NEWBORN INFANT NORMAL NEWBORN ‘ From birth to under four weeks of age (< 28 days), the infantis called newborn (neonate) and that period is called neonatal period™*™, «© Neonatal period is divided into - 4) Early neonatal period (first week of life, te. <7 days) ii) Late neonatal period (7* day to < 28 days) = Term neonate (term baby) «Any neonate born between 37 and < 42 weeks (259 - 293 days) of pregnancy irrespective ofthe birth weight. «= Preterm baby : ‘ Any neonate born before 37 weeks (<259 days) of pregnancy irrespective ofthe bith weight. 1 Post-term baby 4 Any neonate born ator after 42 weeks (294 days or more) of pregnancy irrespective of the birth weight. « Features of normal ‘term? newborn infant are = 1 Length > 50 em!) 1 Head circumference > 34 em = Chest circumference -> 31 em (3 em less than head circumference) 1 Upper segment lower segment ratio ->1.7 0 1.9 1 Heart rate > 120 - 140 per minute'”™="" wt Respiratory rate —> 35 - 40 per minute 1 Attitue—> Flexion!*"” 1 Peripheral cyanosis (acrocyanosis) may be present’! mart? = Urine is passed by 24 hours after birth ‘» Meconium (fist stool) is passed within 24 hours, After that meconium stools (black tarry) can be passed upto 3 days”, On 4°-5* days transitional stools (greenish) are passed. After 5 days regular milk - eae ‘milk stools (golden,yccipital and frontal bones. * The skull shows moulding with parietal bones slightly overriding the 1 There may be pulmonary flow (systolic) murmunto™”,especilly inl 1 Liver spleen and kidney may be palpable". _— mormal newborn and requireso treatment ¢ There are some minor clinical problems which can occur in low birth weight neonates. ‘¢ The problems are - 1. Milia(rora.o taneously. 1 White dots on nose anu face due to distended sebaceous glands. These dseappearsPO” i 2. Erythema toxicumara 2.90 appear spontaneously 1 Exythematous papules on trunk face. Tey appear on 2" & 3cday and disappear spontaneous ‘The following figure in a newborn is showing: 8) Staphylococcus scalded skin syndrome b) Scleroderma ©) Cellulitis ) Normal baby Ans. is‘ ic, Normal baby 2 | ‘© The igure is showing small red splotches with yellow head in the middle —> Diagnosis erythema | toxicum (seen in normal newborn). stewie 3. Mongolian spots"! 1 There are ‘bluish spots most commonly found in pre-sacral area" (mainly in lower back & buttock), but ‘may also be found over posterior thighs", legs, and shoulders. 1 They disappear spontaneously before frst birthday. ‘The newborn given in figures suffering from: a) PEM b) TORCH ©) Telengiectasia 4) None ‘Ans. is'd! Le None | ‘©The given figure is showing mongolian spot, a normal finding in newborn, _ a 4, Storkbites «= Pinkish gray capillary hemangiomas on the nape of neck, upper eyelids, forehead & nose. These disappear spontaneously. 5. Peeling of skin 1» More frequent in post-ferm infants, but can also occur in term infants, 6. Subconjuctival hemorrhages" 1 Disappear spontaneously. 7. Breast engorgment s Due to transplacentally acquired maternal hormones. It is seen on 3“ or 4° day 8, Epstein pearl" 1 Epithelial inclusion cysts, which appear a8 whitish spots. These are of two types - i) Palatal -> On hard palate or on either sie of median raphe, Prepucial —> At the tip of prepuce at 60" clock position.B PRE sores: sere nn Parachute" 8.9 months __ + Ealestrefexto disappear» Rooting reflex. a *Swllowingrefierisearlestt appear > 12-13 weeksof gestation” + Moros reflex develops by 28 week of gesationand dsappearsar6 months of ages" Lett flec tats Persistence of Moro’ reflex beyond 6 months is abnormal" * Unilateral Moros reflex is seen in 1) Exbs palsy" (C.-C, lesion's™s™) ii). Spastic hemiplegia ii). Shoulder dislocation'™!* iv) Fracture proximal humerus or clavicle”, - «Exaggerated Moro’ reflex or persistence of Moro’ reflex is seen in brain (cerebral) damage®re™ ei”, ‘The following figure is showing which reflex: a) Parachute reflex ) Sucking reflex ©) Tonic neck reflex @) Mord’ reflex Ans.is ‘Le, Moro’ reflex ke ener ‘© Thisisa figure of Moro’ reflex. Sudden dropping of head in relation to trunk causes opening. abduction and extension of arm, followed by flexion of upper extremities. f ‘Morgan's Neonatal Neurobehavioral assessment scale «This consists of three parts: (i) Tone and motor pattern ii) Primitive reflexes, and (ii) Behavioral responses. "Stage 1: Deep sleep, eye closed, no eye movement, regular breathing = "Stage 2: Light sleep, eye closed, rapid eye movement, ss | Stage 3: Drowsy or semirowsy. ye opening ad closing (pel tering). | Stage 4: Awake and alert ey open, nial motor avy (movement). _ Sige 5: Wide aa, consid sg) movement "Stage 6: Crying intense and loud, High moto activity, } HYPOTHERMIA «# Anewiorn is more prone to develop hypothermia Because oflarge surface area per unto body weight The protective ‘mechanism for heat generation (thermogenesis) in response to cold environment are i) Peripheral vasoconstriction “i880, 1) "Non-shiveringthermogenesis'in brown ft by adrenaline". Brown fats located around adrenal gland kidney, nape of neck*@!™, and interscapular and axillary regions, ii) Increased heat rate to meet more O, demand. 1» Newborn does not have shivering mechanism for thermogenesis!0%81.% 4199, «# Clinical features ofhypothermia ina neonate are = 3) Peripheral vasoconstriction: Acrocyanoss, coo! extremities, decreased peripheral perfusion, ii). CNS depression: Lethargy", bradycardia" *"™, apnea"%S), poor feedingcones amonone AE iit) Increased metabolism : Hypoglycemia'"®'%", hypoxia", metabolic acidosis”. iv) Increased pulmonary artery pressure : Tachypnea, respiratory distress. ¥) Other: Depressed immunit manifestation. «creased chances of septicemia, seleroma"*™, DIC (due to infection), hemorrhagic LOW BIRTH WEIGHT AND PREMATURITY « Birth weight is the single most important determinant of chances of survival, growth and development ofan infant! "Birth weight should ideally be measured within Ist hour of birth. Average birth weight in India is 27-29 kg (2-8 gyn, «© Most common causes of low birth weight (LBW) in India is maternal malnutrition, Maternal nutrition has linear relation with birth weight Following terms are related to birth weight and maturity of a neonate at birth = 1) Low birth weight 1 Any neonate weighing less than 2500 gm (25 hg) #1" PCMH” beth irrespective of gestational age (WHO definition). But some Indian scientists consider LBW as < 2hg/"M#?, 2) Very low birth weight 1 Any neonate weighing less than 1500 gm (1-5 kg) at birth irrespective of gestational age. 3). Extremely low birth weight # Any neonate weighing less than 1000 gm (1 kg)" at birth irespective of gestational age. 4) Appropriate for gestational age (appropriate for date) 1 Neonate with birth weight between 10° to 90" percentile. 5) Small for gestational age (small for date) f= Neonate with birth weight lee than 10" percentile*'®, These are the baby called as intrauterine growth retardation (IUGR) (6). Large fr gestational age (large for date) ‘= Neonate with birth weight more than 90° percentile 7). Term neonate (term baby) 1 Neonate born between 37 and < 42 weeks (259-293 days) respective of birth weight, 8). Preterm baby = Neonate born before 37 weeks!” (< 259 days), irrespective of birth weight 9) Post-term baby ‘= Neonate born ator after 42 weeks (2 294 days), irrespective of birth weight, Causes of intrauterine growth retardation (small for date) «© Important causes of IUGR are = 1) Maternal malnutrition : Most important cause, 2) Substance/drug intake : Smoking and tabacco™™**", alcohol" ™*", propranolol 3) Maternal factors: Short stature mother, primi or grand mulipara, yound mother («20 years), lo 7 weight. 4) Maternal illness/diseases : Anemia, CRE”, heart disease, malaria, pre-eclampsia, hypertensio 5) Placental factors: Abruptio placenta, excessive infarct, single umblical artery 6) Fetal factors : First born babies, genetic/chromosomal aberrations, twin/muliple pregnancies, intrauterine infection'*"™, ‘Types of IUGR (small for date neonate) ‘© IUGRis classified as 1) Symmetric IUGR ' Reduced growth is symmetric. Head circumference, length and weight are equally affected 2). Asymmetric IUGR 1 Reduced growth is asymmetric with relative sparing of head'**”,pmmetrical IUGR, + Ponder ndes'#Y sas asa indicator fetal growth stats epi 0 ase8 aN Weight (gm) x 100 Ponderalindex =| ————__—_ Length (cm)s + & ponderal index below the 10 percentile may be used to dent IUGR infants correct 0. # A ow neonatal ponderal nds i defined as ess than 1 SD below a mean 2 a define ass than 18D el sna baby who has either normal growth «# Plisuswally less than 2in assymmetric growth retarded baby and 20r more ‘or has symmetrical growth retardation. ¢ Fetal ponderal index can also be calculated by USG examination a found to be predictor of IUGR with the sensitivity and specificity of 76.9 and 82%, respet than ISD, the fetal and neonatal well being is compromised. nd compared with neonatal PI, Fetal PT had been cively Ifthe fetal PTs less Problems of full term small for date infants (IUGR) Birth asphyyia « Hypoglycemiamanese # Meconium aspiration syndrome « Infections # Hypothermia «# Polycythemia & Hyperviscocity «© Head circumference is 3.em more than chest circumference Hypocaleemia ‘ Internal organs like liver, thymus and lungs are shrunken, Features of prematurity ‘¢ Baby is small in size usually less than 47 em long, Jatively lage, sutures are widely separated and fontanelle are large. ‘¢ Face is small and buccal pad of fat is minimal ‘¢ Skin is thin and pinkish and appears shiny due to generalized edema. + Skin is covered with abundant lanugo and there is little vernix caseosal*"™. + Subcutaneous fat is reduced, # The breast nodule is less than 5 mm wide", « The ears are soft and flat with ear cartilage being deficient and pliant’*#™s"e1®, f# Testes are not descended into scrotal sac (Empty scrotum)/*"™, « Scrotal sac is poorly pigmented and has less rugosties « In females labia majora appears widely separated, exposing the labia minora and the clitoris. '* Deep creases are not well developed in the sole", (There may be a single deep crease over the anterior one third ofthe sole). «© Neonatal reflexes such as Moro, Suckling & Swallowing are sluggish, «There is hypotonia with a poor recoil of flexed forearm when extended, ¢ Head is “The figure in question is showing the foot of a: a) Term baby }) Post-term baby ) Preterm baby 4) None ‘Ans. is‘c ie» Preterm baby S absence of deep creases in sole isa Feature of prematurity. ‘The figure in question is showing the genital area of: a) Term baby b) Premature baby ©) IGUR d) NoneComplications of prematurity (preterm baby) ‘© Birth asphyxia ‘© ARDS (Hyaline membrane dis) ‘* Hypothermia © Apenia «© Feeding difficulties ¢ Intraventricular hemorrhage © Hypocaleemia «Infections '* Necrotising enterocolitis © Hypoproteinemia ‘© Respiratory distress ‘© Metabolic acidosis ‘© Theliverofpremature (preterm) neonateis functionally immature that leads to hypo- ‘glycemia, hyperbilirubinemia’™'* 44 (jaundice) and poor detoxification of drugs. Feeding of preterm (premature) neonate We pope sucking eos ag Nopeputivemettnyinthegie ‘merous ’ B= SI en ri evap Ns eannnIGN) OAR OSCR TE = between suck/swallow and breathing _with occasional spoon/paladai feeding ‘Slightly mature sucking pattern Feeding by spoon/paladai/cup 2 34wees Coordination between breathing and repos tbe feeding Spon feeding isnot possible". Breastfeeding NEONATAL SEPSIS «* Pathogenic bacteria gain access into the blood stream and may cause - 1) Overwhelming infection (generalized infection) —» Neonatal septices i) Localized infection to the lung > Pneumonia ill) Localized infection to meninges > Meningitis ‘¢ Systemic bacterial infections are known by the generic term neonatal sepsis which incorporates septicemia, pneumonia and meningitis of newborn, © Two most common causes of neonatal septicemia and meningitis are group B streptococcus (streptococcus agalactic) and E.coli © Most common cause of neonatal septicemia snd meningitis overalls streptococcus agalactie (group B streptococcus) + Most common caus of neonatl septicemia and meningitis fn Inia is E coi 1 1 Most common cause of neonatal sepsis in hospital in India te Klebsiella, 1 Most common cause of neonatal epi in hospital across the worlds E. cl ‘Types of neonatal sepsis 1 Neonatal sepsis can be divided into = 1) Barly onset 11 occurs within 72 hours" of fe and is caused by organism prevalent in maternal genital tract o delivery are. 2) Late onset 1 Ttoceurs ater 72 hours oflife and is caused by organtams prevalent in external environment (from nursery or Iying in ward", Most commonly infection i transmitted through the hands of eare providers" nthePredisposing factors for neonatal sepsis 1) For early onset sepsis, Cutaprer 3 Newborn Infant | | | ¢ Low rth weight or prematurity!™! «© Prolonged rupture of membrane!™ ‘Foul smelling liquor | ‘Multiple per vaginum examination | ‘© Maternal fever ‘ Difiicult or prolonged labor | ‘¢ Meconium aspiration 2) Forlate onset sepsis «© Low birth weight + Superficial infections (pyoderma, umblical sepsis) ‘ Disruption of skin integrity with needle pricks and use of fluids. © Lack of breast feeding’"™ ‘© Aspiration of feeds Clinical features of neonatal sepsis. oT ory onset spt mas eae as pumoia andes commonly spice or mening « Late onset sepsis manifest as septicemia or pneumonia or meningitis. “Tem common and hrc manors san aeration the bis fein behavior aby refuses to suck and becomes lethargic, inactive or unresponsive. « Important laboratory finding are := i) Neutropenia is common (rarely neutrophilia may occur in severe neonatal infection’) ii) Increased number of immature neutrophits*™. ili) Increased ESR and CRP*'™ ‘Treatment of neonatal sepsis « Antibiotic treatment for neonatal infection is 1) Neonatal pneumonia : Ampicillin plus gentamicin *™9” 2) Neonatal meningitis: (i) Ampicillin plus gentamicin plus chloramphenicol or (ii) Cefotaxime plus gentamicin, ot (ii) Ampicilin plus cefotaxime. RESPIRATORY DISTRESS «The principle features of respiratory distress in a neonate ate 1) Tachypnea (fast breathing): Fast breathing is defined as |) Child less than 2 months of age > 260 breaths per minutel®io0 ii) Child aged 2 months upto 12 months + > SO breaths per minute iii) Child aged 12 months upto S years. > > 40 breaths per minute 2). Use of accessory muscles for respiration(°™*"2*1%; Features include use of sternocleidomastoid muscles, nasal alr flare and tracheal tug. 3) Use of intercostal o subcostal muscles'* "for respiration resulting in intercostal or subcostal recession- lower chest wall indrawing. 4) Audible grunting" "60 5) Cyanosis™ 7000 Apne ‘e Apnea may be defined as - |) Cessation of respiration for 20 seconds with o without bradycardia and cyanosis. ma, 4) Cessation of respiration for less than 20 seconds if tis associated with bradycardia or cyanosis 14S. 081,‘¢ Apnea is more common in preterm infants. + Apnea of prematurity occurs in preterm neonates in 2nd to Sth day of life and is because of immaturity of developing brain. * Important cases ofneonat apnesare:ypoghemia™™, metabolic acidosis, ypothermia‘T™ and prematurity" Pulmonary causes of neonatal respiratory distress «© Respiratory distress syndrome (hyaline membrane disease)4"™, ‘© Meconium aspiration syndrome*"™, '¢ Pneumonia. ‘Transient tachypnea of newborn «Persistent pulmonary hypertension «© Congenital malformation —» TER, Diaphragmatic hernia'"****, lobar emphysema, pulmonary hypoplasia. ‘* Upper airway obustruction > choanal atresia, vocal cord palay, lingual thyroid. ‘© Pulmonary hemorrhage Causes of respiratory distress with mediastinal shift in neonates ‘© Diaphragmatic hernia ‘© Congenital lobar emphysema ‘© Congenital mediastinal mass ‘* Pneumothorax ‘¢ Congenital cystic adenomatoid malformation ‘Meconium Aspiration Syndrome ‘e Meconium: is the first stool of an infant, composed of materials ingested during the time the infant spends in uterus, ie intestinal epithelial cells lanugo, mucus, amniotic fluid, bile and water. ‘¢ Meconium aspiration syndrome (MAS) occurs when infants take meconium into theirlungs during or before delivery ¢ It is more common in post-term neonates*'™ but may also occur in term neonates. Consequences of meconium aspiration ‘¢ Three main problems occur due to meconium aspiration - i) Obstructive emphysema or atelectasis™*” —> when aspirated material blocks the airways. ii) Pneumonitis and chemical pneumonia -» because of irritant property of meconium. Defective gas exchange. Clinical manifestations « Respiratory distress within Ist hour with tachypnea, retraction, grunting and cyanosis, ‘¢ Overdistention of the chest. Complications «¢ Respiratory distress syndrome « Pneumothorax ‘Persistent pulmonary hypertensio Radiographic pictures of MAS « Hyperventilated lungs wit patchy infltration, « Flatten of diaphrage. «Increased anteroposterior diameter of chest yi showing hyperinflation with patch infiltration (in post-trm neonate) > diagnosis yn bide= ongenital Diaphragmatic Hernia Bochlek Hernia ¢ Theres herniation of abdominal contents, ie stomach (mostof the time), intestine liver: into thorax through a defey in the diaphragm. ‘* Females are affected more than males. ‘* More common on left side™5 and is posterolateral’™®”. ‘© Components of CDH are = ') Herniation of abdominal contents into thorax ii) Pulmonary hypoplasia 1) Malrotation of intestine ja, omphalocele and CVS I * Associated anomalies may be seen 30% of cases > CNS lesions, esophageal atresia, omphalocele and CV‘ Most cases are sporadic. ns, * CDHisa reconized part of several chromosomal syndromes > Trisomy 21, 18, 13, turner syndrome, Palister-Kllian, ‘inlcal features + CDE may present as 1 Soon (within 6 rs) after birth (most ofthe cases) 2. After neonatal period (small group) 1) Soonafter birth 1 Respiratory distress i a cardinal sign! presents as tachypnes, grunting, chest retraction, cyanosis. *# Scaphoid abdomen") * Increased chest wall diameter ' Bowel sounds may be heard in the chest with decreased breath sound. ' Cardiac impulse is displaced away from the side of hernia, 2) After neonatal period ' Vomiting asa result of intestinal obstruction 1 Mild respiratory symptoms * Occasionally incarceration of the intestine will proceed to ischemia with sepsis and shock, * Most common case of death in CDH is pulmonary complications (pulmonary hypoplasia ™! and pu- monary hypertension). Diagnosis « Prenatal ultrasound can diagnose CDH between 16 and 4 wk. 4 Afierdlivery chest Xray andnasl gastric tube ial that is usually required to confirm the diagnosis, Prognosis ‘* Two most important prognostic factors are pulmonary hypertension( #9511410 ang. 7 Other prognostic factors are: Gestational age at detection'*#™S 14110, 110 and side of defect (ight sie has poor prognosis) Timing of surgery, Management ‘© CDH is no longer considered as surgical emergency child is fi Pulmonary hypoplasia" associated anomalies, size of defect!" is not a prognostic factors 1.411, st resuscitated and stabilized before surgery.Differential diagnosis ‘¢ Pulmonary sequestration. « Pleuropericardial cyst*™””, ‘¢ Cystoid adenomatoid malformation. 