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Tips for doing well in neonatology section of
Pediatric BoardsShantanu Rastogi, MD, FAAP
Neonatologist, Maimonides Medical Center
Assistant Professor of Pediatrics
Mount Sinai School of Medicine
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Some general points
• There are no negative markings and hence no questions SHOULD be left unanswered
• When the answers are not clear in the first reading then try the method of exclusion to get to the best possible answer
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Rastogi’s Rule
• Common presentations of common diseases
• Rare presentations of common diseases
• Common presentations of rare diseases
• Rare presentations of rare diseases
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FETAL WELL BEING
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Biophysical profile
• 5 categories with score of 0 or 2
• NST, fetal body movements, breathing, fetal tone, amniotic fluid volume
• 10 is well fetus, 2 is certain fetal asphyxia, 4 or 6 needs frequent reevaluation for delivery
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Electronic Fetal Heart Rate Monitoring
• Normal – FHRv of 6-15bpm, basis of nonstress test-reactive positive test is normal
• Abnormal patterns– Tachycardia, >160, infection– Bradycardia, <110, head compression– Loss of FHRv, hypoxia– Decelerations
• Early, mirror image of uterine contractions, head compression• Variable, irregular, umbilical cord compression• Late , occur 10sec after uterine contraction and last longer,
uterine placental insufficiency
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RESUSCITATION
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Resuscitation-recent changes• No intrapartum meconium suctioning• Oxygen use
– Can use <100% but if no improvement in saturations, increase to 100%
– If <32w to use pulse oximeter keeping saturations between 90-95%
• Epinephrine IV is preferred but if using ET use x10 dose
• Special use of laryngeal mask, CO2 monitor, and careful temp. control-use of clear plastic bags
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Case
• 28 w baby is delivered vaginally has HR of 90/m and irregular respiration, cyanosis, hypotonia with no reflexes
• WHAT IS THE APGAR SCORE?
• WHAT IS THE FIRST STEP?
• WHAT IS THE SUBSEQUENT STEP?
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Case continued
• After 1 min of IPPV the HR is 60/m
• WHAT IS THE NEXT STEP?
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INFECTIONS
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GBS• The total number of cases of sepsis has gone
down due to the decrease in GBS sepsis, but that from gram negative remain the same
• CDC guideline-recent changes– To screen all women at 35-37 wks of gestation– If GBS positive prior preg. does not mean it is positive in
present pregnancy unless there was invasive neonatal infection
– No prophylaxis required for elective c-section if GBS positive and with no ROM/labor
– Adequate prophylaxis is by completion of 2 doses of penicillin
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GBS• Risk Factors:
– Intrapartum Prophylaxis to mother -if GBS positive OR unknown with <35 weeks GA, ROM 18h, maternal fever 100.4F OR GBS bacteriuria OR previous invasive neonatal GBS
– Rx to baby-Symptomatic OR if mother for IP and baby less than 35 wks/ROM >18h/duration of IP less than 4h.
• Clinical presentation– Early-<7DOL, pneumonia>sepsis>CNS, ascending
infection– Late onset->7DOL, less mortality but more CNS
involvement and sequelae, deep infection as cellulitis, arthritis, osteomyelitis
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Other bacterial infections
• E.coli/Klebsiella sp. Absolute numbers have not decreased and hence the proportion of the neonatal sepsis cases from these organism have increased. Typically progress thru 3 stages of shock
• Listeria- gram + rod, in unpasteurized milk, cheese, raw vegetables and uncooked meat– Early onset: <7d, transplacental, chocolate colored
amniotic fluid, preterm deliveries, sepsis/pneumonia– Late onset: >7d, nosocomial, meningitis with
mononuclear cells
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Other congenital infections
Clinical presentation
CMV Rubella Toxoplasmosis
LBW +++ ++ +
Liver/Spleen ++++ ++ +
Jaundice +++ + ++
Petechiae +++ ++ +
CHD + +++
Cataract +++ +
Retinopathy + +++
Cerebral calcification
Periventricular+ cortical++
Microcephaly ++ +
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Hepatitis B positive mother
Mat. status
Newborn >2kg Newborn <2kg
HBV HBIG HBV HBIG
+ 3 doses, 1st<12h
1 dose, <12h
4doses, 1st<12h
1dose, <12h
unknown 3 doses, 1st<12h
1 dose, <7d
4doses, 1st<12h
1dose, <12h
_ 3 doses, 1st at1-2M
None 3 doses, 1st at1-2M
None
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Congenital Syphilis
Mother Baby Mother Baby
- - - - No or prozone
+ + - - False+
+ +/- + + Mother/B disease
- - + + Treated disease
VDRL InferenceFTA
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Conjunctivitis
• Onset will give the clue– Hours-chemical-silver nitrate– Day 2-5-Nisseria gonorrheae-purulent,
emergency, needs IV antibiotics– Day 5-14-Chlamydia-bilateral, cough
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CHROMOSOMAL ABN.
