wis!"- compartment and binds to tissue proteins in the interstitium.
Hypertrophic pyloric stenosis and other conditions associated with intestinal stasis.
l Further rise of bilirubin
Crigler - Najjar syndrome. Bilirubin crosses blood brain ban'ier
mien syndrome. ,1, .
. Concealed hemorrhages. Gains access into the neurons located

at basal ganglia. hippocampus, auditory nuclei etc.
10. Mdaria.
0 Clinical Features: 0 Clinical Features :
Jaundice. dinicaliy evident upto leg or sole. A. Acute Form:
N99199i°f
Colourless urine. 1. Phasel: a) Poor suck,

Yellow or normal coloured stool. b) Hypotonia.
c) Seizures.
Pallor } in cases of hemolysis 2. Phase II : a) Hypertonia of extensor muscles,
WY b) Opisthotonus
Typical phenotype in Down syndrome.
constlpation. large tongue) c} Fletrocolis
Clinicd feamres oi hypothyroidism (cg. Lethargy. hypotonia, dry skin. d) Fever.
in cretinism.
3. Phase lll : Generalised hypertonia.
I'J Investigations :
B. Chronic Form:
l. LFT:
i. let year of life: a) Hypotonia
a) ‘ To confirm mated hyperbi'imbineflia . b) Active DTFI (Deep Tendon Reflex)
b) Liver enzymes (sect. scPT) usually normal- 2. Beyond 1 year: a) Movementdisordersltremor.choreoathetoid movements)
2. W : led b) Upward gaze palsy, '
3. W count : Ted In cases of hemolysis c) Sensorineural hearing loss.
4. w blood mar : Anisocylosis. Poikilocylosis d) Brownlshstainingolteeth,
mcleatod RBCs, Target cells. e) Various degree of intellectual retardation.
5. Blood grow: of author & baby. El Diagnosis : Kemicterus is a clinical diagnosis. Suggestive clinical
vere unconjugated hyperbilinrbinemia is diagnostic 0' kemictems. features 'In a newborn with
- se-
8. GBPD level
a: QUEST : PAEDIATRICS NEONATOLOGY D Chapter—4 83
‘ ' 3. Baby's position should be changed on 8. off to expose the maximal

0 Prevention I Treatment : arei'otlsiun to light.
because once neuronal damage becomes Irreversrble. no 4. Breast feeding should be continued.
1 Prevention is always better than cure.
I n "we,“
treatment is available to stop the progression of the disease spectrum. D Intensiflcatlon of phototherapy: Phototherapy can be intensified
by following measures —
2. Tintely phototherapy and exchange transfusion can prevent the menace and a so ca a) Reducing distance to 15-20 cm.
early stages of the disease. b) Providing double surface photolherapy by placing the baby on
Biliblanket or LED mattress
CI Sequelae : 1. Choreo-athetoid cerem palsy. c) Using white slings or curtains around the baby which reflect
light on the baby.
2. Intellectual impairment. d) Using Special blue CFL tubes.
3. Sensorineural deafness. ..
Ls .. 0 Complications :
‘. Passage of loose green stools.
0. 51. Phototherapy. [2010. 2015, CNMC-lm Sent, MEMO—9'" Sent]
2. Hypenhermia and dehydration due to Ted insensible water
0 52. Indication and complication of phototherapy. [2008, SOHO-2016} loss.
. Flea-bite rashes on trunk orextremities.
«operators-u
- .-
: Photothera . Risk of opening of Ductus Arteriosus
therapy for neonatal hyperbr
mPhototherapy ha:been accepted widely as a relatively safe and effective Hypocalcemia (due to secretion of melatonin)
Iirubrnemta.
. May cause hemolysis and Ted platelet turnover.
D flechqnlsm of (t t
' . Disturbance in the circadian rhythm of the sex
uncon' ated birmbin a - hormones.
in stoolmand urine. Bitinbin absorbs light maxrmally at wavelength of 42 Decreased mother-child interaction.
with missions at this range lowers serum bilirubin by 3 mechanisms - . Bronze Baby Syndrome (in conjugated hyperb
ilirubinemia)
note-oxidation“ ' v slow and Ineffective)
back to Z-isomers O. 53. Baby of a Rh —ve mother. [Haida-2016]
21L. :hotc-isomenzamZ-isomers to E-isomers. which are not stable and revert
u n u a .
0. 54. Rh-Isoimmunlzation. [IPGIIIIEI‘I-O'fl Sent]
rs produced and II rs excreted
gm: lsonierization (Most effective method. where lumlrubtn
. - m '
3 I Arts : Rh-ISOIHMUNIZATION
. - . .
. without the need for hepatic conjugation).
to Its Indication. Grossly. Tote Rh-isoimmunization or Rh-incompatibility is the most
Indication ' Phototherapy is a drug. which should be used according as laid
fatal of the
blood group incompatibilities causing
of phototherapy. . hyperbilirubinemia in the newborns. This is
Cl Seam Bilirubin (I'SB) > 15 mg/dl is considered as an indication entirely preventable by appropriate measures
the type of Hemolytic Disease of the Newb
orn (HDN) which is
: In term and near-term infants (> 35 weeks). the brlinrbln normograrzr: Sneadfim.s _ in Rh —ve mother.
1 Term infants
' down by MP (America.n Academy ). for starting phototherapy. There
of Pediatricsks) 0 Pathogenesls : FIh-incompatibility occurs
. when a negative mother carries an Fifi-pos
. - - . itive fetus.
Infants at Lower nsk (well Infants 2 38 w Once placental simulation is well established
2.38 wks with nsk factors. like blood after 3 months
ta); Medium risk (well infants of 35-37 wks and infants of pregnancy. fetal RBCs may seep into
etc). maternal circulation.
group incompatibility. G6PD deficiency. asphyxra, sepsis l
ion
c Higher risk : (Infants of 35 - 37 wee ks with .risk factors) Flh antigen of fetal BBC: invoke antibody respo
rapy and exchange transfus nse by the
a $3a Infants : In preterm infants. indication for photothe maternal immune system (Though enoug
h Ab is not produced
dependsonbirfllweight- in first pregnancy. each subsequent pregn
ancies with
Birth W049” Cut-off for PhotothenPY Rh we fetus leads to Ting Ab response and more
severe disease).
l
<1kg S‘n/dl The anti-D antibodies are 196 in type and
1_125kg crosses placenta to reach fetal circulation
7—9mg/d' .
125—151(5) l
9—11mgldl They destroy D we (Rh +ve) fetal FIBCs
1.5—2k9 [Hernolysis].
11—13rngldl a Clinical Features:
2—2.5” 13—15mg/dl ' '
1. Anemia.
>25kg 15—17mgldl z Jaundlce (that usually appears within 1st
24 hours and rapldy Tee in intensity).
3. Hepatosplenomegaly.
' and4 blue CFLe .
:Eachmachrne ’ houseszwhite
4. Urimlscolourtessanddoesn’tstahthediaper
J Prozduclothen s of the baby are removed. except diaper (In male Infants) and
surface of the baby.
eye shield.
filtered in the urlne). (asu
W' tedbitiru " "
b'“ '3 "W edible and not
;: Light m is kept at a distance of 45 cm from the skin 5. Severely affected infants may have
gene ralized anasarca (hydrops fetalis) and
may do in utero.
D Chapter— 4 85
NEONATOLOGYM ...—
I4 QUEST : PAEDIATRICS
6. Associated teatures : 2. Respiratory:

ts in imrnat ure lungs).
a) Hypoglycemia (HBC breakdown product giutathione inactivates circulating insulin —+ Hyper- a) Hyaiine Membrane Disease (due to deficiency oi surfactan
plasia of islet cells oi pancreas —i Hyperinsulinemia —+ Hypoglycemia). b) Bronchopulmonary dysplasia.
b) Lukopenia and Thrombocytopenia (due to increased erythrOpoiesis in bone marrow). 3. CV8 : Delayed closure ol ductus arteriosus-
0 Diagnosis : 4. GI System:
A Cord blood should be sent lor — a) Feeding difficulties (due to poor reflexes)
b) Feed intolerance. regurgitation.
A80 8. Flh typing : Flh we.
c) Abdominal distension (due to decreased peristaltic movements: may prowess '0 Necmllz'w
misinter-
Direct Coomb's test : positive Enlerocolitis).

H) : Low 5. Liver:
Reticulocyte count : Increased a) Exaggeration or physiological jaundice (due to immature coniusraticm System 0' WWW and
. Bilirubin : Increased (Unconjugated hyperbiiirubinemia) also due to relative poiycythemia).
(due to low serum albumin & poor blood
. “eternal Blood : b) Development oi Kemicterus at lower bilirubin levels
brain barrier).
I. Blood Group : Rh -ve
Renal :
2. Indirect Coomb's test : positive.
a) Low GFR (Giomerular Filtration Rate).
0 Treatment:
b) Poor capacity to concentrate mite.
1. Phototherapy : Almost all babies need phototherapy. c) Azotemia.
Day 1 ol life is indicated. it -—
2 Exchange transfusion : Early exchange transiusion on 7. W600 : lraeasedpropensiytodevelm hypothemiaoccus inpreterm
babies duelo-
a) Cord Hb < 10 gm‘ili. a) Excessive heatioesduetolargersurtacearea.
b) Cord Bilirubin 2 5 mgldi. b) Poor generation of heat due to paucity oi brown lat.
3. IVlg—Canbeused. 8. lntections : Preterm inlants are more prone to infections (sepsis) due to —
—vem,arfi-Dhmm(mpgm
D W:Wmflt+vebdrysbomdaRh a) LowlgG level.
given rim. to the mother within 72_hours of delivery. b) Insd'liaen‘ toellularimmunity.
a. 55. Neonatal Jaundice. Issac-20151 9. Metabolic:
a) Hwoglrcenia .
Ans : NEONATAL JAUNDICE b) W3 I Predspose to seizure
al finding during tst week oi tile.
Jauntice is the Mt abnonnai physic c) Metabdic acidosis
0 Causes; See 0. 46 to. Deficiency of micronutrients :
See 0. 47.
0 Diagnosis oi pathological laundice : a) lrondeficiencyanemia(duetolowiron store)
D Management : See 0. 48. b) Viamin E defxziency.
s. [2017-Suppie, RGKMCH-C‘" Sent,
iPGMEH-Qu' Sent, CHUC- c) Osteopenia oi prematurity.
0. 56. W ofpreterm babie
2016] a, 53, Complicabon' ' of email for Geetabonai‘ Age (56A) babies. flPGItER-za 16)
-9" Sent, 2016. "CK-2016]
0. 57. Prabieme of prematurity. [NBS 0. 59. Complication of 1063 babies. [Indicated-2016]
I BABIES
Arte : COIPIJCATIONS OF PRE'I’ER ’ nare Waspr
tatto . etenns_flhe Ans:OOIIPL|OA110NOFSGAiiUGR BABIES
SToontpletedweeksotges
Neomtetoarebornatlessman tcom pitca bon mpr eten nbabtee.” mnmimmsmufltmmretenmbebiesmtauenrgotgowmin—uteroleatirtgto
tems restliittifleren
hmctionaiimmaturiryotvariornsys ‘ntratrtenna' mum" andbirtholbabtes' maresnfltorthe‘aconesponding gestational age When
below—- bhflnreiyfltahbebw1mhpercerflebrflteperioddm.flnyaehmnas SGA(Snallior
1. CNS: . WmtTMWdSGAbabhsmnmlymmmMebhgicallxtonm
Lethargy, reclivily.
eior euweeksoigestatton. trttrauterinegrowthretardatron 9.9 placental mam. dumb hypoxia etc. Comoniy ermflerod
z; Incoming; ‘ andswalowinginbabiesoomb carpiicetiortsare— ,
ry centre).
to immaturity oi the respirato
c) Apnea ol prematurity (due 1. Fashypoxhandimputmdeaflt:0uetophwialdysluctionorisufldency
d) intraventricuiar hemorrhage. z Severebirthasphyxia.
e) PeMntncular leukomalacia.
i) Retinopathy ol prematurity.
86 QUEST : PAEDIATRICS NEONATOLOGY D Chapter-4 or
..
3. Ilecorilum stained liquor: Fetal hypoxia leading to increased stress can cause in-utero passage of b) Enteral feeds. however. should be started as soon as they are hemodynamically stable. with
meconium during birth or just before birth (24-48 hrs). This is known as Meconium Stained Liquor (MSL). choice of feeding method based on the infants' gestational age (as shown below) and clinical
b . fleconlum Aspiration Syndrome (UAS) : Babies may aspirate MSL leading to MAS. which pre- condition.
sents as severe respiratory distress starting on Day 1 of life. preferably within first 6 hours. 2. Healthy infants : Initial feeding method in healthy LBW infants depends on maturation of feeding
5. Polycythemia : skills according to gestational age —
Fetal hypoxia
l Gestational age Maturation of feeding skills Initial feeding method
T Erythropoiotin
< 25 weeks - No sucking IV fluid
l
. No propulsive gut motility
T BBC mass (polycythemia)
2B - 31 weeks - Sucking bursts develop Orogastric (or Nasogastric tube
6. Hypoglycemia : It is more common in IUGR babies than in pretenns. It occurs due to grossly
rirninished body store of glucose in these babies. . No coortination between sudring. feeding)
swallowing and breathing
7- Congenital malformations : including intrauterine infections are common in IUGFl babies.
32-34weeks - Sucking and coordination with Feeding by cup and spoon/
8. Pulmonary hemorrhage : due to unknown cause.
breathing mature slightly paladay
9. Hyperbllirublnemla
> 34 weeks 0 Complete maturation of sucking Breast feeding
10. Thermoregulation : Unsatisfactory thermoregulation may occur due to scanty brown fat.
and coordination with breathing.
1 1 . Vulnerability to infections.
12. Long-term complications : _
U Non-nutritive Sucking (NNS) : All stable LBW infants. irrespective of their initial feeding method.
a) Poor catch-up growth in future (due to decreased nurrber of cells in the body) should be put on their mother's breast. The immature sucking (NNS) helps in ——
b) Increased risk of development of metabolic syndrome X. diabetes rnellitus. hypertension and a) Rapid maturation of their feeding skills.
coronary artery dsease in adult life. b) Improves milk secretion in their mothers.
0 Choice of milk : All LBW infants should receive only breast milk. irrespective of their fearing method.
0. 60. Complication of low birth weight newborn. [BSMC—9th Sam] [2008, 2013-euppfe]
in the form of
0. 61. Limitation of LBW babies. ("firmware-2016) a) Mother’s own milk (best) : Expressed Breast Milk (EBM). or
Ans : COIIPLICATION OF LBW BABIES b) Donor human milk (from milk bank. If available)
Babies with a birth weight of < 2.5 kg are classified as low birth weight (LBW) babies. These include > In case. the mother is sick (and milk bank is not there) or there is any contraindication to
both preterm babies (Le. those born at less than 37 completed weeks of gestation) and term ml for breast feeding. options are -
gestational age (SGA) babies. Clinical problems and prognosis differ significantly In these 2 groups. a) Formula feeds :
0 Complicationsofpreterm:8ee0.56. 57. i) Preterm formula — in VLBW infants (< 1.5 kg).
Cl Cornplicetions ofSGA : SeeO. 58.59. ii) Term formula - in infants weighing > 1.5 kg.
b) Animal milk : 9.9. cow's milk (last option).
0. 62. Feeding of Low Birth Weight (LBW) newborns. [RGKMC-J'” Sam. BRIO-9"I Sam, Kaiyani- Cl Amount offeedfng:
9" Sent, HRS-2016]
1. Infants, who are breastfed are given demand feeding every 2-3 hours. sometimes more fre-
Ana : FEEDING OF LBW BABIES quently.
-
Nutritional management hfluences immediate survival as well as subsequent growth and development 2. Infants. who are not breastfed tile. cup and spoon feeding. tube feeding) : total anount of feed
of LBW infants required per day is calculated and given in divided volumes 0 2-3 hourly.
0 Difficulties : Fearing of LBW infants is relatively difficult because of the following limitations — a) > 1 d5.kg : 60 mlikgiday on day 1. then increasing by 15 miikglday daily into 150 rriikglday
on y 7.
1. meyhavekndequateleechg skisandracureothermedtodsoffeedngoflierthanbreaslfeechg.
b) <15 kg :80 ml/kgidayon day 1.then gradually increasing by 10-15mllkgldaydeiy to reach
2. They are often sick in the early days precluding enteral loading. 160-170 mlikglday at the end of first week.
3. Theyhave hlgherfluid requirements in thefirst week. U NutritionalSupplementa:
4.1heyoflenhavolowbodystoresofvariousmrtrlents.
1. VitarrinD
5. Owlng to gm immatwity. feed intolerance is common. to all LBW Infants.
2. Iron }
0 Decldingthe lnltfalmethod offeeding:
3. Calcium 5. Phosphorus
1. Sick infants : 4_ Foic m } to only VLBW Infants.
a) Often started on IV fluids.
4 89
88 QUEST : PAEDIATRICS NEONATOLOGY E] Chapter—
al age
weight <15 kg and gestation
0. 63. Management of LBW babies. [Kaiyani-2016] 9. Retinopathy of prematurity screening : In a ll babies with birth ilatio n etc.
rece ived 02. vent
Ans : MANAGEMENT OF LBW BABIES < 32 weeks and in selected babies with GA > 32 weeks. who
Unit).
During the early_ neonatal _period (lst week ol life) and also subs‘equenlly. low bll’II't 10. Hearing screening : ll there is prolonged stay in NlCU (Neonatal Intensive Care
. _ _ . ‘ '
weight (LBW)
babies offace venous nti
facets complications
I requmng special care due to th err‘ inherent
' ' ' 11. Screening for intreventricular haemorrhaga : by USG of brain.
handicaps. Dillerent
12. Follow-up : at high risk clinic.
1. Resuscitation :
0. 64. HIE due to birth asphyxia. HACK-2016]
a) Resuscitation-preparedness. as there is a high risk for need of resuscitation.
b) Gentle resuscitation using appropriate-sized small bags (to deliver small tidal volume). Ans : HIE DUE TO BIRTH ASPHYXIA
_ mortality and morbidity in our
Birth Asphyxia or perinatal Asphyxia is the leading cause 0 f neonatal
2. Temperature control : an d ischemic injury to various
country and probably all over the world. Birth Asphyxia leads to hypoxrc
a) Maintenance of warm chain starting lrom warm resuscitation and use of radiant warmer when-
organ systems 01 our body.
ever necessary. I
El HIE:
b) Frequentlure.
monitoring of temperature and education of parents about irn po rt ance oi checking
' is referred to as Hypoxic ischemic
> Neonatal encephalopathy. lollowing severe birth asphyxia
Encephalopathy (HIE).
c) naroo Mother Care. aSphyxia.
> About 25-30% at intents are likely to develop HIE following perinatal
3. Feeding : ,
U Pathogenesis :
a) Choosing appropriate method of feeding according to gestational age:
Perinatal Asphyxia
i) > 34 weeks : Breast teedng. l
i) 31-34 weeks : Cup a. spoon leading. Hypoxia
iii) 28-31 weeks : Tube fearing (Nasogastn'c i orogastric) l
iv) < 28 weeks : lV fluid. Relative isohemia (Existent blood flow not able to maintain adequate 0: supply)
1,
b) Looking for feed intolerance.
Protective mechanisms like Diving Reflex ensues. which redistributes available
c) Sippiementation with micronutrients. blood flow trorn lesser to more vital organs. As a result. blood flow to brain. heart
4. Infection : and adrenals is preserved in the expense of blood flow to kidneys. lungs. GI tract.
liver. skin, skeletal muscles etc.
a) Strict adterence to asepsis. hand hygiene.
> When asphyxial damage is severe and prolonged
b) hittinat handing.
l
c) Low threshold for suspicion of sepsis and start antibiotics (IV) at minimum suspicion.
Compensatory mechanisms overwhelmed
5. Metabolic derangements: - l
a) Hypoglycem ia : Frequent monitoring of blood glucose. particularly in SGA babies 5. VLBW Hypoxic and ischemic damage to the brain.
bdaies. in the tel 48 hours. (Neuronal necrosis)
Infants.
b) Hypocelcemla : Prophylactic calcium gluconate (10%) O 4 mlikgiday in VLBW
6. Hyperlilirublnemla : Cerebral edema (both cytotoxic and vasogenic)
lower blirubln levels than l:I Neuropethology :
a) Early use of phototherapy and exchange translusion at comparatively
their term counterparts. A. in term newborns :
as their skin is more slender and 1. Selective neuronal necrosis (cortical).
b) Phototherapy can be used tpto 10-14 days in preterm infants.
transparent. 2. Status marrnoratus of basal ganglia and thalamus.
. . . . 3. Parasagittal cerebral lniury.
7. Hematologlcelprobieme:
dpartis l exchan geisdo ne.ifne eded.in plethon c babies. B. In pretenne : '
a) Potycythemle:Extrafluidisglvenan 1. Selective neuronal necrosis (sub-cortical).
starting from 6-8 weeks of life to prevent
b) Anemia : Iron supplementation o 2-3 mgikglday 2. Periventricuiar Leukomalacia.
anemia oi prematurity.
3. Periventricular and lntraventricular hemorrhage.
B. Reepirdory problems : a Clinical Features :
and treatment of ROS.
a) Early use of CPAP and suites-tent for prevention 1. Seizures: Mostly within 6-12 hours and invariably by 36-48 hours of birth.
' therapy with caffeine citrate for preven tion of apnea of prematurity in all infants with
b) Prophyladlc 2. Features of CNS irritability. like illteriness. excessive crying etc. primarily occurs.
birtweimi <1.25 kg.
12
90 QUEST : PAEDIATRICS NEONATOLOGY D Chapter-J 91
Later. there are signs oi CNS depression. like lethargy inactivity. apnea and stupor.
99"?!"
6. Hematological :
Iuscle tone : usually hypotonic.
a) Thrombocytopenia.
Anterior lontanetle : may be bulged. due to cerebral edema or NH.
b) Disseminated intravascular coagulation.
lore reflex : hyperactive initialy. followed by incomplete or absent.
7. Endocrine:
0 Staging :
a) SIADH (Syndrome of inappropriate ADH secretion).
Samat and Sam! staging (more elaborate).
b) Transient hypoparathyroidism. leading to hypocaicemie.
2. Levene gradhg (dinicai method. can be used at bedside) : Uses 4 features. namely —
c) Adrenal hemorrhage.
a) Consciousness. 8. Metabolic :
b) Tone.
a) Hypoglycemia.
c) Seizures and b) Hyponatremia. hyperkalemia.
d) Sushi-lg I Breathing. c) Acidosis.
Ct Management :
1. Management at seizures. O. 66. Danger signs of newborn. {NBS-2016, Mir-Supple]
2. Maintenance oi tenperature. glucose and perfusion. Ans : DANGER SIGNS OF NEWBORN
3. Maintenance oi lbid and electrolytes. All health care stalls including nurses. doctors. attendants etc. should be always
vigilant in the meter-
4. Newer Miods. lite ll'terqeeutic hypothermia. nity ward to diagnose neonatal abnormalities at the earliest. Even mother and family
members are also
educated about the possible danger signs. wh’mh should be brought to the notice
a. 65. Organ involvement in pedestal asphyxia. [NBS-8m Sent] at the pediatricians
immediately. Because. if the early symptoms go unnoticed. health of
a newborn may deteriorate rapidly.
Ans : ORGAN INVOLVEMENT Ill PERINATAL ASPHYXIA even resulting in death sometimes.
Perhatai asphyxia (PA) can attest every systems oi the body due to
hypoxia and lschemia. Non-vital 0 Danger signs : The lollowing danger signs are always importan
organs are atlected first due to the dying reflex. whidi redistributes
t as early leatures of severe
blood flow to support the vital organs diseases -
oi the body. 1. Bleeding : From an y site. like - hematemesis.
malena. hematochezia. hematuria. umbilical
1. Haley: loci-nyisti'iemoetcomrnonorgantobelnvolvedinperinata bleeding etc.
l asphyxiaandincldenceol
renalhvolvementisaboutSO‘xinlhelonnol— Jaundlce : Appearance ol jaundice within 24 hours
«907493999’i‘3
or deep jaundice.
a) Acme was: necrosis. Meconlurn : Not passed within 24 hours.
b) Renal vein three-basis. Urine : Not passed within 48 hours.
c) Renal leiure etc. Repeated vomiting or dlan'hoea.
Poor leedingmelusal to suck.
a Brain:PAhvolvesbraininabout)Srdolcases(33%).Bminl
eslonis alsoknownasHypoflc Undue lethargy or excessive crying.
lscl'iemicEncephalopathyME). which may have lollovving manifesta
tions—
a) Seizures. coma. apnea. hypotonia. Excessive frothing or drooling of saliva.
b) Intracraniaihemorrhage. . Respiratory difficulty:
c) Cerebraledema. a) Hurried breathing (RR > GOImln).
d) Longtermneurologicaleequeiae. b} Chest indrawing.
3. Heart:Cardiacinvolvemeuoocursir125%olcases.lnthelonno c) Nasal flaring.
l—
a) Myocardaidamageceusingdysrhythmia. 10. Cyliosts : Peripheral or central.
b) TWW. 11. Apnelc attacks.
c) Congestivecaniaclaiiure. 12. Choking during leedlng.
4. ungszPui'noneryconphetionslnclude— 13. Seisures.
a) Meconiunaspiration. 14. Temperature Instability:
b) SurlecimirimptirncausingRDs. a) Hypothermia - Term < 355°C.
c) Persisterlpuinoneryhypenenslon. b) Hyperttieimta -Terrp > 38°C.
d) WW. 15. Ml Inhctlons:
5.0lTrect: .
a) Mammals.
a) Necroliztmeroooifle(NEC)
b) Pustules.
b) Hepaticdinhncfiori.
c) Oral litush.
c) Paralyticleus.
d) Utfblical sepsis (Redness
and lnduratlon around unbilicus)
T -
92 QUEST : PAEDlATRI NEONATOLOGY 0 Chapter - l 33
cs
o. 57. Neonatal Transport. {2012-Suppk] '
0. 68. Breast milk vs Cow's milk. [2010]
Ans __ NEONATAL TRANSPORT
I . . . . '
Tr! n 5 F : t-
. BREAST
A“There MILK
VS COW S, nutritional
MILKbiochemical and physiological differences between breast milk ow's
' a ndheman
temperature aidmblood goose levels to?1:?bngwbom care. It requrres careful attention to vital parameters,
a y. as well as coordination with the receiving hospital,
are several
D T . 9 is Ideal for the U
calf. while breast milk
milk. Cow's milk is most suited for the biological needs of the
1yp|ee '
.
From peripheral health facilit to the tortmy care centre havrng baby. The differences are — (Composition per 100 ml-)
. mat-hospital transport:
ant). Y NICU
faciity ( i
Nutrients Breast milk (Human milk) COW'S milk
2. trim-hospital transport : Like NlCU to operation theatre. imaging department etc.
. 3-5 gm.
0 TrIShontpor‘l equipments .- ‘ . 1. Protein content : 1.1 gm.
2; his? transport Tithln the hospital can be accomplished by transport incubator. 2. Protein quality:
r a. Whey : Casein — 60:40 20 i 80
I | g '3a include H
b. Whey prorein — Mainly lactalbumin a Mainly Iactoglobulin (allergen)
f? mull-aim. (easily digestible) lactoferrin (bactenostalic)
I) Plastic basket with perforations. amsein is predominant.
c. Casein : lt—casein is more.
E) ”B'mwo' b“ 4.5 gm.
3. Lactose — 7 gm.
M ”M layers 0‘ WHO“ wmpping- (High lactose content helps
v) Skin-to-skin contact. in calcium & iron absor tion
. . . . .. . .
c) When a high-nsk pregnancy ls identified, it is best to transfer the mother to a higher centre. p ) 4 gm.
4. Fat - (content) 3-5 gm.
because uterus is an ideal transport incubator.
0 low-hospital transport : 5- Flt quality -
a. Essential fatty acid — 13% 2 96
> fade-bone : usual indications are as follows —
b. PUFA : Saturated fatty acid - 1.2 : 1 1 :2
1. Preterm irfant < 32 weeks GA or birth weight < 1.5 kg.
2 Respiratory rfistress requiring CPAP or ventltation. 6. Calcium — 35 "19- 140 m9-
3. Severe HIE. 7. Phosphorus — 15 mg. 90 mg
4. Severe sepsis. 3 . Ca I p - ) 2 '
< 2( may or0duce h wow to emia)
.
5. Intractable seizure. 9. Sodium — 0.7 mEq. 2.2 mEq
6. 3| Eng 1e.
10. Potassium -— 1.4 mEq. 3.5 mEq
7_ Severe Jaundrce.
“- Vitamin K - ‘5 #9 60 H9
8. Others (9.9. congenital anomalies. surgical conditions etc.) 350 mosm/L
12. Osmolality - 290 mosmlL
3- rinciplea :
13. Calories _ 57 Kcal 57 Kcal
. Ensure genuine indication for referral.
14. Energy : Protein _ 70 : 1 25 : 1
2. Explain the condition and reason for transportation to the parents I family members.
_ Na. K.
15. Solute load _ (Protein. Low High (may Tdehydration)
3 . Stabilize
" temperature , ainyay
' l , circulation
, breath-n9 ' ' and blood glucose before 1ranspo it.
provrding birth details, need for referral. treatment given etc. Ca. 9 etc.)
4. Precise note should be written
5. Mother shodd be encouraged to accompany the baby. '
' . h , ' f asible. 0. 69. Write your plan of feeding of a premature very low birth weight newborn baby. {2015]
6' A health worker (doctor. nurse. d” etc ) should accompany ' a baby d e A S 062 (F edi ”-w
7. Referralfacilityshouldbehformedinadvance. 91 5:9 0mm ",1 ants)
the fastest possible and "3)- vigil bob
3. Take the baby to the nearest NICU by the shortest route. using 7- < - 9- “'9'?”- 1
af'forddrte mode of transport.
before > let step ‘5 assessment 0' gestational age.
9. Al the eeserrfiel equbments. instalments and emergency dnrgs should be checked i
tr ”pm > Then appropriate lnltlal feeding method is determined.
centre.
10. Referring hospital should be informed about safe arrival at the referral
1'
94 QUEST : PAEDIATFIICS NEONATOLOGY n crisper-4 es
0. 70. Routine care of newborn in the delivery room. p009. flurshidabad-2016] 0. 71. Initial steps of resuscitation of a newborn. [2017, Helms-2016, KalyanI-2016]
Ans .' ROUTINE CARE OF NEWBORN Ans : INITIAL STEPS 0F RESUSCITATION
Each newborn is precious and birth ot every newbom should be taken care 01 adequately. Routine care 'Initial Steps' are a set ol interventions that are done as a part of neonatal resuscitation algorithm.
of newborns at the delivery room includes —
CI Indication: At birth. a newborn is born [delivered
1. Resuscitatbn - Preparedness :
i
a) One health provider (doctor or nurse). who is trained in neonatal resuscitation. must be physi-
cally present during each delivery, irrespective oi the risk status. i) Term gestation ?
b) in high-risk deliveries. 2 persons should be present solely to manage the baby. ii) Breathing or crying ? "359 3 questions are 35k?“-
c) Healh provider designated tor neonatal care should check the resuscitation equipments welI\ iii) Goord muscle tone ?
betore the delivery. r/ \r
2. Standard Asepticmeasures: al 3 answers are 'Yes' any 01 the 3 answers is ‘No'
a) Gloves. mask and gown should be worn by the health provider during resuscitation. i l
b) Observe ‘5 cleans' to prevent sepsis at birth : Routine Care Initial Steps
i) Clean hand. L't Steps :
i) Clean surface.
1. Provide warmth:
ii) Clean blade.
a) My is placed under a heat source. preterably a radiant warmer.
iv) Clean cord-tie.
b) Baby should not be covered to allow lull visualization and to pennit the radiant heat to reach
v) Clean cord-storm (nothing to be applied)
the baby.
3. Preverrtionothypothennla:
a Positioning :
a) Termeratureotthedeliveryroornaround25°0
a) Bdiy is placed on back or side with the neck slightly extended. This brings the posterior
b) Bwy received in pre—wanned linen sheet. pharynx. larynx and trachea on line to Iacilitale breathing.
c) Babyisinmediatelydriedlnclutingheadandlaceandthencoveredtnaseparate.drysheet.
b) To help to maintain this position. a rolled towel or blanket is placed under the shoulders.
4. Ctantplng otthe umbilical cord: elevating them it" to 1" oil the mattress. This is known as ‘shoulder roll'.
a) Usually dehyed tor 1-2 minutes to slow transfer oi additional amount oi blood lrom placenta to 3. CieerAirway:
the inter-a.
a) Secretions are removed lrom the airway by wiping the nose and mouth with a clean cloth or
b)Ciarrpeda12-3crnawaylrorntheabdomen. by sudioning with suction catheter.
c) Clarrped with commercially available clamp or a clean and autociaved thread. b) Mouth is auctioned first belore nose (as alphabetically 'M' comes betore ‘N') to prevent aspi-
d) Cord-sum shared be clean and nothing applied. ration while gasping during nasal suction.
5. Cleaning or the baby : During desiring and viewing the baby. vemix caseosa should not be re- c) 910 olsuction catheter: 12 to 14 Fr.
moved.as itprotectsthe skin andprevents hypothennia.
d) Suction pressure : BO -100 min-Hg.
8. Weight recoding : Baby should be weighed alter stabilization with an electronic weighing scale
(preterabiy) or a ror.rtine weighhg scaiewith 10 gm sensitivity. 4. Dryhg:
Bdry ahead be dried adequately using pro-warmed linen and wet linen is removed away.
7. Heedtotoeexamlnetion:Babyshouldbeexaminedheadtoioeandfrndingsrecordedatneonatal
record sheet. Special attention given to congenital anomarres (e.g. clelt palate. neck masses. 5. m :
ormhalocele. men'ngornyelocele. Morale anus etc.) and birth injuries. Act oi steaming and drying itsell provides adequate stimulation to initiate breating. lithe baby
3. Vitamin K: lnj. Vrt. K (1 mg; 0.5 mg for birth wt. < 1 kg.) is given Law. at antero‘lateral thigh tor al doesn't stil respond. additional tactile stinulatlon provided in the lorm 01
newborns.
a) Filming the back gently, or
9. Wham: EadthtaMnusthaveanidenfifrcationbandcontalningmothersnam. hos-
pld registration no. gender and birth weight b) Fishing the soles.
10.6mlcaflonwlhllnly: Mothermdthetamilymenbersarecornrmnlcatedcleariym: 6. Noting :
a) Gender (rmst be shown also). lI-reposlioriing Is not maintained duringthese manoeuvresbaby is repositiorwdto previous
podium
b) Biliweightand
c) We! being 01 the baby.
NEONATOLOGY u Chapter—4 97
96 QUEST : PAEDtATFttCS
0 Modifications in babies born through [ISL : > So. BMW is indicated. it —

a) Baby is apneic or gasping n.
Babies born through MSL (Meccnium Stained Liquor) 1 even alter initial steps 01 resuscitatio
l b) HR < 100 beats I minute
01 100% ct tree flow 02.
0 HR 2 toolmin c) Persistent central cyanosis despite administration
Ct Contraindicatlon :
ii) Good respiratory elicits —: the air. pumped into litte lung:
iii) Good muscle tone t. in suspected or continued diaphragmatic hernia. because
lree. This art vnll distend the s oma
opening is
also passes into the stomach partly as the
I \i will further compromise lung inflation.
which is more olten in the thoracic cavity and
All ‘Yes' Any 01 the 3 is absent stained liquor (IlSL). because any mic;
2. in non-vigorous babies born through meconium
1 l larynx and trache a will be further pushe d into the lungs. BMV is done only alter trac e
nium in
Vigorous Bury Non-vigorous baby suctioning. il indicated.
i l
O. 73. Newborn Resuscitation. {SOHO-2016]
Usual steps Modified steps
Ans : NEWBORN RESUSCITATION
extent. A:
> Iodfied steps : can prevent asphyxial damage to a large
Prompt and ellective neonatal resuscitation delivery should be wewe
a) Postpone drying and suctioning to prevent stimulation. the cases and thereto re. each
phyxia can only be anticipated in about hall
be observed to manage asphyxra.
b) Removal oi residual meconium from mouth and posterior pharynx by suctioning under direct as an emergency and basic readiness should
visionusingalaryngoscope D Equipments :
c) lrnbation md auctioning ol trachea by applying suction directly to the Endotracheal tine 1. Radiant warmer.
ma-
(10. 12. 14 Fr). central suction [portable suction
(ET tube) and gradually withdrawing the ET tube. 2. Suction equipment : Suction catheters
china
0. 72. indication and Contraindication 01‘ Bag Mask Ventilation. [BSMC-cth Sam] (tor both term and preterm babies). oxygen supply
3. HIV equipment : AMBU bags. Face masks
Ans : BAG a IASK VENTILATION with tubings.
blades no. 0 (preterm) a no. 1 (term).
it. Intubation equipment : Laryngomopes with straight
Positive Pressure Ventilation (PPV) is the single most eflective step in babies who tail to breathe
Endotracheal tubes (2-5 to 4 mm).
normally at birth. PPV is usually given by using a sell-inflating bag a lace mask. together known as Bag
a Mask Ventilation (BMV). 5. Hedications : Epinephrine. NSIFlL.
stethoscope. syringes, feeding tubes (6. 8
6. Miscellaneous : Linen. shoulder roll. gauze. gloves.
D Indication : ‘.
Fr) etc.
Chart on the next page.
Delivery fl a baby 0 Algorithm' : See
inserted)
by Bag 3. Mask or Bag 8- Tibe (ii ET tube is
C] PPV : Positive pressure ventilation is given
ce of ‘squeez e. two. three'.
i) Term gestation ‘? > Rate : 40450 breath/min. ioliowing the sequen
onic: MRSOPA)
i) Breathing or crying ? > Ventilation conectiVe steps: (miem
iii) Good muscle tone ? i) Fla-apply Ilask .
i) Reposition the head and neck.
Answeris‘No' Alltheaanswers are iii) Secretions cleared.
in any oi the 3 ‘Yes' ting.
iv) Mouth kept slightly Open while ventila
i l
Routine Care V) Pressure increased slightly.
Initial Steps
t No Vi) Airway: consider allemative (9.9. ET tube)
1. inultmeouslywith PPV 03:1(chest
HR < toOIm'n. or a a Laboured breathing or 0 ChulComprusion:Chestconpressionisalways givens
persistenicyanosis mression : PPV) and total 120 events in 1 minute (is. 90ched cormressions and 30breaths)
Gasping or apnoeic No
00 solution.
l D In]. Epinephrine : 0.1-0.3 mlg. iv. oi 1:10.0
m —»1w *1" 0!
(Tenn) I CPAP(Pretenn)
13
NEONATOLOGY U Chapter—4 99
' d) Adduction and llexion at shoulders. '

- Term gestation ? ' Routine Care
0 Breathing or crying ? Yes (all 3] r - Provide warmth 2nd phase (Slow)[ e) Flexion at elbows.
- Gard muscle tone ‘? - Clear airway. it necessary l) Closing of hands.
_ L ° D” evaluation
' Ongoing Associated
features
[ 9) Opening of eyes it.
h) Lusty cry.
Initial Steps I J
0 Provide wan'nth. clearairway. - Abnormalities :
dry. stimulated. position No
i) Depressed in asphyxia. sepsis. hypoglycemia etc.
ii) Exaggerated in early meningitis.
- HH < tOO/min ? I No Laboured breathing or persistent iii) Asymmetric in Erb's palsy. # clavicle. t humerus etc.
- Gasping or apneic? cyanosis
- Disappears by 3-6 months.
JrY“ IY 2. Grasp reflexes :

on the palmar
Posruve' ' pressure ventilation 14d improving as a) Palmar grasp : Flexion ol the lingers oi the baby on placing examiner's linger
l \ SPO, monitoring. Supplemental surface.
HR ' 1 No 02 (lerrn) or CPAP (Preterm) b) Plantar grasp : Flexion ol the toes. while pressing the anterior part of the solo
by examiner's
50.100, - [Hn<1oolnm?_J— A linger.
irrproved - Disappears by 2-4 months (palmar grasp) and 6 months (plantargrasp).
Yes
is
>{ Post-resuscitation Care ] 3. Rooting reflex : When baby's cheek is touched softly near the angle of the mouth, head
Ventilation-corrective steps 1'— HR < tOO/mrn
tumed towards that side with deviation ol tongue and angle at mouth to the same side.
lHFi<60Imin _ ' Appears at 32 weeks and disappears by 4—6 months.
Chestconpressionaiongwith aw HR ‘ ‘°°’"“" 4. Sucking reflex : When clean index linger ol examiner is introduced into the mouth. sucking
movement ensues.
lHFkGOlrnin
. . . Consider Endotracheal Intubation at - Appears at 28 weeks and disappears by 4-6 months.
IV adrenaline/epinephrine 4] multiple steps.
5. Glabellar tap : Tapping the nasion is lollowed by closure ol the eyes in infants above 30 weeks
or gestation.
6. Asymmetric Tonic Neck Reflex : (ATNR) Rotation of baby's head to one side causes extension
0. 74. Neonatal Reflexes. [2016]
of upper and lower limbs oi that side and flexion of the limbs at opposite side.
-
An: : NEONATAL HEFLEXES ' Disappears by 5 months ot age and its persistence precludes turning ol the baby lrom
-..-
are brainstem-mediated auto-

“use
swine to prone position.

Newborn babies have a large number of primitive reflexes. which
numerou s such reflexes and all at which disappea rs after a certain age.
matic responses. There are
'
0. 75: Differentiation of Jitteriness from convulsion in neonate. [2018]

1'
L—t‘lm
Ct Woe :
t. The response may be sluggish. exaggerated or normal. which
may point towards ditterent dis- Ans : DiFFERENflATiON OF JITI’ERINESS FROII CONVULSION
ease states . Jitteriness or coarse tremors is extremely common in newborn babies and is a common seizure-
reflex) pointing towards unilateral ab- nirniclrer. it needs to be differentiated from convulsion. as it generally carries good prognosis. doesn't
2. Few reflexes may have asymmetric response (0.9. More
normality. require antiepileptic dnrgs and it may be iound in normal babies also. Dillerentiation many requires
marker of cerebral palsy. iromclonicvarietyolseizure.
3. Their persistence beyond a certain age is an early
D Commonly used reflexes : Jitterlness Convulsion
with head flexed on examiners arm and hand.
t. Iororeflex:Babyisheldhsemiupright position
Head isthen allowed to drop sudden ly by 15-30' and supported by hand again. The response 1- Fast movement (4 . s iarirslsecond) 1. Slow movement (1-3 jerksisecond) _
0—;
'ncludea - 2. To-and-tro movements are at equal speed and 2. Have last and slow components that occur
a) Abduction and extension at shoulders. armimde alernately
1stphase(Ftapid) b)Extensionolebows. 3. Provoked by stirrxlalion 3. Not provoked bystirnulation
c) Openi'rgothandsJollowedby—
4. Can be stopped by restraint! resistance 4. Doesn't stop with restraint
pter—4 101
100 QUEST : PAEDIATRICS NEONATOLOGY D Cha
Convuislon j LONG QUESTIONS

Jmm‘
5. Neurological examination usually normal 5. Neurological examination — often abnormal olism. A 7 day old neonate (term) is havin
g jaundice-
0. 78. Describe in brie! the bliirubin metab
-
ntly uncon lugated). Enumerate the pos-
6. Not associated with eye movements or 6. Often associated with eye movements (tonic The serum bilirubin level is 15 Mg/di (predomina
7 (6+1+3) ”(PC-9th Sent]
autonomic changes. deviation or fixed stare) andior autonomic sible causes. How will you manage the baby
changes (9.9., changes in heart rate) jaundice
One 3 da y old baby presented with
a. 79. Discuss the process of bilirubfn metabolism. nos is and management 7.
ch for th e diag
extending upto the sole. How will you approa
[20131 (3+7) {Kaiyani-Jth Sent)
0. 76 : Baby of 3 days old, mother having chickenpox.
Ans : BILIRUBIN METABOLISM (O. 78 It 0. 79)
Ans : 3 DAYS OLD BABY WITH MATERNAL CHICKEN PC)!
See GI System.
lesions, following
.ten mother of a 3—day old newborn is found to have chickenpox or varicella CAUSES OF JAUNDICE :
ent protocol —-
paints should be considered before deciding the managem listed in Q. 46, except —-
1. 6 day old neonate (O. 77) : All the causes
any evidence of infection
1. Whether the mother developed the rashes on the same day. or she had a) Breast milk iaundice
days ( 129., lst or 2nd post partal days). which was missedfign ored. This is because jaundice)
forthe last 1-2 ‘ usually presents later (causes of persistent
may have occurred before b) Pyloric stenosis
if motherdevelopsrashes upto 2 days alter delivery, the initial viremia
is more severe and fatal). c) Hypothyroidism
delivery. resulting In transplacental infection of the baby (which
d )aundice (l'SB=1 5 mgidl) [0. 78] -
definitely devoid of immunity against 2. 7 day old term neonate with unconjugate
2. Whatever may be the time of onset of rash, mother was patholo gical jaundice (O. 46) except the above 3 causes
which
there is no protectin g Ab against Varicetla Zoster Vims (VZV) in the newborn also. All the causes of unconj ugated
vancela. So. e.
are more susceptible to severe present later 9 Physiological jaundic
3. Gestational age of the baby is also irrportant. as preterm infants > 15 mgidl) (O. 79) —
3. 3 day old baby with sole staining (is. TSB
infection. jaundic e (O. 46). except -
All the causes of patholo gical
0 W- a) Above 3 causes. which present later (>1-2
weeks)
1. Post-exposure prophylaxis — (PEP) b) increased enterohepatic circulation
- fndcations -+ c) Sepsis ] usually present after 3 days
after delivery. [N.B. — also for mothers
a) If mother had onset of rash upto 2 days (1) Metabolic diseas es.
ping varice lla upto 5 days before delivery]. irrespective of GA 0! the baby.
develo I (O. 77 8t 0. 79)
weeks) as the mother have possibly DIFFERENTIAL DIAGNOSIS iAPPROACi-
b) if the baby is preterm (i.e., GA < 37 completed l feature s and investigation) a bout the causes enlisted in'the answer
ity. [N.B. - If GA < 28 weekshveight < 1kg. PEP to [Should include discuss ion (clinica
no evidence of varicela immun
ity]. of that particular question)
be given irrespective of maternal immun
A. Clinical Features :
Options for PEP a jaundice. like — prematurity, LBW. peri-
' 1. Hi0 any risk factors for exaggeration of physiological
) — Most preferred. but it is presently
a) Varlceiia Zoster lmmunoglobuiin (VZIG natal asphyxia etc.
is also prohibitive.
unavailable in India and the cost 2. HIO parenteral nutrition.
e dose.
nce of VZIG; dose is 400 mgikg singl
bi MG - Second option in the abse 3. Urine and steel colour :
truly on day 3. PEP
2. If the baby is term and heal thy and the mother has ens at of rash a) Normalin unconlugated jaundice.
mainly Iound in
is not recommended. b) High~colored urine and white stool In conjugated )aundice (white stool is
breast-feeding is withheld. obstnicttve causes)
3. isolation - Should be done and
other complications
4. Treatment - if the baby subs
equently develops rashes. or any
be started. irrespective
4. Palior : in hernolysls. massive extravasation of blood. infections etc.
phalitis etc). lV Acyc lovir shou ld
(litre pneumonia. hepatitis. ence 5. Plethoric : in polycythemia.
of the PEP status.
and other supportive 6. :Elfle.t'tornegatyy1:”);J hemolysis. infections and metabolic causes (may be associated with
aggressively with oral acyclovir
5. Mother should be treated ation Wmlfi'lli etc.
“WHO. 7. Features oi Intestinal obstruction. like - abdominal distension. constip
nel in
in e a days old neonate. [201
6-9uppla]
m ' "he — “mm“ "“5 WOW anterior lonia
O. 77. Differential diagnosis
oi jaundice
a. mmngzlrrthgomfta.:m' m
CamScanncr
102 QUEST : PAEDIATHICS
NEONATOLOGY El Chapter-4
“Le . 103
B. Investigations :
3. Specific therapy : . ;I t
1. Serum Bilirubin : ' "’h'
a) Antibiotic for sepsis.
a) Total.
b) Exploratory laparotomy for intestinal obstruction.
b) Direct fraction (CB)
c) Kasai operation for Biliary atresia.
c) Indirect traction (UCB) (=Total — Direct)
d) lVIg may be used as an adjunctive therapy in cases
It is the first and foremost investigation in any newborn with jaundice. to differentiate between of immune hemolysis.
unconjugated and conjugated hyperbilimbinemia and also to dicide management strategy. O. 80. Give an outline of bilirubin metabolism . Describe
th e undo I ' '—
When Direct Bilirubin is > 20% of total bilirubin it is known as conjugated hyperbilirubine— ological jaundice in the newborn.
mia (Although UCB > CB). r ymg memwsgrgégz;
‘
- Otherwise. diagnosis remains unconjugated hyperbilirubinemia in all other cases. Ans : BILIRUBIN METABOLISM
2. Blood Group of See GI system.
a) Mother and PHYSIOLOGICAL JAUNDICE : MECHANISM

b) Baby (If mother is ‘O' or Rh —ve) _ See 0. 45 (Etiopathogenesis)
3. Direct Coomb's Test : Positive in immune hemolysis ( :19. A80 incompatibility & Flh-incompat- O. 81. Discuss _Bilirubin Metabolism in relation to physiological jaundice
ibility). ' ' In newt: . M '
the criteria of Pathological Jaundice. (7 + 3) [MRS - 8th Sam] [ ICAzrg- 22’1'33n
4. Hemalocrii : Decreased in
Ans : - Ist Part - Same as Q. 30
a) Hemotysis.
b) Infections (sepsis or intrauterine infections). 0 Criteria of Pathological Jaundice — See 0.47.
c) Massive extravasation of blood. ' a. 82. Describe Billrubin Metabolism. Enumerale the mechanis
m election and side efiects of
. Reticulocyte count : Increased in hemolysis. phototherapy.
m‘lO‘JU’t
(4 + 4 + 2) [MCK o9th Sam]

. GGPD level : For diagnosis of G6PD deliciency. Ans : BILIRUBIN METABOLISM
. Sepsis screen : Positive in sepsis (confirmed by blood culture). See GI system.
. Liver Function Test : Deranged (is. Ted enzymes, led albumin, Ted Prothrornbin time etc.) in PHOTOTHERAPY : MOA & SIDE EFFECTS
cases of - See 0. 51 - 52.
a) Sepsis induced hepatitis.
b) Metabolic diseases. a. B3. (Dre'sc'ribe the physiology of human lactation. Briefly mention
the anti-infective properties
a roast milk. {6 + 4) {MOS-Supplementary]
c) Other causes of hepatitis.
9. TORCH screening : For diagnosis of intrauterine infections. Ans : PHYSIOLOGY OF HUMAN LACTATION
10. Straight X-ray abdomen : For intestinal obstruction. See 0. 26.
II . USG abdomen : For diagnosis of obstructive causes. ANTI-INFECTIVE PROPERTIES OF BREAST MILK
‘I 2. Metabolic screen.
- See 0. 29 —+ Advantages of colostrum (No. 2. 3 and 5)
TREATMENT (o. No. 78) 0 See 0. 30 -—) Microbiological and immunological advantages of breast milk.
Total Serum Bilirubin Level).
Treatment strategy is decided according to the severity of jaundice (i. 9. 0. 84. Enumerate the possible causes of convulsion in a neonate. How will
transfusion.
following the normograms for institution of phototherapy and exchange old newborn brought to hospital with active convulsions?
you approach 2 days
during the initial 7-10' days of tile (2 + 6) [KPC - 2016].
1. Double surface Phototherapy: Usually the mainstay of therapy
3 mechanisms ——
for unconjugated hyperbilinrbinemia. It lowers serum bilirubin level by Arts : NEONATAL CONVULSION : POSSIBLE CAUSES
a) Photo—oxidation. Neonatal convulsion or neonatal seizures are the most frequent and distinctive clinical mantles-
.
b) Photo«isomen'zation a tation of neurological dysfunction in the newborn infant. Etiologies are —
c) Structural isomerization (most effective mechanism)
2. Exchange transfusion : In more severe
cases. when the initial bilirubin level is too high or the t. Hypoxlc tschemlc Encephalopathy (HIE) — Secondary to perinatal asphyxia and the
commonest cause oi neonatal seizure in our country. Subtle seizures are the commonest type of
phototherapy fails to decrease jaundice adequat ely. Selection of blood group for exchange translu-
. seizures Iollowlng HIE in neonates.
sion is done according to the followi ng rule —
2. Metabolic causes -
group at the baby.
a) Rh incompatibility : Rh —ve blood wlth ABO
Rh group of the baby. a) Hypoglycemia,
b) ABO Incompatibility : ‘0’ gram blood with
b) Hypocalcemla.
c) In all other cases. baby's blood group to used.
_ 105
NEONATOLOGY U Chapter-— 4
) SAH . .
c is seen in term ‘well' baby
c) Hypomagnesemia.
d) Rarely. pyridoxine de ende
nc and IEM l
_
d) IVH ls commonly seen in preterm babies.
p y [ nbom Errors 0' Metabolism) 3. General examination -+
3_ Infections _ l hemorrhage
_ 'l' a) Pallor: Seen in intracrania t
a) M y) with polycythernia
. _
etc) b) Plethora : Seen in preterm babies (mainl
terine infections (9.9.. TORCH. Syphnis
_ _
b Meningi ls orphic feature.
] eningoencephalitis secondary to Intrau c) Any obvious malformation or dysm
<
4' lntracramal hemorrhage - 4' CNS examination _} in IVH, SAH etc.
a) Subarachnoid hemorrhage (SAH). a) Bulging anterior iontanelle : Seen
noted.
b) Intraparenchymal hemorrhage,
Common in terms b) Consciousness. tone and reflexes odour may be <
tosplenomegaly or abnormal urine
o) Subdural hemorrhage (SDH). 5. Systemic examination —i Hepa
_., Common in preterms
d) Intraventricular hemorrhage (IVH) suggestive 0' ”EM
- Like neuronal migration detect <
5. Developmental defects of brain
C) Investigations :
al narcotic withdrawal, local anesthetic injec-
6. bliscellaneous - Like polycythemia. matern hic neonatal convulsions etc. 1' Blood sugar—i To detect hypoglycemia; bedside CBG measurement is essential t
atal seizure.
in each case oi neon
tron into the scalp (accidental). benign idiopat calcemia
2. Serum calcium —> To detect hypo
APPROACH excellent tool lor detection at NH and
3. Cranial ultrasound (GUS) —> An SDH. (
. 2 da Id e to detect SAH and
ya 0 nevyborn. _ inlraparenchymal hemorrhage but is unabl mia.
hypoglyce
Active WWU‘S'OHS on presentation. 4. Sepsis screen —+ As sepsis may precipitate c
'
'4 For diagno sing anemi a (hemonhage s) and polycythemia
7' Possible causes in this 0839 -tst 24 hours. but initial subtle seizures may be ignored by 5- PCV sequ elae of HIE and hypoglycemia etc.
6. CT scan / MR! —> To diagn ose SAH. SDH,
1. HIE_(usually present in tude integr ated EEG) has both diagnostic and
him?) 'i. EEG -i (Including aEEG or ampli (
2. Hypoglycemia. prognostic role in seizures. ing substance,
blood pH. ammonia. urinefor reduc
8. Metabolic screening —i Includes (
3. Hypocalcemia. serum and CSF lactate etc. and are done,
is scape-clad.
if IEM
4. lntracranial hemorrhage positive.
5 IEM ' 9. Specific iEiir screening -—) Ii metabolic screen is ‘
6. Pol;cy.hemia' TREATHENT — See Question No.
43 (Flowchart for treatment).
with active
7, Maternal narcotic withdrawal. er weighing 4 kg was brought to NiCU
o. 85 : A 2 day old baby of a diabetic moth ruptu re of membran e andtlie baby was ~
s. Mother had history of prolonged
APPROACH convulsion e "'9
probable “"595 ”0" W5" ybunianag
A) History born by emergency LUCS. Enumerate fl" (2 + 5) [KPC " 8th Sam]
d be obtained from the parentsiiamily
-
1. Complete description of the seizure shoul “5‘ 7 <
members. A” -’ PROBABLE CAUSES
ire about any seizure activity (9.9.. subtle
2. Leading questions to be asked to enqu - Available intormations - ‘
seizure) in the first 24 hours oi lite. 1. infant of diabetic mother (IDM)
2_ Day 2 baby ‘
3' Antenatal “53°”- hypoglycemia and hypocalcemia)
a) Maternal diabetes (leads to both a. Weight = 4 kg (i.e.. LGA)
awal seizures in the newborn infant) 4_ Presentation _ active convulsion
b) Maternal narcotic addiction (leads to withdr
- H/O penn atal asph yxia (9.9.. less fetal movements. prolonged 5. “,0 PROM
4. Natal history cry alter birth etc.). HIO instrumental deliv- . ‘
on. timin g of 6. Born by Emergency LUCS
labour. need for resuscrtati _-
ery (may lead to hemorrhage). . 1
ry - i-l/O asso ciate d letha rgy. drowsiness. vomiting alter breast ' W0 ' _
5. Postnatal histo . s of IBM
Co .ication
feeding may be suggestive of IEM. mental retar-
1- Hypoglycemia
rnpl
inity in parents. family H10 seizures. 2. Hypocalcemia
6. Family history- HID consangu . which is a imown nsk tactor oi E03)
dation or early neonatal deaths may sugg est IEM. 3. Early onset sepsis (as there is Hi0 PROM
B) Examinatlon _ oi LEA)
4' Polycythemia (complicationhemo
5. Others - HIE. Intracranial nhage (as DID of day 2 neonatal seizure).
infants with seizure '
Vital al no -i recordedl inhtall
1
2' G [g d birth
.infants. APPROACH and MANAGEMENT
' "m M "’ w' 9 " preterms. SGA Inianls and LGA SeeQueslion No. 84
Hypoglycemia is more common in
a) . . . -
infants
b) Hypocalcemra is common in VLBW
14
IMMUNIZATION I] Chapter-5 107
.. ' t .— I
i}- ' i
O. 2 : Inactivated polio ccfne. [Burdwan] [SSKM]
CHAPTER — 5 Ans : IPV is available as an effective vaccine against poliomyelitis tor the past five decades, developed by
Jonas Salk in 1950. '
IMMUNIZATION Cl Vaccine :
> It is formaldehyde killed polio virus-grown in monkey kidney cells/bu man diploid cells.
> Currently used IVP vaccine contain 40, 8 and 320 antigen units of type 1. 2 and 3 respectively
o. r.- 806 Vaccination. {zorO-Suppre, 2008-SUppIe] and thus called 'enhanced potency IPV (eIPV)'.
Ans : BCG Vaccine is derived-from the bovine tuberculosis strain and first developed in 1921. > StOrage — At 2-8° C.
El Vaccine : D Protection :
> It is a live attenuated vaccine. I 3* Excellent efficacy in preventing occurrence of polio.
> Most common strain used is Danish 1331. In India this strain was produced at Guindy. Tamil ‘5» Produces secretory lgA antibody and herd immunity though it is lower than OPV.
Nadu. . > Does not cause VAPP (Vaccine associated paralytic poliomyelitis) by sequential administration
> Available as a lyophilized (freeze dried) in a vacuum-sealed dark multidose vial. of IPV with OPV. Sequential administration of OPV and IPV maintain high rates of mucosal
> Diluenl-sten‘le normal saline. immunity and thus prevents VAPP.
> Storage 2-B° C, sensitive to heat and light. Unused reconstituted vaccine is to be discarded after El Dose and route : 0.5 ml. intramuscular or subcutaneous.
4 hours. El Site : Usually anterclateral aspect of thigh.
CI Protection : El Dose schedule: Not recommended in NIP till now.
> Primarily induces cell mediated immunity. IAP schedule : Primary — 3 doses at 6, 10 and 14 weeks
> Protects against severe form of tuberculosis (9.9. Miliary TB, TB meningitis) . Booster — one dose at 15-18 months
_
.
"a"
> Significant reduction of risk of death from TB. OPV at birth, 6 months, 9 months and 5 years and on NIP.
a‘x..-.E.:;_Ll
D Dose routine: 0.1 ml., intradermal. Catch up - upto 5 years.

E] Site : Left upper arm, at the insertion of deltoid to allow easy identification of BCG scar. 3 doses at 0,2 and 6 months
”—1..“
0 Normal Reaction : D Adverse reaction : Local pain swelling.

u..;_v.—. _
Intradermal injection El Contraindication : Known allergy.

l
_.~-_.
or. 3: MMR Vaccine. [2015] _

wheel of about 5 mm
Measles and
-
Ans: MMR vaccine is effective against three complicating infectious disease - Humps.
-‘_.H
l
death have
Small papule by 2-3 weeks Rubella. With the help of widespread measles vaccination. globally number of measles
-u
public health
dropped considerably. But in developing countries measles still continues to be a serious
._...
l
Enlarges to 4-8 mm by 5-6 weeks .problem.
Momps carries
i Globally. most countries use MMR vaccine instead of Measles vaccine only. Because
orchitis.
as much significance in terms of a number of complications like — Aseptic Meningitis. encephalitis.
Ulcerates and heats by scarring at 6-12 weeks to disastrous
oophoritis, deafness. pancreatitis etc. and Rubella during first trimester of pregnancy le ad
[:1 Schedule : consequences known Congenital Rubella Syndrome (CRS).
> At birth or at first contact u Vaccine :
> Catch up can be given till 5 years. > It is live attenuated vaccine.
U Adverse Reaction: 5‘» Strains used are different formulation from different manufacturers.
> Local ulceration or discharging sinus. Mumps component - common strain is Jeryl Lynn strain.- .
L.
if given subcutaneously)
> Axillary or cervical lymphadenOpathy (more likely Rubella component — RA 27/3 strain.
_
_:
Measles Component — Edmonston Zagreb Strain.

«:4.—-_.
> Disseminated infection.

compromised patient. 1» Vaccine is effective with seroconversion role rate is over >95 %.
. _
> Osteomyelitis or scrofuloderma.- in immune

wh-—-.—...
..._._
Cl Contraindication : > ' Storage at 243° C light protected.