'e HMD always occurs in preterm babies often less than 34 weeks of gestation, I! 6 the commonest cause ofr distress in a preterm neonate. Incidence is highest in preterm male and white infant, ‘s HMD disease is due to deficiency of surfactant", Surfactant start appearing in fetal lung by 20 week o) sgestation™™#™, Bat mature levels appear only afer 35 weeks of gestation; therefore LIMD is more common i premature newborns. in amniotic lids surfactant appear between 28-32 week of gestation" Risk factors for HMD ‘e Prematurity (most important)*""*® —_# Cesarean sectionEl Cutarren 3 Newborn Infant © Asphyxia # Cold stress cinco «¢ Ahistory of previously affected infants ‘© Maternal diabetes! 70199 © Multiple birth" Protective factors for HMD © Hypertension ‘© Maternal heroin use «© Prolonged rupture of membrane « Antenatal corticosteroid prophylaxis Morphological changes in HMD * Diffuse alveolar damage is the characteristic histological manifestatio of HMD. # In the acute stage the lings are heavy frm, red and boggy with congestion interstitial and intravalveolar edema, * Thealveolar walls become lined with waxy hyaline membrane. Hyaline membrane consist of fibrin rich edema fluid ‘mixed with the cytoplasmic and lipid remnants of necrotic epithelial cells”, Clinical features of HMD ‘Respiratory distress occurs within the first 6 hours of life" 40%, ‘Clinical features include - = Tachypnea'™'e” 1 Decreased air entry = BP may fall = Retraction" * Fatigue 1 Oliguria } If untreated = Grunting * Pollor wleus = Cyanosis 1 Mixed respiratory & metabolic acidosis" ‘¢ FRC is smaller than closing volume's™s™, X-ray appearance in HMD + The inital roentgenogrom is occasionally normal”*™, with typical pattern developing at 6-12 hours. 1) Reticulogranular pattern! 1 rir mas) 4i) Ground glass opacitiegt™s'4 14 rc1n.tewero ii) Air bronchogran/siss12.16. 17 mans jv) In severe case whiteout lungits121raiv-kesso Prenatal diagnosts of HMD ‘* Prenatal diagnosis of HMD can be made by 1) Lecithin / sphingomyelin (LS) ratio in amniotic fluid 27 ‘= L/S ratio > 2 indicates adequate lung maturity, 2). Shake test Amniotic fluid or gastric aspirate is mixed with absolute alcohol and shaken for 15 seconds and allowed to sete. Copious bubbles are formed in the presence of adequate surfactant indicating extent of lng maturity, Treatment of HMD ‘¢ Neonate should be managed in NICU (neonatal intensive care unit), ‘© Oxygen should be given - Mild distress > Without ventilator ‘Moderate distresi*™™1 5 Continuous positive airway pressure (CPAP) Severe distress > Intermittent mandatory ventilation (IMV) Oxygen tension i hep at 90% (100% oxygen In given because of sk of retlenal broplasa). 4 Intratracheal surfactant therapy i the specific therapy, its indications are: |) Allmeonates less than 28 weeks irrespective of presence or absence of HMD (RDS), ii) Neonates with >28 weeks with severe respiratory distress.Prevention of HMD_ ‘¢ Administration of prenatal glucocorticoids to mother atleast 24 hrs prior to delivery in all pregnancies of less than 34 weeks gestation, reduces the risk of HMD. «© Injection betamethasone (12 mg Im every 24 hours!” for 2 doses) is preferred, Dexamethasone (6 mg Im every 12 hours for 4 doses) is an alternative. Beside reducing HMD risk, corticosteroids also reduces mortality/*™™#™ and incidence of interventricular hemorrhage!s#™*™, increased air bronchogram > hyaline membrane ‘Bronchopulmonary dysplasia (BPD) « Bronchopulmonary dysplasia is usually defined as a need for supplemental oxygen at 36 weeks after conception. BPD is usually defined asa need for supplemental oxygen at 36 wk after conception. + distress persists or worsen ands characterized by hypoxia, hypercapnia onygen dependence and in severe cases right sided hear failure. 4 BPD isa result of ung injury in infants requiring mechanical ventilation and supplemental oxygen. ‘¢ Most ofthe children with BPD are premature and have hyaline membrane disease. But, BPD can also occur in full term newborns with meconium aspiration or persistent pulmonary hypertension. The premature lungmmakes insufficient functional surfantantand the antioxidant defence mechanisms arenotsuficiently mature to protect the lung fom the toxic oxygen metabolites generated from oxygen therapy. «The major underlying pathogenic mechanisms causing BPD are - 4) Oxidant damage by taxi oxygen metaboltes*!™*™. ‘Mechanical trauma! ; Atelecto trauma (alveolar collapse and volutrauma/barotrauma''™ due to ‘overdistension by mechanical ventilation). ii) Pulmonary edema due to capillary dama Severe” = or Moderate supplement0fr28 dys and_Suplement0, for 28 2) and_ Supplement, or 28 das and mio, a * esting = 30% 0, andor i positive presture vento anected GAOT fon ppv at 36 necks ier coneded Gor at schage (whchevercomes ta) ' + Brexting = 30% 0, andor + brathingromatbys6days © <30%0,bySédayspoatal "postive presure (PV) by azmeks * poumulogoratascurge " Sgecrtcichgetehiner 56 ye ssa ag 2 } Bcherercomesint, ereomesfsh dicarge whicheve ees fo ‘Transient tachypnea of Newborn self. limiting disease occuring usually in term neonates and is ue to « Transient tachypnea of the newborn is ab delayed clearance of lung fluid. Its also called respiratory distress syndrome type I. © TIN follows -3] id 3 Newborn Infant i) Uneventful normal preterm or term vaginal delivery ii) Cesarean delivery™™ ae eee «TIN isbelieved tobe secondary to slow absorption of fetal lung ld resulting #2 and tdal volume and increased dead space therefore also known as wel Iw" ‘Clinical manifestations 1 Early onset of tachypnea 1 Sometimes retraction or expiratory grunting # Occasionally cyanosis, 1 Patients usually recover rapidly within 3 days. 1 Hypoxemia, hypercapnia and acidasis are uncommon. «The lags are generally clear without les or shonchi and chest roentgenogram hos = Prominent pulmonary vascular markings = Overaeration’ fa diaphragms fluid lines in the fsure 1 Prominent inter-labar fissures <1 from hyaline membrane diseases dificult. The distinctive Feature of tra ‘= Occasionally pleural fluid «# Distinguishig this disease: stent tachrepaca 1 Mild symptomology 1 Sudden recovery ofthe infant 1 Absence of roentgenographic reticulogranular pattern or air bronchogram' Pulmonary alveolar proteinosis ‘¢ Pulmonaryalveolar proteinosisis a disorder characterized by the ntraalveolar accumulation of pulmonary surfactant. # Itis dueto deficiency of protein-B component of surfactant, which result in imparied spread and absorption of major phospholipid of surfactant ‘# Thus there is functional deficiency of surfactant and failure of expansion of alveoli. ‘© Usually newborn is full term and may have positive family history/si™s1-% «© Child usually present with respiratory distress immediately after birth which does not respond to surfactant «© There may be ground-glass appearance on chest x-ray. «¢ Histopathological examination of lung biopsy specimen is the gold standard for diagnosis. On histopathological examination distal air spaces ae filled with a granular, eosinophillic material that stains positively with periodic acid schiff reagent and is diastase resistant. RESUSCITATION OF NEWBORN «The goal of pediatric resuscitation is to maintain adequate oxygenation and perfusion of blood throughout the body while steps are taken to stabilize the child and establish long term hemostasis. ‘¢ The most common indication for neonatal resuscitation is asphyxia. Second most common indication is extreme prematurity ‘¢ The components of neonatal resuscitation are TABC - Maintenance of temperature*®””; By radient heat source, and by drying the baby with removal of wet linen, 1 A- Airway"; Establishment of open airway by placing the neonate on hi back with light extension of neck by elevating the shoulder 3/4 oF 1 inch ofthe mattress with the help of rolled blanket or towel. Suction of mouth and nose is done. 1 B- Initiate breathing": Tactile stimulation is given and when necessary, EV tube can be used. = C- Maintain circulation'**"” : This is done by chest compression’ *2!©? and/or medications bag and mask ventilation is given or Resuscitation protocol ‘As soon as the baby is delivered, five signs are assessed - 1, Clearance of meconium‘Active breathing or erying Good muscle tone (flexed posture and active movement of baby). Pink color (look at tougue and lips) 5. Term gestation (delivery between 37-42 weeks of pregnancy), is required. 1 IFany of the 5 signs is absent, baby requires resuscitation, '# The baby should be placed under the heat source (radiant warmer) and subjected to a set of intervention known as initial steps. © Ifall signs are positive no active resuscitati Initial steps of resuscitation 1. Positioning 1 The neonate should be placed on her back or side with the neck slightly extended. This can be achieved by putting a rolled blanket or towel under the shoulders, elevating them ¥ or 1 inch off the mattress 2 Suctioning 1 The mouth and nose should be suctioned. The mouth is suctioned first" to ensure that there fs nothing for the infant to aspirate when the nose is suctioned. ' One should not insert the catheter very deep in mouth or nose for suction -> Stimulation of posterior pharynx: during the first few minutes after birth can produce a vagal responce, causing severe bradycardia or apnea. ‘= Therefore, during oral suctioning, a suction tube is gently introduced into the baby's mouth until the 5 em mark!" iat the baby’s lip. During nasal suctioning, a suction tube is introduced upto 3¢m mark! into each nostril. 3. Dry, stimulate and reposition « Aller suctioning, the baby shouldbe dried by using pre-warmed linen to prevent heat loss ‘A briet tactile stimulation in the form of licking the soles or rubbing the back may be provided in case of znon-establishment of good respiratory efforts”. 4. Free low of oxygen 1 Ifthe Baby continues tobe depressed, provide fre Now of oxygen usinga facemask. « Aer providing initial steps, the baby shouldbe evaluated for three signs 1. Respiration 2, Heart rate (HR) 3. Color «¢ Ifbaby has good breathing, HR >100 and pink color, he should be given supportive care. 4 If the baby is not breathing well or HR <100 then bag and mask ventilation is needed. «¢ After the infant has received 30 seconds of ventilation with 100% oxygen by bag and mask, evaluation of heart rate should be done - HR>100 > Discontinue ventilation if spontancous respiration is present *"™, Below 60 -> Continue ventilation + chest compressions «After 30 seconds of chest compressions, the heart rate is checked, HR <60-> Continue chest compression and bag & mask ventilation + initiate medications, HR > 60-> Discontinue chest compression but continue bag & mask ventilation until the heart r Resuscitation in newborn through meconium stained liquor « When baby passes meconivm in utero there isa chance that the mecomium wl be aspirated in init potentially into the trachea and lungs. «Appropriate steps must be aken immediately after delivery to reduce thei of serous consequenses aspiration of meconium. «Intrapartum nasopharyngeal suctioning jus after the delivery of head is no longer recommends oi reduce the risk of meconium aspiration syndrome and, on rare occasions, may cause nasopharyiigeal tru ‘cardiac arrhythmia.==. n-vigrous = 1 The first step after delivery cewborn is vigrous or non-Vigrot 10 identify whether the n A) Vigrous newborn, 2) Good muscle tones initial stepsof resuscitation are provided, signs are present :~ 02 if necessary 3) Non-vigrous newborn 1 Ifany of the above thre signs is present, the ne 1 For non-vigrous child, the initial steps are modified :~ no i) Place the baby under radiant warmer and postpone suctioning to prevent stimulation of posterior sborn is classified as non-vigrous. ‘pharyngeal wall that can cause bradycardia ii) Residual meconium inthe mouth and posterior pharynx should be removed by suctioning wnder direct vision using a laryngoscope. ii) The trachea should then be intubated and mechonium suctioned from the lower airway: Tracheal suctioning is best done by applying suction directly tothe endotracheal tube. 1 Afier providing initial steps, the further management i same as with resucitation for other conditions ‘© Forcildren,uneuffed and straight blade" endotrachealtubelsused. Incubators used for thermal regulation of premature neonates are convection!#""%"2% warmed incubators, ‘ Incases ofbirth asphysla, corticosteroids are not used“. et a ae | ‘© Bag and mask ventltions contraindicated in: Diaphragmatic hernfa™*, Tracheo-esophageal fistula", and ‘meconium aspiration syndrome", pa gs eae Se ‘© Important drugs used for neonatal resuscitation are epinephrine (adrenaline)™""®, normal saline o ringer lactate, naloxone’ and sodabicarbonate". Eee A STORER ES | 000%, ee Dose of adrenaline in neonatal resuscitation: APGAR Scoring ‘© APGAR Score is a quantitative method for assessing infants respiratory, circulatory and neurological status: ‘© Colorofthe body™*”(ay roti a Blue or pale Body pink extremities blue «Scoring for APGAR Score 1 Total score 10 1 No depression 7-10 f= Mild depression 4-6 0-3 1 Severe depression ‘© The test is generally done at one and five minutes after birth, and may be 3€ repeated later ifthe score is and remai low. Scores 3 and below are generally regarded as critically low, 4t 6 fairly low, and 70 10 mca nee «A Tow score onthe one-minute test may show that the neonate requires medical attention ies ee » (e.g, resuscitation 45")but isnot necessarily an indication that there willbe long-term problems, particularly if there isan improvement by the stage of the five-minute test, + Wthe Apgar score remains below 3 at later times such as 10,15 or 30 mintues, there isa risk thatthe child will suffer onger-term neurological damage, There isalso a smal but significant increase of the risk of cerebral palsy. ‘+ However. the purpose ofthe Apgar test isto determine quickly whether a newborn needs immediate medica cae; it ‘was not designed to make long-term predicitions ona childs health! ‘Assessment of respiratory depression {The severity of respiratory distress i assessed by ilverman- Anderson score and Downes’ score. * While the Silverman Anderson Retraction Score is more suited for preterms with HMD, the Downes’ score is more ‘comprehensive and can be applied to any gestational age and condition, ‘Audible with I naked ear A score of>6is indicative of impending respiratory failure NEO! HYPERBILIRUBINEMIA AND JAUNDICI ‘ Bilirubin is the end product of catabolism of hemoglobin. 1 gm of hemoglobin yields 35 mg of bilirubin" ‘A bilirubin lve of more than § mg/d manifests as clinical jaundice or icteus in neonate (i adults jar 2:25 mg/d). ‘Aste bilirubin levels increase, jaundice involves more distal parts of body =and (i) Conjugated. ‘¢ Hyperbilirubinemia may be of two types : (i) Unconjugated ‘A) UnConjugated hyperbiliubinemia "© Conjugated hyperilieubinemia is seen when - 1) Increased production fbilrubinfrom hemoglobin, Sothat byincreased production, ‘© Hemolyticanemia**” > Hereditary spherocytos {Ineffective erythropoless > Thalassemia, Pericious 2) Reduced hepatic uptake of bilrubin from bilbin albumin 3) Impaired hepatic conjugation, € e i) Physiologica jaundice» uwver of aneonae i functional 4 é i Brees a jeundice™ »Prananedtalin breast mikintreres with brubincOnjogeO | it) Genetic defciency of UOPG transferase» Crigler-Nojjarsynaromes" 2% east 1W) Hepatocellular disease -> Vial or drug induced hepatitis, cithosis, ¥) Hypothyroidism, cepholohematoma 8) Conjugated hyperbiliubinemia Conjugated hyperbirubinemiats seen when~ 1) Impaired secretion of conjugated bilirubin ito bile -> syndromenetioa venue, tnecapociyoftvertoconjgetebiirbinis overwhelmed 1s, 66RD deficiency". ‘anemia omplex > OTS immature (¥ UOPG transferase) i sae one 12. 1880, Rotor ‘Dubin johnson syndrome” 1) impaled bile Now -» Obstructive jaundice", primary billary crrhosis, Neonatal cholestasis eg. Extrahepatic biliary atresia" neonate idiopathichepatits, Choledocal est”, Sclerosing cholangitis, Caroli disease, Metaboll (Tyrosinemia, Wolman disease, Nieman pick disease, GalactosemiaFructosemial. ‘Time of appearance of jaundice Jaundice present at birth or within 24 hours of life ‘« Erythroblastoss fetalis (Rh incompatibility)"°7=!