Pediatrics at a Glance UN Panda
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Neonatology1

  1. Prenatal gestational age determination by ultrasound.
In the first trimester, gestational age based on crown-rump length is accurate to within 3 days. From second trimester on, measurement of biparietal diameter is most helpful, until 34th week, is accurate within 10 days. Other helpful measurements are femur length, average body diameter and abdominal circumference. The ratio of head circumference to abdomen circumference may be best indicator of IUGR in third trimester.
  1. Postnatal gestational age determination.
  1. Physical assessment
  2. Neurologic assessment
  3. Examination of lens of eyes
  4. EEG
  5. Nerve conduction velocity
When seven physical and six neurological criteria are combined they can define gestational age with an accuracy of ± 2 weeks. The seven physical signs are skin, lanugo, plantar creases, breast, ear, genitals (male and female) and the six neurologic signs are posture, square window (wrist), arm recoil, popliteal angle, scarf sign and heel to ear.
  1. Fluid requirement in neonates.
• < 800 gm
80–100 cc/kg/day
• 800–1500 gm
60–80 cc/kg/day
• > 1500 gm
60 cc/kg/day
  1. When should sodium, potassium and calcium be given to neonates?
Calcium should be included in the very first IV solution of preterm infants, infants of diabetic mothers and asphyxiated newborns. Sodium and potassium are added at 24 hours of age.2
  1. Diagnosis of shock in neonate.
Shock is not identified by blood pressure reading but rather by a constellation of features like tachycardia, tachypnoea, low pulse volume, poor capillary refil, mottled blue white skin, anuria-oliguria and cold extremities.
  1. What is brownfat?
Brownfat is the site of nonshivering thermogenesis in response to cold stress in newborns. The major sites are:
  1. Between scapulae
  2. Around muscles and blood vessels of neck
  3. Axillae
  4. In mediastinum around trachea, esophagus and internal mammary arteries
  5. Around kidneys and adrenals.
  1. Peripheral nerve injuries in difficult delivery.
  1. Klumpke's palsy (C8T1)—Extended wrist, Horner's syndrome
  2. Erb Duchenne palsy (C567)—Waiter's tip position (90% recover by 1 year)
  3. Phrenic nerve palsy—Mortality 10 to 15% in unilateral and 50% in bilateral
  4. Facial nerve palsy—Excellent recovery in 1 to 3 weeks
  1. Fetal hormones promoting intrauterine growth.
  1. Insulin
  2. Growth hormone
  3. Thyroid hormone
  4. Epidermal, fibroblast and nerve growth factor.
  1. Causes of IUGR
Symmetric
  • Chromosomal anomalies: Down's, trisomy 18, Turner's, Chri-du-chat
  • Genetic disorders: Aminoaciduria, phenyl ketonuria
  • Congenital anomalies: Microcephaly, congenital heart disease, single, umbilical artery
  • Intrauterine infections: Toxoplasma, syphilis, CMV
  • Miscellaneous: Alcohol, tobacco, heroin, haemoglobinopathy
Asymmetric
  • Maternal vascular diseases: Toxaemia, hypertension, diabetes
  • Multiple pregnancy3
  • Placental malformations: Abnormal insertion, haemangioma, infarction >50%
  • Placenta praevia
  • Unknown (in 50% cases)
  1. Ponderal index (PI) and its significance.
PI is used to assess adequacy of intrauterine fetal nutrition; values less than 2 between 29 to 37 weeks gestation and 2.2 beyond 37 weeks indicate fetal malnutrition. Pre-eclampsia, chronic maternal illness and poor nutrition account for low PI.
  1. Morbidity in IUGR babies.
Short-term morbidity: Perinatal asphyxia, meconium aspiration; hypoglycemia, immunodeficiency, polycythemia —hyperviscosity.
Long-term morbidity: Behaviour and learning problems.
