Case study

Case Study -1
• Kavita, who is 40 weeks pregnant presents to Emergency department in labour. She is 32 years old and is G4 P3 and has had
prenatal care throughout her pregnancy. Upon examination, the infant is crowning and delivery is imminent. As the newborn is
presenting, the cord is found to be wrapped around his neck. The physician unwinds the cord before the delivery of the baby.
Infant is delivered by the physician and has poor tone, minimal respiratory effort and central cyanosis.

• Phase I

Baby has occasional gasping respirations with a heart rate of 90 beats per minute. APGAR Score is found to be 3. Skin colour is
still cyanotic with poor muscle tone. You start with positive pressure ventilation with bag-valve-mask on room air at the rate of
40-60 breaths per minute.
• Phase II

• Baby does not respond well to the ventilations and has minimal shallow respirations with a heart rate of 50. Skin
of the baby is cyanotic. You initiate chest compressions with positive pressure ventilation via BVM with 100%
oxygen in ratio of 3:1 (90 compressions/30 ventilations per minute).

• Phase III 

• The physician chooses to intubate the baby. After intubation, he confirms the placement of the tube. Lung sounds
are heard equally bilaterally with good rise and fall of the chest. You establish an IV access. Heart rate is 50 bpm.
 Case Study -2
A 13-year-old child weighing 61 kg with a 1-week history of swelling around the eyes and both legs, and
generalized body swelling. She had a history of fever, cough and decreased urine output. Examination
revealed bilateral pedal oedema (pitting type).

Vital signs were 101.9º F temperature, Pulse rate 132beats/min, respiratory rate 20 breaths/min, Blood pressure 110/54 with
a pain scale of 6 and weight of 61.2 kgs

Laboratory investigations showed protein in urine, reduced serum albumin (2.0 g/dL) with elevated lipid
levels. Although kidney biopsy could not be performed due to economic problem of the family, a diagnosis
of idiopathic nephrotic syndrome (NS) was made based on clinical and laboratory findings.

The patient was mainly treated with furosemide, prednisolone and enalapril. Urine I/O charting
(Intake/Output chart for assessing fluid intake and ability to pass urine in adequate amounts) was done daily
until optimal results were obtained.
Case study 3
• A twenty-seven months old boy reported in ED and presented with a history breathing difficulty,
cough and fever for two days. His physical examination revealed the past case history of grunting,
very severe chest wall indrawing and hypoxemia (SpO2 (peripheral capillary oxygen saturation)
82% without O2) and head nodding. He was clinically diagnosed with severe pneumonia. On
admission, his temperature was 37.4○ C, RR 74 breaths/min, PR 176 beats/min, and SpO2 was
82% without O2. Patient was dyspneic and irritated. On Auscultation, crepitation was present in
both lung fields (right upper zone and left lower zone) and rhonchi was present on upper and
middle side of left lung field.
CASE STUDY -4
 Case Study -4
15 days old female baby, weighing 2.9kg and case of
birth asphyxia delievered via LSCS due to breech
presentation at 38 weeks of gestation was admitted on in
NICU with C/O

⚫ Fits : for 1 day

⚫ reluctant to feed : for 1 day
 HISTORY OF PRESENTING COMPLAIN:

•According to attendent, baby was in usual state of health 1 day

back when she started having fits in the morning. Fits were focal and
involved either one limb at one time with flickering of eyes and lasting 5-
10 secs occuring every 2 to 3 hrs. There was no loss of consciousness,
fecal or urinary incontinence and uprolling of eyeballs.There is no history
of fever and vomiting .Baby is also reluctant to feed since then.
 BIRTH
HISTORY
⚫ ANTENATAL:
 It was a fullterm pregnancy and a booked case at some private hospital
 U/S scan was done twice at 8th and 9th mth
 Mother had no c/o gestational DM, hypertension,fever,rash or anemia
during pregnancy
 She took multivitamins and got tetanus toxoid.

⚫ NATAL:
 Mother underwent LSCS due to breech presentation of baby at 38 wks of
gestation.
 There is no H/O PROM, preeclampsia or any other maternal complication at
birth
of baby.