%*41*) -y most common cause ‘* ABO incompatibility + Concealed hemorrhage ‘© Congenital infections —> Rubella, syphilis, CMV, toxoplasmosis ‘¢ Red cell enayme defects (G6PD deficiency) ‘© Red cell membrane defect (Hereditary spherocytosis) Sepsis” Jaundice appearing on 2nd or 3rd days of life « Physiological” ‘¢Crigler “Najjar syndrome —_@ Early onset breast milk jaundice Jaundice appearing from 3rd to 7th days of life Bacterial sepsis Urinary tract infection ‘© Other infections > syphilis, CMV; enterovirus, toxoplasmosis _« Polycythemia Jaundice appearing after 1st week of life «All other causes of jaundice. Physiological jaundice ‘@ Most neonates develop visible jaundice due to elevation of unconjugated bili ju irubin concent in first week. This common condition is called physiological jaundice. Concentration during thelr «# This pattern of hyperbiliubinemia has been classified ito two functionally distinct periods - 1. Phase one 1s Last for 5 days in term infant with peak bilirubin levels to 12 mg/dl, « Last for 7 days in preterm infant with peak bilirubin levels to 15 mg/dl. 2. Phase two 1 There is decline to about 2-mp/dl, which ats for 2 weeks after which adult values ae attained.Criteria for physiological jaundice 41) Clinical jaundice appears after 24 hours of age, 1) Total bilirubin rises by less than Smal per day (no sudden risey""™, 1H) Peak bilirubin occurs at 3-5 days of age, with atta bilirubin of no more than 15 mg/l 9) Clinical jaundice is resolved by 1 weeks in term infants and 2 weeks in preterm infants", Breast milk jaundice * There i strong association between exclusive breastfeeding and neonatal jaundice. + A few babies who remain on exclusive breast fed develop jaundice in the second week of life and continue well into the third month. Ths is called breastmilk jaundice. © A ilicubin level of over 20 mg/dl may be attained. (It is presumed to be due to inhibitory substances in the breastmilk that interfere with bilirubin conjugation eg. pregananediol and fre fatty acids). * Temporary interruption of breastmilk feeds will dramatically reduce the serum levels of bilirubin and there may be slight increase in bilirubin when breast feeding s resumed, butt never reaches the previous level. ABO hemolytic disease ‘+ ABO hemolytic diseases less common then Rh incompatibility. Itcauses unconjugated neonatal hyperbilirubinemia. ‘+ Hoccurs in neonates having blood group A or B with mother of blood group O. Jaundice appears within 12-24 hours of hfe. ‘¢ Direct agglutination test (DAT) testis postive. * Reticulocytosis and the presence of micraspherocytes!*"™5™ on smeat help to confirm the dagnoss Congenital hyperbilirubinemias ‘Important congential hyperbilirubinemias are 1). Unconjugated hyperbilirubinemia (defective conjugation): Gilbert syndromes YE D nto. snM4 Crigler Najjar Syndrome (type 16 ys!" bane ane, 2) Conjugated hyper Gilbert syndrome «© Gilbert syndrome is an autosomal dominant*™**° congenital unconjugated hyperbilirubinemia!*!*® SI D814 a1 «© All hepatic biochemical tests and liver histology are normal'*"*8”", but in some patients increased lipofuscin pigment may occur. «© There is mild increase in unconjugate bilirubin“! 4%, thus kernicterus does not occur 1 Basic defects a 4) Decreased hepatic uptake of bilirubin. ii) Decreased activity of UDPG transferase!" © Usually no treatment is required", irubinemia : Rotor syndromels!NEEDN811 Pot 96A1¥591.89, Dubin Johnson syndrome, ‘* Phenobatbitone induces the enzyme UDPG transferase; thus it can reduces the level of unconjugated bilirubin by increasing its conjugation. Hemolysis may also occur, ‘# The disposition of most xenobiotics metabolized by glucronidation appears to be normal except for antitumor drug irinotecan. Thus, irinotecan toxicity can occur” ‘8 There is no association with cirrhosis”. Criggler-Najjar Syndrome (CN) ‘© CN syndrome isa congenital unconjugated hyperbilirubinemia!*!™°*"%, Basic fects either reduced or ssc UDPG transferase 1 There are two types of CN syndrome = A) Typel ts Itis an autosomal recessive disorder in which UDPG transferase is absent, Thus phenobarbitone has no effect (as enzyme is absent). 1 Itis more severe hyperbilirubinemia than type Il. There may be kernicterus.| 7 1 LET and ver histology are normal” ®) per seduce, = Itisan autosomal domi ina199 disorder in which UDPG transferase is 0 tosomal dominant"? disorder in whi inducing UDPG transferase. * Phenobarbitone can reduce unconjugated bilirubin” BY 1 LETs and liver histology are normal”) and there is mo Rermicferu" Dubin Jhonson syndrome (045) scans, ‘+ DJS isa type of congenital conjugated hyperbilirubinemia'!"** ‘ Itis autosomal recessive. excretion of bilirubin glucuronides due to mutation in + Conjugated bilirubin is increased because of defective biliary canalicular multidrug resistance protein 2 (MRP 2). Liver function ‘© A cardinal feature of DJS is the accumulation in the lysosome o ‘granular pigment. Asa result, theliver is blackin appearance. This pigmen tests are normal centrilobular hepatocytes of dark, coarsely tis thought tobe derived from epinephrine abolites that are not excreted normally «There is increased urinary excretion ofcoproporphyrine I (normal coproporphyrine IT is more excreted), but tt coproporphyrine level is normal ea there is reflux of conjugated sulfobro- ‘© Gallbladder isnot visualized on oral cholecystography. Afferiv administration, ‘mophthalein (Bromsulphalein, BSP) from liver to circulation. Rotor syndrome _ « Rotor syndrome isa type of congenital conjugated hyperbilirubinemia'™!"™¥#= ANS f Itis autosomal recessive « It is due to decreased biliary excretion of conjugated bilirubin and also due to decrease hepatic uptake & storage of bilirubin. «Differentiating features of rotor syndrome (from DJs) - 4) Liver is not pigmented and liver histology is normal”™"™, fi) Coproporphyrine [is increased in urine but total coproporphyrine level i also increased. iil) Gall bladder is visualized iv) There is no reflux of conjugated BSP. Kernicterus ‘# Kernicterus or bilirubin encephalopathy, is a condition caused by bilirubin toxicity to the basal gan, various brainstem nuclei ‘eI is mainly caused by unconjugated bilirubin“ as unconjugated bilirubin can cross blood brain barrie. ‘Unconjugated bilirubin level of more than 20 mg/dl" increases the risk of kernicterus, # Clinically, kernicterus is described in 3 phases, which may progress over 24 hours to 7 days = 1, Phase > Poor suck lethargy hypotonia‘, depressed sensorium. 2. Phase It > Fevet, hypertonia progressing to opisthotonus', 3, Phase I > High pitched cry, convulsions, death # Long term survivors demonstrate choreoathetoid cerebral palsy*'"”, upward gaze palsy/*'””, sensorineural hearing loss!" and mental retardation. «The toxic effects of unconjugated bilirubin (and therefore chances of kernicterus) are increased by = 1) Hypoproteinemia (4 albumin)*"™ -> Normally unconjugated bilirubin binds to albumin in circulation. Ifthe level of albumin decreases, concentration of free unconjugated bilirubin will increase 2) Drugs (ulfonamidesy*!" 3) Acidosis" 4) Increased FFA (secondary to hypoglycemia, starvation or hypothermia)*""” 5) Asphyxia™! | Displace bilirubin from its binding site on albumin ‘Make neurones more susceptible to 5 eee toxic effect of unconjugate bilirubin 7) Prematurity“""" 8). Infection‘TREATMENT OF HYPERBILIRUBINEMIA, ‘* Treatment options of hyperbilirubinemtia are := A) Drugs (Pharmacological therapy) * Drugs used for hypertitirubinemia are: 1) Barbiturates™'™" (Phenobarbitone): Induce UDPG transferase and enhance conjugation of bilirubin. 2) Metalloporphyrins (Tin: Sn and Zinc Zn): Decrease bilirubin formation by inhibiting heme axyyenase, 3) Miscellaneous : Frequent milk feeding, charcl and agar prevent reabsorption of bilicubin from gut. B) Phototherapy * Phototherapy has emerge as the most widely used form of treatment for unconjugated hyperbilirubinemia. + Phototherapy converts unconjugated bilirubin into isomers that are able to bypass the conjugating system of ler and are excrete inthe bile oF urine. + Thrce types of photochemical reactions occur; in decreasing onder of importance := 1, Structural isomerization **™5*9 ® Bilirubin is converte into lumirubin, whichis excreted inthe bile and urine 2. Photoisomerization 1 Less tox, polar isomers are formed which ae excrete in bile. But, the photoisomer can revert back to ‘unconjugated bilirubin and get reabsorbed from the gut ifthe baby isnot having stools 3. Photo-axidation « Ie convert bilirubin into small polar product that are excreted in urine, 1 "The most ffctve lights for phototherapy are those with high energy output near the maxim absorption ‘peak of bilirubin (450 to 460 nm). Special blue lamps with a peak output of 425 t0 475 nm are the most efficient for phototherapy ‘* Complications of phototherapy are = 1). Bronze baby syndrome™=™, 4) Purpuric rash with transient porphyrinemia. 2). Loose stool. 5) Increase environmental and body temperature*"™". 3). Retinal damage™™, 6) Erythematous macular rash. ©) Exchange transfusion « Exchange transfusion is indicated when bilirubin level is high and chances of brain damage are significant. Indications to start phototherapy and exchange transfusion 1) According to gestational age ‘¢ Teis usually used for premature newborn. 2) According to gestational weight (at birth) fe Tris used when age is not available.Preterm babies 1001-15009, 710 1315 10-12 ia 2001-25009, 245 1820 325009 1518 3). According to age after birth «Its used for full term (mature) neonates. NEONATAL HYPOGLYCEMIA. + Hypoglycemia ina neonate is defined as blood sugar less than < 40 mg/dl”, + According to serum level hypolycemia is defined as serum glucose level < 35 mg/dl between 1-3 hours of life; < 40 ‘mg/dl between 3-24 hours of life and < 45 mg/dl thereafier. Aer neonatal period (especially after 2 months™*") hypoglycemia is defined as serum glucose < 54 mg/dl®™*", ‘¢ Hypoglycemia is the most common metabolic problem in newborns. Important causes of neonatal hypoglycemia A) Due to inadequate substrate enzyme function : Prematurity*™**, small for gestational age (SGA), smaller of twins, espiratory distress syndrome’**™** and infant of toxemic mother. B) Due to hyperinsulinism : Infant of diabetic mother (large for date™5*, erythroblastosis fetalis (Rh incompatibility”, and perinatal asphyxia", ‘Treatment of neonatal hypoglycemia 1) Asymptomatic with blood glucose between 20-40 mg/dl # Direct breastfeeding is started. I neonate is unable to suck, expressed breast milk i given, Expressed breast milk should be fortified by 5g sugar per 100 ml of milk 2). Symptomatic or asymptomatic with blood glucose < 20 mg/dl = Bolus 10% dextrosel#t™™2: ml/kg is given IV. Ponce by continuous infusion of 6 mg/kg/minute. If normogly- cemia isnot achieved within 24 hours, glucocorticoids (prednisone or hydrocortisone) should be administered For intractable hypoglycemia, glucagon, epinephrine or diazoxide can be given, 1 In hypoglycemic seizures, dose of 10% dextrose is 4 ml/kg!"Neonate of diabetic mother '* Neonates of diabetic mother have following problems. 1) Hypoglycemials™s% ra (non-ketoticy*™5%41, 6) Polyeythemia. 2) Macrosomia!** (large for date*™™), 7) Transient tachypnea of newborn. 3) Hyperbitirubinemia’*™sere1, 8) Cardiomegaly. 4) Hypocalcemia'ssses rev, '9) Asymmetric septal hypertrophy. 5) Hypomagnesemia. 10) Increased risk of RDS. ‘* Neonates of diabetic mother are at increased risk for fetal malformation"™'™. ‘¢ Two most common causes of seizures in these neonates are hypoglycemia (most common cause*!"-A™8) and, hypocalcemia (2~ most common cause!" A™), «These infants are at increased risk of developing obesity™*™-4!™ and DM'™5™*" in future. ‘Neonatal hyperglycemia s defined as blood glucose level> 125 mg/ AP or plesma glucselevel> 150mg/d MISCELLANEOUS Perinatal asphyxia ‘e Perinatal asphyxia is an insult to the fetus oF newborn due to lack of oxygen (hypoxia) and/or « | (ischemia), Effects of perinatal asphyxia are 1) CNS : Hypoxic ischmelc encephalopathy, infarction, cerbral edema, seizures's™8*”, hypotonia or ly (generalized, involving all muscles simultaneously*""*™), altered sensorium™*” 2) CVS: Myocardial ischemia, tricuspid insufficiency, hypotension, 3) Pulmonary : Pulmonary hypertension, pulmonary hemorrhage, RDS. 4) Renal: Acute tubular or cortical necrosis. 5) Adrenal: Adrenal hemorrhage. 6). Metabolic: SIADH, Hyponatremia, Hypoglycemia, Hypocaleemia, Myoglobinuria 7). Integument : Subcutaneous fat necrosis. 8) Hematology: DIC. 9) Gastrointestinal : Perforation, Ulceration with hemorrhage, Necrosis.Hyporic ischemic encephalopathy * Encephalopathy progress overtime - 1) Birth to 12 hours -» Decreased level of conciousness, Poor tone, breathing or apnea, seizures», = 2) 12-24 hours More seizuers, Apne spell, jiteriness, weakness 2) fer 24 hours> gptni, | conousen, por fing, brainstem sgn oelomeet) and pop disturbances, decreased spontaneous movement, periodic * Hypotonia is generalized, involves both limbs and trunkand all muscles simultaneously’ Causes of respiratory depression in neonates «Intrapartum asphisa (most common case), ‘ * Drugs: Norotc analgesis (morphine or othe pioldd¥s¥ M0), anaesthetis «Sepsis + Prematurity CNS immaturity, surfactant deflency «Respiratory problems: Diaphragmatic hernia, obstructive sions. * CNS abnormalities: Malformation, eum + Muscle dlsordrs Myopahy, prematurity. Erythroblastosis fetalis ‘© Erythroblastosis fetalis is caused by the transplacental passage of maternal antibody active against paternal RBC antigens ofthe infant and is characterized by an increased rate of RBC destruction. * Although more than 60 different RBC antigens are capable of eliciting an antibody response, significant disease is ‘associated primarily D antigen of Rh group'!®”” and with ABO incompatibility’*™*"”, ‘© Other rare antigens involved are - = Cor E antigen of Rh group*™5"? = RBC antigens - Cs, Cx, Cu, K (kell), M, Duffy, S, B MNS, Xg, Lutheran, Diego and Kida ‘ Anti-Lewis antibodies do not cause disease/™8*, Hydrops fetalis ‘© Hydrops fetalis (fetal hydrops) isa serious fetal condition characterized by abnormal accumulation of fluid in 2or ‘more fetal compartments, including ascites, pleural effusion, pericardial efusion and skin edema. ‘+ Important causes of hydrops are 1) Immune: Rh incompatabilty, 2) Non-immune: Twin-Twin transfusion, chorangloma ofplacenta, congenital heart block", cystic hygroma ‘© mediastinal teratoma, congenital infections (TORCH) and congenital nephrosis>=e™), Microcephaly © Microcephaly is defined as a head circumference (occipitofrontal circumference) that measures more than three standard deviation below the mean'**"? for age and sex, ‘¢ Important causes of microcephaly are :- ‘A) Primary (genetic) 4) Isolated: Autosomal recessive, autosomal dominant, X-linked. ii) Syndrome : Down syndrome (trisomy 21), criedu-chat syndrome, B) Secondary 1) Structural defects: Neural tube defects (anencephaly, encephalocele, 1) Metabolic disorders: Rhenylketonuri'*™%, citrulline methylmalonic ii) Congenital infections : Rubella", CMY, SY, toxoplasmosis syphilis, iv) Teratogens: Alcohol, tobacco, cocaine, heroin, ¥) Others: Maternal dabetes,materal phenylketonuria, hypothyroidism Edward syndrome (trisomy 18), Patau syndrome (trisomy 13) luria, varicella hypopituitrism, adrenal insufficiency.Congenital infections causing microcephaly with intracerebral calcification ‘© Following congenital infections can cause microcephaly, intracerebral calcification and hydrocephalus : (@) Commonly by toxoplasmosis and CMY, and (i) Less commonly by HSV and rubella Hydrocephalus + + + «© Hydrocephalus with intracerebral calcificationin a neonate with history of Spiramycin’ treatment of mother in ‘Pregnancy suggest the diagnosis of congenital toxoplasmosis'*#™#"" A, i [na te, procepbaly f ‘© Head circumference in the given figure is 13-14 cm (normal overage head circumference at birth is about 435 can) > Diagnosis is microcephaly. |___ © Hidrocephalus is the most important cause, Macrocephaly is associated with frontal bossing dolicocephalic shape narrowing of biparetaldiamete anda square shaped face. Macrocephaly '» Macrocephaly is defined as an oceipito frontal circumference greater than two standard (SD) above the mean‘! +9 for age and sex (Note : Microcephaly is three standard deviation below the mean). © Important causes are 4) Syndromes: Fragile-X syndrome, and neurocutaneous syndromes (Neurofibromatosis), tuberous sclerosis, Sturge Weber ii) Increased CSF: Hydrocephalus, choroid plexus papilloma'*!™, Bone disease : Achondroplasia, osteogenesis imperfecta, oteopetrosis. Others : AV malformation, intracranial hemorthage (subdural, epidural, subarachnoid), Tha! hypervitaminosis-A, lead poisoning, pseudotumor cerebri, galactosemia, Canavan’s Ieukodystrop! |The diagnosis in the given figure is: 3) Microcephaly b) Macrocephsly ‘c) Plagiocephaly | 8) Dolichocephaly “Ans is‘D’ Le» Macrocephaly ‘© The figure in question is showing large head with frontal bossing and square shaped face > features of | macrocephaly Fetal alcohol syndrome «High level of alcohol ingestion in pregnancy can cause damage to fetus, known as fetal alcohol syndrome, The harmful effects may be due to alcohol itself or due to one ofits breakdown products, «# Some evidence suggests that alcobol may impair placental transfer of essential amino acids a for protein symthesis, which may account for IUGR. «# Characterististics of etal alcohol syndrome include: 1) TwGRss 8) Facial abnormalities 1 both necessarype | Cuarten 3 Newborn Infant 2). Microcephaly™se 6) Minor joint anomalies 3) Congenital heart defects (ASD, vspysmsse! 