> Cellular immunodeficiency. > Reconstituted unused'vaccine is to be used within 4__‘ho_urs.
wag—W
D Dose Route : 0.5 ml. Subcutaneous "

> Symptomatic HIV.
“nu-y
106
..
__..——.-m
IMMUNIZATION El Chapter-—5 109
108 QUEST : PAEQIATRICS
A
{-j' ,
.1
D Contraindication : (a) Inherited or acquired immuno—deticiency state.
A-
Cl Site : (b) Advanced HIV.
) Anterolateral aspect of thigh.
0. 5: Typhoid vaccine (MCK ) (8th sem)
> Right upper arm [at the insertion oi deltoid) India. To combact
Ans : Typhoid lever Is the major public health problem in most developing cOuntries like
AflJflA—uhfl
CI Schedule : this infection there are 3 types of typhoid vaccines have been developed.
> National programme - At 15-18 months (only in some states) Vaccine -
> IAP : - Two doses at 15 months and 4-6 year. ' Whole cell inactivated typhoid vaccine (TNTAB) —
- Catch up 2 12 months — 2 doses 2 4 weeks apart.
> Contains heat-killed whole cell Salmonella typhr‘ and S. Paratyphi A and B
CI Adverse reaction: > Protected elficacy 50-70% '
2-3 year.
> Fever. > Two doses, 4 weeks apart in children > 6 months old. and reactivation every
3‘» Transient rash. ride vaccine -
' VI polysaccha
> Arthralgia. serum bactericidal action.
> Purified V1 antigen that prevents phagocytosis ol S-typhi and inhibits
> Lyrnphadenopathy. ed and conjugated
> They are oi two types unconjugat
-
> Aseptic meningitis. revaocination every 3 year
> Unconjugated vaccine elicits anti vi—antibodies in children > 2 year and
D Contraindication: Conjugated vaccine has been developed recently immunoge nicity and safety is insulficient to
>
> Immunodeficiency state. recommen d its use.
— immunosuppressive drugs. ' Oral vaccine -
nrx
— Malignancy.
3» Contains live attenuated bacteria of the Ty21 a. Strain of S-lyphr'.
— Advanced HIV. million live lyophilized
> The vaccine is available as an enteric coated capsule containing 2-6
— Untreated tuberculosis. bacteria that induces mucosal immunity.
stomach
> Pregnancy- > Primary immunization consisting of 3 doses given on alternate days on an empty
in children < 6
it Capsules must be swallowed intact so capsule is unsuitable tor administration
A
0. 4.- emrent opv. [BSMC] years.
litis.
Ans : OPV is the vaccine of choice for eradication of poliomye El Adverse reaction — Local pain, swelling. redness for injectable vaccine.
rx
ce : Howeve r OPV, particula rly the serotype 2 is associated with a high risk oi virus regaining I3 Contraindication — (i) Anaphylaxis (ii) Significant immunodeficiency in oral vaccine.
El Relevan
poliomyelitis (VAPP)' in 1 of 1.5 million
its neurovirulence to cause ‘vaccine associated. Paralytic Storage —> 2° — 8°C.
A
OPV recipient.
nce of outbreaks of paralytic poliomyelitis by a 0. 6: Pulse Polio immunization. [2013150]
> Another relatively recent concern is the occurre
of poliovir us lorrned by mutatio n ol OPV. Called the circulating vaccine derived
virulent strain Ans :
Global polio. <
poliovin1s(CVDPV)
to Pulse Polio immunization programme was launched in India in 1995 as a result of WHO
a dvisory group or poliomyelitis in India is ‘
> One of the many strategies proposed by expert Eradication initiative.
from conven tional trivalen t OPV to biva lent OPV (lacking serotype 2) in 2010. as Supplementar y Immunization Activities (SIA) I
switch over This involves mass immunization campaigns known
I3 Vaccine: that includes both National Immunization Days (NIDS) and Sub National Immunization Days (SNIDS)
j
> Live attenuated vaccine. Objective -- PPI was initiated with the objective ol achieving hundred percent coverage with OPV.
rapidly with
s and —20° C tor a year but potency draps These supplementary immunization rounds are intended to complement not to replace routine
> Vaccine is stable at 443° C for 3-4 month . '
fluctuation of tempe rature . immunization.
e vial Monitor (WM) a heat sensitive patch
displayed on
Aim - Aim of PPI is to 'flood' the community with OPV within a very short period of time. thereby '
> Potency is monitored using the vaccin '
the label of the Vial. interrupting the transmission of virus throughout the community.
‘ d I l
Activity - '
D Protection:
d as 'take' oi the vaccrne, pro uces oca > PPI l NID are conducted in two rounds one month apart usually in December and January every
' 'ruses multi I In ut mucosal cells. terme
9 e at infect ion with wide polio virus a nd thus chances cl paralytic year until polio is eradicated. All children < 5 year age ole particular area are given 2 doses cl OPV.
torywlgA. It reducpesy chanc
Vaccine
> secre
poliomyelitis , > Three to live NIDs are usually required to eradicate polio but some countries require more time.
herd immunity. specially where there routine imrnunlzation coverage is low.
> By excretion or stool it also produces
> They are conducted usually during cooler months (December. January) because logistics are
El Dose and Route: 2 drops. oral and supple- simplilied and immunological response to OPV is improved.
tor routine immunization included in NIP
El Schedule: Currently bivalent OPV is not used mop up activities targeting migrant popul
ation > In Sub National immunization day instead ol covering entire country few states / large geographical
and
mentary NIDs (National lmmunizative Days)
and high risk areas.
T‘ —,_‘__*‘—*— _
11D QUEST : PAEDIATFIICS lMMUNIZATlOM El Chapter-5

. . 1!; 111
fi.
areas are covered. Depending upon the epidemiology of wild polio viruses these rounds are con- After 2 months ~ MMR (Preferred) or Measl
es
ducted throughout the year in contrary to cooler months of NID — Typhoid
lntensification - Affer6month — DWP/DTap
> intensification of the PP! programme is accomplished by extra immunization, rounds, adding house — Hepatitis B
to house ‘search 8. vaccinate' component in addition to mass immunization at a fixed date.
a. 9: NIP (CNMC) [Kafycni]
a. 7: oer/a "Pl/[2010} Ans :
Ans : Oral polio vaccine also known as Sabin and inactivate polio vaccine, also known as Salk are two immunization is regarded as the greatest succes
s story of the 20th cent ury. The immunization
affective vaccine for polio eradication for past five decades. Although both are effective against polIo has increased to more than 85% not onfy in developed coverage
but also in developing countries through organiz
viruses there are some differences which are as follows :
\.
natrcnal immunization programme worldwide. ed
Historlal perspective
IPV (Salk)
-
OPV (Sabin)
- The Expanded Programme of Immunization (EPI)
is the first organized global immunization initiative
1. Live attenuated vaccine. - 1. inactivated formaldehyde killed vaccine. . taken- by WHO in 1974 ' India adopted this initiative in 1973
. and -Included B -
2. Intramuscular or subcutaneous. Vaccrne (OPV) and Typhord vaccine chiefly in urban areas. CG' DTWP‘ Oral Folio
2. Administered orally.
3. Local mucosal gut immunity production is much 0 The Universal Immunization Programme (UIP ) was introduc
3. Produces local mucosal gut immunity move ed in 1985 to improve immunization
through secretory lgA. less than OPV but local production of secretory coverage in India. Measles vaccine was includ ed and Typhoi
d vaccine excluded.
lgA. ' Vitamin A supplementation was introduced in 1990
and polio national immunization days were
- - In - -
- unrmmunrzed 4. Heard immunity
_ . production _though is less_ than initiated in 1995.
4. Produces heard Immunity
-
segment of populatron.
OPV
to gut.but It Is there from spill over of antibody - The
. pentavale
' nt. vaccine containing. Haemophilus . Influenza b (Hib) and Hepatrtrs
" B vaccine
' wrth
‘
Diphtherra toxord. whole cell pertusrs and Tetanus toxoid vaccines
were first introduced in 2011
5. Humoral immunity production is less. 5. Produces strong humoral immunity response.
Obleditle - Universal coverage of all infant under 5 children childr
6. Expertise of administrator is required as the - the recommended vaccrne . schedule are the . enat10and16and Io
6. Administration is technically easy. expertise women with objectives of UlP. a 5 pregnant
not required. Dose -— 2 drops. vaccine is given I.M I 8.0 The objectives are -
Dose — 0.5 ml I.M I 8.0 > To increase immunization coverage
7. Ideal vaccine for outbreak control. 7. Not. ideal for outbreak control. > To improve the quality of service
. Not so much heat sensitive.
03
. Vaccine is very much heat sensitive.- > To achieve self sufficiency in vaccine production
on
9. Though very uncommon Live OPV is associ- 9. Not associated with those side effect. > To train health personnel
ated with serious side effect like Vaccine as- > To supply cold chain equipment and establish a good surveillance network
sociated Paralytic Poliomyelitis (VAPP) and
> To ensure districtvtise monitoring
circulating vaccine derived polio virus (CVDPV)
specially with conventional trivalent OPV. Nation Immunization Schedule
10. Cannot be given in severely immun
o- 10. Can be given in immune-compromised patient.
compromised patient like symptomatic HIV Age Vaccines
pafienL
0 (Birth) BCG. OPV. HepB
en unfmmunfzed 2 year child. [2014] 6 weeks
a 8- Enumerate the vaccines that can be given to
DTt. 0PV1. Hes, Hibt
10 weeks DTwP2. opvz. Hepea. H.132
-
Ans :
age not all vaccination doses are mandatory. The following
14 weeks DTwP3. 0PV3. HepB4. Hib3
if a child is unimrnunized till 2 years of 9 months Measles; Vitamin A‘ (First dose)
schedule is to be maintained -
BCG 15 month MMR (in selected states)
At evaluation (tst contact) -
OPV-1 dose 16-24 month DTwP. OPV (Booster 1 dose)
-
Japanese Encephalitis
.’ DTwpl DTap
(in selected endemic districts)
_ Hepatitis B
5 years DTwP (Booster 2 dose)
After1 month — OPV" d0“ 10 years 11'
.. DTWPI DTap 16 year 1T
.. Hepatitis B
FT— T
UM
112 GUEST : PAEDIATRICS
it...
ow
.
with ist dose at 9 month of age with Measles vaccine
I
‘ 5 mega doses of vitamin A at 6 months interval CHAPTER - a
o
0. 10.- 0e [some] INFECTIOUS DISEASES
Ans:
and Tetanus has been reduced significantly in
p
The morbidity and modality due to Diphtheria. Pertusis
since introdu ction and widesp read coverag e of immunization with DTwP under UlP.
India in children. [13]
is composed of Diphtheria and Tetanus toxoids as a. 1: Clinical features and laboratory Investigation of Dengue fever
0 Vaccine - DTwP. popularly known as Triple antigen
p
absorbe d on insoluble aluminium salts as adjuvant.
' well as killed whole cell pertusis bacilli Ans:
> Maternal antibodie s interfere with immune response s to DTP vaccination, particularly against pertusis. 0 Clinical Features of Dengue Fever
0.--!)
t i
To ensure protectio n vaccines should be administ ered within few weeks after birth and require
Dengue lever presents in two ways -
multiple doses. (i) Classical dengue fever
should be discarded.
> Storage at 2° — 8° 0, if accidentally become frozen. (ii) Undifferentiated febrile illness
Dose — 0.5 mi. intramuscular. _
Classical Dengue Fever- Classical features are common.
Site - Anterolaterai aspect of mid thigh.
Cl
incubation Period : Short, 2-? days

and 14 week (primary)
El Schedule — National Programme - DTwP at 6, 10 High grade fever with abrupt onset, lasts for 3-7 days
Boosters — 15 - 18 month and 5. 6. 10 year
Catch up — At 0. 1 and 6 month (if age is < 7 year) Headache
Retro-orbital pain
Adverse reaction —
vomiting. Photophobia
If > Local pain, swelling, redness, fever. anorexia.
Backache
> Serious adverse effect - Rare
Myalgia
' i ? - Persistent crying
Arthalgia _
I Seizures oi “Break-bone-
0 For those above symptoms classical Dengue fever has acquired an apithet
- Hypotonic hyporesponsive episodes (HHE)
of local reactions increase with increasin 9 number of fever”
Frequency of systemic reactions reduce and that
Other symptoms comrrionly seen
doses.
Severe weakness
Contraindications -
Anorexia
at > anaphylaxis after previous dose
ria and tetanus) Nausea, vomiting
t. : > Progressive neurological disease (give only diphthe
within 7 days of previou s dose. Abdominal pain
F“. ' > Enceph alopath y
s dose is associated with — Constipation
Precautions - Precautions should be taken if previou
48 hour. Transient maculo-papular rash over the chest. back and limbs.
> Fever > 405°C within
within 48 hours. Bleeding manifestation — like GI bleeding. Epistaxis during epidemic
In Collapse (Hypotonic Hyporesponsive episodes)
hour within 48 hours Undifferentiated Dengue Fever— This is seen in majority of children with Dengue infection.
> Persistent inconsolable crying for > 3
Mild to moderate fever — similar to other viral illness. a diagnostic challenge.
> Seizures within 72 hours.
0 A transient maculo-papular rash during fever or delervescence
Murshidabad)
0. i 1: National immunization schedule (Kaiyani, Mild respiratory symptoms
Ans : See Question No. — 9. 0 Investigation
I) Complete Blood count including haematocrit
Hb% -+ low in presence oI bleeding
Leukopenia is feature in early phase of illness
Platelet count may drop I
Haematocrit may be raising -) 20% or more rise is suggestive of hypovolaemia.
Raising haematocrit and drop in platelet count is a finding of impendingoomplication of Dengue.
113
?
QUEST : PAEDIATRICS INFECTIOUS DISEASES U Chapter-6 115

114
’ ' ~ “DI
n) Definitive test for diagnosis or Dengue (v) CNS - Acute-encephalitis caused by direct invation of brain by Measles virus or-‘post' infectious
» ‘ . -
Dengue infection in Immune mediated encephalitis are the rare but serious complication.
(i) Virus isolation in cell culture, viral RNA —) Those are the tests to diagnose
phase, before day 5 of illness during febrile period, but disadvantages are that they (vi) Eye — Keratitis may occur. ‘
very early
viral isolation require several
require expensive equipments. reagents. experienced technician and (vii) Cancrum oris, stomatitis names at different site of mouth and face.
in cell culture. Therefore , not used practically .
days to get viral growth (viii) SSPE— Subacule sclerosing Pan encephalitis - May occur as degenerative brain disease due
quick method of detection of
(ii) Viral antigen detection by ELISA —> This test is easy to perform. to persrstent infection by Measles virus after several years (7 year) after primary infection. It
antigen (N31) during early phase of infection, within 5 days. N81 antigen detection kits now
Dengue manifests as progressive personality changes. developmental retardation myoclonic seizure.
hours.
becoming commercially available which yield results within a few EEG and CSF study help in diagnosis.
antigen disappear from
(iii) Detection of Dengue Antibody —> Alter 5 days, dengue viruses and
al tests —- MAC-ELISA and 0. 3 : Complication of Falclparum Malaria (Supple, 2010)
blood with appearance of antibody. Commonly used serologic
hemagglutination inhibition lest. A) CEREBRAL MALARIA —
recent infection.
MAC-ELISA — Measures dengue specific lgG antibodies and indicates Commonesl complication of cerebral malaria. Presents as multiple seizures, unconsciousness.
Te st — Measures lgG antibody impaired sera collected at an interval hypotonia. brainstem signs. Illness may be confused with meningitis, encephalitis.
Hemagglutination Inhibition
acute flavivirus infection.
of 1-2 week. A fourfold increase in antibodies impaired sera sug gest Cause — Blockage (sequestration) of capillaries with parasitized erythrocytes leading to thrombosis
ntiating between primary and and focal damage in brain. Hypoglycemia is frequently associated with cerebral malaria and carries
Quantification of the IgG and lgM antibodies may help in differs
infection. lgG antibodies will be abundant in secondary infection unlike bad prognosis. Mortality is high (15-16%) and surviving children may have maior neurological deficit.
secondary dengue virus
primary infection.
fever. B) MULTIPLE CONVULSIONS -
I ll) Other tests - These are specially indicated in complicated dengue
Multiple complication without other neurological signs of cerebral malaria are the comma
(I) Blood total protein and Albumin — Low in Dengue with shock complication of falciparum malaria.
(ii) Blood SGPT and SGOT — High level seen in DHF Convulsion may be local. generalized or subtle with repeated twitching. eye deviation. irregular
(iii) Blood Urea, Creatinine - High in severe DHF breathing.
effusion, ascites. myocardial
(iv) Chest X-ray, USG abdomen. Echocardiography to detect pleural Causes - Altered cerebral metabolism
dysfunction in complicated Dengue infection. - Hypoglycemia
0. 2 : Complications of Measles (2012 supple, 2010 supple) — Hyperpyrexia
i on by measles account for the
Widespread mucosal damage and significant immuno-suppress Repeated seizures carry a poor prognosis.
frequent complication. .
C) GASTROINTESTINAL ILLNESS -
Most susceptibles - very young age of characterized by marked vomiting. diarrhoea, dehydration
Gastrointestinal complications
- Immunocompromised dyselectrolytemia. Vomiting is usually characteristic of malaria in infancy. -
-Malnourished
is otitis media. D) ALGID MALARIA -
(i) ENT —) Most common complication of measles
nia is an another common complication. Apart In majority of malaria patients hypovolemia. vasodilatation and postural hypotension is common.
—> Post mea sles Broncho pneumo
(ii) Respira tory
ory related complic ations of Measles like, but In some cases specially malaria in the non-immune children peripheral circulatory failure present
from these are some othe r respirat
as shock.
— ,Croup
E) BLACKWATER FEVER —
— Trachilis
Mild haemtilysislis common in malaria but some patients present with sudden severe haemolysis,
-— Empyema are
red smoky urine (hemoglobinuria) andrenal failure. Children with G -6 - P - D deficiency
— Bronchiolitis vulnerable to have this complication.
— Giant cell pneumonia .
F) ANAEIIIA -
-— Flaring up of Tuberculosis Falciparum malaria often presents with severe anaemia (Hb% < 7 gm%) and
this is out of_
a frequent complications, others may occur as
_ (iii) GIT - Frequent or persistent diarrhoea is proportion to the degree of parasitemia. Patient present with palpitation tachycardia. dyspnea
with
- Appendicitis severe palIor. . _
- Hepatitis ' Causes - Haamolysls

cause of dehydration and malnutrition leading
' Post measles persistent diarrhoea is a significant — Dyserythropoies'is
to high mortality. — Hematopoletic Fator deficiency
dary to immunosuppresslon like septlcemia with
(iv) System — Systemic bacterial infection secon
n.
streptococcus is a common complicatio
. j: ____._ __
_-._.... m“; _
- .
H6 ' QUEST ; .PAEDIATRICS INFECTIOUS DISEASES El Chapler~6 117
G) OTHER LESS COMMON COMPLICATION - (a) Impaired consciousness. coma — (303 < 8
— Pulmonary oedema. ARDS (b) Prostration - Severe weakness
— Abnormal bleeding manifestation to) Multiple convulsions - 2 3 seizure in 24 hour
- Acute nephritis
(d) Acidosis ~ PH < 7.25 and H003 < 15 meg/L
O. 4 : Treatment of cerebral Malaria (HMO, 8th sem, Heidi's] (e) Hypoglycemia -— Blood glucose < 40 mg/dl
_Cerebral malaria is a dreaded complication of iaiciparum malaria with high modality rate and high (f) Severe Anaemia — Hemoglobin < 5 mgidl
rncrdence of neurological sequelae. In addition to proper antimalarial therapy there is vital importance (9) Renal impairment — Serum creatinine > 3 mgldl
of supportive management.
(h) Jaundice — Bilirubin > 3 mgidl
I) Supportive Management - (i) Pulmonary oedema
(i) Patient should be ideally - management in PICU. as it is a potentially life threatening illness.
(j) Significant bleeding
(ii) Assessment of airway. breathing and circulation and management accordingly.
(k) Shock -— Systolic pressure < 80 mm of Hg
(iii) Detection of hypoglycemia (Blood glucose < 40 mglL) and treated by W. bolus of 10% or
(I) Hyperparasitemia -— > 10% red cells parasitized.
25% Dextrose.
(iv) Diagnosis of dyselectorolytemia and treatment accordingly. Risk factor —-
(v) Convulsion should be promptly managed with use of anticonvulsant. — Degree of parasitemia
(vi) CSF study to rule out meningitis. If it is not feasible or deferred for some reasons then - Cyto-adherence and sequestration capacity of individual
proper antibiotic coverage to be given. - Age — infants and children are more vulnerable
(vii) Assessment of hydration status and proper fluid management but overhydration should be — Immune status
avoided. - Geographic region
(viii) For hyperpyrexia repeated cold sponglng and use of antipyretics, Paracetamol I.V. - 10 mglkg
Investigation —
fix) Consideration of blood transfusion in presence of severe anaemia.
(i) Hemogram including platelet count
(x) Correction of lactic acidosis with proper oxygenations, tissue perfusion and judious use of
‘ (ii) Smear examination — Presence of P. ialcr'parum schizonts in smear examination is an
sodium bicarbonate. -
indicator of severe malaria.
(xi) A rapidly rising serum creatinine level is an indication of dialysis.
(iii) Blood sugar level
(xii) Raised intracranial pressure is to be managed by I.V. Mannitol or 3% NaCl.
(iv) Serum bilirubin and SGPT
ll) Anti-malarial Therapy - (v) Blood urea. creatinine
Parenteral antimalarial therapy for cerebral malaria. (vi) Urine -— Routine. Microscopic, Biochemical tests for hemoglobin and urobilinogéjt
Anti-malarial drug Loading dose Maintenance dose Treatment - Parenteral antimalarial drug Quinine or Artesunate or Artemether in fuel courSe along
with good supportive management. [Doses -— See Question No. 5]
20 mg salt/kg over 4 hours I.V 10 mg saltikg over 4 hour repeated
(i) Quinine dihydrochloride
every 8 hour 0. 6 : Management of a child with chloroquine resistant falciparum malaria [KPC, 8th Sam]
1.2 mglkg repeated at 12 and 24 Resistance to chloroquine is a common occurrence in case of falciparum malaria in part of the
2.4 mglkg
(ii) Artisunate IV route hour then 1.2 mg/kglday countries. In such situation Artemission derivative based combination therapy is the treatment of
choice.
3.2 mg/kg ’ 1.6 mglkg repeated 12-24 hour.
(iii) Artemether IM route (a) Artesunate + Suliedoxlne - Pyrimethamine
erapy to - Artisunate tablet 4 mglkg daily for 3 days
parenteral drug to be replaced by oralth
‘ Once the child is able to accept orally, . . . Sulfadoxine (25 mglkg body weight). Pyrimethamin (125 mglkg body weight) on first day.
complete 7 days course. .
emc lntrog - Primaquine — oi‘rs mg/kg body weight on day 2
t on pancreatic secretion leading to
‘ Ouinine has strong stimulant effec lty. So,‘ monit oring of blood glucose (b) Artenether-lumel'antdne
cardi otoxlc
hypoglycemia and also cause significant
if quinine is used as antrmalanai. Available as co-Iormulaled tablet of Artemether (20 mg) + Iumefartorine (120 mg)
and electrocardiogram is necessary
CNAiC] 0 5-14 kg (5 month — < 3 year) — 20 mgi120 mg BD fora days
0. 5 : Severe Malaria (MCK) [8th Sam, ion with P. faiciparum. 15-24 kg (> 3 year — 8 year) — 40 rngi240 mg 30 for 3 days
tially fatal condition caused mostly by infect
Severe malaria is a poten
following situations is defin ed as sever e falciparum malaria. 25-34 kg (> 9 year — 14 year) — 60 mgl360 mg 80 for 3 days
As per WHO presence of one or more nce of P. falciparum asexual
W—u..i.
occurring in absence of an ident ified alternative cause and In t he prese ' Primaqulne : 0.75 mglkg body weight on day 2
parasites -
118 QUEST 2 PAEDIATRICS
INFECTIOUS DiSEASES U Chapter—6 119
0. 7: Enumerate CIF of severe talciparum malaria. (SSKM)

Category Type of contact Recommended Post exposure
Severe falciparum malaria can affect virtually any system in body specially— CNS Respiratory
CVS haematological system and cause variety oi symptomatology prophylaxis
(a) CNS - l . Touching or feeding of animals None if hosiery is reliable

o Headache — Prolonged, uncontrolled headache. - Licks on intact skin
s Prolonged, recurrent convulsion —- 2 or more in 2-4 hour
ll . Nibbling of uncovered skin Wound Management + Antirabies
- Unconsciousness
a Minor abrasion without vaccine
Subtle seizure like facial twiching, eye deviation. irregular breathing
bleeding
- Opisthotonus posturing ‘
- Hypotonia ill 0 Single or multiple trans-dermal Wound Management
- Visual difficulty bnes +
- licks on broken skin Rabies immunoglobuiin
(b) Haematological -
+
0 Severe Anaemia ' Contamination of mucous
Antirabies vaccine
membrane with saliva (licks)
- Jaundice
- Bite over the facelhead.
- Passage of dark red smoky urine.
- Abnormal bleeding. petichiae - Application of soap/detergent for chemical treatment and changing the pH of wound
(c) Respiratory — 0 Application of disinfectants like providone iodine, spirit or household antiseptics to remove the
- Rapid, deep breathing remaining virus.
(d) Circulating — El Rabies lmmunogiobulin (RIG) :
- Postural hypotension - RIG is to be infiltrated as much as possible into and around the wound, remaining to be given
as int.
' 3W
- Shock 0 Provides passive immunity in form of readymade antibody to tide over the initial phase of
infection by binding to rabies vims and resulting in neutralization.
(e) G.l. —
- Two types of BIG -
- Vomiting
— Equine FllG — 40 iU/kg body weight
- Diarrhoea
- Human FilG — 20 lU/kg body weight
- Dehydration ..
E] ‘Antirabies vaccine :
(0 Renal -
- Active immunization against rabies infection will be done with antirabies vaccine.
- Oliguria or anuria
' Two types of vaccine.
- Passage of red smoky urine
(i) Cell culture rabies vaccine (CCRV)
(9) Other- -— Human diploid cell vaccine (HDCV)
. Hyperpyrexia— > 385°C bodytemperature is a common feature ofseveretaiciparum malaria.
— Purified chick embryo cell vaccine (PCEC)
a. 8: Prevention of Rabies [Kalyanl, 90! Sam] [13] - Purified vero cell rabies vaccine (Pi/RV)
is not
Rabies is endemic in india primarily a disease of animal and death is common, it prophylaxis (ii) Purif‘ ed duck embryo vaccine (PDEV)
done properly. Prevention of Babies can be done in following ways
-
- There are various schedule for administration of rabies vaccine for post exposure prophylaxis
(A) Post exposure prophylaxis using intramuscular and intraderrnal routes.
(8) Pre exposure prophylaxis ' Site a Anteroiaterai thighldeltoid.
(A) Post Exposure Prophylaxis 0 Dose —) All vaccine — 1 ml except PVEV. Dose for l.M.. PVEV —> 0.5 ml
of a canine animal
Type of post exposure prophylaxis depends on the wound category alter bite - The Intradermal (ID) dose is 114m of the intramuscular dose.
El Wound mana geme nt: . Most common schedule for use -
rabies
- Preper wound management is primary and important step to prevent Essen schedule — 5 doses (1-1-1-1-1) ("4 use)
minutes to diminish the viral load.
. Washing of wounds under running tap water for at least to Single dose on day 0. 3. 7. 14 and 28
lNFECTIOUS DISEASES U Chapter—6 121
‘0' indicates first injection (i) Explosive onset

Updated that-redcross (Updated TRC—lD) Schedule (ID use) 2-2-2-0-2 (ii) Severe otalgia
0.1 ml of reconstituted vaccine per to site and two such ID sites per visit (iii) Toxic appearance
(one on each deltoid area) on 0. 3. 7, 28 day. (iv) High lever
- Tetanus Toxoid & Tetanus lmmunoglobulin - to be given as required. Duration of antibiotic therapy - 10 days
(8) Pro-exposure Prophylaxis -— initial choice — Amoxycillin / Amoxycillin 4- Ole vuiinic acid ‘
Used for persons at high risk of rabies to contact with animals. - Severe case -— injectable third generation cephalosporin.
Dose & schedule -+ LM. 0. 7, 21 or 28 day. Supportive treatment —-
- Adequate hydration ' ‘
booster dose alter 1 year & every 5 years there after.
0.9: Clinical features and treatment of acute otitis media. [2010, supple] -— Oral paracetamol — to relieve pain and lever
- Tympanocentesis — may be required occasionally to relieve severe pain.
t
Acute suppurative otitis media (ASOM) is a common cause of morbidity in children.
c
ASOM is defined as inflammation of mucoperiosteai lining of the middle ear with duration of illness 0.10: Complication of Mumps (Kalyani, 8th Sem)
and young adult.
< 2 weeks. Mumps is an acute, generalized virus infection predominantly affecting children
— Pancreas,
Children are more prone to devel0p ASOM because the eustachian tubes communicating throats Though main organ of affection is salivary glands mumps can infect almost any organ
s. c
with ears are straight and short. testis or ovary. the breast. liver. joint. heart and CNS and cause a number of complication
l
Clinical Features : Common complications are as follows —
Symptom : (i) Orchitis -
or
0 Moderate to high grade lever > Infection can also be established in the testis and epididymis, particularly in adolescents
excessive crying adufls.
Pain in ear in older children, in younger children this is common cause of
> 1-2 weeks after parotitis
- Ear discharge
> Most of the cases unilateral affection
- Sometimes ASOM may cause lower motor neurone facial palsy
> Onset is usually acute
- Hearing loss may occur in older children
> Testicular swelling, tenderness. nausea, vomiting
Signs : 3
3* Testis become two to four times larger and very tender
. Ear tenderness i
> Atrophy may develop latter but sterility is rare.
- Ear discharge . _
be seen as inflammed, bulged with loss (ii) Meningitis and Encephalitis -
- Otosoopic examination -Tympanic membrane will
with fluid in middle ear. . > CNS complication of Mumps include aseptic Meningitis or Encephalitis-
of normal anatomy '
ation in young children, presenting with fever, > Aseptic meningitis is more common. 140% patient
' Otoscopy should be part of routine examin '
with localization and in a setting of URTI it a child is crying excessively. > Meningeal symptoms develop anytime between a week to several weeks after
parotitis
blindness but prognosis is usually "
Treatment : > Encephalitis can be very serious with seizures and cortical
the primary mode of treatment. good.
As ASOM is a bacterial infection antibiotic is Other
‘ > Aqueductal slenosis and hydrocephalus have been associated with mumps infection.
Useful antibiotics —- (i) Ampiciilin CNS manifestations include — Cerebellar ataxia, Transverse Myelitis. G-B syndrome.
(ii) Amoxycillin
(iii) Pancreatitis -
(iii) Amoxycillin + Clavulanic acid
> Another complication of mumps infection is pancreatitis'. occurs in 5% cases.
(iv) Cephalosporin
(v) Macrolides
> It has been implicated as a possible cause of juvenile onset diabetes
.- é]
‘>_ Diabetes may develop few weeks after onset of parotitis.
initiation of antibiotic therapy : osis
iol ic to be started at the time of diagn (iv) Oophoritis-
‘ Children < 2 years of age — antib e starting antibiotics
disease - one can we it 2-3 days befor > lnlection can occur in ovary specially in postpubertal female patients
‘ Children > 2 years of age 'with mild '
> But usually no evidence of impairment of fertility.
- Severe disease at any age
Severe disease is indicated by
INFECTIOUS DISEASES C] Chapter—6 123
a. 12: Clinical manifestations of Tubercuisr meningitis [CNMC] [9th Semi} ,_ _

(v) Deafness —
Meningitis is a serious complication of childhood tuberculosis. It may occur at any age but is 5’99
> Sensory neural deafness may develop after mumps infection
most common between 6 and 24 months. children. not received BCG vaccination at birth are
> Deafness may be unilateral/bilateral. transient/permanent. particularly at risk.
(vi) Other complications — Other less common complications include ~ Clinical features of TB meningitis are divided in three stages. these three traditional stages of
> Myocarditis TBM are not sharply defined and clinical features often overlap.
> Arthritis Stages are as follows :
> Optic neuritis (i) Stage t, Prodromal stage or stage of invasion
> Mastitis (ii) Stage II. stage of meningitis
> Thyroiditis (iii) Stage III. stage of coma.
> Endocardial fibroelastosis Stage i, Prodromal Stage -
0.11: CSF changes in TB meningitis [2009, Supp] > Symptoms are non specific
Tubercular meningitis is the most frequent manifestation of CNS tuberculosis and is a potentially Onset is inci'dious may be acute in infants
VVVVVVV
curable disease if early diagnostis and early institution of Anti Tubercular chemotherapy can be Low grade fever, loss of appetite
done. Otherwise death and permanent neurodisability'is inevitable. TBM is the most important Disturbed sleep
cause of death in children amongst all types of neurotuberculosis. Vomiting. constipation
CSF study is an important tool to diagnose tubercular meningitis as in other types of meningitis. Headache complained by older children
The classical CSF picture of tubercular meningitis is as follows - ‘
lrritability, restlessness. apalhy
less playful
Feature CSF finding
> Photophobia in older children, younger children resents exposure to sunlight
Physi appearance Clear. colour-less cobweb coagulation is As the symptoms are non-specific this stage is often difficult to be diagnosed as TB meningitis and
formed on standing. it appears as basketball disease progress to next stage.
net suspended from upper end of fluid in test
Stage if, Stage of Meningitis —
tube composed of TB bacilli and fibrin
> Alteration of sensortum. drowsiness or delirious
Pressure (mm of H20) (Nomal - 50-80) Usually elevated. ) Signs of meningeal irritation are positive — Neck rigidity and Kernig sign
5 — 500 > Convulsion in 65% cases .3;
Leukocyte (m3)
PMN early Cananial nerve palsy -— squint. vision disturbances. facial asymmetry, plosis; dilated irregular
Normal < 5%. > 75% lymphocytes) >
but lymphocyte predominate (> 60%) through pupils.
most at the course
Paralysis — Hemiplegia, monoplegia or quardriplegia
VV
100 — 3.000 Features of raised ICT like headache. vomiting, visual disturbances. pulse. 8P changes. bulging
Protein (mg/dl) (Normal - 20-45) May be more high in paresence of block in .
fontanelle and separation of sutures (in infant and young children)
CSF flow
> Cutaneous manifestations of autonomic nervous system disturbance-
4: 50 in most cases Stage ill, Stage of Game - _
Glucose (mg/dl)
(Normal > 50 or 75% serum glocose) 3* Deep coma. well marked meningeal signs, progressive neurological delicits
Acid fast bacille almost never seen on smear.
Staining, Microscopy and culture > Dialatedvand fixed pupils to.light
Culture : If CSF volume is' large > 5 ml. > Clem-stokes or Biol type of breathing
<.-..»_
1-.—
organism can be recovered

3* Neck retraction, opislhotonous, decorticate and decrebrate origidity
Adenosine Deaminase (ADA) level and fiaflefium T5 can be deified bit FOR > Central origin of hyperpyrexia
0 , , Death is almost inevitable if the disease progress to 3rd stage.
l TB -
PCB or > 10 UiL is supportive evidence of Tubercular 0.13: Tubercuiin Test] Marriott: Test [2009, KPC, 8th Sam]
meningitis ng the diagnosis
The ttberoutin skin test (Mantoux Test) is the most common test used for establishi
tuberculosis. But in addition
of childiood TB though the test is not sensitive or specific to diagnose
it helps as a supportive test to establish diagnosis. .
to other test
"I
“x
‘\
\‘n
‘\
.._._I
.
i
124 OUEST:PAEDlATFiI lNFECTlOUS DISEASES El Chapter—6 E
I CS
Dose — S TU of PPD-S (Purified Protein Derivative) or 2 TU of Tuberculin PPD RT-23.
. n te n—
Administration — A one quarter to one half Inch. 26G needle and Tuberculin syringe are used Commo Iy affec d orga
to inject 0.1 ml of PPD intradermatly into volar aspect of forearm. > Lung
Reading - After 48-72 hours of injection diameter of induration should be measured transversely > CNS
to the long axis of forearm and recorded in millimeters. _ 3' Lil/9i
Interpretation - > Bone marrow
. . > Pericardium
Size °f'"d"m‘°" Interpretation - CliniCal features - Symptoms of miliary TB can be vague, non specific. often difficult to
'dentily.
< 10mm Ne alive N a t' ' ‘ - child may have
Iit bacteria are intermittently released into the blood stream from a hidden lesron l
g ' ° owe disease
5 — 10 mm . . . Borderline, on and off febrile episode and gradual weight loss
‘
. '29ml:Eéd-
cififilnzfijglcgztsagzriglnlrtTrficggp sI Ive In Other symptoms may develop as per organ . involvement like —
. . .
adult. > Prolonged cough not responding to muItIple course of antIotIcs
. - > Ftes irato distress
> 10 mm PositIve, suggests disease in presence of > H eagacheryvomiting t
clinical features. . '
> Alteration of sensorium ' t
. > Cranial nerve alsies

é. rltfalls — Numerous factors are responSIble false positive or false negative results of Tuberculin > H epatospjenoiegaly I
=
l
est. .
g . 0 False - Negative result (due to diminish tuberculin reactivity) > Jaund'ce

> Anaemia _ y
> Viral. bacterial infection (Measles, mumps, chicken pox, HlV, typhoid)
i > Live vaccination ' > Chest pain
> Features of pericardial effusion
I > Renal, Liver failure, PEM
P Lymphoma. leukaemia - Diagnosis - As in other form of tuberculosis diagnosis is often difficult by demonstrating the
bacilli in fluid or tissue from body. A number oftests have to be done to reach the diagnosis.
> lmmunosuppressive drugs _
> Chest X-ray to detect miliary focus in lung
> Surgery
i > Tuberculin skin test often falsely negative in setting of disseminated or miliary tuberculosis.
> Wrong method of administration, improper dilution, storage
> CSF study-cells protein sugar, PCR. cutture, ADA CBNAT if meningitis is sus'iiected
> inexperienced reader > .
-
CBC with ESFi — High ESFi with high lymphocyte count is suggestive.
' False positive result (Due to cross reactivity)
5* Fluid collected from the affected organ like, pleural fluid, pericardial or joint fluid to
‘3'; > infection due to a typical mycobacteria . . .
. . . demonstrate Mouth and detect cells. protein, sugar, ADA activity.
if' .
; > 806 vaccrnatIon - > imaging studies — CT scan, USG, MRI of the affected organs as required.
‘
0'14' Miliary Tuberculosis in chrfdren. [13} _ Children with miliary TB often have drug resistance tuberculosis. So. as diagnosis of TB. it
Miliary Tuberculosis is another name of disseminated tuberculosis. It is a significant health problem is also important to detect drug resistance to one or more anti tubercular dmgs which will
help in treatment. .
in developing countries specially in areas where BCG vaccination is not regularized. It is a
I . b H1 ”h h m b! 'd st , . Treatment - i
5 poterziallty hf: threatanLicondrtIoz. H b
_ _ _ . . . . .
t. ° cu e o sprea - rge num er 0 u ercu osrs acr I rave roug e co , ream an Category | (2H3R323E3) In IntenSIve phaseand 4H 383 In continuatron
)> Sgiitiercplar drugs
, spread through out the body.
; 0 Risk factors - There are certaIn nsk factors which predIspose the child to develop dissemInated Duration __ 6-9 months ‘
-. Tuberculose. These are - , - . 12 th f TB . ,.
i > Age of child < 3 years ’ C . mzn :Bor .mwng‘t's ' l
i r '
. : > ortrcosteroi - TB “inmglzs
"i > Child with weak immune system. FEM
" > Not vaccinated with BCG ' p S rt' t t per-Ice: I s ‘ rt f t l
. _ .. uppo Ive rea men In cm 0 suppo o organ unction. (lung. kidney, brain] blood
Organs affected MIlIary TB may affect one or many organ in the body. transfusion. drainage of effusion.
-‘.
126 QUEST: PAEDIATRICS INFECTIOUS DISEASES El Chapter-6 127
- Classical Triad —
0.15: Clinical features of Chilrungunya fever [2012, Supple]
> Chorioretinitis
Chikungunya is a viral fever caused by an alphavirus and transmitted by bite of an infected > Hydrocephalus
Aedes aegypti mosquito. The disease is so named because of severe arthritis symptoms, that is > Cerebral calcification
chikungunya (that which bends up). '
Eye and neurological changes may not be present during neonatal period, may be
delayed even
Clinical Features — years. depending upon severity of infectionQNeurological signs and symptoms include -t
Incubation period — 2-12 days > Convulsion
Onset - Acute usually in most cases > Micrecephaly I Macrocephaly
. Setting sun sign
‘7
Classical triad : Fever, rash and arthalgia
Paralysis of extremities
VVV
Fever -
Developmental delay
> Rises abruptly to 103 - 104°F
Intellectual impairment
> Accompanied by rigors and chills
- Other manifestations -
> Associated with headache. fatigue. muscle ache, nausea, vomiting
Prematurity
V‘VVVVVV
> The temperature may remit for 1-2 days after a gap of 4-10 days, resulting in a ‘saddle back’
lUGR
fever.
Jaundice
Rash -
‘ Hepatosplenomegaly
> Flushing of face and trunk followed by characteristic maculo-papular rash. I
Myocarditis
> Trunk and limbs are commonly involved but face, palms and soles also may show lesions Pneumonitis
, > Flashes are itchy Various rashes
- > They may simply fade or desquamate > Sensorineural hearing loss
Arthaigia I Arthritis — Infant may be asymptomatic at birth and letter presents with mental retardation l. deafness.
> Polyarticular, migratory Diagnosis
.1 > Predominantly affect small joints andha'nds, wrists. ankle. feet - Prenatal Diagnosis —
> In acute stage intense pain . (i) Fetal ultrasound — at 2 weeks interval beginning at the time of acute infection of mother
i > Pain is worse in the morning, improved by mild exercise ~(ii) PCR analysis of amniotic fluid — To detect T. Gondi genome
' > Swelling may occur. but fluid accumulation is rare. - Post-natal diagnosis —
- > Arthritis/Arthalgia may persist for weeks to months.
(i) Serological test
1 Other clinical features - Serum lgM - Persistence or rising titre of Tox0plasma lgM antibody in infants senlm.
l _ > lridocyclitis, retinitis Serum lgG — Passively transferred maternal IgG take months and years to disappear.
> Meningoencephalitis (1%) Raising titre —> infection of infant
> Fuiminant hepatitis (2%) Lowering titre —-> Passively transferred matemal antibody
> Mild haemon‘hagic manifestation (3%) (ii) CT Scan — Hydrocephalus
> inguinal lyrnphadenopathy . . .
. - cerem calcification -
Most symptomatic patients complained of a chronic stage of the disease where 10ml pain may (iii) csr= Analysis - Toxoplasma specific lgc, lgM. demonstrate - PCR “for T. 90a in csr.
continue for many months after initial illness In a remission and relapses fashion.
Treatment — Drug of choice is - Pyrimethamine + Sultadiazine
Fatality - is rare and if occur in younger age due to thrombocytopenia and shock,
Dose - Pyrimethamine — 2 mglkglday 80 for 2 days '
0.16: Congenital Tcxcplaemcsfs [Males] i
ngen' tai Tox iasmosls '
' occurs when mother gets primary '
Infection wit' h Toxoplasma
_ gondil 1’ mg/kglday for 2 or 6 months
dCEring plregnanrgrp and there is transplacental transmission of Infection from mother to foetus. Ilf:
will be high if
The rate of transmission is higher during later'stage of pregnancy but severity 1 mg/kg twice weekly PD.
mother acquire Infection during earlier gestation. 4 Sulfadlazine — 100 mglkglday BDPO
CUNICAL FEATURES -
Leukovorine - 5-10 mg given twice weekly P.0.
Duration of treatment — 1 year
> Mild to severe neonatal disease or with sequelee
INFECTIOUS DISEASES Cl Chapter—G
_.
0.17: AFP Surveillance Programme (KPC)
Acute Flaocid Paralysis implies paralysis of acute onset (less than 4 weeks) and affected limb or ° CMQENW phase " '
;__' After two to three days of leaky phase
‘ limbs are flaccid i.e. floppy or limp in a child < 15 year old or paralysis in a person of any age in
r: .L
whom polio is suspected.
leaks step
ig. Surveillance means data collection for action. India is having an effective. widely distributed network
t.
i; of an efficient surveillance system for the very first time in it‘s history to detect all cases of AFP in Repair of vessel wall
'; children < 15 years of age. not only Poliomyelitis.
.1.
AFP rate - In other parts of the world. at least one case of AFP (excluding polio) occurs annually for
Return back of plasma from extravascular to intravascular phase
every 100'000 children < 15 years or age {background AFP rate) i '
: Sensitive surveillance will detect a back ground AFP rate of 1/100.000 children.
Vascular congestion
In India. as the incidence of the conditions. Such as traumatic neuritis and AFP caused by other non- .
1
’
polio enteroviruses is very high. back ground non-polio AFP rate is higher.
that - 531} Clinical features " _ _
f Action Plan - Instruction by the Ministry of health and family welfare to all health facilities
a». " After a febnle penod 0’ 2"? day .
:f - All health facilities clinician are rqed to notify all AFP cases immediately to District " — Signs and symptoms 0' C‘fCU'a‘OW failure d9V9'0P5
1 Immunization officer (DID). by the fastest available means.
.L: ' Posturanpotensron
i — Stool sample must be collected from all AFP cases within 14 days of onset.
' Cold penphery
a — If it is not possible to collect stool specimen within 14 days. specimens should still be collected — Thready. pulse
up to 60 days alter onset of paralysis. — Tachycardia
n. . .
J‘ - Upon verification that the case meets AFP case definition. the BIO initials case investigatio
" Crrcumoral cyanosrs
I DIO must revisit every case of AFP 60 days after the onset of paralysis to confirm the presence _. - - Peripheral pulses difficult to palpate
or absence of residual paralysis.
of 24 to 48 hours apart and ,' ‘ If patient '3 untreated then -—
Stool Sample — Two stool specimens should be collected at the interval thumb sized' 8 gm ’ - Low or unrecordable pulse
‘one
within 14 days of onset of paralysis, sample should be of adequate amount. _ Narrow pulse pressure
ion in reverse cold chain process (to
and to be sent in good condition without any leakage. dessicat , ' _ Progressive oti . to a is
d laboratories with all details.
maintain temperature below 8°C) to WHO accredite
from any stool specimen . _ Uncorrected shoclr
. Confirmed Polio case - only by the isolation of wild polio virus
- DIC
5': ‘Non-Polio AFP' case — APO" from shock, patient .Igo “my,“ ..
' . .
” - If wild polio virus not isolated from adequate stool sample. _- Puffy swollen face
ation AFP case as either non-polio AFP or -
- II stool specimens are inadequ ate final classific
examinatron. if the 69 day fOIIOW _ Generalized a
compatble with polio will depend on the results of 60 day classif ied as non-polro AFP.
' . oedem
ess, the case is
up examination shows no residual weakn — Polyserosrtrs
i
(8M0) . 0 After two three days when looks stop - Signs of vascular congestion appear
5 0-73: Bongo: “'0‘?" syndrome. _ Boundary pulse
e haemorrhagic fever (DHF) are the senous
Dengue Shock Syndrome (053) and Dengu - ' _ Wide pulse pressure
- .
' complication of the dengue infection. . _ High urine volume
from asymptomatic to severe lIfe threatening
Clinical manifestation of dengue infection vary
.. Tachypnea ‘
Pathology - DSS occurs in, two phase. — Congestive Hepatomegaly
‘
. Leaky phase __
Investigation
Intracellular dengue viral killing - High Haematocrit ‘
J, f
' - Low platelet count are usually consistent with 088
Vasculoparhy causing damage to the vessels walls . At this stage patient has
,1. ‘
4 _ Positive Dengue IgM
extravascular space
Extravasation of plasma from Intravascular to .
- Positive Dengue IgG (Preexisting)
(Preexisting Dengue IgG antibody Is a risk factor to deveIOp Dss) I
Shock and Bleeding
17
I
CamScanncr
INFECTIOUS DISEASES Cl Chapter-6
130 QUEST : PAEDIATFIICS 131
0.20: Clinical features and management of Dengue haemorrhagic fever (Midnapore)

Treatment — Guideline to treat DSS (WHO)
Dengue haemorrhagic fever is the severe form of Dengue with high mortality
until and unless
detected and managed at earliest.
DSS
l Clinical Features -
Immediate rapid volume replacement —~ Initial picture is like dengue fever with high fever, with intense headache. backache.
myalgia,
FlL I N3 is bolus —- 20 ml/kg. up to 3 boluses joint pain.
i — Bleeding manifestion commonly as the fever gradually subsides
f l - Positive tourniquet test
Improvement No Improvement
- Prolonged bleeding from venipuncture sites
i
Oxylgen - Fine purpuric rash allover the body
W RLNS fluid rate successively
reducin from 20 to 10. 10 to 6, 6 to 3 - Mild G.I bleeding
g i i l - Severe G.I. or other forms of bleeding in < 10% oases
Haematorist rises Haematocrit falls
Further improvement — Circulatory disturbances
I i
LV coloid 10 mI/kg — Blood transfusion - Giddiness
Discontinue
i - Cold extremities
‘9 Improvement
{—P No improvement ' . Oliguria
i _ Succe‘ssively reducing - Restlessness. irritability
Look for Anaemia, acidosis, myocardial RUNS rate — Other features include
dysfunction and treat accordingly
- Intense anorexia
- Nausea, vomiting
0.19: Warning signs of Dengue in children {SSKMJ - Pain abdomen
Dengue ranks as the most important, rapidly emerged. mosquito born viral disease in recent 0 Hepatornegaly
years and is endemic in all continents. Dengue infection occurs in all age groups of human
Management
population and pediatric age group is found to be mostly affected. Children are also at risk of
deveIOping complicated Dengue infection and high inCidence of mortality and morbidity. Investigation
‘ ' ' ' ortant to detect the cases of dengue fever that are going to develop Haematocrit — Rise of haematocrit > 20% for age and sex is a indication of plasma leiakage
Igrrfipzzziipfisolritkaggetrgt:gilaemorrhagic Fever (DHF) andior Dengue Shock Syndrome (DSS). Platelet count — Low invariable < 100,000 in presence of bleeding
There are some warning signs and symptoms, presence of which can predict the risk of ' Criteria for DHF diagnosis
.
development of complicated Dengue. They are as follows —
t Vomiting . (a) A case with clinical criteria for dengue fever
- Recurren
(b) Haemonhagic tendencies evidenced by one on more of the following
- Pleural effusion / ascites / gall bladder oedema on imaging.
- Minor bleedng from different sites : haemoptysis, haematomyelis. haematuria, gum bleeding etc. 1. Positive Toumiquet Test
- Pain abdomen or discomfort 2. Petichiae, eochymosis or purpura
- Palpitation, breathiessness 3. Bleeding tram mucosa. GI tract or injection site.
rill-:“b -.
0 Hepatic dysfunction or hepatomegaly (> 2 cm) with or without tenderness Plus

- Decrease urine output to) 'Thronbocytopenia (< 1.00000 oelislcm‘)
...e-.
- High haematocrit (> 45%} or increase in 20% Plus

. Rapid fall of platelet count
WML
(d) Evidence of plasma leakage due to 'ncreased vascular penneab

fity. manifested by one or ‘
- Cold. clammy extremities more of the following :
- Narrow pulse pressure t. Ansaofhaematocritforageandaex 220%
-
0 Rapid pulse ' 2. A more than 20% drop In haematocrit following volume replacement treatmen
t
. Hypotension 3. Signs of plasma leakage (pleural effusion. ascites. hypoproteinemia]
- General weakness I lethargy! restlessness Treatment - Voiumo mplacement Is the mainstay of treatment in D'HF.
All patients vvith danger signs are to bed admitted to hospital and need i.v. fluid preferably crystalloids.
INFECTIOUS DISEASES U Chapter—6 133

Followed by stiffness of neck. difficulty in swallowing and rigidity of abdominal muscles.
FLOW CHART FOR VOLUME REPLACEMENT Rigidity of facial muscles lead to sardonic smile or risus sardonfcus
Rigidity of back and abdominal muscle lead to opisthotonos posturing
Rigidity of laryngeal and respiratory muscle lead to airway obstruction and asphyxia.
Haemorrhagic Manifestation
+
Spasms are precipitated by stimulus like bright light nose. touch
Thrombocytopenla Constipation and urinary retention
+ Sympathetic nerve involvement lead to hyperpyrexia. hypertension, excessive sweating.
Hypotension tachycardia.
1 - Localized tetanus ,
IV. Therapy 10 ~ 20 ml/kg/hr RUNS for 1-2 hour > This form occurs less commonly than generalized form.
i > Pain and spasm of the muscle in proximityto site of injury
F— Jr
3* May be followed by generalized spasm of muscles
Improvement No Improvement
I. - Cephalic tetanus
LV therapy by crystalloid successively 1 > This is the rare form
I:
reduced from 10 to 6 mlfkg then 6 to 3 ml/kg
Haematocrit Haematoorit > Usually occurs in children with otitis media
i
' l
Further improvement . fife fall - Neonatal tetanus
> Typically occur within 3-12 days of birth
W Colloid Blood‘
‘1' > This is a serious condition
Discontine, l-V therapy therapy transfusion
10 mlfkg 10 mlfkg 3:» Progressive difficulty in feeding (sucking and swallowing)
Over 24-48 hours
l J > Stiffness and spasm of body and in extreme cases opisthotonos occurs
i > Condition is invariably fatal.
Improvement
i 0.22: Acute Encephalitic syndrome {MCK} [8th Sam]
Crystalloid therapy with Acute encephalitic syndrome (AES) is defined as a person of any age. at any time of year with
successive reduction of rate and the acute onset of fever and a change in mental status (including symptoms such as confusion.
then discontinuation disorientation. coma) and/or new onset of seizuere {excluding febrile convulsion)
Etiological agents - Viral agents are mostly responsible in causing AES as follows-l—
- Japanese Encephalitis virus I
initial phase then rapid volume replacement - Herpes simplex 1 .
‘ If the patient has shock with unstable vital signs from
hour over1 hour.
will RUNS should be done with 10 - 20 mllkgf
- Dengue virus
- Measles virus
(NBMC) [8th Sam]
0.21: Clinical features of Tetanus gram positive. -' Chikungunya virus
exotoxin-mediated infection caused by a
Tetanus is an acute, often, fatal, severe - Epstein-Barr virus
tetan i.
anaerobic, organism, called clostridium oping countries. 0 Human Herpes vims 6
an impo rtant cause 0 I neonatal death in devel
Tetanus occurs world wide and is - West nile virus
Clinical Features - - Nipah virus .
' Incubation period — Around 10 days ' Cerebral malaria. Py enicll’ubercular menin itis ' ' ' ' ' '
forms 0 fTetanus have been described.
' Types - Based on clinical findings, three Acute encephalitic sggdrome but careful histgry. mgieefgrtnirgiggnafl SEE: ESLEE:
on investigation are also helpful to exclude these condition.
V (i) Generalized Tetanus - Most comm
Clinical Features - ~
(it) Localized tetanus
History —
(iii) Cephalic tetanus
- Careful history taking Is very important
- Generalized tetanus -
of generalized muscle. - H/O lever, headache. vomiting. seizure. abnormal posturing."
> Descending pattern of involvement
of masseter muscle
> first sign is Trismus or Locklaw due to spasm
Camscanncr
3...... INFECTIOUS DISEASES Cl Chapter-6 135
'134 QUESTzPAEDlATRlCS
Commonest portal oi entry — Airborne transmission and inhalation

- Prodromal symptoms - Flu like illness, diarrhoea Commonest site oi primary complex — Lung, also called Ghon's complex
- Rash Components - It is characteristic of primary pulmonary TB. composed of -
in surrounding zones
' Residence of child -— epidemic area of cerebral malaria, AES (i) lung parenchyma (after subpleural consolidation)
- HIO seizure disorder (ii) lymphatic vessels draining the area of long parenchyma
- Hi0 trauma, immunization (JE. Measles) (iii) Lymphnode component
Premor’oid illness — )aundice. renal disease, developmental delay.
- Pathology -
' Clinical Examination - Inhalation of airborne droplets
' Level oi conciousness. meningeal signs. abnormal movement i
0 Focal neurological deficit. cranial nerve palsies Bacilli locate in the subpléural mid zone of lung
- Localization of brain dysfunction.
Unrestrained multiplication of bacilli
treatment should
Management - As AES is an emergency condition diagnostic investigation and
condition before
be done side by side. Sometime it is more important to stabilize the child’s clinical Brief acute inflammation — neutrophiles
doing investigati ons and even history and examinatio ns to save the life.
Management Include - 5-6 days - evoke gianuloma formation

l) Rapid assessment and stabilization
2-8 weeks — healing
- Establishment of airway
- Ensure ventilation. oxygenation Ghon focus
- Circulation LV. access and basic blood samples to be taken such as glucose. electrolytes. Fate of primary complex
-
LFT LV. bolus oi isotonic saline il circulatory iailure is present. (a) Parenchymal portion of Ghon's complex ~—) caseous necrosis -+ fibrosis and calcification.
. Control oi seizures-LII. benzodiazepine. phenytoln (b) intensive caseation — centre of lesion liquify — empty the content into bronchus - cavity
ll) Proper history and clinical examination formation and spread of bacilli from primary complex via blood and lymphatics to liver.
lll) Empirical treatment spleen, meninges, lymphnode, bones. lung apices —) disseminated TB.
- Inj. Ceitriaxone (C) Tubercular bacilli may remain viable in lymph nodes even after development of librosis and
calcification — compression oi regional bronchus leading to hyperinflation (partial obstruction
- lnj. Acyclovir
or atelectasis (Total obstruction) or transmission of infection to lung parenchyma. '
- lni. Artesunate (it cerebral malaria is suspected)
IV) Investigations 0.24: Category 1 therapy of 1 year old child with Tuberculosis [KPC, 8th Semi
. All children. diagnosed as having tuberculosis should be registered under (RNTCP - Revised
- CSF cell type. count, protein, sugar, viral profile
Dual Antigen for malaria, dengue antibody National Tuberculosis Control Programme). In this programme all Tuberculosis patients are given
0 Blood complete count. viral profile.
intermittent short course chemotherapy underdirect observation (DOTS)
. - Brain imaging - CT scan. MRI. This Includes the category of treatment -
' Blood gas. Lactate (i) Categoryl
V) Supportive care (ii) Category II
- Control of raised ICP — Mannitol13% NaCl.
' - Maintenance of euglyoemia. control of lever .
Ca tegory l
, .
VI) Definitive therapy - Types of patient Treatment Regimen
definitive antiviral therapy available rs LV.
AES is mostly caused by viral'agents, but only
acyclovir, against Herpes virus. ('1) New Sputum positive pulmonary TB (PTB) intensive phase ' . Continuative phase
year — lOmg/‘kg 8 hourly
Dose : 3 months — 12'years -— 500 mglrn2 8 hourly > 12 (ii) New Sputum negative PTB 2H3H323E3 4H333
treatment. - (iii) New extra-pulmonary TB
Duration : Confirmed cases — 14 — 21 d W
Semi]
0.23: Primary Complex (R. G. Ker) [9th New Case - A patient who has no previous hlo taking ATD or < 4 weeks
TB bacilli into
Primary complex refers to initial tuberculous lesion after entry oi Mycobacterlum Pulmonary TB — Refer to disease involving lung parenchyma
the body. Extra pulmonary TB - Refers to disease involving sites other than lung parenchyma
136 QUEST: PAEDIATRICS 137
INFECTIOUS DISEASES E] Chapter-6
Drug and Doses - iv) Liver Biopsy — various charges

H = lsoniazid - 5-10 mgikg B.wt > Granulomatous hepatitis
Fi = Rifampicin — 10 mg/kg B.wt P Milliary TB
Z = Pyrazinamide - 30-35 mg/kg B.wl
3» Conglomerate tubercle
E = Ethambutoi — 20 mg/kg B.wt
> Portal fibrosis
Duration -
> Kupifer cell hyperplasia
(a) Total 6 months = 2 month intensive phase
A
> Tuberculomas
4 month continuation phase
v) Laparotomy and biopsy of surgical specimen - Needed only when other methods tail.
(b) inadequate or no response (on smear or clinic-radiological basis) at 8 weeks of intensive phase,
(b) Supportive diagnosis — More often, diagnosis of abdominal tuberculosis rests on supportive
nnnnnnn-
extension of intensive phase for 1 more month.
or circumstantial evidences
(c) TB meningitis Spinal TB. Miliary/ disseminated TB- ~continuation phase 3 months more (Total
i) Mantoux test—
9 month). Further extension of more 3 month will be decided by treating physician.
> Positive (more than 10 x 10 mm)‘In 50% to 60%
0.25: Enumerate the diagnosis and treatment of abdominal TB in a 6 year old chiid [Maids] > However negative test does not exclude TB
It is defined as Tuberculosis infection of the abdomen including (Gastro intestinal tract GIT) ii) Chest X-ray P-A view — as an evidence of co-exisling pulmonary disease
peritoneum omentum, mesentry, lymph node and other solid organs like liver. spleen and
iii) X-ray Abdomen — suggestive features are -
pancreas.
> Subacute intestinal obstruction
Diagnosis -
> Calcification of lymph node
Clinical Features — Variable and mimic common childhood illness and difficult to diagnose. Like —
> Mass shadow of omentum
> Diarrhoea
iv) Barium Meal Follow—through - very useful. suggestive findings are
-
> Fever
> Ulceration
> Pain abdomen
> Stricture
> Anorexia
> Hypertrophic segments
> Weight loss
> Malabsorption pattern
- Duration of symptoms vary from two weeks to few years
3‘» Matted intestinal coils
- Clinical signs -
> Fistulous tract
> Distension of abdomen
.nhhshnhrnhl.
3» Compression or separation of coils due to enlarged lymph node
> Visible peristalsis
> Doughy feel on palpation v) Barium Enema— when colonic lesions are suspected. ulceration, hypertrophic segments
and strictures can be diagnosed.
> Ascites
vi) Ultrasound and CT scan —- useful to
) Lump
> Locate pocket of ascites
> Hepatosplenomegaly
> Outlining typical appearance of enlarged lymph node
investigations :
> radioiucent centre indicating caseation necrosis
Two categories - (a) Definitive diagnosis; (b) Supportive diagnosis.
vii)Adenosine deaminase (ADA) activity in peritoneal fluid - Raised many folds in Iubercular
(I!) Definitive diagnosis - peritonitis.
Criteria
Treatment
> Demonstration of AFB in lesion lcultum
Anti Tubercular drug— AbdominaiTuberculosis including peritoneal gastro-intestinal and medial
>_ Demonstration of tuberculous granuloma with caseating necrosis involvement are included under category I of FINTCP.
-From palpable mass in abdomen on use guided
I) FNAC (Fine Needle Aspiration Cytology)- Two phases -
aspiration of material to identify AFB or cell reaction
lesion and biopsy or i) intensive phase — To eitect prompt bactericidal effect.
E) Upper and lower G. | endoscopy— For direct visualization of mucosai
Drugs — H3R323E3
aspiration from the lesion also can be done.
iii) Ascitic Fluid aspiration- For culture and cytology - T WBC with T lymphocyte and
Duration - 2 months
—- T ADA— suggestive of TB
18
r INFECTIOUS DISEASES CI Chapter-6 139
El Passive Immunization
relapse
ii) Continuation phase - To sterilize the lesion to prevent Post exposure prophylaxis with immunoglobulin.
Drugs - H3R3 Indication -
. . .
Duration — 4 months > All immune-compromised individual after contact with active measles case irrespective of
management of complications like ~
Surgery — Role of surgery is limited to tissue diagnosis and their immunization status
> Obstruction > Exposed infants aged 6-12 months
> Perforation Management
> Fistula formation - Diagnosis - Diagnosis is essentially clinical
> Significant bleeding ‘
— May be confirmed by estimating the levels of IgM antimeasles antibody that ap-
pear 3 days after rash
macula-
a. 26 : A 4 yrold child presents with high grade fever, waning nose, red eyes followed by - Treatment —
papuiar rash on face and rest of the body 4 days later. What is the most likely diagnosrs?
Outline the differential diagnoses, complication. prevention and War of the case. > Essentially supportive '
(MMC) (9th Sam.) Antipyretic — Paracetamol is adequate dose 10-15 mg/lrg
VVVVV
Sponging with Iuke warm water if fever is high and persists for prolonged time
Ans : 4 year old child presents with high grade fever, ninning nose, red eyes followed by macul-papular
rash on face and rest of the body 4 days later. Maintenance of hygiene
Most likely diagnosis is — Measles. Adequate intake of fluid and calorie to prevent dehydration and malnutrition
El Differential diagnosis : Though the above symptoms are consistent with typical clinical features of Vitamin A — Single oral dose '
measles, following differential diagnosis to be kept in mind — < 1 year - 100.000 unit
° Rubella > 1 year - 200,000 unit
- Dengue fever Reduces morbidity and mortality
- Roseola infantum > Appropriate management of complications
- Erythema infectiosum M A 5 year old boy while playing in paddy field had a dog bite over the lace. How will you
- Chiitungunya approach and protect the boy from Babies? [2016]
- Interoviral and arbovirai infection Ans : Rabies is endemic in India, primarily a disease of animal. in case of human infection by
bite of
' Drug rash Infected ammal death is inevitable if post exposure prophylaxis is not done property.
- Kawasaki disease > A 5 year old child while playing in paddy field had a dog bite over
the face -
Except kavraeaki disease and drug rash all above differential possibilities are caused by viral infec- According to WHO wound category of Rabies prophylaxis. this
is -- Wound category HP
tion and present with fever and macuio-papular rash. Recommended prophylaxis of wound category III is —
CI Complications of measles - See Question No. 2 (i) Wound management
D Prevention of Measles - Measles is a disease which is largely preventable and potentially eradi- (ii) Rabies immunoglobulin
cable because availability of effective vaccine in universal immunization programme.
(iii) Antirabies vaccine
El Active Immunization
(ivlTetanus prophylaxis
Vaccine : > Measles vaccine > Wound management, Rabies immunoglobulin
> Combined with Mumps and Rubella - MMR vaccine and antirabies vaccine - See Question No.8.
- Tetanus Prophylaxis — Tetanus prophylaxis.
> Both are live attenuated that is adninistration of Tetanus toxoid
and l orTetanus immunoglobulin (TIE) will depend
> Dose-0.5m subcutaneous route tetanus vaccine _ won immunization. Status regarding .
7» Site - Anterolateral aspect of thigh
> Sd-redule - - First dose at 9 month of age as matemal‘immunity may interfere Pactdoaea of TI' 11- - 116
with the (National and IAP Schedule) immune response of vaccine
. " Unknown or < 3 doses Yes Yes
- During outbreak time 1 st dose can be given as early as 6 months of
39°.
. Revacclnation after 4 weeks. preferably at 12-15 months as MMR “ or
> Adverse reaction — Fever. transient macular rash (Measles like illness) 5-10 days Yes if
later 5 year since
last dose
INFECTIOUS DISEASES C] Chapter-6 141
O. 28 : Emumerate the clinical features complication and investigation of AIDS

in children
[Maids] (b) Neoplasm - > Non—Hodgkin's lymphoma
Ans : 22V infection has become 'an important cause of childhood mortality and morbidity in many
develo - > CNS lymphoma
img coun nes.The Human Immunodeficiency virus primarily infects and causes depression of body?s
mune system leading to AIDS (Acqurred Immune Deficiency Syndrome) in advanced stage > Kaposi sarcoma
El Clinical Features ' (c) CNS involvement - HIV encephalopathy
> Vary widely depending upon age and stage of the disease — Progressive multifocal Ieukoencephalopathy
> Initial stage — Symptoms are subtle and non-specific -— HIV associated neuropathy
- LymphadenOpathy Cl Investigation
— Hepatosplenornegaly (i) ELISA - ,
~ Failure to thrive > Detects HIV — 1 antibody - lgG, extremely sensitive and very specific.
of IgG f rom mother to child
-— Chronic and recurrent diarrhea > Not useful until child's age is 18 months as transplacental transfer
— Interstitial pneumonia results in false the result.
- Recurrent and persistent oral thrush (ii) Western Blot—
> Advanced stage — Different opportunistic infections ) Measures antibody (lgM and IgA) to specific viral polypeptides.
— Severe malnutrition and wasting > Can be used as confirmatory test after 6 months.
(PCFt), HIV p“ antigen-
— Chronic parotid swelling (iii) HIV— 1 culture and HIV — 1 DNA and RNA Polymerase Chain Reaction
age.
> Valuable test, detects infection irrespective of child's
t.rxnng'-.
- Progressive neurologic deterioration
5» HIV DNA PCR — Qualitative test that detects the proviral DNA integrated with host cells.
— Severe bone marrow depression leading to anaemia, neutmpenia, thromb-
determines the virAI load.
ocytopenra > HIV RNA PCR — Quantitative test using reverse transcriptase and
sensitive but technicall y complex, expensive and results are not available before
, Cl Complications > Culture is
‘
2-4 weeks compared to 2-3 days with PCR.
'3 r(fiatmpfication of Pediatric HIV infection is mainly opportunistic infections, neoplasm, CNS involve-
pz‘ assay is less sensitive than other virological tests.
VV
PCR test on dried blood
These are as follows - The National program (Early infant diagnosis) now uses HIV DNA
DNA PCR on a whole blood
spot sample, the positive tests need confirmation using 3 HIV
'3 (a) Opportunistic Infections —‘ Recurrent infection with unusual pathogen or with common patho-
sample.
gen but Increasrng seventy rs the most common complication of AIDS and also causes death.
(iv) Other markers of HIV infection -
I > Pneumocystic Carinii Pneumonia — d lymphocyte p‘i‘olilerative re-
> Depressed CD4 + count, increased 008 + count, depresse
- Most common and lethal opportunistic infection in pediatric population sponse to mitogens , marked hypergam maglobu linemia.
- Presents with progressive cough, respiratory distress and hypoxemia [2017]
“fin
0. 29 : Features of HIV in children
> Oral candidiosis -
— Most common fungal infection Ans : See Question No. 29 clinical features & complication
- May cause esophagitis leads to vomiting, fever, dysphagia and anorexia a. so .- Treatment of childhood rs as per eNrcp guideline (KPC)
> Intestinal cryptospon'cfiosis — one ofthe deadliest disease world-
Ans : Tuberculosis continues to be a major public health problem and
— May result in severe chronic diarrhea and malnutrition wide specially in developing countries like India.
.
r complex (MAC) —
> Atypical Mycobacterial infection with Mycobacterium Avium intracellula RNTCP (Revised National Tuberculos is Control Program) since 1993 provides standard treatment
DOTS (Directly
_ - Presents With fever, weight loss, diarrhea, anaemia and granulocy topenia
guideline for both adult and childhood TB to acheive significant cure rate through
Observed Treatment) short course program. . .
> Disseminated Tuberculosis with Mycobacteria TB
.
> Protozoal infection — III Clinical Category-i
in demonstration of AFB
_ - Malaria, Toxoplasmosls of increased severity may occur ‘ The major problem in inclusion of children under DOTs has been a difficulty in adults.
‘1 and classification of different clinical manifestations according to categories described
> Viral infection —
with Herpes Simplex , Herpes Zoster, Cytome galo virus and Recently a concensus statement iointly prepared by RNTCP and IAP
(Indian Academy of Pediatrics)
— Opportunistic viral infection follows - '
describe two clinical category of childhoo d TB as
Measles vims often occur
> Lymphocytic interstitial pneumonia —
with cough, exertional dyspnea,
- It is chronic lower respiratory tract abnormality presents
clubbing and requires chronic oxygen therapy
CamScanncr
142 QUEST: PAEDlATFilCS
I Intermittent (DOTS) Regimen

CHAPTER — 7
I Category I Clinical condition in children ]Dally regimen [Intensive phase Continuation phase
Categoryl (I) 1liigtttsputurn positive pulmonary 2HRZE 2.4333235, 4H3R,
RESPIRATORY SYSTEM
+
0i) New sputum negative pulmo-
LONG ourssrrorrsfl
(iii) New extra pulmonary TB O. 1 : A 3 year old child presented with cough and cold for 5 days and respiratory distress for 5
2SHRZE zssHanan; + 5HJR3E3 days. On examination child look toxic and drowsy with head nodding and central cyanosis.
Category ll fl) Relapse What is the diagnosis as per WHO criteria? How will you manage the case ? (2013, supple)
(ii) Treatment failure 1Hl:tZE 1H3RJZJE,
Ans : D Diagnosis as per WHO criteria -
(iii) Interrupted Treatment + Very severe pneumonia.
5 HRE CI Management —
if Drugs — Drugs used in childhood TB are same as adults. Doses are as per body weight. To assist in Child has danger signs (toxic look ~ drowsiness. head nodding and central cyanosis) along with
1""
cough, cold and respiratory distress. So, following will be outline of management —
‘-h-n_.._.
calculating required dosage and administration of ATDs in children medication are available in tom of
combipacks in patient wise boxes linked to child's weight —- i) Hospital admission is essential
.
- Four weight bands for pediatric population for purpose of treatment ii) Antibiotic — y _
> 6 - 10 kgs - Antibiotic should be given by parenteral route
> 11 — 17 lugs 0 LV Penicillin + Gentamicin are antibiotic of choice
> 18 -— 25 kgs > Ampicillin 50 mg/kg or benzyle penicillin 50.000 units/kg l.V/I.M six hourly for at least
> 26 — 30 kgs 5 days.
0 Suggested pediatric dosage of ATD for intennittent therapy > Gentamicin — 7.5 mg/kg l.V/I.M. once a day for at least 5 days.
Ceftriaxone will be the second antrbiotic oi choice it child does not respond to above
-
[7 Drug Therapy per dose antibiotics.
(Thrice a week) iii) Referral - if patient is received in primary health care facilities then has to be referred to
Ins/k9 higher health care facility for injectable antibiotic and supportive therapyxalter giving the first
dose of antibiotic. .
isoniazid 1O - 15
10 iv Supportive therapy — Mainstay of management in patient with very severe risease.
V
Rifarrpicin
30 — 35 0 Oxygen
Pyrazinamide
-
15 > As patient having central cyanosis oxygen to be given with face maskornasal cannula.
Streptomycin
30 > Monitoring of SP02 to keep it above 90% if facilities available
Ethar'nbutol
- l.V.F —‘
Duration - > Standard duration — 6 months > Should be kept nothing per mouth
) Longer duration - 9-12 months or more for > Maintenance fluid as per requirement
- Osteoarthrlar TB > Avoid dehydration orover hydration '
— Neuro TB - Bronchodralator therapy (Salbutamol/levosalbutamol) -
- Disseminated TB > Bronchodialator inhalation through nebulization il child has wheeze on auscultation.
Cortlcoeteroid — > Not rountinely indicated - Anticonvulsant—
> Useful in following condtions _- where host inflammatory reaction after adminis- > If child has recurrent convulsions
tration of ATDs corflribute significantly to tissue damage - _
' ° Respiratory support —
0 CNS Tuberculosis allure
> it child has progressive increase in respiratory distress going to respiratoryi
- Tubercular pericardial effusion
- Endobronchial TB (Short course of steroid)
then respiratory support in form of mechanical ventilation to be given it iacrlrtres are
available.
> Drug and Duration — Prednisolone 1 - 2 mg/lrg/day for 4 — 6 weeks
143
n’J
RESPIRATORY SYSTEM I] Chapter—7 145
144 QUEST: PAEDIATHICS
‘\
i
‘0. 2 : A :2 year old child admitted with history of fever and cough for last 5 days and developed ' Lesion undergo caseous necrosis (liquefaction) in centre, surrounded by macrophages, lymp hocyleS.
n
respiratory distress for last 2 days. Or examination Tachypnea and chest lndra wing are giant cells and collagen fibres - taming a granuloma called Tubercle'
present. What is the most probable diagnosis ? How do you manage the case ? {CNMQ i
8th Sent] Tubercle travel via draining lymphatic channels to regional lymph nodes (Hilar lymph nodes)
G
Ans : 2 year old child admitted with history of fever. cough, respiratory distress with Tachypnea and i
(I. .
chest indrawing on examination. Involvement of pulmonary parenchyma, draining lymph channels and regional lymph nodes collectively
Most probable diagnosis — Severe pneumonia (according to WHO clinical classification) called ‘primary complex'
il—flufl.
Management - Same as very severe pneumonia in question no. 1. Fate of primary complex — Fate of primary complex depends upon the immune response of the
host. "
0. 3 : A 4 year old boy was presented at the emergency room with acute onset of cough and
the
respiratory distress. He has no fever. His father also suffers from recurrent episodes of i) Fibrosis and calcification - ll host resistance is good -+ the inflammatory exudate around
similar problem. The child has admitted 3 time with similar complications in the preceding primary locus is absorbed —> Healing by fibrosis and calcification.
to multiply
1 year. What is your most probable diagnosis 7 How will you manage this condition? ii) Progressive primary disease — When host immune response is weak —) bacilli continue
—> empty
[2008]. —i lesion steadily increases in size —+ large caseous centre is to mod —} centre liquifies
spreads to
into the adjacent bronchus —> cavity formation (uncommon in children) —) infection
Ans : 4 year old boy with afebrile episode of acute onset cough and respiratory distress with positive
other parts of the lobe or the entire lung —+ consolidation / bronchopneumonia.
family and past history.
iii) Enlarged lymph nodes —
Most probable diagnosis - Acute severe asthma
(LLULQfil—rl—JL
- valve obstruction)
- Compression overthe bronchus -—i Emphysema lormation (partial ball
-..—.—_.._-
- Ilanagement - See question no. 14. or collapse (complete obstructio n)

and respiratory
0. 4 : Describe the pathogenesis ofpulmonary primary complex of childhood tuberculosis. Nan'ate - Enlarged paratracheal lymph nodes compression on trachea a stridor
the fates of this lesion. [2016] distress.
Arv.N§?““:meerT-‘.tzrr.':.‘ttw
Ghon Complex! - Compression on esophagus -+ dysphagia

Arts : Primary complex is the pathogcmonic of pulmonary tuberculosis, also called hial tuberculosis.
Ghon Focus resulting from initial infection from inhalation of mycobacterium tuberculosis
bacilli. - Erosion of the wall of the bronchus by caseated lymph node -} endobronc
---.._- ._
_ of bacilli from lynph nodes to blood stream a involvement

It contains three elements — iv) Haematogencus dissemina tion -+ Entry
s). This late occurs in
- Pulmonary focus / Ghon focus — Located commonly in the lower segment of
middle lobe, (lingula) ‘ of other organs like liver, brain, metastatic foci in lungs (Miliary tuberculosi
and upper segments of the lower lobe very young infants. severe malnourished child and child with immune deficiency.
us reactivation of
r bacilli into the hilar lymph v) Endogenous reactivation - Pulmonary tuberculosis resulting from endOQeno
‘u—u....__‘_
' Lymphadenitis - Caused by lymphatic dissemination of tubercula {I

. primary complex is uncommon in children, may be seen in adolescents.
nodes.
”'4’
c vessels draining the Ghon locus and and respiratory distress for one
- Lymphangitis - Caused by inflammation of the lymphati O. 5 : One eight year old child presented with fever, chest pain
—
is (SO/min, treachea
-
linking hilar lymph nodes. week. On examination the child is febrile, toxic and respiratory rate
._.
.-;:~:-.’r---w-Iwenw
-—~...
on. What is your

in children usually occurs following inhalation shifted to left and story dullness on right side of chest on percussi
Pathogenesis - Primary infection with M. Tuberculosis (2009, Supple]
provisional diagnosis? How are you going to manage this case?
————...
of viable microorganism.
of trachea and
The inhaled viable tubercular bacilli Ans : Child presented with fever, chest pain. respiratory distress with toxic look. shifting chest.
of right
' l story dullness or precussion suggests the diagnosis of —- Pleural effusioniEn'ipyema
Lodge in pulmonary alveoli '
Management -
and upper segments of lower lobe)
(Usual site - Lower segments of middle lobe, lingula
0!)
Investigation -
i - Chest X-ray - First investigation off course
Inflammation with hyperemia and congestion — Obliteration cf costophrenic angle of one side
i - Uniformly dense opacity
leukocytes
Initially infiltration of polymorphonuclear — Shifting of mediastinum (trachea and cardiac shadow) to Opposite side
n
i
nuclear cells - ' Needle Aspiration or Thoracccentesls - As radiology cannot differentiate between nature
Later, replaced by‘macrophages / mono of the fluid needle thoracocentesis is mandatory for diagnosis.
A i
n
' —Done at the level of seventh intercostal space in the midaxillary line.
phagocytosed by macrophages
Bacteria multiple intracellulariy after being - Following differentiating features between two types of effusion/eupyema is as below -’—
l
n
develops in about 2 -4 weeks
Cell mediated immunity (CMI) response
n
l
RESPIRATORY SYSTEM Cl Chapter-7 147
- lnlercostai Tube drainage (Tube Thoracostomy)