  1. Consequence of oligohydramnios.
  1. Pulmonary hypoplasia
  2. Potter facies
  3. Limb positioning defects
  4. Growth retardation
  1. Dietary daily allowance of vitamins for neonates.
Vitamin A
1000 units
B1 to B2
0.1 μg each
B6
0.25 μg
B12
0.25 μg
Folic acid
50 μg
Vitamin C
35 μg
Vitamin D
400 units
Vitamin E
4 μg
Vitamin K
5 μg
  1. Manifestation of vitamin E deficiency in neonates.
Anaemia, thrombocytosis, reticulocytosis, peripheral edema. Role of vitamin E in prevention of retinopathy of prematurity, bronchopulmonary dysplasia and IVH is controversial. Vitamin E intake be 1 mg for each gram of PUFA intake, else red cell membrane oxidation may cause haemolysis.4
  1. Manifestation of zinc and copper deficiency in neonates.
Zinc deficiency: Dry skin, growth retardation, hepatosplenomegaly, poor wound healing, hairloss, perioral—perianal rash, immune deficiency.
Copper deficiency: Hypochromic microcytic anaemia, neutropenia, bony abnormalities.
  1. Viruses transmitted in breast milk.
  1. CMV
  2. HBV
  3. HCV
  4. Rubella
  5. Possibly HIV
  1. Protective elements in human milk.
  1. Macrophages
  2. T and B cells
  3. Growth promoting factors (for fibroblasts)
  4. Bifidus factor (promote lactobacillus growth)
  5. Lactoperoxidase (antibacterial)
  6. IgA and lactoferrin.
  1. Breast milk jaundice.
It is due to elevated unconjugated bilirubin occurring beyond first week of life in breast fed babies. It is probably due to competitive inhibition of glucuronyl transferase by metabolites of progesterone or nonesterified long chain fatty acids or increased enteric absorption of unconjugated bilirubin. Treatment is simple observation or temporary cesation of breast feeding but other causes of unconjugated hyperbilirubinemia be excluded like sepsis, haemolytic disease, hypothyroidism.
  1. What is 60 : 40 formula feed?
This is 60% whey or lact albumin with 40% casein. This ratio makes small curds and is easily digestible. It is associated with decreased levels of serum ammonia and metabolic acidosis as in preterm infants and provides adequate amount of aminoacids, cystine and taurine.
  1. Difference between meconium ileus and meconium plug syndrome.
Meconium ileus is presentation of cystic fibrosis where distal ileum obstruction occurs due to thick tenacious concretions of inspissated meconium. A barium enema 5may reveal microcolon and 25% have associated intestinal atresia. Calcifications suggest intrauterine perforation and peritonitis. Meconium plug syndrome presents as delayed passage of meconium or intestinal obstruction. Barium enema shows normal caliber colon with multiple filling defects. Small preterm infants, infants of diabetic mothers are susceptible.
  1. Necrotising enterocolitis (NEC).
It should be suspected particularly in preterms in presence of vomiting, abdominal distention, bloody diarrhoea, lethargy, hypothermia. Many organisms can be isolated from stool including pseudomonas, salmonella, clostridia and E. coli. Such babies need CBC, abdominal X-rays for pneumatosis, platelet count, blood ABG, culture and electrolytes.
Treatment is:
  1. Nothing by mouth by 1 to 2 weeks
  2. Nasogastric drainage
  3. Parenteral antibiotic (cefotaxime)
  4. IV alimentation
  5. Surgery when clinical condition deteriorates, acidosis or thrombocytopenia are unremitting or peritonitis with intestinal perforation supervenes. Infants who retain 20 cm of small bowel from ligament of Treitz to ileocecal valve (intact) do well.
  1. Significance of pneumatosis.
Pneumatosis besides NEC can be seen in ischaemic bowel disease, neonatal ulcerative colitis, pseudomembranous enterocolitis and Hirschprung's disease.
  1. Ascites in neonate, etiology.
  1. Obstructive uropathy, meconium peritonitis, chylous ascites, bile ascites, CMV, toxoplasmosis.
  2. Associated with generalised anasarea, haemolytic disease of newborn, alpha thalassemia, twin to twin or fetomaternal haemorrhage, pulmonary lymphangiectasia/cystic adenoid pulmonary malformation, chorioangioma of placenta, congenital nephrosis, toxaemia of pregnancy.