7) ‘Hyperkinetle mo 4), Mental retardation) Harlequin color change «This rare but dramatic vascular event occurs in immediat infants. If reflects an imbalance in the autonomic vascular regula “a . When thin iplicedn these theo sbisetd logit Pee PPS a hall cwvor period ands most common in ow birth weigh rory mechanism™— a deep red dependent torent fom eg colo change.) ote: The fetches pp ree thane arent Cephalohematoma « Cepholhematoma i a subperiosteal hemorthage usually involving parietal and temp 12-24 hours. ‘vaccum extraction and prolonged swelling with well d oral bones. It appears within labor, It is soft and fluctuant is more common in forceps delivery, ined margins «A cepholhematoma crossing the midline indicates underlying facture ofthe skll > enclue is Iinear not depressed. # Itdisappears between 2 week to3 months", “The diagnosis inthe given figure is: 8) Macrocephaly b) Microcephaly ©) Cephalobematoma 4) None ‘Ans. is‘©’ Le, Cephalohematoma ‘s_ Swelling not crossing suture line with distinct margins suggests the diagnosis of cephalohematoma. ‘© Neonatal period extends Rec "© Nota finding ie a normal newborn :Central cyanosis (there is peripheral cyanos treatment ts minor nal problem Between 37 neonatal da) manana ld eer "e Common ites of mongolian spots: resacral area lower back & buttocks) legs, shoulder, posterior thighs. Hymentag in aneonate:Notreatment isa normalfinding). = Newborn babies oe obo breathandsuckat the sametime because of High position of layer. jent at bith: Rooting/sucking/swallowing teflexes, crossed extensor, moro’ = TS eflexes appear ater birth: Symmetic tonic neck efles, parachute refes, anda reflex. [Brent spon a Nor rennet eae a ners Of davicle, sho Notamechonism of heat production ianeanote: shivering (neonates respond by nonshivering th ee wuld yis:Birth weightless than 10thppercentle, z = h weight < 2500 gm irrespective of gestational age at birth,Complications of UGR:Asphysa, meconium aspiration, hypothermia, hypoglycemia, hypocalcemia, polycythemia, | Infections. [lint tier nt Head cecunfrencds 3m more than chest Geumferencs, |e Organnotofectedinasymetic UGA |e Infect ogni in lt onset 572) neonatal sept: Fom external envionment frome or hospital most tl esonat snl ae ayn GT ERS EA rnting “@ Nota feature of respiratory distress in aneonate: Wheezing [el Apneain noni for 20Seconds wth wthout radars 20 seconds asioed wih aja |= Mecarum possogtn eect Oost empysem ernthenl neue. [BB ikinepetin sec Sen Falter post fans © Most cornmon case of dean congentl dptragrati hea: Pulmonary complication pulmonary hypoplasia and pulmonary hypertension) 5 Tntervention in CDH: Insertion of nasogastric tube. r + Inpertnt prognostic factors in COH: Pulmonary hypoplasia, pulmonary hypertension, gestatona age sie ste of defect. ata prognostcfatorn COH: Timing of surgery. |e Mostimportatrsktactorforneonatalresptory distress syndrome: Prematurty. [2 Derciencyofsurtactant is seen in: Hyaline membrane disease (HMO). | i |e Hyaline membrane in HMD is composed of Fibrin ich edema fuid mixed with remnants of necrotic cells [20 Fin of newbom presents: Within 6 hours after birth. "© Premature newborn wth respiratory distress and ground glass appearance on chest Xray:HMD of newborn, [el Characteristic raditogical features of HD in neonates: Ground glass appearence and airbronchogram. ‘© Fetal lung maturity is assessed by :LIS ratio; shake test [Wot given in treotment of IMD: 100% 0, (oxygen tension kept at 90% to avoid retolental lopli). "© Dose of betamethasone in prenatal peri to prevent HM of newborn: 12 mg every 24 hours for 2 doses. [oT characterized by: FRC smal than losing volume «© Pathogenic mechonismsin BPD: Oxidant damage by oxygen metabolites, mechanical trauma (atelecto-traumal, pulmonary edema ue to capillary damage. [7 Notinovedn pattogeessn 8°0:Use of theopyline. ‘© Risk factors for transient tachypnea of newborn :Cesarean delivery, gestational age. [o> Choractensticradlogica feature of TIN: Prominent horizontal inte lobar sure, ‘© Respiratory distressina fulterm newborn not responding to surfactant with postive family history Pulmonary alveolar proteinosis. Next step in neonatal resuscitation ater suctioning of meconium :Tactile stimulation by trickling of soles or rubbing the back ‘© Arter bog and mask ventilation, ventilation is dscontnuedif: Heart rate is > 100 with presence of spontaneous respiration. [2° Vigous newborn sclossifedithe hat: Strong respiratory effort good muscle tone, heart rate >100. ‘© ype of endotracheal tube used in resuscitation of child Uncuffed and straight blade. [> incabotor used for thermal regulation in preterm neonates: Convection warmed incubator. «© Treatment for birth asphyxio includes: Glucose, calcium gluconate, normal saline, oxygen anticonvulsants (but-not corticostet [57 209 and mas vention is contraindicated in Diaphragmatic eri, TE tua, meconium aspiration syndrome Dose ofadrenain in neonatal resusctation:0.1-0.3mg/kg diluted 110,000. [Aa icre components are Respiratory ft heat rat, clr ofthe ody muscle one, reflex timation (rims. ‘© Nota component of APGAR core: Respiratory rate ids,FE csseress natoninns © One gram of hemoglobin iberates:35 mg 6f BIiFUBIAL =a Seer * Important congenital cases ocnugetedhypebrbiremia: Roto sydrcne DuboNee) Essay + Imprtant congenitl aves of uncnugatedhypebltinei: rer Nar 7A, '* Jaundice appearing within 24 hours of birth :Erythroblastossftals(m spherocytosis. = 2 ‘+ Peripheral smear of neonate with ABO hemolytic clisease shows:Microspheroofes: ‘+ rug which increases the risk of kerncterusina chil with hyperbiubinemia sulfonamide. '* Nota late feature of kernicterus : Hypotonia (it is an early feature). mn, © Keimictersisdue to: High unconjugated bieubin (not conjugated bilirubin}. a © Drugs used in treatment of hyperbiliubinemia/kemicterus : Barbiturates, metalloporphyrins ( + Meckonism moni reipoansblefor econ of lub by phototherapy Struct omertaion. * ron baby sndrome's due to: Phototherapy * child with hyperbilirubinerio, parameters measured should * Notacause ofneonotal hypoglycemia: Post-term infant + Important causes of neonatl hypoglycemia: rematury, AOS maternal dabetes asphyl, eh Symptomatic neonatal hypostycema should be managed by: 10% dextrose. + Important complications oFneonete of dabeic mother: Hyperilrubinemia, hypocalcemia, heen one TIN. CHO, = 3 '* Nota complication of neonate of diabetic mother: Hyperglycamia (there is hypoglycen «ost pec fetalmefomaten nena of debe nate Cauda eein di * Type of ypogicemiain neonate of diabetic mother: Nonketotic hypoglycemia, — '® Most common cause of seizures in neanates of diabetic mother : Hypoglycemia (most common) followed by hypocalee + Maximum oncenttion ef dextee hat can be eno neonate trough perpen: 125% : Eel epee deed lod scene 25g ele lia S © Neonatal byposlycemiis defined.as:Blood glocose < 4Omg/al or serum glucose < 35mg/dl between 1-3 hours of life, serum glucose << 40 maydl between 3:24 hours fife, serum glucose <45 mg/dl after 28 hous of life. ‘+ Hypoglycemiain infant 2 month old: Serum glucose < 54 mg/l. 4 Resolution of physolgico umbicel herio ocursat: Oth weekot gestation i [npr gest eat egy deren roti Tests used to cierto maternal bid Alka denaturation (Ap. test, ond acid denaturation (Mehauer betes BE=cassaan Aerophasy; esophageal atresia, faulty feeding technique, amniotic fluid est way monitor neontebrethng and apeain incubator for peter ronverticted baby Impedence technique 1 [> Intatonressrerequtedtorhatnteninaeente:2540emH,Olor>1Sseconds. ‘© Organs palpable in anormal neonate: Liver, kidney and spleen. [Pca xine: ten am ro cn ae er ne URGE] Mc coef expt cress pretr nena ! ost common 45) tin zine. Toa bivbin and dire (onl emia. | |® Heartratein anormal neonate: 120-140 per minute. Bestmethod for tonsport of newborn wih maintainance temperature: Kangaroo Mother Care (MC), oyQUESTIONS NORMAL NEWBORN 1, Neonatal period extends upto- (weer Dec12Patem) 2) 21 days oflife 1b) 30days of ie ©) 28days of life &) 35 days oflife 2 Normal findingina newborn-(Atnda Dec13 Pate) ) Length 30cm b) Peripheral cyanosis ©) Central cyanosis 4) Extension of body. 3. Meconium can passed upto --~- days in healthy bady- (All nia Dee Pate) at b3 Os a7 4. ‘The apropriate approach to a neonate presenting, ‘with vaginal bleeding on day 4 of life is- (CET Aug 12 Pater, A105) a) Administration of vitamin K ') Investigation for bleeding disorder12 ©) Nospecifc therapy 4) Administration of 10 ml/kg of fesh frozen plasma ‘over 4 hours 5. Common sites for mongolian spot are-(PGINov15) a) Face b) Neck ©) Lambosacralarea —d) Leg ©) Thigh 6. Ahymenal tag ina newborn is best treated by - (All India De. 14 Pater) a) Steroids ) Surgery ©) Leaving it alone 4) None of the above 7. Newborn babies are able to breathe and suckat the same time due to- (ats or 1) 8) Wide short tongue b) Short sof palate 6) High larynx 4) Short pharynx PRIMITIVE RELFEXES. 8. Which ofthe following reflexes is not present at birth- {AUINS May07. ALO?) 2). Asymmetric Tonic Neck Reflex b) More's Reffex ©) Symmetric tonic neck reflex 48) Crossed extensor reflex 9. Swallowing breathing reflex not seen in fetus for- (Alin ects ater) a) 4 weeks b) 12 weeks 6) 16 weeks 4) Appear in all above period 10, Persistant Moro’ reflexat 6-7 months indicates ~ (@a102.D°60») a) Normal child ») Brain damage 3) Rungey cid 4) Irritable child 11. Parachute reflex disappear at- (A ii ec13 Patten) a) 3months. b) 6 months ©) months 4) Never 12, Child of 9 months, which reflex is most abnormal - (G1 fe 98) a) Asymmetric neck reflex b) Parachute reflex ©) Righting reflex 4) None 13. Ababy on examination shows unilateral moro’s reflex with positive palmar grasp reflex. The site of, lesion is- (ans) 9 C-C, bec oGT OG 14, Atypical moro'srefleis seenin AJE~ (PID 97) a) #clvide ») Sternomastoid tumor ©) Shoulder dislocation 15 mg/d 89. Conjugated bilirubin is increased in ? (CETNou3 Pattern) a) Rotor syndrome b) Gilberts syndrome ©) Criggler Najjar syndrome 1 1d) Crigglee Najjar syndrome 2 90. A child has bilirubin of 4 mg. Conjugated bilirubin ‘and alkaline phosphatase are normal, bile salts and bile in urine are absent. However urobilinogen in urine is raised. What is the likely diagnosis - (AUMS Nov 01) a) Obstructive jaundice b) Rotor’ syndrome ¢) Biliary cholestasis, 4d) Hemolytic jaundice 91, _AS-yearsold male child presents with episodic anaemia and jaundice since birth. He is least likely to have which of the following - (AMS Nov 11) a) Hereditary spherocytosis ) Sickle cell anemia ©) PNH ) G-6-PD deficiency 92, Jaundice at birth or within 24 hours of birth is com- monly due to t195) a) Erythroblastosis bb) Congenital hyperbilirubinemia 93. 94, CONGENITAL HYPERBILIRUBINEM| 93. 96. 7. 100, ton. ) Biliary atresia 4) Physiological Neonatal Jaundice not acause is a) Galactossemia by Rh Incompatibility c) Hypothyroidism 4) Breast milk Jaundice oo ‘aterm neonate with unconjugated hyperbili-ru- tinemia of 18 mg/dl on 20th day, All are common (AMS Ma 07 first time appears in the 2nd week (NEET Dec. 12 Pater causes except - fa) Breast milk jaundice b) Congenital cholangiopathy ©) G6PD deficiency 4) Hypothyroidism Defective hepatic conjugation is seen in all the following except - a) 2) Neondtal jaundice ) Gilbert syndrome €) Crigler-Najar syndrome 4) Novobiocin therapy Allare true about Gilberts syndrome except - (atts D7) 2) Mild conjugated hyperbilirubinemia b) Autosomal dominant ©) Normal liver histology 4) Almost normal live function tests Gilbert syndrome-True is~ (Alina Det Pate) 4) Reduced activity of glucuronyl transferase ') Causes indirect hyperbilirubinemia ©) Not required any treatment &) Allofabove ‘True about criggler najjar type-I syndrome is - (All Inia Des ate) 8) Diglucuronide deficiency b) Dominant trait €) Kernicterus is seen 4) Phenobarbitone not useful A case of jaundince with 50% direct bilirubin, other LFTs normal. Diagnosis is- (aurnssoro a) Rotor syndrome b) Gilbert syndrome 6) Glucurony! transferase deficiency © Primary biliary citthosis ‘Unconjugated hyperbilirubinemia is seen in- (AI india Des 1 Paste) a) Rotor syndrome ») Dubin-Johnson syndrome ©) Biliary atresia 4) Crigler-Najar syndrome Causes of conjugated hyperbilirubinemia is - (NEETc12 a) Rotor syndrome ‘ ) Breast milk jaundice©) Crigler najar 4) Gilbert syndrome 102, Mildly elevated bilirubin, normal liver enzymes are seen in- (All dia Dec Pattern) a) Malaria b) Thalassemia ©) G-6PD deficiency 4) Allofabove KERNICTERUS. 103. False about kernicteres is- (al nia Dec Paten) a) Nolong term effect ) Occurs with bilirubin more than 25 mg % ©) deposition in basal ganglion 4) Opisthotonus 104, In unconjugated hyperbilirubinemia, the risk of kernicterus increases with the use of - ar0s) a) Ceftriaxone b) Phenobarbitone ©) Ampicllin 4) Sulphonamide 105, The ate features of kernicterus include all except = (Altnde Dec 13 pattern) 2) Hypotonia ») Sensorineural hearing loss ©) Choreoathetosis 4) Upward gaze palsy 106. All of the following statements regarding jaundice in ‘a newborn are true, except - ania) a) Physiological Jaundice usually peaks after 48 hours b) Breast milk jaundice usually peaks after day 7 ©). High levels of conjugated bilirubin may cause Kernincterus 4) Allof the above are true ‘TREATMENT OF HYPERBILIRUBINEMIA. 107. Drugs that can be used in kernicterus- (P6106 Ds: 02) a) Barbiturates ’b) Benzodiazepines ©) Phenytoin’ 4) 1Chlorpromazine ©) Carbamazepine 108. Which mechanism in phototherapy is chiefly re- sponsible for reduction in serum billirubin- (IMS ay 05) 2) Photo-oxidation b) Photo-isomerization ©) Structural isomerization 4) Conjugation 109, Bronze baby syndrome is due to - (cree 98) a) Phototherapy ) Wilson disease ©) Chloramphenicol toxicity 4) Hemochromatosis 110. A fall term, 80 hrs old new born baby develops jaun- dice what should be the minimum level of serum m1. 2, bilirubin tostart phototherapy (AIIMS june 9) 2) 20mg b) 125:mgh ©) 18 mg 4) 15mg ‘A 30 weeks premature infants, 900gm weight on the third days. The serum bilirubin is 13 mg%. “The treatment of choice is- (al tada Dex. 15 Pattern) 2) Exchange transfasion b) Phototherapy ©) Waitand watch therapy 44) Pharmacologic therapy ‘What should be measured in a newborn who pres- cents with hyperbilirubinemia - (412000) a) Total & Direct bilirubin ») Total bilirubin only ©) Direct bilirubin only 4) Conjugated bilirubin only NEONATAL HYPOGLYCEMIA 113, m4, 15, 16, 17, 118, Serum glucose levels in children > 2 months with hypoglycaemia is? (CET Aug 12 Pattern) a) <40 mg/dL b) <45 mg/dL. ©) <50mg/dl 4) <54 mg/dL, All ofthe following groups of newbornsare at an increased risk of hypoglycemia except - (ans Nov 02) a) Birth asphyxia b) Respiratory distress syndrome ©), Maternal diabetes, 4) Post term infant A large for gestational age baby delivered at 40 weeks was observed to be lethargic. The blood sugar was measured to be 35 mg/dl. The management is- a) Fortified Breast Milk b) 1086 1V Dextrose 6) Oral Glucose Solution &) Normal Saline Child comes with blood suger 32 mg/dl with convul- sions Treatment is- (AM ata De: a) 5% dextrose 2 ml/kg b) 10% dextrose 2 mirkg bolus €) 10% dextrose 4 mig &) 5% dextrose 4 ml/kg Maximum concentration of dextrose that can be given through peripheral vascular line in neonate - (NEETDee.2 Pattern) as b) 10 28 a5 Administration of glucose solution is prescribed for all ofthe following situations except (IIMS Sty 06) a) Neonates b) Child ofa diabetic mother €) History of unconsciousness &) History of hypoglycemia eter)ne _ vf ree Carrex 3 Newbom infant NEONATE OF DIABETIC MOTHER 119, All of the following are the complications in the new born of a diabetic mother except = _(AIIMSay05) a) Hyperbilirubinemia —_b) Hyperglycer ©) Hypocaleemia 4) Hypomagnesemia 120. Which of the following malformation in a newborn is specific for maternal insulin dependent diabetes mellitus? ares) a) Transposition of great arteries ) Caudal regression ©) Holoprosencephaly 4) Meningmyelocele 121, Infant of diabetic mother with weight 3.8 Kg presented with seizures ater 16 hours of birth. What is the cause - (A111, ATS Nov 09) a) Hypoglycemia b) Hypocalcemia ©) Birth asphyxia 4) Intraventricular hemorrhage MISCELLANEOUS 122, Kangaroo mother care-True is ~ (Allindia Deis Pate) 1) Can also be given by fathar ») Especially for low birth weight body ©) Effective thermal control 4) All ofabove Resolution of physiological umbilical hernia occurs atwhich week of gestation? (CET Aug12 Pattern) a) Gweeks b) Sweeks ©) 10 weeks 4) 12weeks Hyperglycemia in Neonate if blood sugar is above - (MEET De.12 Pater) 123, 124, a) 150 mg/dl b) 125 mg/dl ©) 180 mg/dl 4) 100 mg/dl ‘Anewborn was given a drug in neonatal ICU, but then was found in respiratory distress. The likely drugis? caron) a) Morphine ) Naloxone ©) Salbutamol 4) Soda-bicarb ‘Anew born child developed respiratory depression in neonatal ward. Which of the following drug is the (AIMS Nov 10) 125. 126. cause - a) Opioids b) Barbiturates ©) Diazepam 4d) Propofol Hypoxic Ischemic encephalopathy trueis- (a1 Nov 10) 2) Lower limbs affected more than upper limbs }b) Prox. Muscles > distal muscles ©) Seizure 127. 128. 129. 130. 131. 