Test Transudate Exudate Including Empyema
— To be done without any delay as soon as child is hospitalized and in the same setting of
Clear Straw colored needle aspiration.
1. Physical Appearance
- (Turbid in empyema) — Closed under water seal drainage to avoid cornplication ot iatrogenic hydro pneumotho-
rax or pyOpneumothorax.
2. Cells No calls Lymphocytes
(Pus cells/Neutrophils in empyema) — Tube with wide bore and largest possible size to be taken it nature of the fluid is pus.
— Regular monitoring of collection in bag and movement of pus coiurn within the tube with
3. Pleural fluid protein < 3 gm/di. > 3 ndi. respiration.
> 0.5 - Thrombolytics or Debridement (VATS) or decortication — .
4. Pleural fluid < 0.5
' Serum - Indicated if complication like loculation. pleural thickening is present which prevents lung
expansion. -
- Protein
- Antitubercuior therapy - ii Tuberculosis is proved to be the etiology.
5. Pleural fluid < 0.6 > 0.6
Category | treatment —
' Serum LDH
intensive phase - 2H3R323Ea
6. Pleural fluid pH > 7.2 < 7.2
Continuation phase — 4H3R3
7. Pleural fluid glucose > 40 mg/dl. < 40 mgidl. - Nutrition and chest physiotherapy — To be started as soon as acute phase is over. child is
able to take teed orally and lung starts to expands.
Special tests to detect etiology - rsHonr ouESTIONS :|

> Gram stain. AFB strain — To detect organism including Mycobacteria.
a. 6: Pneumstoceie [2014]
> Culture sensitivity of pleural fluid.
> ADA (Adinosine Deaminase Activity) and NAA (Nucleic Acid Amplificati
on) test - To Ans : Pneumatoceies are thin-walled air filled cysts that develop within the lung parenchyma
detect Tubercular etiology. Etiology-
- USG Chest - 1) Infection : Most common cause of pneumatoceie is infectious-pneumonia. Among the infectious
the collection. agent most common organism is - Staphylococcus aureus pneumonia other less common
— Appearance of fluid depends on the composition of
seen. organism-
— Locuiaiion. fibrous strand and septa are often
- Klebsiella pneumoniae
- Other tests to support the etiology - - Streptococcus pneumoniae
— Complete blood count inducing ESR - Tuberculosis
> T T80 and T Neutrophil — Empyema 2) Others : Non infectious etiology include —
> t Lymphocytes - T.B. - Trauma
> 1‘ ESFi - T.B. 0 Positive pressure ventilation
Sputum for AFB microscopy and NAA for Tuberculosis. - Hydrocarbon ingestion
Mantoux Test. Clinical Features -
Blood culture - To detect organism in empyema. - Pneumatoceles are per se asymptomatic
Treatment - - Patient mainly present with clinical features of primary cause.
sis has been done.
initial treatment is supportive before etiological diagno - Cough. fever. respiratory distress are the presentation it pneumatocele is associated with
n satura tion above 9 0% pneumonia. - . p
Warm humified oxygen to maintain oxyge
atory distres s i.V. fluid to be 9 iven io maintain hydration. - Most common complication of pneumatocele is rupture and development of pneumolhorax
As the patient is toxic. having respir
body weight oral or W (It cannot take orally) to . - Sudden onset severe respiratory distress. shifting of mediastinum to opposite site. hyper resonal
Antipyretic - Paracetamol - 10 — 15 rngfkg
percussion note and diminished air entry to hemithorax in a patient with pneumonia points to-
cornedown fever and chest pain.
wards a diagnosis of nipture oi pneunatocele.
Empirical Antibiotic Therapy - -
Diagnosis —
— To be started as-the patient is toxic.
3rd generation cephalosporin are the right combi- - Chest X-ray P-A view — Chest X-ray is diagnostic in detection of pneurnatoceie ‘
- Ampicillin + cloxacillin or cioxaciilin + > Seen as a thin wall air filled cyst within the lung parenchyma
nation for empirical thera py.
depending upon culture. sensitivity report. > Sometimes patient is asymptomatic and chest X-ray is Showing pneumatocele incidentally.
- Subsequently antibiotic can belchanged
RESPIRATORY SYSTEM U Chaplet—7 149
Treatment — b) USG chest —+ Can be done and appearance depends on composition of collection.
Medical care -— It involves mostly the treatment of the underlying condition. As most common c) Pleural fluid analysis —) This is the definitive way of diagnosis of empyema thoracis.
cause is infection so administration of intravenous antibiotic broad spectrum covering the common Characteristic findings are -—
organisms causing pneumatocele. e.g. staphylococcus aureus.
- Appearance — Turbid yellow
Positive pressure ventilation can result in increase in size of pneumatocele and can cause rupture
- Microscopy - Plenty pus cells
and development of tension pneumothorax. So. careful monitoring and adjustment of ventilatay
0 Pleural fluid protein - > 3 grn/dl
parameters are required if patient requires positive pressure ventilation with underlying
pneumatocele. - Pleural fluid protein : Serum protein - > 0.5
. surgical care -— Surgery is almost never required for pneumatocele. - Pleural fluid LDH : Serum LDH - > 0.6
- Pleural fluid pH < 7.2
0. 7: Laboratory diagnosis of Empyema Thoracfs. (NBS, 9th Sam] - Pleural fluid glucose < 40 mgldl
Ans : Empyema thoracis is collection of pus within the pleural cavity. It is a common respiratory pathology - Pleural fluid gram stain and culture —
in pediatric age group specially for young children. It is a potentially life-threatening condition Causative organism can be isolated.
requiring prompt diagnosis and" treatment. B) Treatment —
LABORATORY DIAGNOSIS Empyema is a medical emergency
1) Chest X—ray P-A view— This is the initial investigation that can be done in suspected cases a) Administration of oxygen to maintain SPOZ > 90%
but findings are similar those with sero-anguinous pleural effusion. Those are —
b) LV Fluid — Proper hydration is to be maintained with age apprOpriate commsition and amount
- Homogenous opacity involving one hemithorax of I.V fluid administration
' Obliteration of the costo—phrenic angle c) Antipyretics -— Most of the child with empyema have high grade fever that to be controlled
' Slifting of mediastinum to opposite side with antipyretics.
USG - USG chest sometimes done in suspected Empyema. The appearance of emphyma d l.V Antibiotics — l.V antibiotic is to be administrated as soon as diagnosis is suspected.
5-.-
2)
depends on the composition of the collection. Initial antibiotic choice should be broad spectrum covering all the common organisms causing
Ultrasound has a major role in enabling targeted thoracocentesis. empyema. Choice of antibiotic —
space, lung
3 CTScan Thorax — Typically appears as a fluid density collection in the pleural - Ampicillin with Cloxacillin
compression, thickened pleura and 'split pleura sign' at the margins of empyema. - Cloxacillin with 3rd generation cephalosporin (Cetotaxime/Ceftriaxone)
Pleural Fluid Analysis— Diagnostic thoraco-centesis and pleural fluid analysis
is the most definitive
4 - Co—amoxyclav with 3rd generation cephalosporin l vancomycin can be given as
way to diagnosis empyema thoracis. antistaphylococcal agent if MFiSA is suspected.
Characteristic findings are as follows — Subsequent antibiotic therapy to be guided by pus culture and sensitivity repo‘Et.
- Appearance — Turbid yellow Duration of antibiotic therapy — Two to three week. if staph. aureus is isolated than 4-6
- Microscopy - Plenty pus cells weeks.
0 Pleural fluid Protein - >’ 3 gmldl e) lntercostal tube drainage — Should be done without any delay as soon as child is hospitalized
- Pleural fluid protein : Serum protein — > 0.5 and diagnosis is confirmed. This is the most important step. Tube with largest possible size
should be used and connected to under water seal drainage. .
' Pleural fluid LDH : Serum LDH - > 0.6
f) Debridemenf (VATS) or decortication — Surgical intervention like debridement and deconicafion
- Pleural fluid pH - < 7.2
is needed if multiple loculation are present and pleural adhesion has been develOped from
-Pleural fluid glucose - < 40 mgldl organization of pus. '
ms can be isolated.
Pleural fluid gram stain and culture - Causative organis
reacta nt (CFlP) - As empyema is a infective'cause high ' a. 9 .- Cllnfcslfsstums ofAcuts Bronchlolfh's (2009, Supple]
5) Complete blood count and acute phase . .. ' ' _ _ .
serum may be supportive for
total WBC with high neutrophil and high C-reactive protein in ' _ .. Ans : BfOI‘ICtIIllS is an acute inflammatory disease of lower respiratory tract. resulting from obstruction
diagnosis. ,
3." of small airways. Respiratory syncytial virus (RSV) is the commonest causative agent. Other
viruses like influenza. parainfluenza, adenovirus. Flhinovirus are also been implicated.
9th Sam]
O. 8 : Management of Empyema morsels (BUG, Clinical features —
Arts: Empyema thoracis is a pole ntially life threate ning condition until prompt diagnosis and treatment
and treatment -— Age -— Affected Infants are between the ages of 1 and 6 months but disease can affect children
is done. Management include laboratory diagnosis upto 2 years.
A) Laboratory Investigation — Symptoms —
bet ween other fluid collection in pleural
a) Chest X-ray P-A view —) Cannot differentiate - Starts with mild upper respiratory infection —
cavity from empyema thoracis.
RESPIRATORY SYSTEM Cl Chapter- 7 151
Treatment -
> Nasal discharge Bronchiolitis is generally a self limiting illness, treatment is essentially symptomatic.
> Cough > Mild disease — Home care in a humid atmosphere
> Sneezing > Moderate to severe illness — Child needs hospitalization.
> Mild to moderate fever - . . Indicators of severity -
> Diminished feeding
irritability feeding difficulty. . Apnea
- After few days difficulty in breathing increases with wheezy cough,
- Poor feeding
Signs -
‘ - Cyanosis
Examination reveals -
o Toxic appearance
- High respiratory rate
nasal flaring may be present 0 Sign of severe respiratory distress such as head nodding
lntercostal and subcostal retractions. head nodding and
depend ing upon degree of respirat ory distress . - SP02 < 90%
- Chest may appear as hyperinflated bilaterally. - Respiratory rate > 70/min
0 Chest usually bilaterally hyperresonant on percussion. a) General Measure — '
ion
- Breath-sounds are barely audible due to bronchiolar obstruct - Humid atmosphere
Fine'crepitations and wheezes are heard in severe cases. 0 Preferably sitting position at angle of 30° to 40° elevation of head end.
0
- Cyanosis is present depending on degree of hypoxemia. 0 Intravenous fluid to prevent and correct dehydration and electrolyte imbalance.
in severe cases. ' Antipyretic. paracetamol to reduce fever
- Baby is usually restless. irritable or sometimes drowsy -
below costal margin due to overinflated lung, b) Oxygen-
Liver and spleen are palpable usually
con'preesing dome of diaphragm. - Moist 02 inhalation is the mainstay of treatment
3-7 days. Those with severe symptoms
Majority of cases there are mild symptoms and recover within 0 Delivered via headbox, nasal progne or facemask.
require hospita lization and take time to recover. ' To be given even in absence of cyanosis
i, 8th Sen-i] - Most of cases require 30% to 40% oxygen but very sick infant may need upto 60%
0. 10 :Management of Acute Bronchi'oiftis [Kslyan
'
serious ' ory in
acute lower respirat ' faction .
. in infants 0 Pulse oximetry regularly to be performed to keep SPOZ > 95%
' ‘ 'is one of
Ans: Acute Bronchi' olrtis the common
litis is mostly clinical by thoroug h history taking
caused mostly by vims. Diagnosis of bronchio C Bronchodilator - Bz adrenergic andlor lpratropium Bromide
V
investigation to support the diagnosis-
and clinical examination. Nevertheless there is role of some - Not routine recommended in every cases
5“”
Investigation - ' Can be given in presence of wheeze and rhonchi .

a) Chest X-ray shows - Nebulized Epinephrine is superior to salbutamol as regards to improvement in clinical
- Features of hyperinflation symptoms and duration of hospital stay.
> Abnonnally translucent lung fields d) Antblotics -
flattened.
> Diaphragm is pushed down and dome became more . Not recommended in every cases as the disease is viral in origin
> Rbs are horizontally placed _ . indication - '
> More intercostal spaces can be counted. > Presence of high grade fever
. Patchy consolidation. atelectasis and abnormal linear shadows. > Toxic appearance
b) Blood counts - til/BC count > Clinical deterioration
- Nomi/slightly elevated > High WBC Count
al Infection
- Gross elevation indicates secondary bacteri > Infiltration on chest X-ray
c) Blood Gas Analysis - e) Steroids-
cases
. Hypoxemia and Hypercarbls in moderate to severe
- Use of steroid is not beneficlal
d) Blood Electrolyte _,
ia l) Antiviral Drug — Rlbavirin .
0 May show hypon atrem
- Limited role in treatment of babies who were previously healthy
9) Detection of RSV infection -
. Using monoclonal antibodies against RSV in new-pharyngeal aspirate. - Can be given in infants with - . '
> Congenital heart disease .
- Practically not done.
RESPIRATORY SYSTEM D Chapter—7 153
:9 Chronic lung disease like Bronchopulmonary dysplasia

Treatment — Treatment is usually symptomatic as in other viral illness
> Pulmonary Hypertension
- Maintenance of hydration - ff child is not able to drink then i.v. fluid is essential.
> Immunodeficiency - Oxygen inhalation — to relieve hypoxia
- Delivered by nebulizer for 12 to 20 hours/day for 3-5 days. ° Care in calm environment. avoid painful procedure as far as possible.
9) Respiratory support — Continuous Positive Airway Pressure (CPAP) or assisted ventilation is 0 Airway management — Mainstay of treatment
needed if there is progressive respiratory distress going to respiratory failure. > lnhational Epinephrine
0. if : Clinical presentation and management of acute bronchialr'tr's [10] > Single dose Dexamethosone I.V.
Ans : See Question 9 and 10 Both are effective in reducing severing and duration of illness.
' Antibiotics — Not required usually
O. 12 :Acute laryngotracheobronchitis {2008, Supple]
0 Hospitalization —
Ans: As the name implies it is the infection of larynx. trachea, bronchus. also named as infectious
> Home care usually 1
croup.
- If child is comfortable
Etiology - Mostly viral agent are implicated
— Stridor is audible only by stethoscOpe (
> Parainfluenza type 1, 2 and 3 - Most common
> Hospitalization
> Other vimses — less common
- In presence of danger signs ‘
° Influenza A and B
- Adenovirus — Progressive increasing severe stridor
— Respiratory distress (
o Respiratory syncytial vims (RSV)
- Measles — Hypoxia
> Few bacteria - can cause — Apnea (
0 Diptheria - Altered sensorium
_
..._>
Ls-—....
- Mycoplasma pneumoniae Complication - Can occur in few cases — <

-,.. .. 4.
ebb-Ir— .. J-—---.-
- Extension of infection -to the other part of respiratory tract like middle ear. lung parenchyma.
_
Clinical features -
.- _.._.-_..._
c
wz'rr."
- Secondary bacterial infection.

' Age group —
> Between 3 months to 5 years. peak dun’ng second year of life.
. Eat-fl wmhh-EEF
O. 13: A305 [2014, Supple]

A. .
Initial 2-3 days - Ans: ARDS'Is pulmonary edema not originating from the heart. ~
will; . _l ____...._
-
'
> Characterised by features of Upper respiratory tract infection It Is defined as inflammatory response to a local (pulmonary) or remote (systemic) insult resulting
in injury to alveolar epithelial and endothelial barriers of the lung, leading to hypoxemia and (
> Pharyngitis
.
respiratory failure.
w: ._-_._
> Rhinorrhea
> Mild Cough Causes — ‘
> Low grade fever 5 Local (pulmonary)
days
- Characteristic symptoms - develops after few Usual:
'.
> Severe pneumonia (most common) ‘

> Barking cough
> Hoarseness _ M
> Aspiration Pneumonia
. . - . ‘
> Strider > Multiple transfusions of blood products
Ion, reduced In upng
night, aggravated by crying and agItat '
They are characteristically worse at Rare: .
position. > lnhalatfonal injury 1
0 Examination - > Pulmonary contusion .
> Hoarse voice ) Drowning . f
ss
> Variable degree of respiratory distre - Systemic
pharynx
> Nonml to moderately inflammed Usual :
sag—4. I
osis is essen tially clinica l

Diagnosis - Diagn ‘steeple slgn'. > Sepsis (2nd most common cause)
——Sho w typica l sub-g lottic narrowing called as
r 5‘.- ———-:r._—..‘:':‘r='"‘\" “-
- X-ray neck soft tissue

> Severe trauma
- Not routinely indicated \
w
RESPIRATORY SYSTEM D Chapter-7 155
ized by recurrent episodes of
Ans : Asthma is a chronic inflammatory disorder of airways character
mo rnlng, reversible with inhaled
Rare : wheezing. breathlessness and coughing mostly at night or early
> Acute pancreatitis bronchodilator.
of severe asthma that fails
> DlC Acute severe asthma also known as Status Asthmaticus is the attack
and that requires admission to
to respond to inhaled 82 agonists. oral or W steroids and oxygen
> Burn
hospnaL
:9 Head injury
Management of Acute Severe Asthma
essentially clinical with detailed history
Pathology - A) Diagnosls - Diagnosis of acute severe asthma is
Local or systemic cause (recurrent cough, breathiessness, allergy. trigger. family history] and thorough clinical examination.
cyanosis. presence of wheeze or absent
1 (patient's consciousness. degree of respiratory distress.
ry circulation breath sound on auscultation).
Increased permeability oi alveolar capilla
in following cases —
l - Chest X-ray — Not mandatory in all cases but should be done
Aggregation ol leukocytes > Children with first episode of wheeze
l > Evidence of parenchymal disease
et activating factor Those requiring PICU admission
Release of 02 free radical and platel )
l > Suspected complication e.g. Pneumothorax.
Iniury to vascular epithelium B) Treatment -
l . General treatment
tion
Edema and hyaline membrane forma > Children should be admitted to hospital prefera
bly in PICU
l respiratory monitoring
> Continuous pulse oxymetry and cardio-
Fibrosis e
> Sedation should be strictly avoided becaus
Clinical routines — -— Difficulty in CNS assessment in sedated patient

is severe enough
ARDS if underlying local or systemic Most sedatives are respiratory depressant
- Any age is vulnerable to develop -
- Initially symptoms are less - Fluid — I.V.F. to be given to maintain euvolemia
d first
ases > Dehydration is common. if present should be correcte
*- After 6-8 hours. breatheless incre
lt refra ctory hypoxia and hypercarbia develops > Avoid overhydration
0 After 12 hours of insu ion > 95%. W
- Oxygen — By nasal cannula, by mask to maintain saturat
- Profuse frobhy secretion e pattem depending on patients response.
. - Medication — Medication should be given stepwis
Investigation — -
ARDS develops fully Stepwise medication as follows
0 Che st X-ra y -— Bilat eral reticular opacities when
ratio is diag nost ic.
- ABG -— Very high PaOz I FiOz
tegies will be as follows muons
Treatment— Treatment stra
- Control of causative factors
(Sepsis. shock) . |
V l l
' Mechanical ventilation - Corticosteroids
3: MOM“ Anticholinerglc
- Careful fluid administration Drugs - Hydrocoriisol stat a 6
(Maitstay of therapy) .
' 01119 . lpratopium Bromide hourly. 51o mgfkg
- Salbutantol continuous Inhalation
> Nitric oxide (250119) nebulization - Switch to P0-
by Mobilization pl’fldl‘liSOlOI'lB when
every 20 min uplo 3
> Surfactant 0-15 " 0-5 "W“
doses. stable 1-2 mglkg for 5-
> Corticostewid - Salbutamol MDI 4-8 puff
. Subwtanoous or W Terbutaline - Repeat 6 - 8 hourly 7 days
- Supportive therapy -
> Analgesia - Cont nebtiization 4-6 hourly.
> Sedation ._
l
> Nutrition Not respOnding- '
Sam]
a In children (Clinic, 9th
0 14 ' Managem ent of acute severe asthm
Chapter- 7 157
156 QUEST 2 PAEDIATFIICS RESPlFlATORY SYSTEM U
- LV. Magnesium sulphate infusion at a rate of 10 - 20 mglkg/hour Drugs —

- LV. Theophylline or Aminophylline -— bolus 1) B; Agonist—
Not responding to all above drugs — ° Short acting — Commonly used
Mechanical ventilation — Cardiopulmonary anest I Severe hypoxia! rapid deterioration of
> Salbutamol
mental state.
> Levosalbutamol
. Antibiotic — Not indicated routinely in every cases. To be given if followings are present —
> Adrenaline
> High lever
> Pumlent secretion - Long acting
> Consolidation in chest X-ray > Salmeterol
> High leukocyte count > Formoterol
2) Anticholinergic drugs —
0. 15 : Staging of Bronchial Asthma in children. (HMO, 9th Sam]
- lpratopium Bromide
Ans : Asthma is a chronic inflammatory disorder of airway. Successful management of asthma requires
staging of asthma. according to frequency andseverity of symptoms and functional impairment. Mechanism
Staging is done by asking question and objective measurement of airflow limitation by PEFR.
Aerosol particles (size varies) from MDl or nebulizar (1 —5 mm)
Criteria includes -
l
- Frequency of symptoms Inhalation
0 Effect on day to day activity of child l
- Need for medication Aerosol reach bronchioius
0 Hospital visit l
- Hospitalization Bronchodialator with short onset of action
- PEFFt (Peak Expiratory Flow Rate) measurement by spirometer in children older than 5-6 years
Advantage - Bronchodialator aerosol therapy is the primary mode of treatment of childhood as
of age with diurnal variability.
well as adult asthma worldwide in acute as well as preventive therapy.
Based on the above criteria. asthma can be classified into 4 groups as follows —
' Instant onset of action
Stage Symptoms Night time PEFR 0 More effectivity in bronchodialation than oral route
symptoms - Lesser systemic side effects of drugs
- Severe persistent Continuous limitation Frequent g 50% predicted. variability > 30% Disadvantage -
of physical activity . - ..
asthma - Though very much efficacaous MD! has problem in proper drug delivery specially in young
0 Moderate persistent Once a day Once a week > 60% < 80% predicted, variability children because of need for Breath-Actuation co-ordination. To eliminate the problem use of MDI
asthma > 30% should follow the guideline below —
More than once a > W a month > 80% predicted, variability 20% > Children < 4 years - MDI
0 Mild persistent asthma +
week but < tiday - 30%
Spacer
- lntemiittent Less than twice a <Twice a month > 30% predicted, variability < 20%
'
+ t
week.
Facemask ‘
Brief exacerbation
> Children > 4 years — MDI ‘
+
- '
0. 16: Bronchodialator aerosol [2012, Supple] - Spacer
of respirable range
Ana : Aerosol are the minute particles suspended in genome medium. Aerosol size > Children > 12 years — MD!
AAA
is 1-5 mm. +
and dialate the airways and

Bronchodialators are the group of drugs that relax smooth muscles Spacer (preferably)
wheezy bronchitis.
provide symptomatic relief in patient with bronchial asthma and other - Nebulizer - Requires high flow 6-12 Umin to produce aerosols of respirable range
asthma.
Bronchodialator aerosol therapy is the mainstay in treatment of bronchial Selection of device -
therapy is
' done through [1) MDl. Meterdos e inhaler
‘ whic
' hdeltvers
Dovlcor— Aerosol bronchodialator - Acute asthma ’_ .
Nebullzer-release aerosol
a fixed amount of medication in aerosol form each time it is activated. (2)
> Short acting Ba agonist and anti Cholinergic drug ‘ ‘
particles from liquid form of drug.
KK-
._~‘
xx
\
RESPIRATORY SYSTEM El Chapter- 7 159
> Mild to moderate - MDl + spacer ' Causes for poor control —
) Poor compliance
> Severe — Nebulizer
' Preventive therapy - MDI + Spacer > Wrong technique 0' inhalation
> Long acting 82 agonist. > Continued use of empty canister
> Inappropriate doses
3* Moderate to severe persistent asthma
> '"'°°_“°" (Otitis media, sinusitis)
0. 17: Assessment of asthma control [(PGMER, 9th Sam]
assessment ) Contlnuous ”905”” ‘0 allergens
Ans: Continuous assessment at few interval is the integral part of asthma control This > Under assessment of illness
nt.‘
should be In details with history. clinical examination and objective expiratory tlow measureme
. > Associated co-morbidities like Allergic Rhinitis. GERD.
. Frequency of assessment = 4 _ 12 weeks interval
. History _ a. 18: Management of Foreign Body In Respiratory tract [2017]
> Frequency of symptoms Ans: Foreign body inhalation in respiratory tract is a common occurrence in pediatric age group
3.. Sleep disturbance Young children between 1 to 5 years of age are especially prone to aspirate small objects'In their
air passages.
> Physical activity incidence of foreign body location is similar in the right and left side.
> School absenteeism
> visit to doctor ”'"9°'“°"' "
_ - Diagnosis - Diagnosis of foreign body aspiration requires high index at suspicion. Unless
recognized and treated these children have significant morbidity such - recurrent wheeze persistent
) for F’réndu-OdiaIaELd t he
> PEFR vanatlon ('1 race a me) . cough, pneumonia and bronchiectasis
._,. Clinical
> Exposure to trigger .
> Inhalation technique and compliance.
Foreign body in airway
0 Clinical examination - l
> Presence of wheeze Checking. gag. cough or wheeze
) Allergic rhinitis
i
Adverse d s Subsequently course depends on size,
> _ effect of mg t
' location and nature of foreign body
3’ Height. ”9‘9” measuremen I( \l
0 PEFR/ Pulmonary function MS! - '
. 2 Partial obstruction of airwa y Oomflete¢ obstruction of aimsy
> " Possib'e for older children be i
ment control of asthma can
Based on these history. clinical examination and PEFFI measure
mm as ‘ ‘ localized hyperinflation Localized alalectasis
(i) Controlled
:3 . am ”my-
(ii) Partially controlled
(“0 UWO'W- > Radio-opaque foreign body can be seen chest X-ray or its complication like unilateral
alelectasis. hyperinflation. pneumonia.
Uncontrolled . CT Scan chest _
Features Controlled (All at Partially controlled (Any
“'9 following!) feature present in any ) ) Indicated when there is persistent syn-mom
Three or more ) Detects ea uelae
, None More than twicelweek can be
An features of partially ) Radio [339"
° Day time WWW” I‘m" body seen.
y controlled asthma
' Limitationofaclivifies None ' Bronchascqoy -
a Nocturnal awakening None AW present in any
week > Bronchoscopy is needed for diagnose and therapeutic purpose
d for rescue None (twicetor less! More than twiceiweek s the dagnosls even
> Should be undertaken it the clinical and radologlcal features suggest
. treatment ' week) i history of foreign body is not forthcoming.
in i . N l ( 30% predicted
One or morelyear One in any week ' > For diagnosis of foreign body flexible bronchoscopy is beneficial.
. Lung '
. Exacerbation None
RESPIRATORY SYSTEM D Chapter-J 161
Treatment -
Diagnosis -
. Heimlr'ch Maneuver —
Diagnosis is usually clinical by -
> Can be done even outside hospital setting by a trained person
- History of provocative event
> If sudden onset checking
- Stereotyped pattern oi events
> Severe respiratory distress
0 Color changes proceeding the loss of conciousness
> Child is unable to speak or cry
Investigation — Usually not required — May be done to rule out serious illness.
. Oxygen _
' EEG — Electroencephalogram if seizure is suspected and history is conlusing
> If patient has respiratory distress with or without cyanosis ° ECG — If associated with pallor then ECG should be done to rule out arrhythmia
- Nebulizatrcn - Management -
> If suspicion of foreign body. nebulization should not be done. otherwise that may be ' As the condition is benign in nature but events are extremely frightening to parents. 80
pressurized to more inner side reassurance is the major part of treatment.
- Rigid Bronchoscopy — - Explanation to parents about —
> For removal of the foreign body Benign nature of illness
VVVVV
> Consultation with otolaryngologist and pediatriclcardio thoracic surgeon Self limiting course
- Antibiotic - To remain calm during the event
> No immediate eltect To distract the child's mind when they will start to cry.
> Given when there is late consequence like pneumonia from secondary infection. To avoid pick up the child (since this decreases blood flow to the brain)
3* To turn the head to apposite side so that secretion can be drained out.
a. 19.- Breath Holding Spell {2010, Supple, HRS, 9th Sent]
0 ll child has pallor then iron supplementation should be given. It may have role in prevention
Ans : Breath holding spells are benign paroxysmal nonepileptic disorder typically initiated by a of recurrence of spells.
provocative event that causes pain. anger, frustration, trauma causing the child to cry.
- Occurs usually In healthy children O. 20: Clinical features of severe pneumonia (CHIC, 9th Sam]
Ans : Acute lower respiratory tract infection (LFtTI) is a leading cause of death in children below 5
- Age-— Flare before 6 months of age, peak at 2 year and usually abate by 5 years.
years of age specially in developing countries.
- Usually equal incidence in boys and girls.
WHO has recommended some clinical criteria to diagnose and classify AFII at the primary health
- They are benign events. pose no long term risks for the child. centre to reduce mortality from ARI.
Events - According to WHO clinical classification -
Provocative events Severe pneumonia -
l - Cough
Excessive crying - Increased respiratory rate
l < 2 month old — 2 ISO/min
Crying stops at full expiration
' l 2 - 12 month old — 2 50/min
- Color changes — cyanosislpallor 12 - 60 month old - 2 40lmin
- Apnea - Chest in drawing
- Loss at consciousness
- Occasionally seizure a. 21: Bronchial Breath Sound [Murshidebad]
l Ans: Bronchial breath sounds are the respiratory sounds that are heard on the large airways (Tracheal
Within orle minute and part of chest which are close to large airways. ,
0 They have following characteristics —
. nesunption of normal activities
. Inspiratory and expiratory phases are equal with the expiratory phase is louder
. Regaining of conciousness - It has a 'Tubular' quality— Similar to air being blown through a hollow tube
Types - - The sound is considered abnormal if they are heard at a distance from larger airvvays.
breathing '
. Depending upon the color changes at the peak at holding . Usually high pitched and a pause is present between inspiration and expiration.
- Cyanotic spell
- Pallid spell
RESPIRATORY SYSTEM U Chapter-7 153
162 QUEST : F'AEDIATRICS
0 Cyanosis may be present

E] Site and condition when bronchial breath sounds are heard -
- Evidence of staphylococcal infection in other parts of body
- Normal ~
Pathology -
> Over the trachea
— Pneumatocele'Is the pathological hallmark of staphylococcal pneumonia.
.> Part of the chest that are close to larger airways
— Pneumatoceles result from diffuse pneumonic process followed by suppuration and
— Between the scapulae bronchoalveolar destruction.
- At lung apices especially on the right Complication —
Abnormal — Complication occur in untreated cases following extension of infection
> When heard over the chest away from large airways - lntrapulmonary - lung abcess .
> Consolidation with patent bronchus —- En'pyema Thoracis
> Collapse with patent bronchus — Pyopneumothorax
> Lung cavitation. - Extrapulmonary — Pyopericardium
> Tension pneumothorax — Metastatic abcess in muscle, bone, liver, brain
— Osteomyelitis. meningitis
0 Types of bronchial breath sounds —
Diagnosis -
Depending upon the quality of sound they are of three types —
- Suspicion in infant or young child with respiratory distress. toxic look and evidence of staphylo-
' Tubular type
coccal infection elsewhere In body
> Low pitched. sticky quality a Characteristic complication — Pyopneumothorax. empyema, pyopericardium
> Heard in consolidation
' ' Chest X-ray — Presence of pneumatocele as thin walled cyst {Pneumatoceles are also seen in
- Cavemous type ' klebsiella pneumonia)
> High pitched, hollow in quality - Pus staining and culture if empyema present
> Heard in lung cavitation Treatment -
' Amharic type - Immediate hospitalization.
> Metallic quality 0 Moist 02 to releive cyanosis and dyspnea
> Heard in tension pneumothorax - Antipyretic — in adequate dose and frequency
en ' l.V. Fluid - To maintain hydration
o. 22: Staphylococ Pneumonia in Childr
ce In in tents and. young children in whom the illness - Antibiotic therapy —
Staphylococcal Pneumonia occurs with high inciden
— Promptly started
is more severe and highly fatal. is
lly Methicillin resistant staphylococcal pneumonia - Initial choice co—amoxycillin or cloxacillin and ceftn'axone
incidence of staphylococcal pneumonia especia
increasing over past 20 years. — Modified by culture sensitivity report (Puslblood culture) when vancomycin/linezolid or
hyrna. Teicoplanin may be necessary
Source: ' Primary infection of lung parenc
. Secondary- From staphy loccal infection in other parts of body - Duration of antibiotic therapy -
— Furuncle, carbuncle. impetigo 2 weeks in uncomplicated cases

4-6 weeks"In empyema or pneumothorax.
- Osteomyelitis, septic arthris
— Following intial therapy, the remaining course can be corrpleted with oral antibiotics.
- Septicemia
Staphylooowal mlded skin syndr
ome — Treatment of complication like drainage of empyema lpyopneurnothorax I pyqaericardium.
-
les, influenza
Risk Factor :0 Viral infection - Meas
- Cystic fibrosis
- MalnutritBOn
. - Diabetes _
Clinical Feat ures : Usua lly a seve re course
Start s with coug h and cold follow ed by progressive respiratory distress
-
and febri le
- Child is usually toxic
ter-8 165
CARDIOVASCULAR SYSTEM [1 Chap
CHAPTER - a Jr
There is T PVR
CARDIOVASCULAR SYSTEM i
re
T RV pressure due to backward transmission of PA pressu
fi—
i
R sure radiant _., RBVBI’SBI Oi shunt (in
0. t : Pathophysioiogy of large VSD and the future changes in hemodynamlcs it remain untreated.
“W" Vpresi 9 #‘J advanced stage)
Mention the complications of VSD. Outline the treatment of VSD with CCF [2013] (5 + 3 + 2) l
O. 2 : Describe hemodynamlcs of a large VSD in children. Describe the management olan infant L -) R shunt i as (i ed shunt murmur)
presenting with VSD with cardiac failure. [Nat-l0, 9th Sem} {5 + 5) i (Eisenmenger’s
l Volume overload of LA and LV syndrome)
Ans :
PATHOPHYSIOLOGY I HEMODYNAMICS OF LARGE VSD l
H93“ size retums 1° +— l LV size (only RVH and prominent PA segment)
» Ventricular septal defect (VSD) is the most common congenital heart disease in children. normal
- Shunt — Defect in the ventricular septum causes left to right shunt oi oxygenated blood from LV
to RV. as LV pressure is more than the RV pressure throughout the systole. COMPUCATIONS OF V50
l1il-
o Magnitude of the shunt depends on — 1 Congestive Cardiac Failure —> Due to increased blood flow through pulmonary circulation.c
U
a) Size of the defect and dren may develop features of CCF with respiratory difficulty.
_ 2) Pulmonary vascular obstructive tfisease (PVOD) -> It develops in untreated long-standing VSDs
b) Level of pulmonary vascular resistance (PVR)
with irreversible changes in pulmonary circulation. Ultimately, there is reversaloi shunt causing
a In a small defect (usually < 5 mm) which is pressure-restrictive. shunt magnitude doesn't de- cyanosis (known as Eisenmengei’s syndrome)
pend on PVR. Whereas, in a large non-restrictive defect (usually > 10 mm), there is complete
transmission of LV pressure to RV and the shunt depends largely on PVR (Dependent shunt).
3) lnfective Endocarditis -> VSD is the commonest cardiac lesion complicated by IE.
80, large stunt doesn't owur until the infant reaches 6-8 weeks of age, when PVR falls to normal. 4) Infundibular stenosis —> May develop due to the hypertrophy of the RV infundibulum, causing
- Hemodynamics —
iv ed magnitude of L a R shunt.
5) Aortic regurgitation —+ Due to prolapse of the aortic valve leaflet through outlet VSD.
1) Generally. flow of blood occurs through the defect throughout the systole (when RV is also
contracting). Thus. extra blood goes to the PA and spares the RV from being hypertrophied. MANAGEMENT OF LARGE VSD WITH CCF
Chambers enlarged in small and moderate VSD are — PA. LA and LV (discussed later)
- Investigations —
But. in large VSD, there is direct transmission of LV pressure to RV. Thus. RV also becomes
enlarged in addition to PA, LA and LV. So, there is Biventricular hypertrophy in large VSD. 1. CXR-
2 Shunt murmur in VSD is usually pansystolic. But in large VSD (non-restrictive), pressure a) Cardiomegaly (involving LA. LV and RV)
v
gradient is depleted early. 30, late systolic component of murmur is abolished. producing b) Prominent main PA segment
long systolic murmur. c) Increased pulmonary vascular markings
3 There is extra blood flowing through pulmonary valve. which may produce ejection systolic 2. ECG-
U
murmur at pulmonary area. a) Biventn'cular hypertrophy (BVH)

early A2. On
4) LV blood has 2 outlets (Aortic valve and VSD). So, it empties early producing b) LAH
in P2. Thus,
the other hand. pulmonary valve handles extra amount of blood, causing delay
82 is widely split. P2 is loud due to T PA pressure. 3. Echocardiography —
pulmonary plethora a) Identifies the number. size and exact location of the detects (VSD).
5) Increased volume otblood passes through pulmonary circulation. causing
and repeated chest infections. b) Estimates PA pressure .
6) This increased amount of blood reaches LA causing its enlargement (LAH) c) Identifies other associated detects (e.g. aortic valve prolapse. aortic regurgitation,
murmur of infundibular stenosis etc)
7) Extra blood passes through Mitral valve, which may produce delayed diastolic
Mitral Stenosis at apex. _ d) Picks the direction of flow through the shunt
8) Finally. LV has to handle that extra blood. which causes LVH. - Treatment —
the pulmonary
- Left untreated — It large VSD is left untreated, irreversible changes occur In 1. Treatment of CCF —
vasculature, causing pulmonary vascular obstructive disease (PVOD). a) Propped m posltlon
l b) Moistoz Inhalation
164
CARDIOVASCULAR SYSTEM ['3 Chapter-8 167
— Valvar
contraindication for enteraI
c) It! fluid - Should be used cautiously and if there is absolute as there is — Supravalvar (Branch PA stenosis)
requirement.
feeding, 9.9.. severe tachypnea. Usually given 6 50% of total c) LV outflow —
volume overload.
by oral feed or nasogastric tube feed. i) Aortic stenosis (AS)
d) Enteral feeding - Preferred method: given
— Subvalvar (Membrane)
e) Diuretics —
oral) according to severity is - Vaivar
n Frusemide G 1-4 mg/kglday in 2 divided doses (i-v. or
the lst choice. - Supravaivar
d. ii) Coarctation of aorta
ii) Spironolactone may be added, if require
f) ACE inhibito rs— (Enala pril) reduce s after load B) Cyanotic heart disease —
9) Digoxin -— rarely needed 1. Reduced pulmonary blood flow —
h) Correction of anemia . a) Tetraiogy of Fallot (TOF)
i) Treatment of any associated LRTI. b) Pulmonary atresia
ve endocarditis.
and antibiotic prophylaxis against infecti c) Tricuspid atresia
2. Maintenance of good oral hygiene
3. Closure of VSD —— d) Ebstein anomaly
indications — 9) Double outlet RV (DORV) + PS_
a) CCF in infamy f) Single ventricle (SV) + PS
05 -+ Systemic
> 2 : 1. (Op —> Pulmonary blood flow. 2. Increased pulmonary blood flow -—
b) Large L -> R shunt with 0,. : Os _
blood flow) a) Transposition of Great Arteries (TGA)
or AR.
c) If there is associated PS. PAH sal of shunt) b) Persistent truncus arteriosus
menger’s syndrome (Severe PAH with rever
Contraind icatio ns — Eisen c) Total anomalous pulmonary venous retum (TAPVR)
Options —
in relatively older children d) DORV without PS
re (best suited for mu scuiar VSD
a) Non-surgical device closu 6) SV without PS
> 8-10kg)
a patch.
C) Coronary lesions —
b) Surgical closure —> with 1. Anomalous origin of left coronary artery frompulmonary
artery (ALCAPA)
embryo logic al basis ofpetent ductus
rt Disease. Mention briefly the 2. Coronary AV fistula
a. 3 : Classify Congenital Hea clin ical futu res and management of this
con dltion. (2+2+4+4) . ..
srterlosus (FD A). Out i'ne the

EMBRYOLOGICAL BASIS OF PDA
[Maids — 2016]
persistence of patency of DA. which normally
ITAL HEART DISEASE PDA or Patent Ductus Arteriosus is the abnormal
Ans.
CLASSIFICATION OF CONGEN closes after birth.
_ ’
Disease: tion between aorta and pulmonary artery,
A) Acyanotic Heart - Ductus arteriosus : Ductus arteriosus is the connec
shu nts -— which acts as an important shunt in fetal circulat ion.
1. Left to righ t
s aorta. _ _
a) Pre —tr icuS pid > - Structure — Conical structure with broader end toward ary
rn (PAPVR) (La. PA to aorta) in fetal circulation, as pulmon
pulmonary venous retu > Flow — Flow in ductus is mostly R —+ L
i) Partial anomalous
D) vascular resistance is high.
ii) Atrial septal defect (AS
(VSD) Closure of ductus -
tricular septai detect -
b) Ventricular - Ven birth
> Functional closure - by 10-15 hours after
c) Great artery — .
riosus (PDA) > Anatomical closure — by 2 to 3 weeks
i) Patent ductus arte -
win dow. > ' Factors for closure —
ii) Aorta-pulmonary ) or Endocardiai cushion
defect (ECO) the strongest stimulus for closure of DA.
ricu iar septa! defect (AVSD i) Oxygen - Postnatal increase in‘ PaOz is DA PGE1 level toe
:1) Complex -' Atriovent results in constriction of
ions —
ll) PGE, — Decrease In level of PGE‘ after birth
. Obstructive les the to -
triatum
a) inflow — Cor tria ) 1) Removal of placental source of PG
w — Pu lmonary stenosis (PS
b) RV outflo
bvalvar)
_ infundibular (Su
189
QUEST : PAEDIATRICS CARDIOVASCULAR SYSTEM U Chapter—8
168
b) Increase in pulmonary blood flow — effective removal of PGE1 from circulation. - Treatment —
- Persistence of Ductus (PDA) - 1. Supportive measures -+
i) Hypoxia and acidosis (as in perinatal asphyxia. sepsis. HDS. MAS etc.) relax ductal a) Treatment of CCF with anticongestive measures (Diuretics)
smooth muscles and results in delayed closure of DA. infants with PDA
b) Fluid restriction (50-60% of maintenance) in case of preterm
ii) Premature infants have poor constrictor response of DA to oxygen and increased PGE1 c) Treatment of LHTIs with antibiotics (oral/iv.)
levels. which results in more incidence of FDA in preterms. Preterm PDAs reapond well
d) Endocarditis (IE) prophylaxis. if indications arise.
to NSAID treatment.
2. Definitive treatment —)
iii) Few cyanotic heart defects have duct-dependent circulation (like - Pulmonary atresia).
for closure of
Thus. PDA is essential for their survival. a) Pharmacological closure — Use of NSAIDs (Indomethacin or Ibuprofen)
FDA is usually effective in preterm infants before the age of 2 weeks and not useful in
iv) Lastly, term infants without any risk factors can also have PDA. which have genetic.
term infants.
environmental or other unexplained causes. Term PDA poorly responds to NSAID
treatment (unlike preterm PDA). > Mechanism of Action — NSAIDs inhibits the production of PGE1, which maintains
patency of FDA.
CLINICAL FEATURES OF FDA > Dose —
PDA results in left to right shunt from aorta to PA through ductus. which results in all the features i) lndomethacin - 0.2 mg/kgldose x 3 doses 12-24 hours apart. (oralfl.v.)
described below — ii) Ibuprofen -10mg/kg on day 1. followed by 5 rng/kg on day 2 and day 3 (oralliy)
- Symptoms —- > Contraindications -
1. Patients are usually asymptomatic. when ductus is small with small left to right shunt. Hepatic or renal insufficiency
i)
2. When shunt is large. it causes — it) Thrombocytopenia or bleeding tendency
a) Repeated LRTI (Fever. cough and respiratory distress) b) Catheter closure — By use of coils or occlusion devices has become popular now-a-days.
b) Congestive cardiac failure (Tachypnoea and poor weight gain) c) Surgical closure — Indicated in -
c) Exertional dyspnoea in older children or feeding difficulty with sweating in infants. i) Small infants with large ductus
I All
- Signs - ii) Very large ductus (> 10 mm)
1. Tachycardia and tachypnoea (with/without retractions) in infants with CCF iii) Devices are not affordable
2. Bounding peripheral pulses with wide pulse pressure (water hammer character) > Indications of closure — Hemodynamically significant PDA with CCF. recurrent LFlTI
3. «Precordium is hyperactive on inspection and palpation or poor weight gain
> Contraindications of closure — Eisenmengei’s syndrome- 3
4. Systolic thrill may be present at upper left stemal border
5. P2 is usually normal (intensity may be accentuated in the presence of pulmonary hypertension) 0.4: Enumerate the defects of Fattot's temlogy. Outline the hemodynamics In this disorder.
or upper left
6. A continuous (Machinery) murmur best audible at the left infraclavicular area Describe the management of cyencttc spell. (2+3+5) (RGKMC — 2016, SDMC — 2016)
stemal border
FDA DEFECTS OF FALLOT’S TETHALOGY
. Rumbling diastolic murmur at apex (Functional MS) may be heard in large
Ans. .
‘1
right to left with cyanosis at lower 1. Large non-restrictive ventricular septal defect (V80)
8. When Eisenmenger's syndrome develops. shunt becomes
half of the body (known as differential cyanosis). . 2. Flight ventricular outflow tract (RVOT) obstmction. [Commonly lnlundibular P ulmonary Stenosis]
MANAGEHENT 0F FDA 3. Overrlding of the'aorta -
- Investigations - 4. Flight ventricular hypertrophy [FWH)
1. Chest X—ray -> HEMODYNAHICS OF TOF
a) Cardiomegaly (Dilatation of LA. LV)
Tetralogy of Fallot'ITOF) ls the-most common cyanotic congenital heart disease in children. It
b) T ed pulmonary vascular markings (pulmonary plethora) consists of 4 defects or abnormalities (enumerated before).
2. ECG -tr LVH or BVH (with large PDA) . Impedance of different detects - From physiological point of View. 2 defects are essential for
3. Echocardiography —+ ‘ the development of TOF hemodynamics —
_ . 9s...
a) Confirms the diagnosis of FDA a) A VSD large enough to equalize systolic pressures in both ventricles. and
b) Assesses the chamber enlargements (LA. LV) b) FIVOT obstruction (infundibular PS. valvular P8 or both)
c) Picks the direction of shunt
22
CARDIOVASCULAR SYSTEM CI Chapter—8 171
- The other 2 defects, like —- > Investigations - As cyanotic spell can be diagnosed clinically in a lcnownc/o TOF,
investigations are not warranted. Undue blood sampling may further aggravate the condition.
c) RVH occurs secondary to RVOT obstruction and
If done. ABG shows acidosis. l P02 and T P002.
d) Overriding of aorta varies widely and it may not be present in all cases.
> Treatment—
> Magnitude of shunt/disease severity — Magnitude of 'R —+ L shunt through VSD and
1) The baby is held in a knee-chest position. Benefits are -
resulting cyanosis (due to passage of deoxygenated RV blood into the aorta) depends
solely on the severity of pulmonary stenosis. a) Pressure over aorta — T SVR
More severe stenoels (PS)
b) Pressure over IVC — I venous return
2 Humidified 02 may be provided. but not much useful. (Better to avoid. if child is restless
V
/
More R -> Lshunt from
\
Less pulmonary blood flow
due to 02 mask)
3) Calm and quiet environment
4) Correction of hypovolemia or dehydration —-> with NF.
RV to LV and aorta
[N.B. — with mild stenosis 5) Injection Morphine Sulfate (0.1-0.2 mg/kg 8.0. or i.m.) —> Supresses respiratory centre
\ / shunt may be L —> R (like and breaks the vicious cycle.
. VSD) with no cyanosis. This 6) Injection Socium Bicarbonate (t mqkg i.v.) —-> Corrects metabolic acidosis and eliminates
. is known as Pink TOF or the respiratory centre stimulating effect of acidosis.
More cyanosrs Acyanotic TOF}
7) if the spell continues despite all these supportive measures. following mediCations may
- Hemodynamics — be useful.
1. As VSD is large and non-restrictive. systolic pressures are identical in both the ventricles. a) Vasopressors (like phenylephrine) -> Increases systemic vascular resistance by a,
Shunt (Fl —-) L) occurs proportional to the severity of PS. But, there is no shunt murmur. stimulation.
2. As pulmonary artery pressure is low, flow of blood across pulmonary valve from RV to PA b) Propanolol —> Acts by decreasing heart rate (it, blockade) and increasing SVR ((32
produces Ejection Systolic Murmur (ESM) of PS. This is best audible at mild-left stemal blockade).
border (infundibular stenosis) or upper left stemal border (valvular PS).
c) Ketamine -) It simultaneously sedates the patient and increases SVR.
3. Intensity of ESM is inversely proportional to the severity of PS, as with more severe PS. less
8) Surgery —> Reserved for refractory cases and includes —
blood flows through pulmonary valve and more shunt occurs through V80.
a) Emergency modified BT shunt (Blalock - Taussig shunt : Subclavian artery to PA
4. RV hypertrophy, which occurs due to P8 is concentric due to pressure overload. but there is
anastomosis)
no volume overload as RV blood flows freely to LV and aorta. Thus. CCF never occurs in
TOF and heart size is also normal in TOF. b) Balloon pulmonary valvuloplasty
5. Because of low pressure in PA. P2 is soft and often inaudible, resulting in a single 32.042). A2 > Prophylaxis — Primary or secondary prOphylaxis to prevent cyanotic spells can be achieved
is louder than normal due to anterior displacement of aorta. . wrth propanolol (daily oral dose). 3A
CYANOTIC SPELL 0.5: Enumerafe the causes of congestive cardiac failure (CCF) in children. Outline the
Cyanotic spell (also known as Tet spell or Blue spell) is an important and occasionally life- management of CCF. (5+5) [8M0 - 8th Sam]
threatening complication of TOF. It is more common in younger children (infants and toddlers). 0.6: Enumerate common causes, describe clinical features and outline the management of heart
> Mechanism -— Most important mechanisms precipitating the cyanotic spell are tachycardia failure in children. (2H4) ' [NBMC - 8th Sam]
and lowering of systemic vascular resistance (SVR). Ultimately a vicious cycle sets in with 0.7: Define heart failure and enumerate important causes of heart failure in neonates, infants
hyperpnoea and increasing cyanosis. and children. Discuss in brief the management of heart failure. ( fur-5) [BSMC - 2016]
Tachycardia or isvn ——> IPBF (Pulmonary blood flow) Ana. HEART FAILURE : DEFINITION (0. No. 7)
I .
Heart failure is a complex clinical syndrome that can result trom any structural or functional
RV volume
cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.
overload
CAUSES OF HEART FAILURE
L T Systemic ”MUS I 1 P051 P002, i PH ] A) Congenital heart disease:
r return . 1) Left to right shunt
T Negative intrathoracic \ / a) VSD
pressure Stimulation of respiratory centre
b) PDA
Chapter-B 173
CARDIOVASCULAR SYSTEM CI

d) Large FDA
c) ASD 9) Critical AS/PS
d) AVSD (Atriovenlricular septal defect) f) Arrhythmia
2 Cyanotic heart disease with increased PBF — 9) Severe anemia (in all age group)
v
a) TGA Infants—
v
b) TAPVR {total anomalous pulmonary venous retum) a) VSD
c) Tmncus arteriosus b) PDA
3 Obstructive lesions — c) AVSD
v
a) AS d) d-TGA
b) PS e) 00A
0) Coarctation ol' aorta (COA) f) Unobstructed TAPVR
4 Fiegurgitant lesions Children—
V
a) AH a) Rheumatic lever
b) MFI b) RHD
8) Acquired heart disease : c) Cardiomyopathies
1) inflammatory— d) Myocarditis .
a) Myocardtis (Viral) e) Congenital HD with complications [9.9. infective Endocarditis)
b) Acute Rheumatic Fever with canitis
c) Kawasaki disease CLINICAL FEATURES OF HF (0. Ho. 6)
:1) Cl-Iaga's risease Symptoms —
2) Rheumatic heart disease (RHD) -— 1. Poor weight gain [growth failure
a) HR 2. Fast breathing with ct'restwall retraction (worsens during feeding)
b) AR 3. Feeding diffrcuity —+ (in infants)
c) MS a) Poor feeding
3) Cardiomyopathy — b) Fatigue during feeding
1|) Ditatedcardiomyopathy (DCM) c) Perspiration over forehead
b) Muscular dystrophy d) Suck-rest-suck cycle (repeated small amount of feed with rest in between)
9) Doxorubicin induced 4. Exertional breathlessness, orthopnea
4) Tachyarmwrmia - SVT. VT etc. 5. Persistent cough or wheezing } (in older children)
5) Hypertension 6. Swollen feet or putty eyelids
0) Extracardiac causes : Signs -
1) Metabolic— 1. Signs of left heart failure (Pulmonary venous congestion) —i
!) Severe hypoxia and acidosis a) Taohypnoea
bi Hypocalcerria b) Retractions (suboostal and intercostal)
2) Em“ - Wmmm c) Wheezing
3) Severe anemia d) Pulmonary crepltations (Basal)
CAUSES OF HF ACCOHHNG TO AGE OF PRESENTATION (O. No. 7) 2. Signs of right heart failure (Systemic venous congestion) —)
1) Neonates —
a) Hepatomegaly—usuallywith asoci- ted tenderness
1:) Pedal edema! Presacral edema (in lying‘patients
a) Perinatal asphyxia ) - suggest dependent edema
b) TAPVR (obstructed) c) Engorgedneckveins 7
c) Large use d) Hepatoiugular reflux I Abdominojugular reflux
CARDIOVASCULAR SYSTEM I3 Chapter—8 175
es) —+ b) lnotrepic agents ~ They improve myocardial contractility and4include -—

3. Signs common to both (Result of compensatory respons
' Dobutamine (preferred)
a) Cardio megaly
- Depamine
b) Tachycardia
' Adrenaline
c) 83 gallop rhythm
c) Digitalis - Digoxin also have inotropic action but its use is limited due to various life-
d) Weak and thready pulse
threatening side effects.
a) Occasionally cyanosis
d) Afterload-reducing agents These agents combat the compensatory vasoconstriction
-
MANAGEMENT OF HEART FAILURE that may be deleterious to failing ventricle. Examples are —
done to — - Arterial vasodilator - Hydralazine
- Investigation — Heart failure can be diagnosed well clinically. So. investigations are
- Venodilatcr — Nitrates
a) Confirm the diagnosis in dubious cases and
b) Identify the cause of heart failure
' Mixed - ACE inhibitors (Enalapn'l, captopril etc)
1. CXR - Cardiomegaly is found in almost all cases of HF
o) Others - B-blockers (like Carvedilol, Metaprolol) are useful in chronic HF, especially
. due to DCM. B-blockers are usually contraindicated in acute decompensated HF.
2. ECG —- May help in identifying cause (like arrhythmia)
the cause and also assess seventy N.B. - ACE inhibitors and B-blockers are believed to have long-term preventive
3. Echocardiography - Most helpful investigation to identify effect on
cardiac remodelling.
of HF.
I, .
4. Natriuretic peptides — ANP and BNP are elevated in HF. a. 8 : Write in brief about pathogenic basis of major clinical manifes
tation of Rheumatic fever.
Give an outiine of pharmacological management of CCF in children
Tmtment — . (5+5) [BSMC - 9th
Sam]
A) Treatment of underlying causes —
1. Surgical correction of congenital heart defects and rheumatic heart diseases Ans. MAJOR CLINICAL MANIFESTATION OF RHEUMA'HC FEVER
2. Control of hypertension or arrhythmia. .
According to Revised Jones criteria, major clinical manifestation
of Acute Rheumatic Fever (ARF)
B) Treatment of contributing factors — Factors which precipitate heart failure in a susceptible includes —
child should be dealt with to control HF. like —
1. Arthritis,
1. Infection - by appropriate antibiotic
Carditis,
9:59!“
2. Anemia — to maintain Hct > 35%
Erythema Marginatum
3. Fever - control with antipyretics.
Subcutaneous nodules and
G) Control of HF state -
Chorea '
1. Propped-up position - to combat orth0pnea ..
o Pathogenesis - ARF. is believ

_ ed to be an immunological response occu
2. Moist o2 inhalation Streptococcal (GAS) infecti rrin9 after Group A
on of the pharynx, but not of the skin. There is
3. Salt restriction (< 0.5 grit/day) — about 1-5 weeks (average - 3 weeks) between a latent period of
GAS pharyngitis and onset of ARF, suggesting
i) Avoid extra salt (table salt) and supporting the Immunological theory
. Supporting evidences for immune-med
pathogene sis are ~ iated
ii) Avoid salty snacks (9.9., chips)
. Adequate calorie intake — upto 120 — 130% of RDA a) Identical seasonal variation of GAS
infection and ARF.
39’9”“
Restricted IVF - 050.60% of total requirement. only it absolutely needed. b) Epidemics ofstreptococcal infection are follow
ed by higher incidence of rheumatic fever.
Respiratory support - for patients with respiratory failure 0) H10 proceeding sore throat is available
in about 50% of patients of ARF.
Drugs - - , d) Latent period between GAS infection and
ARF
a) Diuretics — Drug of choice in any HF. They act by reducing preload and thereby e) Streptococci are never isolated from rheum
atic lesions in joints. heart or skin
relieves congestive symptoms. _ 1) Penicillin prophylaxis for streptococcal
infection prevents recurrence of rheum
' Loop diuretics - Frusemide G 1-4 mg/kglday 9) More than 85% of patients show eleva atic fever
ted levels of A80 (anti-streptolysin 0
- Thiazides — Hyd'rochlorothiazide (rarely used) 7 Ab)
- Potassium sparing diuretics — Splronolactone acts as add-on therapy with lmsemlde
to enhance action and also reduce side~effects (like hypokalemia)
176 QUEST : PAEDIATFIICS CARDIOVASCULAR SYSTEM CI Chapter— 8 177
‘Rheumatogenic' GAS infection in pharynx

(GAS pharyngitis) ..$. GAS I snonr NOTE]
I 0. 10 :Madr'l‘r'ed Jones Criteria. [2014, 2003 — Supple, RGKMC — 9m Sam. BMC - 9"? 39'": “PC '
GAS antigens (M protein. cell wall Group-A ® GAS A9 em Sem, NBMC — em Sem, CNMC — 2016]
carbohydrate. capsular hyaluronate etc.)
are presented to Antigen presenting cells (APC) Ans. MODIFIED JONES CRITERIA
I Modified Jones Criteria or Fievised Jones Criteria is used for the diagnosis of Acute Rheumatic
Production of Ab against GAS Ags by B cells Fever. These guidelines were originally suggested by T. Duckett Jones and are later revised by
American Heart Association and WHO. it consists of major. minor and essential criteria -—
0 Major Criteria -
There antibodies cross-react with various ‘A A A
host tissues(e.g.. heart. joint. skin. brain) . . . 1. Carditis (includes pericarditis. myocarditis and endocarditis)
because of common antigenic 2. Polyarthritis (usually migratory)
determinants in these tissues. 3. Chorea
[Example — Certain M proteins share epitopes with human tropomyosin and myosin in heart] 4. Erythema Marginatum
I 5. Subcutaneous Nodules
Activation of cellular immune respons e with involvem ent of 00“». 003+ T cells and Macrophages - Minor criteria —
l CfiOkines (IL-2. IFN-a. lFN-y)

A) Clinical
1) Fever
Inflammatory response\
2) Arthralgia
B) Laboratory findings —
1) Elevated acute phase reactants (ESR. CRP)
2) Prolonged PH interval on ECG.
0 Essential criteria - (Supporting evidence of antecedent Group A streptococcal infection)
Pancarditis Migratory Erythema
Marginatum Subcutaneous 1. Positive throat culttire. or
Nodulee 2. Positive rapid streptococcal antigen test. or
b) Myocarditis
Sydenham’s 3. Elevated or rising streptococcal antibody titre
c) Endowrdrtis
Chorea [Antistreptolysin-O (ASO). Anti DNA-ass B]
- Diagnosis — High probability of acute rheumatic fever is suggested by the presence of essential
PHARMACOLOGICAL MANAGEMENT OF CCF
criteria with —
See Question 5 to Question 7 (Management — Drugs) a) 2 major criteria, or
child with moderate sized b) 1 major + 2 minor criteria
til it stale and mana ement of 3 years old
y 9)! 9 (3+5) [CNMC——2016] . Limitations I Exceptions -—
O 9 3253"“ the pa OP
1. Arthralgia or prolonged PR interval cannot be used as minor criteria. if arthritis and caiditis
Arte. MODERATE 5|o vso respectively, are used as major criteria
the following differences —
- Plthophyelology- Similar to large V80 (0. 1). with 2. Chorea may occur as the only manifestation of rheumatic fever and in that case. often essential
1. Moderate sized VSDs are usually 5-10 mm in size criteria are also absent.
shunt magnitude doesn ’t depend-on
PVH and
2. They are usually pressure-restrictive. so 3. Recurrences of rheumatic fever may not fulfil the Jones Criteria fully.
' depends on size of the detect. 4. Partial treatment with NSAIDS may supress full manifestations of rheumatic fever and make
pressure is greater than FlV pressure
3. LV and RV pressures are not equalised. Thus. LV diagnosis difficult.
tolic.
throughout systole. Munnur is usually pansys
re eve rload in RV. Chambers enlar
ged a. 11 :Dlagnosle of Rheumatic Fever. [Kfllyani - 8th Sent]
is no volume or pressu
4. FM-l doesn't occur. as there Same as 0. 10.
Ans.
are- PA. LA and LV.
increase in intensity of P2.
5. PA pressure is mildly elevated causing slight O. 12 :Rheumatlc Cardltls [MMC — 8th Sem]
- Ilanagement - Samea s large VSD {0 1).
CARDIOVASCULAR SYSTEM D Chapter- 8 179
173 QUEST ‘ PAEDIATRICS
- Treatment :
Ans : RHEUMATIC CARDITIS
1. Benzathine penicillin — to eradicate streptococci.
within the ist 2 weeks of
Carditis in acute Rheumatic Fever is an early manifestation occuring 2. Complete bedresl — during active carditis.
. . ..
onset._ 3. Anti-inflammatory therapy —
: Carditis occurs in about 50-60% of patients of acute RF. But. subclrnical cardrtis
- Incidence a) Aspirin alone — for mild to moderate carditis without CCF
iography)
may be present in another 30-40% of patients (diagnosed by echocard b) ASpirin + Prednisolone — for severe carditis with CCF
: Molecular mimicry of cardiac tissue Ag with Gr. A streptococ cal antigen (M protein)
- Pathology 4. Anti-CCF measures —
l
a) Diuretics (Frusede)
Anti-streptococcal Ab produces inflammatory reaction
1, Pericarditis b) Digoxin (used with gution)
Development of pan carditis < Myocardiiis O. 13 :Rheumatfc Chores [2009] {2016 Supple], [Midnapare - 2016]
Endocarditis
Ans. RHEUHATIC CHOREA
Clinical Presentation :
1. Pericarditis- Rheumatic chorea (also known as Sydenham's chorea or St. vitus’ dance) is a late manifestation
a) HIO chest pain of Rheumatic Fever. occurring around 3 months after the onset of acute RF.
b) Pericardial friction nrb on auscultation - incidence — About 15% of patients with ARF present with rheumatic chorea. Prepubertal girls
causes tamponade. May present (8‘12 years) are more affected than boys.
c) Pericardial effusion is usually mild and almost never
. with muffled heart sounds. - Pathology - Molecular mimicry of brain tissue (including basal ganglia) with GAS Ag.
2. Myocarditis — . i
.. a) T cardia (out of proportion to the degree of fever) Anti-streptococcal Ab cross-reacts
'i 3 Jr
1 b) Cardiomegalv .
5I c) 8' ns of congestive heart failure in severe cases (53 gallop. Tachypnea. Hepatomegaiy. Inflammatory reachon
; TEVP) - Clinical features - It is a neuropsychiatric disorder.
T 3 itis _ 1. Neurological signs -
Pansystolic murmur a) Chorea — Jerky. semi-purposeful movements of limbs involving major joints.
a) Mitrai Regurgitation (most common) —
b) Aihetosis — Writhing movement of small joints of hands (Athetoid movement) may be
b) Aortic Regurgitatio n
associated
diastolic murmur due to fl ow across inflamme
d and
c) Carey Coomb's murmur (delayed c) Hypofonia and weakness
thickened mitra l valve )
d) Drops things he or she carries
d) Triouspid regurgitation (very rare)
2. Psychiatric signs —
a) Emotional iabrlrty
l I l
1 Acute Phase Reactants- T ESR. 109?

‘ :
b) Hyperactivity
2.' CXH --
c) Personality changes
a) Usually show cardiomegaly
CCF) - Diagnosis —_
b) 1‘ Pulmonary vascular markings (in "> By revised Jones Criteria. but isolated chorea is difficult to diagnose.
3. ECG — > Only 66% of patients with isolated chorea have elevated ASO titre.
a) 1 PR interval > They have elevated anti-neuronal antibodies against basal ganglia tissues (90%).
is)
b) Global ST elevation (in pericardit a Treatment —
found (in myocarditls)
c) Various arrhythmias may be for subciinlcal carditis. 1. Anti-Inflammatory therapy - usually not needed
ory for rheumatic cardrtls a nd diagnostic
4. Echocardiography - Confinnat a lniection Benzathine penicillin — to eradicate streptococci
a) Detects pericardial effusion 3. Reduction of physical and emotional stress
b) Assesses Ejection Fraction 4. Dnrgs — indicated for severe cases only and includes —
t chambers
0) Picks up dilatation of hear a) Phenobarbitone -
e involvements.
d) Diagnosis of different valv
180 QUEST: PAEDIATFIICS
CARDIOVASCULAR SYSTEM [3 Chapter—8 181
b) Haloperidol
d) Propped up position
c) Carbamazepine
6) Treatment of chorea -
d) Diazepam
a) Reduction of physical and emotional stress
5. Lastly, counselling and reassurance about the self-limiting nature of the disease.
b) Counselling
a. 14 :Management of Acute Rheumatic Fever. [MMC - 9th Sem] c) Drugs (e.g.. Phenobarbitone. Haloperidol etc) in severe cases only.
Ans. MANAGEMENT OF ACUTE RHEUMATIC FEVER 0. 15 :Prevention of Acute Rheumatic Fever. [8M0 — 8th Sem, Murshidabad - 2016‘]
- Investigation — if history and physical examination suggests acute rheumatic fever, following O. 16‘ :Prophylaxis of rheumatic fever. [IPGMER - 9th Sem, IPGMER - 2016]
investigations are done to confirm the diagnosis —
Ans. PREVENTION I PROPHYLAXIS OF RHEUMATIC FEVER
1. Complete blood count
2. Acute phase reactants — A) Primary prevention — Primary prevention of rheumatic fever includes treatment of
8) E88 streptococcal pharyngitis with appropriate antibiotics to prevent the first attack ot RF. However,
it is not possible to give primary prevention in every patients because of high incidence of
b) CRP
subclinical infection. Options for primary prevention are -
. Throat culture
749990.)
1) Iniection Benzathine Penicillin G - Single dose

A80 titre a) 6 Lac lU deep i.m. (< 27 kg)
ECG b) 12 Lac IU deep i.m. (> 27 kg)
Chest X—ray 2) Penicillin V — 250 mg ODS x 10 days (orally)
Echocardiography 3) Azithromycin — for 5 days
- Treatment - 4) Cephalexin - for 10 days
1) Bed rest— Recommended in any cloacute rheumatic fever, but the duration varies from B) Secondary prevention - Patients with documented history of rheumatic fever (including
1-2 weeks (for isolated arthritis) to 4-6 weeks (for severe carditis). Bed rest is generally rheumatic chorea) should receive secondary prophylaxis to prevent recurrent attacks of RF.
followed by a period of indoor ambulation before normal daily activity (like going to school) But. isolated elevation of A80 titre is not a criteria to start secondary prophylaxis. Drugs
is resumed. used for secondary prevention are -
2) Salt restriction - needed only in cases with features of congestive cardiac failure. 1. Injection Benzathine Penicillin G — every 3 weeks at same dose as primary prophylaxis. (6
3) Injection Benzathine Penicillin - 6 Lac l U (for children < 27 kg) to 12 Lac M (for children > 27 Lac IU / 12 lac lU deep i.m.)
kg) deep i.m. is given when diagnosis is confirmed to eradicate streptococci. This dose also 2. Penicillin V — 250 mg 80 (orally)
serves as the first dose of penicillin prophylaxis. '
3. Erythromycin — 250 mg 80 (for patients allergic to penicillin)
4) Anti-inflammatory therapy- (Total duration — 12 weeks) . - Duration of secondary prophylaxis -
a) For carditis with CCF — Prednisolone @ 2 mglkg/day for 2-3 weeks a) For RF without carditis — 5 years or until 21 years of age (whichever is longer)
i
b) For RF with carditis (but without Rheumatic Heart Disease) — 10 years or until 21 years
Slow tapering over next 2-3 weeks of
age, whichever is longer.
+
c) For RF with carditis with RHD — 10 years or until 40 years. whichever is longer;
Aspirin a 50-60 mg/kglday often lifelong.
b) For isolated anhritis — O. 17 :Canstrictive pericarditis. [20 14 - Supplementary]
—> Aspirin 0 100 mg/kg/day for 2-3 weeks Ans. _ CONSTRICTIVE PERICARDITIS
i Chronic pericardial inflammation with fibrosis. calcification and thickenin of
Tapered to 50-60 mglkglday the ericardium.
::::?rl1ngl:fltIjrrini‘alredcardiac diastolic filling. :5 known as constricti
ve pericardigtis. It is 03mparatively
c) For carditis without CCF — Steroid preferred over aspirin alone
5 Treatment of CCF - - Etiology —
v
a) Diuretics (Frusemide) 1. Infective —

b) Digoxin a) Recurrent viral pericarditis
0) MOST 02 b) Tuberculous pericarditis
c) Incomplete drainage of purulent pericarditis
CamScanncr
CARDIOVASCULAR SYSTEM [3 Chaplet—8 183
tez QUEST : PAEDIATRICS
’ :bl "" 'V
2. Hemopericardium -i Fall in intralhoracic pressure
3. Mediaslinal irradiation for lymphoma

4. Cardiac surgery Pooling of blood inside thoracic cavity
- Pathogenesis -
Chronic inflammation of the pericardium /
t ed filling of RV
\
t ed tilting of LA and U;
l (as pulmonary vessels
(as systemic veins are
Fibrosis. thickening and calcification extrathoracic) are intratho racic)
l .
Stiff pericardium
l l SBP and l pulse vol during <___ l in stroke volume
l ed distensibility inspiration and cardiac output
l
Impaired diastolic filling of heart 5-1 0 mm Hg. When
- Normally, difference between expiratory SBP and inspiratory SBP is around
l this difference exceeds 10 mm Hg. it is known as pulsus paradoxus
. _
Diastolic dysfunction
- Causes —
- Clinical features - 1. Cardiologicai causes -
Elevated JVP a) Rapidly developing pericardial effusion and cardiac lamponad
e.
spore-
ar Reflux
Hepatomegaly with positive Hepatojugul b) Chronic constrictive pericarditis
\
Ascites and peripheral edema left stemal c) Restrictive cardiomyopathy
bling opening snap. commonly heard at
Pericartflal knock - a diastolic sound resem 2. Respiratory causes —
border a) Bronchial asthma
s may be found
Pericardlal rub and distant heart sound b) Pulmonary embolism
min
c compromise.
e - in sever e cases . there may be more signi iicant cardia '
. Cardiac tamponad 3. Miscellaneous -
resulting in —- a) Obesity
a) Hypotension b) Superior mediastinal syndrome
b) Tachycardia in the above cobal_ t'ons causing
- Pathophyslology - The normal phenomenon is accentuated
c) Pulsus paradoxus pulsus paradoxus. because —
funher {which is already elevated in
- Investigations - a) During inspiration. intrapericardial pressure rises . .
ons of pericardium e in venous return and cardiac output.
1) CXR - May show calcificati tamponade) causing decreas
a fixed diastoli . As RV filling is
ge. T-wa ve inversion or flattening b) There is corlpetition between 2 ventricles to occupy
c volume
2) ECG — Low ORS volta gy section) . LV filling is further oornpromised.
more during inspirat ion (as shown in physiolo
3) Echocardiography — of intrathoracio pressure due to obstruction to
c) In respiratory causes. there is wide variations
a) Thickened pericardium airflow. .
b) Diastolic dysfunction SBP
0 Measurement - BP cuff is inflated well above the
e sensitive
4) Cardiac CTIMRI - Mor l
my Slowly deflated
- Treatment - Pericardiecto {2012] *5
1 l
a. 18 :Pulsus paradoxus. ‘ . . At first. Korotkoff’s Sounds are heard only during expiration
PULSUS PARADOXUS :r l
'7 Diference between
.
Ana. sus normalia
should beltor be called "pul in
Pulsus paradoxus is actu .. _ ally a misnomer and it of a phy siolo gical phenomenon. “ms taken”- Funher deflation enables the sounds to be heard
eita gge ratlo n . both expiration and inspiration
it is not hing but the
exaggeralus". because d pressure . (Doubling oi the rate)
is physiological variation in
pulse volume and systolic bloo ‘ '
PI] Y3“" 09? - There exp irati on)
different phases of respiration( i.e.. inspiration and sed
If difference > 10 mm Hg I—t [mus paradoxus is diagno
a '
(SBP) during
CamScanncr
Dnnnr‘r‘ninnnnmitt
184 QUEST : PAEDIATFllCS
fl. CARDIOVASCULAR SYSTEM U Chapter-B 135
0. 19 :Common causes of hypertension in children [2013 sample] In general, younger the child and more severe the hypertension, more likely that an underlying
Ans. COMMON CAUSES OF HYPERTENSION cause is identified.
' Evaluation of childhood hypertension encompasses the following facets. namely —-
Hypertension in children is defined as systolic and/or diastolic BP greater than 95'h percentile
1. Identification of potential causes
for age and sex on at least 3 occasions. Hypertension is generally classified into 2 types —
2. Evaluation of co-morbidities
a) Primary or Essential hypertension —- when a specific cause cannot be identified; common)
associated with obesity and positive family history. 3. Screening for extent of target-organ damage.
y
b) Secondary hypertension — when cause can be identified. Common causes in children are _ 1) identification of potential causes - [Common secondary causes include -—
renal parenchymal disease. renovascular disease and coarctation of aorta. A) Renal parenchymal disease.
- Causes of secondary hypertension - B) Renovascular disease-and
1. Renal- C) Coarctation of aorta.)
a) Acute Glomenrlonephritis (e.g.. Post-streptococcal GN) a) Routine evaluation (done in all cases of proven HTN) -
b) Chronic kidney disease i) History (including sleep history. family history. dietary history. H/O addiction etc.)
c) Pyelonephritis ii) Physical examination
d) Obstructive uropathy (9.9.. hydronephrosis) iii) Blood for CBC. Urea. Creatinine, Electrolytes (NaIK)
e) Hemolytic uremic syndrome iv) Urine for Fl/E. CIS.