  1. Role of phenobarbitone, phototherapy in hyperbilirubinemia.
Phototherapy is very helpful in reducing serum unconjugated bilirubin in the newborn. It eliminates need of 6exchange transfusion in infants with physiologic and nonhaemolytic jaundice. In contrast phenobarbitone is effective in enhancing bilirubin excretion and is useful for treatment of conjugated hyperbilirubinemia.
  1. Exchange transfusion.
Exchange transfusion is started depending on birth weight, bilirubin level (mg)/dL and risk factors.
Birth weight (gm)
< 1250
1250–1500
1500–2000
2000–2500
> 2500
Standard risk
13
15
17
18
20
High risk
10
13
15
17
18
High risk criteria are birth weight < 1000 gram, 5 minute Apgar score < 3, PaO2 < 40 mmHg, pH < 7.15 (both after 1–2 hour of birth), rectal temp < 35°C for > 4 hours, serum total protein < 4 gm/dL, serum albumin < 2.5 gm/dL.
1 exchange removes blood volume by 63%, 2 volumes 87% and 3 volumes 95%. Although 87% of infant's bilirubin is removed in a 2 volume exchange, serum bilirubin falls to 45% of pre-exchange level which rises to 60% in ½ hour. Albumin infusion prior to exchange transfusion increases amount of bilirubin removal.
  1. Mechanism of phototherapy effect.
The spectral range used is of 460 to 500 nm. The minimum irradiance that is effective for reducing serum bilirubin is 4 µwatt/cm2/nm. Photoisomerisation of bilirubin to lumirubin occurs in nano second (ZZ form to ZE form), lumirubin is rapidly excreted in bile. Loose green stools are common effect of phototherapy. Bronze baby syndrome can develop when lumrubin is not excreted.
  1. Kernicterus.
Deposition of toxic unconjugated bilirubin in basal ganglia (bilirubin encephalopathy) causes kernicterus characterised by lethargy, opisthotonus, rigidity, high pitched cry, fever and seizure. Survivors have chorioathetosis, hearing loss and often mental retardation. Hypoglycemia, hypoxia, acidosis, sepsis, hypothermia, haemolysis are known to increase risk of kernicterus.
  1. Manifestation of hypocalcemia, hypomagnessemia and hypoglycemia in neonates.
Hypocalcemia: Jitteriness, seizure, high pitched cry, laryngospasm; positive Chvostek's sign (facial muscle twitching on tapping), and Trousseau's sign (carpopedal spasm).7
Hypomagnessemia: Same as hypocalcemia. It should be suspected in any hypocalcemic infant (< 7 mg%) not responding to calcium.
Neonatal tetany is often due to hyperphosphatemia (due to milk) that depresses serum calcium.
Hypoglycemia: Lethargy, high pitched cry, apnea, seizure, cyanosis, hypotonia.
  1. Hypoglycemia and its causes.
Hypoglycemia is defined as serum glucose less than 35 µg/dL in term neonate and less than 25 µg/dL in preterm or low birth neonate during first 3 days of life. Beyond this age glucose below 45 µg/dL is considered abnormal.
Causes
Glucose production abnormality
Hyperinsulinemia
1.
Prematurity
1.
Infants of diabetic mothers
2.
Small for date
2.
Rh incompatibility
3.
Asphyxia, hypothermia, sepsis
3.
Nesidioblastosis
4.
Cyanotic heart disease
4.
Tocolytic therapy with sympathomimetics
5.
Deficiency of GH,T3,T4
5.
Beckwith Weidmann syndrome
6.
Galactosemia
7.
Tyrosinosis
  1. Treatment of hypoglycemia.
  1. 2 cc/kg 10% dextrose IV bolus then 6 to 8 mg/kg/min infusion.