132, 133, 134, 135, ) Trunk involved stephyxial injury in aterm baby is characterized by res 3 it ia (lower limbs > upper limbs) ») Differential hypotoni ©) Altered sensorium 9) Difficulty in clearing oral secretions ‘Arnewborn with eyes closed Ghrs after birth ustily crying no chest retraction and movements ofall Print ibs. Neonatal behavioral response grading . (AI Nor) a) State 1 b) State3 ) State 5 a) States ‘Aneonate requires how much pressure for frst inflation ? (CET Non. 12 Pater 2) 25 mmof Hg b) 25cm of H,O ©) 25cmof Hg 4) 25mm of HO Vomiting on the first day of baby’s life may be caused by al ofthe following except - a) Pyloric stenosis b) Oesophageal atersia ©) Aerophagy 4) Amniotic gastritis ‘Anon ventilated preterm baby in incubator is under ‘observation. Which i the best way to monitor the baby’s breathing and detect apnaea? ao a) Infrared throraric movement study ') Capnography ©) Nasal digital temperature monitoring 4) Impedence technique ‘Which ofthe following agents is likely to cause cere bral calcification and hydrocephalus in a newborn whose mother has history of taking spiramycin bat ‘was not complaint with therapy - 08) a) Rubella b) Toxoplasmosis ©) CMV &) Herpes A pregnant lady had no complaints but mild cervical lymphadenopathy in first trimester. She was pre- scribed spiramycin but she was noncompliant. Baby was born with hydrocephalous and intracerebral calcification. Which of these is likely cause? (aii iy" ata, b) Toxoplasmosis , 4) Herpes Microcephaly is defined as head circumference? (CET Aug. 12 Bate") ais 2) < ISD for age and sex ) 28D forage and sex © $38 forage and sex 4) <4SD forage and sex136, Hydrops fctalis may be caused by the following, except: (All nda Dec 14 Pater) 4) Congenital heart block ) Cystic hygroma ©) Congenital varicella syndrome 44) Congenital nephrosis 137, Fetal alcohol syndrome is characterized by all ex- ee (ALIMS No 03) 2) Microcephaly : b) Low intelligence ) Large proportionate body 4) Septal defects of heart 138. Test used to differentiate maternal from fetal blood? (AUIMS Nov 10) a) Osmotic fragility test b) Water bulb test ©) Apttest @) Kleihauer Betke test 139. Macrosomia is - (att ndia ec Pate) a) Large size baby ) Big mouth ©) Large head @) Large tongue QUESTIONS OF VARIOUS OTHER EXAMINA- TIONS, 140, Grasp reflex develops by - pmer 11) a) 20. weeks b) 24 weeks ©) 28 weeks d) 32 weeks 141, The following is of serious pathological significance in infants - (Ucarmaaka 88) a) Loss of weight ') Palpable left kidney ©) Palpable spleen 4) Deviation of trachea from midline 142, Harlequins Skin change in the newborn is seen in- ipmer 93) a) Autonomic dysfunction b) lethyosis ©) Septicemia 4) Polycythemia 143, Ina new born, what is the normal respiratory rate? (UPSC-1108) a) 10-20 breaths/minute ») 30-40 breaths/minute ©) 40-60 breaths/minute 4) 60-80 breaths/minute 144, The newborn heart rate is about - anon a) 120-160 /min b) 160 - 180 /min ©) 180 - 200 /min 4) 200-220 /min 145, “Microsomia” is defined as- (tart 05) a) Birth weight below 90% percenti b) Birth weight below 10 percent 4) Birth weight below 50° percentile M6, v7. 148. 149. 150. 151, 152, 153. 154, ‘Most common newborn rash which presents at 24- 48 hours of life is- (PSC 1109) a) Erythematous papular pustular lesions b) Milia ©) Transient neonatal pustular melanosis 4) Haemangioma ‘Which one of the following medical disorders leads to delayed foetal lung maturity (UFSC07) a) Heart disease ) Diabetes ©) Thalassemia minor) Epilepsy ‘Most common cause of respiratory distress after birth in first 24 hours is- 1PMER5) a) Neonatal sepsis ) Meconium aspiration ©) Bacterial pneumonia @) Airembolism Cephalhematoma usually disappears within - (ne MER 80, UPSC82) a) 3.5 months b) 2-5 weeks ©) 3-5 weeks 4) 5-7 weeks Which one of the following is true of Transient ‘Tachypnea of Newborn (T7NB) - (wrsc97) a) Itis the commonest respiratory disorder caused by absence of surfactant ') In premature babies, iti often fatal ©) Onset of respiratory distress is immediately after birth and it rarely lasts beyond 48 hrs 4) It often leads to chronic lung disease ‘days old neonate with extensor posture- (99) 4) Cerebral palsy 1b) Hypoxic ischemic encephalopathy (©) Malnutrition 4) Infection ‘A 26 year ol third_gravida mother delivered a male baby weighing 4-2 kg at 37 weeks of gestation through an emergency caesarean section, for obstructed labour. The child developed respiratory distress one hour after birth. He was kept nil per orally (x?0) and given intravenous fluids. He ‘maintained oxygen saturation on room air. No antibiotics were given. Chest radiograph revealed {luid in interlobar fissure. Respiratory distress settled by 24 hours of life. What is the most likely diagnosis? (0PSC06) a) Transient tachypnea of the newborn 'b) Meconium aspiration syndrome ©) Persistent fetal circulation 44) Hyaline membrane disease “The foetal length is affected ifthe mother has undernutrition during the - (urscss) a) First trimester b) Second trimester ©) Third trimester 4) Any time during the pregnancy Meconium contains all except - (cise) a) Lanugo ) Bacterial flora ©) Epithelial debris 4) BilirubinCuapreR 3 Newborn Infant 155. 156. 157, 158, 159. 160. 161. Which of the following is best for transport of the newborn with maintainance of warm temperature ~ ary a) Kangaroo Mother Care (KMC) b) Transport incubator ©) Thermacol box ) Hot bottle In Rh Jso Imunisation, exchange transfusion is indicated if- (alts 39) 8) Cord blood hemoglobin is less than 10g % 'b) Gord bilirubin is more than 5 mg, ©) History of previous sibling affected 4) Hydrops fetalis Indications for exchange transfusion are all except pmer03) 4) Unconjugated bilirubin > 18 mg/100 ml 'b) Cord hemoglobin < 10 mg/100 ml ©) Gord bilirubin <5 mg/100 mal <) Bilirubin protein ratio > 35 Jaundice in the new-born is physiological when - (075038) 2) The infantis visibly jaundiced in the frst 24 hours of birth }) The total bilirubin concentration in the serum increases by 1 mg/dl per day ©) The total bilirubin concentration is above 15 mg/dl 4) Jaundice persists for more than one week in a term infant In a neonate, jaundice appears for the first time in the 2nd week. The following isnot acause- (DPC 10) a) Galactoseria b) Rh Incompatibility ©) Hypothyroidism ) Breast milk jaundice Which ofthe following is not true about late onset Hemorrhagic disease of newborn (HON? (MH 10) a) Begins between 2-7 days of ife 1) Intracranial hemorshage is common ©) Biliary atresia can predispose <4) Warfarin therapy is associated Which of the following subtance is toxic to neurons- ipmeR 95) 4) Unconjugated bilirubin 162. 163. 164. 165. 166, 167, b) Bilesalt ©) Haemoglobin ) Melanin oe jour old full-term breast- rn Spina 31005 presents with clinically evident Jeondic. Physical examination is otherwise tal bilirubin is 11.0 mg/dl witha ct bilirubin of 04 mg/dl. What would be the correct treatment - (uescon SP Continue breast feeds and review after 48 hours B) Stop breast feeds and review after 24 hours ©) Continue breast feeds and stat blue-light phototherapy 4) Arrange for a double-volume exchange transfusion Fetal lang maturity assessed by all except-—_(UPos) 2) Measurement of a-feto protein +) Lecithinphingomyelin ratio c) Measurements of amnotic fluid creatinine & Phosphatidyl choline concentration in amniotic fluid Respiratory rate in a2 month old, to label it tachy- pneais- (DPGEECS) a) 40 b) 50 9 6 @) 70 ‘The blood sugar in.a neonate shortly after birth reaches the lowest level of 30 mg/dl at the age of - (orcee os) a) Lhour b) 3hours ©) Ghours ® Shours ‘Which of the following is NOT the correct sign of ‘good attachment of a baby to the breast (U#SC!0) a) Baby's mouth wide open ) Lower areola more visible ©) Baby's lower lip everted <4) Baby's chin touching the breast Which is an abnormal finding in a neonate? (Diath FG FO) 8) Glycosuria ) Bacteriuria ©) WBCS in urine 4) HyperbilirubinemiaANSWERS NORMAL NEWBORN 1 2 5 Ans. is ©’ Le., 28 days of life [Ref O.P. Ghat 8*/e p. 124 & ep. 96) «From birth to under four weeks of age (< 28 days), the infantis called neonate, Ans. is ‘©’i.e., Central cyanosis (Ref: O.P. Ghat 6¥ep. 145 & 7%e p. 113] ‘There is peripheral cyanosis (not central cyanosis). ‘ Length is approximately 50 cm and the attitude of body is in flexion (not extension) Ans. is ‘b’ Le. 3 days [Refi Textbook of maternal & women health care] ‘The baby may pass meconium in utero or soon afer birth, but all healthy babies must evacuate within 24 hours. After that, in normal breastfed baby meconium stools can be passed upto 3 days and on 4* and $* days transitional stools are passed. After 5 days regular milk stools are passed. Ans. is‘©’ ie., No specific therapy [Ref O.P. Ghai 6% p. 147] ‘¢ Menstural-like bleeding (vaginal bleeding) may occur from the third to seventh day of ie. ‘© Thisis attributed withdrawl of maternal hormones aftr birth, + The bleeding would subside after 2-3 days and no therapy is required. to Leg & © i.e Thigh [Ref Nelson 18%e p. 2662], ‘© Mongolian spots are blue or slate - gray macular lesions wich occur most commonly in pre-sacral area (mainly in lower back & buttocks) but may be found over the posterior thighs, legs, and shoulders. ‘¢’i.e,, Lumbosacral area; Ans. is‘c’ie., Leaving it alone [Ref 0.P. Ghai 6%e p. 146, 147] ‘¢ Hymenal tags around margins of hymen is normal finding. Ans. is‘© ie., High larynx [Ref: Gray's 40*/e p. 584; Andrew Grayson p. 82] The infant larynx differs markedly from its adult counterpart. Although it is about one - third adult size, it is proportionately larger. Its lumen is short and funnel - shaped and disproportionately narrower than that of adult. It lies higher in the neck than the adult larynx. At rest, the upper border ofthe infant epiglottis is at the level of the second or third cervical vertebra; when the larynx is elevated, it reaches the level ofthe frst cervical vertebra, This high position enables an infant to use its nasal airway to breath while sucking, PRIMITIVE REFLEXES 9. Ans. is © ie., Symmetric Tonic neck reflexes (Ref: Nelson 18%Ve p. 2439; O.P. Ghai 8%/e p. 142 & ep. 114; Meharban singh 3/e p. 71; Chedda 3fe p. 31) A. Reflexes present at birth 1. Rooting, sucking & swallowing reflexes 4.Crossed extensor 2.Moro reflex 5. Asymmetric tonic neck reflex 3. Palmar grasp (grasp reflex) B,_ Reflexes appear after birth 1.Symmetric tonic neck > appears at 4-6 months 2,Parachute reflex > appears at 8-9 months 3.Landau reflex > appears at 10 months Ans. is ‘Bie. 12 weeks [Ref Nelson 18% ch. 6.1] ‘¢ Swallowing reflex appears at 12-13 weeks of intrauterine life|= | Ciapter 3 Newborn infant 10. ML. 12, 14. 15. 16. HYPOTHERMIA ‘Ans. is ‘Le. Shivering [Refi O.P. Ghai 8% p. 143 & 7/e p 115] 17. to appear by 12-13 week of pregnancy “The suck-swallow relx is one ofthe first flees to appr I yP«aI Deptt : a —— Clinical pediatrics jicts graceful movements By 13-14, breathing and swallowing motions apes and tte sila? clicits graceful movement Ans. is‘ sai ep. 145, 146.6 78e. 114) .e., Brain damage (Ref: 0.P. Gh Primitive reflexes (eg- Moro’) Absent ‘Abnormal persistence , Dysfunction of CNS or PNS- Dysfunction of CNS [Ans is‘ ie, Never [Ref Nelson 18%e 2438; Meharban Singh 3%e P71] « Parachute reflex appears at 8-9 months off and remains throughout Iife after that. ‘Ans. is a iien Asymmetric neck reflex [Refi O.P. Ghat 8*/ep. 142 & 7¥/e p. 114 Nelson 18%e p. 2439; Meharban singh 3"Ve p. 71; Chedda 3%/e p. 31) « Asymmetic tonic neck reflex is prominant between 2nd and 4th months. 2B poeNnce ot tis rellex beyond the age of 6-9 months or a constant tonic neck posture are abnormal and usually indicate spastic cerebral palsy. Ans. is Bt i.e. C,-C, [Ref O.P. Ghai 6*/e p 146; Nelson 18*7e p. 2439, 721] ‘© Unilateral Moro’s reflex is seen in 1 Erbs palsy (C,-C,) damage ‘8 Fracture of humerus or clavicle. Spastic hemiplegia 1 Shoulder dislocation ‘# Exaggerated Moro’s reflex is seen in - cerebral damage. Ans.is‘b’ Le, Sternomastoid tumour (Ref: O.P. Ghat 8%/e p. 142 & 6*/e p. 146] ‘Ans. is'€” Le., 6% month (Ref: Tachdjian p. 371; O.P. Ghai 8%e p. 142 & 7*/e p. 114] “In normal infant the Moro reflex begins to fade at three months of age and gradually disappears at 4-6 months When it persists beyond 6 months it indicates delay in CNS development” Tachdjian “Moro reflex disappears by six months ir normal infant” - Ghai ‘Ans. is 2’ Le. Moro's [Ref: O.P. Ghai 6*/ep. 145 & 7%/ep. 114] ‘¢-Moro’s reflex disappear at 3-6 months and never reappears. $ Grp ee, sot refs, plamenal fe and slg rele ae normal ibid by ronal lab be hid ‘grows, But these ae released from inhibition in frontal lobe damage. So, these reflexes can be seen in persons with frontal lobe damage. SE —_ Grasp reflex, sucking reflex, snout & ‘bom ———*_‘palmomental reflex present ritamnitomitty 5 | Child grows. ———+ Disappearance of these reflexes Lssthnition | Frontal lobelesions. ——~——+_Reappearance of these reflexes Always remember that newborn cannot produce heat by shivering”18 Ans. is‘ L.e., Uncontrolled Shivering [Ref O.P. Ghai 8%ep. 143 & ep. 118] "Neonates Respond by Non-shivering thrmogenesis” LOW BIRTH WEIGHT 19. Ans. is ‘sie, < 10 percentile for gestational age [Ref O.P. Ghai 6¥e p. 136 7%e . 123] * Appropriate for gestational age (appropriate for date) Babies with birth weight ranging between 10th to 90th percentile on such a chart are considered appropriate for date. + Small for gestational age (small for date) Babies with birth weightless than 10th percentile are categorized as smal for dates. * Large for gestational age (large for date) Babies with birth weight more than 90th percentile are categorized as large for date. is @ ie, <1 kg [Ref Ghat 7e p, 128] «+ Low birth weight newborn Any neonate weighing les than 2500 gm at birth irrespective ofthe gestational age. + Very low birth weight newborn ‘Any neonate weighing less than 1500 gm at birth irrespective ofthe gestational age. ‘+ Extremely low birth weight newborn Any neonate weighing less than 1000 gm at birth irespectve ofthe gestational age. 20. A 21, Ans. is‘ ie, Diabetes [Ref O.P. Ghat 8% p. 155 & 7/e p. 128] ‘© InDM, theres large for date baby (not small for date: IUGR). Other three are causes of IUGR. 22. Ans. is‘©’ ie. Weight less than 10% percentile [Ref O.P. Ghai 8%e p. 138-140 & 7 p. 103] ‘First let me differentiate the following three terms i) Lowbirth weight neonates ii) Preterm infant (Premature infant) il) Small for gestational age (small for date) i) Lowbirth weight 1 Any neonate weighing less than 2500 gms at birth irespective ofthe gestational age. i). Preterm infant (premature infant) 1 Any neonate born before 37 weeks of gestation irespective of the birth weight. 1 Because birth weight isa function of gestation, a preterm baby is expected to have less weight. iii) Small for date (IUGR) 1 Babies with a birth weight less than 10 percentile for that gestational age. These may be preterm (born fore 37th week) or term (born between 37 to 42 weeks). ‘So, both preterm infant and small for date neonate have low birth weight, ——— Pre term«———————— Small for gestational age (IUGR) Full term «Low birth weight neonates will have following problems - 4) Problems of small for date babies i) Problems of preterm babies 23, Ans. is‘ ie, Thick ear cartilage (Ref: O.P. Ghai 8% p. 138-140 & 7%e . 109] «e The ears in a premature neonate are soft and flat with ear cartilage being deficient and pliant (and not thick). 24, Ans. is ‘sie. Suffer from jaundice of hepatic origin [Ref O.P. Ghai 8% p, 156 & 7% p. 129-130] «# The liver of premature (preterm) neonate is functionally immature that leads to hypoglycemia, hyperbilirubinemvia (jaundice) and poor detoxification of drugs.25. Ans. I'a Le, Hypoglycemia [ke 0. Ghat ep 1560 7*/ep. 129-130) ‘¢ Small for date babies are prone to hypoglycemia. ¢ Intraventricular hemorthage occurs in preterm infants oot in fll term, small for date babies. 26. Ans. is‘b’ i,, Head circumference is 3 cm more than chest circumference [Ref O-P. Ghai S*/ep. 156 & 6%/e p. 156) JUGRIs synonymous with 1 gestational age infants - Serre weal dace Corona wre of 1G ina) some important etree ‘The difference in the head and ches circumference ‘Internal organs like Liver, thymus and lungs are shrunken, alt Hepatomegaly) «+ Pulmonary alveoli are matures patient is ses is more than 3.¢m. though pulmonary alveoli appear mature... No not premature but only LBW or SED —> No ARDS p. 129; Nelson 18%7e p. 702, 703] Ans. isd ie. Brain [ Ref: O.P Ghai 8% p. 156.6 7% IUGR is classified as ) Symmetric IUGR ‘ Reduced growth is symmetric —> head circumference, «Has earlier onset aeeaey ere aiseases that seriously affect fetal cell number, such as conditions with chromosomal, genetic malformation, teratogenic, infectious or severe maternal hypertensive etiologies. Asymmetric IUGR ‘© Reduced growth is asymmetric with relative sparing of head growth 1 Has late onset. Is associated with poor maternal nutrition or with late onset / exacerbation of maternal vascular disease (preeclampsia, chronic hypertension). length and weight equally affected. 28. Ans.is‘a ie, 1.6 [Ref O.P Ghai 7%e . 108] Weight (gr) x 100 nderal index = Ponderalindex = Es em ‘¢ The Plof the baby in question is - 2000 x 100 (soy « That means the baby is having assymetic TUGR (PI <2). 