0 SLE nephropathy v) Renal ultrasound — to look for congenital malformations of kidney (9. g., polycystic kidney.
ectopic kidney etc). renal scarring. hydronephrosis etc.
2. Vascular—
vi) Chest X-ray
a) Renovascular hypertension (9.9.. renal artery stenosis, renal artery/vein thrombosis)
vii) ECG
b) Coarctation of aorta
viii) Echocardiography
c) Takayasu arteritis - b 2nd line investigations (done in selective cases on the basis of findings in history and
'h—f
3. Endocrine-— examination) — For example. these extensive studies are not indicated in adolescents with
a) Cushing's syndrome mild hypertension and positive family history of essential hypertension.
b) Pheochromocytoma i) Excretory’ urogram — to exclude obstructive uropathy and vesiocu reteric reflux (VUFl)
ii) Plasma renin activity
c) Congenital adrenal hyperplasia (e.g.. 1113 hydroxylase deficiency. 17a hydroxylase
iii) Flenovascular imaging —- USG with colour doppler, angiography of canal vessels.
ll
deficiency)
radionucleotide scan. - ’
d) Hyperaldosteronism
iv) Aldosterone levels in serum and urine
Anhhhhl‘nfr
e) Hyperthyroidism v) 24 hours urine for catecholamines (adrenaline and noradrenaline) and their metabolites
f) Hyperparathyroidism (VMA).
4. Neurogenic— vi) Serum cortisol level
a) Raised ICT 2) Evaluation of co-morbidities -
b) GB syndrome i) Fasting blood glucose
5. Drugs— ii) Lipid profile
a) Sympathomimetic (9.9., cough remedies) iii) Polysomnography — for sleep disorders
b) Steroid 3) Screening for target-organ damage —
c) NSAID l) Heart L Echocardiogram

ii) Fletina - Fundal examination
d) OCP
e) Cocaine, Amphetamine a. 21 :Coerctation of sorts. [CNMC - 8th Sem]
runs - 20151 COARCTATION OF AOHTA
O. 20 :Dr‘egnostic workup for childhood hypertension Ans.
TENSION Coarctatlon of Aorta (CoA) is a congenital obstructive lesion of the aorta. where there is a shell-
DIAGNOSTIC WORKUP FOR CHILDHOOD HYPER
causes. Ilke proiection inside the lumen of the aorta producing obstruction to aortic flow.
or idiopathic) or secondary to other
Childhood hypertension can be primary (esse ntial
24
186 QUEST : PAEDIATRICS CARDIOVASCULAR SYSTEM El Chapter-3 187
- Epidemiology - 2. Definitive-
1. More common in males than in females (M : F = 2 : 1) a) Balloon angiOplasty
2. 00A is a common association in Turner’s Syndrome. b) Aortoplasty.
3. About 85% of patients with CoA also have Bicuspid Aortic Valve. itis [Maids — 2016]
a. 22 :Afodlfied Duke's criteria for the diagnosis of infective endocard
- Pathophysiology — Coarctation is almost always in a juxtraductal position (i.e.. at the site of
ductus arteriosus attachment). Ans. MODIFIED DUKE’S CRITERIA
_ ventricular
1. In fetal life . right blood passes through the ductus to su pply the lower part of the endocardium. particularly
.
. lnfective Endocarditis (IE) is characterised by acquired infection of the
body and maintains forward flow through descending aorta. at the diseased portion of the heart. The modified Duke's criteria help in the
diagnosis of IE.
2. After birth. when ductus starts to close. forward flow to the distal aorta is hampered producing 0 Major criteria -
symptoms.
1. Positive Blood Cultures -
3. severity of the cheeses and symptoms depends on -
a) 2 separate cultures for a usual pathogen
a) Severity of coarctation. and I
b) 2 or more cultures for less typical pathogens
b) Extent of collateral simulation development during the fetal life (which maintains blood 2. Evidence of Endocardr'tr‘s on Echocardiography
-
flow to the lower extremities). in the absence of an alternative
a) Oscillating intracardiac mass on a valve or other sites
- Clinical features — anatomic explanation.
A. Symptoms— b) Abscess
among patients with 00A
1. Age of presentations and clinical spectrum varies widely c) Partial dehiscence of prosthetic valve
.
and depends on severity of the disease.
d) New valve regurgitation
2. Most children are asymptomatic
of the lower limbs after exercise. e) Regurgitant flow near a prosthesis.
3. Older children may complain of pain or weakness
t with - - Minor criteria -
4. Symptomatic infants may presen
drug user
1. Predisposing heart condition or injection
a) Poor weight gain rature > 38°C)
2. Fever (Tempe
b) Dyspnoea
ities. oliguria. paleness. cyanosis etc) 3. Vascular phenomena -) like —-
0) Features of shock (cold. clammy extrem
a) Major arterial emboli
8. Signs— b) Mycotic aneurysm
lis pedis
of the lower limbs (9.9.. femoral. dorsa inatous or hemorrhagic legions on palms and
1. Absent or weak peripheral pulses c) Janeway's lesions (painless. small. erylhe
etc) soles)
2. Hypertension in the arm 4. immunological phenomena -) like -
al notch.
3. Systolic thrill in the suprastem a) Glome‘rulonephritis
in the left iriterscapular area in-the back. ermal nodules in the pads of fingers and toes)
4. Systolic murmur may be audible valve) b) Osler‘s nodes (Tender. pea-sized intrad
tion (associated bicuspid aortic
regurgita es with pale centres locatednear the optic disc)
5. Diastolic murmur of aortic c) Ftoth's Spots (oval retinal hemonhag
or infants with severe
e or heart failure in newborns
6. Features of circulatory failur d) Rheumatoid factor
disease.
5. Microbiological evidence —
Investigations - meet major criteria)”
- a) Positive blood culture (but doesn't
organ ism that is consistent with IE.
1. 0X3—
ly enlarged
. b) Serologic evidence of active infection with
a) Heart size normal or mild itis (IE) is likely in the presence of -
rib) in older children due to
dilated collaterals - Diagnosis - Definite endocard
b) Flib notching (4th to 8th 1. 2 major criteria. or
.
. .
_ 2. E06 — LVH 2. 1 major + 3 minor criteria. or
gm phy .- Dia gno stic I confirmatory
I ' ‘ 3. Edrocardio 3. 5 minor criteria
phagus —- “3 sign" there Is —
4. Barium study of eso . El lE is possibie (not excluded). if
.
or
- Treatment — tus arteriosus a) 1 major + 1 minor criteria.
ptomatic new borns to reopen the duc
1 PGE, infusion -— in sym - b.) 3 minor criteria.
‘-
188 QUEST : PAEDIATFIICS CARDIOVASCULAR SYSTEM U Chapter—8 189
0. 23 : Treatment of congestive cardiac failure in children [2011 - Supple} i) VSD

0. 24 :Management of CCF in children (KPC — 9th Sem] ii) MR WW
msm‘mwm
Ans : See 0. 5 - Q. 7 (Management) iii) TR
iv) FDA (in newborns)
0. 25 :Clinical features of GOP in to years old boy. [2016] c Early systolic -i St
‘-'
a. 26 :C/F of heart failure in infancy. [2017 — Supple] i) Small VSD.
'Ans : See 0.5 - 0.7 (Clinical Features)
ii) VSD with pulmonary hypertension
0. 27 :Differential diagnosis of a systolic murmur audible over the precordium [KPC - 2016] iii) TFl with normal FlV systolic pressure. 51 32
Ans. " DID 0F SYSTOLIC MURMUR OVER PRECORDIUM d Late systolic -+ =
U
i) MVP
Most heart murmurs are systolic in children and they occur between $1 and 82. Systolic murmurs
can be differentiated according to the following 4 characteristics — ii) Coarctation of Aorta (CoA) St
1. Location (of maximum intensity), (Interscapular area at the back; represents murmur of 00A itself and not due to collaterals)
2. Timing . Transmission : Includes conduction and radiation of murmur —

3. Transmission and a) Apical holosystolic murmur of MFI transmits well to the left axilla and back.
4. Quality b) AS murmur transmits to the neck.
1. Location : . Quality :
a)_ Apex of the heart —t (Mitre! area) 3) MR. VSD —} High-pitched, blowing
i) Mitral Regurgitation (MR) b) AS. PS —t Rough, grating.
it) Mitral Valve Prolapse (MVP) c) Innocent murmur —) Vibratory, low-pitched, humming
b) Lower left stemal border —) (Tricuspid area) El Further coniinnation is done by investigations, like —>
i) ventricular Septal Defect (VSD) 1. Chest X-ray,
ii) Tricuspid Regurgitation (TR) 2. ECG and finally
iii) Hypertrophic Obstructive Cardiomyopathy (HOCM) 3. Echocardiography (for confirmation)
-
iv) Still's murmur (Vibratory innocent murmur)
0.28: Hemodynamlcs of VSD.
c) Upper left stemal border —> (Pulmonary area) [BSMCf 8th Sem]
O. 29 : Hemodynamics of Large VSD. [lPGMEH 1 8th Sem]
i) Pulmonary Stenosis (PS) - valvular
Ans: See Question 1, Question 9.
ii) Pulmonary Artery Stenosis
iii) Patent Ductus Arteriosus (PDA) - more prominent at (L) intraclavicular area 0. 30 : Complications of VSD
{2008, Burdwan - 2016]
iv) Atrial Septal Defect (ASD) Ans : See Question 1. (Complications)
v) Pulmonary flow murmur in newborn (Innocent) 0. 31 : Hemodynamics of FDA.
[Kafyani - 9th Sent]
d) Upper right stemaf border-i (Aortic area)
Ans: HEMODYNAMICS OF PDA
i) Aortic Stenosis (AS) - valvular
ii) Supravalvular AS PDA or Patent Ductus Arteriosus is a communication between the pulmonary artery and the
aorta.
iii) Sub aortic stenosis. This communication (Ductus Arteriosus) is an integral part of fetal
circulation and it normally closes
after birth. Its persistence; in postnatal life is called as PDA.
2. Timing : -
Shunt : As pressure in the aorta is greater than pulmonary artery
a) Midsystolic (also known as election systolic murmur) - (PA) in both systole and diastole,
there is a left to right shunt through PDA from the aorta to the PA both during
i) Ps systole and diastole.
. ' So, shunt murmur is a continuous murmur. ‘
ii) AS Magnitude of the shunt : Determined by 2 factors ->
iii) Innocent murmurs. 1. Resistance offered by ductus (depends on the length,
31 ' S2 arteriosus), when it is small.
diameter and tortuosity ol ductus
b) Holosystolic (Pansystollc) -> .
- f CARDIOVASCULAR SYSTEM [J Chapter-8 191
190 QUEST : FAEDIATHICS
_ _ .5. -,
ductus is large. its PVR increases.
2. Level of PVR (Pulmonary Vascular Resistance). when the 2' Pulmonary stenosrs ('35); .. -" i
_ """
s due to decrease in the pressure gradient (Depende nt shunt).
shunt decrease
/ l ‘ ‘ I l
. Hemodynamlcs : -
systolic as well as diastolic led pulmonary bl°°d flow
1. Left to right shunt from aorta to pulmonary artery (PA) causes Ejection i W ”dun“? overioad
overloading of the PA. So. PA enlargement coaurs. Systolic . l
left atrium (LA), resulting in
2. Increased amount of blood after passing through the lungs, reaches
. . ' _ . Murmur (ESM) EWE: Fi —> L shunt through
LA enlargement. communication ‘
resulting in delayed diastolic murmur
3. This Increased blood passes through a normal mrtral valve, ‘
of MS at apex. degree of PS-
and delayed closure of 3- Cyanosis and severity 0' "19 disease ‘5 (“foo“)! Proportional lo the
4. Large volume of blood in the LV causes LVH and prolongation of systole 4. As FiV is readily decompressed by the communication, FIV volume
overload never produces
oi 52. if shunt is large
aortic valve. Thus, A2 is is delayed. which may cause a paradoxical split ' heart failure.
‘
enough.
5. As severity of PS increases. pulmonary blood flow declines and the intensity of the murmur also
! Whioh results in an ejection SYStOlio murmur 0' AS.
5. Increased blOOG flows through aortic valve, continu ' s.
decline
ous murmur of FDA.
but the murmur is clinically drowned by the . Examples:
dilatation of the ascending aorta, and an
6. Large LV volume is ejected into the aorta causing 1. TetraIOgy 0‘ Fallot (TOF)
before the start of the continuous murmur.
aortic ejection click. Ejection click is audible 2' d-TGA + VSD + PS
ous) starts after 81, reaches its peak at $2 and ends at or around
7. The shunt murmur (continu
mid-diastole.
in the shunt magnitude. :- Trio-:3; :31; :ih PS
: B. If left untreated. there is increase in the PVFl. which results in decrease
Decrease in the shunt magnitude 5. Double outlet av + vso + PS
- I; . 6. Single ventricle + PS .
3; . \
- . Common findings:
1. Main presentation is cyanosis with occasional cyanotic spells
Murmur becomes SYStOlio Vo'Umo overload 8‘ ‘9“ 2. Ejection systolic murmur at pulmonary area
I side of heart decreases
and gradually shortens
(LA‘ W Aorta) 3. No/minimel cardiomegaly (Boot-shaped heart in-CXFi)
i Wrth further 1 in law;
l 4. led pulmonary blood flow
5. Heart failure rare. ‘.
There is R -> L shunt and _ —
appearance of cyanosis Heart size decreases [BUG - 9!!! Sam]
' _ 0. 33 : DID a! Faffat's Tetrafogy
(Eisenmenger Syndrome)
(”"5 ‘ 9‘“ 59”] Ans : pro OF FALLOT’S TETRALOGY
0. 32 : Fallot’s physiology decreased pulmonary blood flow.
_ Fallot's tetralogy is a congenital cyanotic heart disease with
A” -' FALLOI’S PHYS'OLOGY characterised by 4 defeas _
pattern.
is a comm on physiological pattern or hemodynamlcal a) Large non-restrictive VSD
Fallot’s physiology or VSD-PS physiology nary blood flow.
tic heart diseases with decreased pulmo b) lnfuncfibular PS
that is present in multiple congenital cyano s physio logy are characterized by 2 _.
defects included in Fallot' I
.. Essential characteristics : All the c) Overriding 0' aorta
on hemod ynaml cs -
essential features. which dictates their comm icle) that is large enough to equalize
_ d) FNH
ventricular level (9.9., VSD. single ventr ology comes under the DD oi Fella-s “3
t-
1. A large communication at ' 's physi
cavity. ° [W : All theg'heart defects that follow Fallot
pressures ln LV and RV lnlundlbular or subvalvar investigations like CXFI and ECG. These
blood flow (9.9. , valv ar PS, as they are difficult to differentiate clinically and by routine
Vary ing degrees of obstnlction to pulmonary m _ .
2-
-
PS. supravelvar PS) t. d-TGA + VSD + PS
. Hemodynamlcs : - .
2. r -TGA + vso + PS
1, Free communication between 2 mm” 3. DORV + VSD + PS
’
- - ’n LV and RV 4. Tn'cuspid Atresia + PS
Equa'm'm °ipressures I 5 . Single ventricle + PS
No shunt murmur
‘x.
192 QUEST : PAEDIATFIICS 193
CARDIOVASCULAR SYSTEM E] Chapter-B
- Common hemodynamics : See 0. 32 (Hemodynamics) B) Signs —

- Common findings : 1. Progressive cyanosis
Main presentation is cyanosis with occasional cyanotic spells.
sew—- 2. Tachypnea
Ejection systolic murmur at pulmonary area 3. Temporary disappearance or decrease in intensity of the systolic murmur.
Nolminimal cardiomegaly (Boot-shaped heart at CXR) - investigations :
Decreased pulmonary blood flow . Treatment: } See Question No.4 (Management of cyanotic spell)
5. Heart failure is rare.
0. 35 : Management of Cyanotic Spell in TOF. [.2072]
- Differentiation : Differentiation between these defects need advanced investigations like
Echocardiography. cardiac catheterisation etc. Echocardiography remains the mainstay of diagnosis, 0. 36 : Management of Cyanotic Spell. [RGKMC — 8th Sem, MCK - 8th Sent, MMC — 8th Sam,
as it is non-invasive and can delineate each of the above defects in experienced hands. SSKM — 2016, MCK - 2016] ‘
Ans: See Question No. 4 (Management of Cyanotic Spell).
a. 34 : Cyanotlc Spell [2010 - Supple], Hypoxia ‘blue' spells. [2017 - Supple}
O. 37: Write briefly management of shock in children. [KPC -— 9th Sem]
Ans : CYANOTIC SPELL
Ans : MANAGEMENT OF SHOCK IN CHILDREN
Cyanotic spell, also known as hypercyanotic spell, hypoxic 'blue' spell and tet spell, is an important and
occassionally life-threatening complication of Tetralogy of Fallot or other TOF — like defects (that follow Shock is a clinical state of acute disruption of circulatory function, resulting in inadequate tissue perfusion.
Fallot's physiology). , Shock is classified into the following categories according to the etiology —+
— Commonly occurs in children < 2 years of age. 1. Hypovolemic shock
- Pathophysiology : Cardiogenic shock } These 3 types are common in children
were.»
Spells are typically initiated by the stress of feeding, crying, or aJtter awakening from a long sleep. Septic shock
l . Distributive shock
l l Systemic Vascular . Obstructive shock
[1THFt and TCardiac outputJ Resistance (SVR)
- Treatment consideration of individual types :
l
1. Hypovolemi'c shock —>-
a) Mainstay of treatment is replacement of lost intravascular volume by fluid bolus with NS/RL.
CYCLE b) Blood transfusion may be indicated in Case of hemorrhagic shock (whole Blood/EH30)
FtV volume overload
2. Cardiogenr'c shock —+
l
a) Smaller fluid bolus given (5-10mllkg) in suspected cases; there may be deterioration alter
[TR —+ L shunt from FlV to aorti‘ fluid resuscitation.
l b) inotropics (Dobutamine preferred over Dopamine) are started early after giving 1 or 2 fluid
ipoz. tpcog. tPH (Acidosis) —> Cyanosis bolus.
l 3. Septic shock -—) Early administration of broad spectmm antibiotics is considered, itseptio shock
Stimulation of respiratory centre is suspected, in addition to the routine therapy.
i - Management algorithm : Recognize in children as early as possible
TNegative inkathomw- Ting
pressure ' rala and de P th of re 30 iration l 1
Maintain airway, give 02, establish IV access.
- Clinical Features : l
3‘ NS bolus (es) of 20 mn upto 60 mllkg (maximum)
A) Symptoms—
" Begin antibiotics for septic shock
t. Hyperpnoea
Increasing cyanosis F'Uid shock
'93P°"3i"° { Fluid resistant shock]
9"???"
Can progress to limpness and sycope

i i
Rarely. seizures, hemiparesis and death
Older children may assume squatting position Observation
25
CARDIOVASCULAR SYSTEM D Chapter— 8 195
194 QUEST : PAEDIATFHCS
4. Signs of inflammation are present (9.9.. heat. swelling, redness, pain. tenderness
and limitation
Start Depamine O 10 pgfkglmin of movement) in the involved joints.
(Prater Dobutamine O 10 ugikglmin in cases 5. There is dramatic improvement at arthritis with salicylate therapy (Aspirin) at adequate dose.
of suspected cardiogemc ShOCk) 6. Hi0 sore throat (streptococcal pharyngitis) 1-5 weeks before the onset of symptoms is often
Dopamine l present.
responsive shock [33mins resistant shoci]
- Laboratory diagnosis : Investigations done are ~—
1 a7 \ 1. CBC
. or and Warm i Cold shock 2. CRP, ESR -§ Elevated (acute phase reactants)
finale dose l l 3. ECG —) T PR inlerval
SI ' Norepln” ephrine Start Epinephrine 4. Echocardiography —t to look for cardiac involvement (Rheumatic carditis)
l I 5. A80 titre -—> > 33 Todd unit is diagnostic
[ L 6. RA factor, ANA -+ to exclude other causes of arthritis.
W
- Final diagnosis : Diagnosis of Rheumatic arthritis or Acute Rheumatic Fever
. I l real i 'ne-resistant shock_] is confirmed by
Modified Jones Criteria (See Question No. 10)
i We Give iniedron Hydmnison
maid t e’ if LONG QUESTION?
_ . - d
adrenal "150mm '5 SUSpeCte .
0. 39 : A 6 year old grrl presented with fever. migrating joint pain for last 5 days. She had a past
1 H/O sore throat. What is your provisional diagnosis and how will you investigate
Shock persists and
manage this case ? (12) [BSMC - 8th Sent]
/ i \ _ Ans :
Warm I l with Gold sl :I with low Cold shock With normal - Provisional diagnosis is Rheumatic arthritis l Rheunatic fever-
low 8P 8P 3: ' - Investigation and Management — See Question No. 14 + Question No. 10 (for Jones Criteria)
l l,
. _ Add vasodilators or . . .
a. 40 : An 8 year old boypresented with migratory type olartilntism . .
Trtrate _ Trtrate epinephnne votvrng tug joints, palpitation
inodilstars and bipedal swelling. What is the most probable diagnosis ? Pathogen
naepmepl'lme esis? Hour will you
make a final diagnosis? Management ? (1+2+3+4) [RICK - 2016]
' Ans : ‘.'
. Canaan VW used ‘7 l . Diagnosis — RF, Pathogenesis - Question No. 8. Final dagnosis — Question No. 10.
a) Niroprusnde (Artery > 9‘"
. - Management — Question No. 14.
WW (Vein > Artery)
lator = Inotropic + Vasodrlator]
Carmen Minor: used -i [lnodi
3’ mm } Win inhibitor
{2012]
fltrflia.
to nosis olnheumaflck
0. 38: Diag
‘
DIAGNOSIS OF RHEUIIATIC ARTHRITIS
'
Ana :
t 70% of cases.
of Rheumatic Fever, occurring In abou
' the most common manifestation
Arthriti 5 is
wrists. elbows etc.) of the body.

. cum
1. Usua “1‘9
“ lly invol ves :large joints (9.9., knees, an.ides.
“0‘“
joint (Monoarthrttls)
(Polyarthrttrs). But, involvement at a single
2. Often more than 1 joint is involved
usly. Migratory
nt involv19t can oowreithe rin succession' (Migratory) or simultaneo
can ‘8’30' m"
of rheumatic arthritis.
3' mmgis is the classical teature
r— 9 197
GASTFlO-lNTESTINAL SYSTEM Cl Chapte
(b) Viral serology to detect etiology —- igM HAV Antibody.

CHAPTER — 9 HBsAg, HBeAg, Anti HBC antibody AntiHCV
El Treatment :
GASTRO-INTESTINAL SYSTEM (a) Adequate rest and avoid undue physical activities.
(b) Nutn'ous diet to provide adequate calories.
(c) Avoidance of Hepatotoxic drugs - lNH. Valproate.
fiche ouesnoiisj (d) Fever - if present should be managed by Tepid Sponging and paracetamol half of the recom-
of Acute Viral Hepatitis in children complication of Acute mended dose (if necessary).
0. 1 : Mention the causative organisms [BMC, 9th Sent}
Viral Hepatitis and its management. (a) Constipation ~ Oral Lactulose — 0.5-2 ml/kg/dose. 6 hourly to ensure bowel clearance.
of liver that lasts for less than 6 months. (f) Water soluable vitamin preparation.
Ans : Acute hepatitis refers to any inflammatory process
Viral Hepati tis : (9) Cholestasis - if present (specially in older children and adolescents) should be treated with oral
El Causative Organisms of Acute Ursodeoxycholic acid.
Common Hepatotropic Viruses : (h) Nausea and vomiting — treated by antiemetic
(i) Hepatitis A (Most common) (i) Ascites -— if present, to be treated with short course of spironolactone.
(ii) Hepatitis B (j) Hospitalization - not required for all cases
(iii) Hepatitis C
indications -
(iv) Hepatitis D
— Persistent vomiting
(v) Hepatitis E & G
— Fluid retension
Less common : - Altered sensorium
(i) Epstein-Barr virus -— Bleeding manifestation
(ii) Herpes simplex virus
0. 2: An 8 month old baby has presented with Acute watery diarrhea. He has been diagnosed to
(iii) Coxsasckie B virus
have severe dehydration. Write the clinical features that suggested dehydration. Given an
(iv) Cytomegalo virus A outline of rehydration therapy for this child.
. . (R. G. Kar, 9th Sam]
Cl ComplicationofAcuteViralHepatitis: ns :
complication may
Majority of Acute \firal Hepatitis in children are self limiting illness. But in few cases Cl Clinical Features of Diarrhea with Severe Dehydration
occur. These are— 1. General condition -— Lethargicldrowsy/unconsciousness
(a) Hepatic Complication — 2. Eyes - Shrunken
— Acute liver failure 3. Tears — Absent
- Chronic hepatitis (hepatitis B. C and D) 4. Tongue - Very dry
- Sub-acute hepatic failure
5. Thirst — Not able to drink
Prolonged cholestasis
6. Skin Pinch — Goes back very slowly on palpation.
— Prolonged hyperbilirubinemia
0 Rehydration Therapy for severe dehydration :
(b) Extra Hepatic Complication -
The primary objective is to quickly rehydrate the child in a hospital with
— Glomerulonephritis facilities for I .V fluid therapy.
- Guillain-Barre syndrome Preferred Fluid :Hinger's Lactate
- Myocarditis Alternative : Normal saline
— Pericarditis L Total Volume: 100 kg
. Duration: Over 6 hour in infant < 1 year
— Polyarthritis
- Aplastic anaemia Over 3 hour in older children
D Management of Acute Viral Hepatitis :
Infant (< 1 yr) cider children (>1 yr)
As other viral illness majority of. Acute Viral Hepatitis are self limiting illness. There are no specific
therapy targeting the causative organisms. Hence management is supportive. .
Volume of Ringer’s Lactate 30 ml/kg Of body weight T” hour 30 "‘n 0' body M- -> 3‘2 hour
Management includes -
70mllkgofbodyvreight—> next5hour 70 ml/kg
Cl Investigation of body wt. —) next 2% hr.
(a) Complete liver function test including Prothrombin Time and NH Monitoring
- Todelect degree of liver dysfunction - Assessment for improvement every 1-2 hour
- Not improving. give l.V. fluid more rapidl
y.
196
n“ .
GASTHO-INTESTINAL SYSTEM C] Chapler— 9 199
" — Eye examination —.Kayser — Fleischer ring in Wilson's disease.- cataract in Galactosemia.
status and choose appro.
- After 6 hours (infants) and 3 hours (older children) assess hydration - Thyroid. Joint exam nation -) To rule out thyroiditis or arthritis that-may coexist with auto-
priate plan for hydration (A, B or C). immune hepatitis.
0. 3: A 7 year old boy having jaundice for 6 months with hepatornegaly admitted for massive Relevant Investigation :
such a
haematemesis. Mention the diagnostic possibilities. Write how will you evaluate Investigations of a child with CLD include determination of etiology and evaluation of liver function.
case to confirm the diagnosis. [IPGHEE 8th Sam]
(a) Complete blood count -—> Anaemia in Wilson's disease. auto-immune hepatitis or related to
Ans : Jaundice for 6 months + Hepatomegaly + Massive haemalemesis. blood loss.
Together point towards the diagnosis of chronic liver disease. Possibilities are -— (b) Liver function test including prothrombin time 8. NH — To assess degree of liver function
(a) Infection —> impairment
Chronic Hepatitis 8 (c) Ultrasonography of abdomen —- For echotexlure of liver, ascites, collaterals in portal hypertension.
Chronic Hepatitis C (d) Upper G.l. endoscopy —+ For esOphageal varices in portal hypertension.
(b) Metabolic -+ (9) Specific investigations —
Wilson disease — Viral markers : HBsAg. HBeAg, HBV DNA Anti-HOV
Galactosemia ~ Auto-immune markers : SMA, ANA, SLA
Fructosemia — Serum ceruloplasmin and 24 hour urinary copper to diagnose Wilson's disease.
Gaucher disease - GALT for Galactosemia or Fructose intolerance test for fructosemia.
(c) Drug induced —> (i) Liver biopsy - For etiological confirmation and presence of active inflammation/fibrosis.
INH, Methotraxate. Valproate o. 4 : Name the common causes orgeneralised oedema in children. Describe the paths-physiology
(d) Auto-immune -—) oi oedema in children. (MB, 2015}
Auto-immune Hepatitis
Ans: El Name the common causes of generalised oedema -
Primary Billiary Cirrhosis
0/0 or causes of AnasarcaiGeneralised swelling :
(e) Hepatic venous outflow tract obstmction
Budd chiari syndrome a) Chronic Cardiac Failure
Venn-occlusive disease b) Renal cause —
, — Nephrotic syndrome
(f) Cryptogenic - No‘ cause found
d chronic liver disease for diagnosti c confirmation _ - Renal failure
El Evaluation of a patient of suspecte
— Acute glomerulonephritis (AGN) - less common
History :
c) Chronic liver disease
CLD
(a)Jaundice 9 Duration —-) 2 6 months arise the possibility of d) Protein-energy malnutrition
g or static or decreasing
Progression ~+ Whether jaundice is progressively increasin e) Allergic or angioneurotic edema
with Hepatropic virus
Past history —> Previous history of jaundice may indicate infection D Pattie-physiology of oedema in children.
persistent liver dysfunction due to any
in) Hi0 fever 4 Mostly point towards infections cause but There are different patho-physiological mechanism for development of oedema in children depending
prone to repeated infection.
etiology may cause depression of immunity and make the child upon the underlying cause — '
ascites.
to) Pain abdomen and swelling -> Due to liver enlargement and (a) Diminished plasma oncotic pressure —
chronic Hepatitis BIC infection. .
(d) Past history of blood transfusion -> More possibilities of Normally fluid is retained in intravascutar compartments due to interaction between oncotic
raise the possiailrty of
(e) Family history —> History of affection of sibling or death from jaundice pressure (indrawing force) and hydrostatic pressure (out driving force) in plasma.
metabolic liver disease or auto-immune cause. Oncotic pressure in plasma is maintained by adequate amount of protein (albumin) in plasma.
cular, anticonvulsants.
(0 Drug history -—> Prolonged intake of hepatotoxic drugs — antituber Any factor causing decreased plasma protein leads to less oncotic pressure hence fluid cannot
tion.
(g) Immunization history —> Status of Hepatitis B Vaccina be retained In intravascular compartment and develonment of oedema. Now less plasma pro-
tein concentration may be due to : '
Clinical Examination :
i) Decreased protein production (Albumin) -
- Degree of jaundice
with enlarged left lobe -) Progression e.g. in chronic Liver disease. PEM.
Uver -—> Enlarged —> in chronic liver disease. Shrunken . ii) Increased excretion of protein e.g. In Nephrotic syndrome.
to chirrhosis.
-
(b) increased sodium and water retenslon by kidney -
— Ascites
_ . Hypertension. around the unbilicus.
in portal
- Caput Medusae - Cutan eous portosystemic shunts In some pathological condition there is increased sodium and water retension by kidney. Sec~
mune Hepatit is (Auto- immune haemolytlc anemia) ondary to dininished renal perfusion. This excess sodium and water retension lead to develop-
Anaemia —- May significantly present Auto-im
ia). ment of oedema by activation of Ftenln Angiotensin system.
or Wilson cfisease (Coomb's negative anaem
ctasla, palmer erythema.
Other manifestation of CLD — Muscle wasting. facial telangle
200 QUEST : F'AEDllltTFiIGS1
GASTRO-lNTESTlNAL SYSTEM U Chapter-9 201
(innnnnnnn----
9.9. — Cardiac failure Source : Heme containing protein
Acute Glomerulonephritis
(a) Haemoglobin 80%
to) increased venous & capillary hydrostactic pressure —
(b) Other compounds 20% — Myoglobin. cytochromes, catalase. peroxidase.
Increased hydrostatic pressure in venous and capillary system lead to outward movement of
D Acute ler Failure :
flurd from intravascular compartment to interstitium .
e.g. — Cardiac failure. A multisystem disorder in which severe impairment of liver function (INFi > 1.5 with encephalopathy or
NH > 2 with or without encephalopathy) occurs in association with hepato-cellular necrosis with no
(d) Increased vascular permeability —
recognized underlying chronic liver disease, within 8 weeks of the initial symptoms.
increased vascular permeability due to chemical medicator like histamin and bradykin is culprit '
for developing oedema in few Specific condition. E] Clinical Features of Acute Hepatic Encephalopathy :
9.9. — Angioneurotic oedema. Most important presentation of Acute Liver Failure. Clinical apperance and severity depend on extent
and-rapidity of hepatic damage. degree of pone-systemic shunting and precipitating factors.
a. 5 : Outline Billirubr'n Metabolism. Define acute liver failure. Write briefly the clinical features of Depending upon the severity of clinical features, Acute Hepatic Encephalopathy are divided into four
Acute Hepatic Encephalopathy. _ (SSKM) stages-
Ans : - Billirubin Metabolism— Earliest marker — (i) Behavioral alteration
(ii) Changes in sleep pattern
F Haemoglobin Other heme containing (iii) Motor in coordination
l compounds
Stage Clinical manifestation
Reticulo- Heme
endothelial CO Stage I (i) Slowness in mentation
cells I ‘ Heme Oxygenase (ii) Dieturbed sleep wake cycle
ron (iii) Motor incoordination
(iv) No asterixis
Biliverdin
Stage it (i) Drowsiness, confusion
Biliverdin Heductase
(ii) Disorientation
i l
(iii) Inappmpriate behavior

Bilirubin (iv) Easily elicited asterixis (+)
+
Stage Ill (i) Very sleepy but arousable
Albumin (ii) Unresponsive to verbal command
(iii) Markedly confused
i (iv) Delirium H
Unconiugated (v) T Reflex. Jerks
Bilirubin (UCB) (vi) Babinski sign ++
—
-nnnnnrnn
(vii) Asterixis ++
' t
Stage lV (i) Unconcicus _
U08 4- Ligandin (7 protein) (ii) Deoorticaleldecerebrale posture i No response to pain
i (iii) Asterixis usually — ve
Transport
c
.
. a. 6: Write briefly the physiological basis of ORT in acute diarrhea in children.
What are the
advantages ol' hypo-osmolar OHS over standard WHO ORS. Mention the indications of
UCB + Glucoronic acid parenteral fluid therapy in children.
2-0
3! J, UDP Glucoronyl transferase' n in childhood
a Ans: OHS is the worldwide accepted oral solution to prevent and treat dehydratio
é’
O
Conjugated Bilirubin (c e) diarrhea.
0 Physiological basis of ORT In Acute Diarrhea
.9. in stool to
‘56a. B Glucorortidase Intestinal Bacteria Objective ol OHT in acute diarrhea is to replace the water and electrolyte that are lost
Small
o Intestine prevent dehydration and electrolyte disturbance.
I mucosa by
Urobillnogen a Sterclobllin In diarrhea there is active secretion of water. sodium and chloride in stool from intestinal
9o \ —— ucd effect of toxin produced by causative vims or bacteria. But at the same time some
nutrients such as
‘6 glucose, amino acids are absorbed continuously without difficulty.
Stool
“3
26
.l
202 QUEST: PAEDIATHICS GASTRO-INTESTINAL SYSTEM El Chatter—9 203
"it": ‘~-" * '~«

Glucose absorption in the intestinal cells is an enzyme-mediated active process which remains active 50% —+ Isomatremic dehydration , ECF sodium content remain normal (about_140 mqL)
despite of loss of water and electrolyte through gut mucosa. Glucose reabsorption mechanism is also 5% —-) Hypernatremic dehydration - ECF (serum) sodium become eleVated (> 150' mEq/L) specially
linked with reabsorption of sodium despite of its active loss and sodium absorption is associated with if the child has given fluid with more salt.
absorption of water. Thus despite active loss from gut mucosa. sodium and water they can be replaced - Diarrheal stool contain large amount of potassium. Therefore hypokalemia eventually develops if
in adequate amount through oral rehydration therapy.
diarrhea continue for prolonged period and more severe if the child has malnutrition. Hypokalemia
El Advantages of Hypo-Osmolar 085 over Standard ORS - WHO Eatpert Group (2004) that hypo- leads to abdominal distension, paralytic ileus and muscle hypotonia.
osmolar ORS should be the universal solution for all causes of diarrhoea and at all ages. 0 Since there is loss of Bicarbonate. in diarrhea stool acidemia usually appear in moderate to severe
The major difference in composition between hypo-csmclar OHS and standard OFtS is concentration cases leading to deep and rapid breathing (Kussmaul breathing).
of sodium and glucose which two are the major determinant of osmclarity of a solution.
El Skin turgor:
Standard OHS Normal skin turgor or elasticity is maintained by presence of water and fat in tissue. As sodium is major
Hypo-Osmolar OFlS
determinant of ECF osmolarity in lSO and hyponatremic dehydration. due to less osmolarity of ECF
Sodium (rnmol/L] 75 90 water comes to intra cellular compartment (ICF) from ECF causing shrinkage of ECF volume. Thus
111 causing loss of skin elasticity and skin after pinch goes back slowly to original position.
Glucose 75
In hypematremic dehydration water comes from lCF to ECF and partially masks the loss of skin turgor.
245 311
Osmolarity El Pulse, 8P. Urine output :
As ECF volume is depleted blood volume is reduced leading to weak. thready pulse and fall in BP.
or stool output. Be-
Standard OHS due to its high osmolarity cannot decrease diarrheal duration Because of less renal blood flow urine output is reduced. in severe cases renal failure may occur.
and causes undue
cause of its high osmolarity it itself draw water from gut mucosa to lumen Urine output is a good indicator of severity of diarrhea.
n of thanheal duration. Hypo-osmo lar OFlS does not cause prolongatio n of diarrhea.
prolongatio D Assessment of Severe Dehydration :
OHS is due to high concentrat ion of
- Another advantage of hyp o-osmolar ORS over standard See question 2.
non cholera type of diarrhea if
sodium. There is risk of developing hypema tremia in patient with
treated by standard OFlS. ln OFiT with hypo-osmolar OFt 8 there is minimum
risk of hyponatremia in u Outline the Treatment of Severe Dehydration in a 4 year Old Boy of Body Weight 16 kg.
therapy to be given properly. See question 2.
reduction in stool output. lower
Trial with low osmolarity OFlS revealed reduced needs for W. fluid. Amount of FiL to be transfused —> 100 nil/kg = 100 ml x 16 = 1600 ml Total
vomiting and no significant hyponatremia. let ‘5 hour = 30 ml/kg = 480 ml
safe and efficaecous i n treating children
For these above reasons hypo-osmolar OHS is found to be 2nd 2% hour = 70 mllkg = 1120 ml.
with diarrhea.
— 0. a : Discuss briefly the clinical features'and prevention of Hepatitis B infection in a 4 yearold child.
Cl Indications of parenteral fluid therapy in children [Haida]
sion or shock. when immediate volume replacement is life saving.
i) Severe dehydration. hypoten Ans:
to oral feeds.
it) Persistent vomiting. with poor tolerance I] Clinical Features of Hepatitis B infection
ss. status epilepticus. severe respiratory
iii) Critical medical / surgical illness e.g.. unconsciousne d due to risk of aspiration. .
not possibl e or contrai ndicate ' Incubation period - 60 - 180 days
distress etc when oral feeding
that require fine tuning of fluid intake. - Spectmm of clinical features of Hepatitis B infection is wide starting from Asymptomatic infection
iv) Systemic disorders 9.9:. renal failure or CCF
to development of chirrhosis and I or Hepatocellular carcinoma.
0.7' Discuss the physiologica f Disturb
ances caused by Acute diarrhea. How will you assess 0 Asymptomatic Infection — In many cases. without evidence of jaundice or other features of liver
year old boy of ‘
the treatment at severe dehydration in a 4
severe dehydration? Outline dysfunction diagnosed only by viral markers in serum as carrier stage.
[Marshldabad]
Body weight 16 kg. 0 Acute hepatitis -— Occurs in 10 — 15% cases
Ans : - frodromal phase—marked by anorexia. fatigue. weakness. nausea. vomiting. with or without
ever. -
Cl Physiological Disturbances In Diarrhea: ' I 0 ed in M
) content In body. This fluid is dtstnbut ‘

u I
u
n -
— lctetic phase - jaundice. hepatosplenomegaly and intense fatigue.
of a child's body weight is due to fturd (water
o
About s
cornpa m'nent (ECF) and intra cellular compartment (ICF). ECF include — Extrahepatic manifestation — in some cases of acute Hepatitis B infection there are some extra
compamnt ' The extracellular lyte conten t of the extra cellular compart-
s regula te the electro hepatic manifestation like urticarial rash. arthritis, glomerulonephritis, aplastic anaemia.
blood intestinal fluid and secretion. Kidney .
ment. El Choronlc hepatitis or chronic liver disease -
Fluld and Electrolyte Loss : water soluble Some cases of Hepatitis B infection turn into chronic hepatitis or chronic liver disease with clinical
losses contain large amount of water and features of liver dysfunction. Such as - persistent or recurrent jaundice. ascites, bleeding manifes-
- Diarrheal losses come from ECF. This olyte there is a huge loss of Sodium.
s. Amon g the electr tation. growth failure. hepato—splenomegaly. muscle wasting. palrner-erythema.
electrolytes and metabolite mic dehydration.
to excessive sodium loss —> Hyponatre
40 — 45% —-> Hyponatremia occurs due
GASTRO—INTESTINAL SYSTEM CI Chapter~9 205
204 QUEST : PAEDlATFilCS
CI Cirrhosls andior hepatocellular carcinoma — - Pale stool

-— Tender hepatomegaly
A few cases of Hepatitis B infection may tum into development of cirrhosis or Hepatocellular carcinama
Convalescance phase —-
in adult life. with feature of liver dysfunction. shrunken liver and portal hypertension in cirrhosis and
Hard nodular liver in hepatocellular carcinoma. - Duration 12 months after acute infection
-
— Jaundice decreases
Ct Prevention of Hepatitis B Infection in 4 year Old Child
— Appetite returns
General Measures :
- Size of liver decreases
. Avoid unnecessary needle pricks the causes of extra
O. 10 :Whatare the features of extra hepatic portal hypertension? Write do wn
0 Use of disposable needle if parental injection is needed at all out of extra hepatic
hepatic portal hypertension. How will you manage upper GI bleeding
- lf blood transfusion is needed then-transluse propedy screened blood WCK}
portal hypertension.
Immunization:
Aug:
- Active — Since the child's age is 4 year and it is expected that primary immunization has been
completed then no more active immunization needed. D Features of Extra Hepatic poI'ial Hypertension -
the liver.
Primary immunization —) i.m. 3 doses sub unit HBV vaccine Extra hepatic Portal Hypertension (EHPVO) indicates obstruction in the portal vein outside
Features are -
— 0, 1 and 6 months
or — Gastro-intestinal bleeding in form of haematemesis or malena. usually not severe.
- Birth, 6 and 14 weeks - Splenomegally, size varies with the duration of obstruction.
or ‘ Splenomegaly is the universal feature of EHPVO
— 6.10 and 14 weeks . - Jaundice
Catch up - Complete 3 doses. second dose is given a 4 weeks and 3rd dose 2 8 week after — Ascites
Absent
1st dose. - Abdominal veins (caput medusae)
0 Passive - If the child has exposed accidentally to HBV infected material then passive, — Liver is not palpable
immunization with Hepatitis B immunoglobulin. D Causes of Extra Hepatic Portal Hypertension —-
Dose — 0.06 ml/kgldose as soon as after exposure. (p referably within 24 hours, not late than (a) Congenital — Cavernous malformation of portal vein.
7 days)
(b) Acquired - Thrombosis of portal or splenic vein due to
0. 9 : Briefly discuss on liver function test. Write etiology, clinical features and management of (i) Infection — Omphalitis in neonatal period
Acute Viral Hepatitis. [CNMCI — Infection at the associated drainage are intra-abdonmal‘ Iy like appendicitis, peritonitis.
Ans : Cl Liver function test —+ Question 22. (ii) Trauma Io abdomen
Etiology and Management — Question No. 1 (iii) Hyper coagulable state — Nephrotic syndrome, polycythernia
CI Clinical Features of Acute Viral Hepatitis : (iv) Neoplasia — Neoplastic lymph node obstructing the portal vein
Acute Viral Hepatitis has three classical stages. (v) Other causes
-
- Prodromal phase — Intervention at portal vein — e.g. umbilical vein catheterisation during neonatal period (Exchange
- Icteric phase transfusion)
- Convalescence phase - Sepsis
Prodromal phase - — Dehydration
- Duration 2-7 days D Management of Upper G.I. Bleeding from Extra Hepatic Portal Hypertension — .
- Nausea. vomiting Causes of bleeding — .
- Abdominal pain specially at right hypochondrium (i) Ruptured esophageal varices at the lower end of esophagus (Esophageal varices) and proximal
- Passage of high coloured urine stomach (Gastric varices) '
— Fever (it) Congestive gastropathy
- Profound anorexia
(iii) Gastric erosion
Icteric Phase -
Duration 7-14 days usually Bleeding from EHPVO is usually less severe than. intra hepatic portal venous hypertension due to
of icterus absence of associated coagulation abnormality from liver dysfunction.
- Prodromal symptoms usually decrease and disappear with onset
Management includes —
— Jaundice
O
— Deep mustard coloured urine
206 QUEST : PAEDIATRICS GASTFiO-INTESTINAL SYSTEM Cl Chaim—9 207
_ Gastric verifies can be managed with endoscopic injection of tissye adhesive glue.
(a) Immediate haemodynamic resuscitation
(b) Cessation of variceal bleeding and relieve the portal hypertens
ion IV. Surgical Methods - ' " '
- When all the above measures fail
(c) Prophylaxis
~ Transjugular intra hepatic pone-systemic shunt (TIPS) Temporary shunt is created be-
(a) Immediate Resuscitation
-
tween branches of hepatic and portal veins to decompress portal pressure
- Assessment of vital signs (pulse. BP, respiration)
- Devascularization or transection of esophagus which blocks blood flows to varies
— Vital signs usually change with minimum 20% of blood volume loss (c) Prophylaxis
normal saline) till blood is available.
— Volume replacement with crytalloid fluid (like ringer lactate.
Administration of B blocker (Prepranolol 1-2 mg/kg/day) reduces risk of recurrent bleeding.
— Blood transfusion as per requirement.
— Monitoring of pulse, blood pressure, urine output, 02 saturation
(SPOZ) 0. 11 :A seven year old child with history of exchange transfusion in neonatal period, presents
with haematemesis. Physical examination is unremarkable except for splenornegaly (6 '
— Oxygen administration if SPO2 falls
‘1 cm). What is your differential diagnosis ? Describe steps of management in this child [10]
— FFP, platelet transfusion if required
— Adminis tration of H2 blocker/p roton pump inhibitor — Ranitidin e / Pantoprazole W. Arts: Seven year old child with history of exchange transfusion in neonatal period, presents with -
Hyperte nsion haematemesis and splenomegaly (6 cm) - suggests diagnosis of Extrahepatic portal hyperten-
(b) Cessation of Variceal Bleeding and Fiellve from Portal sion. (Due to portal venous obstruction as a result of exchange transfusion during neonatal period).
I. Pharmacological Therapy —
splanchnic vasoconstriction. 0 Management — See Question No. 21.
Vasoconstrictive drugs decrease portal venous flow by c ausing
These are — [ snonr oussnonfl
— Vasooression
o. 12 : Use of zinc in Diarrhoea. [Supple, 2016]
- Vasopression analogues like — Terlipression
— Somatostatin Ans : Zinc plays a critical role in metal coenzymes. polyribosomes cell membrane and cellular function.
— Octreotide > Zlnc deficiency is common in developing countries due to —
Side effects — Due to concomitant arterial vasoconstriction - Intake of predominant vegetarian diet.
- Peripheral vascular ischemia s High content of dietary phytale (in cereals, nuts. legumes) which reduce absorption of zinc
-— Myocardial ischemia from gut.
Flenal tubular damage
-— 0 Increased fecal losses of zinc during diarrhoea which aggravates preexisting zinc defi-
ues ciency.
More with vasopression and their analog
> Effect of zinc deficiency - ~_j_
Prevention -
- Affect immune mechanisms and host resistance-to several pathogen by
Concomitant administration of arteriolar
‘ Lymphoid atrophy
Vasodialatcr - Nitroglycerine
" Decreased cutaneous delayed hypersensitivity response
ll. MechanlcalTherapy-
ns for direct compression of varies ' Lower thymic activity
— Mechanical modes include inflatable balloo ' Decreased number of antibody producing cells
— Songstaken-Blakemore tube 3» Zinc supplement in diarrhoea -
— Complication - 0 Improve absorption of water and electrolytes by helping early regeneration of intestinal
- Aspiration mucosa.
- Esophageal perforation ' Restoration of enteric enzymes
- lschemic necrosis of mucosa Clinical benefits —
h diagnostic (detect location and extent) and thera-
u Endoscopic Therapy — Endoscopy has bot ' Faster recovery
peutic role. ' Fleduced stool output
apy and ligation.
Include endoscopic variceal sclerother . WHO and IAP — Recommendation : zinc supplementation during dian’neal episodes
starting as
cal meth od — succ ess 80 - 95% .
Most effective non-surgi absol ute alcohol early as possible after onset.
' of highly irritant solution. Such as ethan olaml ne.
-— Sclerotherapy — lnj action bosis/fibros is of vertx Dose : 10 mg/day for < 6 month old infant
lea ding to throm
into and around the vanx and followed by 20 mglday for > 6 month child
of varix with rubber band occlude the varix
- Ugationibanding — Banding Duration: 10-14days
_ .
fibrosis.
g08 QUEST : PAEDIATFNCS
GASTRO—INTESTINAL SYSTEM U Chapler~9 209
o . ~__
Formulation — 3 different zinc salts are equally effective —-

Treatment :
- Zinc Sulfate
Mild Form — low milk formula feed
- Zinc Acetate
Moderate Form - cereal based feeds
- Zinc Gluconate. Severe Form: - Resuscitation
0. 13 : Low Osmoiar OHS - Partial parenteral nutrition, parenteral anti-microbials
[2017, Supple 2011}
- Nutritional rehabilitation from 5 days onwards
Ans :
indications of Antimicrobials —
Low osmolar ORS has been adopted as single - universal OFIS to b e used for ll
- - - Presence of gross of blood in stool or pus cells > tOIHPF
diarrhea. Since 2004. based on WHO/UNICEF and lAP recommendation. a ages and types 0f
- Resistant shigella/salmonelta in stool culture
Composition of Low Osmotarty ORS - Associated systemic infection
- Severe malnutrition-
Low _ Low Indication of protozoa] — it Giardia or Entamoeba histolytica trophozoites in stool.
Osmolar GramlLrtre Osmolar mmollL Vitamins and minerals — About twice recommended daily allowance. zinc supplementati
on.
CBS 085
O. 15 : Oral Rehydration Therapy (Kalyani) {8th sent], (KPC) [9"? Sem}
Sodium chloride 2-5 Sodium 75 1
Ans:
Glucose, anhydrous 13.5 Chloride 65 with the
Concept of Oral Rehydration Therapy (ORT) has revolutionized the management of diarrhea
Potassium chloride 15 Glucose. anhydrous 75 discovery of coupled active transport of glucose and sodium in the small bowel, with passive
absorp-
tion of water and other electrolyte and nutrients even continuing loss in cepious diarrhea.
Trisodium citrate 2-9 Potassium 20 in
Citrate 10 CRT is the mainstay of management of acute diarrhea in diarrhea of all type and all ages specially
children, as dehydration and electrolyte imbalance is the most important cause of mortality from
Total Osmolarity 245
diarrhea.
OFtT includes :
Advantages of low osmolarity OFtS over standard ORS
(a) OFIS solution of recommended composition.
See Question No. 6
(b) Solution made from sugar and salt, if prepared correctly (Sugar 40 gram, salt 4 g)
0. 14 : Persistent Diarrhea in children. (2011, Supple) to) Food based solutions with appropriate concentration of salt like lentil soup. rice. kanji. butter
milk.
Ans : Prolongation of acute diarrhea and dysentry for more than 14 days with associated weight loss is
termed as persistent diarrhea. - ‘ ((1) Plain water along with continued feeding-
Causes : - Persistent infection with one or more enteric pathogens. Oral Rehydration Salt (OHS) Solution :
This is the standard recommended preparation to prevent or correct dehydration and electrolyte
0 Secondary malabsorption of carbohydrate and fat. used over
imbalance caused by diarrhea. Previously available preparation was WHO standard OHS,
0 intestinal parasitosis. three decades has saved millions of lives. From 2004 onwards. based on WHOIUNICEF recommen-
v infrequently allergy to dietary protein. dation low osmolar OFiS is universally accepted for OFtT.
Pathology: Composition of low osmolarity OHS — See question 9.
Prolonged cell mediated immune damage to small intestinal mucosa by variety of noxious stimuli ORT In Dlarrheal dehydration management —
Loss of
such res-nutritional. infective. allergic causes malabsorption of carbohydrate. protein and fat. Plan A -— To prevent dehydration.
in food intoler-
brush border enzymes and direct absorption of macromolecules foreign proteins result
ance and allergy. Age Amount of ORS (after each stool punge)
Clinical Presentation : . < 6 months Quarter glass or cup (50 ml)
loss and dehydration.
(a) Mid Form : Characterised by several motions/day without significant weight 7 months -— 2 year Quarter to halt glass or cup (50 - 100 ml)
weight loss but without
(b) Moderate Form : Characterised by several motions/day with marginal Hall to one glass or cup (100 ~ 200 ml)
2 —- 5 year
dehydration.
ance to milk and cereals. As much as the child can take
(0) Severe iomi : Characterised by dehydration. weightless and non-toler Older children
Diagnosis:
infection should be assessed. Plan B -— To correct dehydration
— Emergency risk factors arising out of dehydration. malnutrition and 4 hours.
and pH examination. 50 — 100 mtlkg body weight (average 75 milky). over a period at
— Stool for culture. reducing sugar
27
QUEST: PAEDIATRICS GASTRO—TNTESTINAL SYSTEM U Chapter—9 211
210
O. 16 : Differential diagnosis of Ascites in chifdren. [CNMQ 9th Sam] Tests are as follows -
(l) Complete blood count - Detects/suggests infections
Ans :
T TO WBC, T PMN — Bacterial infection.
Ascites isdefined as pathological accumulation of fluid in peritoneal cavity.
T Lymphocyte. T ESR —) Tubercular infection.
Differential diagnosis of Ascites can be broadly devlded into two groups -
(ii) Liver function test —-including plasma protein, alternation suggest hepatic etiology
(a) Associated with portal hypertension
(iii) Complete urine examination Proteinuria (grade 3+, 4+) suggests nephrotic syndrome as‘etiology.
-
(b) Other causes
(iv)Serum Amylase and Lipase — Elevated in pancreatitis
(a) Associated with Portal Hypertension :
(v) Chest and abdomen plain X-ray —
(i) Extra hepatic disorder:
- More than > 500 ml of fluid is required to diagnose ascites from plain X—ray
— Splenic vein thrombosis
- Detects pleural effusion if associated with ascites
— Pertal venous thrombosislcavemous malformation
c The lateral liver edge is medially displaced from the thereon-abdominal wall — Most-specific
— Bidd-chiari syndrome sign. (Hellmer’s sign), Mickey Mouse Sign — Symmetric densities on both sides of bladder.
- Inferior vena cava obstruction (vl)Ultrasound abdomen '
-
(ii) lntra hepatic disorder: a Can detect fluid as little as 100 ml.
— Biliary tract disease like - Also visualises liver. billiary tract, portal vein, spleen, pancreas and detect abnormality as
' Extra hepatic biliary alresia . cause of ascites.
- Choledochal cyst - Lollipop I Arcuate appearance of small bowel loops, Septal Fine or coarse internal, eches.
' Sclerosing cholongitis (vlf) CT and M RI abdomen -
- Hepatocellular disease like - Ascites can be well-demonstrated in CT, MFtl
- Chronic Hepatitis BIC ° 'Small fluid collection in peritoneal pouches can be detected well
- Vlfilson disease - Evaluable other structure as well like liver, pancreas.
- Autoimmune hepatitis (viii) Upper G.I. endoscopy - To confirm esophageal/funda varices.
' o: i antitrypsin deficiency (ix) Abdominal Paracentesis -
- Toxin like a Most rapid and cost effective method of diagnosis of ascites and its cause.
- Ethanol a Following tests can be done on ascitic fluid
° Methctrexate Appearance —
(b) Other Causes — —- Translucent - Normal
(i) Congestive heart failure - Turbid — Infection
(ii) Nephrotic syndrome — Brown — HyperbilirubinemialBiliary perforation
(iii) Tubercular peritonitis Grossly bloody — Malignancy, Trauma
(iv) Bacterial peritonitis Black I tea colour — Pancreatic Ascites.
(v) Severe Malnutrition Cell type and count -
(vi) Pancreatitis — t wec & t PMN — Bacterial peritonitis
(vii) Rheumatoid arthritis — T WBC & T Lynphocyte - TubercularlFungal peritonitis
(viii) Chlamydial infection — T FIBC — TB peritonitis. trauma. malignancy
(ix) Malignancy Gram stain and culture -
(x) Protein-losing enteropathy Comfimi bacterial peritonitis and organism.
[2009 Sam]
a. 17 : Laboratory evalutfon afAscftes of: child. ADA and CBNAT —
Ans : Diagnose tubercular peritonitis.
Laboratory evalution of ascites should aim - Proteln and SAAG -
(a) Confirmation of the presence of ascites SAAG = Serum-Ascites Albumin Gradient.
SAAG > 1.1 gmfdl — Ascites from portal hypertension.
(b) Finding the cause for ascites
SAAG < 1.1 gmldl — Non-portal Hypertension cause
(c) Assessing any complication due to ascites
GASTRO—lNTESTlNAL SYSTEM U Chanel-9
' 0.
.
LDH — Detects spontaneous bacterial peritonitis
These are as follows —
Amylase — Markedly elavated in pancreatitis or gut perforation.
[Marshidabad] (a) HBsAg (Surface Antigen) :
0. 18 : Shifting dullness in abdominal examination.
Marker important for screening test.
Ans : chronic
Only a marker of exposure to the virus and therefore positive both in acute and
Shifting dullness is reliable test to detect free fluid in abdomen clinically. infection
Sensitivity — To detect ascites by shifting dullness there should be at least 1500 mi of fluid in perito. Appears 6 weeks after infection
neal cavity.
Disappear by 3-6 months
Procedure —
Persistence > 6 months —-> indicates chronicity
- With the child in supine position. purcussion to be done at midline abdomen above downwards
to find maximum resonant area (b) Anti HBs antibody :
. From this maximum resonant area purcuss to either right or left upto a point of first dullness. Protective antibody appears soon after disapperance of HBsAg
0 Now ask the child to tum opposite side and give 1 minute time to shift fluid from one side to Persists life long
other. Positive after effective immunization
- Repercussion over the same areas alter 1 minute will reveal the resonance over previous dull (c) HBeAg :
area and dullness over resonant area previously.
Marker of infectivity and active viral replication
False negativeshifting dullness -
Detected soon after appearance of HBsAg
(i) Massive ascites where there is no scope for shift
Disappear by 6 weeks
(ii) Loculated fluid
Persistence indicates progression to chronicity and active infection i
(iii) Multiple adhesions.
(a) Anti l-c :
(iv) Fluid is low < 1500 ml.
Not a protective antibody _ C
0. 19 : Laboratory investigations of Acute Viral Hepatitis - [Murshidabad]
It appears after disappearance of HBeAg
Ans : Laboratory Investigation of Acute Viral Hepatitis : Seroconversion indicates good response to treatment C
(i) Liver Function Test — (e) HBcAg (Core Antigen) :
Bitirubin - Unconjugated and conjugated both fraction are elevated. Detected in hepatocyte as ground glass appearance C
AST and ALT -— Characteristic elevation is twice the upper limit of normal and fall during recov- Not detected in serum
ery ALT > AST
(0 Anti HBe: i
Serum Protein & Albumin — Usually remains normal in Acute Viral Hepatitis.
Not a protective antibody
(ii) Urine for bile salts and pigments - usually positive (
lgM indicates recent infection
(iii) Complete blood count
if patient is hospitalized. may be altered depending upon lgG indicates past infection
(iv) Blood urea creatinine
patie‘nt’s clinical condition. (9) DNA: I
(v) Blood glucose
Can be assessed qualitatively or quantitatively
(vi) Blood for prothrombin time &1NR —> assess liver function and prognosis.
Presence indicates active viral replication 4
(vi) Blood for HBsAg -+ Important screening test to mle out Hepatitis B virus infection.
(viii) Blood for lgM HAV —+ As most common virus causing acute viral hepatitis is HAV
(ix) Blood for serum ceruloplasmin, upto lgM EUSA, Widal test, urine for copper excretion -+ To rule
out. HBsAg HBeAg Anti HBe Anti HBc Anti HBs DNA Remarks ‘
\Mlson disease, Leptospira infection, Enleric fever respectively which present with clinical features + + _ - lgM / — High Acute Hepatitis
of acute viral hepatitis.
.. .. +1- lgG/ + - Recovery
(x) Ultrasonography of liver -+ - To assess liver echotexture, intra hepatic cholestasls
0 To rule out gall stone. liver abcess . _ - — + - Vaccination immunity
-
a. 20: Viral Markers of Hepatitis B infection. 4. + +I- lgG + High Chronic Active Hepatitis
Ans : There are different types of antigen of Hepatitis B virus. These antigens. antibody against few + - +i- IgG - Detected Carrier
al
antigens are released in blood in different phases of infection. — Thus they are the serologicalivrr
markers of Hepatitis B infection status.
.-.-...l-
[CMQ 9th Sem] CHAPTER — 1o

ren
0.21 : Hepatitis infection in child
HEMATOLOGICAL DISORDERS
Ans:
n t —+ Question 1.
Cl Causative organisms. manageme
Cl Clinical features -> Question 17. ‘ [—LBNG oussncfifl
[BSMQ 9th Sem] note on bleeding-
physiology of hemostasr's. Write a brief
O. 22 : Briefly discuss on Liver funct
ion test: a. f : Define hemostasis. Describe the [2014 supple]
disorders. (2 + 4 + 4)
Ans: nt of the patient with HEMOSTASIS
are helpful in evaluation and manageme Ans:
There are few biochemical test which proces s that 0 lots blood in areas of-blood vessel
injury. yet
liver dysfunction. These are helpfu
l to Hemostasis is defined as the active
to the areas of injury.
nction and extent of damage simultaneously limits the clot size only g is impaired.
(i) Confirmrpresence of liver dysfu system. restoring no rmal blood flow. it clottin
of etilogy Over time. clot is lysed by the fibrinolytic lications ensue. Hemostalic response
(ii) Diagnosis if clottin g is exces sive, lhromb olic comp
hemorrhage occurs, and
(iii)Response to therapy maintains this balance by rapid and regula
ted response.
are used to evalude liver function -
'
There are a battery of tests which

PHYSIOLOGY OF HEMOSTASIS
__'.- H-
and Conjugated Fraction : process are -

(i) Bilirubin (Total), Unconjugated The main components of the hemostatic
In any liver disease bilirub in will be increased. s; 4. Anticoagulant proteins; 5. Fibrinolylic system
1. Vessel wall; 2. Platelets; 3. Coagulation protein
"Us.
< 1 mg/d l elium is the primary barrier against hemorrhage

El Process of Hemostasis — Intact vascular endoth
Norm al biliru bin level ->
.
hyper bilirubinemia
30% of lot al bilirubin. Unconjugated es are set into action.
cascad
Conjugated bilirubin level -) upto and coagulation. After vascular injury. following
_.. __‘
rarely occurs due to liver disease

per so.
tion ofplat elet plug - Platele t plug forms immediately and stops bleeding temporarily.
y tract disease. 1. Forma
binemia a llways implies liver or biliar
-."._"—"-——-1—_.._
lation pathwa y.
In contrast conjugated hyper biliru till true clot is formed by coagu
detox ificati on funct ion of liver.
This test denotes excreratory and Vascular Injury
(ii) Liver Enzymes :
) -> Protein found in blood in liver dama
ge. specific tor liver
(a) Alanine Transaminase (ALT r limit of normal. increased Vasoccnstriction
.
the n two times of uppe

I.
t if it is more
disease. Level is significan
._.____
l
se.
both in acute and chronic liver disea thelial matrix proteins.
) -+ Thou gh this enzyme is not specific for
liver disease von Willebrand Factor (vWF). coming in contact with subendo
(b) Aspertate Transaminase (AST a;
two times of uppe r limit 0 f normal, both in acute and changes conformation
but increased in blood more then
chronic liver disease. disease and also in lb llX complezrt)
Level increased in live r. biliary tract Activated vWF binds to platelet receptor for vWF (Glycomotein
(c ) Alkaline Phosphatase (ALP) -> 1.
bone disease. '
ction which constitute the major Binding of vWF to platelet
min 8: Prote in —+ As the source of albumin produ
(iiiJS erum Albu
album in level decre ases in liver dysfunction.
liver. 3 0 serum
portion of plasma protein is album in is long as 21 days. Platelets are activated by
ase as the half life of Platelets are tethered
specially in chronic liver dise intracellular signalling
to the site of injury
INR :
(iv)Phrothrombin Time and
rs like II. VII. IX. X coagulation
site of prod uction of some coagulation facto Secretion from storage granules
As the liver is the
prothrombin time which is Waters Adhesiofl
nction. More specifically it is the (ADP. Serotonin etc)
time is prolonged in liver dysfu me eleva ted leading lo high risk of
and INR value beco L
characteristically prolonged
spontaneous bleeding. Glyooprolein llbllllareceptors
are switched on
t
. .
Fibrinogen binds to GPllbllIla

“FJ‘iUTMiung
Cross-linking of
platelets . “— receptors of platelet
l
Platelet AggregationJ (Platelet plug)
215
T
216 QUEST : PAEDIATFIICS HEMATOLOGICAL DISORDERS D Chapter-IO 217
_ «3.. .
2. Coagulation Cascade — All the 13 clotting factors are involved in this cascade. BLEEDING DISORDER I
A child with bleeding disorder presents with some sort of bleeding (9.9.. skin. mucous membrane.
Vascular injury deep-seated etc.)
I- ——————— “I i D Etiology—
) (INTRINSIC PATHWAY) ( Exposure of Tissue Factor (TF) {Factor III] 1. Defeclln vessel wall - HSP, SLE. Scurvy etc.
I XII ———> XII a I 2. Defect in Platelets —
Kallikrein
L ______ .1 a) Qualitative -— (Platelet Function Defects)
VII -—> VII a (EXTRINSIC PATHWAY) i) Bernard Soulier Syndrome
[ ‘ This portion ii) Glanzmannthrombasthenia
doesn't take part b) Quantitative — (ThrombocytOpenia)
in physiological XI --—> XI 8 J
i) lTP
coagulation. but
involved in PTT Platelet phospholipid (PL)
ii) Infections (Malaria. Dengue etc.)
measmement] IX ____’ PL. Ca Calcium (Ca) iii) Dwgs (Penicillin. Valproate. NSAID etc.)
iv) Microangiopathy (HUS. TTP)
VIII —> VIII a
. v) Malignancy (Leukemia)
vi) Hypersplenism
x——>- 3. Defects in clotting factors —

a) Congenital —
i) Hemophilia A and B
ii) von Willebrand disease
' Thrombin —; is a mrlt'potent iii) Specific factor deficiencies
Thrombin (Ila) <—— Prothrombin (II)
enzyme which acts by-
b) Acquired ——
I
a) Coverting Fibrinogen to i) Liver disease
fibrin
ii) Vitamin K deficiency (Hemonhagic disease of newborn)
b) Activathg Factor V. VIII. Xi
Fibrinogen (l) ——> Fibrin monomer iii) Warfarin overdose I
and XIII
iv) DIC
c) Aggregrating platelets Xilla l
(Activation of factor Xi El Clinical evaluation —
amplifies thrombin eration FIBC . 1. Age of onset of bleeding -) Congenital diseases (Hemcrphilia) usually present early
and dot formation)gen Stable hemo- <———— Cross linking and clot retraction [Exception — von Willebrand disease often presents late]
static plug Platelet "C
2. Type ofbleeding /site ofbleeding -> Differentiates well between platelet disorders and
coagulation defects.
3. Role ofanticoagulantproteins - 4 clinically important anti-coagulants regulate the extension

Characteristics Platelet disorders Coagulation defects
of the clotting process —
a) Antithrombin III (AT III) — inhibits Xa and Ila (thrombin) (a) SiteoiBleeding—r Skin and mucous membrane Deep-seated bleeds (joint.
b) Protein C (oral cavity. GI tract) muscles. soft tissues)
inactivates factor Va and Villa
0) Protern S (b) Petechiae —-) Yes No
Vlla and TF.
d) Tissue Factor Pathway Inhibitor (TFPI) - limits activation of factor X by factor
4. Ffbrfnolytic system - Once a stable lib rin-platelet plug is formed. fibrinolytic sysem limits
its (c) Bleeding after minor Yes No
trauma —> ‘
extension and also lyses the clot to re-establish vascular integrity.
(d) Bleeding after surgery -r Immediate. but mild Delayed (1-2 days). often severe.
' Acti tor PA _ G . .
Plasminogen “SSW Plasmrrrogen -‘ m (T ) :— Plasmrn 4—_———-—Antiplasmrn
. Preclpftatfng factors - Spontaneous or after surgery.
Streptokrnase
urokin'ase 7451:01nHlO antecedent lnfectlon - lTP. HUS
G . Rash - HSP, SLE. Dengue
Plasminogen Activator Fibrin———-——> Fibrin Degradation lcterus - Liver disease
lnhibitor(PAl) (Clot lysis) Products (FDF') Renal failure — HUS
28
HEMATOLOGICAL DISORDERS Cl Chapter-10 219
‘ e- 3"? . a. 2: Outline the Metabolism of iron in the body. Compare the laboratory findings of iron
8. HIO Drug intake ' [2010]
disease deficiency anemia and thalassemr‘a (4 + 6)
9. Family history — Disorder affecting only boys in family suggests X-Iinked recessive
(Hemophilia) Arts : METABOLISM OF IRON
10. Splenomegaiy -— Malignancy, SLE, Malaria, Hypersplenism. Iron is an important micronutrient, needed for synthesis of hemoglobin, myoglobin. cytochromes etc.
Total body iron is 3-5 gms and 2/3rd is present in blood (as Hb mainly).
CI Laboratory Evaluation— 1. BT.CT. 2. Platelet Count, 3. PT.aP1T
D Source - There are 2 major sources of food iron —
1. Home tron - Highly bioavailable and absorbed intact within the porphyrin ring. Its
(BT measures defect in (PT measures extrinsic pathway
Bleeding child absorption is not influenced by the inhibitory factors in the diet. It is present in animal
formation of platelet plug and and aPTT for intrinsic pathway)
proteins. like meat. fish, egg and also in blood products.
CT measures coagulation
defects) Bleeding Time (BU 2. Non heme Iron - Present in foods of plant origin and often complexed with phosphate,
phytate etc. So. absorption is poor.
Clotting Time (CT)
[1 Absorption — Maximum absorption of iron takes place in duodenum. 2 steps are involved in the
iron absorption —
1. Entry from intestinal lumen to enterocyte.
BT prolonged CT prolonged
2. Passage from the enterocyte into the plasma.
l l
[ Platelet count] Prothrombin Time (PT)
/ \ Activated partial thromboplastin A0!) = Anemia of Chronic
time (aPTT) Diet Disease
I l Platelet count I I® Platelet count I

l l Nonheme Heme fl Heine
Causes of - Vascular causes Iron Iron —' Iron
Thrombocytopenia 0 Platelet function
I Cytochrome b
defects (Qualitative
disorders of platelet)
Fea”
l l Stored as
J.—
Abnormal aP'l‘I' Ferritin (Fe3*)
79H?!
Abnormal PT and Abnormal PT and

Normal aPTT - Normal PT
aPTT Feb
s
l l
i
",3'35'W'i' ...._ ,.
- Liver disease (early) - Hemophilia A and B {f 4-- Fr:2+

' DIC Ft2+
- Factor VII deficiency - von Willebrand disease
. Liver disease I Hephallstin
' Vit. K deficiency - Anticoagulant therapy
,j
a
2
r: 0 N.B.
erropo n (Transferrln)
1. 010 (Disseminated lntravascuiar Coagulation) -
. Fe“
a) i Platelet count
b) T ET
d) T PT
9) T aPTT
is
Hepcidin
c) T or I) l Fibrinogen, FDP (in ACD)
2. von-Willebrand disease —
a} T BT. TCT Intestinal ..Enterocyte
b) T aPTT, Normal PT
i7
et type VWD)
c) Platelet count — Normal (except — platel I Iron Absorption I
e and thus PT is prolonged first in early days
3. Liver disease — Factor VII has lowest half-lif ged.
prolon
oi liver disease. but later both PT and aPTT are
220 QUEST : PAEDIATFIICS
——_~.
HEMATOLOGICAL DISORDERS CI Chapter —10 221
Cl Regulation of Iron absorption —
Iron absorption in gut is finely regulated
needs of the body. depending on the
#— Laboratory Markers IDA Thalassem l 3
bran stores I T Body irgl
l _ 4. Mentzerlndex -t High LOW
(MCWFIBC count)
T Transferrin saturation
i 5. HOW (Red Cell Distribution High. as norrnocytes are also Normal
T ‘Messenger’ iron in enterocytes Width) —> present with microcytes.
[Measure of Anisocytosis]
l
T Production of 6. Polkilocytosis ——i + ++
7. Peripheral Blood Smear—i Microcytic, Hypochromic. M/C, H/C. Aniso. Poikilo (+)
Fe“ —————__.; Ferritin(Fe3*) [storage form] Anisocytosis, Poikilocytosis Fragmented RBCS, Tear drop cells,
Target cells etc.
8. Ferrltin —> Low(<10 — 12 mg/ml)
l ed absorption Discarded with desquamation Normal initially- High in later stages
into plasma of the disease.
of cells
9. TIBC —> (Total Iron Binding High Normal (initially) to low (late stage)
- Similariy, Iron absorption is increased with — decrea Capacity)
sed iron stores, increased erythropoietin ——
activity and during pregnancy.