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Trisomy 21
• Recurrence risk- If no translocation- 1% risk till mat.age of 37y, if mat. translocation-10-15%, if pat. translocation-5%
• Types- 94% non-disjunction,3-5% translocation, 2% mosaic. Commonest cause in both old and young mothers is non-disjunction
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Trisomy 21
• Defects– Cardiac (40-50%)-Endocardial cushion defect,
VSD– Extremities-single palmer crease, 5th finger has
hypoplastic middle phalange and clinodactyly– Face-slanting palpebral fissure, Brushfield spots,
epicanthic folds, short neck, flat occiput– GI- duedenal atresia, Hirschsprung Disease– Neurology- hypotonia, MR, – Other –hypothyroidism, leukemia, hip dysplasia
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Other chromosomal anomalies
• Trisomy 13 (Patau-MIDLINE deformities)– Holoprosencephaly,cleft lip/palate,coloboma,
sloping forehead, cutis aplasia, VSD, polydactyly, hyperconvex nails, persistence of fetal Hb
• Trisomy 18 (Edward)– Cardiac (common, VSD, PDA, PS),clenched hand,
overlap of 2nd over 3rd and 5th over 4th finger, rocker bottom feet, small mouth/eyes/palpebral fissures, short sternum, hernia, cryptorchidism
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PULMONARY
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Case• 28 wk preterm baby was delivered and intubated
and placed on settings of RR 40, PIP of 25, PEEP of 5 and O2 of 100%. Decision was made to give surfactant.
• WHAT IS THE NEXT EXPECTED CHANGE IN THE VENT.SETTINGS?
• If surfactant was not given as the O2 requirement decreased to 50% and was clinically observed.
• WHAT CHANGE WILL NEED TO BE FOLLOWED FOR PREDICTING IMPROVEMENT?
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RDS-Surfactant Def.• Clinical course: Peak-1 to 3 d and recovery starts with
diuresis• Risk Factors: Low GA, male, Mat. DM, perinatal depression• RDS in term: SPB def, Mat. DM, Beckwith Weideman
syndrome, congenital syphilis• Pathology: Hyaline membrane (cellular debris in fibrinous
matrix)• Treatment-surfactant replacement, fluid/electrolyte and
respiratory management• Complications: pneumothorax as sudden decompensation • DD for reticulogranular CXR- GBS pneumonia, PAPVR
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Congenital malformations
• CCAM– cyst of lung tissue with small communication with
bronchial tree, blood supply from pulm. circulation– Can present IU (hydrops, polyhydramnios, pulm.
hypoplasia) or neonatal ( resp. distress) – 3 types
• I - large cyst, good prognosis • II- medium size cyst, 50% associated anomalies,
prognosis ??• III- large lesion with multiple small cyst, usually present
IU, poor prognosis
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Congenital malformations• Congenital emphysema
– Commonest lesion, commonest in left upper lobe– Over distention of lobe due to loss of cartilage in large
airways– Variable clinical usually mild respiratory distress
• Sequestered lung– Non functioning lung tissue with systemic b.s.– 2 types:
• Intralobar - mostly left lower, few other anomalies• Extralobar - mostly between LL and diaphragm, many associated
anomalies
– Often asymptomatic, rarely can present in utero
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Case
• FT BB delivered by stat c/s for bradycardia required resuscitation by IPPV. Improved but soon developed progressive respiratory distress and poor perfusion. ABG showed 7.1/72/42/-5/18 on 100% oxygen.