  2. Refractory hypoglycemia be treated with corticosteroid (reduce peripheral glucose utilisation and promote gluconeogenesis), glucagon (promotes hepatic glycogen breakdown and gluconeogenesis), epinephrine (promotes glycogenolysis/glyconeogenesis) and diazoxide.
  1. Beckwith-Weidemann syndrome.
Features include gigantism, macroglossia, and omphalocele associated with severe hypoglycemia, often with hypocalcemia and polycythemia. Hemihypertrophy and nephroblastoma may be associated.
  1. Abnormalities associated with infants of diabetic mothers.
  1. Metabolic: Hypoglycemia, hypocalcemia, polycythemia, hyperbilirubinemia.8
  2. Congenital anomalies: Septal hypertrophy, limb defects, CNS and genitourinary defects.
  3. Functional abnormalities: Respiratory distress, renal vein thrombosis, small left colon.
  1. Pattern of organ system damage in perinatal asphyxia.
CNS: Haemorrhage, anoxic encephalopathy, edema/necrosis.
CVS: Myocardial dysfunction, right to left shunt, cardiogenic shock.
Respiratory: Respiratory distress, pulmonary bleed.
GI: Necrotising enterocolitis.
Urinary: ATN.
Endocrine: SIADH, adrenal haemorrhage.
  1. Neonatal hypoxic ischaemic encephalopathy.
•
Selective neuronal necrosis
Hypoxemia
•
Status marmoratus
Hypoxemia
•
Parasagittal injury
Ischaemia
•
Periventricular leukomalacia
Ischaemia
•
Focal/multifocal ischaemic brain necrosis
Ischaemia
  1. Significance of hyperpnea and tachypnea in neonates.
Hyperpnea refers to deep relatively unlabored respiration at mildly increased rate. This occurs in presence of reduced pulmonary blood flow (e.g. pulmonary atresia) and results from ventilation of under perfused alveoli. Tachypnea is shallow labored and rapid breathing in a setting of low lung compliance (e.g. pulmonary edema, primary lung disease).
  1. Difference between apnea and periodic breathing.
Apnea is cessation of respiration for > 10 to 15 sec with or without cyanosis, pallor, hypotonia, bradycardia or for < 10 sec accompanied by bradycardia. Periodic breathing is respiratory pauses of 5 to 10 seconds followed by 10 to 15 seconds of rapid respiration as seen in preterm infants. It is not associated with bradycardia.
  1. Causes of apnea, on first day of life.
Prematurity, infection, impaired oxygenation, metabolic disorders, hypothermia, GE reflux, intracranial bleed/dysfunction, drugs, bronchopulmonary dysplasia.9
  1. Risk factors for respiratory distress syndrome (RDS).
Increased risk
Decreased risk
Prematurity
Maternal toxemia
Maternal diabetes
PROM
Male sex
Glucocorticoid to mother
Cesarean section
Perinatal asphyxia
History of RDS in sibling
  1. Indication of mechanical ventilation in RDS.
Clinical: Intractable apnea, cyanosis, severe retraction.
Laboratory: pH < 7.2, PCO2 > 60 mmHg, PaO2 < 50–60 torr despite FIO2 of 0.7 to 1.
  1. Causes of cyanosis in RDS.
  1. Ventilation-perfusion mismatch due to atelectasis.
  2. Intrapulmonary shunting of blood due to pulmonary vasoconstriction secondary to acidosis and hypoxemia.
  3. Shunting across foramen ovale/ductus arteriosus.
  1. Optimal PEEP.
It is the endexpiratory pressure at which oxygenation is maximum. In practice PEEP is 10% of inspired oxygen concentration.
  1. Hyperoxia test.
In patients with cyanosis, the hyperoxia test can be performed to distinguish among primary lung disease, cyanotic heart disease (CHD), and persistent pulmonary hypertension (PPH). The child is put on 100% O2 briefly and O2 tension is measured. PaO2 > 100 mmHg means primary lung disease. To distinguish between CHD and PPH 100% O2 is administered while hyperventilating the patient. If PaO2 rises above 100 mmHg—PPH is likely. Treatment of PPH is hyperventilation and tolazoline but resultant alkalosis and hypotension may be troublesome.