' 10. Transferrin Saturation -) Low
El Transport — Iron circulates in combination with Normal to high
transferrin. Circulating transferrin binds with the
receptors in the cells where iron is needed (erythroblasts).
It is then endocytosed. converted to 11.FEP (Free Erythrocyte High (in the absence of iron,
ferrous form (Fezf) and used in Hb synthesis. Protoporphyrin) —)
Normal
protoporphyrin rings are free in
Ci Storage — Excess iron is stored as ferritin in FIE cells FIBCs)
(Reticulo endothelial cells) and can be
used later. if needed.
0 Daily loss — Iron is lost from the body mainly through 12. Hb electrophoresis —+ Normal pattern
iaeces and through menstruation in T HbF. T ”DA-2
females.
13. Response to iron Good
COMPARISON OF LAB FINDINGS OF IDA AND THALASSEMIA Poor. (Iron contraindicated)
therapy -)
Iron Deficiency Anemia (IDA) and Thalassemia (commonest form of Chronic
Hemolytic Anemia)—
both produces microcytic hypochromic anemia (i.e., l MCV, l MCH, I MCHC).
But. there are basuc
differences in pathogenesis. IDA causes decreased heme production due to iron a. 3 : Enumerate the coagulation cascade. Desc
deficiency. 0." the ribe the clinical pictures of hemo
other hand. thalassemia causes defective synthesis of different globin chains (a, [5 etc.) management. (4 + 4) philia and its
leading to [CNMC - 8th Sam.)
hemolysis of FiBCs. Ans : Coagulation Cascade — See Question No. 1 (First
_ Part)
Different laboratory markers that can be used to differentiate between these two conditions are
described below — HEMOPHILIA
Hemophilia is the commonest con genital coagu
lation factor deficie ncy disease. It is of two
Hemophilia A (Factor VIII deficien cy) and Hemo types -—>
Laboratory Markers philia B (Factor IX deficiency).
IDA Thalassemia
D Clinical Features — In hemophilia, there is deficien cy
of coagulation facto
r VIII or IX, which are
1. BBC Count —-) Low Normal or High important factors in intrinsic pathway. So. the
dise ase mainly manifests as bleed
from different sites. ing episodes
2. 'Reticulocyte Count -«) Increased (> 2%). but is proper-
_ Significantly T ed (usually > 5%). 1. Family history is usually positive. As it is in herited as X-lin
tionate to degree of anemia. disproportionate to the degree of are affected in a family and females act as carrier.
ked recessive manner, only males
anemia
2. Severity of bleeding depends upon severit
3. Heticulocyte Index -) y of disease —>
Close to 1" (Normal) > 1 (Raised) a) Severe disease — Spontaneous bleeding
. HCT
[Bet] count% X “4—5- b) Moderate disease Bleeding after trauma
-
(I-ICT = Hematocrit)
c) Mild disease — Bleeding after surgery or injury.
HEMATOLOGICAL DISORDERS El Chapter-10 223
bleedings’. ii) Avoid contact sports and outdoor games

3. Deep seated bleedings are mostly seen with hemophilia as opposed to cutaneous
Joint and Muscle hemorrhages are hallmark of this disease entity. iii) Hepatitis B immunisation (to prevent transfusion — bcurnue infection)
around 9 - 18
4. Symptoms usually occur when the child learns to cruise. walk and run (usually iv) lntranasal Desmopressin Acetate — releases patient's endogenous factor VIII
months). in mild hemophilia A. It is not effective in moderate to severe Hemophilia A and
knee. elbow and ankle. all forms of Hemophilia B.
5. Hemerthrosis (Joint bleeding) — Most frequently affected joints are
Joints become swollen. warm. tender and have limitation of movements. 3. Prophylaxis —
to damage to the joint
El Target joint - Repeated bleeding into the same joint eventually leads i) In severe hemophilia. prophylactic factor replacement 2-3 times/week is
termed as ‘Target
cartilage and syncvium. This results in chronic. painful arthritis and the joint is recommended to reduce bleeding episodes (primary prophylaxis) and improve
Joint '. . quality of life.
6. Muscular hemorrhage Presents as localised pain and swelling. Bleeding into a large ii) In older children with target joint. secondary prophylaxis is often initiated to
loss of a large volume into the
-
muscle (3.9.. iliopsoas) may become life-threatening due to stop further damage.
' muscle. Patient may land into hypovolemic shock. 0. 4 : Outline the mechanism of hemostasis in children. Briefly write the managementof recently
GU bleeding. easy or spontaneous
7. Other bleeding manifestation include — GI bleeding. diagnosed case of acute ITP. (5 + 5) [IPGMEH - 9th Sent]
bruising, bleeding from oral mucosa etc. Ans: Mechanism of hemostasis - See Question No. 1 (First Part).
8. Life-threatening bleeding — lntracranial hemorrhage.
MANAGEMENT OF ACUTE ITP
D Management - ‘ Idiopathic Thrombocytopenic Purpura (ITP). now renamed as Immune Thrombocytopenia. is the
a) investigations - commonest cause of acute onset of thrombocyIOpenia in an otherwise wellchild. Recent evidences
1. CBC -—) Within normal limits with (N) platelet count. suggest autoantibody-mediated platelet consumption in the pathogenesis of ITP.
BT—) Normal El Investigations -
Pit-"PP!“
CT-i Prolonged Common for both 1,. Complete Blood Count —

pT ., Normal hemophilia A and B
a) Platelet Count — Low (usually < 20.000lmm3)
..
aPTT —+ Prolonged b) Platelet morphology - Platelet size is normal or increased, reflective of Ted turnover.
s the diagno sis of hemop hilia (A
Specific factor assay—i (forfactcr VIII and IX) confirm 0) Hb% - Low (Proportionate to the degree of bleeding)
and also helps in assess ment of severi ty of the disease —
and B) d) WBC count — Normal with normal Differential Count (DC).
i) < 1% — Severe a) Abnormal cells — Nil
ii) 1 - 5% — Moderate BT — Prolonged
9‘99”!“
iii) > 5% (6 - 24%) -— Mild CT — Normal _ 1:
.. '
b) Treetment— factor PT. aPTI' - Normal
for both hemophilia A and B Involves
1. Factor Replacement -—> Treatment Bone Marrow Examination - Increased Megakaryocyles-
levels.
replacement to raise the factor to hemostatic _ in the. 35- - Indications — To exclude possibility of allemative diagnosis
'
‘ to moderate bleeding. ' levels are
hemostatic
- culatr‘on of dose —> For mild d arm to achieve
hemorrhages, dose shoul a) Abnormal WBC counts or DC.
5063196 range. But. in severe or life-threatening .
levels of 100% activity. b) Abnormal cells on peripheral blood smear,
in F-VIII level x body weight (kg) x 0.5
i) Dose of F-VIII (IU) = % of desired rise c) Severe anemia disproportionate to the degree of bleeding,
rise in F-IX level x body weight (kg) x 1.4
ii) Dose of F-IX (IU) = 96 of desired d) Findings on history and clinical examination suggestive of a bone marrow failure
' calculated dose should be given ‘ every 12 . hours (F-Vlll) to syndrome or malignancy.
. ti of the —+ This
rding to the seve nty of bleeding episode. 6. Others — ANA. HIV screening in adolescents with new-onset ITP.
gffiog (F—lxfigfa-‘I days acco
0 Mode of replacement -+ ble.
CI Treatment -' Acute ITP is usually a self-limiting disease and hate a course of 2-4 months before
ideal. but is costly and often not availa
..
spontaneous remission. But. appropriate treatment helps in more rapid rise of platelet count to
i) F-Vlll or F-IX concentrate is ls absent in
alternative for hemo philia A (but F-IX > 20.000/mm3 and thus decreases incidence of life-threatening bleeding episodes.
rgs—
ii) Cryoprecipitate -— Effective

- I) For children with only skin bleeding (like petechiae. ecchymosis etc) without any mucosal
..-
..
crappt) . and It contains all

ma )- Most widely available option bleed and platelet count > 20.000imm3. cldse observation with serial platelet count suffices.
iii) FFP (Fresh Frozen Plas
the factors of coagulation. 2) For children with active mucosal bleeds. treatment options are -—
- a) lVlg— Intravenous Immunoglobulin (Wig) is the treatment ofchoice. but is very expensive.
2. Supportive therapies subcutaneous. as far as
i) Avo id IM inje ctio n s and vaccines (should be given
possible)
225
‘
ter- 10
HEMATOLOGICAL DISORDERS [3 Chap
linnnnnnnnnnnm
Dose is 1 gmlkglday lor 2 consecutive days. It acts by downregulating Fc-medialed Type of Anemia Low Reticulocyte Count High Reticulocyte Count
phagocytosis of antibody-coated platelets. i) Thalassemia syndromes
1. Mlcrocytfc i) Iron deliciency anemia
b) Prednisolone —~OraI prednisolone G 1-4 mglkgiday for 24 weeks followed by slow tapering
induces rise in the platelet count in most of the patients. It is indicated for patients who anemia —’ ii) Sideroblastic anemia ii) HbC. HbE diseases
can't afford IVIg. iii) Lead poisoning (Hemoglobinopalhiesl
c) lVanti-D lmmunoglobulin - Useful only in Fth-positive patients @ 50-75 pgllig, but causes Iv) Thalassemia trait
mild hemolysis.
Anemia of chronic disease i) Antibody—mediated-hemolysis ~
3) In severe. life-threatening hemorrhages (like intracranial bleeding). multiple modalities may 2. Normocytlc i)
be used, including platelet transfusion, corticosteroid (oralllV) and Mg. anemia -> ii) FiBC aplasia (Infection. Drugs etc) (Autonmmune/ Allormmune)
4) Platelet transfusion - Generally avoided in ITP. except in life-threatening bleedings.“ iii) Leukemia ii) Hypersplenism
5) Counselling and education of the family members are of utmost importance in the management iv) Flenal failure (i EPO production) iii) Microangiopathy(HUS.TTP)
of ITP. iv) Membranopathy (Hereditary
v) CDAtypell
spherocytosis)
O. 5 : Discuss about physiology of coagulation. Outline the management of ITP. (5 + 5) v) Enzymopathy (GSPD, PK
[CNMC — 9th Sem, Haldia - 2016]
deficiency)
Arts: Same as Question No. 4.
3- Macrocyfic i) Folate deficiency i) CDAtypelandIll
0. 6 : Define Anemia. Classify anemia according to RBC morphology citing examples. Describe
the peripheral blood pictures of chronic hemolytic anemia. ‘(2 + 5 + 3) anemia—i ii} Vit. B“Z deficiency ii) Active severe hemolysis
[RGKMC - 9th Sen-i] iii) Orotic aciduria
Ans : ANEMIA iv) Hypothyroidism
v) Congenital aplastic anemia
Anemia is defined as a reduction of the hemoglobin concentration or red blood cell (RBC) volume (Diamond-Blackfan anemia)
two standard deviation (280) below the mean for that particular age and sex.
As per WHO, cut off values for diagnosis of anemia at different ages in children are as follows -
- Abbreviations -
a) 6 months—6 years : < 11 gm%
EPO = Erythropoietin
b) 6— 14 years : < 12 gm%.
CDA = Congenital Dyserythropoietic Anemia
CLASSIFICATION OF ANEMIA ACCORDING TO HBO MORPHOLOGY
HUS = Hemolytic Uremic syndrome
Classification of anemia on the basis of RBC morphology is an age-old method. It can be done TTP = Thrombotic Thrombocytopenic Purpura _
in narrowing
easily by simple test (like microscopy of peripheral blood'smear) and is very useful
down the diagnostic possibilities. PK = Pyruvate Kinase
Aflflflflhflnli
- HBC morphology can be assessed by two ways —> GSPD = Glucose 6 Phosphate Dehydrogenase
a) Examination of PBS - by microscopy PERIPHERAL BLOOD PICTURE OF CHA

b) Determination of RBC Indtces - - CHA or Chronic Hemolylic Anemia is characterised by chronic ongoing hemolysis (intravascular
i) MCV (Mean Corpuscular Volume) [Normal range is 80-95 fL] or extravascular) due to various intrinsic defects of RBC and also by external insults.
ii) MCH (Mean Corpuscular Hemoglobin) [Normal range is 28-32 pg] - Common causes of CHA are —->
30-36%]
iii) MCHC (Mean Corpuscular hemoglobin Concentration) [Normal range is 1. Intrinsic :- a) Membrane detect (e.g., Hereditary Spherocylosis), b) Enzyme defect (e.g.,
-l GGPD delimency. Pyruvate kinase deficiency. c) Hemoglobinopathy (e.g. Thalassemia
- Anemia can be classified into 3 types according to FIBC morphology, namely HbC. Sickle cell disease etc.) ' '
1. Microcytic (l MCV) —+ Usually Hypoohromic (l MCH, 1 MC HC) also. ‘ 2. Extrinslcg— a) Autoimmune Hemolytic Anemia (AIHA), b) Paroxysmal Nocturnal
2. Nonnocytic (Normal MCV) -+ Usually Nonnochromic (Normal MCH and MCHC) Hemogloblnuna (PNH), 0) Micro angiopathic Hemolytic Anemia (e.g.,' HUS. TTP etc).
3. Macrocyfic (T MCV). - Peripheral Blood Picture—
(High/Low).
.- Each of these 3 types can be further classified according to Fleticulocyle count 1. HBO series -
In the body. Low
Increased Reticulocyte count is found in cases. where 9805 are destructed
reticulocyte count in the presence of anemia suggests decreased erythropolesis.
8) RBC morphology-
I) Microcytic hypochromic in thalassemia syndromes
- Examples —
ii) Nonnocytic in most of the other causes of hemolysis
29
226 QUEST : PAEDlATFllCS HEMATOLOGICAL DISORDERS U Chapter-40 227
iii) Macrocytic, it there is acute severe hemolysis by any cause (due to pouring out oi Ans .' HEMOGLOBIN SYNTHESIS
Immature RBCs from bone marrow) Hemoglobin (Hb) is synthesized in the developin g 8803 in' the normoblastrc' sta e me
' ed ' t
b) immature RBCs — normoblasls). Each molecule of Hb contains 4 haem and 4 globin chains (protein). 9 ( t rm 'a e
i) Fieticulocytes are the last stage in .erythropoiesis inside bone marrow and are D Heme Synthesis -
normally found in PBS @ 0.5 — 2% at Total RBCs. Fieticulocyte count increases
Glycine + Succinyl-COA -—-> a—amino B-keto adipic acid
(>2%), whenever there is anemia due to increased erythropoietic response in BM
(exception — hypoplastic l aplastic anemia)
ALA synthetase
- But in CHA, reticuiocyte count is much more increased (usually > 5 - 6%) 6-ALA
is corrected
— Heticulocyte index (RI) is a better parameter to show BM response, as it
‘ (fi-Amino Levulinic Acid)
. . . HCT .
reticulocyte count for degree of anemia HI = RC /° X 75— . Ftl > 1 in CHA. fi-ALA dehydratase
under normal
ii) Normoblasts are more premature R805 and are never found in PBS
numbers in
condition. But, in CHA, normoblasts can be found in considerable Porphobilinogen Ill
PBS.
in CHA are l Porphobilinogen deaminase
C Abnormal FiBCs - Various other abnormal RBCs found
be
cells — are seen spontan eously or after sickling test in Sickle cell disease.
i) Sickle Hydroxymethyl Bilane
ytosis. Immune hemolytic anemia
E) Spherocytes — can be found in Hereditary Spheroc Non-enzyniatii/ \iroporphyri nogen Ill CoSynthase
etc.
iii) Elliptocyte — in Hereditary Elliptocytosis. This details may Uroporphyrinogen l Uroporphyrinogen Ill
(Microangiopathic Hemolytic Anemia)
iv) Schistocyte I Helmet cells — in MAHA
be omitted or cut
d, uniform in size, numerous spicules
v) Echinocyte — RBCs with regularly space short it marks l Uroporphyrinogen decarboxylase
(Echinocytes) are seen in PK deficie ncy. are less.
vi) Target cells } Coproporphyringogen l ' Coproporphyrinogen Ill
Seen in thalassemia syndrome and
- -
. es .in other hemolytic anemias also
V“) Tear drop ce lls
" sometim
viii)Fragmented R805 . .
_ Coproporphyrinogen Oxidase
2. W80 series —- CHA (mainly In GBPD
after acute hemolytic episodes in
a) Leukocytosis — Can be seen .
deficiency) ia) Protoporphyrinogen IX
plica tion of thala ssem
rsplenism (a com
b) Leukopenia — Seen in hype nism. I Protoporphyrinogen Oxidase
seri es - Thro mbo cytO penia is also seen in hypersple
3. Platelet
it
Protroporphyrin iX
fies OWEWIW
Feafll Ferrochelatase
“s acids in a chain pattern (141 5a in ct-

. (d) El Globln Synthesis - Giobin is a protein containing amino
(c) ' . (9)
(a) (bi Echmocytes Target ce from DNA by transcription andtransiation

Elliptocytes Schistocytes chain, 146 Ea f'n fl-chain). It is synthesized in the BBC
Sickle Cells methods.
binds to the globin chain via the nitrogens
ormal RBC shapes El Formltion of heinogiobln - The iron (Fea) in heme and 87" histidine in a-chain, 63"_ and
Figure 1 : Different abn of the hlstldine residues of the drains in 2 sites (9.9.,
58"
lassemil.
pathophysioiogy o fthe 92"“ histidine in B—chain) l
e is. ‘Brfefl mention thewith severe pailor and hepato-
gre sen tfng
the 8m” 0:21:52?! 3M boy [Kaiyani—t Soul]
0' 7: How toate
Enumer will ?!” "
spienomeglly ? (2 + 3 4' 5)
———-———-—-T
Cl Chapter-10 229
228 QUEST: PAEDIATRICS HEMATOLOGICAL DISORDERS
l T We Mfg/i
One'haem + one globin chain form one T HbF ((1272)
subunit
1 i i
a-chain in fl-thalassemia)
Excess of the normally produced globin chain in BBC (9.9..
4 such subunits together ionn one Hb l
molecule
Forms insoluble inclusions [at in B—thalassemia. .BtiHbH)
in BBC precursors in a-thalassemta]
PATHOPH‘I’SIOLOGY OF THALASSEMIA l
Thalassemia syndromes are a heterogeneses group of disorders inherited in an autosomal recessive I
manner. The hallmark of thalassemia is decreased or absent synthesis of one or more globin chains
.
(Ineffective Damage cellmembranes Decreased BBC deformability
(:1 or (3). ‘1'
erythropoiesis) Destruction in spleen
a) a-thalascemia - When synthesis of tat-chain is affected, the disease is known as re lntramedullary death of cells
thalassemia. i i
_
- There are 4 a-giobin genes in chromosome 16. According to the number of genes Bone marrow expansion (hemotytic tacies)
affected, there are 4 types of clinical presentation for u—thalassemia —
i) Silent carrier (1gene affected) V t
i) a—Thalassemia trait (2 genes) T Meduuaw } _ _ . T Unconjugated Bilinrbin (Jauncice)
erythropoiesis 4-— T EPO secrehJon (Erythroporehn) , Splenomegaly
ifl HbH disease (3 genes)
iv) Hydrops ietalis (4 genes) .7
b) B—thahssemia — It is characterised by .L ed/absent synthesis of B—globin chains (3° mutation Extramedullary erythropoiesis
— Absent synthesis, (5‘ mutation — 1 ed synthesis ) l
4 types
- Zfl-gtobin genes are represented on chromosome 11. B-thalassemia also have Hepatomegaly
of presentation -
0 Silent carrier ((5+ mutation) } 1 gene affected (Heterozygous)
in B—Thalassemia trait (5° mutation) APPROACH
ii) fivThalassemia Intennedia ((3“ mutation) 2 genes affected (Homozygous) - 12 month old boy
- Severe pallor
iv) B—Thalassernia major (B° mutation)
of Hb that can be found in children - Hepatosplencmegaly
E] Pathophysiology of clinical features - There are 3 types
and adults a El Common possibilities —
above 1 year of age. 1. Chronic Hemolytic Anemia —r (Cl-M)
a) HbA (Adult l-b) -r 02|32 :9096 of total Hb in children
b) HDA2 a (1262; < 2 - 3% of total Hb in children a) B-thalassemia (major! intermedia)
tes > 70% of total Hb in newborns. b) Sickle cell anemia
c) HbF (Fetal Hb) -+ 0.212; main Hb in total life and constitu
c) Hereditary Spherocytosis
Gradually l ed to almost undetectable level after 1 year of age d) l-IJE disease I E-B thalassemia
2. Hematological lililgmncios —r
I—Thalammla Syndromefl a) Acute leukemia (ALL. AML)
b) Non-hodgldn lymphoma (NHL)
l
3. infection: a
l ed productions! either of the globln chains (ail!) a) Disseminated TB
l
b) Malaria
Imbalance between 2 types of globin chain, whlch
c) Kala-azar
are normally present in 1 : 1 ratio In Hb.
230 QUEST : PAEDIATRICS HEMATOLOGICAL DISORDERS U Chapter-10 231
4. Metabolic—r 5. Osmotic Fragility Test —+ T lragility in HS.

a) Gaucher’s disease _ 6. GGPD level —r led in GBPD deficiency
' Rare 7. Bone marrow examination —) - Lymphoblasts in Leukemia (ALL)
b) Mucopolysaccharidosis
Causes
5. Connective tissue disease —; ' Myeloblasts in AML
a) SLE ' L0 bodies in kala-azar (55-85%) [Splenic aspiration can show
b) Systemic-onsetJlA. LD-bodies in > 85% cases]
. - Gaucher cells in GB
Cl Differential diagnosis —
‘ 8. CXR —> - Lesions in lungs in TB .
a) From history -;
- Enlarged mediastinal lymph node (Mediastinal widening) may be seen in NHL [HRCT
1. HO fever— in inlectious causes. leukemia; may be present in CHAs or Iynphcmas also.
is more sensitive]
. Bleeding manifestatim - seen in leukemia. malaria
«ignorance»
. Jaundice — in CHA. malaria. kala-azar 9. FNAClBiopsy from LN —> In case at lymphadenopathy. diagnostic for lymphoma. TB.
Recent weight loss — in malignancies (leukemia. lymphoma), disseminated TB. 10.8putum tor AFB and CBNAAT a (Gastric aspirate in this child) positive in TE.
. Joint pain — leukemia, connective tissue disease. 11.Mantoux Test —> may be positive in TB.
__
Bone pain — in leukemia tZMalarial dual Ag —> positive in Malaria (Vivax or Fatciparum)
. H/O blood transfusion — may be found in CHAs.
.I
t3.Fll(-39 Ag —> positive in Kala-azar.

8. Family history — positive in CHAS ; contact history in TB
X
14.lnvestigatlons to define spread in malignancy —

~.»—
b) From examination —)
.
(a) CSF study - in leukemia

i‘
1. Signs corroborative of symptoms — like raised temperature (fever), bleeding spots

3
.
(b) USG (abdomen) l CT Abdomen — in lymphoma.

(petechiae, purpura in skin and mucous membrane). icterus etc.
t'
=3
(c) Bone scan

'."'
Lwnphadenopathy — seen in leukemia. lymphoma. TB

saws-saw
' _. 'v-:
15.For connective tissue diseases -

n
Hemolytic facies — in CHA (mainly thalassemia]

"
Abnormal findings in chest auscultation - usually found in disseminated TB (8) RA factor — may be we in JIA
".3
Meningeal signs — may be positive in disseminated TB (b) ANA- in SLE or JIA

i
I--
"
Ascites — in TB, may be found in lymphoma and leukemia (NHL) (c) anti-ds DNA — SLE
<‘
“
. Stemal tenderness —- in lukemia. (d) CFtP - Positive

'_
NJ
‘
"
c) From investigations 4
'_
0. 8 : Describe the mechanism of normal haemostasis. Enumerate diseases in children which can
:‘tt-':.':’_ _'
i .' ‘7:...;;;r-.-.
1. Complete blood count - Most important investigation occur due to defects in coagulation. (7 + 3) I“; [KW-2016]
a) BBC morphology - ' Microcytic hypochrcmic in CHA (Thalassemia) Ans:
0 Normocytic normochromic in most of the others
..
."‘.‘.’ .‘-
Mechanism of Normal hemostasis

an
r Spherocytes in HS
See 0. 1 ‘
'7-
b) Reticulocyte count - T T in CHA

a.“ 1'
COAGULATION DEFECTS
{Elfin-nut
c) Nucleated RBCs - in CHA

Detects in coagulation or coagulopathy comprises of deficiency or detect in the proteins involved in
d) Total WBC count — 0' Leucocytosis in Acute leukemias
gm. ..»
coagulation cascade (includes both procoagulant and anticoagulant proteins).

- Leucopenia in Iukemia. kale-azar
«3-.
v~
A. Detects in procoagulant proteins: Manifests with bleeding

.
e) Diflerential count - - Lymphocytic predominance in ALL

“Wane
1. Congenital -
0 Relative lymphocytosis in kala-a'zar and TB
0 Predominance of polymorphs in AML (a) Hemophilia A (Factor VIII def.)
l) Platelet count - l in leukemia, kala-azar (b) Hemophilia B (Factor IX def.) “inked W

AML) (c) Hemophilia 0 (Factor XI det.) — Autosomal Hemphilia
g) Abnormal cells — Blast cells in acute Ieukemias (ALL and
tissue diseases (d) AfibrinogenemialDysfibrinogenemia (Factor I def.)
2. ESR —- Raised in TB, malignancies, connective
(Thick and thin films required) (e) Other factor deficiencies (9.9. II. VII. X, XIII etc.)
<1 .._
3. Malaria parasite — Can be lound in peripheral blood smear

.u;
s) 2. Acquired-
4. Hb Electrophoresis (for hemoglobinopathie
(a) Uver disease
- T HbF, T HbA2 in Thalassemia
(b) Hemorrhagic disease of newborn (vii. K deficiency)
- T HbS in Sickle cell disease
0 T HbE in HbE disease
Chapter-10 233
HEMATOLOGICAL oisonoens C]
-- bleed 'IS accorn D aniedb y muscle gua

. - _ When a large jornt rding and swelling,
(b) Immobilrsation maximal comfori and
(c) Disseminated Intravascular Coagulation (DIC) position 01
be done at the
immobilisation of the joint by plaster of parts can
(d) Drug overdose — Warfarin, Heparin maximal joint space.
ting pain.
B. Defects in anticoagulant proteins : Manifests with thrombosis - maximally d islended with excrucia
to) Aspiration — indicated. when the joint involved is ek pre—
replace ment D 2 time slwe
1. lnheritedlCongenltal — 4. Prophylaxis : Primary / secondary prophylaxis
with factor
C.
(a) Factor V Leiden mutation (MC) — Resistance of Va to inactivation by activated protein vents hemarth rosis and chronic arthropa thy of target jOlntS.
raises.
started within 2-3 days followed by active exe
(b) Protein C deficiency 5. Rehabilitation : Isometric exercises should be
will you investigate a case of iron deficiency
(c) Protein 8 deficiency
O. 70 : Discuss in brief the iron metabolism. How [Murshldabad-2016]
(d) Antilhrombin deficiency anemia (lDA)? Outline the treatme nt of IDA. .(4+3+3)
(e) Prothrombin gene mutation (GZOZIOA)
Ans :
(f) Hyperhomocystinemia
Iron Metabolism
2. Acquired -
See 0. 2.
(a) Nephrotic syndrome
IRON DEFICIENCY ANEMIA (IDA)
(bj Antiphospholipid antibody syndrome (APLA) includes 3 facets —- General markers,
D Investigations : Investigations of a case of suspected IDA
0. .9 : Outline the physiology of hemostasis. Write briefly the management ofjoint bleed in a child ry causes.
[IPGMER, 2015] confirmation of diagnosis and identification of possible seconda
with hemophilia A. (5 + 5)
A. General markers - Corroborative with IDA
Ans: 1. Hb & Hematocrit — Decreased.
poikilocytosis. presence of
Physiology of Hemostasis 2. RBC morphology — Microcytic, hypochromic. anisocytosis,
abnormal cells (Target cells. pencil shaped cells etc.)
See 0. 1
MANAGEMENT OF JOINT BLEED IN HEHOPHILlA-A RBC count — Decreased
msneso
HemOphiIia A is an X-Iinked recessive disorder of coagulation due to deficiency of factor VIII. Most Reticulocyte count — Normal / mildly elevated
common presentation is hemarthrosis orjoint bleeding. MC joint affected is knee joint, followed by MCV, MCH, MCHC — Decreased
elbow, ankle, shoulder and hip joint. Management of hemarthrosis includes the following -— . new (Red cell distribution width) — > 14.5% [® upto 13.5%]
1. Prevention and early recognition : 8. Confirmation of diagnosis -
(a) Prevention of trauma — avoidance of contact sports and high-risk behaviours. 1. Serum ferritin — It is the first marker to be abnormal in iron deficient state, as it denotes
(b) Education of parents - regarding the disease iron stores. Serum ferritin value of < 12 nglml is highly specific for iron deficiency. Ferritin
(c) Respect the early symptoms described by patients - like pain. funny feeling of the joint, is falsely elevated in inflammatory conditions (acute phase reactant).
tingling, feeling of warmth etc. Start treatment at the earliest to improve outcome and lessen . Serum Iron - Fleduced
review»
duration and cost of treatment. . Total Iron Binding Capacity (TIBC) - Increased
levels of factor VIII
2. Factor replacement : In mild to moderate bleeding. values of hemostatic Transferrin Saturation —- Decreased [< 16%)
includes 35-50% range.
Free Erythrocyte Protoporphyrin (FEP) - Increased
° Dose (IU) = % of desired rise in FVIII x Body wt. x 0.5 Soluble Transferrin receptor (STIR) : Ferritln - Increased in IDA. It is the most sensitive
every 12 hrs to acheive
0 So. for hemarthrosis, around 20-25 IU/kg of factor VIII will be required indicator of iron deficiency by distinguishing it from anemia of chronic disease.
hemostosis. C. Identification of possible secondary cause -
- Options for replacement - (fl FVIII concentrate 1. Stool for NE, OPC — Identities GI infection (eg. Giardiasis)
(ii) Cryoprecipitate
2. Tests for malabsorption
(iii) FFP
is given every 3. Identification of source of ongoing blood loss —
- Treatment is continued for 3-5 days. till syn'ptoms subside. Then additional treatment (a) Stool for occult blood — it we — upp er GI endoscopy and colonoscopy
alternate day for another3-5 days (optional).
(b) Urine for occult blood .
3. Supportive therapy:
(c) CXFl — for diffuse alveolar hge (DAH)
(a) Control of pain — Commonly used analgesics are -
0 Treatment :
(i) Paracetamol
1. Treatment of secondary causes - Hookworm infestation is the most common cause of
(ii) Pentazocine
occult GI blood in children in niral India. So, routine deworming should be done in all such
(iii) Morphine/Pethidine (non-responsive cases) cases. Other causes. if identified. are treated accordingly.
[0 NSAIDS are contraindicated]
HEMATOLOGICAL DISORDERS E] Chapter—10 235
3. Poor absorption of Iron -

2. Oral therapy—
(a) GI infections (9.9. Giardiasis)
(8) Dose — 4-6 mg/kg/day oi elemental iron
(b) Malabsorplion syndrome
(b) Preparation - Ferrous suliate. Ferrous iumarate
and gastric HCI helps in 4. Chronic Blood loss -
(c) Timing with food - As food interferes with iron absorption
' (a) Worm infestations (9.9. Hookwonn)
absorption, it is best taken on an empty stomach or in between meals.
after complete correction oi anemia to replenish (b) Peptic ulcer disease
(d) Duration -— filmed for 2-3 months
the stores. (c) Inflammatory bowel disease (130)
discomfort etc.
(e) Side effects - Nausea. vomiting. constipation. diarrhoea, epigastric (d) Cow's milk protein allergy
used preparation.
3. Parenteral therapy - Iron dextran complex is the most commonly (e) Pulmonary hemosiderosis due to DAH
. - I] Clinical Features :
- lndicatlons— (i) Intolerance to oral iron
fii) Malabsorption 1. Most children are asymptomatic. and identified by routine screening
(iii) Noun-compliance . Irritability and anorexia are early symptoms to develop in children with IDA
PNQQPQM
0v) GI bleeding Lethargy, weakness. leg cramps
- Total dose — wt. (kg) x Hb deficit (gm/d1) x 4 Breathlessness and tachycardia (when there is CCF)
there are features
4. Blood transfusions - Vlfith concentrated BBC is generally avoided, unless Impaired growth
of congestive heart failure or Hb < 3 gm% . Compromises cognitive development and scholastic performance
5. Response to therapy -— Pica - Ingestion of non-nutritive substances
(a) 12-24 hours - Replacement of intracellular iron enzymes — led irritability. Ted appetite Signs - Include pallor. occassionally splenomegaly and signs of GOP in advanced cases
(b) 36-48 hours - Bone marrow response (initial) 9. Nail changes - Koilonychia. platynychia etc.
(c) 48-72 hours - Fleticulocytosis D Laboratory diagnOsisl Investigations :
(d) 4430 days — T in Hb level 0 Treatment : SeeQ.10.
(9) 1-3 months — Flepletion oi iron stores

O. 14 : Autoimmune hemoiytic anemia. [CNMC - 8th Sent]
Short Notes : Ans :
a. 11 : Common causes and laboratory diagnosis of iron deficiency anemia in children. [2014] AUTOIMMUNE HEMOLYTIC ANEMIA
Autoimmune hemolytic anemia (AIHA) is an extrinsic_ cause of hem 0 l tc . ' caused by au _
‘ anal-31a
10A in children. [Midnapore - 2016] FlBCs.
O. 12 : toantibody to the
O. 13 : Clinical manifestations olA in children. [Kaiyani - 8th Sent] El Classification : There are 3 common types of AIHA. namely -
1. AIHA due to ‘warm' antibodies
Ans :
2. AIHA due to 'cold' antibodies
IHON DEFICIENCY ANEMIA (IDA)
There is decrease in
3. Paroxysmal Cold Hemoglobinuria (PCH)
Iron deficiency anemia (IDA) is the mos 1 common cause of nutritional anemia.
and cause IDA. D Etiology:
iron content of the body. which is severe enough to diminish erythropoiesis
1. Warm Abtype AIHA—
' Causes :
of the most important (a) Idiopathic (Primary)
1. Inadequate dietary intake - Low overall dietary intake of iron is one
factors responsible for IDA in our country. (b) Immune disorders - (i) SLE
2. Poor bloavailabllity- ._ - (ii) Lymphoproliferalive' disorders
phos-
(a) There are various dietary factors which inhibit iron absorption, e.g. phytates. (iii) lmmunodeficiencies ‘
phates and tannates. (c) Drug-Induced- (I) Hapten mechanism (9.9. Penicillin)
than those
(b) Infants consuming bovine milk are more likely to develop Iron deficiency (ii) Temary complex mechanism (cg. Ouinine)
on breastmilk, because - 7 (iii) True autoantibody (eg. Methyl dope)
(i) Iron in cow’s milk has lower bioavailability. 2. Cold Ab type AIHA —
n.
(ii) Higher calcium concentration. which competes with iron for absorptio (a) idiopathic cold agglutinin disease (Primary)
(iii) Cow's milk allergy causes GI bloodless. _ (b) Infections (e.g. Mycoplasma. EBV. CMV. etc.)
“
\.
23$ QUEST: PAEDIATRICS HEMATOLOGICAL DISORDERS D Ci‘apter— 10 237
3. PCH -('a) Idiopathic (Primary) Characteristics

—-_.._...__,_"
Warm Ab Type Cold Ab Type PC”

(b) Donath Landstelner hemolytic anemia (after acute viral syndromes)
6. Direct Coomb’s Test
CI ltltilizril‘céllyr29:31::u2lfease is characterised by acute onset hemolysis. manifested by ~ (Common
(a) at 37°C lgG :t: 03 c3 03
(a) Weakness. postration (b) at 4°C Not needed C3 [96 + Ca
(b) Pallor
7. Ab titrc Low High Moderate
(c) Jaundice
8. Treatment — Steroid — Avoid cold ' — Avoid cold
(d) Dark urine (cola-coloured)
(e) Splenomegaly - lVlg — Plasmapheresis -— Steroid
- Another presentation with prolonged and chronic course is seen in infants (< 1 yr.) and > 12 yrs 9. Outcome May be chronic orlprolonged Short-term Short-term
adolescents, which have a poorer prognosis.
- Cold Ab type AIHA and PCH are usually self-limiting a. 15: Prognostic Factors in ALL. [IPGMEFl-Bth Sem, Meir-20161
U Investigations: Ans:
(a) Normocytic. normochromic anemia PROGNOSTIC FACTORS IN ALL .
(b) High reticulocyte count and presence of normoblasts in peripheral blood smear. ALL or Acute Lymphoblastic Leukemia is the most common childhood malignancy, accounting
,,
(c) Spherocytes may be seen for about Us" to 'A" of all childhood cancers. Overall prognosis of ALL is better than most of the
.u-rq..r.
.4.-_4...
childhood malignancies with about 80% long-term sunrivors in developed countries. The 2 most
(d) Ll-‘r —r 1 Indirect and total bilirubin. t LDH important prognostic factors include - (at) age at diagnosis and (b) the initial leukocyte count. But.
vi-'r
(e) Hemoglobinuria (urine for occult blood we, no RBCs) there are several markers which determine prognosis, which are as follows -
v'l-v—‘D-u -....
(f) Direct Coomb's Test - Positive (Detects Ab-coated RBCs)

"‘"
-
Features Good Prognosis Poor Prognosis

El Treatment :
_...‘h".r_
1 Prednisolone - 1-2 mgfkglday for 4 weeks. followed by gradual tapering over 3 months is 1-10 yrs <1 year. > 10 yrs.
-
1. Age-
.
_ ....
_
-.\.',....
I effective in 80% of warm Ab type AIHA and occassionally for cold agglutinin disease. 2. Sex- Female Male
1
2. lVlg - May be used as a second line therapy, but response is often not sustained. < 50,000 / mm" > 50,000 1 mm3
3. Initial wec count
we
3. For chronic cases - Treatment options are —

..‘.|r
at presentation -
au‘ul‘mup
(a) Splenectomy
r.-.._q.n>
4. Hepatosplenomegaly— Absent Massive f;

spharride , Cydosprine etc.)
(b) Other'urmuno expressive therapies (9.9. Azathioprine, Cyclopho
-..
Absent - . Massive
I __ I;
5. LymphadenOpathyf
_.‘__.
4. Infection-associated cold agglutinin disease —

I
..
care may be enough. Absent Present

(3) Usually have a self-limiting course and only supportive
6. Mediastinal mass-
-¢. .,. _
F's-ram.
pheresls Absent Present

(b) Severe cases may need Plasma
u- ...
7. CNS Involvement-
rill ‘ '.'ttf.f.;;‘§ :i
anemia Mature B cell Au. T-cell ALL

PRBC Transfusion - May be necessary for severe 8. Phenotype— Pre-B cell ALL
oi secondary Al HA is of paramount importance.
6. Treatment of the undet'lyin9 disease in case 9. Ploidy- Hyperploidy Hypoploidy
JI.
urn;
. .‘
J 10. Immune M510 chemistry CD-to (common ALL Ag or CD-10_negative

.1.
_
CALLA) positive
pr...
(IHC) -
.l.
AIHA :
".
N.B. : Differentiation between 3 types of (a) it9 ;- 22) [philadelphia chr.]

mmrgflfimfi
11. Cytogenetics — _ (a) Trisomy 4 81 10

PCH
Characteristics Warm Ab
_
Type Cold Ab Type IgG (b) t(12 ; 21) orTEL-AMLt moon (b) tit; 1 1) [intarrtiie ALL]-
lgaM 4°C (6) Hox11 Rearrangement (clfilfli 14) [Burtit leukemia]
lgG
1. Ab lsotype
' ’ 37°C 4C (d) in ; 19)
2 Temperature Yes
12. Response to treatment- V Good early response Poor early response
(Threshold tor hemolysis) P Ag
Variable Yes PDsifiVQ f: .
3. Cornplement fixation 13.Mlnlmal Residual Disease Negative
I r
Flh Ag lfi A9 (MRD) after first induction -
4. Ag specificity lntravascu a
Extravascular lntravascular '-_
5 ' Site of hemolysis

x...-
‘._‘
-.
Scanned
Scanne d by CamScanner
it
1“
“us-um.
HEMATOLOGICAL DISORDERS El Chalet-10 239
41..
- Dose - 30 mglkgfday
a. 16: Chelation therapy In thalassemia. [HMO-9U! Sam, MEMO-8th Sam]
”'
' Adverse effects — (a) Skin rash, (b) Nauseafvomiting (c) Renal and hepatic toxicity.
Ans .-
4. Combination therapy -— Additive and synergistic effects of combination of iron chelators can be
CHELATION THERAPY IN THALASSEMIA explained by ‘Shuttle' hypothesis. A bidentate (Defen‘prone) or tridentaie (Deferasirox) ligand acts
in chronic hemolytic
Thalassemia is a type of congenital defect in globin chain production. resulting as a shuttle to mobilize iron from tissue to blood. where they get bound to a larger hexadentate
of thalassemic children. as It rm-
anemia. iron chelation therapy is an important aspect of treatment (Desferrioxamine) ligand for excretion.
proves life extectancy and quality of life. a. 17 : Clinical manifestations of ALL in children. [CNMC — 9th Sam]
El Rationale : l‘lhalassemia I Ans :
CLINICAL MANIFESTATIONS OF ALL
‘ ALL is the hematological malignancy that arises from clonal proliferation of abnormal hematopoi-
° Chronic hemolysis etic cells of lymphoid series (Lymphoblasts).
’ 'D Pathogenlsis : Clinical features of ALL are mainly attributed to two factors —
° Ineffective erythropoiesis
(8) Bone marrow failure due to infiltration by leukemic cells.
Need for recurrent (b) Extramedullary involvement.
Blood transfussions El Manifestations:
Ted iron absorption 1. Duration of symptoms may vary from days to weeks to few months (in some cases).
through GIT
2. Anorexia, fatigue, irritability and weight loss are often present with occassional low-grade
fever. (Prodromal symptoms).
3. Pallor, fatigue with exercise intolerance (due to depression of BBC series) is a common
IFiON CHELATORS
L‘L—
, l
presentation.
e 4. Recurrent or continuous fever (due to depression of WBC series) may be found with signs
of infections.
l - ' l . . .l . 5. Petechiae, bruising or epistaxis (due to depression of Platelet se ries).
I i l
dysfunction
Hypoparathyroidism Cardiac dysfunction Liver 6. Musculoskeletal involvement —
Hypopituitarism Diabetes Hypothyroidism
(a) Bone painI that may be severe enough to wake the child at night (objective sign —
l Stemal Tenderness)
- Growth failure (b) Joint swelling 1 Arthritis - may be tst presentation. 1..
- Delayed sexual maturation 7. Extramedullary involvement— (Reticulo endothelial system)
.
accumu lation in the body; _
usually
' of chelation : Depends on amount of iron
'
(a) Hepatomegaly
tion rs Serum Ferritrn > 1000
D armggg ro‘r’ gmm sfus ion is given for 1.2 yrs. Classrcal Indica (b) Splencmegaly > in > 60% cases
1500 pglL. .
. . (c) Lymphadenopathy
lators : Com mon ly used tron chelators are —
0 Iron Che al practice, adml nlstered parenter- 8. Respiratory distress — May be due to severe anemia or compression of trachea by thymus
earliest iron chelator used in clinic
1. Desferrloxamine - It is the [large mediastinal lymph node. (Superior Mediastinal Syndrome)
ally, and most effective. 9. SVC Syndrome — It may be a part of SMS or may occur alone with- compression of SVC
S.C. for 5 days in a week.
- Dose — 40-60 mg/kglday OVGI' 8-12 '1 ours at night (Superior 'Vena Cava) producing —
tions
° Adverse effects - (a) Local reac (a) Facial puffiness
(b) Auditory and visual toxicity (b) Dilated neck veins.
(c) Growth retardation (c) Conjunctival congeticn etc.
‘ costly than desferrioxamine.
less
iron chelator, less effective an d - 10. CNS Involvement — (5%)
2. Deterlprone - it is an oral
(a) Signs of raised lCT.
0 Dose — 75-100 mgrkg/day (b) Cranial nerve palsies
Arthropathy .
- Adverse effects - (a) " (c) Seizures
(b) NeutropenialAgran uloc ytos rs
' comparable to desf errioxam lne. 11.Testlcular involvement - (<1%) Firm. painless. unilateral or bilateral testicular swelling.
with efficacy
also an oral chelating agent cellular deposits of iron. 12.Tumor lysls syndrome — Seen in patients with high tumour burden and presents with
' h'gh
3' rs . both intracellular and extra
r l;';:fectilviesfor iron and chelates oligurla and azotemia.
240 QUEST : PAEDIATFIICS HEMATOLOGICAL DISORDERS CI Chapter—IO 241
nnnnmnnA/‘Anm
Management of HP.
[asuc - 9th Sent, NBMC - 9th Sam} E] Radiological features : Includes marrow hyperplasia. osteopenia 8. extramedullary hematopoiesis.
0. 18:
{MCK - 9th Sent} I. X~rays —
0. 19 : Diagnosis ofacute fTP.
(a) Skull (Lateral View) - Widening of the diploic space (medulla) with a thinning of the
Ans: -
tables (cortices) occur. frequently with completed obliteration of outer table.
MANAGEMENT OF ITP ' New bone formation beneath periosteum with thickening of the Irabeculae are seen
See 0. 4 as bony spicules.
DIAGNOSIS OF ACUTE ITP
' These features together forms classical “hair on end" appearance over the frontal
laboratory diagnosis.
Diagnosis of acute ITP involves both clinical diagnosis and supportive and parietal bones.
0 Clinical diagnosis : Diagnostic clinical features include— (b) Thoracolumbar spine (AP view) — Generalised osteopenia with thickened primary
etc.) in a healthy
1. Sudden onset of bleeding (petechiae. bruises. epistaxis. gum bleeding trabeculae results in striated appearance of vertebral bodies.
child of 1-5 years age. (0) Obliteration of pneumatization of paranasal sinuses.
may be found.
History of a preceding viral infection 1-4 wks prior to the onset of symptoms (d) Premature fusion of the epiphyses may be seen.
99°03
Pallor may be present, but will be proportionate to the degree of bleeding. 2. USG (Abdomen) - May show gallstones.
should be there.
No significant hepatosplenomegaly. lymphodenopathy or bone pain 3. CT Scan I MRI — Indicated to detect iron overloadl iron deposition in liver and heart.
bony anomalies or hyperpigm entation.
5. There are no dysmorphic features, 0 Other features :
El Laboratory diagnosis : See 0.4. (Investigations) l. LFT — Elevated unconjugated bilirubin.
of Thalassemia Major.
0. 20 : in vestigation ate 1 year old child with clinical diagnosis 2. Ferritin — Increased (upto > 1000 — 2000 in later stages after multiple transfusion).
[KPC- 8th Sent] 3. Serum Iron, Transferrin Saturation — Tes simultaneously with ferritin.
4. Screening for Bloodvbourne infections - HBV. HCV. HIV etc.
[BMC - 2016]
Hematological and radiological changes in fl-thalas
sernr’a.
a. 21 : [N.B. For answering Q. 19. where age is 1 year. complication like iron ovedoad, hypersplenism
[Murshidabad - 2016] etc. should be omitted from answer.]
a. 22: Radiological changes in fi-thafassemia major.
O. 23 : Clinical features of Chronic Hemolytic Anemia. {Midnapore, 9th 39m]
Ans :
INVESTIGATIONS 0F THALASSEMIA MAJOR Ans:
emia Syndromes. characterised by chronic ongo- CLINICAL FEATURES OF CHA
Thalassemia major is the severe form of Thalass
from bone marrow.
ing hemolysis and ineffective erythropoiesis Chronic Hemolytic Anemias are characterised by—chronic or ongoing hemolysis usually since
ll
birth. as the causes are mostly hereditary. Common causes are - thalassemia syndrofites sickle
D Hematological features :
cell anemia. hereditary spherocytosis. HbE disease etc. + I
1. Hb% - Low (2-8 gmidl)
El Symptoms :
2. RBC count - ® or increased
‘AAAA-tnn
by t. Egogrrgsssirlitéeugzll—or — It IS the most common presenting feature of CHAS. Accompanying
penia may be found in cases complicated
3. TLC - Leukocytosis is the usual finding. Leuko
hypersplenism. (a) Easy fatiguability
ure leukocytes occassionally.
4. DC - Un markable. except - presence of immat (b) Weakness
m.
5. Platelet count - Low in do hypersplenis (c) lrritability
- Elevat ed (5-8% ).
6 . Reticulocyte count (d) Anorexia
microcytic and hypochromic
7 . Peripheral Blood Smear— (a) RBCs are (e) Shortness of breath (in severe pallor)
(b) Nucleated RBCs seen.
sional. . Growth failure (t for age. lht for age)
SOPNPSnfhwrx-i
(c) Fragmented cells, Tear drop cells -— occas
. . Recurrent Infections with fever
(d) Basophilic stippling may be found
Decreased scholastic perfomtanoe
IT.
a. nec lndlces — ucv I. MCH l. MCHC t, FIDW— ® Need for recurrent blood transfuslons
9. HPLCIHb Electrophoresis j- Enlargement of abdomen
(a) HbA - Decreased r Absent Jaundlce
(b) HbF — Elevated Hyperplgmentation (in later stages due to iron overload)
(c) Hb‘A2 - Elevated Recurrent painful episodes (including chest in limb a‘ ' ' . .
sickle cell anemia pa ' p '"'°"ap'5"‘ etc-l-espwallym
31
-—=‘-a'~=+fi§
242 QUEST : PAEDIATHICS HEMATOLOGICAL DISORDERS U Chapter—10 243
5. aP'l'T - Prolonged
0 Signs:
with severe anemia, like — 6. vWF assay - for confirmation and classification
1. Anemia — Mild to severe; signs of heart failure in cases
CI Treatment :
(a) Tachycardia. Tachypnoea. Water hammer pulse
1. Type 1 vWD — may benefit from intranasal desmopressin acetate (DDAVP)
(b) Gallop rhythm
2- Type 2rrype 3 vWD — u sually "99d VWF rl‘ilJlacement therapli (commonly done with cryo-
(c) Systolic flow murmur precipitate)
(d) Tenderness in liver
O. 25 : 0/0 of microcytic hypochromfc anemia. {MCK - 9th Se
(9) Raised JVP, Edema
ted liver disease sets in ( due to blood- 0. 26: Microcytic Hypochromr’c Anemia.
2. lcterus -— Usually mild; may be severe. it associa [KPC 20:3;
boume infections) Ans : MICROCYTIC HYPOCHROMIC ANEMIA
3. Hemolytic Facies - (also known as “Chipmunk facies")
In peripheral smear examination wh m' cc -
' . .
(a) Frontal bossing

RB
hromic, 't '5 termed as

I an
microcytic hypochromic anemia.

C
CS appear l ytic and hyp
(b) Prominent maxilla
[J Confinnatlon : Confirmed by measurement of RBC indices .—
(c) Hypertelorism
(a) MC)! - Low (Microcytic)
(d) Depressed nasal bn’dge
(b) HCH - Low (Hypochromic)
(e) Dental malocclusion
(c) MCHC - Low
4. Hepatomegaly — Usually firm. moderate to
severe.
of hepatomeg aly (Thus, combinely called 0 Causes : 1. Iron deficiency anemia (IDA)
5. Splenomegaly — Firm. more than the degree
2. Thalassemia syndrome
splenohepatomegaly)
e commonly known as "triad" for CHA. _ :45. Hemoglobinopathies (HbC, HbE disease. Sickle cell anemia)
El Anemia. Jaundice and Splenomegaly er . nmnycahgnfigomc inflammation or disease (more commonly normocytic and
[Malda - 2016]
a. 24 : von-Willebrand disease.
VON-WILLEBFIAND DISEASE 5. Sideroblastic anemia
Ans : it is inherited 6. Lead poisoning ] (Flare)
common hereditary bleeding disorder, and
von Willebrand disease (MD) is the most ' El Differential diagnosis:
n equall y.
autosomally. So, it affects men and wome rand Factor (vWF). - Mlcrocytic, Hypochromlc Anemia
to deficient or defective action of von Willeb
D Pathophysiology : vWD occurs due are as follow s — (MCV < co fL. MCH < 28 pg. MCHC < 30%)
stasis . which
vWF has significant roles in normal hemo the injured site.
ged) and helps in platelet adhesion to l
1. vWF adheres to the endothelium (dama fibrinogen to Normal or Low «— _—+
ets, which intera cts with High
n by activating platel
2- vWF helps in platelet aggregatio
form cross-linkin g. l " l
for plasma factor VIII. l '0" studies
3. It also serves as the carrier protein et plug tonna-
Hb Electrophoresis or HPLC
in vWD, there are-(a ) defective platel
' Thus. during deficient activity of vWF
of F-Vlll .
tion and (b) secondary deficiency Low Iron A n" : ll
Low Ferritin ’ Low Iron “Mm Iron H I . HbS)
0 Classification : ”“1 “BC Ill/Him Femtin N/LowTIBC (HbC. HbE, thy
tion of vWF (MO: > 85%)
1. Type 1 W10 - Quantitative reduc t type vWD) Low TS (Transferrin saturation) M0" “80
abnormal vWF. (includes platele ., l Him Ferritin
— '-
i
2. Type 2 WW — Qualitatively
3. Type 3 vWD - Absent vWF vWF activity, most of the
m
I _ _ ESFt, CRP 1' -
MC, where there is only reduction of
(Iron deficiency) A Hb Electrophores rs or H PLC
is
CI Clinical Features : As type 1 vWD ly symptomatic. _ .
or mild
patients remain asymptomatic bmis ing, epista ids, meno nhag ia etc. _
are seen inducing excessive 1? Elevated Normal
(a) Mucocutaneous haemonhages extraction , tons illect omy etc. Free Erytlmcyte Pmloporplwm
' (FE?)
parlicularty after tooth . J, I Abmflnal ”0"“31
(b) Post-operative hemorrhages. 3 detect.
r blee ding, like intra cran ial haemorrhage is seen only with type Inflarrmatory Anemia of 1
(c) Majo J,
0 Laborawttgry‘ findings : > 70 note >160 pgldl “m” m”"°'“°
se
Thalassema‘ Sideroblaslic'
-type vWD 1 1 suggests
et count — Low in platelet
Syndome Anemia
.
' ' (Ring sidemblasls.
-_- t lronstain'nBM)
\. ‘-
\
'I-
. #TV}
dentscanner
r_.____¥
HEMATOLOGICAL DISORDERS [3 Chapter —10 245
[2009] 4. Iiriidney biopsy - Confirms diagnosis of HSP. SLE, if associated ranal involvement is
a. 27 : Vascular Purpura.
ere.
Ans :
VASCULAR PUHPURA 5. Cortisolvlevel - Raised in Cushing disease.
wall or its supporting 6. X-ray of limbs - show features of scurvy.
When purpura occurs due to vascular causes, :29. disorders of the vessel
structures, it is known as vascular purpura. O. 28: NutritionalAnemla. [Haida - 2016]
El Causes : Ans:
1. Vasculitis- NUTRITIONAL ANEMIA
(a) Henoch Schonleia Purpura (HSP) ygsntional anemia refers to the types of anemia that can be directly attributed to nutritional disor-
(b) Systemic Lupus Erythoneatosus (SLE)
(c) Microscopic Polyangitis (Micro PAN) El Types : 1. Iron Deficiency Anemia (MC)
2. Abnormalities of Collagen - 2. Megaloblastic Anemia — (MA)
(a) Ehler Danlos Syndrome (Hereditary) [EDS] (a) Vitamin B“, deficiency
(b) Scurvy (b) Folic acid/Folate deficiency
(c) Cushing disease El Pathogenesis : (a) lDA —- iHb synthesis, (b) MA - iDNA synthesis -— lcell division
(d) Prolonged use of corticosteroid [I Etiologies:
(e) Severe malnutrition . 1. Inadequate dietary intake —
3. Vascular malformati ons — Hereditary Hemorrhag ic Telengieclasia. (a) iron - Poor intake of iron-rich foods
e of normal hemostasis,
Ct Pathology : As vessel wall is an important component in the maintenanc (b) Bu - Lactovegetarians, Lacto-ovo-vegetarians, Vegans suffer from B deficiency
s of the vessel wall cause bleeding manifestati ons (like purpura, petechiae and (c) Folate — Goat milk feeding
abnormalitie ‘2 l
Thus, defects in
eochymosis). Collagen matrix Supports blood vessels and maintains its integrity. (d) Generalised malnutrition (PEM)
collagen also result in purpura.
2. Poor bioavallabillty—
El Diagnosis:
with purpura, when- (a) Phytates, Phosphates and Tannates in diet impair bioavaila
1. Confirmation of diagnosis - Vascular purpura is suspected in any child bility of iron
(b) Bovine milk ingestion results in poor iron bioavailability
(a) Platelet count — Normal ' .
3. Poor absorption - Fe B and FA - .
(b) Platelet function — Normal malabsorption syndromes. 12 are poorly absorbed In association with various
(c) BT - May be prolonged 4. WEISS anemia — Lack of lntnnsic Factor (IF) in gastric
secretion leading to poai'absorption
(d) CT, PT, aP‘iT— All normal
' Skin biopsy often helps in diagnosing vascular pathologies. El Clinical Features:
I
2. Differential diagnosis— 1. Symptoms and signs of anemia —
(a) From clinical features - . (a) lrritability '
arthritis, abdominal pain
1. HSP - Palpable purpura in lower limbs and buttocks, with (b) Easy latiguability
and oocassio nally renal involvem ent. (c) Weakness
renal involvement, serosi
SLE - Photo sensitivity, malar rashes. oral ulcers, arthritis, (d) Pallor .
tis etc. suggest SLE. (9)
(r) Poor
Impaire
attention
d gr(Wh5o an and scholastic
ility, scarring etc. suggest ‘ performance
I
EDS -— Hyperelastic skin, Lax joints with easy sublaxab
.
EDS. (9) Breathlessness (in severe anemia)
Scurvy - Gum bleeding, loosening of teeth, bone pain, scorbutic rosary are associ-
‘ were-sore Pica ‘ ,
ated in scurvy.
Nail changes I m IDA
5. HID Corticosteroid use for prolonged period.
Glossitls, Stomatitis
6. Malnutrition
Hyparpigmantation of Knuckles J in MegaloblasticAnenfia
(b) From investigations -
1. Acute phase reactants - (ESFI, CFlP) Ted in vascuiitis. . Neurological signs-
2. Antinuclear antibody (ANA) —- Positive in SLE. (a) Loss of position and vibration sense (earliest
sign)
3. ANCA — may be positive in Micro-PAN. (b) Memory loss, confusion etc. .
246 QUEST 1 PAEDIATRICS
Cl Laboratory Evaluation:
1. Complete Hemogram — CHAPTER — 11
-
(a) Hb% - Low
(b) RBC count — Low GENITO — URINARY SYSTEM
(0) RBC morphology— (i) Microcytic in IDA
(ii) Macrocytic in Megaloblastic Anemia
[ions oussnofi
(iii) Anisocytosis > in both
(iv) Poikilocytosis 0. 1 :Describe the c]! and War of minimal change Nephrotr'c Syndrome
. (2013 supple)
((1) W30 - Hypersegmented Neutrophils in MA Ans: 95% of childhood nephrotic syndrome is primary or idiopathic.
(e) Platelets — May be reduced in MA 80% of these idiopathic Nephrotic Syndrome shows minimal or insignifica
nt changes under light
(f) RDW — High microscopy, they are called Minimal Change Nephrotic Syndrome.
(9) NOV — Low in IDA (< 80 fL). High in MA (> 100 fL) 0 Clinical Features : Usual age of presentation 2 to 6 years.
2. Confirmation of IDA - Symptoms :

(a) Ferritin — Low > Onset lncidious
-
> Facial puffiness specially at morning then progressing to involve
(b) Iron — Low whole body ~generalised
swelling.
--
(c) TlBC -— High

4" if.
) Diminution of urine output.