• WHAT IS THE PROBABLE CAUSE?• WHAT NEEDS TO BE DONE NOW?
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Air leak syndromes• Pneumothorax
– Air between parietal and visceral pleura– Risk Factors-Aspiration synd.,lung diseases (RDS,
MAS), ventilation (high PIP)– Presentation can be with tension (severe RD,
bradycardia, apnea, hypotension with mediastinal shift), large leak or small leak.
– Complication: IVH by dec. venous return, SIADH– Diagnosis: asymmetrical air entry, transillumination– Rx: EMERGENCY if tension-needle aspiration
followed by chest tube, supportive
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Airleak Syndromes• Pneumopericardium- air in pericardial sac
– Usually associated with other airleak syndromes– If large- muffled HS, venous congestion, decreased CO– Rx if symptomatic-pericardial aspiration, high mortality
• Pneumomediastinum- air in mediastinum– Usually after IPPV or difficult intubation, high PIP– Muffled heart sounds, CXR-sail sign– Usually need supportive treatment
• Pulmonary Interstitial Emphysema-air in interstitial space– Usually preterm with RDS and on ventilation– Rx: decrease MAP, if unilateral-selective intubation/blocking of
bronchus
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Chronic lung disease Vs BPD
• BPD- 36 w of GA with oxygen requirement• Mechanical trauma to susceptible lungs (preterm
lungs) leading to inflammation, injury is increased with decreased antiproteases and antioxidants in the preterm
• Poor compliance, increased WOB, pulmonary hypertension, RVH
• Radiographic classification I to IV• Rx- nonspecific as supportive care, good nutrition
(120-150cal/kg/day), diuretics, bronchodilators, steroids
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Apnea
• Cessation of air flow for >20s with cyanosis/bradycardia
• Types: Central (no effort, no air flow), Obstructive (no airflow despite effort), Mixed
• Cause: prematurity (usually after 12h of life), infection, maternal med.(narcotics, magnesium), infant med.(Indomethacin), CNS disorders (IVH)
• Treatment: Treat underlying disease, methylxanthines (caffeine) , CPAP, ventilation
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Transient Tachypnea of Newborn
• It is a diagnosis of exclusion
• Cause: delayed clearing of lung fluid
• Risk factors: elective c/s, maternal DM, perinatal depression, precipitous delivery
• Usually resolves 2-3 days
• Treatment: oxygen/ CPAP
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Meconium aspiration syndrome
• Definition: MSAF+RD+CXR changes• Clinical: usually post-term, severe respiratory
distress• Complications:pulmonary hypertension, airleak
syndromes• CXR:snow storm appearance• Prevention: ??intrapartum suction of meconium• Rx: respiratory support, correcting acidosis,
antibiotics, surfactant
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Case
• FT AGA BB was delivered to mother with GDMA2 not well controlled. AS were 8,9 developed respiratory distress with cyanosis within few hours of being in the WBN. Vitals are stable with tachypnea associated with saturation of 70 in the right hand and 45 in the left leg. CXR shows lungs with decreased blood flow.
• HOW TO CONFIRM THE DIAGNOSIS?• WHAT IS THE DRUG OF CHOICE?HOW IS ITS
TOXICITY MONITORED?