  1. Bronchopulmonary dysplasia—causes and treatment.
Causes include immaturity, barotrauma, oxygen toxicity, infection, CHF and growth failure.
Treatment is with steroids and diuretics.10
  1. Estimation of lung maturity prenatally.
  1. L:S ratio
  2. Phosphatidyl glycerol
  3. Foam stability test
  4. Fluorescence polarimetry
  5. Optical density at 650 nm.
LS ratio is the gold standard but optical density is rapid and readily available. LS ratio ≥ 2 carries a low risk of RDS, 1.5 to 2 carries 40% risk and < 1.5 75%, risk of RDS.
  1. TTN, RDS type II and Wilson Mikity syndrome.
Transient tachypnea of newborn (TTN) is respiratory distress of nonasphyxiated mature newborn due to delayed resorption of lung fluid. X-ray shows fluid in interlabor fissures and central hypervascularity.
Chronic pulmonary insufficiency of prematurity (CPIP) As name suggests prematures of less than 1250 gram have delayed onset (after 3 days) of apnea, atelectasis and increased O2 requirement probably due to poor surfactant turnover, persistent secretion of fetal lung fluid.
Wilson-Mikity syndrome The baby usually less than of 36 weeks gestation, who is born normal develops gradually, cyanosis and retraction following days only to improve on its own.
  1. Pulmonary interstitial emphysema (PIE).
It presents either as diffuse (intrapulmonary) air collections or localized subpleural disease. It is thought to arise from mechanical ventilation. Reduction of peak inflating pressure and higher ventilator rate avoid this complication.
  1. LVH and RVH in neonates. ECG features.
LVH:
R in V6 >17 mm in first week, > 25 mm first month
T inversion in V6 or V1
RVH:
qR in V1, RV1 > 28 mm
SV6 > 13 mm
Pure R in V1 > 10 mm
Positive T in V1 after 5 days.
  1. Prenatal factors and cardiac disease in neonates.
1.
Diabetes mellitus
VSD, septal hypertrophy, AS
2.
SLE
Heart block
3.
Rubella
PS (peripheral), PDA
11
4.
Alcohol
PS, VSD
5.
Lithium
Ebstein anomaly
6.
Betablockers
Asymmetric septal hypertrophy
  1. The 5 ‘T’s of congenital heart disease.
  1. Tetralogy of Fallot
  2. Transposition of great vessels
  3. Truncus arteriosus
  4. Tricuspid atresia
  5. Total anomalies pulmonary venous connections.
  1. Differential diagnosis of neonatal cyanosis.
  1. CHD with right-left shunt with ↓ pulmonary flow—TOF, tricuspid/Pulmonary atresia
  2. CHD with right-left shunt with ↑ pulmonary flow— d-transposition, anomalous pulmonary venous return
  3. CHD with CHF and V:Q mismatch—Large VSD, coarctation, SVT
  4. Primary pulmonary disease—RDS, pneumothorax, pneumonia, meconium aspiration
  5. Metabolic disease—Hypoglycemia, methaemoglobinemia
  6. Polycythemia—IUGR, twin-twin transfusion
  7. Infection—Sepsis, myocarditis
  8. Persistent fetal circulation—Maternal salicylates
  9. CNS disease—Intracranial bleed, seizure disorder
  1. CHF without a murmur in neonate.
  1. Myocarditis
  2. Cardiomyopathy secondary to asphyxia, hypoglycemia, hypocalcemia
  3. Pompe's disease
  4. A-V malformation (vein of Gallen)
  5. Sepsis
  6. Cardiac arrhythmia
  1. Indications and side effects of PGE1.
Indications
Ductal dependent flow to (a) pulmonary circulation as in pulmonary or tricuspid atresia with intact septum or to (b) systemic circulation (coarctation, hypoplastic left heart, aortic arch interruption, (c) in infants with suspected CHD without a firm diagnosis.