(d) Transferrin saturation - Low
Signs :
-!
3. Confirmation of MA —
> Oedema present; pitting type. Pedal. parietal, facial oedema, scrotal
(a) Vit. B,z Assay swelling.
>Ascites present usually
(b) Folate Assay > Blood pressure is normal.
(0) Bone Marrow Examinations - Megaloblasls .
>Hydrotherax may be present.
(d) Schilling Test — For diagnosis of vit. B12 malabsorptron El Management :
(1F deficiency in Pernicious Anemia) (a) .lnvestigation :
. .
0 Treatment : ' Routine urine examination :
1 For IDA - Iron supplemen tation with oral Iron, IV iron or blood transfusion
> 3+ to 4+ (Nephrotic range) proteinuria.
2. For MA — (a) Vit. Bu — 250—1000 (19 IM daily x 1-2 wks —> weekly > Hyaline. granular casts.
(b) Folate — 1—5 mg orally daily x 3-4 wks. > Pus cells +l— .
3. Dietary supplement - of Iron. B12 li- FA. it possible. 0 Urinary culture and sensitivity : To rule out or confirm infection.
' Blood cholesterol, albumin:
> Cholesterol (> 200 mg/dl), Triglyceride and LDL increase.
> Total protein and albumin decrease < 2.5 grn/dl and < 1 grnldl
in severe cases.
' Blood urea and creatlnine : '
> Usually normal.
' Blood Calevel : Normal.
' Renal Biopsy : Not routinely indicated in all cases to confirm diagnosis
.
Indication : Atypical features :
(l) Age < 12 months .
(ii) Gross or persistent microscopic hematuria
(iii) Hypertension
(iv) Low blood C3
(v) lnpaired renal function
a... \H 247
‘\
Chapter-11 249
248 QUEST I PAEDlATFllCS GENITO-URINAFIY SYSTEM U
Effacemenl of Diffuse proliferation of all components of glomeruli

Finding : Light microscopy — No significant abnormality. Electron microscopy —-
epithelial foot processes.
Obliteration of glomerular capillary lumen
AAA‘AA-
' Chest x-ray, Mantoux test. ESFl — to exclude TB. l
Less renal blood flow to glomeruli
Cl Treatment : t
- Steroid : Mainsfay of treatment of nephrotic syndrome is oral steroid, prednisolone. Less GFR.
Dose —+ 2 mg/kg in divided doses daily for 6 weeks then 1.5 mg/kg as single morning dose on D Pathogenesis of PSGN:
alternate days another 6 weeks. Clinical features :
0 Antacid or H, blocker or proton pump inhibitor: To counteract the gastritis inducing side effect ‘ ' Oedema -) Earty morning periorbital to generalised oedema latter
of prolonged steroid therapy. ' Haematuria -} Gross or microscopic
' Diet : High protein diet and adequate calorie. ' Hypertension «9 May present with complication of hypertension like heart failure,
encepha-
> Salt should be restricted to the amount usual in cooking, no extra salt. lopathy
0 Infection : If any to be treated before starting steroid therapy. ' Oliguria —i May progress to frank renal failure
0 Tuberculosis : Should be ruled out before starting steroid therapy. 0 History —-) Pharyngitis to - 14 days back. Skin infection 2-3 wks back in form of pyoderma.
Basic pathology and pathogenesis :
' Diuretic : Usually not recommended in every cases.
Basic pathology — Glomemlar injury responsible for symptomatology of PSGN.
> Restricted use for patients with significant oedema
spirono- Mechanism - The exact mechanism of glomerular injury is not known. Probably it is immune
> Frusemide (1 «4 mg/kg/day in divided doses) orally alone or with Aldactone antagonist
“Ann
complex mediated.
lactone (2-3 mg/kg/day in 2 divided doses). Oral routine is preferred than parenteral.
Streptococcal M antigen
> Should be used judiciously and cautiously. l
very low serum albumin.
' Albumin infusion : If significant ascites and refractory edema with Antibody to M antigen
with 20% albumin transientl y increase serum albumin.
therapy 1
Response to steroid therapy : Usually within 10-14 days. Immune complex formation
> Diuresis l
> Loss of edema Molecular mimicry between streptococcal antigen and glomerular tissue (autoantigen)
> Abolition of proteinuria
I.
urine heat test. pulse, blood pressure (in Immune complex formation and deposition in glomerular tissue
Monitoring : Daily measurement of urine output, weight,
hospitalized patient).
I”.
nce of therapy Activation of complement system and inflammatory cuscade
Parent education : Very important to ensure the complia
therapy , regular urine examination for proteinuria t .
> Education is about the disease, duration of
Damage to glomerular basement membrane and adjoining cell component —> Haematuria
n
Ac.PSGN? Describe the undenying patho-
0. 2. What is glomerufar filtrat ‘on? How it is affected in l
nism for the c finicaf picture of PSGN. [2008]
genic mecha Diffuse proliferation of glomeruli leads to obliteration of glomerular capillary lumen
A
the mecha nism by which fluid composed of crystalloids, low i
Ans : Cl Glomerular Filtration : It is amino acid are filtered from glomerular
molecular weight substances such as urea, glucos e,
h glomerular filler, composed of endot helia
.
l cells j
Decreased GFFl
P Oliguria and renal failure l
A
capillary tuft to bowman's capsule throug
m2. ‘
Normal Glomerular Filtration Flule (GFR)
— 100 to 125 ml/min /1.73 Enhanced Na‘ and water retension in distal and collecting tubules -—>
t
rulonephritis there is symmetrical enlargemen l
Glomerular Filtration in Ac.PSGN : In acute glome
‘
d. There is esse ntially diffus e and generalized proliferation of Expansion of extravascular fluid volume
of kidney. Glomeruli appear enlarge
of inflammatory cells like PMN. T lymphocyte, l
all cell components of glomeruli with invasion
‘
Hypertension
macrophages.
to
ion of glomerular capillary lumen leading
This diffuse proliferation of glomeruli causes ob literat ion of fluid leading to reduced Complication
of filtrat
‘
less blood flow to glomeruli and consequently reduc tion
— Hypertensive cardiac failure '_
glomerular filtration.
— Hypertensive encephalopathy.
32 ' «-3
250 QUEST : PAEDIATRICS GENITO—URINARY SYSTEM El Chapter—11 251
O. 3. Define Nephrotic Syndrome. How do you investigate and manage a case of let attack of — Asciles
Minimal change Nephrotic Syndrome. (MCK, 8th sem) — Pleural effusion
- Anasarca.
Ans : III-Definition : This is a syndrome characterised by heavy proteinuria (> 40 mgim‘ihour). hypoalbu-
mrnemia (serum albumin < 2.5 gmidl). hypedipidemia (serum cholesterol > 200 mgidl) and oedema. Treatment:
El Investigation and management: See question 1. 0 Steroid itself acts as diuretic but takes 5-10 days to work.
- Frusemide :l: spironolactone orally.
0. 4. What is Nephrotic Syndrome? Pathogenesis of oedema formation in Nephrotic Syndrome. in urine.
Discuss the management of Frequent Relapse Nephrotic Syndrome and complications asso- - IV 20% albumin — For refractory oedema but effect is transient as albumin rapidly lost
s diuretic therapy in larger dosescan cause hypovolem ia and precipitate
ciated with Nephrotic Syndrome. Caution : Overzaleou
|
renal failure. '
Ans : D What is Nephrotic Syndrome : See question 3.
I3 Pathogenesis of oedema formation in Nephrotic Syndrome : (ii) infection : Frequent complication of nephrotic syndrome.
Exact mechanism of oedema formation in Nephrotic Syndrome is not clearly understood. However Cause:
proposed theory is as follows. - Urinary loss of factor B and immunoglobulin.
Massive urinary protein loss — Defective opsonization.
i — Prolonged immunosuppressive therapy.
Decrease in plasma oncotic pressure Organisms - Steptocoocus pneumonia.
l I - Gram negative organismsivaricella.
Escape of fluid from intravascular to interstitial space. Mycobacterium Tuberculosis.
i Clinical Presentation - Cellulitis
Diminished intravascular — Peritonitis
v'olume - Pneumonia
— Meningitis
l
l l -— Urinary tract infection.
preferably guided by
Stimulation of Antidiuretic Treatment - Prompt initiation and adequate course of antibiotic therapy
Diminished renal perfusion report.
hormone release culture sensitivity
pressure for 4-6 weeks.
i. immunization - Pneumocoocal and varicella vaccines. once the patient is off steroid
1
n ol nephtrotic
Activation of renin angiotension- Act on collecting tubules (iii) Coagulation abnormality : Thrombosis of major veins and arteries is a complicétio
J, ‘
aldosterone system syndrome.
Increased absorption Causes:
- l
Tubuler reabsorption of sodium
of water — Urinary loss of clotting inhibition (protein C and S) protein.
J — Increased platelet aggregation.
and water
l — Aggravated by use of diuretics. hypovolemic state.
t
Clinical Presentation :
——> Oedema
- Renal vein is the commonest site.
Management of Frequent Relapse Nephrotic
Syndrome : - Major arteries (femoral. mesenteric) axillary and subclavian veins.
Cl
ement of steroid dependent nephrolic syndrome). — Cerebral veins.
See question - 12 (Same as manag s) in
(urine albumin 3 + [4 + on 3 consecutive sample — Pulmonary venue thrombosis.
Frequent Relapse - Two or more relapses
initial 6 months-or more than three relapses in any 12 month s. Treatment :‘ 5
— Correction of dehydration
:
E] Complications of Nephrotlc Syndrome - Use of heparin followed by oral anticoagulant.
me.
is a frequent complication of nephrotlc syndro
(i) Oedema : Massive oedema and anasarca e whlch in turn causes (iv) Acute Renal Failure : It is not frequent complication of Nephrotic
Syndrome.
s, dimini shed inlrav ascul ar volum
Cause: Massive urinary protein loss cause Causes:
sodium and water retenion.
— Acute gastroenteritis with huge amount of fluid loss.
Clinical Features :
- Over treatment with diuretic.
— Massive oedema .\
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[3 Chapter-11 253
252 QUEST : PAEDIATHlCS GENITO-URINARY SYSTEM
Clinical Presentation : (viii) Chest x-ray P-A view:

Prelrenal type of acute kidney injury. — Prominent - vascular marking due to hypervolemia.
- Abdominal pain - Cardiomegaly. pleural effusion may be present.
— Hypotension (ix) USG abdomen :
—Tachycardia — Bilaterally enlarged kidneys.
-Cold extremities — Mild parenchymal changes.
Oligurialanuria.
—- (it) Renal Biopsy: Not routinely indicated.
Treatment ~— Rapid infusion of normal saline. El Complications:
(v) Steroid Toxicity : On long term steroid-therapy. (a) Hypertensive Encephalopathy : tension
ofAcute PSGN. Undiagnosed hyper
A complication and often a clinical pr esenlation halop athy.
results in encep
— Growth retardation or a consequence of failure to monitor blood pressure
- Hypertension Clinical feature :
- Cushingoid features — Repeated convulsion.
— Bone demineralization. - Unconsciousness
— Posterior subscapsular cataract. - Very high blood pressure.
(vi) Acute fiypovolemic shock : Precipitated by vomiting. loose motion over enthusiastic diuretic Treatment:
use. —— Control of seizune by anticonvulsant.
- Sublingual/oral Niledipine.
a. 5. A 7 year old boy presented with the swelling of the whole body starting in the face and
- l.v LabetalollNitroprusside.
scanty reddish urine for last 3 days. There is No tears pustules oi the leg 3 weeks back. a:
What is your provisional diagnosis? What investigation you like to do? Name the dreaded (bl Left ventricular failure and pulmonary oedem
tation or complic ation of disease. It occurs due to
complication of the disease. Briefly outline the management of the patient. This may present as manifes
(’BSirll"I Semi - (i) Hypertension
Ans : Cl Provisional Diagnosis : Acute Post streptococcal Glomerulonephritis. (ii) Hypervolemia
El Investigation: Clinical features :
(i) Urine analysis : -— Respiratory distress.
— Tachycardia. gallop rhythm.
- Mild to moderate proteinuria. usually upto 300 mgldl (1+ or 2+) __
— Basal crepitations in lung.
— Dysmorphic BBC. BBC cast. WBC. hyaline cast.
Treatment— |.v Furosemide 2-3 mghcg.
- White cells indicate glomerular inflammation rather than UTI. (c) Renal Failure : Patient may present with progressive oliguriai
anuria or frank renal failure.
(ii) Blood Urea, Creatinine : Treatment — Mild to Moderate — Conservative manage
ment.
— Increased with increasing oliguria. Severe — Dialysis.
-— May be normal.
El Management of PSGN :
(iii) Blood Electrolyte :
(a) Hospitalization:
d at home.
—_-.
- Hyponatraemia
a Mild — Mild oliguria and Normal blood pressure can be manage
-—.-
- Hyperkalemia a Severe —- Children with moderate oedema

and impairment of renal function.
— They develop as there is increased oliguria - Anuria or oliguria.
(iv) Haemoglobin : - Hypertension andlolr its complication.
— Usually low due to hemodilution. - Renal failure.
‘
(v) Serology for streptococcal infection : Hospitalization is needed.
cases
(b) Rest : Strict bed rest is not essent ial in mild to moderate case but necessary in severe
— Asotiter increased
— Anti—DNase B is likely t 0 be elevatedas this
case of PSGN is following skin infection. with complications.
ess and urine out in 24 hours.
(vi) Throatswab culture: (c) Fluid intake: Restricted to insensible waterl .
should be restricted in presence 0| oliguria
— Likely to be negative for streptococci. (it) Diet : Protein. sodium and potassium intake -
hypertension and renal failure.
(vii) Complement 03 level :
.
- Usually low but usually normalized by 5-6 weeks x.“-
“-..
(BENITO-URINARY SYSTEM El Chapter—11 255
254. QUEST : PAEDIATRICS
- Facies : Facial pulliness likely to be present.

(e) Diuretics : Mild to moderate oedema — restricted salt and water intake and oral Furosemide
1-3 mglkg. . Pallor : Present.
Pulmonary oedema — l.v. Furosemide 2-4 mglkg. - Oedema : Present but usually turgid type.
(0 Hypertension : Mild Hypertension — salt and water restriction. ' JVP : Raised in presence of pulmonary oedema and heart failure.
Antihypertension — Calcium channels blocker (Amlodipine. Niledipine). 0 Respiration : Tachypnea in pulmonary oedema.
— Atenolol - Pulse : High in left heart failure.
— Furosemide - Blood pressure : Likely to be increased.
Hypertensive Emergency _ I.V. Labetalol/Nitro preusside.
‘ - Skin : Marks suggestive of streptococcal skin infection-may be present.
Gentle-urinary System : BIL kidneys can be palpable if grossly enlarged.
(9) Left ventricular failure : Fluid restriction and LV Furosemide. on following inves-
n is good choice. investigation : After taking detailed history and thorough clinical examinati
(h) infection : If present promptly treated with antibiotics. AmpicillinlAmoxycilli
above with monitoring of tigations can be done to confirm the diagnosis.
(i) Renal failure : Mild to moderate — Conservative treatment as mentioned
Investigations — See question no 5.
blood urea. creatinine and electrolytes.
periorbitai region with decreased urine
Dialysis : Indication — a. 7. A 5 year aid male child presented with puffiness of
week back. Discuss diagnostic
- Severe Hyperkalemia output following an episode of fever and cough one
approach and treatment. [SDMC]
- Acidosis
d urinary output following an episode of
— Uncontrolled hypertension Ans : 5 year old male with periorbital puffiness with decrease
fever and cough one week back.
- Pregressive renal failure. lo-nephritis.
Provisional diagnosis : Acute Post Streptococcal Glomeru
ap-
cola-cola ured urine with oedema. How will you
0. 6. 5 year old boy presented with oliguria, El Diagnostic Approach : See question no 6.
proach this case? [BSMCKs‘ Sem) El Treatment : See question no 5.
urine + oedama.
Ans 5 year old with oliguria + cola-coloured
: duration. Discuss the possible differential
me/Acute Glomerulonephritis. a. 8. 4 year old girl presented with haematuria of 1 week
Provisional Diagnosis : Acute Nephri Syndro
tic
diagnos is and manage ment of UTI. (CNMC) , (8" Semi
El Approach : 1 week in a 4 year old child are -
Ans : 0 Possible differential diagnosis of haematuria for
0 History : Causes of Haematuria - See question no 22.
,.
' Oliguria : Duration 0 Management of UTI : See question no. 24. u-
.
Amount (if possible) of urine in 24 hours Nephron. Mention the laboratory diagnosis of
in AGN. 0. 9. Describe the functions of different parts of
Mild to moderate oliguria is common nephrotic syndrome. (2017)
o Cola-coloured urine : Duration
of AGN. Ans: - Parts of Nephron
Cola-colour urine is characteristic
0 Oedema : Dura tion Nephron
— Site of first appearance I
. ' '
F t
— Progression morn ing peno rbltal puffi- Flenal Tubule
ma in early stage prese nts as early Malpigian Corpuscle
In acute nephritis syndrome oede |
involve the legs.
ness to gradually progress to n like I , l 1
diagnose impending complicatio
ulsion, respiratory distress — to Proximal Convo- Loop olHenle Distal Nephron
c History of headache, conv failure.
.
Glomerulus :‘Bowman's
or heart
hypertensive encephalopathy to diagnose acute glomerulo- ’ Capsule luted Tubule I
tion. skin infection - in recent past, likely
' History of throat infec F— l, l
l infection.
nephritis after streptococca ”Descending Hairpin Ascending
Examination : limb bend loop
l l
General examination : . I
nose encephalopathy. Distalconvaluted Connect Collecting
0 Higher function : To diag hypertensrve heart failure/p
ulmonary
ing tubule system
us : Change s with pres ence of tachypneo due to ' tubules
' Decubit
oedema.
CamScatmer
I
i
GENITO—URINARY SYSTEM EJ Chapter—11 257

t
I
l 256 QUEST: PAEDlATFiICS
Part of Nephron Maior Function (ii) Hydronephrosis

(iii) Wilm's Tumour
1. Glomerus (tuft of capillaries with afferent - Blood circulate in glomerular capillaries.
and efferent arteriole). (iv) Drug : Cyclophosphamid, I.V contrast
- Glomemlarfiltrale (ultratiltrate of plasma, containing glu-
cose. Na'. Cl‘. urea) us formed from plasma inside the (v) Haematological disorder — Thrombocytopenia. Haemophilia
glomerula, capillary tuft by capillary hydrostatic pressure. (vi) Alport syndrome
2. Bowman's Capsule (surrounding the — Receives the glomerular. filtrate from glomerular (vii) Polyarteritis nodosa
glomerules) capillaries through filtration membrane. (viii) SLE nephritis.
3. Proximal convoluted Tubule (continuous — PCT is the most active part of the renal tubule. Diagnosis :
with Bowman's Capsule).
— Reabsorbs about 65% of the glomerular filtrate. Diagnosis of a case of haematuria will depend upon proper history, thorough clinical exami-
nation and relevant investigation.
— Most of the solutes like Nat, Glucose, K‘, urea, Ca”,
protein in small amount are absorbed from PCT. History :
— It is freely permeable to water. (a) Haematuria : Duration

— Passage of frank blood.
4. Descending limb of I00p of Henle. — This is the site of simple diffusion of substances
and water. (b) Oliguria : Glomerulonephritis. HUS
5. Ascending limb of loop of Henle and early — Reabsorbs significantly Na‘, K' and Cl'. — Amount in 24 hrs.
distal tubule. (Ascending limb is thicker part — Impermeasable to water and urea. — Duration ‘
of the loop). (c) Dysuria : UTI
- This area is important of urinary concentration as
due to differential permeability of solutes result in ac- (d) H/O Fever : Infection (UTI, Pyelonephritis).
cumulation of Na* in medullary interstitium, (e) History abdominal mass — Wilm's tumour, Hydronephrosis.
necessary for urinary concentration. (0 Joint pain : HSP. SLE
6. Distal Tubule (latter part). — This part is involved in aldosterone controlled Na' (g) Rashes : HSP. poltarteritis nodosa. SLE
reabsorption and K‘ selection.
(h) History of vision or hearing defect : Alport Syndrome
7. Late distal part and collecting system- - Contain specialized cells which actively secrete (i) Facial puffiness, oedema — Acute glomerulonephritis
hydrogen ions against concentration gradient and (j) Bleeding from other sites of body — Bleeding disorder.
responsible for urinary acidification.
(k) Recent past history : Respiratory tract infection (1-2 week back for AGN. 1-2 days for
" Jaxtra-glomerular appparatus (composed of — Involved in systemic blood pressure regulation. lgA nephropathy). G.l infection for HuS.
afferent and efferent arteriols and specialized — Maintains electrolyte homeostasis. (l) Drug history : l.V contrast agent. cytotoxic drug like._cyclophosphamide.
cells of distal tubule the macula densa) — Control tubuloglomerular feedback mechanisms. (m) Seizure. irritability : AGN with hypertension, HuS. '
l
(n) Difficulty in breathing : AGN with hypertensive heart failure.
Renin angiotensin system regulator. '
Examination:
General :-
- Laboratory Diagnosis of Nephrotic Syndrome — See question no 1.
(i) Higher function : Altered in AGN with hypertensive. encephalopathy. Hus.
O. 10. A five year old child presents with painless haematuria. Mention the causes and diagnosis (ii) BP : High in AGN.
of such case. (Supple, 2017)
(iii) Temperature : High in infection AGN.
Ans : Causes Common : (iv) Pallor: Significant in Hus. bleeding disorder, SLE. HSP.
(i) Post Streptococcal Glomerulo-nephritis.
glomerulo (v) Oedema : AGN.
(ii) Other form of glomerulonephritis like Membranoproliferative, local segmental
(vi) T JVP : AGNiwith hypertensive heart failure.
nephnfis.
(iii) Henoch — Schoolein purpura
(vii) Skin lesions:
(iv) lgA nephropathy Purpura - HSP. Thrombocytopenia.
(v) Haemolytic Uraemic Syndrome Butterfly rash. Discoid rash : SLE
(vi) UTI (viii) Joint swellingI tenderness : SLE, HSP
Less Common : (ix) Visoin and hearing assessment : Alport syndrome _
(i) Pyelonephritis (x) Signs of heart failure : AGN with hypertensive heart failure.
‘\
33
q
253 QUEST : PAEDIATFiiCS

GENITO-URINARY SYSTEM U Chapter—11 259
(Benito-urinary System :
(i) For abdomen mass at lumbar region : Wilm’s tumour. hydronephrosis. Euonr QUESTIONS]
(ii) Abnormal external genitalia : Ambiguous genitalia in Wilm‘s tumour associated syndrome
like WAGR syndrome. 0. 12. Steroid dependent Nephrotic Syndrome. (R. G. Kar, 8th Sam)
Investigation : Ans : E] Definition : Two consecutive relapses when on altemaie days 01 steroid therapy or within 14
(a) Urine RE/lilE : days oi its discontinuation.
Haematun‘a : > 5 FtBC/ml of urine D Management :
Difference between glomeruiar and non-glomerular haematuria Patients having steroid dependence require repeated courses of prednisolone and may develop
ieatures of steroid toxicity, including cushinged ieatures (obesity. hirsutism. striae), hypertension,
_ Glomerular Non-glomerular growth retardation, glucose intolerance. posterior subcapsular cataract. Management protocal is
as follows —
(i) RBC casts+ (i) RBC casts absent-No cast! or Steroid dependence or Frequent Relapse
epithelial cast + -
i
(ii) Albumin ++lmore (ii) Trace or +
Alternate day prednisolone to maintain remission. Assess steroid threshold.
(iii) Phase contrast microscopy (iii) .< 15%
i
-— Deformed RBC > 15% '—<5% i 1
- Acanthocytes > 5%
Threshold < 0.5 mglkg on Threshold > 0.5 mg/kg on
ailemate days alternate days or steroid
o Painless haematun'a is most likely Glomerular origin. i toxicity
(1:) Urine culture sensitivity: Suspected UTl.
Alternate day prednisolone ‘L
(c) Blood: Complete blood count - iv Hb%. T WBC (TC 1‘ Neutrophile), Platelet low T ESH —
for 9-18 months Levamsole Cyclophospha-
-
Vasculitis, SLE mide MyCOphenoiate
- Urea creatinine —> High in renal impairment - AGN. HUS. motetil Tacrolimus.
- Semm Total protein, albumin Cyclosporine
-
— Serum electrolyte Long-term alternate day prednisolone :
- Serum cholesterol Following treatment of relapse. prednisolone is tapered to maintain remission on ailemate day
(d) Special diagnostic test : dose of 0.5-0.7 mgikg for 9-18 months.
- Semm Ca- Glomeruionephritis. lgA Nephropathy Levamisole:
- Serum Aso titre. Post Streptococcal Glomerulonephritis. After inducing remission Levamisole'is administered at a dose of 2-2.5 mg/kg on alternate days
for 1 -2 years.
— Serum ANA - SLE
In addition alternate day prednisolone 0.3-0.5 mg/kg for 3-6 months.
(e) Renal imaging :
Cyclophosphamide : Alter remission cyclophosphamide is given at a dose of 2-2.5 mglkg day for
— Common renal imaging — 12 weeks. Prednisolone is co-administered at tapering dose for 6 months.
USG - Hydronephrosis. Pyelonephritis. Wilm's Tumour. Cyciosporine, Tocrolimus — Prolonged therapy with prednisolone.
(1') Renal Biopsy :
o. 13. Complications or Nephrotr'c Syndrome. (2011,5upple}
- Persistent haematuria
Ans: See question no 4.
(g) Hearlng Assessment:
— Suspected Alport Syndrome.
0.14.1.abomtorydiagnosisoichlldhood Nephrotic Syndrome. (zomsoppro)
had peda l oedema, a. 15. investigation in F case olsuspected Nephrotic syndrome. 1 (Kalyani, rut Sent)
-.0 11. A seven ear old irl presents with convulsion in tnage room. She
'
ions of the
decrease; urinarygutput What is your diagnosis? What are the other complicat Ans : Both question no.1.
investiga tion you want to perform to arrive at your diagnosi s?
disease? What relevant 0.16. Urine Heat Test.
-[NRS}(8" Sam)
complication (Hypertensive Ans: Urine Heat test is a satisfactory semiquantitative bedside test fer assessment of presence of urinary
Arts: 0 Provisional Diagnosis : Acute Nephritic Syndrome with protein.
' Encephalopathy).
Procedure: 10-15 ml of urine to be collected in a test tube and upper ponion oi the time column
question no 5.
El Other Complication oi Nephrltlc Syndrome : See is to be boiled. Ii turbldity appears 3 drops at concentrated acetic acid to be added toihe sarrple
El Relevant Investigatio n : See question no 5. and it will be boiled again.
M" "
r-11 2—61
260 QUEST: PAEDIATFIICS —_-
GENITO-URINARY SYSTEM Cl Chapte
Interpretation : lf turbidity persists after boiling with added acetic acid. this turbidity is due to Alternate day prednisolone to maintain
presence of protein in urine. Depending upon the density of this cloudiness or turbidity proleinuria remission
I ° Alternate day prednisolone 1.5 mg/
can be graded from 0 to 4 +._ kg for 4 weeks. 1
0 or Nil : No turbidity seen.
l—
1 + : Slight turbidity through which a fine print can be read out. l
Significance — Proteinuria 30 to 100 mg/dl. Threshold < 0.5 mglkg. on
Threshold > 0.5 mglkg on alternate
days or steroid toxicity.
2 + : Turbidity present through which print is read out with difficulty. alternate day
l l
Proleinuria — 100-300 mg/dl.
Levamisole.
3 + : Turbidity with fine precipitate and print can not be read out. Alternate day predinisolone Cyclophosph amide
Proteinuria : 300-1000 mg/dl. for 9-18 months Mcphenolae mofetil
4 + : Dense turbidity with precipitate and print cannot be read through this. Tacrolimus, Cyclosporin.
Proteinuria > 1000 mg/dl.
3* and 4' indicates heavy proteinun'a with Nephrotic range. O. 19. Clinical Features ofAcute Post Streptococcal Glomerulonephritis [We] (8“ Sam).
a. 17. Management of oedema in Nephritic Syndrome. Ans : Cl Clinical Features of Acute PSGN :
Ans : MANAGEMENT OF OEDEMA IN NEPHHOTIC SYNDROME Typical manifestations of acute PSGN occur after streptococcal infection in body either pharyn-
gitis or pyoderma with a latent period of
«1 Mechanism: Excessive Na* and water retention secondary to diminished renal blood flow and
consequently glomerular filtration. . 10-14 days — Pharyngitis
- Management: 2-3 weeks — Pyoderma.
(i) Fluid intake to be restricted to insensible loss and urinary output. (i) Oedema — Starts as early morning periorbital oedema, progressing to generalised body
(ii) Restriction of salt intake limited to adding salt only during cooking and no extra salt thereafter. swelling. Edema is due to increased Na+ and water retension.
Avoid salty snaks.
(ii) Haematuria — Passage of dark reddish brown colour urine is a typical clinical picture of acute
(iii) Moderate oedema : To be treated by oral Frusemide 2-4 mg/kg. Oedema usually disappear PSGN. Haematuria can be gross or microscopic, classically called cola-coloured urine.
with return of renal function. Add Spironolactone 2-3 mg/kg with higher doses. lf inadequate Haematuria is due to damage to glomerular basement membrane.
response then add metolazone/Hydrochlorothiazide.
(iii) Oliguria or anuria — Another typical clinical manifestation of acute PSGN is diminution of urine
(iv) Pulmonary oedema : Pulmonary oedema in acute nephritic syndrome should be managed
with |.V. Frusemide at a dose of 2-3 mglkg given as slow |.V pushes. Resistant/pe
rsisting volume that may progress to anuria and renal failure occurs to due diminished GFR.
over 1-4
edema — If all above methods fail then give Albumin infusion 20% with frusemide. (iv) Hypertension — Blood pressure is usually high in acute PSGN. This high pressure ca'fi be
hour, on alternate days. asymptomatic. detected during examination or patient may present with complications of hy-
0. 18. How will you manage steroid sensitive nephrotic syndrome. pertension like -
of minimal change nephrotic syn- Hypertensive Encephalopathy with recurrent convulsion, unconsciousness, headache.
Ans : Steroid sensitive nephrotic syndrome includes 1st episode
drome, frequent relapse. infrequent relapse and steroid dependence. —Hypertensive left heart failure with tachypnea. tachycardia, basal crepitations in lung,
distended jugular veins. Blood pressure usually normalizes by 3-4 weeks.
Management :
' First Episode 0. 20. Difference between clinical features of Nephrotic and Nephn'tic Syndrome.
Nephrotic Syndrome
Ans : Nephrotic syndrome and nephritic syndrome or acute glomerulonephritis are two most common
l entities occurring in pediatric age group with clinical features. lhat are sometimes difficult to be
Prednisolone 2 mg/kg daily for 6 weeks followed by. differentiated. _
1.5 mg/kg alternate day for 6 weeks However following are the usual differentiating clinical features between nephrotic syndrome
and acute glomerulonephritis — -
I
F l '
Infrequent Relapse Frequent Flelapse Steroid depen-
l dence
Therapy: '1'
Alternate day prednisolone to malntaln
- Prednisolone 2 mglkg daily until
remission them remission
262 QUEST : PAEDIATRICS GENlTO-UHINARY SYSTEM Cl Charla-11 263
Features Nephrotic Syndrome Nephritic Syndrome 0 Haematuria : Red cells > 5IHPF
In most of the cases gross haematuria present Specially in moderate to severe cases.
1. Age first presentation most commonly 2 Usually older children 5 - 12 years.
6 year. ' Proteinuria : Protein content is mild to moderate Grade 1 + to 2 + (upto 300 mg/dl)
Nephrotic ranges proteinuria (374‘) is usually absent.
2. Proceeding hilay be history of minor respiratory 0 History of skin infection. (Streptococ. - Casts : RBC casts ++
history illness. cal pyoderma] 3-6 weeks back.
Dysmcrphic RBC «H which is indicative of glomerular origin of the disease.
- History throat infection (Streptococ-
-
cal) 2 weeks back. — Hyaline. granular casts may also be seen.
WBC/Neutrophil — initially neurophile count is high due to glomerular inflammation which is
3. Oedema . Usually significant oedema at v Mild to moderate oedema. severe often mistakenly diagnosed as urinary tract infection.
presentation to start with mild oedema is rare.
oedema - progress to moderate . . 0. 22. Causes of Haematuria {SDMC}.
to severe ° Oedema l5 relatively tough or turgid.
Ans : Haematuria is defined as presence of 2 5 red blood cellslml of urine.
' Oedema is pitting type
Haematuria can be gross or microscopic.
4. Haematuria Gross haematuria is absent Gross haematuria present — WK- El Causes of Haematuria :
colafred urine. (a) Glomerular:
(i) Primary Glomerular:
5. Hypertension 0 Absent during first presentation Usually present and patient may
. May occur subsequently as a represent with complication of hyper- -Post streptococcal glomerulo-nephritis — Most common cause of haematuria in children
suit of prolonged steroid therapy tensron 'Hypertenswe Emergency'. -lgA nephropathy
—Alport Syndrome
6. Oliguria May be present if oedema is severe Very common as a result of renal
-Membrane proliferative, membraneous, focal segmental glomemlcvnephrifis
leading to diminished renal blood insufficiency
flow. Frank renal failure is very rare. Acute renal failure may occur, eCresentic glomerul-nephritis.
(ii) Secondary Glomerular :
7. Fever, mal- Uncommon Common
- SLE nephritis
aise lethargy
- H.S purpura
8. Loin pain Uncommon Common —Poly arteritis Nodcsa'
9. Heart failure Does not occur Common due to hypervolaemia or by-

-Haemofy1ic Uremic Syndrome.
pertension. (b) Non-Glomerular: ' ‘'
10..Hyperten- . Does not occur usually Common feature. presents as hyperten- (i) Kidney :
sive crisis . Flarely may occur as a result of swe encephalopathy or heart failure. - Pyelonephritis — bacterial
steroid toxicity -Tubulo-interstitial nephritis
— Hydronephrosis
11. Acute renal Flare May occur - Multicystic and polycystic kidney disease.
failure
- Wilm's tumour.
12. lnfective Frequent Uncommon (ii) Renal vasculature :
complication - Renal vein or renal artery thrombosis.
(iii) Uretor, bladder. urethra :
13. Thrombotic Common Does not occur.
— Urolithiasis
complication
- Cystitis.
(iv) Crystalluria : Oxaluria. Idiopathic hypercalcuria. Uric aciduria.
0. 21. Urinary Findings of Acute Post Streptococcal. 10
(v) Trauma _
Glomerulo-nephrltfs/Urfne analysis ls PSGN. [Murshldsbsd]
(vi) Drag induced : Cyclophosphamlde causing haemorrhagic Cystitis.
Ans : El Urinary Findings of Acute PSGN :
264 QUEST : PAEDIATRI$ GENITO-URINARY SYSTEM El Chapter-11 1E5
(c) Haematological : investigation :

- Thrombocytopenia ' (i) Complete blood count:
— Haemophilia ~ Low Hb%
— Disseminated intravascular coagulation. — Broken and distorted red cells on peripheral smear.
— High reticulocyte count
a. 23. Haemolytic Uremic Syndrome. (CNMC, 8th Sem) (NRSMC 2011)
— Thrombocytopenia
Ans : Haemoiytlc Uremic Syndrome is a disorder characterised by triad of Micro-angiopathic
— High neutrophil count.
haemolytic anaemia, Thrombocytopenia. acute renal insufficiency.
(ii) Coomb's test: Negative
. Sub group : Two broad sub-groups are identified :
(ill) Serum LDH level : High
(i) D‘lTypicai Hus : Associated with diarrheal disease (Common).
(lv) Urine Analysis :
(ii) D‘l’Atypical Hus : Not associated with diarrheai disease (Rare).
— Haematuria +
0 Site of affection : Kidney, Brain (Sometimes). - Proteinuria (Mild)
0 Etlopathoiogy: (v) Blood urea, creatinine : High depending upon the severity.
The diarrheal disease proceeding 0* Hus usually caused by - (vi) Renal Biopsy : Usually not indicated. if indicated, findings are -
— E.Coli (0.157 : H7) verotonin producing. Swollen endothedial cells and capillary lumen are narrowed by swollen endotheliai cells, blood
—ShigelIa-dysenteriae t (in Indian context). cells and fibrin thrombi.
Hus : Insidious onset
Cytotoxins from enteric pathogen
- Severe hypertension and progressive renal insufficiency.
l — Predisposing factors, infection (Pneumococcal. HIV) systemic lupus. cobalamin deficiency.
Injury to endotheiium in renal vascuiature Treatment :
i - Correction of anaemia
Loéalized coagulation and fibrin deposition - Treatment of hypertension
i -— Peritoneal or hemodialysis in severe renal insufficiency
_ I l l — Plasma pheresis in D" Hus.
Sequestration of platelets Thrombosis in glomeruiar Damage to red cells
J, capillaries mechanically a. 24. Clinical features and treatment of UT! ofchildren (Haldia).
I ThrombocytopeniaJ l - . l Ans: CLINICAL FEATURES OF UTI :

Decrease in glomeruiar Micro-angiopalhic Depends on child’s age severity and site of infection in urinary tract.
filtration rate (GFR) haemolytic anaemia Newborn period : Features of sepsis with fever. vomiting diarrhea. jaundice, poor weight gain,
l lethargy. shock.
I Renal insufficiency ] Infant :_ Nonspecific symptoms like diarrhea, vomiting, failure to thrive, unexplained fever. cry-
ing dunng voiding. -
Older children :
. Clinical Features : - Lower UTI presents with dysuria, hypogastric pain, frequency. urgency.
- Younger child (2-3 yr) are affected usually. - Pyeionephritis presents with fever with chili, regor. flank pain. vomiting, toxic appearance.
- HlO Diarrhea — dysentry. Treatment : Antibiotic therapy — Promptly started. choice of initial antibiotic therapy will
— Sudden onset pallor. depend on — Child’s age.
— Diminution in'urine output (oligurialanuria). — CliniCal condition.
— Haematuria may be present. - Associated structural anomaly if any.
- Irritabiiity, weakness. Once culture report become available antibiotic therapy will be modified depending upon
culture sensitivity report. '
- Altered consciousness.
Neonate and infant : Neonate and infant (Specially < 3 month) UTI is a part of generalised
- Convulsion. sepsis.
v-III-I-
GENITO-URINAFIY SYSTEM El Cfrapterntt 267
Imaging Studies:
ide (Amikacin. Gentamicin).
Choice of antibiotic : Ampicillin + Aminogiycos Three type of imaging studies are done alone or in combination depending
on child's age.
tion cepha lospor in alterna tively. on
- 3rd genera (a) Renal Ultrasonography : To get informations
(Ceiotexime. Ceftriaxone). - Kidney size, number, location.
Duration : 10-14 days. - Hydronephrosis
clinical severity of UTI.
Older children : Management depends upon — Urinary bladder abnormalities.
ion of therap y is crucial. —- Post voidal urine volume.
Pyelonephrltis : Prompt institut
eral therap y. once toxicity subsid es antibiotic can be given orally. (b) DMSA scinflgrapny : A sensitive technique to detect
— Initially parent
idelSrd generation cephalosporin.
vParenteral therapy Ampicillin + Aminoglycos — Renal parenchymal infection.
—- Cortical scarring.
- Duration - 10-14 days.
Distal UTl : Oral antibiotic therapy is usually
sufficient. (c) Micfurating Cysfo-urethrograply': Provides information regarding —
- Choice of antibiotic - Anatomical details of bladder and urethra.
— Vesico ureteric reflux (VUFl).
— Amoxiciliin,
—- Cephaiexin
First urinary tract infection
— Co-amoxyclav
I i i
- Cefixime
— Ciprofloxacin Age < 1 yr ultrasound, Age 1-5 yr ultrasound 8. DMSA Age > 5 yr ultrasound
MCU & DMSA scan scan Ii ultrasound abnormal
- Ofloxacin.
— Duration of therapy — 7-10 days. MCU if ultrasound or DMSA MCU and DMSA scan
. scan is abnormal
Response : Mth appropriate antibiotic therapy
culture becom e sterile within 24-48 hrs.
Symptoms disappear and
Failure to respond —— Timing of imaging study :
— insensitivity to drugs 0 Ultrasound — Soon after diagnosis of UTI.
- Non-compliance 0 MCU — 2-3 weeks later.
tive uropathy.
— Presence of complicating factor as obstruc
- DMSA scan — recommended 2-3 months after treatment.
General Measures :
> Antipyrefics —> Control of fever. a. 26. Evaluation of urinary tract infection. (lPGfiEfl, 8th Sem)
raly
) Hydration —> Fluid intake orally or parente Ans : Evaluation of urinary tract Infection includes followings :
> Antiemetic —) If persist ent vomitin g.
(i) Confirmation of infection.
Imaging Study : Mandatory if (it) Detection of any underlying urologic anomaly. (Obstruction or vesico-ureteric reflux).
- Child presents with UTI in early infancy (iii) Involvement of kidney (pyelonephritis).
— Recurrent UTI Confirmation of Infection :
ity despite adequate antibiotic therapy.
- Persistence of symptoms and culture positiv (i) Urine routine and microscopic examination :
t recurrent UTI and risk of renal scarring.
Prophylaxis : - if child's age < 2 year to preven Diagnosis of UTI is suggested in urine RE. ME as follows -
Choice of Antibiotic —- Co-trimoxazole - Mild Proteinuria
— Nitrofurantoin - Leukocyte count (> SIHPF in centrifuged urine and >. 10 WBClmma in uncentriiuged urine].
tract is completed. -Bactsria on gram stain. _
Duratio n — 6 months -2 yrs until appropriate investigation of urinary
(KPC) - Bacterial enzyme nitrate reductase; leucocyte esterase test — These are the rapid tests for
U'li.
0. 25. How will you Investigate a child on follow up of culture proved diagnose UTI. .
positive UTI to detect underlying structural
Ans : Alm : The aim to investigate a child after a culture e or involvement of kidneys.
(ii) Urine Culture Sensitivity test :
ts at high risk of renal damag
anomaly and identify patien For proper culture sensitivity of urine clean collection of urine is necessary.
should be investigated but chiefly
Indication : Ideally all culture positive UTI cases Collection of urine : Methods of urine collection depends upon the age.
- Child < 1 yr of age < 2 yrs —> Suprapubic' aspiration or urethral catheterisation.
'— Recurrent UTI Older children - Clean catch mid stream urine sample should be needed.
uction.
- Suspected VUH or urinary tract obstr
Chapter-11 269
GENITO-URINARY SYSTEM U
at a close of 30-50 mglkg elemental

Management : (a) Oral calcium gluconate or carbonate
Bacterial colony count : ca cium.
will depend upon the method of de gel and diet containing low
Bacterial colony count to confirm the diagnosis of UTI (b) HYpefphOSphatemia —+ Treated with aluminium hydroxi
collection. phosphate.
are considered as significant.
in general to diagnose UTI the following colony count (c) Dialysis in refractory hyperphosphatemia.
sample.
Bacteria of single species a 10l urine — tn clean catch
O. 28. lndlcations of Renal Biopsy in Nephrotr'c Syndrome (2018).
2 5 x lO‘lml urine : ln urethral catheterisation. ome (MCNS)
Ans : Renal Biopsy is not routinely indicated to diagnose minimal chan ge nephrotic syndr
Any number of - ln suprapubic aspiration bacteria. me renal biopsy is
is every cases. However. in presenc of atypical features in nep hrotic syndro
‘ A colony count between 10‘ to 10l may be significant. if the child has polyurialother
tion. Indicated. Indications are listed belonr —
symptoms of UTI or received antibiotic, require reevalua
ent of kidneys. A) At onset :
Detection of Urologic anomaly llnvolvem
anomaly or i) Age of onset less than 1 year
This evaluation is needed in child alter a culture proved UTI to detect urologic
ii) Gross haematuria or persistent microscopic haematuria
involvement of kidneys by imaging studies.
iii) Low serum Ca
lmaglng studies — See question 25.
iv) Persistent Hypertension
(MCK)
Cl. 27. Electrolyte abnormality in Acute Renal failure. v) Renal failure not due to hypovolemia
of the body, in acute renal failure vi) Suspected secondary cause of nephrotic syndrome.
Ans : As kidneys play a vital role in maintaining electrolyte balance
of electroly te abnorma lities are noted as folloWs —
a number B) After initial treatment :
and dangerous electrolyte, abnor-
(i) Hyperkalemia : Increased serum potassium is a common i) Proteinuria persisting despite 4 weeks treatment with daily prednisolone
mality occurs in acute renal failure. ii) Before treatment with Nephrotoxic drugs like Cycl05porine A or Tac rolimus.
(Kr).
Cause : (a) Diminished renal clearance of potassium
acidosis.
(b) Shift of K' from intracellular space due to metabolic
(0) Tissue breakdown and Hypercatabolic state.
Clinical features : Mild to moderate : Non specific
Severe —) Cardiotoxicity occurs.
xicitly occurs.
Management: (a) I.V Calcium, gluconate —-> If cardioto
(b) I.V Sodium bicarbonate.
uptake of K’.
— lnsulin and Glucose infusion - To increase cellular
ge resins (Calciu m Resoniu m) orally or by enema.
- Exchan
(c) Avoidance of potassium rich foods.
s any time during the course with serum
(ii) Hyponatremia : Can be present initially or develop
sodium < 130 mqL
administration -+ Dilutional Hyponatremia.
Cause : Most important cause is excessive fluid
-— Increased sodium loss (rarely).
with altered sensorium. convulsion (if
Clinical features : Profound hyponatremia is associated
serum Na' < 115-120 mEq/L)
y mode of therapy.
Management : (a) Fluid restriction —> Primar
tremia with CNS symp toms — 6 mllkg 3%
(b) Infusion of 3% NaCl solution - in severe hypona
s. Sodium admini stration is hazard ous in patient wi th excessive body
NaCl over 30-60 minute .
and conge stive heart failure
water and can cause hypertension
la, hyper magn eseml a and Hypoc alcem la : lf ARF persists for few days.
(Iii) Hyperphosphatem
hate and magnesium.
Cause : (a) Reduced renal excresion of phosp
d production of calcitrlol by kidneys and
(b) Hypocalcemia is thought to be due to reduce
ted calcium phosph ate deposi tion in tissues. c) Tissue breakdown
hyperphosphatemia media
and hypercatebolic state.
ic due to associated acldosls but alkall-
Clinical features : Hypoc alcemia is usually asymptomat
therapy may precipitate tetany or convuls ion.
CNS Cl Chapter—12 271
Symptoms :
CHAPTER - 12 a) ll-D-lfeadatihe — Persistent headache specially in early morning is the leature often bioccipital or
i ronta .
CNS b) Vomiting Usually projectile
-
— Often in early morning
Usually not associated with nausea.
[ LONG QUESTIONS]
-
c) Increase in head size -— Seen in children below 2 years at age
d) Personality changes - Irritability
0. 1 : Describe the iormation and circulation of CSF in brain. Describe the clinical features of _
raised intracranial pressure of a 6 year old child. Give an outline of treatment at such a — Lethargy
patient. {20141 - Apathy
Ans : CSF is the fluid which fills the ventricles of the brain. central canal of the spinal cord, the subarachnoid - Disturbance in speech
cistemae and subarachnoid space. e) Visual disturbances - Decreased visual acuity
0 Formation — —
Diplopia
— From choroid plexus — Squint
— By process of ultra filtration and active secretion. l) Convulsion — Recurrent convulsion may occur
0 Circulation - Signs :
Chomid plexus a) Alteration of sensorium. drowsiness, unconsciousness.
b) Children < 2 years of age - Increase in head size
In lateral ventricles
Fullness of anterior trontanelle
l
Interventricular loramine of Monro - Separation of sutures
-— Macewen sign in skull
3rd ventricle - Sunsetsign in eyes
‘ Macewerr sign — Percussion over the skull nearjunction of frontal. temporal and parietal
Aqueduct ct Sylvius bones wrll produce cracked pct sound indicating separated sutures.
l Sunset sign - Eyes appear driven downward due to upward-gaze paresis
4th ventricle c) Eye signs - Papilledema --j_
— Enlargement of blind spot ‘
Foramina of Luschka and Magendie- Central canal of spinal cord I.
— Squint
l
Lateral gaze palsy
-
V Subarachnoid space
d) Cashing Triad — Seen in lite-threatening severe rise of ICP
D Absorption - CSF in subarachnoid space - Bradycardia
i
- Hypertension
Arachnoid villi
l — Irregular respiration
e) Hemiation syndrome — Severe rise of lCP causes herniation in which part of the brain may
Cerebral venous sinus
get Impacted in abnormal location.
(Mainly to superior sagital sinus)
Features. of Hemlation —
-
El Clinical Features of raised intra-cranial pressure (lCP) o Impaired consciousness
Normal CSF pressure - -’ Abnormality ol Pupil size
In older children and adult : 10 —- 15 cm of H20
0 Hyperionicity
Younger children :73 — 7 cm of H20.
' Paresis
Raised lCP when lCP > 15 cm H20 at any age.
lCP > 40 cm of H20. - Decerebrate or decorticate posturing
Severe life threatening intra-cranial hypertension is called when
- Cardiovascdlaroollapse '
Clinical features —
270
T
272 QUEST: PAEDIATRICS CNS El Chapter—12 273
Cl Treatment- Protein — 20-45 mgldl

1) Maintain Airway, breathing and circulation — Most important as raised lCP is an emergency Glucose - 45-80 mg/dl OH
condition. 75% of serum glucose
2) Head position — Fiaise head end 15° — 30° Management of TB Meningitis :
— Keep in midline Management of a 2 year child with TB meningitis include diagnosis and treatment.
~ This position ensure better venous drainage thus better drainage of CSF. CI Diagnosis — TB meningitis is a potentially serious illness. if not diagnosed or treated properly may
3) Temperature —- Normal body temperature to be ensured lead to high mortality and permanent disabilities. Following investigations are suggested -
- Raised body temperature increases metabolic rate and thus increase lCP 1) CSF Analysis
4) Blood pressure — To be maintained as normal for age, High BP in raised CP reduces blood flow I - Pressure — usually elevated
to brain. - Cells — 10 - 500I predominantly lymphocytes
5) Seizure control — Midazolam, Iorazepam, phenytoin — to be given till seizure has been controlled ' Protein — 100 - 3,000 mg/dl, higher in presence of block in CSF circulation.
s Seizure increase cerebral oxygen consumption and increases ICP - Sugar — low in most of the cases
6) Fluid — Maintain Nonnovoiemia v Organism - may be detected by PCR
— isotonic fluid is the choice. ' Smear for AFB - positive if CSF volume is large.
7) Paralysis and sedation — with judicious use of sedative and muscles relaxant for paralysis - CSF culture -—
(specially during controlled ventilation) Conventional culture —- requires longtime to yield positivity (8 - 12 weeks)
- Sedation decreases sympathetic overactivity BACTEC culture - requires less time (1 — 3 weeks)
8) Osmotherapy— ’ 0 Nucleic Acid Amplification test — helps in rapid diagnosis of TB from CSF and also detects
c Mannitol (20%) — 0.25 - 0.5 mgikg as below and may be repeated 4-6 hourly dmg resistance.
- Furosemide — 0.5 - 1.0 mg/kgllV alone or with mannitol - ADA (Adenosine deaminase level) - produced by lymphocytes and monocytes in presence
9) 3% NaCl — if Mannitol is contraindicated of tubercular bacilli thus elevated in T3 meningitis.
— Hypotension Normal level in CSF - 1 to 10 UlL
— Hyperosmolar state 2) Contrast Enhanced CT scan l MRI helpful in diagnosis of TBM characteristics charges
_ olTBM
-
are as follows —
10) Hyperventilation - Short term reducelP - 30 sec - 8 min.
-— Basal enhancement
—
Causes vasoconstriction and decreased cerebral blood flow
- Presence of exudates
11) Environment — Patient should be protected from external stimulus, noises
~ Communicating (60%) or obstructive (20%) hydrocephalus
12) Resistant, severe raised ICP —
— Periventricular infarcts
— Barbiturate coma
- Tuberculoma
- Decompressive craniotomy
3) Supportive investigations - to detect evidence of extranural TB
- Operative treatment for mass lesion
i) Chest x-ray - Parenchymal or nodular lesion
- Ventricq-peritoneal shunt
ii) Ultrasound abdomen
- Neuromuscular blocking agent
- To detect retroperitoneal lymphadenopathy
0.2: Describe formation, circulation, absorption and composition of CSF of a normal child. - Matted bowel loops
Give outline of management of Tubercular meningitis of 2 year old child. [2011]
iii) Tuberculin (Mantoux test) — > 10 mm induration consider as positive
reaction
Ans : CSF is the fluid in brain which fill the ventricles. central canal of spinal cord. subarachnoid cisternaes iv) Sputum/Gastric Aspirate — For nucleic acid amplification test.
and subarachnoid space. '
D Treatment— ’
Formation._circulation and absorption — Question No. 1.
a) Aniitubercular treatment — It is the cornerstone of effective treatmen
Composition — It is important to know the normal composition of CSF to diagnose various infectious t of TBM
and nonvinfectious diseases of CNS. ATD should be started as soon as TBM is suspected or diagnose
d by definitive and supportive
evrdence. ' '
Appearance —— Crystal clear
Duration — At least 12 month is preferable according to IAP
Pressure — 50-80 mm of Hg
Though RNTCP advocates 6 month regimen
Cells (leukocytes) - < 5 lmm3
-
> 75% lymphocytes
274 QUEST : PAEDIATRICS CNS El Chapter-i2 275
Regimen Intensive
_ phase Continuation phase Status Epilepticus
IAP 2HFiZE 10H RE i
r I
8.
RNTCP 1) Airway Breathway Circulation Blood 1) History. examination and
9mm“ 0"" G'g‘me " 'ess) investigation to ascertain cause
Streptomycin (30 - 4o mgfkglday) i.m. to be given initially for 2 - 3 weeks.
Dose : 2) LV. DiazepamlLorazepam Fiepeal
after 10 min if needed
lsoniazid -— 5 mg/kglday maximum 300 mg/day
. J.
Fiilampicin - 10 mg/kglday maximum 600 rug/day
3) LV. Phenytoin llFOSphen y‘toin
Ethambutoi - 15 - 20 mglkglday
Pyrazinamide — 30 mg/kglday 4) W. Valproate/llv. Phenobarbitone
All the above drugs to be taken orally -
-
J, mg/kg eve ry 6 hours LV. 5) Midazolam infusion
‘ - Parenteral Dexamethosone 0.15
b) Steroids
i
c b ral oedem a subsided 6) Phenobarbitone comet intubalion +
ere i
Mechanical ventilation
Oral prednisoione
i
1) initial stabilization -
6 weeks
- Airway — Mouth open, oropharyngeal suction.
MOA - Steroid causes- _
_ Breathing - Oxygen, manual BMV if needed
- Reduction olcerebral oedema Circulation — LV. access, NS bolus if circulation is poor
noiditis
- Reduction of risk of development at arach LV. Dextrose in CBG is low, to - 25% Dextrose
— CBG—. Capillary blood' glucose estimati' on and _
-
- Reduced fibrosis and spinal block ‘ .

2 mlmg
this condition
ortive there has an important role in TB meningitis as
I - -
- u
seizure m status epilepticus

n e
S
2) Benzodlazapine _ ist modality to control
-
.
-
ermanent disabilities. weight
gafiifinpggefigztifiyhigh ltEtE’rtitliiies andpg Dose _ w Diazepam 0.1 _ 03 mg/kg body
nvulsa nt drug for seizur e mg/kg body weight ”7:“-
._ Antico Flectal Diazepam 02 _ 0.5
_ Mannitol for raised intracraniai pressure - LV. Lorazepam 0.1 mglkg body weight
Correction of dyseiectrolytemia 3) Phenytoin — It seizure not controlled with Benzodiazepine then next drug is I.V. Phenytoin
- intravenous fluid/N asogastric feeds
, vitamin_ and mineral supplement .
Dose — 20 mglkg body weight. 1mg/kg/min infusion
cephalus.
Ventriculo peritoneal shunt tor hydro 4) VaiproatelPhenobarbitone — Alter Phenytoin. Dmg of choice to control seizure is Valproate or
’0’ "'0” ' Phenobamitone
. h' d has been brought to emergency with convulsion PerSi'Sfiflg
ento;25:13; Dose 20 mg body weight Valproate
the managem
M 3:75;3:13:33? lint you will diagnose the case? Briefly narrate
-
0189- ' , 10 — 20 mg/kg body weight Phenobarbitone
Ans ; . ' _ 5) Midazolam infusion — ll status is still persisting it is needed to give midazolarn inlusion.
Dose - Starting 1pglkg/min can be increased upto 18 pglkglmin.
El Diagnosis - Status Epilepticus ' ' I ’sodes of seizure lasting
- - - '
multip 9 am . But higher doses_ causes respiratory depression and needs ventilatory support.
Status Epileptlcus (SE)
. '5 defined
. as prolonged
- - ' seizure ' orbetween.
single .
_
_
midazolam .
- infusion then there
for more than 30 minutes Without regaining of
conclousness tn
6) Phenobarbital Com) a _
If seizure is intractable
_ . and persistent despite
_
l tential life threate ning complications with time, the cut all time value ts need to produce. Balbituraie coma With Thlopental and patient needs intu bailon and mechanical
' 0f developmen t ‘3 it"?
Due to nsk I n u c
. u a to 5 ”fin 88.
‘ ‘ . . . _ . .
ndition so patient's stabilization and ventilation at {”5 stage.
has been dimmlsned cus is an emergen-cy oo - Examination
7) History, ascert and Investigation -- History. examination and relevant investigations should be
0 Management - As 5talus Epilepti . . - - se to be done done '0 ain the cause .
and investigations to diagnose the oau
control of seizure shou Id be the first pnonty
simuflaneouslr- a) History — Proper history regarding
— Onset
-
In..."
e \
.
_
. v .'. ’ - ..1 ..
'
.s -. .A, z- . ,__
. -‘
_t_.— n -
____.____....__ . . ... —A_
-
EL
275 QUEST : PAEDIATRICS CNS El Chapter—l2 277
- Duration
0) Pain - Causes reflex stimulation of spinal or motor neurones and causes increase In muscle
- Type of convulsion (Focal / generalized) tone.
— Any previous history d) inhibitory intemeurones — There ae inhibitory interneuranes in grey matter of spinal cord
— Birth history and they have maintenance of muscle tone in selective group of muscles. Such type of
- Developmental history interneurone is Renshaw cells that connect to or motor neurone.
— History of fever Activation of or motor neurones
— Other relevant history i Inhibition of same a
b) Examination - motor neurone
Activation of Renshaw cells >
- Detailed neurological examination should be done alter seizure is being controlled
B) Supra-segmental control -—
— Other system examination
Supra—segmental signal to maintain muscle tone operate from different parts of CNS and operate
0) Relevant investigation — by influencing segmental strech reflex or or motor neurones situated in Spinal cord.
-— Electrolytes (Na+. Kt. Ca“) in blood seizure can occur from dyselectrolytemia These are as follows —
- LFT. FIFT (Urea creatinine) to detect failure of vital organ function a) Cerebral cortex— It sends inhibitory influences mainly either directly by Cortico-spinal pathway
— Complete blood count or through the extra-pyramidal mechanism.
— Peripheral smear for malariafDual antigen if associated with fever _ b) Basal ganglia — They have inhibitory influences on muscle tone by extrapyramidal pathways.
- CSF study — if meningitis is suspected 0) Cerebellum — Cerebellum as such inhibits muscle tone by inhibitory influences on vestibula-
— Arterial blood gas analysis Spinal mechanism.
- Any other tests — as clued from history or clinical examination. d) Brainstem - Brainstem contains the reticular formation and its derivatives like vestibular
nuclei. Reticular formation has both inhibitory and excitatory influences on muscle tone.
0.4: A 3 year old child with generalized seizure for > 45 min. What is your provisional diagnosis?
C Other influences — There are some other influences which also take part in maintenance of
V
How will you manage the case? [2012 supple] muscle tone —
Ans: Diagnosis —r Status Epilepticus a) Anxiety state — increases muscle tone through extra-pyramidal pathways.
Management — Question No. 3 b) Different tonic and postural reflexes along with vestibular apparatus influence muscle tone.
0.5: How the tone of a child is maintained? What are the causes of hypotonic child? Write the 0) Sleep and unconsciousness — Muscle tone diminishes during state of
sleeping and
Wm of GB syndrome. unconsciousness. .
[2012 supple]
d) Drugs — Different types of dnrgs, mainly sedatives decrease muscle tone by
Ans : The state of partial contraction of a muscle at rest is called Muscle Tone. their action on
CNS. ‘7‘;
Muscle tone is like a background activity over which muscle contraction becomes more easier and Causes of Hypotonic child -
a muscle with normal tone can contract more effectively than a muscle with abnormal tone.
Elaypotonia is called when there is little or no resistance against passive moveme
Mechanism of maintenance of muscle tone - nts. It is also called
cidity.
Mechanism of maintenance of muscle tone is complex and involves segmental and suprasegmental
Causes — Hypotonia is typically found in lower motor neurone
mechanism as follows — paralysis. Lower motor neurone is
composed of —
A) Segmental (Spinal control) - Various mechanisms operate at the level of spinal cord to maintain
f) Anterior horn cells of spinal cord.
the muscle tone like —
2) Peripheral nerve
a) Segmental stretch reflex - It has a pivotal role in maintenance oi muscle tone through stretching
of muscle spindles which are the sensory organs found in skeletal muscles. Afferent nerve 3) Neuromuscular junction
from muscle spindle send impulse to spinal cord 4) Muscle.
l So. lesion to any above these structure leads to
hypotonia. as follows
Reflex firing of the a motors neurone in spinal cord
-
LMN lesion —-
l 1) Anterior Horn cell lesions —
Contraction of muscle fibre
— Poliomyelitis
- Spinal muscular atrophy '
Increase in muscle tone
b) Golgitendon organs - Stimulation of Golgi tendon organs by severe stretching. inhibits 2) Peripheral nerve
muscle tone by inhibition of or motor neurones in segment of spinal cord. - Demyelinating neuropathy like Guilla
in Barre Syndrome
3) Neuromuscular Junction —
._ 5-."
\x
u.
\.
CamScanncr
CNS D Chapter—12 279
Ans : 3rd cranial nerve is the occulomotor nerve that supply most of the extra-ocular muscles except
- Myasthenia Gravis lateral rectus and superior oblique.
- infantile Botulism Following are the extra ocular muscles supplied by 3rd nerve with action -
4) Muscle— 1. Medial rectus — causes adduction of eyes
Myopathy 2. Superior rectus - causes elevation of abducted eye
— Muscular dystrophy 3. Interior rectus — causes depression of abducted eye.
— Myotonic dystrophy 4. Interior oblique - causes elevation of abducted eye
— Metabolic and endocrine myopathies [Mnemonic : Rab r’.e., Flectus are the elevator and depressor in abducted eyes, reverse is true
Others — for oblique muscles]
of hypotonia in children.
Apart from LMN paralysis there are few other causes
Superior rectus inferior oblique
— Unconsciousness due to any cause
-— Dyselectrolytemia
t A
- Cerebellar disorders
Management of Guillain Barre Syndrome -
D Dlagnosis-
Guillain Barre Syndrome is a post infectious polyneu
- CSF studies —
ropathy involving mainly motor nerves.
@ Superior oblique
Inferior rectus
— Cell count normal
Temporal side Nasal side
Protein-more than twice the upper limit of normal
-
— Glucose normal
iation and is diagnostic of GB syndrome. Diplopia towards looking nose — Muscle involved is Medial Flectus
This finding is called Al bumino-cytological. Dissoc
(NCV) - Greatly reduced . Causes of 3rd nerve palsy - Oculomotcr nerve can be involved in any disease process affecting
Motor Nerve Conduction velocit y study
lrogtynerve nucleus in mid brain, throughout its course upto orbit and causes features of 3rd nerve
condu ctor Velocity study — Slow pa .
- Sensory nerve
ation of muscle
0 EMG (Electromyography) - Acute denerv Causes can be divided as follows —
- MFlI (Gadolinium Enhancemen t) - i) lschemia — ThrOmbosis
ecal nerve roots.
- Thickening of cauda equine and intrath - Emboli
tests not practic ally done to (fiagno se GB syndrome are —- ii) Haemon'hage
Other
iii) Compressive - Aneurysm
5» Muscle biopsy
- Tumour (like meningion'ta)
> Sural nerve biopsy
iv) lnfillrative — Leukaemia causing brain metastasis
> Antiganglioside antibodies . v) Inflammatory — Cavernous sinus thrombosis (by granulomatous inflammation)
.
El Treatment — ascending — Orbital cellulitis
sion should be done and observation for
- Acute onset, in early stage hospital admis vi) Trauma
paralysis vii) Connective tissue disorder — SLE
n respi ratory failure
on as in cases with rapid progressio
0 Monitoring for respiratory muscle functi viii)DemyeIination
lop
and respiratory arrest may deve
rator y failure develops
Resp irator y support if respi a. 7: A three year old boy has been brought to the ER with convulsion persisting for more than
us Immu noglobulin (lvlg) — 30 min.
Dmg of choice is Intraveno
Dose — 0.4 gmlkg/day for 5 days a) What Is the probable diagnosis?
ctive
r lmmunosuppresslve drugs ls Ivlg is Ineffe
- Other modality - Plasmapheresis and/o and spon taneous remission
h) Outline the management of such patient ?
ld be ob serve d for stabi lizatio n
- Patients with slow progression shou Ana: 3) and b) - See question no. 3.
without treatment.
y?
are the causes of 3rd nerve pals
AAAA‘ND
280 QUEST: PAEDIATRICS CNS C] Chapter-12 251
a. 8 : 2 year old boy presented with acute onset weakness of both lower limbs. Discuss the 3) Transverse Myelilis
differential diagnosis. What is AFP surveillance ? [2008, Supple] 4) Traumatic Neuritis
Ans : Acute onset weakness of both lower limbs in children is classically known as Acute Flaccid Paralysis AFP Surveillance : See Infectious disease chapter.
(AFP).
Cl Definition — A case of AFP is defined as any child aged less than 15 years who has acute onset of
[ snonr QUESTIONS ]
flaccid paralysis for which no obvious cause (such as severe trauma or electrolyte imbalance) is O. 9: Febrile Convulsion [2011, NBMC —— 8th Sam, MMC — 9th Sam]
found or paralytic illness in a person of any age in which polio is suspected.
Differential diagnosis — Ans : Febrile convulsions are generalized. tonic-clonic brief and sell limited events that occur in the presence
of fever and in absence of underlying neurological diseases. Occurs between 6 months to 5 years of
1) Polio age.
2) Gullian Barre Syndrome (GBS) Types - Febrile convulsion can be classified as follows.
IM__-A__
i) Simple febrile convulsion —
Polio GBS Transverse Traumatic
Myelltls Neurltls - Primary generalized, usually tonic-clonic
Etiology Polio virus i, ii 5. ill lmmuncgenic Usually unknown Trauma Lasting maximum 15 min
-
(Entero virus) - Not recurrent within a 24 hour period.
ii) Complex febrile convulsion -
Onset of paralysis 24 to 48 hour Hours to 10 days Few hours to Few hours to
four days four days - Focal in character
- Lasting more than 15 min
paw Acute Usually acute. Acute. symmetrical Acute. asymmetrical
Asymmetrical mainly symmetrical & cistal affecting one limb - Recurs within 24 hours.
proxinal only Risk Factors - There are some risk factors for recurrence of febrile convulsion.
.,
[din-lull
a.
i) Age <1 year

nus—1"-“uum“-
Mlfidfl Tone Reduced or absent Global hypotonia Reduced Reduced to absent

in affected I'wnb ii) Duration of fever < 24 hour
iii) Fever 38 — 39°C
Deep tendon reflexes l or Absent Absent usually Absent — early l or absent iv} Family historyof febrile seizure
Hyper reflexia late
«was-a...
v) Family history of epilepsy

Sensory involvement Myalgia backache Tinding Anesthesia in pain in gluteus vi) Complex febrile seizure
.'u-
hypoesthesia lower limbs with

El Diagnosis - Diagnosis of febrile seizure is usually clinical considering history, clinicalfexamination
'I'l'Dn-nu
sensory level
and by exclusion of underlying neurological illness presenting with fever and convulsion.
Cranial nerve When bulbarl Often present Absent Absent ° Lumber Puncture - indication —
involvement bulbospinal involve- — If neuro infection is suspected
ment is present
First episode of febrile seizure within first year.
-
Respiratory When bulbarl In severe cases Absent Absent o imaging of brain —
insufficiency bllbospinal involve- — Not indicated in simple febrile convulsion
ment is present
- Helpful to detect underlying CNS abnormality
Autonomic syn'ptoms Dysautonomia + Present frequently Hypothennia in Absent ' EEG -
and aims affected limb
— After 2 weeks of acute episode
— Usually normal in simple febrile convulsion and usually not indicated
csr= Study Wee t Protein - was < 10 Normal or slightly Normal
Normal or slighuy t Protein - T T protein CI Treatment — This includes -
i) Treatment of fever —
Bladder involvement Absent Transient Present Never
- Frequent monitoring of temperature
NOV Anterior horn cell Abnonnal No diagnostic value Abnormal. - Uses of antipyretic — Paracetamol 15 mglkg
disease Myelination (Normal or Axonal damage — Hydrotherapy for immediate control of body temperature
abnormal)
I] Management of acute episode —
EMG at 3 weeks Abnormal Normal Normal Normal - Use of benzodiazepine-Diazepam or lorazepam I.V.
-‘_ \.
\_ ,
CNS E] Chapter-12 233
— Intranasal Midazolam spray also available and can be used in control of recurrent - Prophylaxis Prophylaxis therapy has role in febrile seizure to reduce risk
of recurrent attack or
-
convulsion as home based therapy future epilepsy. Prophylaxis may be intermittent or continuous.
D Prophylaxis - Can reduce chance of recurrence i) Intermittent prophylaxis —
i) lntemiittent - — Best way of prevention

~ Oral diazepam, lorazepam or clobazam for 1st 3 days of fever
- Oral diazepam, clobazam. lorazepam for first 3 days of fever
ii) Continuous — — Reduce recurrence by 80%
— Phenobarbitone or Valproate are used for continuous prophylaxis — Lesser side effects
ii) Continuous prophylaxis —
— Duration : at least 1 year of seizure free period or till 5 years of age.
- Given to whose who does not respond to intermittent prophylaxis or having risk factors
a. 10 : Management of febrile convulsion [N35] suggesting possibility of future epilepsy.
Ans : Management of febrile convulsion includes investigation, treatment and prophylaxis. — Drugs : Phenobarbitone or valproate
-v—q—d4'.___
D Investigation - Diagnosis of febrile convulsion is usually done by history. clinical examination and — Duration : Optimum duration is at least one year of seizure free period or till the age of
by exclusion of more serious neurological disease like CNS infection when suspected. Followrng 5 years
investigation can be done on basis of requirement. - Due to continuous therapy risk of side effects are high.
- Lumber Puncture — 0. 11 : Simple Febrile Convulsion [IPGMER — 8th Sem, R. G. Kar — 9th Sem]
—- lf neuro infection is suspected
— It first episode of febrile seizure occurs. Under 1 year of age as clinical Signs of CNS Ans : Febrile seizures are the commonest provoked seizures experienced in childhood. They are brief,
infection are subtle in this age group self-limited events that occur in presence offever and in absence of underlying neumlogical disease.
The convulsions are not related to the degree of temperature rise but are frequent if temperature
- Brain imaging - (CT or MRI scan)
rises abruptly.
- Not recommended in evalution of tst episode of simple febrile convulsion
Simple febrile convulsion
individualized.
- For evaluation of complex febrile seizure need for imaging are to be
' They have following characteristics —
° Electroencephalogram (EEG)
neurologically — Usually generalized in nature
Not indicated in first episode of simple febrile convulsion or if the child is
— Occur within 24 hours of the onset of fever
healthy.
_ — Last maximum upto 15 min
— Cannot predict future recurrence.
— There are no post-ictal neurological deficit
- if indicated should be done after 2 weeks of an acute episode.
D Diagnosis - .
- Blood studies
-
' should
. um and complete blood count — They are benign in nature, diagnosed from history and nature of convulsion
- Blood glucose, sodium, potassium, calcium, magnesi
management accordingly.
be done as work up of all cases of febrile convulsron and ' Lumber puncture — If child‘s age of first episode less than 1 year then LP should be
done to rule out CNS infection
El Treatment-
e Brain imaging and EEG Not indicated in simple febrile convulsion
-
- Fever —
of convulsion in febrile seizure. Ct Treatment— I
Reduction of body temperature is the mainstay of control
0 Treatment of fever
- Frequent temperature monitoring.
. Reduction of raised body temperature is the mainstay of treatment for simple febrile
— Hydrotherapy to reduce body temperature quickly convulsion ‘
g body weight.
— Use of antipyretic; Paracetamol - 15mg/k Frequent temperature monitoring and prevention of rapid rise of temperature
- Control of acute convulsion -— Hydrotherapy
bly l.V. route
— Short or long acting benzo-diazepine prefera Antipyretic --) Paracetamol 15 mglkg. Dose repeated dose may be required.
-
-— Diazepam 0.3 mg/kg l.V. ' Control of seizure -—
Lorazepam 0.1 mg/kg l.V. .
— Acute control of seizure by W. diazepam (0.3 mg/kg) or lonazepam (0.1 mglkg)
then per rectal dlaze pam 0.5 mg/kg
lf l.V. access not possible — If I.V. access not possible then per rectal diazep'am 0.5 mg/kg
y also availa ble now a days to control acute seizure can be
— lntranasal midazolam spra
used on home basis.
CNS [3 Chapter— 12 285
Deafness (Sensory neural)