⚫ POSTNATAL:
 Baby had delayed and weak cry.
 There was peripheral cyanosis.There was no jaundice.
 Baby had episode of fits half hr after birth.They took the baby to Jinnah
hospital and upon their refusal to admit due to lack of incubators, they took the
babyto Naseem centre.The baby was admitted there as a case of perinatal
asphyxia for 9 days.No fits were observed during this period.Platelets and FFPs
were tranfused.Baby was on tanzo and vancomycin and was discharged on 9-9-
⚫ VACCINATION HISTORY:
No BCG vaccination done.

⚫ FEEDING HISTORY:
Baby was kept NPO after birth.Breast feeding was
started at 8th day of life and she was taking feed
normally. She is reluctant to feed for 1 day.

⚫ FAMILY HISTORY:
Baby is 5th product of cosanginuous marriage.She has
3 normal siblings.There is no significant family history of
any illness.

⚫ SOCIOECONOMIC HISTORY:
 Their socioeconomic status is average.
 They use unboiled water for drinking.
 EXAMINATIO
N
GENERAL PHYSICAL EXAMINATION

⚫ VITALS
Heart 142/min
rate:
Respiratory rate: 48/min
Temprature:
98.6F

Capillary refill time: <2 sec

O2 saturation: 92%
RBS: 86mg/
dl Anemia: -ve
Cyanosis: -ve
Jaudice: -ve
Dehydration: -ve
Edema: -ve
⚫ ANTHROPOMETRIC MEASUREMENTS
Length: 53.5cm
2.9 kg
Weight
FOC: 37.5cm
:
 HEAD TO TOE
EXAMINATION
⚫ HEAD:
Anterior fontanelle was wide open
⚫ EYES normal
⚫ NOSE
⚫ MOUTH AND PALATE no cleft lip and
⚫ palate
EARS normally placed,no
⚫ LIMBS deformity normal
⚫ BACK normal
 Systemic examination
⚫ RESPIRATORY SYSTEM
NVB,equal bilateral air entry

⚫ CVS:
s1+s2+0

⚫ ABDOMEN:
soft, nontender, no liver or
spleen palpable, gut
⚫ CNS:sounds audible
Ton increased
eREFLEXES brisk
Moro incomplete
Suckig fair
Rooting fair
Grasping po
DIFFERENTIAL
DIAGNOSIS??
DIFFERENTIAL
DIAGNOSIS
⚫Hypoxic ischemic
encephalopathy
⚫Meningitis
⚫Sepsis
 INVESTIGATI
ONS
CBC
2 ND Day 4th Day
Hb 13.3 12.60
MCV 103.8 101.5
MCH 36.4 36.8
MCHC 35,1 35.2
HCT 37,9 38.9
TLC 9400 6200
Neutrophils 47 45
Lymphocytes 33 32
Basophils 0 0
Eosinophils 15 11
Platelets 298000 371000
ELECTROLYTES
Na 137 140
K 4.8 4.1
Cl 103 104
BUN 11 2
Creatinine 0.5 0.3
Total bilirubin 0.31
Direct bilirubin
ALP 173 150
SGPT 51
PT
control 10.5
test 9.7
INR 0.92
APTT 26.9
Calcium 14.4 9.8
CRP 0.30
 CSF DR
⚫ AMOUNT: 1.5ml
⚫ APPEARANCE: clear
⚫ Ph: 7.3
⚫ PROTEIN: 5.3mg%
⚫ GLUCOSE: 34mg/dl
⚫ RBCS: 1-2/HPF
⚫ WBCS: 5/CMM
⚫ GRAM STAIN: no organism seen

CSF CS
⚫ No bacterial growth

BLOOD CS
⚫ no bacterial growth seen
⚫ X-RAY SKULL:
 Widening of sutures and anterior fontanelle suggestive of
raised
ICP

⚫ U/S brain:
 no solid or cystic lesion seen
 mild hydrocephalus with dilated all 4 ventricles
 brain edema
 grade 2 parenchymal and IVH including germinal matrix
IMPRESSION:
 Grade 2 intracranial hemorrhage