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Pulmonary Hypertension
• Cause– Maladaptation- normal vasculature but
vasoconstriction (hypoxia, hypothermia, polycythemia, pneumonia)
– Maldevelopment-abnormal structure of pulmonary vascular bed (chronic intrauterine hypoxia, pulmonary hypoplasia)
• Rx- respiratory support (no hyperventilation), correcting acidosis, NO, ECMO
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Congenital diaphragmatic hernia
• Types-Posterolateral thru Foramen of Bochdalek (L>>R) and central thru Foramen of Morgagni
• In-utero as hydrops, after birth as RD due to lung hypoplasia, scaphoid abdomen
• Complications-related to lung hypoplasia and pulmonary hypertension (PH)
• Treatment strategy-IMMEDIATE intubation, stabilizing the PH and delayed surgical repair
• Usually delivered in ECMO centers as may be needed for treating PH
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Hypoplastic lungs (Potters sequence)
• Causes – Intrathoracic compression (CDH, CCAM)– Thoracic (neurological ds. as Werdnig Hoffman
syndrome)– Extrathoracic (common, causes of
oligohydramnios specially kidney diseases)
• Clinical- related to primary cause but usually present with severe respiratory distress
• Rx: respiratory support and treatment of the cause
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Neurological ds. causing RD
• Werdnig Hoffman- usually in neonatal period as hypoplastic lungs/hypoventilation
• Brachial plexus injury- with h/o shoulder dystocia and LGA, can be associated with Horner's Syndrome, chest fluoroscopy -eventration of the diaphragm
• Injury after cardiac surgery-recurrent laryngeal nerve injury mild distress with stridor, direct laryngoscopy will show ipsilateral vc in cadaveric position with no movement with crying.
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CARDIOLOGY
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Congenital Heart Disease-Some Facts
• Incidence 8/1000 live births (excluding PDA in PT newborns) with 25% with other associated abnormalities
• VSD- commonest CHD• TOF- commonest cyanotic HD beyond neonatal
period• TGA-commonest cyanotic HD in first week of life• HLHS- 2nd commonest cyanotic HD in first week
of life and commonest cause of cardiac mortality during that period
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Congenital cardiac disease
• When to suspect-murmur, cyanosis with minimal respiratory distress
• IMMEDIATE need for ECHO, consider starting PROSTAGLANDIN. 3-5% babies with PG have apnea- might require intubation
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Presentation of CCHD
• 5T’s, DO, ESP- TGA, TOF, TAPVR, Tricuspid atresia, Truncus arteriosus, DORV, Ebstein’s Anomaly, Single ventricle and Pulmonary atresia
• HLHS Vs sepsis: usually HLHS presents after the duct is closed by 48-72 h and baby presents with cardiac failure to the ER with no murmur. If no high risk factors for infection always consider the diagnosis of HLHS
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PDA• Normal course-physiological closure 12-15h ,
anatomic closure several months, about 4% of term, 10% of 30-37 wk and 50% of <30 wk do not close by 72 h and considered PDA
• S/S-– Term-asymptomatic, machinery murmur, if large have
bounding pulse, CHF– Preterm can also have decreased bf to the gut-NEC,
Pulmonary h’age. and prolonged intubation
• Treatment-Fluid restriction, maintaining hematocrit, ibuprofen (indomethacin), surgical correction
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Maternal conditions and CHD
• Maternal drugs– Aspirin/Indomethacin-PH/PDA closure,
Lithium-Ebstein’s anomaly, Ethanol-VSD
• Maternal diseases– Lupus-Cong. Heart block (anti Ro, anti La
Ab), Diabetes (VSD-commonest, TGA, ventricular hypertrophy-most specific)
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NEUROLOGY
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SCaLP Injuries
• In SubCutaneous tissue- caput succedaneum, soft, crossed midline/sutures, usually with molding, resolves over several days
• Beneath Galea Aponeurotica in Loose areolar tissue- subgaleal, can move to neck and behind ear, can cause anemia, hypotension, jaundice, resolves in 2-4 wk
• SubPeriosteal- cephalhematoma, confined to suture lines, firm, 10% have skull fracture, jaundice, resolve in weeks to months
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Intraventricular Hemorrhage
• From where-germinal matrix, usually involutes by 34 wk
• Incidence increases with PT e.g. <1kg 30%, 1-1.25kg 15%, 1.25-1.5kg 8%
• Timing- 50% in 24h and 90% in 72h present as S/S of anemia + CNS involvement.