Side Effects
Apnea, pyrexia, flushing, seizure, hypotension.12
  1. Persistent fetal circulation (PFC), and its clinical features.
PFC refers to combination of pulmonary hypertension and right to left shunt at foramen ovale/ductus arteriosus in absence of structural anomaly. Features are cyanosis, tachypnea.
  1. Significance of fetal Hb, Bart Hb and Gower Hb.
HbF is α2δ2. Transition from HbF to HbAn starts at 32 weeks intrauterine life, at birth 50 to 65% of Hb is HbF. Bart Hb in γ4, its level is increased in alfa thalassemia and HbH disease. Gower Hb is of embryonic origin present between 10 to 12 weeks gestation. It is usually absent at birth and its presence especially Gower-2 occurs in trisomy 13.
  1. Manifestation and complications of neonatal polycythemia.
Manifestations: Lethargy, hypotonia, cyanotic look, tremulous, myoclonic jerk, hepatomegaly.
Complications: Respiratory distress, CHF, convulsion peripheral gangrene, priapsim, necrotising interocolitis, ileus, renal failure.
  1. Risk factors for polycythemia in newborn.
  1. Infants of diabetic mothers
  2. IUGR
  3. Perinatal asphyxia
  4. Twin-twin transfusion (recipient)
  5. Delayed cord clamping
  6. Beckwith's syndrome
  1. PT, TT and PTT in neonates.
Prothrombin time reaches adult values by 1 week of age, while PTT attains normal values by 2 to 9 months of age. Thrombin time of term infant is that of adult value.
  1. Haemorrhagic disease of newborn and its prevention.
Haemorrhagic disorder of first few days of life is due to deficiency of vitamin K dependent factors (II, VII, IX and X). It can be prevented by IM 0.5 to 1 mg of vitamin K1 to newborn shortly after birth.
  1. Apt test.
Apt test distinguishes fetal blood from maternal swallowed blood. A pink colour persisting over 2 minutes 13indicates fetal Hb. Adult Hb gives a pink colour that turns yellow in 2 minutes.
  1. Klelhauer Betke test.
In cases of suspected fetomaternal haemorrhage, this test is used to detect presence of fetal cells in maternal circulation. This acid elution technique is based on the property of fetal haemoglobin to resist elution in an acid medium. In a stained maternal blood smear the fetal cells stain darkly and the % of fetal cells can be determined.
  1. Rh antigen complex.
It is made up of six possible antigens C, c, D, d, E, e but isoimmunisation causing serious neonatal disease is mostly due to incompatibility with D antigen.
  1. Reason for direct Coomb's test negativity in ABO incompatibility.
Mother of ‘O’ group bearing A or B positive fetus causes haemolysis in newborn. There are fewer A or B antigenic sites on the newborn red cells and they are distantly placed.
  1. Causes of hydrops fetalis.
  1. Severe chronic anemia as in Rh isoimmunisation, homozygous alpha thalassemia, twin to twin or fetomaternal transfusion.
  2. Cardiac failure: severe congenital heart disease.
  3. Hypoproteinemia of congenital hepatitis/renal failure.
  4. Intrauterine infectious: CMV, toxoplasma, syphilis.
  1. Clinical presentation of neonatal sepsis.
  • Lethargy, irritability, hepatomegaly, jaundice
  • Hypo/hyperthermia, apnea, cyanosis
  • Leukocytosis is not essential feature of neonatal sepsis
  • Immature to total neutrophil ratio is dependable indicator, neutropenia is frequent and bears poor outcome
  • Acute phase reactants (C reactive protein, fibrinogen, haptoglobin, orosomucoid) may be of use.
  1. Common pathogen of sepsis in newborn.
E. coli, group B streptococci, coagulase negative staphylococci. PROM, chorioamnionitis and prematurity are the risk factors.14
  1. Relatively specific finding in perinatal infections.
Chronic
  • Rubella: Cataract, cloudy cornea, pigmented retina, PDA, PS.