. Prophylaxis — Mental retardation
proper
PrOphylaxis therapy usually not required in simple febrile convulsion. Advice for Systemic complications
of the cases.
fever treatment with paracetamol and hydrotherapy is enough in most
In cases where parents are anxious or resident of far way from health facility intermittent a) Shock —
for
prophylaxis can be adviced in form of oral diazepam or Ionazepam or clobazam Causes of shock may be —
first 3 days of fever. — Septic shock specially in neonate, infant
[IPGMER - 9!: Sam] — Adrenal insufficiency (N. meningococcal meningitis)
0. 12: Complication of bacterial meningitis in child
b) Myocarditis -
meningitis caused by bacteria
Ans: Any type of CNS infection is a dreaded illness in pediatric age group
of complications - involvement of myocardium in patients with meningitis is a serious complication
is a serious illness which if not treated in proper time that may lead to a number
with high mortality or serious neurolo gical deficits. - Patient presents CCF and/or arrhythmia
Complications of Bacterial Meningitis - 0) Status Epilepticus -—
—- Status epilepticus may be precipitated in patients with meningitis
CNS complications
- Treated bylong term anticonvulsant
A) Immediate-
d) Inappropriate ADH secretion —
a) Subdural effusion or empyema —
- Collection of reacfive fluid (effusion) or purulent material (Empyema) in subdural space ~ Patient with pyogenic meningitis may secrete ADH excess in amount causing SlADH.
.
- Young chfldren and infants are particularly susceptible to develop this complication — Diagnosed by history. clinical examination and measurement of sodium. potassium
Occurring in 40% — 60% cases _ . and osmolality tests of blood and urine.
- Seizure. irritability, increased head size. Ietherge bulging frontanelle are features O. 13 : Pseudotamour Cerebri
— Diagnosis by USG brain or CT scan.
Ans :
b) Ventricul‘rtis— - Also known as Benign lntracranial Hypertension or idiopathic intracranial hypertension.
— Spread of infection into the ventricles of brain is a serious complication of bacterial - It is characterized by headache, papilledema. raised intracranial pressure without any cause.)
meningitis normal CSF components, normal ventricular sizes on brain imaging.
.
- infants and young children are vulnerable and a well known feature of gram negative
meningitis. 0 Etiology — Following are the possible causes -
c) Aracl'inoidifis — a) Drug —
- Spread of infection to arachnoid layer of meningitis Nalidixic acid
—- Presents with tingling, pain and neurological symptoms. Tetracycline

Nitrofurantoin
d) Brain abscess -
to brain parenchyma
Pyogenic meningitis is often complicated by extension of infection Steroid
forming abscess. Phenothiazines
development of local
Persistence of fever, altered mental statue. neck rigidity, b) infection —
neurological signs point towards development of brain abscess. GB syndrome
- Diagnosed by imaging of Brain (CECT scan or MFII) Roseola infantum
e) Hydrocephalus - Lateral sinus thrombosis
— Another complication of pyogenic meningitis. c) Metabolic and endocranial —
~ it can be communicating or non-communicating (obstructive) Hypervitaminosis A
(communicating) or
- Exudate formation may cause interference in CSF obstruction Vitamin A and D deficiency
obstruction of CSF flow at the level of aqueduct of sylvius (obstructive)
lapse of few days. Addison's disease
B) Late complication — Some neurological complications may develop after Hypoparathyrofdism
Those are :
Pseudohypoparathyroidism
- Herniplegia
- Aphasia Growth hormone therapy
- Ocular palsies 002 retention
- Blindness
235 QUEST '. PAEDIATRlCS CNS [3 Chapter—12 287
Lumber puncture —
d) Haematological—
— Raised CSF pressure
— Poiycythemia
— Normal composition
— Iron deficiency anaemia
EEG - Slow wave activities
— Leukaemia
Assessment of vision
- Non-Hodgkin's lymphoma
0 Treatment -
e) Vascular-superior vena cava obstruction
initial LP is diagnostic as well as therapeutic to release excess CSF pressure
f) Trauma-Minor head injury
Acetazolamide — 5 mgfkg/day following lumber puncture
9) Miscellaneous—
Prednisolone — 2 mg/kg it above measures tail
— DPT immunization
Low salt diet and weight reduction in obese patient.
- Bell's palsy 0 Lumboperitoneal shunting it above measures to decrease lCT
- ' ' i ns
Visual monitoring to prevent visual impairment.
0 Pamogmessfilfflitef:ctomechanism of developing pseudotumour cerebri is controversial. Possible
theories are — . 0. 14 : Clinical features of pyogenic meningitis in children
[2008]
— Alteration of CSF absorption and production . . Ans : Acute Bacterial (pyogenic) meningitis is a major cause of mortality
as well as morbidity in children.
— Cerebral oedema which is due to increased cerebral blood volume and impaired CSF It is more common in neonates and infants than older children.
absorption. .
I] Clinical features -
- 'Decrease cerebral flow and venous obstruction resulting in venous engorgement Symptoms - Symptoms of pyogenic meningitis are -
El Clinical Features- — Onset usually acute
Symptor'ns - - Fever : Moderate to high grade for variable duration
0 Onset — Acute or gradual - ' — Headache : Either diffuse or in frontal region often spreading
to neck and eye balls.
- Common symptoms —- Headache, irritability, drowsiness . diplopia. - Vomiting : Child may have recurrent vomiting may be projectile
in nature due to raised ICT.
- Shrill cry. irritability : Child may have shrill cry or excessiv
- Less common symptoms e irritability
— Refusal to food : in infant and young children occurs early
— Transient visual obstruction in course of illness.
— Photophobia : Marked photophobia is usually a feature
- Nystagmus occurs due to raised lCT
- Seizure or convulsion : These are common symptom.
Neck stiffness may develop at the onset or during
the course of the illness.
-
— Ataxia — Alteration of sensorium : Drowsiness or unconsciousnes
s may develop during the course
- Seizure of illness.
- Movement disorder — Bulging Frontanelle : Fullness or buldging of anterior
frontanelle in young infant is a
prominent feature and noticed by parents. V
—- Paresthesia
D Signs -
5'91” Anterior lrontanel full in infant and young children Alteration of sensorium is common. in form of irritabili
ty. drowsiness to unconsciousness.
- Maceweri sign positive in older children Signs of meningeal irritation positive
'
- Papilledema. early optic nerve atrophy ' Neck rigidity
- 6th cranial nerve palsy . ' Kernig sign
o Consciousness is preserved - Bmdzinski sign
0 No local neurological signs Bulging frontanelle with opening of sutures in infants
indicate raised intra-cranial pressure.
. Muscle power is usually preserved. sometimes hemipa
' No risk of herniation resis may develop.
by exclusion Generalised hypeitonia may be preSent.
El Diagnosis - Pseudotumour cerebri' diagnosis is usually diagnosis
Reflexes are nonnal. diminished or exacerbated.
- CT scan or MRI brain .
Cranial nerve palsies may be present
— Normal with small ventricle size Hemianopsia
—- Obliteration of normal sulci markings
CatnScanner
CNS ['1 Chapter— 12 289
d.
ma'if intracraniai pressure is raise ° Antiviral
— Fundus examination — Papillaede
Late stage — . . — Oral Acyclovir or Valacyclovir as most common is Herpes simplex or Zoster virus
—
intracranial pressure infection
Cushing tn'ad — From severe alarming use of
lar respiration — To be added with prednisone. alone acyclovir is not effective
(a) Hypertension (b) Bradycardia is) irregu
' Physiotherapy
- Circulatory failure and shock.
[2011] — Physiotherapy to facial muscles is recommended in cases with poor recovery
0. 15 : Bell's Palsy ' Ocular drop .
palsy that is not associated with other cranial
Ans - Bell’s palsy is an acute unilateral facial nerve — Ocular lubricant eye drop (methyl cellulose) to prevent exposure keratitis of eye of
neuropathies or brain stem dysfun ction affected side.
— All age groups can be affected. .
El Prognosis —
- Abrupty develop s 2 weeks after a system ic viral infection
—- The prognosis is usually excellent
El Etiology - — 85% recover spontaneously with no residual weakness
- Common -— — 10% have mild facial weakness
-— Herpes Simplex Wrus (Type 1) infection upto 80% of cases — 5% are left with permanent severe facial weakness.
— Herpes Zoster infection
0. 16 : Status Epilepticus — causes and management [2014, supple]
- Less common infection —
Ans : Status Epilepticus is a medical emergency and that should be anticipated in any patient who presents
Otitis media with acute seizure.
-
— EB virus infection it is defined as continuous or recurrent seizure activity without regaining consciousness lasting for
— Cytomegalovirus infection >30 min.
_ Munps 0 Causes - There are many causes of status epilepticus in children as follows —
- Less common cause — - Metabolic
- Trauma - Hypoglycemia
— Tumour — Hyponatremia
- Guiliain-Bane syndrome — Hypocalcemia
— Drugs - Ribavirin, Interferon — Hypomagnesemia
— Intranasal influenza vaccine 0 Stroke
- Ischemia (arterial or venous)
El Clinical manifestation -
— Haemorrhage
0 Features of unilateral facial nerve palsy of LMN type — Flapid onset of mild weakness to total
paralysis within hours to days - - Systemic
- Absence of frowning ~ Hypertensive encephalopathy

- Hepatic encephalopathy
- Unable to close the eye of that side
Excessive watering from eye — Renal encephalopathy (uremia)
—-
. Infection
- Drooping of comer of mouth
— Meningitis
- Inability of whistle
- Encephalitis
Taste on the anterior 2/3“ of tongue is lost or involved side in 50% of cases.
— Cerebral Malaria
— lpsilateral numbness in few cases.
. Drug
D Treatment -
— Withdrawal or overdose of antiepileptic drug
- Oral steroid — Tricyclic antidepressant
— Prednisoione - 1 mgikg/day for 1 week followed by tapering over next week . Trauma
- Best resuit when started within 3-5 days - Brain tumour
290 QUEST: PAEDIATHICS CNS U Chapter—12 291
- Chest x-ray — supportive evidence of TB

- Flare causes
‘ Manloux test — supportive evidence of TB
— Pyridoxine deficiency
- EEG — To detect seizure disorder-
—-Inbom error ct metabolism
- Braln
' imaging
' (CT Scan / MRI) — For structural anomaly. cerebral oedema
— Brain malformation
— Neurodegenerative disease O. 19: Status Epilepticus
[BSMQ 9th Sent]
- Epileptic syndrome Ans: Status Epilepticus is define '
0 Management — See Question No.3 more than 30 minutes omitiégifiiiiggfiiffo'isiiéi‘é’feié iifii’t'feifi‘fié‘is t§L§°““’° “3"”9
'
(R. G. Ker, 8th Sent] El Etiology- Etiology of childhood status epilepticus is vast which incl ude lollowmg—
. metabonc
0. 17 : Treatment of Status Epilepticus p as.
Ans : See Question No. 3
lsions —
Hypoglycemia
on in a 2 year old febrile child with convu
O. 18 : Etiology and relevant investigati [KPC. 9th Sent] —
Hyponatremia
- Hypocalcemia
in a 2 years febrile child -
that can be possible for convulsion — Hypomagnesemia
Ans : There are multiple etiologies
f lschemic or haemorrhagic stroke
CI Etiology -
- CNS infection
1. Febrile convulsion / Simple . — Meningitis
Atypical '
— Encephalitis
lever
2. Seizure disorder, triggered by - Cerebral Malaria
' '
3. Meningitis Systemic— Hypertensive! Renal/Hepatic encephalopathy -
— Bacterial
- Viral
+ E Status
- Tubercular pflepficus
ephalitic syndrome
4. Enwphalitis [Acute Enc N Ensure
Hist W
' 00’ .-
5. Cerebral Mala
6. Brain abscess
ria
..
'rway {Suction}
- . 0 us
)
. i. an ve'l
history and other relevgfliniemal
El Investigations .
' Examination
stabilization — .
A) Basic investigation for corroded I.V. Dtaz
DM'EF' neurological and elite
0 Blood glucose - Hyp oglycemia if present should be %fléfl?epam’
ium , . ia. Hypocalcemia and
Hyponatrern
.
systemic examinatlort
.
iumCalc ium , Mag nes
ulsron Repeat after 10 ml if needed
Blood electrolyte —- Sod
0 accordingly because conv ' investigation _.
checked and managed
magnesemia should be imbalan ce. Not cont all
out correction of these elec troly te
r ed - Senm Glucose, Electrolytes
cannot be controlled with l.v. Phenytoin — LFI', an '
rmin e the cause -
B) investigation to dete Not controlled _- CBC
cou nt -
' Complete blood se I.V. Valproa'te
‘ :9fiphetal smear + Dual
neutrophil Bacterial cau
- High TC WBC with high 02$: dy
-
l in origin LV. Phenobarbitone
lymphocyte - Mostly vira - it
Low TC WBC with high Not controlled _ _ A33
gestive of tuberculosis
High ESFI — may be sug LV. mt zolam infusion — Any other test
parasite
ect presence of malarial
Peripheral smear — To det ipa rum
plasmodium viva x and lalc Not controlled
Dual Antigen — Against Ima gin g
stion no. 6 and Bra in Phenobarbitone coma
CSF analysis — See que lnttbation + Mechanical ventilation
B and antibody
Blood for Viral PC igation lor TB
A Te st — supportive invest
- Sputum of AFB , NA
nnnnnnnnnm.
A a
O Drug -- Withdrawal
I l Of AED CH AFTER _ 13
. Trauma
. Brain rumour MISCELLANEOUS
- Flare cause
— lnbom error of metabolism
— Brain malformation. IE
an emergenc y condition so patient's stabilization and _ . . . , ,
._ bcu 5 Is and
D Mamzmggtzumfijflimgfggppmfiw investigations to diagnose the etiology ‘0 be done 0. 1 . Clinical features and treatmenrof scabres In children. [2009]
con .
Ans . SCABIES - -
simultaneously.
{SDMC} Scabies is caused by the mite Sarcoptes scabei var. hominis. There Is burrowing and release of term
0. 20 : CSF finding 0' T""¢"°""’ Meningitis substances by the female mite. which cause the skin lesions.
— It is transmittedby close contact with infested humans.
Ans : See question no. 2
Clinical Features :
1. Intense pruritus. which is most severe at night.
2. lst sign of infestation is usually 1 to 2 mm red papules.
3. Classical scabies lesion is the thread like serpentine burrows with a papule at the end.
. In infants. vesicles and pustules are commoner than the classical burrows.
(DUI-h-
. Secondary lesions include — pustules, eczematized lesions and nodules.
. Preferred sites — lnterdigital spaces. wrist flexors. anterior axillary folds. umbificus, groin.
(l
buttocks, ankles and genitalia. Head. neck, palms and soles are generally spared. except in
infants.
7. Secondary infection with streptococcus causes pyoderma and may result in glomerulonephritis.
{I
Cl Treatment :
1. Smblcides (Topical) - Topical scabicide should be applied all over the body below neck.
[I
including the free edge of nails. genitals and soles after hydrating the body with a bath. Scalp
treatment is warranted in infants. in whom there is affection of scalp.
II
l
Medication is left on the skin for 8-12 hours (usually overnight)
(I
l
Scrub off next morning with bathing
(I
l
May be re-applied after 1 week. if necessary
n
- Medications: (a) 5% Permethrin (Treatment of choice)
(b) 10% Crotamiton
n
(c) 25% Benzyl benzoate
(d) 1% Gamma Benzene Hexaohloride
f'l
2. Oral scabicide —> Single dose of lvermectin (200 rig/kg) may be used as additional therapy and
in case of epidemics (in children > 5 yrs.)
A
3. Antlblotlcs —> for secondary infection.
. Antlhlstaminlcs —> for pruritus
A.
5. Treatment of contacts —> To eradicate the scabies mites fully. addtional steps undertaken are _
n
(a) Treatment of all the close contacts (family members). even “asymptomatic.
(b) Washlng of all the clothes. bed linens. towels etc.
A
"'u.
-H‘
\“
293
l
MISCELLANEOUS-CI Chapter~13 295
(b) Systemic - Systemic antibiotic therapy (oraltparenteral) is needed. it the pyodenna is wide-
(lCAFlE - 2016] [RGKMC - 9th Sent]
O. 2 : Kwashiorlror dermatosr's. spread. there is associated lever, or in very small intents with signs of systemic infection
(Parenteral therapy may be considered in newborns. infants and children with significant mal-
Ans : nutrition etc.). Oral antibiotics used are —
KWASHIOHKOR DERMATOSIS
_ . edema. Severe
' d by pitting (i) Amoxycillin + Clavulinic acid
' a form of proteln
Kwash'lorkor Is ‘ energy malnutn"tlon (PEM), characterise to
association with adequate calorleintake can lead (ii) Cephalexin
protein and essential amino acid deprivation in
orkor in childre n of post-w eaning age. Accord ing to the Wellcome trust classrficatlon. weight for (iii) Cephadroxil
kwashi '
is called Kwashiorkor.
age < 80% of expected with presence of edema 2. Scabicides - (a) Topical
e is known as Kwash iorkor derma tosis or nutritional
- Skin changes associated with this diseas . . (b) Oral Same as 0.1 (Skin) - Treatment pan
dermatosis. 3. Antihistaminics
ncies of tyrosine. niacin. zinc and vitamin s are attributed In the patho-
El Pathophysiology : Deficie 4. Treatment of contacts
genesis oi these skin changes.
El Features : ~
in colour, RHEUMATOLOGY
hyperpigmented. eryth ematous or jet black
1- The skin becomes hypopigmented. . ‘ .
with desquamation. Q. 1 : Classification of Ju venite idiopathic Arthritis. [SSKM-201 6. MRS-2016]
g is the classical cutan eous findin g. known as Flaky Palnt
2 Diffuse fine reddish brown scalin Ans :
Dennatosis'. Classification of JIA :
d, like dorsum of the feet and hands.
a Sun-exposed skin is relatively spare ement of the trunk Juvenile Idiopathic Arthritis (JlA) is the most common rheumatic disease in children. it represents a heter-
ks. perineum and upper thigh. with involv
4 The distrbution is typicalty on buttoc . . ogenous group of disorders sharing the clinical manifestation of arthritis.
.
is less often. - ILAR (International League of Associations for Ftheumatology) Classification of .llA : The
. which ls ulcerated and
s are found in the flexures and grom
5 In severe cases cracked lesion atos is’.
term JlA was coined by lLAFt to replace the previous term JFtA (Juvenile Rheumatoid Arthritis) and
' ' ' ‘ raz Pavement Derm included various other categories of arthritis into it (e.g. psoriatic arthritis. enthesitis-related
diphtheria. may also
ay trit ium : [1:19) :tnd bacteria.‘ especially cutaneous artheritis etc.)
6. m
occur. El Common criteria -
' . . d dark bands may
. 1. Age at onset < 16 yrs.
7. Nails are thin and soft.
2 Minimum duration 2 6 wks.
ilrni-Irtlgguate nutrition. This
ealp iggz ltitrf’:piggfiigeasdgttleat‘emalfi
. 8- figufiiip::r:t:$ greg 3. Presence of arthritis [swelling or effusion, or the presence of 2 or more of the following signs : (a)
is known as "Flag sign’. Limitation of movement. (b) Pain or tendemess on motion. (c) Increased heat] in: 21 ioint(s).
‘ Management: El Classification-
malnutrition.
1. Treatment of Underlying 1. Systemic onset JlA —> Arthritis. with or preceeded by ieverfor'al least 2 wits, and presence at z 1
n and trea tme nt of secondary infection - of the following - ' '
2. Preventio rapidly. as serum zinc level is
often
therapy may heal the lesmns (a) Evanescent erythematous rash
3. Topical and systemic zinc
deficient. (b) Generalised lymphadenopathy
[20151 (c) Hepatomegaly or splenomegaly or both
O. 3 : Treatment of infected sca
'
bies .
(d) Serositis (£8. peritonitis. pleuritis or pericarditis)
2. Oligoarticular JIA —) Arthritis affecting 1-4 joints (5 4) during the 1" 6 months of disease. in the
Ans : TREATMENT OF INFECTED SCABIES -
ies. Lesions of scables may absence oi systemic signs.
var. hominis is known as scab5. streptococci). resulting in
Skin infection by the mite sarcomas scabe‘ . staphylococci 3. Polyarticular .lllt -) Arthritis affecting 2 5 joints during the 1* 6 months of disease. in the absence oi
gram positive bacteria (e.g
get secondarily infected by systemic signs. '
multiple pustules (Pyoderrna). 4. Psoriatic Arthritis —» Arthritis and psoriasis. or arthritis and at least 2 units following —
Cl Treatment: n, if there is'secondary infec- (a) Dactylitis
Top ical - Top ical antibiotics are routuinely give pro lcally in children
V.
1 . AntI'blotics -+ (a) ' are prescn'bed . phylact

' ics (b) Nail pitting and onycholysis
Sometimes. topl'cat anti' biot
‘
' ' ' hyg lene ls que stlo nable.
ance of (c) Psoriasis in a 1"degree relative _
. fi:es:gos-£os
rf:r:i:sstatus . where mainten
f0 mfi
fm' 5. mitts-rotatedutluitlsrean) —) Arthritis and enthesitis or. arthriis and at least 20fthefollowing—
-
Options are — a) Mupirocin (a) Sacroiliac ioint tendemess.
fii) Fusidic acid .
h.
ne lod ne (Be tad lne)

(iii) Povido \
‘\ -c
e.
MlSCELLANEOUS El Chapter-13 297
(b) HLA-Bz7 antigen, . Gastric lavage is contraindicated for the risk of aspiration aggravation.
(c) Onset of arthritis in a male > 6 yrs, . Oxygen, if respiratory distress or cyanosis is present.
(d) Anterior uveitis, . Antlpyreties (Paracetamol @ 15 mg/kg/dose) for fever.
(e) HIO ERA, ankylosing spondylitis, inflammatory bowel disease, Fleiter syndrome or anterior . Sucraliate —+ for local gastric mucosal protection.
uveitis in a 1" degree relative. . Antibiotics —+ when there are signs of pneumonitis.
. Undifferentiated arthritis —> Arthritis that fulfils criteria in no category or 2 2 of the above categories. Nebulisation —+ usually coatraindicated, for the enhancement of aSpiration-risk.
Observation -+ for at least 24 hours. as full blown picture oi K.oil poisoning may appearupto 24
hours alter ingestion.
a. 1 : Kerosene poisoning in toddler. [MRS—2016, 2016-Supple)
Ans:
0. 2 : Management of Neurotoxic Snake (Cobra) bite. {2016, Supple)
KEROSENE POISONING IN TODDLER Ans:
Kerosene oil poisoning is the commonest accidental poisoning in children in india and toddlers (1-3 El MANAGEMENT OF NEUROTOXIC SNAKE BITE (Cobra)
years) are at the greatest risk due to their curiosity. Neurotoxicity is the feature of bites by cobras and kraits; sometimes mssels viper. Apart from local
El Causative factors : swelling. pain and necrosis. Cobra bite causes descending paralysis. Earliest signs to be appearent
1. Easy availability of kerosene oil in most of the households and more so in the poor house- are ptosis. diplopia or ophthalmoplegia, followed by bulbar palsy and respiratory paralysis.
holds. A. General measures :
2- Storage of Koil in containers meant ior drinking water. 1. Airway —> Paralysis ofjaw and tongue can lead to upper airway obstruction in neurotoxic snake
3. Easy accessbility to toddlers (is. kept in accessible places). bite. Airway maintenance is done by - (a) Head tilt, chin lift and jaw thmst manoeuvres.
4. Carelessness of parentslcaregivers. (b) Different airways (crepharyngeal. laryngeal)
D Pathophysiology: 2. Breathing —> In case of respiratory muscle paralysis, there may be inadequate breathing.
occur dur-
1. Respiratory - The principal threat from K.oil poisoning is aspiration, which can which is treated by assisted ventilation.
ing ingestion or following vomiting, due to its volatile nature. 3. Circulation —+ Maintained by WP and lnotropic agents, if required.
l 4. Reassurance a To the patient, if he/she is conscious.
Contact with respiratory mucosa initiates a 5. Toumiquets —> Should be removed slowly under strict supervision and distal pulses lelt for
strong inflammatory response (Chemical pneumonitis) their presence.
'3‘.
as G.l. irritant and may

2. Gastrointestinal - Absorption through GI. tract is negligible. K.oil act 6. Pain —> Local pain should be managed by Paracetamol.
result in increase in peristalsis and local gastritis and esophagitis. 7.- In]. Tetanus Toxoid —> If indicated (not needed in children who are fully immunised)
.
3. CNS —> CNS involvement occurs secondary to hypoxia. B. Clinical Evaluation:
CI Clinical Features: 1. Look for ptosis and external ophthalmoplegia
. Burning pain in the throat 2. Test for bulbar paralysis
”PVP‘ms-some
. Choking sensation 3. Test for reSpiratory paralysis -+ single breath count. paradoxical respiration
. hypoxia/cyanosis.
Nausea, vomiting 0. Investigation:
Abdominal colic, diarhoea 1. 20 minute whole blood clotting test (20 WBCT)
. Cough, breathlessness . Hb%. platelet count
Jason:
Fever (very common) PT, aPTi’
lhesetestsare more useful in
. Cyanosrs. in re cases . Urine for occult blood. BBC Viaerine(hemati:rtoxic) bites
Coma, seizures 5. Serum urea, creatinine. electrolytes
. Characteristic odour in breath 0. Treatment :
10. Diffuse rhonchi and crepitations on chest agscultatlon 1. Anti Snake Venom:
for signs of pneumonitis.
Cl Investigations : Only relevant investigation is chest X—ray to look
appear late). ptosis external
(to.etc.) - muscle
_ . W“th a lm Oplegra,
CXR is usually done after 6-8 hours of ingestion (as radiological changes Name
. lndluflonam paraly "embe
sis. °'inabilit y to rmds!head
only supportive measures are
0 Treatment : No definitive treatment/Antidote is available; so. (ii) Cardiovascular abnormalities (e.g. hypotension. shock,
undertaken. arrhythmia etc.)
1—.
38
MISCELLANEOUS El Chapter-13 299
298 QUEST '. PAEDIATRICS
(in the 9. Cardiac defects : Include Bicuspid aortic valve (most common). coarctation of aorta partial
more than hall of the bitten limb anomalous pulmonary venous return (PAPVFI) etc.
I
(iii) Severe local swelling involving
absen ce of toumiq uet) double renal elvis uret ' ' '
10.Renal defects : include horseshoe kidney u
, e
-
p ropehric “who" Ob
(iv) Ftapid extension of swelling. struction etc.
1 hour (iv). Further
5-10 milkg of NS/5% Dextrose over 11. Sensorineural hearing loss.
' Dose —+ Initially 10 vials dissolved in 20 vials for neur otox ic bite in case of no
ally upto
doses can be given (5-10 vials) maxim 12. Hypothyroidism (due to antithyroid antibodies).
improrement. 13. Pubertal development : Sexual maturation usually fails to occur with no thelarche
and
on. 2 regimens —>
- Premedication —) to prevent ASV reacti puberohe. though adrenarche may occur early. There maybe primary amenorrhoe
a.
1. (In). Hydro cortis one + In]. Promethazine) lM
s Investigations:
Adren aline SC
0R 2. In). 1. Karyotyping —> Conlinnalory investigation.
mended.
- Skin Test I Test dose —i Not recom anticho- 2. USG of heart (Echocardiography) and kidney -
bite should receive a trial oi
children with neurotoxic snake
2. Antichollnesterase —+ All mg/kg (IV). 3. USG of gonads —> (a) Streak ovaries
e 0.04 mgfkg (IM) + Atropine 0.05
linesterase with Neostigmin
.1, Observed for next 30-60 mins. (b) Hypoplastic uterus
4. LH, FSH 4 Levels are increased. (Hypergonadotrophic hypogcnadisrn).
If there is improvement
5. Antlthyroid antibodies -> May be positive.
l
6. Audiometry —-> For evaluation of hearing
Neostigmine 0.01 —- 0.04 mglkg
Every 2-4 hours lV - Treatment :
+
1. Growth Hormone therapy -> is useful; it may increase final adult height by
8-10 cm.
upto 8-12 hours
Atropine 0.05 mglkg around 13-14 years of age to induce puberty.
ts) 2. Estrogen‘therapy -> usually started
(to block the muscarinic effec of estrogen
3. Cyclical therapy with estrogen and progesterone —> started after 6-1 2 months
therapy; maintains menstrual cycle.
I GENETIC DISORDERS |
4. Counselling and Behavioural therapy
[CNMC - 81h Sam]
chifdren.
0. 1 : Tamer Syndrome. 0. 2: Describe the clinical manifestations and diagnosis of Down Syndrome in
[Maids "CH-2016]
Ans :
Ans:
El TURNER SYNDROME mosomal constitution (Le. abse
nce ,-
omal disorder having 45 X0 chro El DOWN SYNDROME ..

Turner syndrome is a chro mos
_ births.
of 1 X chromosome). Down syndrome is the most common chromosomal disorder. with an incidence of about 1 :000 live
ence : Abo ut 1 in 1,500 - 2,000 live born females. It rs also known as Tnsomy 21. because of the presence of an extra chromosome 21.
- Incid rome may be of following types—
gements in patients oiTumer Synd
. Genetics : Chromosomal arran ' Genetics :
1. 45. X (Most common, > 50%
) (a) True trisomy 21 (is. presence of 3 copies of chromosome no. 21) —> 95% (Most common)
XX (Mosaicism with normal cell line) (b) Mosalcs —) 1% '
2. 45. X l 46.
aicism with isochromosome] (c) Translocatlon -+ 4% [Most common translocation is 1(14. 21)]
Pam < 3. 45. XI 46, X. i(Xq) [Mos ]
[Mosaicism with ring chromosome
”mm 4. 45. X I46. X. r(X) - Clinlcal manifestations:
Clinical Features: at the 1. CNS -i (a) Mental retardation
- s and feet. and loos 9 skin folds
edema of the dorsum of hand (b) Developmental delay (social 'develooment relatively spared)
1. At birth : Characteristic
to the diagnosis.
nape of neck may give clue . (c) Hypotonia -
ure : The card inal finding in almost all girls.
Short stat 2. Cranlofacial —> (a) Brachycephaly with flat occiput
Pflg’sfifiwm
. Short neck with webbing. . (b) Flat facial profile

Low posterior hairline. high arched palate. (c) Upward stanting of eyes
inent ears, epicanthal folds and
Facles : Small mandible, prom ced nipp les (d) Epicamhic folds
g the illusion of widely spa
Broad shield-like chest givin (e) Bmshfield spots over iris
carrying angle.
Cubitus valgus : Increased (f) Small nose with flat nasal bridge
rpal s and metatarsals.
Short 4" metaca
Jorl‘a
MISCELLANEOUS El Chapter—13 301
malignant cells are prone to

(g) Protruding tongue Etiology : Lymphoproliferative disorders with rapidly multiplying
(h) Short hard palate develop TLS. like -
(i) Small, dysplastic ears
t. Burkitt's Lymphoma
2. ALL
3. Musculoskeietal —> (a) Hypertlexibility of joints
(b) Hands are short and broad 3. AML
Pathophysiology: Rapid cell breakdown
(c) Simian crease (single transverse palmar crease)
t
__0___0
(d) Clinodactyly (Hypoplastic middle phalanx of 5" finger)
(e) Sandal Gap (Wide gap between t" & 2"d toe) Release of intracellular ions (K'. PO‘, Uric acid)
(f) Atlantooocipilal sablaxation J,

4. CVS -) (a) Endocardial cushion detect (MC) Renal excretion capacity is overwhelmed
in) VSD J,
LJ l_(l__()_t Lit—(LBJ
(c) ASD (ostium secundum) Renal failure
(d) PDA - Clinical Features : Typically manifests 12-72 hours after the initiation of chemotherapy.
5. GI -a> (a) Duodenal atresia 1. Cardiological —+ Arrhythmias (due to T K‘. 1‘ PO‘)
(b) Annular pancreas 2. Renal —> Oliguria or anun‘a
(c) Hirschsprung disease 3. Neurologiml -+ Seizures, tetany {i Ca“)
(d) Tracheo—esophageal fistula Diagnosis :
6. Eye 4 (a) Congenital or acquired cataract 1. Laboratory TLS -+ Presence ol 2 2 of the following -
(b) Nystagmus (a) Uric acid -> Above the upper limit at normal tor age
(c) Strabismus (b) Phosphate —+ > 6.5 mg/dl in children
(d) Refractory errors (myopia) (c) Potassium —«> > 6 mEq/Lt.
7. Ear —+ (a) Congenital or acquired hearing loss (d) Calcium —+ < 7 mg/dl.
(b) Serous otitis media 2. Clinical TLS -+ Laboratory TLS (+) any 1 of the following end-organ involvement—
8. Endocrine —> (a) Hypothyroidism (a) Kidney — (i) Serum creatinine > 1.5 times the upper limit oi normal. -or rise of 0.3 mgldl
(b) Obesity over baseline
(c) Infertility (ii) Oliguria (< 0.5 mlfkglhr) for-6 hrs
9. Growth retardation (b) Cardiac- Arrhythmia
to. Recurrent infections (sinusitis, pneumonia etc.) (c) Neurological —— Seizures

Treatment and Prevention : .
it . Malignancy -) Most common is transient lymphoproliferative disorder.
Chromosomal
- Diagnosis : The diagnosis of down syndrome is continued by Karyotyping and 1. Hyperhydration —> It is the cornerstone of prevention as well as treatment of TLS
—
analysis in children having suggestive clinica l features. Additional investigations include (a) IV fruid @ 2-4 times of the maintenance to be started 48 hours prior. and continued till 72
hours following the initiation of chemotherapy.
(a) Echowdiography
(b) Fluid should contain saline and dextrose without potassium and calcium.
(b) Thyroid function test
(c) IV frusemide added, if urine output is below 2ml/kglhour. even with IVF.
(c) Lateral neck radiograph
2. AlIOpurinol —+ It is xanthine oxidase inhibitor. which lowers uric acid level. Initiated
(d) BER?) prophylactically 48 hours prior to initiation of chemotherapy.
(e) Test for refractive errors 3. Treatment of hyperkalemia —;
MALIGNANCY (a) 10% calcium gluconate (cardiac membrane stabiliser)
I . [lPGMEH-c Sam] (b) Insulin + Dextrose
0. 1 : Tumour Lysis Syndrome. (intracellular shilt of K+)
(c) Salbutamol nebulisation
TUMOUR LYSlS SYNDROME
Ann
Ans -'
rised by hyperkale- (d) Exchange resin (eliminates K+ from body)
Tumour Lysis Syndrome (TL8) is a Iifethreateni ng oncological emergency. characte
ry to rapid break-
mia. hyperphosphatemia, hyperuricemia. hypoca lcemia, and/or azotemia, seconda
down at tumour cells after initiation of chemother apy or. rarely spo ntaneously.
1‘
MISCELLANEOUS U Chapter—13 303
- Treatment:
4. Treatment of hyperphosphatemia -+ 1. Maintain airway. breathing. circulation
(a) Hydration 2. Monitoring otvitals
(b) Oral phosphate binder (Aluminium hydroxide)
in symptomatic patients. 3. Antibiotics—
5. Treatment at hypocalcemia —y IV calcium gluconate only
(a) 1'l line - Piperacillin-Tazobactamlcetoperazone-sulbactam t amikacin
6. Dialysis —) Last measure for unresponsive patients.
Kt. PO‘. uric acid) (b) 2"” line — Meropenem + Vancomycin
(a) Reduces the load of metabolic products (urea. creatinine.
(b) Maintains euvolemia in anun‘c children (c) 1" dose of antibiotics should be given without delay
[MCK - 2016] (cl) 2"“ line antibiotics given, when fever continues for 48-72 hours.
a. 2 : Febrile Neutropem‘a.
(9) Antitungals - added. it fever continues after 4-7 days of antibiotic therapy.
Ans : 4. Supportive therapies -— Blood transfusion (Hb < 8 gm%). platelet transfusion (Pit < 10.000!
FEBRILE NEUTROPENIA mm3 or < 20.000 [mm3 with bleeding). G-CSF etc.
is encountered in children during the
Febrile Neutropenia is the most common emergency that 5. Maintenance of strict asepsis - Hand washing. restriction of invasive procedures (or do it
cy and it remains a significan t cause of morbidity and mortality.
treatment of malignan with meticulous aseptic measures).
or a temperature of 2 100.4°F for 2 1 hour,
. Definition : A single temperature reading of 2 101°F.
as febrile neutropenra. [ ENDOCRINE SYSTEM j
with an absolute neutrophil count (ANC) of < SOC/mma is known
- Etiology : It commonly occurs in children with -
(a) Acute lukernia
LONG oussrrons : ]
(lo) Lymphoma
‘
a. 1 : Discuss briefly the synthesis of thyroid hormones. Outline the clinical tea tures and treatment
(Sr-3+2) [2012]
(c) Solid tumours (Neuroblastoma. Fletinoblastoma etc.) oicretr'nism.
(d) Aplastic anemia a. 2_ : Outline in brief about thyroid hormone syn thesis and its control by higher centres. Outline
- Clinical Featurelvaluation : the clinical picture of cretirrism and its management. (3+2+3+2) [Midnapore - 2016]
.
A. History —> 1. Fever — onset. duration. severity Ans:
respiratory, GI. mus-
?_ Associated localizing symptoms — ear, nose. throat. THYROID HORMONE SYNTHESIS
culoskeletal. urinary. nervous system.
0 Thyroid gland secretes 3 hormones. namely —
3. Phase of chemotherapy — intensive / nonointensive
_ (a) Thyroxine or Tetraiodothyronine (T‘),
4. Recent hospitalization and antibiotics received
Examir fitlon :1. Vitals (Tempe rature, HR. BB. BP. Saturation) monitored at regular interval (b) Tri»iodothyronine (T3), and
B.
focus of infection.
2. Detailed systemic examination-to search for the (c) Caicitonin _ _
ed - Oral cavity.
3. Sites that need special attention and are comrnonty overlook - T, a T. are secreted from the follicular cells or acinarcells. have similar biological activity. and are
site of bone marrow
ear. sinuses. skin, nails. perianal area. sites oi IV access. termed asé‘thyroid homrones'. Whereas. calcitonin is secreted from parafollicuiar '0' cells and is
aspiration etc. involved in calcium metabolism along with parathonnone. .
0 Investigations: _ ° Steps of thyroid hormone synthesis :
Corrrplete blood count (inducing DC at ANC) 1. Iodine uptake - Iodine is present in the blood in the iorrn oi Iodide. which is taken up by the
PPS-9!“?
Eledrolytes. urea. creatinine acinar cells through active transport with energy expenditure. because it has to be moved
Blood culture against electrical and concentration gradient. This active transportis done by Nat : l‘
symporter (NIS) and is stimulated by TSH. This I‘ is carried across the apical membrane by
Chest X-ray
stool. urine. CSF. sputum. bronchoalveolar another transporter named ‘Pendrin.'
Cultures from other sites. as clinically relevant -
2. Oxidation and organificatlon of iodine — The iodide it) taken up by the cells is converted to
lavage. skin or pus
other forms oi iodine by the enzyme thyroid peroxidase in presence of H202. before it can
. Flick Stratification : (Low risk/High risk) combine With tyrosine residues of thyroglobulin, which is present inside colloid.
Low m High risk _ Thyroid
Intensive I + H201 Peroxidase t + H0l+ EOI
1. Phase of chemotherapy - Non-intensive
Clinically unstable/ co-mor’oldity 6
2. Clinically stable. no co-morbidity - ' These terms at iodine fr'odinium (l‘). Hypoiodons acid (HOI) & Enzyme-linked hypoiodate (EOi)]
3. No focus oi infection Focus $ combine avrdly with tyrosine residues without enzymatic intervention to to rm Monoiodotyrosine
4. ANC -+ 2 foofmm3 ‘ <100imm’ (Mil’) and Diiodotyroslne (DIT).
5. Anticipated neutropenla -y < 7 days > 7 days
Wu.
__——
K
\ K'-
MISCELLANEOUS El Chapler~ 13 305
(i) Tyrosine + Iodine (at position 3) -) MIT (3-MIT) 2. Negative feedback — Increased secretion of T3 and T. leads to inhibition of TSH secretion
by pituitary and reduction oi TRH receptors on pituitary (thus, reduction of TRH action).
(ii) 3-MIT + Iodine (at position 5) —) 3.5 —- DIT
whereas it
3. Autoregulation - When iodine content increases, thyroid gland is depressed.
3. Coupling -> Pairs of iodinated tyrosil residues couple together to form T and T . This is -
J 4 becomes hyperactive in the iodine-deficient state.
called oxidative coupling. and it is catalyzed by thyroid peroxidase.
(i) 3, 5 - on + 3-MIT fl» 3. 5. 3‘-Tri-iodothyronine (r3) CRETINISM
con-
Cretinism is a condition of severely stunted physical and mental growth owing to untreated
(ii) 3, son + 3. 5-017 32+ 3, 5. 3‘5'-Tetra-iodothyronine a.) genital deficiency oi thyroid hormone (congenital hypothyroidism). Most common
cause of con-
gland).
(iii) In some of the reactions. DIT may forrn the outer ring of T3 instead of MIT. producing genital hypothyroidism is thyroid dysgenesis (aplasia, hypoplasia or ectopia of thyroid
therefore. difficult
Reverse T3 (RTE). which Is physrologically inactive. Ci Clinical Features : Features of congenital hypothyroidism are non-specific and
3-MIT + a, 5-bit 139—» 3. 3 z 5 ' - Tri-iodothyronine (RT.) to identify in the neonatal period. They become prominent with increasing age.
increased due to
4. Storage and release —) The hormones. thus synthesized. remain attached to the thyroglo- 1. Birth weight and length are normal. whereas head size may be slightly
myxedema of the brain.
bulin molecule and is stored as thyroid colloid. till it is needed by the body for use. During the
need for release of the hormones. thyroglobulin is endocytosed within the cell. 2. Prolongation of physiological jaundice may be the earliest sign.
3. Scalp -> (a) Anterior and posterior iontanelles are widely open
i (b) Scalp is thickened
Fusion with Iysosome to iorrn phagolysosome (0) Hair is coarse. brittle and scanty
t (d) Low frontal hairline
Hydrolysis by proteases 4. Facies —>(a) Edematous facies with swollen eyelids
t (b) Wide apart eyes. with narrow palpebral fissures
Release of T... T‘. MIT. DIT (c) Depressed nasal bridge
(d) Mouth is kept open with protruding thick. broad tongue
/\
T.I and T. are secreted MIT and DIT are deiodinated
5. Affected infants cry little. sleep much. have poor appetite and sluggish movements
6. Skin —) (a) Rough. dry skin
.
(by iodotyrosine dehalogenase) (b) Hypothermia

into the circulation
7. Abdomen -? (a) Large abdomen
(b) Umbilical hernia
Released iodine is re-utilised _.
(c) Constipation (Refractory to treatrnenl)
ral
T3 is about 3 times more potent than T.. periphe ertrophy of muscles occur (Kosher-
5. Peripheral conversion of T. to Tr’ As , 8. Generalized hypotonia. with occasional pseudohyp
rts T. to T3 ~—
tissues especially. liver and kidney , conve Debré-Sémélaigne Syndrome)
5' ~deiodinase 9. Pallor. due to macrocytic anemia
4 T3
'10. Delayed deveIOpmental milestones
T. and convert
except brain and pituitary, which take up 11.Growth retardation and stunting
0 Target tissues usually takes up this T3. In untreated long-standing cases
it to T3 within their own cells. 12. Delayed dentition of congenital Hypothyroidism
13. Delayed puberty and sexual maturation
D REGULATION OF SECRETION :
1. Control from higher centres — 14. Mental retardation with very low IQ
hypothalamus. El Management
TRH (Thyrotropin releasing hormone) from
' Investigations:
1. Free T. —» Low
2. TSH —i (a) Usuafly high
st imulating hormone) release from anterior pituitary (b) Low in central causes of hypothyroidism
| Dopamine. Somatostafl —O—>TSH (Thyroid 3. Other Investigations to look for etiolo
gy —>
lo (a) Thyroid scan {radionu cleotide uptake)
Thyroid hormone (T3. T.) synthesis from

thyroid gland (stimulates all (b) use of thyroid gland
the steps exce pt perip heral conv ersion of T. to T3) -..,_.
\
"\.,
‘5. _.
39
AI—fl-J— Junk“ .. ;_-_-7
MISCELLANEOUS CI Chapter-13 307

(a) Primary TSH method - T. is measured only it TSH > 20 plU/ml. This approach is likely to miss
(c) Thyroglobulin level
central hypothyroidism. thyroglobulin deficiency and transient hypothyroxinemia of prematurity.
(d) Antibodies (anti-TSH receptor. anti-TPO) (b) Primary T. method — Likely to miss milder/subclinical cases. where T‘ is initially normal with
_ -
- Treatment : elevated TSH.
(T.) -+ Replac ement of thyroxin e is the mainstay of lherap y. Ior congenital
1. Thyroxine (c) Concomitant TI and TSH method — Most sensitive approach. but it incurs higher cost.
hypothyroidism (CH) or cretinism .
' Role of Free T. (FT‘) : FT. measurement is costlier than T... but it provides better estimate in preterm
> Dose - Starting dose varies with age -— infants (low levels of TBG) and thyroglobulin deficiency (TBG).
(a) Newborns -+ 10-15 pglkglday - Further evaluation :
(b) Infants —> 6-10 pglkg/day I
(c) Children —) 3-5 pglkglday ‘ Abnormal Tfl-‘il.TSH

In children who are well-controlled with
> Duration -i Usually lilelong treatment is needed.
3 yrs to rule out transient forms of CH.
therapy. discontinuation lor 4-6 wks is tried at the age 0 i l
> Monitoring —> Thyroid function tests to be repeated —
(a) lst 6 months -> Monthly/6 weekly
(b) 6 months — 3 years —+ 3 monthly i
. Normal uptake
(0) > 3 yrs —+ 6 monthly No uptake Ectopic uptake
ment should precede thyroid replace ment. as it
2. In central hypothyroidism. cortisol replace l l t
could precipitate adrenal insuffic iency. )Ultiound (<3G) j Measgrggent oi
of thyroxine. How will you screen for conge
nital
O. 3: Discuss different steps of synthesis (5+5) [NBS — 9th Sent]
hypothyroidism?
No thyroid Normal thyroid
Ans : gland gland Normal Absent
Thyroxine Synthesis: _
l i l l
See 0. 1. 0.2 (Thyroid hormone synthesis).
Thyroid _ Ab to TSH Dyshormonogenesis. TBG synthetic
OIDISM Agenems receptor . Iodine deficiency defect
SCREENING OF CONGENITAL HYPOTHYFI
subtle and
on of congenital hypothyroidism (CH) due to
- Necessity : Difficulty in early ide ntiticati the disastr ous consequences of
th e neona tal '
period . along with
non-specific clinical features in have led _ .1:
delayed diagnosis and treatment in the loan of impai red neuro—intellectual development Positive Negative
to introduction of neonatal screening of CH. . i l '
‘ .
. Timeline: Transient CH Thyroid hormone
sample
postnatal age of 3-4 days With dried blood biosynthetic detect.
1. Universal screening is ustially done at due to maternal Ab
collection. TSH receptor detect
other
ing. it screening is done only for CH and not for
2. Cord blood can also be used for screen _ . '
inborn errors of metab olism.
ing.) for DH is currently being done in
(universal screen
0 Indications : Routine newborn screening indications for screening are -
sal screening.
may parts of the world. In the absence of univer 0. 4 : Clinical features and management of Congenital Hypothyroidism. [curve 4 lllh Sam]
. . ‘ .
(a) Family history of CH Ans: See 0. 1. 0. 2.
roid medicm e intake in the mother '
(b) History of thyroid diseas e or antithy
-
ence of associated CH. like — Down syn- a. 5: Diagnosis ofHypothyroidism in infant. [MMC - 8th Sent]
(c) Presence of other conditions with higher preval ins syndrome etc.
y 18. Neura l Tube defect s. Pierre -Robb Ans: See 0. 3 (Screening & Flowchart) + Q. 1. 0.2 (Investigations)
drome. Trisom g.
' m toms of CH. '
like —— prolon ged jaund ' cons tipatlon. poor feedin
ice. .
e of Si‘ nsls atous a dry skin etc. 0. 6: Congenital Hypothyroidism. [2008, 2014 — Supplementary]
open posterior tontanelle. edem
(d) Eglfifiggl hernig, mairoFglossia. wide
for screening of CH — Ans .- CONGENITAL HYPOTHYROIDISM
- Methods : There are 3 approaches Congenital Hypothyroidism is one of the most common preventable causes of mental retardation.
(a) Primary TSH, back-up T. (MC used strategy)
‘ Incidence: 1 :4,000 live births (worldwide) '
(b) Primary T“ back-up TSH
(c) Concomitant T. and TSH
———
CHAPTER - 14
Causes :
A. Permanent - APPROACHES
asia. (c) Ectopia (MC cause)
t. Thyroid dysgenesls — (a) Aplasia, (b) Hypopl
2. Thyroid hormone biosynthetic detect
since 6
3. Iodine deficiency (Endemic cretinism) 0.1: 2 years old child weighing 8 kg presented with H/O recurrent respiratory distress
y,
4. Central hypothyroidism [Defects in pituitary (TSH)
or hypothalamus (TRH)]. months of age. On examination, there is tachycardia, tachypnea and tender hepatomegal
but no cyanosis. What is yourprovisional diagnosis? How will you approach the case for
B. Transient — [MCK — 2016]
mother management ? (1 + 7)
1. Transplacentat passage of TSH receptor Ab from
2. Exposure to goitroge ns (Iodide. Antithyr oid drug) Ans: PROVISIONAL DIAGNOSIS
3. Transient hypothyroxinemia of. prematurity lnformations available —
4. Sick Euthynoid syndrome t. 2 years old child
Clinical Features : O. 1 ‘ 2. Weight = 8 kg. [Expected weight at 2 years = 2 x 2 + 8 = 12 kg; this child weighs 67% of
Screening : 0.3 expected —> Grade II malnutrition according to IAP classification].
Treatment: 0. 1. . Hi0 recurrent respiratory distress since 6 months of age.
4. Tachycardia. tachypnea and tender hepatomegaly on examination. suggestive of congestive
RECENT UPDAEI cardiac failure (CCF).
[2017 Supple] 5. No cyanosis excludes congenital cyanotic heart diseases as possibility.
ization.
0.1: Recent recommendation of polio immun Provisional diagnosis : 2 years old child having FTT (failure to thrive) with I-IIO recurrent respiratory
last few years,
Ans: In the light of remarkable achieve
ment i n the field of polio eradication in India over distress (probably due to recurrent respiratory tract infection) and CCF without cyanosis suggests
tial tPV — OPV schedu le has been recomm ende d. This will pave the way to ultimate diagnosis of -)
now sequen za-
ring the inevitab le cessation of OPV from immuni
adoption of all IPV schedule in future conside paralyti c poliomyeiitis) and
Congestive cardiac failure due to acyanotic congenital heart cfisease (e.g.. VSD, PDA. ASD etc.)
i.e.. VAPP (vaccin e assoc iated
tion schedule owing to it’s safety issue. APPROACH FOR MANAGEMENT
CVDPV (circulating vaccine derived polio virus).
This child is suffering from CCF and common causes to be considered are left to right shunts. Like —
Recommended schedule : Birth dose - OPV
. 1. Ventricular Septal Defect (V30)
- Primary doses of IPV at 6, 10 8. 14 weeks
2. Patent Ductus Arteriosus (PDA) and ..
- OPV at 6 and 9 months and at 5 years.
3- Atrial Septal Defect (ASD) (Least common possibility, as ASD usually presents at g‘tater
-IPV (Booster) at 15 - 18 month. age .
Additional doses of OPV on all Nl & SlAs A) History — In addition to l-t/O failure to thrive and recurrent RTI. There may be history of —
-
minimum 3 doses.
- OPV in place of IPV, if IPV is unfeasible. 1. Exertional dyspnea 4 Which manifests as feeding difficulty in young infants. Mother
8.0 may complain of typical “Suck-Hest-Suck" cycle during feeding.
- OPV —» two drops oral. IPV — 0.5 ml [M or
is given
in few states of India. In West Bengal OPV 2. increased sweating —> Over forehead typically during feeding/exertion (due to
However IPV is currently included in NIP only
le. Sympathetic stimulatlon)
in national programme as previous schedu
3. Orthopnea —) T ed breathlessness on lying down.
B) Examination -
1. Anthropometry —) Usually points toward chronic malnutrition.
a) l ed weight for age
b) i ed height forage
c) l ed Head circumference for age (sometimes)
d) 1 ed MAC. chest circumference.
2. Signs of respiratory distress --)
a) Tachypnea (already mentioned) with —
309
APPROACHES Cl Chapter-14 311
3 varieties.
c) Cardiomegaly: If the lesion is significant. seen in all
b) Chest retractionsl Indrawing. d) Apex: RV-type (upturned apex) in ASD, LV-type in VSD
and FDA
c) Nasal flaring. } may be present
3. ECG -)
d) Head nodding - RBBB (Flight Bundle Branch
a) ASD: Right Axis Deviation (RAD), RVH. sometimes
3. Signs of heart failure —> Block) and FIAH (Right Atrial Hypertrophy)
a) TaChYCa'd‘a- ] already mentioned b) VSD : Biventricular enlargement
1;) Tender hepatomegalv. c) PDA : LVH and LAH (Left Atrial HypertrOphy)
anomaly requires echocardiography.
c) Raised JVP. } may be present 4. Echocardiography -) Final diagnosis of the cardiac
d) BlL basal crepitations in lung It also —-
dation or bronchopne umonia may be a) Delineates the size of the defect,
4. Othersigns of RT! 4 like lever. features of consoli
found in addition b) Assesses different chamber enlargements.
etc.
5. Cyanosis —) absent c) Measures the degree of pulmonary hypertension
6. Clubbing 4 absent
D) Treatment -
7. Examination of CVS -) 1. H, of CCF 4 With diuretics, digoxin. ACE inhibitors
ing pulse) in PDA: even pulsation
a) Pulse -Water—hammer pulse (high volume collaps
is easy palpab le. 2. fix of RT! —i With appropriate antibiotics (oralllV)
of Maria Dorsalis Pedis
3. Surgical correction of the defect —)
b) BP— Wide pulse pressure in PDA
a) Device closure, or
c) Apex Beat—
only outward shift b) Open surgical correction
i) Position — Down and out (LV type apex) in VSD and PDA.
(RV type) in ASD 4. Providing adequate nutrition -) Pre and post-operatively.
ined) in VSD and PDA. both.
m Character— Hyperdynamic (Forceful. ill-susta purpuric spots a ver difierentparts
the degree of RV enlargement) O. 2 : A nine year old girl presented with mild pallor, multiple
d) Parasternal pulsation/ lilt/heave — (Depending on of the body. Clinical examination did not reveal any significant
lymphadenopathy or
found in VSD and A80 s ? [MEMO—8th Sent]
hepatosplenomegaly. How do you approach the case for diagnosi
in A80
e Epigastn'c pulsation — Usually prominent
H
Ans : APPROACH
1) Palpable P2 - in VSD
g Thrill - Best palpable at - - Available informations —
V
0 Lower Left Stemal Border : VSD 1. 9 year old girl child

i) Pulmonary area and Left intraclavicular region
: FDA 2. Presentation - Mild pallor and multiple purpuric spots all over the body.
in) Rare in ASD 3. No lymphadenopathy
h) Heart Sounds - 4. No hepatosplenomegaly
i) Loud S1 in PDA - Possible causes! lferentiaf diagnosis -—
i) P2 is accentuated in all three A) Thrombocyfopenla (low platelet count) —>
:Wide and variable split in VSD; Reverse 1) immune Thrombocytopenic Purpura (HP) or immune mmmbocytopenia « Most common
ii) Splitting of 32 : Wide, fixed split in ASD l
cause (provisional diagnosis) _
splitting in PDA.
left stemal border in VSD, Continuous . i
i) Murmurs - Pansystolic murmur at lower 2) Aplastic anemia
left infraclavicular region in PDA. i
machinery murmur at pulmonary area and 3) Bone marrow infiltration - Acute leukemias (may present initially without lymphadenopa
thy
nary ejectio n systol ic murm ur in ASD. ~
pulmo or hepatosplenomegaly)
sound at femoral artery, Duroziez’s .
j) Others — Other vascular signs, like — Pistol shot 4) Infections 4‘ Like
murmur etc may be found in PDA. a) Septicemia. Meningococcemia. '
_
C) Investigations —- b) Viral hemorrhagic fever (Dengue),
there is
nuclear leukocytosis may be present, If c) Rocky mountain spotted fever
1. Complete Blood Count -+ Polymorpho
active RTl. 5) Consumption -
2. Chest X-ray -+ a) Microanglopathy (HUS. TTP) _ '
es may be found in cases of RTl.
a) Consolidation or bronchopneumonic chang b) DIC
: In all L -) R shunts.
b) Pulmonary congestion / hyperemia
l
Chapter~14 313
APPROACHES El
312 QUEST: PAEDlATRlCS
6) Drug-induced — like Aspirin. Phenytoin. Sulfonamides etc

- Lymphocytes T ed in viral infections and ALL
7) von-Willebrand Disease (Platelet type or Type 28). 0 Blast cells may be seen in ALL
B) ”trombasthenia -) (Platelet count - Normal. Platelet function — Defective) 0 Neutrop enia in aplastic anemia. ALL
t) Congenital (9.9.. Bemard-Soulier Syndrome and Glanzmann's Thrombasthenla) d) Platelet count —9

in Bernard-Soulier Syndrome
2) Acquired (9.9.. Uremia) - Low in all causes of thrombocytopenia and also
(833)
C) Vasculopatby—r )
' Normal in the rest (Vascular causes. thrombasthenias
1) Henoch-Schonlein Purpura (HSP)
e) Platelet size - usually large in 888
2) Scurvy (Rarely presents with purpura)
2) Coagulation profile —
. Diagnostic approach —
a) Bleeding Time —+ Raised in all causes of purpura (usually)
A) History—r es)
b) Clotting time -> Raised in MD. DIC. infections (sometim
1) Fever — is associated with infectious causes. lukemias. aplastic anemia etc.
c) PT —-) Prolonged in DIC
2) Joint pain — in HSP. ALL. Dengue etc.
d) aPTT —> Prolonged in vWD. BIG
3) Severe pain abdomen - in HSP. Dengue, Meningococcemia
9) Fibrinogen level —-> low in 010
4) W0 recent infection - in lTP
f) D-dimer assay —9 Positive in BIG.
5) H/Oreounent bleeding- in congenital causes. like congenital thrombasthenias. vWD. Scurvy of lTP. ALL and
(mainly gum bleeding) 3) Bone Marrow Examination - When there is confusion between diagnoses
blood count.
aplastic anemia due to disparity in clinical features and peripheral complete
6) Drug history— may reveal intake of drugs causing thrombocytopenia. bone marrow aspiration is done. It is confirmatory in the diagnosis of these 3 diseases.
series
B) Examination—r ’ a) lTP —> Normal/increased number of megakaryocytes. erythroid and myeloid
1) General state of well being- are normal.
a) Chfld looks otherwise healthy in lTP b) Aplastic anemia —) Hypoptastic marrow with depression of all the 3 series and increased
fat spaces.
b)_ Child appears sick with fever and constitutional symptoms in infectious causes. Aplastic
anemia and ALL. c) Leukemias -> Adequate number of blast cells (> 25% lymphoblasts in ALL. > 20%
myeloblasts in AML) are present.
2) Distribution of purpura -
4) Acute phase reactants — (ESR, CRP) raised in infections and malignancy (ALL)
a) All over the body with occasional small ecchymoses is seen in lTP and most of the
other causes of thrombocytOpenia. 5) Platelet Function Tests - for diagnosis of congenital thrombasthenias (BSS, Glanzmann‘s
thrombasthenia) .-
b) Symmetrical distribution over bilateral lower extremities is seen in HSP.
6) Blood Culture — Positive in septicemia
3) Palpabie purpura - in HSP.
7) Serology—
4) Necrotic hemorrhagic rash - i.e.. eochymosis around necrotic patch, is characteristically
seen in meningococcemia. 3) 19M l lgG ELISA for Dengue (NS1AG for early detection)
5) Features of shock — i.e.. tachycardia. hypotension. delayed capillary refill etc. are seen'in b) Also helpful in confirmation of meningococcal infection and rickettsial infections.
dengue. meningoooocemia etc. 8) Renal Function Test— Abnormal in uremia. HUS
6) Hess Capillary Test- Positive in vascular causes (T ed capillary fragility) including dengue. 9) vWF assay — for diagnosis of vWD
C) investigations —) 10) Skin biopsy — for confirmation of diagnosis in HSP
1) Complete Blood Count— 11) Vitamin C level — Low in scurvy
a) Hb% —+ Mildly low 12) Radiological changes — characteristic in scurvy.

b) Total Leukocyte Count -+ flit 4 year old child presented with pallor. fever. gum bleeding and 1.5 cm palpable spleen.
- Normal in lTP Mention the diagnostic possibility and investigations to confirm diagnosis. (3 + 5)
0 High in infections. ALL [2012, 2014 supplementary]
' Low in aplastic anemia. ALL Ans: DIAGNOSTIC POSSIBILITY -

[N.B. ALL may have both high and low TLCs]
' Available lnforrnatlons -
0) Differential count —>
1. 4 year old child
- Polymorphs T ed in bacterial infections
2. Presentation — Fever. pallor. gum bleeding
an.
40
"\
‘* .
314 QUEST : PAEDIATRICS APPROACHES El Chapter—14 315
3. OlE -— Splenomegaly (1.5 cm) 8. Severe headache and myalgia -— ln dengue (Older patient may even complain of classical
retro-orbital pain)
4. Duration — Not known
9. Night sweats -— Common in Hodgkin's lymphoma
- Differential diagnosis -
10. Hyperpigmentation — ln kala-azar
1. Hematological mallgnancles - Most probable diagnosis
11. Oliguria — May be seen in leptospirosis
a) Acute Ieukemias (ALL. AML)
B Examination —t
h.-
b) Lymphoma (Non-Hodgkin > Hodgkin)
1. General appearance —-
2. Infections-
a) Toxic/Sick looking in sepsis. leukemia. enteric lever. disseminated tuberculosis.
a) BflCfGfifll—i
dengue.
i) Sepsis
b) Relatively well-appearing in kala-azar and viral hepatitis
ii) Disseminated TB
. lcterus ~ Corroborative to jaundice in history.
parapet-hum
iii) Enteric fever with complications
. Malnutrition - Corroborative to weight loss in history
iv) Leptospirosis . Lymphadenopathy— ln lymphoma. leukemia and TB
b) Viral—i . Coated tongue — In enteric fever
i) Viral hemorrhagic fever (e.g., Dengue HF)
Gum hypertrophy — ln AML
fi) Acute viral hepatitis Tachycardia, Hypotension (Shock) - in Dengue. Sepsis
c) Parasitic —) Kala-azar
. Hepatomegaly— In almost all cases
3. Others (Rare) — .Signs of respiratory distress, crepitations— ln TB
a) Hypersplenism (in chronic hemolytic anemia)
10. Meningism- May be found'In TB Enteric fever. leukemia
b) Connective tissue disease
C investigations 4
H
c) Storage disease with intercurrent infection
1. Complete Blood Count-
APPROACH a) Hb% -> Low
(In this question. only investigations are required. But. anytime language of the question may change. b) TLC —>
So, lull diagnostic approach is being included in the answer) . High in sepsis, leptospirosis
A) History-a - Lowin kala-azar
t . Intensity of fever- - HigMow/Normalin leukemia. TB. entericfever
3) High-grade in sepsis. enteric fever. leptospirosis and dengue HF. c) DLC —I>
b) Low-grade in TB. viral hepatitis. kale-azar. - Polymorphonacleer in sepsis
2. Fever pattern - 0 Relative hrmphoqrtosisinTB. ALL. enteric fever. kale—azar.
a) Evening rise of temperature in TB d) Platelet count —> Usually low in leukemia sepsis and dengue; may be low'In kala-
azar. enteric fever. lymphoma and TB.
b) Double rise (Saddle back pattern) in a day :typicaliy seen in kale-azar.
e) Abnonnal cells —>
c) Step-ladder pattern : seen in Typhoid (Flare in children)
in T8. kale- ' Lymphoblasts in ALL
3. Jaundice — Significant jaundice in viral hepatitis and leptospirosis. may be found
azar. lymphoma, leukemia. c Myeloblasts in AML
4. Altered bowel habit— - Hypersegrnented neutrophils in sepsis
a) Alternate diarrhoea and constipation in enteric fever 2. 533- -Very high In TB and malignancies
3. LFT— Abnormal in viral hepatitis leptospirosis: may beabnomtal'In malignancies. sepsis.
b) Constipation may be associated with TB (Abdominal TB)
enteric fever. dengue
c) Diarrhoea occasionally seen in kale-azar. 4. RFT- May be abnormal in leptospirosis with renal involvement
ed with superior
5. Cough and respiratory distress — In TB, leukemia/lymphoma complicat 5. Blood culture - May be positive in sepsis and enteric fever
medlastinal syndrome.
6. Chest X-ray—
6. Weightioss- In malignancies. TB, kale-azar.
a) Miliary shadow'In mtliary TB
7. Appetite - Relatively preserved in kala-azar b) May show pleural effusion In TB. malignancies. dengue fever
QUEST : PAEDIATRICS APPROACHES El Chapter—14 317
316
c) Mediastinal widening in lymphoma, TB B) infections ->

7. Bone Marrow Examination - t. Sepsis
3) Presence of blast cells (> 25% lymphoblasts in ALL. > 20% myeloblasts in AML) is 2. Disseminated TB
confirmatory tor the diagnosis of acute Ieukemias. There is also variable depression
of RBC and platelet series. ' 3. Kala-azar (chronic)
b) LD Bocfies (amastigote forms of the parasite) can be demonstrated in bone marrow in - Approach - Same as Question No. 3 (approach). except —
viral hepatitis
60-85% of patients with kala~azar. I. Exclude the points for enteric lever. leptospirosis. dengue and
and juvenile CML in history. examina tion and investigation.
0) Depression oiali 3 series with resulting pancytopenia may be seen in bone marrow 2. Add discussions about CML
involvement due to lymphoma. TB. kala-azar. CML
8. Lymph node biopsy—
ristics —
a) Diagnostic of lymphoma CML or chronic-myelogenous leukemia has the following characte
b) Ditferentiates between Hodgkin and non-hodgkin lymphoma A) History—i

1. Fever
0) Tubercles or AFB is seen in TB
me a N
Weight loss
d) LD bodies in 60% cases of kala-azar
kala-azar. Night sweats
9. Spienic aspiration - Highest yield of LD bodies (90-95%) in cases of ‘
Bone pain
10. Serology —
Early satiety (due to splenomegaly)
a) Widal test — Positive in enteric fever (after tst week of fever) ‘
6. Lt. upper quadrant abdominal pain
b) Agglutination test — For detection of leptospiral Ah
B) Examination -+
(Hepatitis B), Anti-HOV Ab etc. .
0) For viral hepatitis -— Anti HAV Ab (Hepatitis A), HBsAg I. Sternal tenderness
of fever ‘
d) Dengue NS, Ag — Positive in the 1515 days 2. Features of hyperleukocytosis (e.g., respiratory distress,
visual disturbances. priapism etc.)
e) Dengue lgM ELISA — Positive alter 5 days C) investigations —>
.
stic test) “
I) RK-39 Ag — Positive in kala-azar (Rapid diagno 1. Peripheral blood —
T in TB.
11. Sputum/Gastric Lavage Obtained to demonstrate AFB or to perform CBNAA a) Anemia-normocytic. normochromic
-
to
positive or negative in disseminated TB due
12. Mantoux test— Positive in TE (may be weakly b) Leukocytosis (often > 50,000/mm3)
low immunity in the patient) c) Thrombocytosis (chronic phase) or thrombocytopenia (blast
phase)
13. CSF study- cells in peripher al smear (e.g., myelobla st. myelocy te, mét‘amyelocyte.
d) Early'myeloid
meningism ‘
a) For diagnosis of TB meningitis, enteric nucleated RBCs). blast cells may be found during blast phase.
involv emen t in ALL. g
b) To look for CNS 2. Bone marrow —
-
n revealed severe a) Hypercellular with elevated M : E ratio
d with lever for 20 days. Examinatio
' A two year old child has presente s all over the body . Write the differential b) Blasts (Myeloblasts) < 5% in chronic phase and > 30%
in blast phase of CML (
purp uric spot
pailor, hepatospienomegaly and [2011]
to reach th e final diagnosis. (5 + 3) c) Cytogenetics show Philadelp hia chromos ome (19 :22)
diagnosis. Suggest investigations
JCML l
DIFFERENTIAL DIAGNOSIS
Ans :
known as JMML (Juvenile Myelomonocytic
JCML (Juvenile Chronic Myelogenous Leukemia) is now
- Informations available — Leukemia). Characteristics are -
I. 2 year old child A) Presentation 7)
2. Fever x 20 days spots all over the body. 1. Flashes. ‘
3. Examination — Severe pallor.
Hepatosplenomegaly and purpuric
2. Lymphadenopathy,
- Possible causes - 3. 7 Splenomegaly and
A) Malignancy —> 4. Hemorrhagic manifestation
AML) ‘
1. Acute leukemias (9.9., ALL. 5. Age < 2 years
-
2. Lymphoma (9.9., NHL > HL) B) investigations —)
nile CML) I
3. Chronic leukemias (CML, Juve 1. Peripheral Blood —
‘ \
31B QUEST : PAEDIATFIICS APPROACHES El Chapter-14 319
a) Anemia. O. 7 : A 4 year old child is admitted with severe respiratory distress, pellor and generalized
lymphadenopathy. Enumerate the possibilities. How will you investigate such a case?
b) TTLC.
(3 + 5) [KPC -9th Semi
c) Monocytosis (Absolute monocyte count > 1000lpL). Ans : POSSIBILI‘HES
d) Thrombocylopenia.
- Available information -
e) Presence of erythroblasts.
1. 4 year old child
2. Bone Marrow —>
2. Severe respiratory distress
a) Less than 20% Blast cells.
3. Pallor
b) Absence of Philadelphia chromosome.
4. Generalized lymphadenopathy
c) Myelodysplastic pattern
- Diflerentlaldiagnosis-
3. HbF—) Increased
1. Lymphoma —i
3 a. 5 : An 8 year old boy presen is with is ver, epistaxis, severe pailor, generalized a) NHL - Cause of respiratorydistresse
l lymphadenopathy and hepatosplenomegaly. What may be the most likely diagnosis ? Give b) HL i) SuperiorMediaslinalSyndrome(MC)
' the 0/0. investigate the case to arrive at diagnosis. {1 + 2 + 5) [MMC - 8th Semi]
2. Acute leukemia» ii) pleufal effusion
O. 6 : A 4 year old boy presented with fever for 3 weeks, associated with pailor, epistaxis, a) ALL iii) Pneumonia
generalized lymphadenopathy and 2 cm palpable spleen. Mention the diagnostic b) AML
l ossibilities and necessa in vestigatlons to confirm the diagnosis. (3 + 5) .
3. Disseminated tuberculosis or Hillary TB
p ry [RGKMCH — 2016}
4. Others (rarely) ->
Ans : DIAGNOS110 POSSIBILITIES a) CML
- Available lnformatlons - b) SOJIA
1. 8 year old! 4 year old boy c) SLE
Fever (3 weeks in Q. 5)
shears
INVESTIGATIONS
. Pallor (severe in Q. 5) Same as Cl. 6.
Epistaxis
Generalised lymphadenopathy 0. 8 : A 6 year old child presented with 2 weeks fever with pallor,
iymphadenopathy and
hepatosplenomegaiy. Discuss the possible 0/0 and investigations for
6. Hepatosplenomegaly l 2 cm splenomegaly conglmlation of
diagnosis. - (4 + 4) [NR8MC.-.9th Sam]
- Diflemflal diagnosis - Ans .' DIFFERENTIAL DIAGNOSIS
1. Acute leukemia —}
- Avallableinformations-
a) ALL (Most likely diagnosis)
1. 6yearold child
b) AML
2. Fever-2weeks
2. Lymphoma a
3. Pallor
a) Non-Hodgkin lymphoma
4. Lymphadenopathy
b) Hodgkin lymphoma
5. Hepatosplenomegaly
3. Disseminated tuberculosis
- Posslblllties-
4. Others (Rare possibilities) -)
1. Acute leukemia-
a) Kala-azar (chronic) [Lymphadenopathy is rare]
a) ALL,'-
b) Chronic leukemia (CML, JMML)
b] AML
c) Connective tissue diseases (Systemic onset JIA. SLE)
2. Lymphoma—
.INVES‘I’IGATIONS a) NHL.
See 0. 3, Q. 4 and O. 9 (for informations about SOJIA and SLE) b) HL
3. Infections-
320 QUEST : PAEDIATHICS APPROACHES EI Chapter-14 32_1
a) Disseminated TB 4. Pharyngitis with marked tonsillar enlargement, occasionally with exudales / white membrane
b) HIV infection. over tonsils
0) Infections mononucleosis 5. Petechiae at the junction of hard and soft palate
4. Others (rarely)— 6. Rarely, maculopapular rash
a) Chronic leukemia, C) Investigations —i
b) Connective tissue disease. 1. CBC-
0) Chronic kala-azar. a) Leukocytosis with relative lymphocytosis
b) 20-40% of atypical lymphocytes
INVESTIGATIONS I APPROACH
c) Mild thrombocympenia (but without manifested purpura)
Like Question No. 3 - Question No. 6. + lnforrnations about HIV infection and infectious mononucleosis, 2. LFT- Elevated liver enzymes
which are given below—
3. Definitive diagnosis -
0 HIV Infection - a) Heterophile Antibody Test - Paul-Bunnell Test
A) History —) b) Antibodies to EBNA, EA and VGA (M0 = IgM-VCA).
1. FaiIUre to thrive or chronic malnutrition (not gaining weight)
2. Chronic diarrhoea/recurrent diarrhoea. a. 9 : A 10 year old girl presents with is ver for 4 weeks along with anemia, hepatosplenomegaiy
and swelling of both knee and ankle joints. What are the differential diagnosis? Write
3. Recurrent RTI (Respiratory Tract Infection) briefly the clinical and laboratory evaluation to reach the diagnosis. (2 4- 6) [SSKM -— 2016]
4. Oral thrush
Ans : DIFFERENTIAL DIAGNOSIS
B) Examination ->
1. Findings corroborative of histories - Available infonnatlons —
2. Parotid swelling 1. 10 year old girl child
3. Generalized Iymphadenopathy 2. Fever — 4 weeks
4. Hepatosplenomegaly 3. Anemia
4. Hepatosplenomegaly
C) Investigations —>
1. 080— 5. Swelling of both knee and ankle joints (Arthritis)
- 0 Possibilities -
a) Anemia,
b Leuco enia May be present alone or In 1. Systemic onset JIA
) p ' combination -2. SLE
c) Thrombocytopenia
3. Acute leukemia (ALL)
2. Definitive diagnosis - Test for antibody against HIV - 1 and 2 by means of rapid test and
ELISA lest. 4. Polyarticular JIA (may have systemic features)
- Infectious Mononucleosis - Caused by Epstein—Burr Virus (EBV). DIAGNOSTIC APPROACH