29, Ansis‘b’ i., Orogastric [Ref: Handbook of pediatric nutrition p. 50-60] Feeding of a preterm neonate «# The aim of nutritional management ofa preterm infant isto achieve full enteral feeding as soon as possible. «# For preterm infants of more than 34 weeks of gestation, iti possible that breast or they should be able to coordinate sucking, swallowing and breathing. arr Heding ca beanie «But for those younger infants who may have compromised respiration orb “ration or be neurologically less well developed, this south (oro-gastric tube) or the nose (naso-gasric tube). Naso-gastec tube increases th ane ed ‘work of breathing, therefore, orogastric tube is preferred over nasogastric tube —— = «# Breast milk i the food of choice as iis best tolerated and includes other benefits as ‘well as nut TPN is given to VLBW infants who cannot tolerate gastric tube feeds, are is not possible or just while enteral nutrition is being established, Ou ‘mature/LBW infants which include Infants with; ° (i Significant respiratory distress required assisted ventilation, (ii) Shock requiring inotropic support. (ii) Seizures, renal/cardiac failure have gastric disease, enteral feeding (by tbe) ther important indication for TPN is sick pre"(8) Symptomatic hypoglycemia/hypocalcemia, electrolyte abnormalities. (9) Surgical condition of GIT, NEC, hydrops ‘Even in these sick infants, enteral feed should be started as atly as possible. Alogrthm for feeding ofa preterm infant Siiveas Irae bres foding Obcereir {Poctotng and atachmentare good 2LABletmekefethel an long eough (aor i-tS my Sawer Fe 1 Sur feet} poonpalaat fain | Obseneit ng wll iho ing Sushing = aAietceptadenneanom —— [283T we] a No Start feed by OGING tube + Observe if 1. Vomiting / abdominal <28 weeks distension occurs 2. The prefeed aspirate exceed >25Meof feed volume Yate ‘Gastric tube feeding TEN Coming to question ‘s Best answer ofthis question is feeding by spoon or paladia, However these are not provided in options. ‘s Amongst the given options orogastric tube is the answer of choice,| > | Carter 3 Newborn Infant NEONATAL SEPSIS 30, 31. 32. 33. 35. 36. 37. 38. Ans. is @ ie 72 hours [Ref Ghai 7e p. 136] ‘+ Early onset neonalal sepsis occurs within 72 hours of life ; are ofthe new born the, Meharban Singh] mn 72 hours and late onset sepsis Occuring air Ans. is ‘bie., E.coli [Ref O.P. Ghai 8%e p. 163 e+ 74e p. 136: ‘ew born sepsis canbe clasfed int early onset sepsi-occurting wih 72 hours. Early onset sepsis - ‘ Itis caused by organisms prevalent in the genital ‘In the west it is mostly caused by group B streptococcus ‘In our country its mostly due to gram negative organisms: «© Majority ofthe neonates with early onset sepsis manifest as respiratory Late onset Septicemia: ring ka wd « Late onset septicemia is acquired as nosocomial infection from the nursery or lying) NAN 1 The onset is delayed for 48-72 hours afer birth. ‘i 3 inmost cases symptoms appear by the end offist week or during second week of ie {About two thind cases of ate onset septicemia are caused by gram negative bacl Klebsiella pneumonea, entero bacteria, E.Col, poeudomonss aeruginosa alkaligenese fcalis, salmonella tyhimurium. proteus, citobacter and serrata, ‘Ans. is’ Le., Local nursery environment [Ref O.P. Ghai 8% p. 163 & 7*/ep. 136) 4 Late onset sepsis is caused by organisms of the external environment of home or hospital and the infection is transmitted most frequently by the hands of the care-provider. ‘Ans. is‘b’ e., Klebsiella (Ref: OP Ghai 8%e p. 163 & ep ‘graduate medicine (JPGM)] | tract or in the labor room and maternity operation theatre. and Ecol coi Klebsiella and enterobactor sp. “istress due to intrauterine pneumonia, (cherbaan Singh 6*/e p. 209 and Journal ofpost- ‘© Most common cause of neonatal sepsis in hospitals in India is = Klebsiella ‘© Most common cause of neonatal sepsis in hospitals across the world is» E.coli ‘© Most common cause of overall neonatal sepsis > Group B streptococci ‘Ans. is ‘a’ i.e., Genital tract [Ref Nelson 184%e ch 183] «© Gram positive CAMP positive coccus is group B streptococcus (Str agalactiae), the most common cause of neonatal meningitis, «Its habitat in human hosts is female genital tract and rectum, ‘Ans. isb’i.e., Neutrophilia [Ref O.P. Ghai 8% p, 164 & 7% p. 137; Nelson 164/e p. 548] Ans. is's Le, Group B streptococci [Ref OP. Ghat 8% p. 163 6 7/e p. 136] ‘Ans.1s"b’ ley Streptococcus agalactiae [Ref O.P, Ghal 8% P1636 7%e p. 136, ‘Ans. is ‘b’ ie, E. coli [Ref Nelson 18% p. 747] 'P-136; Nelson 18% p. 747) 1 E.coli & streptococcus agalactie (group B streptococci) are the two ‘meningitis, 10st common cause of neonatal sepsis an39 Ans. is’¢ Le, Ampicillin and Gentamicin [Ref O.P. Ghai 8e p. 171 & 7H/ep. 138] * Antibiotic therapy for neonatal pneumonia includes ampicillin plus gentamycin. RESPIRATORY DISTRESS 40. Ans. isa’ i.e., Wheeze [Ref Nelson 18%/e Chapter 101.4] * The principle features ofthe respiratory distress n'a neonate = 1 Tachypnoea: Rates of> 60 breathsimin > 50 breaths/min and > 40 brethsin for youn infants (0-59 day), infants (60-365 dys) and childhood (1-3 ear). 2 Use of acessory muscles for respiration : Features include us of sternoledomastoid muscles, nasal ala Mae and tracheal ug, 3. Use of intercostal or subcostal muscles for respiration resulting in intercostal or subcostal recession - lower chest wall indrawing. 4. Audible grunting 5. Cyanosis Al. Ans.is ‘a ie., Apnea [Ref O.P. Ghai 6¥/e p. 169 & 7%/ep. 146) ‘# Apnea may be defined as - '). Cessation of respiration for 20 seconds with or without bradycardia and cyanosis. 48) Cessation of respiration for less than 20 seconds if itis associated with bradycardia or cyanosis 42. Ans. is‘ i.e., 20 sec [Ref See above explanation] MECONIUM ASPIRATION SYNDROME. 43. Ans.is‘’ie., Obstructive emphysema [Ref Dutta 4/ep. $11; .P. Ghai Yep. 170 Te. 144-145; CPDT 184% 20,21] Consequences of meconium aspiration ‘© Three main problems oceur duc to meconium aspiration - 4) Obstructive emphysema or atelectasis -> when aspirated material blocs the aia. ii) Pneumonitis and chemical pneumonia -» because of irritant property of meconium, iii) Defective gas exchange. “b’i.e., Meconium aspiration syndrome [Ref Nelson 18%/e p. 742; O.P. Ghai 8*/e p. 170 & 7/ep. 144- 44. An 145] ‘# Meconium stained liquor (amniotic fluid) with respiratory distress soon afer birth suggests the diagnosis of meconium aspiration syndrome. «The important clues in this question are 1) Baby is full erm —> MAS occurs in term or post term neonates. fi) Respiratory distress soon after birth —> MAS presents lke this iil) Liquor is meconium stained —> supports the diagnosis of MAS « In transient tachypnea of newborn and hyaline membrane disease (surfactant production) amniotic uid will not be stained with meconium. 45, Ans. is‘b’ ie, Meconium aspiration syndrome [Ref Ghai 7 p. 142] 1 Tachypnea (or respiratory distress in post erm» Meconium aspiration syndrome, Sree types ecus in peters ote baby nd HMD ocasin peter baby. CONGENITAL DIAPHROGMATIC HERNIA 46. “Ans. is‘ ie, Pulmonary hypoplasia [Ref Nelson 184%e p. 748] «¢ Most common cause of death in congenital diaphragmatic hernia is ~ Pulmonary complications Sa most common cause of death in congenital diephragmatic hernia in S Intestinal obstruction47. Ans. is‘b’ i.e., Diaphragmatic hernia [Ref: Nelson 18*/e ch.101.9) ital diaphragmatic hernia. aeeeae ar ai aerencad aot abamen sigs cngeral SAPNAERANS NS 48, Ans.is‘¢ ie, Insert a nasogastric tube [Ref Schwartz 7%€. 1720] Management of congenital diaphragmatic hernia , «Eater congenital diaphragmatic hernia was consideredto be affect ofhernlated viseera the major factor in cardiorespistOry COMPFOTNS 1 and pulmonar « Now itis recognized that mjor ads ofcarcocspttorcompromiseisPumonar? ype y Iypoplasia. seit « Somnov the patient is ntaly resuscitated before surgery is penformed. TMs ress 8) Stabilization by mechanical ventilation with 100% O, b) Nasograstre suction wide adequate oxygen deli « Ventilation prevents the development of pulmonary hypertension and provide adequate O=78en N= Now days infants are ventilated by high frequency oscillation. 4 Nasogastric tube is used for suction to aspirate swallowed which would further compress the hing. , ‘© So both option ‘c’ & i are preoperative procedures in congenital diaph should be performed fist ease ee cc sucton is performed fistin a case of CDH unless the patient presents with flowing symptoms» a)Cyanosis, b) Apnea, _¢) Respiratory disease «Here in the question the patient does not complain of any of the above symptoms so be the first priority 49, Ans. is‘ Le, Put a nasogastric tube [Ref See previous explanation] scaphoid abdomen with respiratory distress suggest the diagnosis of congenital diaphragmatic cal emergency It was believed that the mass tation consists of air and to prevent distension ofthe herniated owe, ragmatic hernia. The question is which nasogastric suction should © Mediastnal deviation, hernia (CDH). «The resuscitation of CDH patient consist of: a) Stabilization by mechanical ventilation with 100% 02. by Nasogastrc suction «This child has already been intubated. «© Now nasogastric suction should be done to aspirate swallowed air and to prevent distension of the herniated bows ‘which would further compress the lung. 50. Ans. is‘ i.e., Confirm the position of endotracheal tube [Ref Nelson 18%e p. 746-748] ‘This sa case of congenital diaphragmatichernia ‘The clinical features suggesting this are: wt Respiratory distress afer birth with decreased air entry onthe lft side 1 Scaphoid abdomen ‘# Mediastnal shift s atiesbne gueion mes sf cured aes bgnd sk vention and endothe ibton So there is @ possibility of wrong endotracheal intubation (ie, endotra i So there poss ff intubation (i, endotracheal tube entered esophagus instead of ‘e This caused distension of stomach with gas which resulted in medias position of the endotracheal tube should be done. i mediastinal shift. So the confirmation ofthe ‘ If the endotracheal tube is in proper position the next immediate treat it decompression ofthe gastric distension by nasogastric tube imrertion. ment modality in this patient would Pe 51. Ans.is b’ Le, Remove tube & reattempt intubation [Ref Read below «© Dont get confuse with answer of previous question, «Theres difference between option of previous question and option‘ Previous question -confim the potion ofendatachea tube: This question - confirm the position of ET tube by chest x-ray. « Best answer would have been, confirm the position of endotrach ‘© But, chest x-ray cannot distinguish between tracheal and es — of the ET tube in trachea. Chest x-ray is done to confirm the, of this quest iPhageal intubation and cat ation and cannot confirm the position Correct length of tube (not the position).‘Method to confirm tracheal intubation |, Tests which suggest tracheal placement (not confirmatory) ‘= Symmetrical Bilateral chest movements when reservoir bag is squeezed. ' Equal breath sounds over hung fields when reservoir bag is squeezed. 1» Absence of gurgle over lung fields when reservoir bag is squeezed. 1 Misting ofthe tube (water vapour deposition) during expiration. 1 Feeling of correct lung compliance and refilling of bag during expiration. 2.Confirmatory tests 1 Capnography ~> Measures end tidal CO?2 in expired gas. 1 Esophageal detector device. ‘¢ None ofthese method has been mentioned inthe options ofthis question. ‘+ Amongst the given options, best course of action i to remove the tube and reattempt intubation : - "there is any doubt about tube placement the tube should be removed” == Lee. Neonatal respyatry ditess Signs of CDH GSeaphold abdomen, medias! shit) Immediate ET Intubation Signs of improper positioning of tube Proper positioning of tube ‘ Dysfunction. gress or PNS. Confirm the: pstion of tube Remove the tube & reattempt intubation > Nasogastric tube insertion todacomppess bowel Chest srayto confirm he Diagnosis of COH Surgery as required 52, Ans. is‘ Le, Nasogastric tube insertion [Ref See above explanation] | 1 Here “removal of tube and reatempting intubation’ is not provided amongst the option, : ‘©The nent best stept isto decompress the distended stomach by nasogastic tube insertion, So, the same question has three different answers depending on the options provided 1) Confirm the positon of BT tube (not by chest x-ray) Best answer 1i) Removal ofthe tube and reattmpting intubation ~ If previous one snot provide as an option i) Nasogasri tube insertion -> If previous two are not provided in option. "Note : In previous three explanations I have explained the management protocol of CDH in which intubation has already been used. But you should keep in mind that nasogastric suction should be the frst procedure except in “Apnea, cyanosis and respiratory desease, where intubation is preferred initially. ‘Ansis‘b’ i.e Delay in emergent surgery [Refi Nelson 18%e p. 748; Fundamentals of pediatric Surgery p. 535, 536] ising of surgcal repair has gradually shifted from an emergency repair, policy of stabilization using variety of ventilatory strategies prior to operation, ‘# Current recommendation is to adopt a conservative approach and dela surgical repair of the CDH until the infant stablizes from a hemodynamic and respiratory point of view. Prognostic factors in CDH «Prognostic factors canbe divided into ‘Primary prognostic factors (Pathophysiological) i eer ue te mont important progaetic factor which fect morbidly and mort,| = | CHapTER 3 Newborn infant These factors are i) Pulmonary hypoplasia (most important) ii) Pulmonary hypertension (2nd most important) predictors (diagnostic/clinical) factors are: B)_ Secondary or relativ 1 These poor prognos a) Antinatal i) Detection at an early gestational age (< 24 wks) Associated extradiaphragmatic congenital anomalies iii) Liver herniation into thorax (Liver above diaphragm) ¥) Stomach herniationinto thorax (Stomach above diaphragm) vi) Presence of polyhydraminios vii) Small lung to head circumference ratio (LHR ratio) Viii)Small fetal abdominal circumference (< than 5* percentile) b) Postnatal 4) Early age (< 6 hours) of presentation ii) PO, and PCO, unresponsive to ventilation ili) Need for extracorporeal membrane oxygenation (ECMO) ©) Side of defect 4) Right sided defect 54, Ans. is‘a’ i.e, Pulmonary hypertension [Ref Sabiston 18%e p. 2073] ‘Compression of the lung results in pulmonary hypoplasia involving both lungs, with the ipsilateral lung being the most affected. In addition to the abnormal airway development, the pulmonary vasculature is distinctly abnormal in that the medial muscular thickness of the arterioles is excessive and extremely sensitive to the multiple local and systemic factors known to trigger vasospasm. Thus, the two main factors that affect morbidity and mortality are pulmonary hypoplasia and pulmonary hypertension.”.Sabiston 18%Ve p2073 HYALINE MEMBRANE DISEASE 55, Ans. is‘c’ie., Prematurity [Ref: Nelson 18%/ep. 731, 732] ‘+ HMD always occurs in preterm babies often less than 34 weeks of gestation. 56. Ans. is‘c’ie., HMD [Ref: O.P. Ghai 8*/e p. 169 & 7%/e . 143; Nelson 184e p. 731] ‘© Surfactant deficiency (decreased production and secretion) is the primary cause of RDS. 57. Ans. isa’ ie., In the first 6 hours of life [Ref O.P. Ghai 8%/ep. 169 7%/e p. 143; Nelson 18%/e p. 732] «¢ Respiratory distress occurs within the first 6 hours of life. 58, Ans. is‘b’ ic., Hyaline membrane disease [Ref O.P. Ghai 8%/e p. 169 & 7%/e p. 143; Nelson 18%/e p. 731, 732] Respiratory distress in a preterm infant and X-rays showing ground glass appearance with air bronchogram suggest the diagnosis of neonatal respiratory distress syndrome (RDS) also called hyaline membrane disease. “Hyaline membrane disease is the commonest cause of respiratory distress in a preterm neonate”, — Ghai About other options «© Meconium aspiration syndrome usually occurs in full-term or post-term newborn, ‘© ARDS is adult respiratory distress syndrome. 59, Ans. is‘a’i.e., Hyaline membrane disease [Ref: Ghai 7" p. 143] 60, Ans. is‘b? ie., Air bronchogram on chest x-ray [Ref Nelson 18%/e p. 733; OP Ghat 8%/e p. 169 & 7¥/e p. 143] “The chest x-ray of an infant with RDS is characterized by atelectasis, air bronchograms, and a diffuse reticular- ‘granular pattern commonly referred to as “ground glass’. The chest x-ray may progress to a complete “white out” with severe disease. ‘About other options « Antenatal corticosteroids are given in pre-term (pre-mature) pregnancies not in term pregnancies. Further, antenatal ‘corticosteroids are given to prevent RDS (HMD) —» after antenatal corticosteroids administration, risk of HMD is reduced.+ Respiratory distress occurs within first 6 hours. ‘¢ HMD occurs in pre-term neonate. 61, Ans. is a Le,, L/S ratio [Ref: O.P. Ghal 8%e p. 169 e+ ep. 144] Rrenatal diagnosis of HMD can be made by - 1) Lecithin / sphingomyelin (L/S) ratio in amniotic fluid —> LIS ratio > 2 indicates adequate lung maturity 2) Shake test —> Amniotic tuid or gastric aspirate is mixed with absolute alcohol and shaken for 15 seconds and allowed to settle. Copious bubbles are formed in the presence of adequate surfactant indicating extent of lung maturity. 62, Ans.is‘c’Le., Phosphatidyl glycerol estimation isa reliable method of diagnosis [Ref: O.P. Ghai 8% p. 169 & 7/e p. 143-144) ‘¢ In HMD surfactant is reduced and its measurement can be used for diagnosis eg. in shake test. # Constituent of surfactant are - dipalmitoyl phosphatidylcholine (lecithin), phosphatidylelycerol, apoproteins (surfactant proteins SPA, SPB, SPC, SPD) and cholesterol. 63. Ans. is ‘€’ Le, Is treated by administrating 100% oxygen [Ref O.P. Ghai 8%e p. 169 ¢- 7/e p. 143-144] « Premature infants receiving high concentrations of oxygen may develop rtrolentalfibroplasias. So generally oxygen tension is kept approximately 90% and not 100%. 64, Ans. is‘a' Le, CPAP [Ref Neonatology by Eval 47e p. 59] ‘ Specific treatment for HMD is intratracheal surfactant therapy This therapy requires endotracheal intubation, which also may be necessary to achieve adequate ventilation and oxygenation. 1 Less premature infants (those > 1 kg or > 28-30 weeks gestation) and those with lower O, requirements (Fi02 < 40 - 50%) may respond well to supplemental O, alone or to treatment with nasal continuous positive airway pressure (CPAP). 