• Grading- I thru IV• Prognosis- Poor in grade III/ IV• Complication- hydrocephalous/PVL
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Periventricular Leukomalacia
• Where- periventricular white matter usually focal
• Risk factors-prematurity, hypotension, IVH• US shows bilateral periventricular
echodensities• Outcome usually as spastic diplegia with
associated cognitive and visual defects
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Birth Asphyxia• Definition
– pH <7, AS<3 at 5min, neurological sequelae (HIE), multiple organ dysfunction
• HIE staging ( Sarnat Stages)– Stage 1-usually hyperactive CNS with
sympathomimetic activity, 100% normal– Stage 2-decreased CNS activity, lost reflexes,
parasympathomimetic activity, seizures, 80% normal
– Stage 3- variable presentation, seizures rare, burst suppression EEG, 100% severe sequelae
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Cerebral palsy• Non progressive neurological deficit• Incidence:2-5/1000, increase with dec. GA• Clinicopathological correlation
– Selective neuronal necrosis-common after HIE, diffuse damage, Quadriplegia, MR, seizures
– Parasagittal cerebral injury-due to dec. perfusion, necrosis in watershed areas of carotids, weakness of proximal muscles U>L
– Focal or multifocal ischemia- usually in FT, meningitis, trauma, thrombotic syndromes, as hemiplegias, seizures, cognitive defects
– Status Marmoratus- kernicterus, HIE, basal ganglia, spasticity, choreoform movements
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Brachial plexus injury
Erb-Duchenne Klumpke
Roots C5-7 C8-T1
Incidence Common Rare
Typical S/S Waiters tip Ape hand
Differentiate Palmer grasp + -
Associated C4/5 (phrenic nerve), C7 (scapular winging)
T1( Horner’s syndrome)
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Neural Tube Defect
• Incidence: variable geographically, more with folic acid def., maternal diabetes, valproate intake
• Intrauterine diagnosis- inc. alpha fetoprotein and cholinesterase in amniotic fluid
• Prognosis-level of involvement e.g. no ambulation with cervical, thoracolumbar involvement and with sacral can ambulate without braces
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Hydrocephalous
• 2 types– Obstructive- common, commonest cause is post
hemorrhagic HC, others are aqueductal stenosis, Dandy-Walker Syndrome (cystic dilatation of 4th ventricle, 70% have other abnormalities), rarely masses
– Communicating-usually after bleeds, infections, NTD, Arnold Chiari malformation
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Case
• Mother is rushed in for stat c/s for abruption. Apgars are 2, 3, 8- improving after IPPV, chest compression and fluid resuscitation. Improves and admitted to NICU. Mother had uneventful antenatal course. Baby develops generalized tonic clonic seizures and bradycardia at 12h of life- controlled by phenobarb.
• WHAT IS THE CAUSE OF THE SEIZURES
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Siezures
• Types– Subtle-most frequent, oral, facial ocular activity, may
be associated with changes in HR, resp. BP and sats. – Multifocal clonic-one limb migrating to another– Focal clonic- may represent focal disease– Tonic-change in posture, more in preterm– Myoclonic
• Many causes- usual asphyxia, metabolic (Ca, glucose etc), infection, trauma, malformation
• Initial drug of choice is phenobarb
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METABOLIC/ENDOCRINE
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Inborn errors of metabolism• When to suspect: just about any S/S specially
if the initial usual diagnosis e.g. sepsis is not responding to the usual forms of treatment e.g.antibiotics.
• Specific smells– Sweaty feet-Isovaleric acidemia/Glutaric aciduria– Male cat urine-Glycinuria– Maple syrup odor-Branched chain aa(MSUD)– Musty odor-PKU
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Flow chart of IEM-with hyperammonemia
• Acidosis+ketonuria-MSUD, Lactic acidemia, glutaric aciduria, glycinuria
• Acidosis without ketonuria-Fatty acid oxidation problem• Without acidosis or ketonuria-urea cycle defects, check
citrulline– Very high-Argininosuccinic Acid (ASA) Synth. Def.– Absent- check urine orotic acid
• High-Ornithine transcarboxylase def.• Low/Normal-Carbamyl phosphatase synthetase def., N-acetyl glutamate
def.