A) History-> A) History -)
1. Fever ( may be acute/prolonged [> 1 week] ) 1. Age of onset-
2. Prodromal symptoms (e.g., malaise, fatigue, headache etc) a) SOJIA can occur at any age
3. Sore throat b) ALL is more common at a younger age (2-5 years)
4. Pain and discomfort at left upper quadrant of abdomen (due to rapidly enlarging spleen) c) SLE is more common at prepubertal age (10-12 years) -
B) Examination —> ‘
2. Sex predilection -'
1. Generalized lymphadenopathy a) No sex predilection for ALL and SOJIA
2. Splenohepatomegaly b) Females are more affected in SLE (9 :1) and polyartic
ularJlA (5 :— 1)
3. Distribution of LN involvement - 3. Fever - Usually high-grade In SOJIA and low-grade
in others, like ALL. SLE etc.
a) Cervical nodes are commonest 4. Rash -
b) Axillary and inguinal LNs — rare a) Evanescent, salmon-coloured rash in SOJIA
0) Epitrochlear LN — specific b) Malar rash. discoid rash and photosensitivity are
seen in SLE as skin manifestations
41
5.“
APPROACHES U Chapter—14 323
r
d) Platelet count —
c) Purpuric rash may be found in ALL.
be encountered in SOJIA and SLE. - Elevated in JIA
Bleeding manifestations —— More common in ALL. may
9°?49’S"
. Low in SLE and ALL
Bone pain — Characte ristic for ALL
ESFl - Raised in all the diseases.
“NP’P‘PPP
Pallor— More severe in ALL CRP- Elevation of ESR is very high in ALL in respect to CRP
Joint involvement — Ferritin -— High in JIA
a) Mainly involves large joints in ALL and SOJlA Renal function - (urea, creatinine) may be high in SLE nephritis.
polyarticular JIA.
b) Both large and small joints are involved in SLE and Urine R/E ~ Shows proteinuria, hematuria. casts in SLE
—} mainly in polyarticularJlA.
c) Axial joints and temporomandibular joints involved 03 level -— Usually low in SLE nephritis
toid factor (RF) +ve variety of ‘
d) Symmetric joint involvement in SLE and Rheuma . X-ray ofjoints —
polyarticular JIA. a) JIA: Soft tissue swelling. osteoporosis and periostitis as early changes and varying
.
ia. HTN. edema etc. are seen in SLE. degrees of bony destruction with loss of cartilage in advanced stages.
.
9. Renal involvement— In the form of oliguria. hematur

....
10. Neuropsychiatric manifestation - In SLE, b) SLE/ALL: Non-erosive arthritis

III—l_|lh"|n|7
11.Aiopecia - Non-scarring in SLE. 9. Chest X-ray-

a) Pleural effusion in ALL, SLE
B) Examination —> b) Pneumonic changes in ALL
redness. swelling and limitation
1. Classical signs of arthritis — Including tenderness. warmth. c) Ground-glass opacity of interstitial lung disease in SLE
ly seen in JIA. There may be only painless swelling of joints in SLE.
of moments are common
less common in SLE and usually absent in d) Usually normal in JIA
2. Lymphadenopathy— Common in ALL and SOJIA.
polyarticular JIA. 1'0. Connective tissue profile —-
3. Stemai tenderness - Positive in AU_. a) ANA—
and SOJIA (i.e., distant heart sounds, - Sensitive marker of SLE (positive in 95-99% cases)
4. Signs of pericardial effusion May be seen in SLE
-
pericardial rub etc.) - Not very specific for SLE
5. Oral cavity- - Positive in 40% cases of polyarticular JIA
a) Oral ulcers common in SLE - Usually negative in SOJIA.
b) Oral thrush may be seen in ALL b) Anti ds-DNA Ab
} Specific for SLE (done if ANA is positive)
6. Respiratory system — Signs suggestive of - c) Anti-Smith Ab
a) Pneumonia or pleural effusion in ALL d) Rheumatoid factor — Positive in 10% cases of polyarticular JIA. FiF we cases show
b) Pleural effusion or interstitial lung disease in
SLE more aggressive disease. ._
e) Anti-COP (Cyclic citrullinated peptide) Ab — Specific for JIA and is also a marker of
7. Ocular manifestation -
more aggressive disease
a) Scleritis in SLE
1 1 . 305::$1.1m:s‘nlrrnatron — Presence of adequate nunber of blast cells (> 25% lyrrphoblasts)
b) Uveilis in RF negative polyarticular JIA
polyarticular JIA
8. Rheumatic nodules — May be seen in RF «we 12. and toyfacci’l‘ijtsa’tfe
Kidne bi Usuall neSefggégms:s
—gradingyof ' of SLE nephritis ‘ ' pattern
' ' to know the histological
C) Investigations 4
13. :oflnyggaégggdgprgoomsmgfi fifpsy — In cases of diagnostic dilemma and there is
1. CBC —
a) Hb% - Low in all, very low in ALL
b) TLC - fl :1! 9 month old infantpresented in the children ward with acute respiratory distress. Mention
' Elevated in JlA the common causes. How will you proceed to manage the case. (R. 6. Kat 8th Sam]
- Low in SLE Ans: 9 month old infant with acute res irato ‘ - - - - -- -
o Elevatedflow in ALL respiratory and other systems ofthe bidiffiisesszaa: t2: If::l)|omrrl:r::E diagnostic possrbrlrtres “0a
c) DLC -— A) Respiratory System - ' '
o . Upper.-
- Lymphopenialn SLE
° Relative lymphocytosis in ALL - Group or Laryngotracheobronchitis
- Abnormal cells (lymphoblasts) in ALL - Acute Epiglottitis
— Foreign body
\
'x.‘
APPROACHES El Chapter-14 325
- Lower—
' Clubbing -— May be present in cyanotic heart disease. empyema.
— Bronchiolitis
- Neck vein — Engorged in heart failure
— Pneumonia
- Febrile and toxic look — Epiglottitis/pneumonia. Empyemafpneurnonia
- impacted foreign body in lower respiratory tract
Respiratory -
— Pneumothorax
- Empyema - Upper respiratory - Laryngoscopy to rule out croup/Epiglottitis/Foreign body in larynx
Wheeze associated lower respiratory tract infection/hyperactive airway diseaSe
— ° Lower respiratory -— Beta and degrees of reSpiratory distress.
- Bilateral hyperinflation ~ Bronchiolitis/Hyperactive airway disease
B) Cerdio-vascular system -
- Unilateral restriction of respiratory movement. Pneumonia/Empyemaaeumothorax
- Cardiac failure — Acyanotic heart disease (ASD, VSD, PDA)
' Shrfting of mediastinum — Empyema/Pneumothorax to opposite side
- Cyanotic spell — Cyanotic heart disease
- Dullness on percussion = Pneumonia/Empyema/Collapse (foreign body)
C) Central nervous system - 0 Hyperresonant on percussion— Pneumothorax
- Guillain barre syndrome ' tlilti’rghifishedlabsent breath sound— Pneumonia/Empyema/PneumothoraxlCollapse (foreign
- Neurotoxic snake bite V
o CNS depressant drugs - Crepitation -— Unilateral — Pneumonia. Basal bilateral — Heart failure
D) Metabolic- ' Flhonchi - Bilateral — WALFtl/Hyperactive airway disease/Bronchiolitis
. Metabolic acidosis due to any cause Unilateral localized — Foreign body impaction
- Strider - Upper reSpiratory pathology — Croup/Epiglottitis/foreign body
Management
Cardiovascular —
Management of a case of acute respiratory distress involve simultaneous clinical assessment, rel- - Apex-shifting character — ln acyanotic heart disease
evant investigation and early initiation of supportive treatment regardless the causes.
0 Murmur- For VSD, PDA, ASD or TOF
A) Clinical Assessment-
CNS —- For weakness or paraplegia — GB syndrome, Ptosis — snake bite
History—
B) Investigation - Relevant investigation should be done if patient's condition permits
— Onset duration. progression of distress
a) Chest X-ray — (i) Hyperinflation :
- History of associated fever
- Past history of same episode
- History of known allergy. atopy HYPERINFLATION
- History of night cough

- Famfly history of same illness
- History of cyanosis or cyanctic spell Unilateral Bilateral
History of persistent feetfing difficulty . farsign body I b - Bronchiolitis
— History of weakness of any part of the body ay or may no e . H eractive a'
— History of any drug intake seen in X-ray) digase [may
History or suspicion of foreign body intake
— History or suspicion of snake bite (ii) Unilateral opacity —
Examination —- Detailed examination should be done. o :I: Airbronchogran without mediastinal shifting
General survey - — Pneumonic consolidation
- Consciousness - Shifting of mediastinum to same side
— lrritability restlessness —+ Hypoxemia Collapse (foreign body impaction)
-
snake bite / depres- - Shifting of mediastinum to opposite side + obliteration of costophrenic
- Unconsciousnessldrowsiness —r respiratory failure/neurotoxic, angle
sant drugs — Empyema
y distress
Decuibetus- Propped up position/orthOpnea indicate degree of respirator (ill) Unilateral hypertransluoency + shifting of mediastinum to opposite
side- Pneumothorax
g chronic illness. 0.g.,—i
Anthropoiemetry — Gross wasting or malnutrition indicates underlyin (iv) Pulmonary oedema + Cardiomegaly— Heart failure
Congenital heart disease (v) Pulmonary oligemia— —Cyanotic heart disease
Cyanosis— Cyanotic heart disease or with severe respiratory Illness b) Thoracocentesis/Needle aspiration — Helpful in suspected empyem
Pallor- Underlying chronic illness- congestion-cyanotic heart dlsease
alpneumothorax
Pallor or congestion
\
‘.
_ 2Eh‘hn‘ 1.: l
CamSCanner
APPROACHES i] Chapter-14 327
olic acidosis, - Pneumonia It Bacterial

c) Arterial blood gas analysis -— pH, and H 003 —-) Metab . x;
Viral
l PaOz -a> HypoxemiaiTypel respiratory failure - Pneumothorax
ca rbia) ventilatory support needed.
l PaOz + T PaCOZ _ Respiratory failure Type II (Hyper ma
- Empyema thoraxis ‘
phil — PneumoniaiEmpye
Complete blood count -— High TC WBC and neutro
— Pleural effusion
d)
oscopy — If foreign bod y is strongly suspected - Acute attack of asthma
e} CT scan chest and bronch
syndrome. Approach
f) CSF study and MRI spine -— Suspected GB
— Epiglottitis — ii) Steeple sign — Croup Approach should be pr er hist t ' ‘ ' - -
X-ray Neck (AP/lateral view) — i) Thumb sign
9)
without any delay.
tion (if needed) to reach thcepdiagnocsrig. akmg' thorough Clinical examination and relevant investiga-
C) Treatment— Treatment should be started
cannula 0 History
s and maintain saturation > 90% through 02 mask/
- Moist oxygen To releive distres
-
1. Fever
° I.V.F.
- Duration
i — Oral feeding should be stopped
lyte balance - Type
LV. fluid to maintain proper hydration and electro
Baby should be nourish ed in proppe d up position preferably i n mother's lap — Grader if documented
Position —
Subsided by medication or not
- Nebulization —
ation} in suspected croup and Bronchiolitis . Cough
— Epinephrine (preferably race mic prepar
nebulization in bronc hiolitis . WALFil or hyperactive airway disease - Duration
— Levosaibutamol
body and pneumothorax. - Dry or moist
— Not to be done in suspected foreign
ion — In suspe cted pneum othora x by clinical examination and/or X—ray a ~ Sputum if any
- Needle insert
intercostal space in mid clavicular line to releive — Drumal variation of cough. e.g., — Night or early morning cough in asthma
wide bore needle to be inserted at 2nd
air pressure in pleural space. - Cough intensity change with postural change. 9.9., - Postnasal dri
ma
Thoracocentesis and lntercostal tube
drainage — Suspected and confirmed empye - Bouts or paroxysm of cough. 9.9., — Pertusis infection P
-
-, Antibiotic - . Diiticuity in breathing -
first dose of antibiotic - Duration
- Pneumonia - Onset
- Progression
— Err-pram
— Cloxacillin + Cettriaxone - Whether associated with audible wheeze
me
Epiglottitis - CeftriaxoneiCefotaxi . History of cyanosis
@mwpmh
active airway disease
LV. Steroid - Hydrocortisone — In hyper Past-history of recurrent respiratory distress. e.g., - Asthma
- Dexamethosone — Group Family history of respiratory distress — e.g., Asthma
removal . History of allergy or slow — Important in asthma.
' Bronchoscopy — For foreign body PaCOz T
failure inspite of all effort PaOz l and
0 Ventilatory support - If respiratory . History of taking medication or inhaler therapy at home (it any)
progressively. . Difficulty in swallowing and phonation. e.g.,— Epiglotittis.
0 Other therapies — Clinical examlnatlon -
ne in confirmed s nake bits.
— AVS and Injection Neostigmi Higher fugction — Irritability. restlessness = hypoxemia
in GB syndrome. ‘. _
— Intravenous lmmunoglobulin Dro ' - .
fever and cough for 3 days and '
ented in emergency with history of - -
“P 903 we OrthOpnea indicates de' gree 0f respiratory dlstress
M: A 3 year aid child pres Enumera to diflerenti ai diag nosis. How do you approach . -
respiratory distress for 1 day. Cyanosrs - Indicates severity of distress
[20151 (MEMO, 9th 59m]
such a case (or diagnosis ?
ss for 1 day. ,
cough for 3 da ya and respiratory distre
Ans : 3 year old child with fever and Presence oi accessory muscle of reSpiratory use. 9.9. - Head nodding
CI Differential diagnosis — Examrnation oi upper re sp irat cry tract by laryngoscopy-
epiglottitis I Red and swollen epiglottis = Acute
0 Upper respiratory tract -
Biateral hyperinflated chest — Asthma
- Epiglotittis
. Unilateral restriction of respiratory movement — Pneumonia iPneumotho raxi Empyema
— Group or laryngotracheobronchitis
Unilateral hyperinflation i Buldglng — Pneumothoraxl Empyerna i Eftusion
- Lower respiratory tract ~— -\
‘g
\
‘u
APPROACHES C] Chapter-tr 329
Mediastinai shifting to opposite side - Pneumothorax I Empyema I Effusion ii) Blood count — May be informative to diagnose the following
Oederna of chest wall with localized swelling — Empyema - l WBC — Suggestive of viral infection
Dullness on percussion - Empyema I Effusion I Pneumonia. Hyperresonant on percussion = - T EosinOphils — Allergic rhinitis I Hyperactive airway disease
Pneumothorax - T WBC —- Suggestive of bacterial infection.
Diminished breath sound —— Pneumonia I Empyema I Effusion I Pneumothorax investiga-
The above baseline investigations are sufficient to diagnose cough and cold. Further
and there is
Bronchial breath sound — Pneumonia tions are not needed usually. However if the above investigations are not informative
follows - -
- Adventitious sound — persistence of symptoms. next line investigations can be planned as
studied for eosinophil counts, in cases of allergic rhinitis.
Crepitation = Pneumonia iii) Nasal cytology - Can be
Rhonchi = Asthma iv) Throat culture - For bacterial growth and sensitivity pattern
and culture sensitivity
Strider = Group I Epiglottitis v) Bronchoscopy and bronchoalveofar lavage — For bacterial growth
vi) Serum lgE — Serum lgE level is elevated in presence of atopy and allergic rhinitis
Cl Investigation —
History and thorough clinical examination reduce the necessity of investigation. The basic in- vii) Sputum examination - Examination of sputum is effective and informative
vestigation that can help to confirm the diagnosis : - Physical examination —- SerousIPurulent/hemonhagic
i) ChestX—ray- - Abnormal content - Pus cells/eosinophil count
Unilateral opacity with/without air bronchogram and no mediastinal shifting — Pneu- - Gram stain -— For bacteria
monia (Lobarlsublobar)
0 Culture sensitivity.
Unilateral opacity with mediastinal shifting to opposite side - EffusionIEmpyema
tion, patient looks
- Bilateral patchy opacities -— Bronchopneumonia O. 13 :A chifdp resented with respiratory distress for last2 days. On examina
cause for this
Unilateral hypertranslucent lung field with mediastinal shift to opposite side — Pneu- toxic and there is dullness on th e right side of chest. Name 2 important
[2011, Supple]
mothorax condition. How do you proceed for diagnosis of the case.
right side of the chest.
- Hyperinflation bilaterally - Asthma Ans : Child with 2 days of respiratory distress. toxic look and dullness on the
ii) X-ray shift tissue neck (AP/lateral View) — D Causes
- Thumb sign — Epiglottitis (Swollen Epiglottis) 1. Pneumonia (consolidation)
- Steeple sign — Croup (Subglottic narrowing of trachea) 2. Ernpyema Thoracis
n
iii) ThoracocentesrLs/Needle aspiration = EmpyemalEffusio investigation.
Approach -— Diagnosis wit depend on history, thorough clinical examination and relevant
e blood count— Leukocy tosis in empyem aipneum onia. be difficult to
iv) Complet A. History - Detailed history should be taken on following but from history it will
with
Write the differential diegnosis. Suggest differentiate between two above conditions. i.e., both Pneumonia and Empyetna can {Siresent
0. f2 : A childsged 1 yearpresented with cough and cold. [8th Sent, BMC] similar clinical history.
‘
the investigation to reach the final diagnosis.
1) Respiratory distress —
Ans: 1 year child with cough and cold. - Onset
El Differential diagnosis — - Duration
i) Common cold — Progress
ii) Allergic Rhinitis — Associated feeding difficulty
iii) Wral copper respiratory tract infection 2) Fever - if present
iv) Bronchiolitis ' - Duration
tract infection
v) Wheeze associated lower respiratory - Type
vi) Laryngotracheobronchitis or croup — Grade, if documented - Usually high grade in both conditions.
These are as
tigation can be don e to reach the diagnosis. — Subsided by medication or not
0 Investigation - Some base line inves is tobe taken
follows : 3) Cough — Any history of cough before or in associated with respiratory distress
-
carefully
i) X-rey -
-‘ Duration
- Chest X-ray P-A view - lung fields—
d patchy atelectaesls in
> Hyperinflation with flattened diaphragm an
- Dry or moist
— Character of sputum (if any)
Bronchiolltis
disease
> Hyperinflation - Hyperactive airway area
4) Cyanosls
tissu e neck (AP view) - Steeple sign — Narrowing of the subglottic
X-ray soft
"-..
- "‘s
‘1
h“.
42
‘——H
APPROACHES El Paper-14 331
330 QUEST : PAEDlATHlCS
i
(ii) Needle Thoracocentesis - Aspiration of pus confirms the diagnosis of Empyema.

B. Clinical Examlnatlon — Thorough examination of respiratory system to reach the diagnosis.
Fluid/Pas analysis -
- Respiratory rate. degree of respiratory distress —- Presence of subcostal. intercostal suction
or head nodding - Pus cells
- Unilateral restriction of respiratory movement —- both in pneumonia and empyema. — Protein > 3 gm/dl
- Unilateral bulging of the chest - Empyema — Pteral Fluid : Serum Protein > 0.5
- Oedema of the chest wall with or without localized swelling — Empyema - Pleural Fluid : Serum LOH > 0.6
- Mediastinal shift —- -— pH < 7.2
— No shift — Pneumonia (consolidation) - Glucose < 40 mgidl.
- Shift towards opposite side -— Empyema (iii)USG chest: Can be done to confirm the diagnosis but usually not required
° Dullness unilateral - both in penumonia and empyema (iv) Blood count : T WBC & T Neutrophil — Both in Pneumonia and Empyema
- Dullness with tenderness of the chest well during percussion — likely to be empyema.
- On auscultation — a. 14 : A 4 years old child has been bought to emergency with severe respiratory distress. There
— Unilateral abcesenoe/diminished breath sound — both in pneumonia and empyema is H/O recurrent attacks of cough and cold from early infancy. What are the possibie
causes and how will you manage the child? (KPC)
— Bronchial breath sound — Pneumonia
- Crepitation — Pneumonia Ans:
- Vocal resonance - Diminished — both in pneumonia/empyema — Increased - 4 years old child with respiratory distress and history of recurrent attacks of cough and cold from
Pneumonia early infancy.
To summarise the clinical findings - Possible causes —
(i) Asthma
— Toxic look - Toxic look (ii) Congenital heart disease with left to right shunt
- Respiratory distress - Respiratory distress 9.9. - VSD. PDA presenting with pneumonia or heart failure
— Unilateral building of the chest wall - No buldging/depression of the chest (iii) Congenital lung defect with superadded infection.
—- i Oedema of the chest wall - No edema of chest wall MANAGEMENT
_ i Localized swelling - No shifting of mediastinam
Management includes investigation and treatment. Before that proper history about previous epi-
- Shifting of mediastinal to opposite side ' Du""ess 0" percussion sode and thorough clinical examination is mandatory to guide investigation and tegatment.
_ Unilateral Dullness - Diminished / absent breath sound/bronchial
breath sound INVESTIGA'HON
. . . _ _
- Diminished/absent breath sound - Crepitation 1. Chest X-ray P—A view : It is the first investigation to be done in a patient presenting with respiratory
N dded sound .
— Diminished/increased vocal resonance distress. Suggestive findings are -—
.. ca . . _ .
- Diminished vocal resonance - Pneumoniafconsolrdation) ' Asthma
- Empyema - Bilateral hyperinflation of the lung fields.
— Localized area of consolidation may be present.
be done to differentiate between two ' Congenital heart disease with left to right shunt —
C. Investlgation -— The following investigations and to
conditions - - Cardiomegaly or increased cardio-thoracic ratio
conditions can be diagnosed.
i) Chest X-ray P-A view — first investigation to be done and both the - Congestion of pulmonary vessels with cephalization suggestive of pulmonary edema.
- Localized area of consolidation or diffuse bilateral involvement suggestive of
Pneumonia pneumonia.
Empyema
- Congenital lung lesion —
Unilateral homogenous opacity — Unilateral opacity, may be homogeneous
- - Unilateral hyperinflation
— No shifting of mediastinum .
— Shifting of mediastinum to opposite side - Unilateral localized opacity
- Obliteration of the costo-phrenic angle — No obliteration of the costo-phrenic angle
332 QUEST: PAEDIATFIICS APPROACHES E] Paper—14 333
2. ECG —Ventn'cular hypertrophy Ans : 6 year old male child admitted with severe respiratory distress and unilateral decreased breath
Leftibiventricular in VSD/PDA sound.
Right ventricular in A80 a) Differential diagnosis —
3. Echocardiography - Shows 0 Pneumonia (Lobar)
— Nature of the lesion - Pleural effusion
— Ventricular hypoirophy
' Empyema
— Pressure gradient
° Pneumothorax
- Status of the major vessel
' Hydropneumothora'ii/ Pyopneumothorax
4. Complete blood count —
b) Relevant investigation -
— High WBC with high Neutrophil — Suggestive of recent infection both in case of Asthma/CHO
- Chest X-ray P-A view — First investigation to be done
- High Eosinophfl - Supportive of Asthma diagnosis
Findings —
TREATMENT ~ Unilateral opacity (may or may not be homogenous) without any mediastinal shifting and
giggment of this patient includes supportive and specific management depending upon the underlying without obliteration of costophrenic angle — suggestive of pneumonia.
- Unilateral homogenous opacity with mediastinal shifting to Opposite side and oblitera-
- General treatment — tion of costophrenic angle - suggestive of Pleural Etfusion / Empyema (Chest X-ray
cannot differentiate between these two conditions)
i) Admission —) Hospital admission and preferably in ICU if facility is available.
Unilateral Hyperiranslucency without visible bronchovascuiar marking. collapsed lung
ii) Moist oxygen —> Oxygen should be given through face mask to maintain saturation above 90%. border and mediastinal shifting to opposite side — suggestive of pneum othorax.
iii) I.V. fluid - Oral feed will not be permitted '
Findings of pneumothorax above and effusion below with horizontal fluid level - suggests
— i.V_F to maintain Euvolemia and electrolyte balance. Hydropneumothorax/ Pyopneumothorax.
iv) Position —-) Propped up position in mother’s lap or in bed. USG chest -> Can be done can differentiate above conditions and provide information
0 Specific treatment — Specific treatment will depend upon the underlying cause detected. regarding nature of fluid-effusion i Pus {Fibrinous exudate)
i) Asthma - - Needle aspiration or thoracocentesis — should be done in suspected effusion/empyema
to examine the nature of the fluid and find the etiology
> Nebuiization with 82 agonist (salbutamol). anticholinergic (lpratropium)
See : Respiratory system, question no. 5
) l.V. Steroid — injection Hydrocortisone
0 Other supportive investigation — These are needed to findout the etiology, sometimes
> Severe cases — Injection Magnesium sulphate, injection AminOphyiiine suggestive rather than confirmatory __
ii) Congenital heart disease — in congenital heart disease acute respiratory distress occurs due to i) CBC - T WBC count — Pneumonia, Empyerna
pneumonia or heart failure. T Neutrophil — Pneumonia. Empyema
> Pneumonia - Empirical antibiotic therapy with Co-amoxyclavi3rd general cephalosporins T Lymphocyte and T ESR — Pleural effusion caused by tuberculosis
+ cloxaciilin.
ii) Mantoux test. Sputum for AFB/NAA test -— To detect TB etiology of effusion.
> Heart failure —
iii) Blood culture — Often yield the organisms causing pneumonia/empyema.
Injection Frusemide it no circulatory insufficiency
—
c) Outline the treatment —
injection DobutamineiDopamine — In presence of shock
—
is secondary bacterial infection. As the child presents with severe respiratory distress priority of treatment should be stabiliza-
iii) Congenital lung deiect— Cause of acute respiratory distress tion of the patient. Specific treatment will be started after confirmation of diagnosis and finding
positive and gram negative organisms.
:9 Empirical antibiotic therapy covering gram of etiology.
with history of sudden onset of Patient should be admitted in lCU preferably if facilities are available.
0. 15 : A two year old child presented in the emergency room -
will you diagnose and manage
difficuihr in breathing. What is the probable diagnosis ? How (2018)
° Propped up position is to be maintained.
the case? . Humified oxygen with high flow to maintain oxygen saturation above 90%.
- If respiratory distress is so severe that oxygen saturation cannot be maintained child will
Ans : See Question No. 10.
be put on ventilatory support.
tory distress and unilatem! decreased
0. 16 : A 6 year old male child admitted with severe respira (Supple, 2016) - l.V fluid bolus and ionotropic agent should be started if circulatory insufficiency is present.
breath sounds : If tension pneumothorax is suspected a wide bore needle should be inserted instantly in
a) Discuss the ditteren tiai diagnosis the 2nd intercostal space at the mid-clevicuiar line to relieve distress.
b) Relevant investigations to confirm the diagnosis
c) Outline the treatment.
—.i
~———-——-—o—u——-—.--—
334 QUEST : PAEDlATRICS APPROACHES El Paper—14 335
- If empyema and large amount effusion is diagnosed immediate arrange will be made to — Cold extremities
drain pus/fluid by water seal drainage system. ~ Tachycardia
0 Empirical l.V. antibiotic therapy to be started without any delay latter guided by culture Low blood pressure
-
sensitivity report. (iv) Skin rash —
- Anti tubercular therapy to be started it TB is detected as etiology. ~ Type-Petechial/Polymorphus
- Distribution
O. 17 : 9 year old girl presented with excessive sweating restlessness and cold extremities
preceded by high grade fever and bodyache and skin rash. The child abruptly detoriorates — Blanching or not
her general condition. Clinical examination reveals petichial spots altered sensorium, (v) Chest - Localized area of dullness with diminished breath sound with rnediastinal shitting
extreme dehydration and very feeble pulses. How will you approach to diagnose the case — Suggestive of pleural effusion. commonly associated with complicated Dengue.
(Maids)
and manage the condition. (vi) Abdomen - Ascites — commonly associated with complicated Dengue.
Ans : - Hepato or hepatosplenomegaly may be present
by restlessness. extreme
9 year old child with high grade fever. body ache, skin rashes followed (vii) CVS - Signs of heart failure may be present
pulse.
dehydration. altered senson'um. petichial spots. cold extrimities and very feeble . Above history and clinical examination findings are high suggestive of Dengue haemorrhagic fever
APPRO ACH wrth shock. (Dengue shock syndrome llIilV)
A. History — C. investigation—
(i) Fever — Duration (i) Complete blood count
- Grade - Hb% & PCV - Low in bleeding
fever with body ache is
— Associated headache. body ache, eye pain. High grade High in shock
-
suggestive of viral illness. - Both may occur in Dengue haemorrhagic fever with shock
(ii) Skin rash - Type - WBC - Usually low in Dengue as in other viral illness
— Duration - . Platelet count - Usually low in critical Dengue in presence of bleeding
Distribution (ii) NSl antigen — ELISA method.
-
— Change in character Positive if done with 5 days of onset
papular.
specially in Dengue where initially maculo
0 Skin rash may be present with viral illness illness .
— Highly suggestive of Dengue though that may be positive in some other llavi virus infection.
ric character in next phase of the
Type of rash changes to purpu (iii) Dengue antibody —
(iii) Altered sensoriurn — lgM — Positive in acute infection. it done after 5 days of onset
- Duration lgG — Positive and that indicates previous dengue infection
— lrritabilitylrestlessness/drowsiness (iv) Liver function test —
—- Convulsion, if any Sometimes positive with elevated bittirubin and liver enzymes in Dengue with liver
.
nities - Duration. involvement.
(iv) Excessive sweating. cold extrir y sugg estiv e of Dengue
ficient peripheral circu lation . highl (v) Urea. Creatinine -
- These are the feature of insuf
with shock. Elevated in Dengue with prolonged shock affecting renal perfusion
be taken - vomiting
(v) Other important history to MANAGEMENT
- Bleeding from any site of body Patient will be shifted to pediatric intensive care unit with facilities for continuous monitoring.
— Urine output (i) Oxygen — To be given with mask/02 cannula to improve tissue oxygenation and maintain
saturation above 90%
B. Clinical Examination—
(ii) Fluid — fFluid management is the mainstay ottreatment in Dengue shock syndrome.
(t) Higher function -
— Preferable fluid is normal saline/ringer lactate (For shock correction}
- Alteration of sensorium
— In critically sick children it is preferable to establish tvvo I.V lines. one for FtLiNS
— Flestlessnessidrowsiness and another tor 5% dextrose and potassium.
(ii) Feature of dehydration — (iii) Blood and blood component transfusion -
h goin9 back very slowly.
— Dry tongue. eyes. skin pinc - Fresh whole blood or fresh packed cells is preferable for transfusion in
presence of
(iii) Feature of shock — severe bleeding. .
- Feeble pulse -. .V“
.\_
336 QUEST : PAEDIATFIICS Paperwtll 337
APPROACHES CI
Assessment of Shock
O. 18 : A 2 year old child with running nose and cough for 2 days, develops lever followed by 6105'.
Outline your approach for management of seizure in the emergency and what advice will you
l
V l give to the parents of the child . [2003, 2010, sapple]
Hypotension [DSSIII] BP unrmordfble (DSSIV) Ans:
l 2 year old child with running nose and cough for 2 days. develops fever followed by GTCS. point
Ringer lactate (FlLilNS Ringer lactate (RUINS bolus towards the diagnosis of febrile convulsion.
10-20 milkn 20 mgitrg upto 3 boluses
Management : Convulsion should always be treated as emergency where treatment and some baseline
I ‘ Assessment _ _l .
management to be done simultaneously.
t
t [3 Base line investigation :
I
Improved No imprfvement ° Capillary Blood glucose Hypoglycemia if present to be treated I.V. dextrose infusion.
-
-
t - Blood electrolytes - Sodium, potassium, calcium. magnesium to be measured according to
it .i available facility and treat accordingly.
Gradual decrease in infusion
Haematocrit increased Haematocnt decreased 0 Moist oxygen and oral suction of secretion.
rate with 2 houi'ly assessment
D Control of acute convulsion.
Colloid 10 mllkg Blood transfusion
BL 10 mtlkglhr - Short or long acting benzcdiazepine preferably in U] route.
'L Assessment
J, — Diazepam 0.3 mglkg I.V.
RL 5 mtlkglhr _
.I. t - Lorazepam 0.1 mglkg I.V.
l
No improvem ent
Same dose can be repeated after 10 min if seizure not controlled.
RL 3 nlllkglhr -
— If |.V. access is not possible then per rectal diazepam 0.5 mglkg can be given.
Assessment of anaemia acidosis,
'
Continua ti ° nof W fluid until -
myocardial dysfunction -— Now a days intranazal midazolam spray is commercially available that can be used In emer-
stable tor 24 hours gency situation if LV. access is difficult.
D Control offever-
-
ce to support of the benefit of platelet transfu - Reduction of body temperature is the mainstay of control of convulsion in febrile convulsion.
0 Platelet concentrate — There is little eviden
ng.
sion in presence of petecha or minor bleedi — Hydrotherapy to immediately reduce body temperature. ‘
- — Use of antipyretic - Paracetamol — t5 mglkg body weight.
Indication of platelet transfusion —
ce of bleeding.
Platelet count less than 10000/CU.mm.in absen El Brain imaging and EEG -
openi a.
Severe bleeding, even without thrombocyt — These are usually not recommended in 13! episode of simple febrile convulsion.
- Cannot predict future occurence.
0 Fresh frozen plasma - .
of fresh whole blood Or PFtBC.
In severe bleeding and unavailability ADVICE TO PARENTS
sheik. holutlerveggsgfiris‘fepegj
stay of management of Dengue
(iv) lonotrops : Fluid is the main ort sue afaboticl: acidosis . Advice to parents to prevent future recurrence is a important step in management of febrile
n
nt Ionot ropic supp
sists despite adequate fluid mana geme . convulsion.
0 me
be considered after correction
Dobutamine. lnj adrenaline can ed — Though it is a benign condition there is every possibility of recurrence of convulsion when-
__"\
in case of susp ecte d supe radd
antibiotics are only indicated
(v) Antibiotic : Broad spectrum ever there is lever upto 5 years of age.
bacterial infection. managed accordingly. - Fever should be aggressively managed to prevent recurrence.
ey dysfunction if present, to be
(vi) Organ sapport: Liver or kidn to be mon itored - 4 Hydrotherapy and paracetamol — 15 mglkg body weight.
treatment. Following are
(viflMonttoring : Crucial part of — Intermittent prophylaxis with oral diazepam l clobazam for tst 3 days of fever help to reduce
— Heart rate chance of recurrence by 80% that can be adviced to parents.
— Respiratory rate — It convulsion can not be controlled by home base management then immedate attention to
hospital. _
- Pulse pressure
— Blood pressure O. 19 :A 10 month old baby having high fever since morning and developed generalized tonic
— Urine output clonic seizure persisting for about 5 hrlns. and become well alert after that episode. Wis
the most possible diagnosis? w do you manage the case? (CNMC) (9th am.)
—- Central venous pressure
CamScanne;
QUEST : PAEDIATRICS APPROACHES E] Paper-14 339
338
. Pyogenic
Ans : Viral Tubercular
5 min and becam e well alert after that eplsod e. Meningitis Meninge—encephalitls Meningitis
10 month old baby with high fever and GTCS for
Cell count (mm’) 100-1 0,000 PMN T rarely > 1000 cells
Most possible diagnosis — Febrile convulsion. 10-500 PM nearly but
predominate . lymphocyle throughout
Management — See Question No. 18. the course
ing for2 days. Chit:
the emergency with high fever and vomit Protein (mg/dl)
’ O 20: A 10 year old boy presented in ness. Enem erate the etiology an
100.500 50-200 1003.000 Higher in
by unconcious
. had one episode of GTCS followed [CNMC] presence of block
management. Sugar (mg/dl) < 40 mgidl of < 50% Normal or decreased (< < 50 in most cases
serum sugar 40 mg/dl)
Ans :
unconciousness.
ng. generalized convulsion folio wed by PFBSSUfe Usually elevated Usually elevated or Usually elevated
10 year old boy with high fever. vomiti
le -— normal
Etiology Multiple etiologies are possib
-
ADA Normal May be normal Usually elevated
(i) Bacterial meningitis —
(Adenosine deaminase)
— Streptococcus pneumonlae
Gram stain culture May identify the Normal Normal
- N. Meningitis organisms
— H. lnfluenzae
Viral profile-Antibody, Nomal May be positive Norrnat
(ii) Vlral meningo-encephalitis - PCFt
- Herpes simplex PCR for Tubercular Normal Normal Ma be 't'
Japanese encephalitis bacilli/NM test y pm we
-
- Dengue
— Entero virus - Management of pyogenic meningitis -
- Mumps Management of pyogenic meningitis patient is an emergency situation and patient should be man-
aged overall by supportic care. antibiotic therapy and treatment of complications and investigations are to
— Measles
be done simultaneously.
(iii) Cerebral malaria
El Supportive care —
(iv) Tubercular meningitis
ered by fever - Patient is ideally managed in ICU if facilities are available.
(v) Seizure disorder. trigg
— Establishment of airway. breathing and circulation are of prime importance
(vi) Brain abscess
Question No. - 22 and 23. — Raised intracranial pressure : ‘
D Management — See s. and sudden?
grade fever for last. 2 day > LV mannitol (20%) - as osmotherapy and is administered 4-6 hourly
temer ncy with, high the differential diagnosis
lgnaic semis: for last 10 minutes. What aref menin
ogenic[0M0 gitis? > W 3% NaCI in conditions where mannitol is contraindicated.
a. 21: A
onset maleeralise
10 orofgen d tonigtce
child pres
ent condition and manage
mento
, PY ] (9th Semi ' Lumber puncture should be done very causiously in presence of raised intracranial tension.
Describe the CSFpicture of differ
— Convulsion :
> To be managed by preper AED
utes. The
Ans : den onset GTCS for 10 min
male chil d with .
high .
gra de fever for 2 days and sud > W Benzodiazepine (DiazepamiLorazeparnfMidazolam) are the first choice
10 month old > Followed by Hi phenytoinlvalproate '
differential dlagno sis —
following are the possible
Antileptic drugs can be stopped after 3 months if brain imaging and neurological exam'netion is
(ii Atypical febrile convulsion
>
normal.
(ii) Pyogenic meningitis — Fluid and electrolyte homeostasis
litis
(iii) Viral meningo-encepha > Hypotonic fluid is to be avoided
(iv) Cerebral malaria > Serum electrolytes level should be maintained in normal level
ns -
D CSF picture of different conditio — Hypolenslon ' '
> Proper use of vasopressors like Dopamine/Dobutamine
'-._
’x“.
'-.
340 QUEST: PAEDIATHICS APPROACHES Cl Paper—14 341
Cl Speciflctherapy— U History ..
— Initial empiric therapy — Fever
(i) Third generation cephalosporin — - Type of fever
> 'Ceftriaxone (100-150 mg/kg/dayJICefotaxime (150-200 mg/kg/day) — Grade

— Diurnal variation — low to high grade evening rise of temperature favours the diagnosis
(ii) A combination offirilpiéfllin (200 mg/kg) + Chloramphenical (100 mg/kg/24 hrs.) are also effec- of TB meningitis .
tive as iniflgerrtmbim.
— Chill and rigor - specially in older children raises the possibility of malaria.
- lf fever or meningeal signs persist after 48 hour of therapy. LP should be repeated with
review of antibiotic therapy.
Convulsion-type '
- Whether focal or generalized
— Specific antibiotic — If specific organism can be detected by blood/CSF culture.
— Duration of each convulsion
> Meningococcal meningitis — Penicillin
Alteration of sensorium. drowsiness, unconsciousness in between the episodes of convulsion.
v CefotaximelCeftriaxone
Headache
H.lnfluenzae meningitis — CeftriaxoneICefotaxime
— Type of headache
Staphylococcal meningitis - Vancomycin — Whether associated with fever
(If methicillin/Penicillin resistant strain is suspected)
Vomiting
Gram negative bacilli - Cefotaxime/Ceftriaxone/Ceftazidime — Combination Ampicillin + — Recurrent vomiting associated with headache may occur in raised intracranial tension.
Aminoglycoside Photophobia difficulty in vision
Pseudomonas meningitis — Ceftazidime and Aminoglycoside combination — Suggests raised ICT
- Meropenem/Cefepime Symptoms of other system involvement before or at onset
— Duration of therapy - — Like cough, diarrhoea. skin rash (Measles). parotid swellig (Mumps)
Staphylococcus I Gram negative organism — 3 weeks. Contact history of TB in family
Rest organisms — 10—14 days. Perinatal history
response, but not recom- — H/o perinatal asphyxia may be present in seizure disorder
‘ Repeat CSF examination is indicated only in delayed or partial clinical
mended routinely. History of prolonged cough / weight lose
Steroid Therapy -— -— ln TB meningitis
-
Developmental history
— Specially helpful in Haemophilus meningitis.
— Any delay or regression may raise the suspicion of presence of focus of seizure
— Reduces neurological complication like.
l disturbances. lmmunization ‘ it.
Sensorineural deafness/Hydrocephalus/Behaviora
ethasone 0.15 mg/kg LV 1 6 hourly - Whether properly immunized with BCG, Hib. JE vaccine
Dmg of choice — LV Dexam
Whether patient is a resident of the zone where high prevalence of malaria or high incidence of
— Duration 2-4 days
vrral meningoencephalitis. '
dose of antibiotic.
1 st dose to be given simultaneously or with tst
lastmy
iabora Clinical Examination -
nicaii y and
convu by for
lsion two
is ver for 7 days and recurrent
(fl' A 4 years old child presented no'01 No for diagn osrs cii {2013 ] General examination —
days and headache. How will you proceed > Pallor -— in cerebral malaria, TB meningitis.
investigation 7 > Anthropomelry — Wasting, stunting malnutrition in T8.
the diagnostic
ent convulsion and headache. Following are
Ans : 4 years old child with tile fever. recurr . .. . . > Cyanosis — Cyanotic heart disease as risk of developing brain abscess.
ossibilities - .
pneumoniae, N. meningitidis, H. influenzae) > Vital signs — Alteration of pulse rate, respiration and blood pressure in raised intracranial
P i) Bacterial Meningitis (Streptococcus les, Mump s, Enter o virus) tension. ‘
, Herpe s. JE Deng ue, Meas
ii) Viral Meningo-encephalitis (Commonly > Cervical neck glands - Palpable. firm often matted cervical lymph nodes may be palpable in
iii) Tubercular Meningitis TB. .
iv) Cerebral Malaria > Skin rash
ulsion (Atypical)
v) Fever triggered seizure I Febri le conv 0 Macularl Maculopapular rash-Measles. Dengue. Enteroviral infection
vi] Brain abscess - Vesicular lesion -— Herpes group of infection
both clinically and by 7
have to proceed for diagnosis
Keeping these above possi bilities in mind we - Haemonhagic lesion in meningococcal meningitis.
-
Laboratory investigation —
APPROACHES U Paper-14 343
Pyogenlc Viral meningo- Tubercuiar Meningitis

CNS Examination - encephalitis
Meningitis
> Higher function
— Drowsiness to coma Cell count (rnm3} 100 ~ 10.000 PMN T . rarely to — 500 PMN early but lym-
Predominate > 1000 cells phOCyte throught out course
- GCS score
ki sign.
> Meningeal signs — Neck Fligidity. kemig sign. Brudzins Protein (mgldi) 100 - 500 50 - 200 100 — 3.000 higher in presence
halitis oi block
- Positive in any type of meningitis or meningoencep
> Cranial nerve palsy Sugar (mg’d) < 40 mg/dl Normal < 50 in most cases
— 6th nerve palse commonest OR OR
< 50% serum sugar decreased (< 40 mg/dl)
—- Other cranial nerve palsy may be present
> Convulsion Pressure Usually elevated Usually elevated Usually elevated
- Direct observation of type local or generalized OFl -
Norrnai
> Head cirwmference
microcephaly
- Seizure disorder, may be associated with
- Motor. sensory function - as affected ADA Normal May be normal Usually elevated
Other system examination - Gram stain May identify the organism Normal Normal -
TB
> Hepatosplenomegaly — Malaria. disseminated culture .
— Cyanoti c heart disease like Tetralogy o i Fallot in Brain abscess.
> Cardiovascular system May be positive Normal
l meningitis with pneumonia (Pneumococcus. Viral profile Normal
> Respiratory system -— in suspected TB, bacteria Antibody. PCFi
Hib)
PCR for tubercular Normal Normal Ma be ' '
El Laboratory investigation bacilli INAA Test y posrtwe
- Complete blood count -
Hb% -Severe Anaemia - Malaria. TB
O. 23 : 0/0 of fever and con vulsicn in 2 year old child. How will you manage the case ?
T ESR - TB (Human)
T TLC with T Neurophil - Bacterial infection
Ans: There are multiple differential diagnosis oi convulsion in a child of 2 years and fever: They are
l TLC with relative lymphocytosis — Viral or TB
oi malarial parasites t) Febrile convulsion/V Simple
Peripheral smear - Ring or trophozoite
- Dual antige n study - Cereb ral malari a Atypical
- CSF study (see chart on the next page) 2) Seizure disorder. triggered by fever
alitis
yield positive resu It in viral meningo enceph 3) Meningitis
Blood for viral antibody and PCR —+ May
osis — Bacterial
Sputum tor AFB, NAA - To support TB diagn
- Viral ._
- Mantoux test — Tuberculosis
— Tubercular
. Chest X-ray - Tuberculosis
(CT Scan/MRI) diagnosis 4) Encephalitis i Acute encephalitic syndrome
Brain imaging — Useful aid to reach the
suggestive at T8 5) Cerebral malaria
- Hydrocephalus. Basal Exudate — highly
cing lesion with thick wall and parties ional oedema. Brain abscess. T uberculoma 6) Brain abscess
" Fling enhan
ral lobe
Abnormal signal intensity in bilateral tempo D Management - As convulsion is an acute emergency so management includes control of convulsion
supportive treatment as well as investigation needed to stabilize the patient and detect the cause:
Herpes Encep halitis
D Investigation - See question no. 22. '
— Vascular compression (ischemia)
El Treatment -
In any type of meningitis.
r. a) Ensure Airway. breathing and circulation.
ver normal report does not exclude seizure disorde
EEG - To detect seizure disorder. howe
.\
v
\‘I
‘x .
TCamScanner
344 QUEST : PAEDIATRICS APPROACHES Cl Paper~14 345
- Oropharyngeal suction, airway or intubation ° Clinical features of TB meningitis - Clinical features of TB meningitis are divided in three
— Oxygen. positive pressure ventilation if needed stages, these three traditional stages of TBM are not sharply defined and clinical features often
overlap. '
- LV. access and infusion of normal saline bolus for rapid restoration of circulation.
b) Hypoglycemia — 086 to be checked and if hypoglycemia present then 10% dextrose Stages are as follows :
infusion 2 mlikg body weight. i} Stage I (Prodromal stage) -
c) Anticonvulsant - l.V. Benzodiazepine l(Diazepami
_ Lorazepam) 5* Symptoms are non specific.
Onset is insidious, may be acute in infants.
VVVVVV
I.V. Phenytoin
Low grade fever, loss of appetite.
l
Disturbed sleep
W. Valproate i Phenobarbitone
Vomiting. constipation
J.
LV. Midazolam infusion Headache. complained by older children
i lrritability. restlessness and apathy
Phenobarbitone coma > Photophobia in older children. younger children resents exposure to light.
lntubation and Mechanical ventilation As the symptoms are non specific this stage is often difficult to be diagnosed as T8 meningitis
and disease progress to next stage.
Above anticonvulsant are to be given in succession if convulsion not controlled.
promptly ii) Stage II (Stage of Meningitis) -
d] Electrolyte imbalance — Hyponatremiai Hypocalcemia if present should be treated
and Paracetam ol. ' > Alteration of sensorium, drowsiness or delirious
e) Control of fever - Sponging
7f) Reduction of ICP - If there are signs of raised > Signs of meningeal irritation are positive — Neck rigidity and kemig Sign.
lntracranial pressure then > Convulsion in 65% cases
— 30° - 40" head elevation > Cranial nerve palsy -— Squint. visual disturbances, facial asymmetry, ptosis, dilated
irregular pupils
— Antioedema measurement like Mannitol. 3% NaCl.
definitive causes as revealed in > Paralysis — Hemiplegia, monoplegia or quadriplagia
9) Specific management — According to suspected or
investigation — > Features of raised I.C.l
- Febrile convulsion i Seizure disorder iii) Stage III (Stage of Coma) -
sufficient
- Anticonvulsanls and supportive treatment is > Deep coma, well marked meningeal signs. progressive neuro-deficits.
Meningitis i Meningo encephalitis > Dialated fixed pupil -
-
hours if needed)
-—Pyogenic - Caftriaxone + Vancomycin (after 72 > Cheyne-strokes breathing i Biot type breathing
antiviral dmg.
- Viral - Apart from Acyclovir there is no > Opisthotonous. decorticate and decerebrate rigidity.
i Meningo encep halitis is suspected
Acyclovir to be added if Herpes meningitis > Central origin of hyperpyraxia
- Tubercular — ATD for 9 to 12 months. Death is almost inevitable if disease progress to 3rd stage.
- Cerebral malaria - l.V. Quinine or Misunale Laboratory dlagnosis - See CNS question no. 2.
0 Brain abscess vancomycin D. 25 : A 4 year old boy presented with anasarca with history of similar illness 6 months back.
with 3rd 9 eneration cephalosporin and
— I.V. antibiotic -> Empirical therapy Mention the DID and how to prmed to the diagnosis. (one, 9th Sent]
— LV. Metronidazole Ans:
- Duration of therapy — 4-8 weeks rior fossa) [1 DD or causes of AnasarcaiGenerallsed swelling :
uired (large > 2.5 cm. located in poste
- Surgical drainage of abscess if req (a) Chronic cardiac failure
absorptio Mention
n.
(0.5. F.) Formation, circulation and
O. 24 : Discuss the Cerebraspinal Fluid ding the labo rator y diagnosis of this (b) Renal cause —
lar meningitis inclu
the clinical presentation of tubercu . (2017, Supple) — Nephrotic syndrome
condition. the subarachnoid - Acute glomerulonephritis (AGN)
al canal of spinal c ord,
the ventricles of the brain. centr
Ans : CSF is the fluid which fills - Renal failure
cistemae and subarachnoid space.
no. 1. (c) Chronic liver disease
n of CSF — See CNS question
- Formation. simulation, absorptio
44
.A
346 QUEST ‘. PAEDIATRICS APPROACHES u Paper-14 347
(i) Ascites — should be assessed by careful examination.

(d) Protein—energy malnutrition
(j) Others signs of CLD —) Palmer erythema. Telangiactesia.
(e) Allergic or angioneurotic oedema
Investigation: '
D How to proceed to the diagnosis :
examination and relevant (a) Complete blood count ——> For anaemia
Diagnosis will be based on proper history taking. thorough clinical
investigations. (b) Liver tunwon test —> Any alteration suggest chronic liver dysfunction.
History : (c) Chest X-ray. Echocardiography —y To detect cardiomegaly and cardiac dysiunction.
(a) Oedema > Duration — how long the oedema is present. (d) Uttrasonography abdomen -+ To detect hepatomegaty. change in hepatic echotemtre or renal
> Onset ~+Acute — in allergic/angioneurotic oedema/AGN. parenchyrnal disease. ascites.
insidious — in rest of the illness. (e) Blood biochemistry -> Cholesterol, albumin. urea. creatinine, C level to detect renal etiology of
anasarca. a
> Progression -> Progression of oedema from the site of first
appearance may provide
clue to diagnosis.
ally then progress
9.9. — ln renal cause oedema usually first appears in face, penorbit
down wards.
then spread upward
In carcfiac failure oedema appear first in feet and
accumulation is peritoneal cavity
-
— In contrast in liver diseas e or PEM first place of fluid
and child presents with ascites.
chest pain. point towards the cardiac cause.
(b) l-fistory of citficutty in breathing cough or
occurs in renal cause of anasarca.
to) History of diminution of urine output
hepatic etiolog y.
(d) History of jaundice indicate
exclude PEM as the
(e) Feedng history to be taken carefu lly to calculate. Protein and calorie intake to
etiology.
cause of allergic oedema.
past shout d be taken carefully as a
(f) Dmg and Food history of recent
Clinical Examination:
(a) Sites of oedema -
- Dentin of foot
— Ankle
- L99
-— Thigh
7 Scrotal l Labial
— Abdominal wall
— Chest wall
— Eyelids
bulatoy patient).
Pre-sacral region (in non-am
-
of liver cause.
(b) Jaundlce — more chance ed oedema.
se heart failure I eading to generalis
(c) Pallor — Severe pallor may cau ct PEM .
assessment -— to dete
(d) Anthropometry and nutritional reactions.
urticaria and other allergic
(a) Skin examination — For .
abnormal heart sound.
For tachycardia. murmur,
(0 Cardiac examination -— liver with change In consistency.
n -> For presence of enlarged
(g) Gastrointestinal examinatio
surface, margin.
.
palpable kidneys if any
(h) Renal examinatio n — For
Cha‘pier- 15 349
ADDITIONAL ANSWERS OF 2013 (SUPPLEMENTARY) Cl
CHAPTER - 15 Manloux test interpretation :
Size of induratlon Interpretation

ADDITIONAL ANSWERS OF 2018 (SUPPLEMENTARY) - < 5 mm Negative/no active disease.
° 5 — 10 mm Consider positive in immunocompromised, malnutrition
and positive contact history patient.
O. 1) : Diagnosis of childhood pulmonary tuberculosis — RNTCP guidelines.
' 2 10 mm Positive. suggests disease in presence oiclinical features.
Ans : Tuberculosis is still a major cause of morbidity and mortality for children worldwide. especially in
developing countries : O. 2) : Fluid management of Dengue Shock Syndrome.
Diagnosis of TB in paediatric age group is really challenging because of following reasons — detected and ‘
Ans : Dengue Shock Syndrome is a form of severe dengue with high mortality rate if not
i) Clinical features are often non-specific managed at earliest phase.
capillary
ii) Chest X-ray and Mantoux test are difficult to interpret and do not give confirmed evidence for The pathogenesis of DSS is wide-spread endothelial damage leading to increased
cy.
the disease. permeability, subsequently haemoconcentration and circulatory insufficien
iii) Paucibacillary nature of the illness makes it difficult to diagnose the disease by direct The algorithm of fluid management in severe dengue is as follows
-
demonstration of mycobacterium organisms in various clinical Specimen.
Severe Dengue
So diagnosis of TB in children is based corroborativeiy on clinical signs. symptoms. chest eay.
'
Mantoux test and history of contact with adult patient of tuberculosis. Assessment of shock
C
is defined as any child who lives in a household with an adult, taking
Contact history : Contact
antitubencular therapy or has taken such therapy within past 2 years. l— l f
RNTCP (Revised National Tuberculosis Contract Programme) proposed
diagnostic algorithm- Hypotension Unrecordable blood pressure i
for diagnosis of pulmonary TB in children as follows — l i
Fever and l or cough > 2 weeks 088 ill DSS IV
+ l- loss of weight or no weight gain l _
t _
+ /— history of contact with suspected 5 Crystalioid - Crystallord 20 ml/kg bolus .
or confirmed case of active TB 1 — upto 3 bolus.
O 20lmI/kg/hr
; Assessment {—
i
l 1
Sputum Examination Improved No improvement
preferably 2 sputum smear l
l
l t . . Gradually decrease rate Check haematocrit
F of infusion 2 hourly *— J
2 negative
1 or 2 positive Haematocn't Haematocrit
i ‘l’ -
for AFB increased decreased
10 mi/kg/hour
Oral antibiotics for 10-14 days
J,
1 Symptoms persists 5 mI/kg/hour Colloid infusion Blood transfusion
l 10 milkg 1 0-15 mlikg
Chest X-ray and Mantoux test
3 mlikglhour L—t Assessment 9—J
l
I l . |
0 Abnormal chest X—ray - Mantoux negative or positive . ‘1' 1
Continue |.V. fluid until
- Positive Mantoux test 0 Chest X-ray normal stable for 24 hour improved Not improved
l l
l
' I diagnon
investigati lunher for TB and
osis Assessment for Acidosis. anaemia. myocardial
_., Treat for Tuberculosis l l other
dysfunction and treat accordingly
348
3'9:
CamScantter
ADDITIONAL ANSWERS or: 2013 (SUPPLEMENTARY) El Chapter—15 351
' Erythema infectiosum - Also known as 'Fifth Disease' is a common illness in childhood
Type of fluid - Crystalloid — Normal saline I Ringer Lactate
Rash - Character is erythematous
Preferably two I.V. line to be established one for crystalloid and one for dextrose
—
and potassium - Starts on face in ‘slapped cheek' appearance
Monitoring — During fluid therapy following parameters are to be monitored carefully - Rapidly spreads to trunk and extremities and rapidly undergoes a central clearing
leaving a lacy or reticulated pattern of rash.
- Heart rate
— Fades over 1-3 week period.
‘ Respiratory rate
- Roseola infantum — Also known as Sixth Disease
- Blood pressure
Rash — Character is maculopapular
- Pulse pressure
First appears on trunk. within 24 hour of fever
- Urine output
Spreads to face. neck and proximal extremities
Management of fluid overload -
0.1 — 0.5 mg! Fades by 3-4 days.
- If the patient is stable and is out of critical phase a Oral or W. Furosemide
kg/dose once or twice daily. - Dengue fever —- increasing incidence now a days.
of LV. fluid
- If the patient is stable but still in critical phase (Plasma leakage) —> Reduction Rash — Usually erythematous or maculopapular type
rate. — Rash appear in different phases of illness
0. 3) : Characteristics of skin rashes in different exanthematous
fever in children - Initial rash is transient flushing erythema of face within ist 24-48 hours of
paediatri c age group and really a diagnostic symptoms.
Ans : Exanthematous fever is a common problem in
in diff erent illness help to diagnose — Second rash appear 3-6 days of onset of fever
challenge to pediatrician. Clinical characteristics of rashes
the conditions. - — Irgéecovery phase some patient have a rash of “islets of white in the sea of
cteristics of the rashes are as follows —
Common exanthernatous fever in children with chara r .
- Measles Common and serious illness
O. 4) :A six year old child presented with severe anemia without any Lymphadenopathy or '
-
Rash — Character - Maculopapular Visceromegaly. Mention the differential diagnosis and how will you approach to diagnose
- Appear on the 4th day of rise of fever the case 1’ (2 + 6)
posterior aspects of cheeks
lst appear behind the ear, along the hairline and Ans : DIFFERENTIAL DIAGNOSIS
y spread s to face, neck. chest. arm. trun k. thigh. legs over the next 2-3
Rapidl
days. - Informations available :
of appearance and leaves a branny
- Starts to disappear in the same order t) 6 year old child
amati on and brown ish disco louratio n which fades over 10 days.
, desqu 2) Severe anemia
illness
- Vancella (Chicken pox) - Common 3) No Iymphadenopathy or visceromegaly (i.e.. hepatosplenomegaly)
of rash
Rash -— Classical Vesicular type - Differential diagnosis :
-
- Appea r 24-48 hour after prodro mal symptom
l) Nutritional anemia -
- First appear on tmnk a) hen Deficiency Anemia (IDA)
type ras has first appear as macule and
Though characteristic rash is vesicular b) Megaloblastic Anemia (MA) —> dueto
progress to papule. vesicle and crust.
the i) Vitamin B12 deficiency
s in varyi ng stages of evolution is
-— Simultaneous presence of skin lesion ii) Folic acid deficiency -
characteristic of varicella.
2) Anemia of chronic disease (ACD) - 9.9.. Osieomyelilis. Bronchiectasis. Ulcerative
—- Lesions usually crust by 6-7 days
ted rashes that persist for days to Colitis etc.
es leave behind hypo and byperpigmen
-— Rash 3) Chronic Renal Failure (CFlF)
weeks.
in children 4) Aplastic anemia ,
Rubella — Mild exanthemaious fever
u—h
-
ble in size
AI
Character -— Discrete maculopapular. varia 5) Blood loss —) .

vu-
Rash
a) Acute - 9.9.. Esophageal varices, Rectal polyp. Peptic ulcer. Hemangioma.
-
ds rapidly to trunk
— It appear fst on face and sprea
Herriarlhrosis in hemophilia etc. '
- Last for 3 days
ence of appearance without
significant b) Chronic — Occult blood loss. 9.9., in hookworrn infestation. Meckel's diverticullum
— Rapidly disapp ear with sequ
desquamation. .x
-.
—
PLEMENTARY) Cl Chapter— 15 353
ADDlTlONAL ANSWERS OF 2018 (SUP
C) investigations:
6) Pure Red Cell Aplasia
1) CBC —r
[\fim
7) Chronic lead poisoning
a) Hb% — Low (Anemia)
APPROACH b) TLC — Low in Aplaslic anemia
A) History — c) DC -
sis in aplastic anemia
1) Dietary history —§ i) Neutropenia with relative iymphocyto
phils may be found in MA
8) Prolonged consumption of cow's milk instead 01 breast milk in infancy and ii) Hyper segme nted neutro
delayed weaning may lead to iron deficiency. — Low in aplast ic anemi a.
'L
d) Platele t count
b) Pure vegetarian diet may lead to vit. B12 deficiency 2 Fielicuiocyte count —>
V
c) Goat's milk ingestion (as main lood) often lead to folic acid deficiency a) Increased in hemorrhage
MA)
2) We Chronic diarrhoea —> Can lead to malabsorption and various types of nutritional b) Normal in nutritional anemia (119.. IDA and
red cell aptasia
anemia (IDA. MA). 0) Low in aplastic anemia and pure
3) We bleeding manifestations —> , MCH, MCHC) —+
3 Red cell indices (MCV ning
, l MCH. ~|r MCHC) -) lDA, Lead poiso
V
a) Anemia proportionate to bleeding - a) Microcytic, Hypochromic {L MCV orrhage, anemia
MCV and MCH) -) Haem
i) HematemesisiMalena —> in peptic ulcer or esophageal varices b) Normocytic, Normochromic
(Nor ma I
ii) Hematochezia —) in rectal polyp of chronic disease. CFlF
stic anemia
iii) Hemarthrosis, Epistaxis, Gum bleeding —> in coagulation disorders, like c) Macrocytic (T MCV) -«> MA, Apla
hemophilia 4) HOW —> Increased in IDA and MA
in aplastic
b) Anemia disproportionate and more severe than bleeding ~> seen 5 Ferritin —->
U
anemia a) Low in IDA
4) Past H/o bleeding/easy bruisability —> in hemophilia b) High in chronic inflammation
5) Family history -) positive in hemophilia 6 Serum iron —) Low in IDA
6) Drug history —) in IDA
7 Total Iron Binding Capacity (WHO) —> High
predispose to folic acid in lDA (> 80 pgldl). very high (> 160
a) Phenytoin. Phenobarbitone, Methotrexate —+ can 8) Free Erythrocyte Protoporphyn'n (FEP) —> High
deficiency. . ~
pgidl) in lead poisoning
suppression
b) Chloramphenicol -—> may cause bone marrow 9) Bone marrow examination -)
7) We pica —> in lDA. a) Megaloblasts are seen in MA
B) Examination : b) Depression of erythroid series in pure red cell aplasia
1) Nutritional assessment -9 c) Depression of all 3 the series in aplastic anaemia
a) PEM may be associated with nutrition al deficien
cy anemias, 9.9.. IDA, MA or ‘ 10) Vitamin B12 and Folic acid level —> to find out the etiology of MA.
mixed (dimorp hic). 11) Flenal Function Test —> Abnormal in CHF
nic renal failure. bronchiectasis etc.
_ b) Failure to thrive is associated with chro 12) Stool for GET—b to look for chronic occult blood loss.
c) Signs of rickets may be seen in CHF. 13) Upper Gf Endoscopy —) to find outcause of hematemesis or malena
be found in aplastic anemia or
2) Bleeding spots —-> (Purpura, ecchymosis) may 14) Colonoscopy -i_ for hematochezia. -
coagulopa thies .
15) Coagulation profile (er, cr, PT, aPTl) —-) for coagulopathy
3) Hypertension -) in CFlF. 16) Technetium 9.9m scan —) if source of bleeding is obscure.
c diseases leg. migratory coarse
4) Systemic manifestations -+ in various chroni
crepitations in bronchiectasis).
in MA.
5) Hyperpigmentation of knuckles —>
6) Blue line in gums -+ in lead poison ing.
7) Nail changes -—> (koilonychia) in IDA.

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QUEST

Dr. Shatanik Sarkar MBBS, MD (Paediatric Medicine)

Dr. Debasree Guha MBBS, MD (Paediatric Medicine)

First edition 2018

Price : Rupees three hundred only

WBUHS QUESTION PAPERS 2018 – 2015 XI – XIV

Chapter 1 : GROWTH AND DEVELOPMENT 1 – 9

Chapter 2 : NUTRITION AND MICRONUTRIENTS 10 – 35

Chapter 3 : FLUID AND ELECTROLYTE 36 – 42

Chapter 4 : NEONATOLOGY 43 – 105

Chapter 5 : IMMUNIZATION 106 – 112

Chapter 6 : INFECTIOUS DISEASES 113 – 142

Chapter 7 : RESPIRATORY SYSTEM 143 – 163

Chapter 8 : CARDIOVASCULAR SYSTEM 164 – 195

Chapter 9 : GASTRO-INTESTINAL SYSTEM 196 – 214

Chapter 10 : HEMATOLOGICAL DISORDERS 215 – 246

Chapter 11 : GENITO-UNINARY SYSTEM 247 – 269

Chapter 12 : CNS 270 – 292

Chapter 13 : MISCELLANEOUS 293 – 308

Chapter 14 : APPROACHES 309 – 347

Chapter 15 : ADDITIONAL ANSWERS OF 2018 (SUPPLEMENTARY) 348 – 353

- Standing Height — For child > 2 years

> Measuring tape against a wall.

- Correlates closely with stature.

é . é 1'2 - it‘s best practice to plot head circumference on growth charts.

' ghosts: Different Types of Growth Charts :

main-1 t..,,.tt.s.l|..,._ ll-

> Bme Age > crronological age.

Causes - Thrrotoxioosis BMl for age

- Precocious puberty Skin told thickness [or age

Going upstairs I" alternate feet. 0. 10 :Developmental milestones at 9 months of age. ]

diiterent target tissues include —

b) Timing of the day

2. In rickets. the cartilage cells go on mulli plying

matrix at the growth

6. Coarse trabeculation of the diaphysis. Watery rickets]

a) Growth hormone increases serum Ca" due to increased absorDllon 70f“ 9 -

c) Vitamin D dependent rickets :

1B QUEST : PAEDIATFIICS NUTRITION AND MICRONUTRIENTS U Chapter-2 19

Ans: BALANCED DIET

by-products oi nal in the rhodopsin prosthetic group.

b) [V Fluid only in shock.

classification. ' 3) Potassium supplements

b) Maintain hand hygeine SHORT NOTES :

a) Initiation of feeding. as early as possible. Ans: CLINICAL FEATURES OF OF RICKETS

Dyselectrolytemia Unmineralized matrix at the growth plate.

O. 17 : Role of vitamin D in children. [BMC - 2016]

0. 23 : Vitamin A prophylaxis. {BMC - 2015] Ans: See 0- 9 (complications)

0. 3f : Age Independent criteria of malnutrition. {BSMC—Bth Sem. 9th Sem SUMO-2016]

Abdominal distension. iv) Home economist etc.

Ascites. > Activities:

:1 Diagnosis: Acceptls orally Clinically better. but not accepting orally

Complementary teed : Give at least 1 Kalori serving at a time of mashed rotifbread/biscuit

in) Total protein : 4-6 gmlkg/day.

0. 38 : Diet of 1 year old infant. [2011, 2014-Supple]

our traditional bulky

Loss of Sodium e) Coma

l ' - b) “Cutaneous loss (Bum)

lntracranial hemorrhage <- Tear in the bridging vessels of brain