65. Ans. is‘c’ie., Prevents hyperbilirubinemia [Ref: O.P. Ghai 8% p. 170 & 7/e p. 144) Prevention of HMD ‘© Prenatal steroids are effective in preventing HMD. ‘¢ Steroids acts by enhancing lung maturity. Benefits 50 percent reduction inthe incidence of respiratory distress syndrome (ROS) 50 percent reduction inthe incidence of intraventricular hemorrhage (VH) © 40 percent reduction in mortality. Indications fe Allmother at risk of preterm delivery between 24 and 34 weeks of gestation. © Cases of preterm premature rupture of membrane atlessthan 32 weeks of gestation inthe absence of overt clinical chorioamniontis, contraindication "> Clinical chrioarnnionitis, (Maternal hypertension and diabetes mellitus are no ‘contraindications. Careful monitoring and management of hypertension and hy- peralycemia should be ensured), Treatment schedule 2 In} Betamethasone 12 mg IM every 24 hours, 2 doses (preferred). Inj. Dexamethasone 6 mg IM every 12 hours, 4 doses (only ifbetamethasone can not be arranged). Timing of effect ‘© Optimal effect occurs after 24 h of initiating treatment. fe Theeffect of one course lasts for 7 days. 66, Ans-Is‘b' Le, 12:mg every 24 hours (Ref: See above explanation] 67. Ans is‘a'Le., FRCis smaller than closing volume (Ref: Hand book of pediatric intensive care Me p. 138] “Hyatne membrane disease reduces compliance and cases a fll n FRC (tees blow the normal closing volume ofthe lung)”. = Handbook of pediatric intensive careBRONCHOPULMONARY DYSPLASIA. = p71 Pep 146; Nelson 18% p. 737, 738] 4¢» Theophylline use [Ref: 0.P. Ghai 8% Bronchopulmonary dysplasia (BPD) yen ; «© BPD isa result of lung injury in infants requiring mechanical ventilation and tee . ae _ + Most ofthe chldeen with BPD are premature and have hyaline membrane disease. DY in. term newborns with meconium aspiration or persistent pulmonary hypertension: Pathogenesis, «The premature lung makes insufficient functional surfantant sufficiently mature to protect the lung from the toxic oxygen met .nd the antioxidant defence mechanisms are not taboites generated from oxygen therapy. ‘Premature newborn + Immature lung (surfactant) + Hyaline membrane disease 4 ee ‘oxygen therapy to newborn 4 cee Generation of oxic oxygen metabolites (neta is : cnn darage tong bzaus promt ——o neve aia eee mechan ovens are not sufficiently mature ‘tenn a $$. rune er, naman & pray wey os onder . Bronchopulmonary dysplasia 69, Ans. is‘a’ Le., Mild BPD [Ref Nelson 18%/e Chapter 101-4] Mild Moderate Severe’ Supplement 0,{for28.dey3)_ Supplement 0, for28 days) Supplement 0, for28 da) and and and atbinh sethingroomatt3eweeks—Besthing with < 308 0, at” Breathing > 30% 0, conected GA or at dscharge 36 weeks corrected GA of at pouttive pressure ver Gvhihevercomes fst. dlicharge (whichever come fpPU}i™ = nt 36, we first). corrected GA or at dischar (whichever come first) = 32weeksGAatbirth Breathingroomairby 6 days <30%0, by 56 days postnatal postnatal age or at discharge age orat discharge (whichever (whichever comes first), comes first). Breathing 2 30% 0, and/or Positive pressure ventilation (Pv) by 56 days postnatal age orat discharge (whichever ea 4 The baby in question falls in category < 32 weeks gestation age at birth, « Simply looking at question, answer seems tobe sever BPD as mechanical has included only in diagnostic criteria of sever BPD, ventilation (positive pressure ventilation)‘ But this question is not as simple ait is looking, Is tricky one. ‘In baby with > 32 gestation age at birt, we wil have to see the respiration at 36 weeks corrected gestational age: = This baby was born at27 weeks of gestation and required mechanical ventilation for 4 more weeks, i.e. upto 31 weeks corrected gestational age. After that he maintained at room aie. Thus, at 36 weeks corrected gestaional age, baby is breathing at room air > diagnostic criteria of mild BPD. TRANSIENT TACHYPNEA OF NEWBORN 70. Ansis‘c’i.e., Elective caesarean section [Ref O.P. Ghai 8p. 171 & 74/e p. 146; Various articles of Obs & Gynae] * In text books, both elective caesarian section and normal preterm or term vaginal delivery have been mentioned as isk factors for transient tachypnea of newborn. «But the best answer is caesarian section ~ “Delivery by caesarian section and gestational ag are the risk factors for TTN”._— Articles Obs & Gymae 71. Ans.is‘c’Le., Prominent horizontal fissures [Ref: O.P. Ghai 8p. 171 & 7*/ep. 146; Nelson 18%e . 741] ‘+ The lungs are generally clear without rales or rhonchi and chest roentgenogram shows 1 Prominent pulmonary vascular markings = Overaeration ' Fluid lines in the fissure 1 Flat diaphragms = Prominent inter lobar fisure = Occasionally plewral fluid. 2. Ans. ise Le, Interlobar fissure effusion [Ref O.P. Ghai 8p. 171 & 7 p. 146; Nelson 184/e . 741] PULMONARY ALVEOLAR PROTEINOSIS 73. Ans. is‘ ie., Neonatal pulmonary alveolar proteinosis [Ref: Nelson 18*/e p. 1821] “Respiratory distress in an infant along with a positive family history of similarly affected newborn infants strongly suggests, pulmonary alveolar proteinosis”. RESUSCITATION 74. Ans.is‘@ ic. Trikling of sole [Ref O.P. Ghai 6%/ p. 128 & 7*/ep. 98-99] ‘© Afier suctioning, the baby should be dried by using pre-warmed linen to prevent hea loss. © Abi mulation i licks subbing the back ma ded in case of non- establishment of good respiratory efforts 75. Ans. is‘s’ie., Discontinue ventilation [Ref O.P. Ghai 8% p. 127 7/ep.99© Clearance of meconium 2 Active breathing or crying (ont 9 Good muscle tone [a > Routine care Color -> Pink Term gestation J Anvortiveisasent Initial steps ‘9 Provide warmth 2 Positioning 9 Good muscle tone o Clear airways ~> suctioning <2 Dry stimulate —» flicking sole or rubbing back 2.O,if necessary | Evaluate 1 Respiration Breathing, ‘ Supportive care Color HR>100 & Pink Heart rate (HR) Apnea or HR< 100 Positive pressure ventilation | Breathing, oe | resting. ongoing care by bag and mask HR>100 & Pink eas vceo | foaoeo ‘9 Continue bag & Mask ventilation] 9 Chest compressions HR<60 oa Epinephrine 76. Ansis‘b’ i.e., Ist mouth suctioning done & ‘c’ ie, suctioning is upto 5 cm [Ref O.P. Ghai 8%/e p. 128 & Suctioning during resuscitation ¢ The mouth and nose should be suctioned The mouth is suctioned first to ensure that there is no suctioned that the thing for the infant to aspirate when the nose is + One should not insert the catheter very deep in mouth or nose for s ¢ for suction -> Stimulation of posterior pharynx during the frst few minutes after birth can produce a i er ape m vagal responce, causing severe bradycardia «# Therefore during oral suctioning, atthe baby5 ip. + During nasal sutioning suction tubes intoduced upto 3m mark into each nose 77. Ans.is‘b’ie., Colour [Ref O.P. Ghat 8% p. 126 & ™e p. 100) «A newborn is classified as vigrous if 1). Strong respiratory efort 2) Good muscle tone 3) Heart rate greater than 100 ‘Max. length of nasal suctioning is upto 3 cm and mouth ‘ep. 98-99; Manual of neonatal care p. 68, 385] ‘suction tube is gently introduced into the baby’s mouth until the 5 cm markis ie has all the three signs are present :-78, Ans. isa! ie. Check pulses (Ref: O.P. Ghai 8%/ep. 126 & 7 p. 100] * After airway has been opened and two rescue breaths provided, determine the need for chest compression. For this check the pulse in carotid (in children) or branchial artery (in infants). * Ifthe pulse is not palpable or heart rate is <60/min, begin chest compression. Ans. is‘C’ie, Diaphragmatic hernia [Ref O.P. Ghat 8% p. 129 & 7 p. 100,153] * a diaphragmatic hernia, the abdominal contents heriating into thoracic cavity have already compromised vent- tion. * Giving bag and mask ventilation to this patient will worsen the condition of the patient as ai will also enter in the stomach and further compress the ngs. ‘+ Indications of Bag and Mask ventilation. ' Bag and mask ventilation is indicated if even ofter tactile stimulation. 8) The infant is apneic or gasping ') Respiration is spontancous but heart rate is below 100 beats/minute. Remember ‘Bag and mask ventilation causes abdominal distention as air or oxygen not only enters the lung, but also escapes into the stomach via esophagus, Distended stomach presses on the diaphragm and compromises ventilation. Therefore if ventilation continues for more than two minutes, an orogastic tube should be inserted and left open to decompress the abdomen, 80. Ans. is’ Le, Convection (Ref: O.P. Ghat 8% p. 128 & 7/e p. 117) “Convection warmed incubators are being routinely used for thermal regulation of the premature neonate’s ambient sir" Ghai %e 154 81. Ans. is ‘b’ ie., Dexamethasone (Ref: This isan extract of the book PAEDIATRICS FOR DOCTORS; Frank Shann ‘and John Vince; hapi/www.developmentgateway.com.au/health/pacdiatrics/PaediatricForDoctors_pg236-242 pd] ‘Corticosteroids should not be used” - Paediatrics for doctors - Frankshann & John Vince ‘Management Protocol ‘The management protocol of babies with asphyxia: 1.Oxygen. In the absence of continuous oxygen saturation monitoring, it is reasonable to give nasopharyngeal ‘oxygen (0.5 lite/min) until the baby recover. If monitoring is available, oxygen is given as appropriate 2-Thermal control Babys body temperature should be kept inthe normal range of 36.5-37.2"C (sometimes the babies become hyperpyrexic) 3. Correction of shock, I peripheral perfusion is poo, itis reasonable to give 20 ml/kg of normal saline initially perfusion remains poor, the use of dopamine should be considered, 4. Fluid balance. Give IV fluids at 2/3 maintenance. Use 10% dextrose 5. Monitor blaod glucose with dextrostix nd do not et it fall below 2.2 mmal (explains glucose administration) {6.Prevent/control convulsions. In less severely affected babies, phenobarbitone should be given when there is snyuspicion of actual or impending convulsions (phenobarbitone loading dose 20 mg/kg IM or 1Omg/kg slowly TV, then 5 mg/kg daily orally). 7.Treat hypocalcaemia iit occurs (or more practical (explains calcium gluconate administration) ithe baby has uncontrollable fitting with anormal dextrosti), ws 82. Ans, is‘b’ Ley 1 [Ref Nelson 18%Ve ch. 94.3] ‘¢ Grimace is given score-1 in APGAR score. Respiratory effort None Slow iregular Good, crying‘+ Color of the body (Appearance) |* Muscle tone (Activity) ‘© Reflexstimulation Grimace) No response Grimace oF putting catheterin nose 83. Ans.is“d ic., Respiratory rate/minute [Ref O.P. Ghai 8% p. 126 & 7*/ep. 107) «Breathing effort (not respiratory rate) is used in APGAR score. 84. Ansis‘s? ie, APGAR at 7 min indicates neonatal mortality depression [Ref Avery’ pediatrics] « Later times APGAR score (after 5 minutes) indicates about longterm neurological damage (not neonatal morality) Interpretation of APGAR Score ‘© The test is generally done at one and five minutes after birth, renee en ne et allot rl low and 10 generally normal ‘© A low score on the one-minute test may show that the neonate requires medical attention (e.g. resuscitation) but isnot necessarily indiation that there wl be long-term problems, particularly if there isan improvement bythe stage ofthe five-minute test. Ifthe Apgar score remains below 3 at later times such as 10, 15 or 30 mintues, there isa risk thatthe child will suffer longer-term neurological damage. There is also a small but significant increase of the risk of cerebral palsy. However, the purpose ofthe Apgar testis to determine quickly whether a newborn needs immediate medical cre; it was nt designed to make long-term prediction ona childs health. C02 transport across placenta + CO, iscleared by placenta by simple difsion. CO, i produced abundantly in the fetus, and the PCO? of fetal blood is higher than maternal blood. CO, therefore diffuses from fetal blood, through the placenta, into the maternal Circulation, andi disposed by explation from mothe’ lng. Anaerobic metabolism causes acidemia due to lactate (lactic acid) production ‘¢ Anoxic perfusion causes an increase in glucose consumption which is more than two fold higher than that seen in the oxygenated perfusion, resulting finally in placental uptake of glucose not only from the maternal but from the fetal circulation. «# Lactate production i increased during the anoxic perfusion, while the inal tissue energy value lie between the values ebserved for eh issue and for the oxygenated perfusion. The shift to aneroble metabolism shown by pl Cental tissue in anoxic conditions enables continued functioning ofthe tissue over the 2-h perfusion period butit appear that under anoxic conditions the tissue may incur an energy debt not observed in oxygenated perfusions. 85. Ans. is‘c’ Le., 5 [Ref Meharban Singh 6*/e p. 262] ‘and may be repeated later ifthe score is and remains ‘« A score of >6 is indicative of impending respiratory failure. ‘¢ Now analyzing our question data : i) Upperchest. Lagoon inspiration present <> moe ii) Lowerchest. —- No retraction meses Xiphoid = No retraction ary iv) Nasal flaring Present ees ¥) Grunting = Present eed + So, total score is 5. 86. Ans. is ‘d’ie., All of above [Refi Nelson 18%/e . 100} ‘¢ Drug used during neonatal resuscitation: (1) Epinephrine/Adrenalin, 2) NS; val dium-by- eo ite, Dose of Adrenalin 0-03 mllkg of I: 10,000, @)NS or RL (3) Naloxone and (4) Sodium-by87. Ans.is‘c’ie.,0.1-0.3 ml/kg in 1:10,000 [Ref O.P. Ghai 8*e p.132& 74/e p.103] Dose or adrentains 0.1 mig to 0.3 ml/kg diluted (1:10,000) Routs: (1) Intravenous (umbilical vein) or (@) Endotracheal Indication - IR < 60/min after 30 sec. of positive pressure ventilation & chest compression HYPERBILIRUBINEMIA & NEONATAL JAUNDICE 88. Ans.is W Le., >15 mg/dl [Ref Ghai 7/ep. 147] 89. Ans. is‘a'Le., Rotor syndrome [Ref Harrisons 17*/e Ch Table 43-1] + Conjugated hyperbilirubinemia is seen when - 1) Impaired secretion of conjugated bilirubin into bile > Dubin-johnson syndrome, Rotor syndrome. i) Impaired bile low > Obstructive jaundice, primary biliary cirrhosis, Neonatal cholestasis, ex. Extrahepatic biliary atresia / neonate idiopathic hepatitis, Choledocal cyst, Sclerosing cholangitis, Caroli disease, ‘Metabolic (Tyrosinemia, Wolman disease, Nieman pick disease, Galactosemia, Fructosemia). 90. Ans.is‘d’ic., Hemolytic jaundice [Ref Chatterje Shinde 4%/cp. 593; Chandrasoma 34/e p. 635] ‘¢ Important clues provided in question are ~ 1) Increased total bilirubin 2) Normal conjugated bilirubin «« Amongst the given options, only hemolytic jaundice causes increased unconjugated bilirubin. 4 Remaining three cause conjugated hyperblirubinemia, 91. Ansis‘c’ ice, PNH [Ref Read below] ‘© Causes of Jaundice since birth are:- 4) Rhincompatibilty(erythroblastossfetalis) ABO incompatibility ‘Congenital infections (TORCH) iw) Sepsis ¥y) Concealed hemorrhage vi) Red cell membrane defect (hereditary spherocytosis) vii) Red cell enzyme defect (GEPD deficiency) «© So, option a & d can cause jaundice since birth. {In sicke cell anemia, affected infants do not develop symptoms inthe frst few months of life because the hemoglebin produced by the developing fetus (fetal hemoglobin) protects the red blood celisfrom sickling This fetal hemoglobin disappears after 5 month of age so that by 5 months of age, the sickling of the red blood cll is prominent and symp } 50, unconjugated bilirubin toms begin. ‘© PNH is manfested in adults. «So, both PNH and sickle cell anemia does not cause jaundice since birth, 4 But among these two I would prefer PNH as the answer because itis manifested in adulthood while the patient in ‘question is a 5-years old child. «Sickle cell anemia symptoms develop at the age of 5 months and its one of the cause of jaundice (en.wikipedia.org); | ms REC SY 92. Ans. is‘a'ie., Exythroblastosis [Ref Nelson 18%/e p. 758] ‘© Erythroblastosis fetalis (due to Rh incompatibility) is the most common cause of jaundice pr 24 hours of fe 93. Ans. is‘b’ie., Rh incompatibility [Ref See above explanation] ‘* Jaundice of Rh incompatibility appears at birth or within 24 hours. 94. Ans. is‘b' ie, Congenital cholangiopathy (Ref: 0.P. Ghai 8*/ p. 172 & 7*/e . 1491 ‘This child has unconjugated hyperbilirubinemia, while congenital cholangiopathy causes hyperbitirubinemia resenting at birth or within conjugated CONGENITAL HYPERBILIRUBINEMIA 95. Ans. isd’ ie., Novobiocin therapy [Ref Robbins 7 p. 887, 888] Physiological jaundice ofnewborn Decreased UGT activity CiiglerNaliar syndrome Genetic deficiency ofbirubin UST activity ; el wna eae Abe vor ees mminant / Decreased UGT activity 96. Ans. is ‘a! i.e. Mild conjugated hyperbilirubinemia [Ref: Robbin’ 7%/ep. 888; Harrison 174/e p. 1929] «© Gilbert syndrome isa type of congenital unconjugated hyperbilirubinemia. # Itis autosomal dominant. ¢ Hepatic biochemical tests are normal « There is normal hepatic histology, but in some patients increased lipofuscin pigment may occur. # There is mild increase in unconjugated bilirubin. 97. Ans.is ‘die, All of above [Ref Nelson 18%e ch. 354] ‘In Gilbert syndrome there is unconjugated (indirect) hyperbiirubinemia due to decreased activity of UDPG transferase. ‘¢ Usually no treatment is required. But phenobarbitone can be used to reduce the evel of unconjugated bilirubin. 98. Ans. is‘b’ ie, Dominant trait [Ref Harrison 17%/e p, 1928] ‘Inheritance ‘Autosomal recessive ‘Autosomal dominant © UverHistology Normal si TE Normal et UDPG transferase ‘Absent RSET eee Hemolss ipgecis Absent Sr Ta | 99. Ans. is‘s’ie., Rotor sydrome «# 50% direct bilirubin means conjugated hyperbilirubinemia, ‘ Normally the direct (conjugated) bilirubin is less than 15-20% of total bilirubin, “oan Cao SteCuarrer 3 Newborn Infant, ‘So, this child has - {Conjugated hyperbiliubinemia ii) Other LFTs normal ‘ Amongst the given options, Rotor syndrome and Primary biliary cirrhosis cause conjugated hyperblirubinemia. ¢ In Primary biliary circhoss, other LFTS are also abnormal, eg, SGOT and SGPT ae rised. + Now we are lft with Rotor syndrome which causes conjugated hyperbilirubinemia, Other LFTS are normal. 100. Ans. is‘ ie., Crigher-Najjar syndrome [Ref Nelson 18% p. 2084; Ghai 7/e p. 320] 101. Ans. is‘a’i.