– Normal or slight increase-check ASA• Present-AS acid lysase def• Absent-check arginine, if inc.-arginase def., if normal or low-transient
neonatal hyperammonemia
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Galactosemia• AR, galactokinase or Galactose-1-PO4ase
uridyltransferase def.• Presents when feeds are introduced as lethargy,
hepatomegaly, liver failure, renal tubular acidosis• Can have cataract at birth• Increased risk of infection specially E.coli• Lab-elevated LFT’s, galactose in urine (reducing
substance positive with negative glucose oxidase test )
• Rx- elimination of all galactose and lactose in diet
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PKU and Homocystinuria• Classic PKU-AR, def. of phenylalanine
hydroxylase, mousy or musty urine odor, severe MR and siezures if untreated, diagnosed by NBS, Rx by low phenylalanine diet
• Homocytinuria-AR, commonly by def. of cystathianine synthetase, usually asymptomatic in neonatal period, has downward dislocated lens (D/D Marfans), myopia, osteoporosis, scoliosis, arachnodactyly, dec.joint mobility (D\D Marfans), MR seizures, thrombotic episodes, Rx Dec. methionine, supplement cytiene, folate, pyridoxine
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Glycogen storage disease
• 8 types, 1,2 3 are common• Type1 –von Gierke, Glucose 6 PO4ase def.,
has lactic acidosis, hepatomegaly, diarrhoea, bleeding disorder, poor prognosis
• Type 2-Pompes, lysosomal glucosidase def., muscle weakness, cardiomegaly, CHF, poor prognosis
• Type 3- Forbes, low glucose, hepatomegaly, muscle fatigue, usually after neonatal period, good prognosis
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MPS and Lipidoses
• MPS- dysostosis multiplex, AlderRielly bodies in WBC and urine MPS– Hurler-iduronidase def., cloudy cornea, HSM, coarse
features, short stature, kyphosis– Hunters-iduronidase sulfatase def., Xlinked, only MPS with
retinal abn.
• Lipidoses– Gauchers-glucocerebrosidase def., Gaucher cell in bone
marrow, normal retina, type I-normal CNS, type II, profound CNS loss
– Niemann Pick-sphignomyelinase def., foam cells in bone marrow, Type A cherry red spot, profound CNS loss, Type B normal retina, normal CNS
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Temperature Regulation• Neonates more prone to heat loss as
– Dec. skin thickness-radiant+conductive loss– Dec. subcut. Fat– Dec. peripheral vasoconstriction leading to dec. heat
conservation– Immature autonomic nervous system– Increased BSA to wt.-radiant heat loss
• Convective Incubators-large radiant loss(dec by double wall)+ small evaporative loss(dec by inc. humidity) and small conductive heat loss (dec by rubber mattress)
• Radiant Warmer-large convective and evaporative loss, reduced by plastic sheet
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Hypothyroidism
• Commonest cause-thyroid dysgenesis• Early presentations-prolonged jaundice,
large post. fontanelle• Others-umbilical hernia, macroglossia,
hypotonia, goiter• Diagnosis- by newborn screening-low
T4 and high TSH • Rx-levothyroxine sodium
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Case
• Baby delivered after difficult vaginal delivery to a mother with gestational diabetes poorly controlled by insulin. Baby was 4300g and was send to WBN where he developed tachypnea with occasional jitteriness.
• WHAT IS THE D/D FOR TACHYPNEA IN THIS BABY?
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Hypoglycemia- IDM
• Commonest presentation of IDM and can primarily present as tachypnea (Other causes are RDS, TTN, CHD (VSD) , birth asphyxia birth trauma and hypocalcemia)
• Other common presentations are hypocalcemia, polycythemia and jaundice
• Specific malformations-Hypertrophic Obstructive Cardiomyopathy d/t asymmetrical ventricular septal hypertrophy and caudal agenesis syndrome
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Hypocalcemia
• Types– Early (till 72h) maternal causes (DM,
hyperparathyroidism), perinatal causes (prematurity, asphyxia, infections)
– Late (after 72h) hypoparathyroidism, hypomagnesemia, vitamin D def.