⚫ CT SCAN brain:
 Extensive white matter edema invlving the subcortical regions
of frontal,parietal and temporal lobes causing effacement of
 right lateral ventricle.
 No hemorrhagic density identified

IMPRESSION:
 Ischemic encephalopathy involving frontal,parietal and temporal
regions.
 FINAL DIAGNOSIS

HYPOXIC ISCHEMIC
ENCEPHALOPATHY SECONDARY
TO BIRTH ASPHYXIA
 TREATMEN
T
⚫ Pt was kept NPO initially ,then mother feed was given 2cc 2hrly
via N/G
⚫ Inj 1/5th in 10% D/S 150cc/kg/day
i.e 450cc in 24 hrs
⚫ Inj cefotaxime 150mg/kg/day
i.e 225 mg iv B.D
⚫ Inj amikacin 15mg/kg/day
i.e 22 mg iv B.D
⚫ Tab phenobarbitone 30 mg
¼+¼
⚫ Inj diazepam 0.3mg/kg iv sos
⚫ Inj Phenytoin 20 mg/kg loading dose
i.e 60mg iv stat,then 10mg iv BD in infusion
⚫ Neb with N/S 6hrly
 HYPOXIC
ISCHEMIC
ENCEPHALOPATH
Y
•Hypoxic-ischemic encephalopathy, is
characterized by clinical and laboratory
evidence of acute or subacute brain injury due
to asphyxia. The primary causes of this
condition are systemic hypoxemia and/or
reduced cerebral blood flow (CBF).
RISK
FACTORS
 PATHOPHYSIOLOG
Y
⚫ The cerebral blood flow (CBF) of adults is typically maintained at
constant levels despite fluctuations in the systemic blood pressure.
⚫ In the infant, CBF autoregulation is not as responsive; therefore,
when hypoxia occurs, the infant's initial systemic response is to
maintain perfusion to the brain and end organs with increased heart
rate and the endogenous release of epinephrine.
⚫ These measures can only maintain CBF for a short time
(minutes), and when the hypoxic state persists, the systemic blood
pressure falls and neuronal cells are damaged through progressive
intracellular energy failure and eventual cell death via apoptosis.

⚫ THIS IS THE FIRST PHASE OF HYPOXIA.

⚫The second or latent stage of this process,
which occurs 6 to 24 hours after the initial
insult, is the recovery of cerebral circulation
and oxygenation leading to a progression of
inflammatory response and significant
cerebral edema, onset of seizures, secondary
cytotoxic edema, and additional cell death.
 INCIDEN
CE
⚫ In the United States and in most developed countries,
the incidence of hypoxic-ischemic encephalopathy is 1-
8 cases per 1000 births.

⚫ The incidence of hypoxic-ischemic encephalopathy is

reportedly high in developing countries.
 SIGNS AND
SYMPTOMS
CNS MANIFESTATIONS
⚫ Clinical manifestations and course vary depending
on hypoxic-ischemic encephalopathy severity.

Mild hypoxic-ischemic
encephalopathy
 Muscle tone may be slightly increased and deep
tendon reflexes may be brisk during the first few days.

 Transient behavioral abnormalities, such as poor

feeding, irritability, or excessive crying or sleepiness.

 The neurologic examination findings normalize by

3-4 days
of life.
 Moderately severe hypoxic-ischemic
encephalopathy

⚫The infant is lethargic, with significant hypotonia and diminished

deep tendon reflexes.

⚫The grasping, Moro, and sucking reflexes may be sluggish or absen

⚫The infant may experience occasional periods of apnea.

⚫Seizures may occur within the first 24 hours of life.

⚫Full recovery within 1-2 weeks is possible and is associated with a

better long-term outcome.
 Severe hypoxic-ischemic encephalopathy
⚫ Stupor or coma is typical. The infant may not respond to any physical
stimulus.

⚫ Breathing may be irregular, and the infant often requires ventilatory support.

⚫ Generalized hypotonia and depressed deep tendon reflexes are common.

⚫ Neonatal reflexes (eg, sucking, swallowing, grasping, Moro) are absent.

⚫ Pupils may be dilated, fixed, or poorly reactive to light.