¢., Rotor syndrome {Ref Nelson 174 Chap. 352] 102. Ans. is‘ ie, All of above [Ref Ghai 7%ep. 304] ‘Mildly levated bilirubin especially indirect and normal liver enzyme seen in hemolytic anemia, 1 In above question all causes hemolytic ane KERNICTERUS 103. Ans. is‘a’i.e., No long term effect &'b’ie., Occurs with bilirubin more than 25 mg % [Ref: Read below] «© Long term survivors demonstrate choreoathetoid cerebral palsy, upward gaze palsy, sensorineural hearing loss and ‘mental retardation. ‘¢ Kernicterus occurs when bilirubin level is > 20 mg/dl or > 20 mg %. “Itis generally believed that unconjugated bilirubin level of more than 20 mg/dl may lead to kernicterus ——Clinical pediatrics “Risk of kernicterus increases with bilirubin levels more than 20 mg/dl and this became the conventional cut-off point for therapeutic intervention in term neonates” —— Pediatric essentials ‘* Unconjugated bilirubin causes toxicity to basal ganglion and various brainstem nucle ‘© Opisthotonus is seen in phase Il of kernicterus. 104. Ans. is‘ Le., Sulfonamides (Refi KDT 5*/e p. 644; Goodman Gilman 10*/ep. 1176] 105. 106, Ans. is © ie., High levels of conjugated bilirubin may cause Kernincterus (Ref: O.P. Ghai 8*e p. 17 The administration of sulfonamides to newborn infants, especially if premature, may lead tothe displacement of Bilirubin from plasma albumin. In newborn infants, free Bilrabin can become deposited inthe basal ganglia and subthalamic nuclei of the brain, causing an encephalopathy called kernicterus. Sulfonamides should not be g to pregnant women near term because these drugs pass through the placenta and are secreted in milk Kernicterus is due to unconjugated hyperbilirubinemia, ‘Ans. isa Le., Hypotonia [Ref Ghai 6%ep. 172] ‘¢ Hypotonia is an early feature (in Phas I). ie 7¥ep. 147) «© Kernincterus is caused by high levels ofun-conjugated bilirubin. TREATMENT OF HYPERBILIRUBINEMIA 107, Ans, is‘? Le., Barbiturate [Ref O.P. Ghai 6*/ep. 172, 173 & 7% p. 150] Barbiturates (Phenobarbitone) ‘tis effective only if given to mother before delivery. 1 itacts by inducing the conjugation of bilirubin -> Phenobarbitone isan enzyme inducer 108. Ans. is ’ ie., Structural isomerization [Ref: Manual of Neonatal Care 5*/e p. 208) 109, «e “Structural isomerization is the intramolecular cyclization of bilirubin to lumirubin. It is the most important pathway forthe lowering of serum bilirubin level"- Manual of Neonatal Care Se, p 208 ‘Ans. is ‘aie, Phototherapy [ Ref: O.P. Ghai 8 p. 175 & 6¥ep. 173] Bronze baby syndrom ee refers to dark grayish brown discoloration ofthe skin in infants undergoing phototherapy. Almost all infants ob served with this syndrome have hada mixed type ofhyperbilrubinemia with significant elevation of direct reacting bilirubin and often with othe evidence of obstructive liver diseaseES 110. Ans. is ‘a’ ie, 20mg% [Ref CPDT 184/e Figure (1-3); Nelson 18%/¢ P- 764) + (i) 2 15 mg/dl in 24-48 brs. aft «In full term newborn phototherapy is indicated when total serum bilirubin level's: (V8 1 at birth i) > 18 mg/dl in 48-72 hrs. afer birth; and (i) > 20 mera ae erates 111, Ans.is ‘a’ ie., Exchange transfusion [Ref O.P. Ghai 8*/ep. 175-176 7/EP TO hcg ge (0 3h we andsordng weigh (1000 graben oft newborn (13 Mor my dl) is an indication of exchange transfusion. 112, Ans. is a’ ie., Total and direct bilirubin [Ref Nelson 18*/¢ p. 758] 1 Measurement of total and direct bilirubin wil make savallable with ll he three parameters Le direc, indirect, toa bilirubin levels These wil help to asi jaundice ito its respective type and ain diagnosis. NEONATAL HYPOGLYCEMIA 113. Ans. is‘ Le, 12.5% dextrose infusion through peripheral line because of risk of thrombophlebitis, (Prefer central line) 118, Ans.is‘¢’ ie. History of Unconsciousness + Neonates are susceptible for developing hypoglycemia during the first 2-4 hours of life. «Ifthe breast-feeding is not started within ¥% an hour of birth about 10% of normal neonates are likely to develop hypoglycemia «This hypoelyemia coz herby tating eat feding or by administering glucose, . Saaee Ce ‘mother is prone for hypoglycemia —> glucose solution is given if the child develops symptoms of + Ina child wit history of hypoglycemia, glucose administration is indicated if the symptoms of hypoglycemia recut NEONATES DIABETIC MOTHER. 119. Ans. is‘V ie. Hyperglycemia [Ref OF Ghai 8p. 181 & 7p, 156, Nein Pedatics 17 p. 613-614 4 At birth the separation of placenta suddenly interrupts glucose infusion into the neonate with tonal effect on the hyperinsulinism, causing. te without a propor = Hyoglycemia -> which is nonketotic = Decreased lipolysis # In addition these infants have following abnormalities: 1 iyperbirbinemia 1 Transient tachyapnea of the newbort rin vthenia 1 Higher incidence of respiratory distr cre foes ess syndrome : oa * Asymmetric septal hypertrophyue. Ans is Le, Cada Repreaon 6 Read below] diab Ean foe n Gouda! raion ome ae the mot pil sen ness of maternal (Caudal regression: * eonasiestion syndrome (CRS) is araremaformative syndrome seen mainly incase of maternal dabetes wth 121. Ans. is ‘a’ Le., Hypoglycemia «Bc dtc nding hypyoma nd ypc commen in siton iin otal moter andy a ee : ‘# Sorry friends, I could not find any reference which has directly mentioned that hypoglycemia is a more common cause Soap ee “iota he ea So hema iheu ead eae. - ln ets mae vee i eater cere ee a ae =e MISCELLANEOUS. 122. Ans.is‘’ ie, All of above [Ref NNF manual] Kangaroo mother care (KMC) # Special way for LBW body 1 Benefit 1) Eftective Temperature control 5) Weight gain 2). Breast feeding ©) Apnea decreases 3) Infection control 7). Mother satisfaction 4). Parental bonding = Component 1). Skin to skin contact 2) Exclusive breast feeding ‘The KMC procedure «The baby should be placed between the mother’s breasts in an upright postion. 1 The head should be turned to one sie and in a sightly upturned postion. This position helps in breathing of ana allows eye-to-eye contact between the mother and her baby. 18 The legs and arms should be folded. 18 Baby’ abdomen should be atthe level of the mother’s upper abdomen. 1 Support the baby bottom with asing/binder. 123, Ans.is‘? ie., 10 weeks [Ref: Abdominal Wall Hernias: Principles and management by Robert Bendavi. 594) ‘During development the intestinal oops lie outside the abdominal cavity in the umbilical cord called the physiological ‘umbilical hernia. «# The loops go back into the abdominal cavity by 10% week of gestation. 124. Ans. is W i.e, 125 mg/dl [Ref Indian Pediatrics 2008; 45:29-38] ‘¢ No established definition of neonatal hyperglycemia and upper safe limit of blood glucose has been determined 1 Various researches has suggested Whole blood glucose > 125 mg/dl Plasma glucose > 150 mg/dl 125. Ans. is ‘a’ Le., Morphine [Ref': Avery’s disease of newborn 8%/e p. 442] ‘¢ Morphine and other opioids can cause neonatal respiratory depression.ee 126. Ansis‘a! Le, Opioids [Ref Cloherty Yep. 720,737; Auer’ disease ofthe newborn Sep 412 127. Ans.is'e he, Seizure [Ref: OF Ghat 8/e p. 167 <7 pl Neon 18%/p. 718: CPDT 18%E. 2) Clinical features of hypoxic ischemic encephalopathy «Encephalopathy progess overtime - 1) Bt fo 13 hoe Det lee of conus por toe decease spin breathing or apnea, seizures 2) 12-24 hours > More seisuers,Apnec pels, jteriness, weakness \eous movement, periodic 3) After 24 hours > Hypotonia, 4 conciousness, poor feeding, brainstem signs (oculomotor) and pupillary disturbances, 128. Ans. is ‘b’ i.e., Differential hypotonia (lower limbs > upper limbs) (Ref. 0.P. Ghai 8*e p. 166, 167 & 7 ‘fe p. 139-140; Nelson 184e p. 718] ‘During asphyxia the infant may remain hypotonic or change fo " ‘may appear normal. These changes are seen simultaneously and the change in muscle tone is also of the both the Hibs 1m: hypotonia to extreme hypertonia or their tone same degree in 129, Ans.is‘d’ ic. State 6 [Ref: Brazelton TB. The Neonatal intensive care unit network neurobehavioral scales procedures. Pediatrics 2004; 113:641-67] «© Crying lstily with all limbs moving (child in question), straight away goes in state 6, 130. Ans. is“b’ie., 25 cm of H,O [Ref Textbook of paediatric emergency medicine - Peter Cameron, George Jelinek, Ian Everitt p. 48: Obstetrics: Normal and problem pregnancies by Steven G.Gabbe, Jennifer R. Niebyl p. 486 | ‘* Higher inflation pressure of about 25 to 40 cms of H,O and higher inflation time > 1.5 sec. may be required for first several breaths (=8) + The volume of first breath is between 30-67 ml « Residual volume after first breath: 4-30 ml (average: 16-20 ml). + By around 30 minutes most neonate achieve normal FRC. 131, Ansis‘s'ie., Pyloric stenosis [Refi Neonatology by Meharban Singh p. 108] «© Alarge number of normal babies vomit on frst day due to iritation of stomach by swallowed amniotic fluid ‘© The regurgitation / vomiting in a neonate is due to ~ faulty feeding techniques or, aerophagy «© Eosophageal atresia may present with vomiting on the frst day. « In hypertrophic pylori stenosis vomiting characterstcaly occurs after 2 weeks of age. (2-3 weeks), 132, Ans. is di. Impedence technique [Ref: Care of the newborn by Meharban singh 6% p, 30, 280) + The respiratory monitor based on impednace technique measures changes inthe electrical resistance duting beat ‘The electrode is fixed on the chest wall pick up signals which ae displayed as respiratory rte + Capnography - It isa simple noninvasive method toassess arterial CO, «¢ Itis used to assess the placement of ET tube in esophagus or trachea, 133. Ans. is ‘b’ie., Toxoplasmosis [Refi Moffet’s 4¥/e p. 463] ¢ This question is straight forward spiramycin isin pregnaney is given for toxoplasmos Tgondii may infect the brain and retina of the fetus and can cause chorioretineis ne ‘and hydrocephalus. ‘© Cerebral calcification and hydrocephalus may also occur with congenital CMY not given for these infections, Prenatally acquired tinitis, intracerebral calcifications and HSV infection, but spiramycinis 134, Ansis‘b’ Le, Toxoplasmosis [Ref Williams 23%%ep. 53] 135, Ans. is‘c’ Le. < 38D for age and sex [Ref Nelson 194%e p. 2007] # bicroephaly i defined asa ead circumference that measures more han thee stand oe lard deviation thetows the mea136. Ans. is © i.e., Congenital varicella syndrome (Ref Nelson 18% p. 70] Causes of Hydrops fetalis “immune “© Rhincompatabity Nom-immune © Anemia thalassemia, GPO deficiency * Cardiacdysarhythmias Supraventricular tachycardia, AF, congenital heart block ‘+ Structual cardiac de- Ticuspidinsuficiency, ednocardial cushion defect. cardlomyopathy,hypoplastcleftheart, a remature closure of foramen ovale © Vascular Chorangloma of placenta, Twin-Twin transfusion, umblical artery aneurysm, thrombosis, ‘of renal or umblical vein or VC © Lymphatic Lymphangiectaia, cystic hygroma, Noonan syndrome (2 Ns Encephalocele, intracranial hemorrhage © Thorasic ‘Mediastnal teratoma, diaphragmatichernia © Teratomas CChoriocarcinoma,sacrococcygeal teratoma © Tumor & storage dis- Neuroblastoma, hepatoblastoma, Gaucher disease, eases t Niemann Pick disease, Mucopolysaccharidosis '* Chromosomal Tisomy 13,15, 16, 18,21 © Bone diseases Osteogenesis imperfecta, skeletal dysplasias “© Congenital infections CMV, rubella Toxoplasmosis Syphilis, Parvovirus, Leptospirosis, chaga’s disease Others Congenital nephrosis, Myotonic dystrophy, Infant of diabetic mother, Maternal therapy with indomethacin, Hepatic fibrosis 137, Ans. is‘C i.e Large proportionate body [Ref Nelson 18%e p. 781] «© Characterististics of fetal alcohol syndrome include :- 1) TUGR (not large proportionate body) 4) Mental retardation 2) Microcephaly 5) Minor joint anomalies 3) Congenital heart defects (ASD, VSD) 6) Hyperkinetic movements 2). Facial abnormalities —» Short palpebral fissures, epicanthal folds, maxillary hypoplasia, micrognathia, low set cars, smooth philthrum, thin smooth upper lip. 138, Ans. is‘c>d’ Le., Apt test > Klethauer Betke test [Ref: Perinatal transfusion medicine 2/e p. 218] Source of sample _ Maternal or neonatal qi ‘e Both Apt test and KB test are used to differentiate maternal blood from fetal blood, So, two options are corre. ‘J However, we have to choose one option and according to me Apt test is best here because Apt testis used specifealy for differentiating maternal and fetal blood while KB testis used to quantify fetomaternal hemorthage 139, Ans. is ‘a’ ie., Large size baby 1s Macrosomia refers to newborn with excessive weight, ie. large for date, Causes are maternal diabetes and maternal obesity ANSWERS OF VARIOUS OTHER EXAMINATIONS 140, Ans. is‘c’ ie, 28 weeks [Refi Meharban Singh 3/ep. 71}141. 142, 143. 144 145. 146. 147. 148, 149. 150. 151. 152. 153, 154. 155. Ans. isa! Le., Loss of weight [Ref Nelson 18*/e p. 220, 2210] ‘* An infant should gain weight progressively, except forthe first few days of life oe « Liver, spleen and kidney may be palpable in normal newborn. ‘# Sometimes trachea may be deviated from midline without any significance. Ans. isa’ Le., Autonomic dysfunction [Refi Nelson 18%/e p. 2262] «© Ifreflects an imbalance in the autonomic vascular regulatory mechanism. Ans. is'b' ie, 30-40 breaths/minute [Ref: OP Ghai 6/e p. 145 & 7*/ep- 108] (¢ Heart ratein neonate 5 120-140 per minute. eRespirstoryrate 35 to40 per minute. Ans. is ‘a! .e., 120-160/min [Ref: O.P. Ghai 6*/e p. 145 & 7*/e p. 108] Ans. is ‘b’ i., Birth weight below 10 percentile [Ref: Internet] ‘# Microsomia means smal for date baby, i. newborn baby with a birth weight less Ans. is‘a'Le., Erythematous papular pustular lesions [Ref: Dutta 6*/e p. 446: Gupte S. 8*/e p. 522] ‘Common newborn rashes ‘¢ Erythema toxicum —> Most common ‘* Acne neonatorum ‘Transient neonatal postural melanosis. Ans. is b’ Le, Diabetes [Refi Has been explained] «© Maternal diabetes predisposes to HMD. Ans. is b Le. Meconium aspiration ‘# Most common cause of respiratory distress in aterm or post-term neonate -> Meconium aspiration. ‘ Most common cause of respiratory distress in a preterm infant -> hyaline membrane disease. Ans. is’ Le., 5-7 weeks [Ref O.P. Ghai 8%/ep. 141 & 7/e p. 112; Nelson 18*/e p. 714) 4 It disappears between 2 week to 3 months. ‘Ans. is‘¢’ Le., Onset of respiratory distress is immediately after birth and it rarely lasts beyond 48 hrs [Ref O.P. Ghai 84/e p. 171 & 7*/ep. 146] Ans. is ‘a ie, Cerebral palsy &‘b’ Le., Hypoxic Ischemic encephalopathy [Refi Internet) ‘¢ Normal posture of full term neonate s flexor posture, « Extensor posture may be seen when there is brain damage as in hypoxia -> hypoxic ischemic encephalopathy and cerebral palsy Ans. is ‘a! Le., Transient tachypnea of newborn [Refi O.P. Ghai 84/e p. 171 & 7/e p, 146] «Respiratory distress, which resolves within 24 hours without any respiratory su i : fon chest X-ray suggest the diagnosis of TTN. Peon aoe feed fo ebb ee ‘Ans. is‘ Le., Any time during pregnancy (Ref: Read below] ‘Fetal growth is affected by maternal nutrition during any trimester in pregnancy. «Fetal growth isaffectd even by nutritional status of mother prior to pregnancy, ‘Ans. is B Le», Bacterial flora [Refi Has been explained] ‘¢ Meconium contains - 4) Intestinal epithelial cells i) Mucus Bae ii)Lanugo iv) Amniotic uid i) Water ‘Ans is ‘¢’ Le, Kangaroo Mother Care (KMC) [Ref O.P. Ghai 8% p. 145, 148 & >4/e n 10 c ‘Agrawal Ip. 104] BUMS, 148 & Ye p12, 158 KD “Preferably mothe shoul accompany and baby canbe transported in KMC peton Eve, transport if mother can not acompany. é than 10* percentile. father can provide KMIC dariet KN. Agniwel156. 157. 158, 159, 160, 161. 162. 163. 164. 165. 166. 167, Ans. is‘a' i.e, Cord blood hemoglobin i less than 10 g %;‘b’.e., Cord bilirubin is more than 5 mgs ‘© Le. History of previous sibling affected [Ref Nelson 18%/e p. 771] Indications of Exchange transfusion © Cordhemoglobin < 10g/dl, ‘Bilirubin protein ratio> 3.5. ¢ Prematurity *Cordbilirubin > Smgid ‘ Reticulocyte count > 15% * Previous kernicterus or severe erythroblastosis in a sibling ‘Ans. is‘¢ i.e, Cord bilirubin <5 mg/100 ml [Ref: Nelson 18*/e p. 771] Cord bilirubin 5 or more is an indication, Ans. is ‘bie, The total bilirubin concentration in the serum increases by 1 mg/dl per day [Ref: 0.P. Ghai 8%/e p. 172 & ep. 147; Nelson 174/e p. 594] © Rate of rises ess than Sighs Ans. is‘b’ Le., Rh Incompatibility [Ref: O.P. Ghai 8e p. 174 & 6*/e p. 172; Nelson 18*/e p. 758] Ans. is‘ Le., Begins between 2-7 days of life [Ref: Care of Newborn by Maherbansingh 6"/e p. 336; Nelson 18%ep. 773] Hemorrhagic disease of the newborn ‘ Early onset > 0-24hr ‘© Classical disease = > 2-7 days # Late onset > 46months ‘Ans. is‘ Le., Unconjugated bilirubin [Ref: Has been explained] Ans. is ‘Le. Stop breast feeding and review after 24 hours [Refi Cloherty 5*/e p. 187] «© Thisisa case of breast milk jaundice. «© Temporary interruption of breast milk feeds will dramatically reduce the serum levels of bilirubin and there may be slight increase in bilirubin when breastfeeding is resumed, but it never reaches the previous levels. ‘Ans. is‘? L., Measurment of. - fetoprotein [Ref: Nelson 18%/e p. 695] ‘Ans. is © Le., 60 [Ref: O.P. Ghai 8%/e p. 381 & 6%/e p. 352] Tachypnea © <2 months + 6Oormore RR/min © 2-12 months + 500r more RR/min 12-60 months > 49ormore RR/min ‘Ans. is ‘Le. 3 hours [Ref: Nelson 184/e p. 655] ‘© Blood glucose reaches its nadi in initial 2-3 hrs. of life ‘Ans. sb’ Le,, Lower areola more visible [Ref O.P. Ghai 8%/e . 154 & 7%ep. 126] Signs of good attachement of baby’s mouth to nipple 1. The baby’s mouth is wide open 2. Most of the nipple and areola in the mouth, only upper areola visible, not the lower one. 3. The baby's chin touches the breast. 4. The baby’s lower lip is elevated. ‘Ans. is ‘b’ Le. Bacteriuria [Ref O.P. Ghai 8*/e p. 468 &- 6 p. 443; Smith General Urology 17*/e p. 49}