• S/S-If symptomatic as jitteriness, high pitched cry, Chvostek/Trousseau sign, siezures, prolonged QTc
• Rx- Underlying cause, Ca, Vit. D, low PO4
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Congenital Adrenal Hyperplasia
• Commonest cause-21 hydroxylase def. (followed by 11beta hydroxylase def.)
• S/S with 21OH-salt wasting in 2nd week with inc.K, dec.Na and hypotension with pseudohermaphroditism in females and males may have precocious puberty.
• Diagnosis-elevated 17OHP in amniotic fluid or serum
• Rx-Antenatal-maternal glucocorticoid, Postnatal-replacement of GC/MC
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HEMATOLOGY
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Cord compression
• Usually presents as variable decelerations
• Most common presentation is anemia due to mild to moderate compression compresses the umbilical vein leading to pooling of the blood in the placenta leading to anemia usually seen in CBC done 4-6h of life.
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Twin to twin transfusion(TTT)• Discordant twins: when the weight of the twins differ by
15-25%• One of the causes of DT is TTT• Usually TTT takes place in monochorionic, mono or di-
amniotic twins, mortality can be 50%• Donor twin is anemic and develops hypovolemia and
oligohydramnios• Recipient twin is polycythemic and may develop
hydrops• When donor dies- blood flows from recipient leading to
its demise soon after the donors hence need for STAT c/s
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Isoimmunization-Rhesus factor
• Decreased incidence due to use of Rhogam• Mother is Rh- i.e. dd (Rhesus An has 3
components C, D, E with D as the major component). Baby is Rh+ i.e.DD or Dd.
• Initial pregnancy usually induces IgM which do not cross placenta, but repeat exposure induces IgG which crosses placenta easily causing hemolysis of fetal RBC.
• Prevented by giving Rhogam to Rh-mother at 28 wk GA and at birth of Rh+ baby.
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Isoimmunization-ABO
• Incidence same in first or subsequent pregnancies
• Mothers with group A or B produce IgM antibodies and that of O produce IgG which easily crosses placenta
• Usually milder than Rh as the antigen is on all the tissues and they capture the antibodies transferred from the mother
• Usually indirect Coombs is positive• Has spherocytosis with B-O incomp.
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AAP guidelines for bili management
• To measure bilirubin in hours of life
• Aggressive phototherapy and specific follow up depending on the zone in the hourly bilirubin charts
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Phototherapy
• Mechanism of action– Photo-isomerization-configurational 4Z15Z to
4Z15E– Photo-isomerization-structural-lumibilirubin– Photo-oxidation
• Blue light- effective wavelength (710-780nm) and penetrates skin well.
• If phototherapy given to baby with high direct bilirubin -bronze baby syndrome
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Jaundice related to breast feeding Vs Breast feeding jaundice
• Jaundice related to BF– Usually exaggerated physiological jaundice due to
decreased intake
• BF jaundice– Prolonged with peak of 20-30mg/dl by 2 wk and
than normalize over 4-12 wk– Rapid decrease after cessation of breast feeding
and rises 2-4mg/dl after resuming BF– Can cause kernicterus
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Thrombocytopenia• Sick Vs Well baby• Commonest for well babies is Alloimmune and
Autoimmune, and for sick babies is sepsis/DIC• Autoimmune
– Transference of antiplatelet antibodies as that of lupus, ITP– Maternal and newborns platelets are low
• Alloimmune– Transplacental transference of maternal antibodies ( like
Rh disease), with normal maternal platelets– Severe, can have IC bleed, death in 20%
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Case
• BB delivered at home with precipitous delivery was admitted to WBN and discharged with mother. Was exclusively breast fed. Found to have fresh bleeding per rectum on DOL 4. There is no other site of bleeding or pertinent history. Clinical examination is normal.
• WHAT NEEDS TO BE DONE IMMEDIATELY?
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Hemorrhagic Disease of Newborn (Vit.K def.)
• Vitamin K needed for carboxylation reaction which activates the clotting factors
• Newborns are predisposed as have no bacterial flora intestine to produce Vit.K and also has liver immaturity
• Decreased placental transference if maternal intake of anticonvulsants, warfarin and ATT or when exclusively breast fed.