⚫ Seizures occur early and often and may be initially resistant to conventional
treatments. They are usually generalized.

⚫ Irregularities of heart rate and blood pressure (BP) are common during
the period of reperfusion injury, as is death from cardiorespiratory failure.

⚫ Infants who survive severe hypoxic-ischemic encephalopathy;

 The level of alertness improves by days 4-5 of life.

 Hypotonia and feeding difficulties persist, requiring tube feeding for

weeks to
months.
 DIAGNOSI
S
⚫ Serum electrolyte levels
⚫ Renal function studies
⚫ Cardiac and liver enzymes - These values are an
adjunct to assess the degree of hypoxic-ischemic
injury to the heart and liver
⚫ Coagulation system - Includes prothrombin
time, partial thromboplastin time, and fibrinogen
levels
⚫ Arterial blood gas - Blood gas monitoring is used
to assess acid-base status and to avoid hyperoxia and
hypoxia, as well as hypercapnia and hypocapnia
⚫ Cranial ultrasonography
Findings include global increase in cerebral
echogenicity and obliteration of cerebrospinal fluid
(CSF) containing spaces suggestive of cerebral edema.
⚫ Head CT scanning
A CT scan of the head shows cerebral edema,
manifested as narrowness of the lateral ventricles
and flattening of gyri. Areas of reduced density that
indicate evolving zones of infarction may be present.
Evidence of hemorrhage in the ventricles or in
the cerebral parenchyma may also be seen.
⚫ Brain MRI
MRI is the imaging modality of choice for the
diagnosis and follow-up of infants with moderate-
to- severe hypoxic-ischemic encephalopathy (HIE).
Demonstrates the injury pattern as area
of hyperintensity
⚫ Amplitude-integrated electroencephalography
(aEEG)
aEEG performed within a few hours of birth can
help evaluate the severity of brain injury in the
infant with hypoxic-ischemic encephalopathy.
 MANAGEMEN
T Initial management
⚫ 1. Transfer the baby to special care newborn unit.
A baby who fails to initiate and sustain respiration at birth is at
risk of hypoxic brain injury and needs regular monitoring. All these
babies should have a cord gas analysis performed.
Infants with moderate asphyxia (Apgar score 4-6 at 1 minute of
age) may be transferred to the mother. However, these infants should
also be monitored frequently in the first 48-72 hours for features
suggestive of HIE.
Infants with severe asphyxia (Apgar score 0-3 at 1minute or need
for prolonged bag and mask ventilation >5 minutes) should be
transferred to a special care newborn unit for observation and
treatment.
⚫ 2. Maintain temperature
Place the baby under the radiant warmer after drying the baby.
⚫ 3. Check vital signs
Immediate clinical assessment should be made by
recording respiration, heart rate, blood pressure, capillary refill
time, temperature and oxygen saturation. Urine output
monitoring should be done.
⚫ 4. Start intravenous fluids
⚫ 5. Check blood sugar, hematocrit and blood gases.
Check blood sugar (to detect hypoglycemia or
hyperglycemia), hematocrit (to detect anemia and
polycythemia) and blood gases (to detect metabolic acidosis,
hypoxia,hyperoxia and respiratory failure).
⚫ 6. Consider infusion of volume expander
If the capillary refill time is more than 3 seconds or if there
is metabolic acidosis, volume expansion with normal saline (or
Ringer’s lactate) 10 ml/kg over 5-10 min should be instituted.
This may be repeated.Maintain the mean BP above 35 mm
Hg
(for term infants). Dopamine or dobutamine can be
used to maintain adequate cardiac output.
 SUBSEQUENT
TREATMENT
a) Maintain oxygenation and ventilation.

b) Maintain adequate perfusion: Use saline, Ringer’s lactate and blood to maintain
intravascular volume.

c) Vasopressors: Dopamine and dobutamine are the drugs of choice.