• Types:– Early-less than 24h, maternal drugs– Classic- 2-7days, exclusive breast feeding– Late-2w-6m, hepatobiliary disease, inc.ICT
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GASTROENTEROLOGY
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Esophageal atresia
• 30-40% with associated abnormalities specially as VACTERL
• 4 types-commonest upper end atresia and lower end with fistula to the trachea
• H type is rare but commonest one for the exams- S/S as cough during feeding and recurrent aspirations
• Rx-surgical-primary or delayed as in stages.
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Case
• Baby is delivered to mother with history of polyhydramnios. Mother had irregular antenatal care. Baby did not tolerate feeds and started to have non bilious vomiting. OG tube could be passed to the stomach. AXR was ordered.
• WHAT WOULD BE THE LIKELY AXR PICTURE
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Double bubble sign
• Associated with duodenal atresia
• High rate of association with trisomy 21, other malrotation and CHD.
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Case
• 24 week PT AGA BG has had relatively uneventful course in NICU. At 8 weeks of life when tolerating full feeds developed abdominal distention. Feeds were stopped and AXR showed pneumotosis intestinalis. Antibiotics were given and no surgical intervention was required. Baby recovered.
• WHAT IS THE COMMONEST SEQUALAE THAT NEEDS TO BE WATCHED FOR?
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Necrotising Enterocolitis
• 10% of those less than 1500g
• Predisposing factors-prematurity, feeds, infection
• AXR- pneumotosis intestinalis
• Outcome-high mortality, morbidity-small gut syndrome if surgery is done, strictures if medically treated
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Congenital Hyperplastic Pyloric Stenosis
• 3/1000 births, male x5
• Related to decreased NO production
• Hypochloremic, hypokalemic, metabolic alkalosis
• Barium-string sign, US-bull’s eye sign
• Rx-Pyloromyotomy
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Case
• 2D old FT Baby in WBN develops distention and has not passed meconium since birth. PMD orders an AXR which shows large dilated stacked loops with absence of air in the recto-sigmoid region.
• WHAT IS THE NEXT STEP?
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Case continued
• If it reveals gradual narrowing of the sigmoid
• WHAT IS THE LIKELY DIAGNOSIS AND HOW TO CONFIRM IT?
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Hirschsprung’s Disease
• 1:5000, usually male, 80% rectosig. only• Associated with trisomy 21• Failure of cranial to caudal migration of neural
crest cell-dec. parasymp. innervation• Diagnosis-XR, biopsy-absent ganglion cells• Complication-Acute bacterial colitis• Rx- single stage pull through or initial
colostomy followed by correction
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Meconium Plug vs. ileus vs. peritonitis
• Plug– benign variation of Hirschsprung’s disease– Delayed passage of meconium – Usually has small colon, IDM
• Ileus– 90% have CF– bilious vomiting, obstruction, AXR-bubbles in the intestinal lumen– enema successful in 60%
• Peritonitis– In utero perforation– Secondary to ileus, atresia, volvulus, gastroschisis– Usually seal spontaneously or can require surgery
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Omphalocele vs. Gastroschises
Omphaloc. Gastroch.
Incidence Common Rare
Chrom. Abn. Common Rare
Midline Yes No (usu.Rt)
Covering Yes No
Umb.cord Involved Normal
Assoc.Abn. More Less-intest.abn
M/M More Less
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DERMATOLOGY
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ERYTHEMA TOXICUM
• Most common 30-70%• Onset DOL 2-3• 1-3mm erythematous
macule/papule-pustule• Fades in 5-7 days• May reoccur• Benign, has eosinophils
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PUSTULAR MELANOSIS
• More in dark skinned• 3 stages-non-
inflammatory pustule, ruptured pustule with scale, hyperpigmented macule (up to 3m)
• Benign, has neutrophils• No Rx
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Mystery Case
• Baby boy born with oligohydramnios, Potters Sequence, and hypoplastic lungs requiring ECMO. Had B/L hydronephrosis diagnosed antenatally and the voiding cystourethrogram shows-
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