d) Maintain normal blood glucose

e) Treat seizures:
The anticonvulsant of choice for controlling seizures is phenobarbitone.The initial
dose is 20 mg/kg, intravenously slowly over 20 minutes.Two additional doses of 10 mg/kg
can be given every 15 minutes. The maximum loading dose is thus 40 mg/kg.
If convulsions are still uncontrolled, phenytoin sodium should be added in a dose of
20 mg/kg intravenously slowly over 20 minutes. Maintenance therapy of both
phenobarbitone and phenytoin is started 12 hours later in a dose of 5 mg/kg/day in a
single dose.
For intractable seizures Clonazepam, Midazolam, Paraldehyde, and Valproate
may be
tried.

f)One promising modality on the horizon is cerebral hypothermia.Mil dreductions in

temperature of the body as a whole or of the head (brain) has been shown to minimize
the effects of hypoxic ischemic encephalopathy.
 DIE
T
In most cases (particularly in moderately severe
and severe hypoxic-ischemic encephalopathy), the
infant is restricted to nothing by mouth (NPO)
during the first 3 days of life or until the general level
of alertness and consciousness improves. In addition,
infants undergoing hypothermia therapy should
remain NPO until rewarmed. Enteral feeds should be
carefully initiated about 5 mL every 3-4 h.
⚫
PROGNOSIS
In severe hypoxic-ischemic encephalopathy, the mortality rate is 25-50%. Most
deaths occur in the first week of life due to multiple organ failure or . Some
infants with severe neurologic disabilities die in their infancy from aspiration
pneumonia or systemic infections.

⚫ The incidence of long-term complications depends on the severity of hypoxic-

ischemic encephalopathy.
⚫ 80% of infants who survive severe hypoxic-ischemic encephalopathy
develop serious complications, 10-20% develop moderately serious
disabilities, and 10% are healthy.
⚫ Among the infants who survive moderately severe hypoxic-ischemic
encephalopathy, 30-50% may have serious long-term complications, and 10-
20% have minor neurological morbidities.
⚫ Infants with mild hypoxic-ischemic encephalopathy tend to be free from
serious CNS complications
⚫ Complications include
• Cerebral palsy - 30%
• Epilepsy - 16%
• Blindness - 14-17%
• Severe hearing impairment - 6
THANK YOU
Scenario- 1
• A twenty-seven months old boy reported in ED and presented with a history breathing difficulty,
cough and fever for two days. His physical examination revealed the past case history of grunting,
very severe chest wall indrawing and hypoxemia (SpO2 (peripheral capillary oxygen saturation)
82% without O2) and head nodding. He was clinically diagnosed with severe pneumonia. On
admission, his temperature was 37.4○ C, RR 74 breaths/min, PR 176 beats/min, and SpO2 was
82% without O2. Patient was dyspneic and irritated. On Auscultation, crepitation was present in
both lung fields (right upper zone and left lower zone) and rhonchi was present on upper and
middle side of left lung field.
 Scenario-2
A 13-year-old child weighing 61 kg with a 1-week history of swelling around the eyes and both legs, and
generalized body swelling. She had a history of fever, cough and decreased urine output. Examination
revealed bilateral pedal oedema (pitting type).

Vital signs were 101.9º F temperature, Pulse rate 132beats/min, respiratory rate 20 breaths/min, Blood pressure 110/54 with
a pain scale of 6 and weight of 61.2 kgs

Laboratory investigations showed protein in urine, reduced serum albumin (2.0 g/dL) with elevated lipid
levels. Although kidney biopsy could not be performed due to economic problem of the family, a diagnosis
of idiopathic nephrotic syndrome (NS) was made based on clinical and laboratory findings.

The patient was mainly treated with furosemide, prednisolone and enalapril. Urine I/O charting
(Intake/Output chart for assessing fluid intake and ability to pass urine in adequate amounts) was done daily
until optimal results were obtained.
Scenario-3

A newborn female infant was delivered through planned cesarean section due to large
occipital encephalocele diagnosed antenatally. The pregnancy was unplanned and the
mother did not take folic acid prior to conception. Birth weight was 3.41 Kg. Upon
delivery, the newborn was healthy, with an Apgar score of 8. The physical examination
revealed 2 large pouches; one was over the occiput, and the other swelling was located
over the nape of the neck. Brain MRI revealed large occipital encephalocele and
cervical myelomeningocele. The 2 defects were repaired separately, with an uneventful
postoperative course.