  • CMV: Microcephaly, periventricular calcifications.
  • Toxoplasma: Hydrocephalus, chorioretinitis.
Late Sequelae
  • CMV: Hearing loss, mental retardation.
  • Rubella: Autism, juvenile diabetes, thyroid dysfunction precocious puberty.
  • Toxoplasma: Chorioretinitis, minimal brain dysfunction
  1. Parot's pseudoparalysis.
It is the painful pseudoparalysis associated with the bony changes of syphilitic osteochondritis and periostitis. Upper extremity is more commonly affected than lower. The baby is irritable and does not want to move the involved limb.
  1. Cerebral calcification in congenital infections.
  1. Toxoplasmosis
  2. CMV infection
  3. HSV
Periventricular calcification in CMV, diffuse white matter calcification in toxoplasmosis and massive bilateral hemispheric calcification in HSV encephalitis.
  1. Listeriosis in newborn—clinical presentation.
Clinical presentation is variable including jaundice, seizure, respiratory distress, myocarditis, meningitis skin and pharyngeal lesions. Listeriosis should be suspected in presence of:
  1. Maternal history of stillbirth or repeated abortions
  2. Chorioamnionitis or placental villous granuloma
  3. Neonatal hepatosplenomegaly with granuloma of skin and pharynx.
  1. Associated findings of bilateral renal agenesis.
Oligohydramnions, Potter's facies (micrognathia, low set ears, epicanthic fold, mongoloid slant) and pulmonary hypoplasia. Other associations are single umbilical artery, GI agenesis and Meckel's diverticulum.15
  1. Seizure like behavioural states in neonates.
These include jitteriness, movements during REM sleep, rowing and bicycling movements, decorticate and decerebrate posturing, and autonomic dysfunctions.
In jiterriness movement is exquisitely stimulus sensitive, with tremor (not colonic) and movements cease with passive flexion of limb, not associated with gaze or eye movement.
  1. Neonatal seizures: time relationship.
0 to 24: hours
Hypoxic ischaemic encephalopathy, intra-cranial haemorrhage, CNS dvelopmental defects, drug withdrawal.
24 to 72: hours
All above pulse hypoglycemia, hypocal-cemia.
After 72 hours
Intracranial infection, hypocalcemia, development defects, drug withdrawal.
  1. Treatment of neonatal seizure.
With hypoglycemia
  • 10% glucose, 2 ml/kg IV followed by 4 to 8 mg/kg/min
Without hypoglycemia
  • Phenobarbitone 20 mg/kg IV start, 2nd dose if necessary
  • Phenytoin 20 mg/kg/IV
  • Calcium gluconate 5% 4 mg/kg IV (under ECG monitoring)
  • Magnesium sulphate 50%, 0.2 ml/kg IM
  • Pyridoxine 50 to 100 mg IV
  1. Subdural effusion.
Subdural effusion results from transudation of fluid in meningeal inflammation. Its protein content is higher (40 mg/dL) and comprises of 60 to 70% albumin that differentiate it from CSF.
  1. Classification of periventricular-intraventricular haemorrhage (IVH).
Grade I
Germinal matrix haemorrhage only
Grade II
IVH without ventricular dilatation
Grade III
IVH with ventricular dilatation
Grade IV
Grade III plus intraparenchymal bleed.
IVH is predominantly a lesion of premature infants; 50% having onset on day 1 of life, 25% on day 2 and 16another 45% on day 3. An US study on the 4th day followed by another after 5 days to determine maximal progression of bleed is recommended.
  1. Difference between ventriculomegaly and posthaemorrhagic hydrocephalus.
Both ventriculomegaly and hydrocephalus may follow IVH. While ventriculomegaly is due to periventricular cerebral atrophy secondary to white matter hypoxic injury, hydrocephalus results from disturbances in cerebral CSF dynamic (i.e., flow or absorption).
  1. Prognosis of neonatal seizure.
Babies of hypoxic ischaemic encephalopathy, hypoglycemia and bacterial meningitis with seizure have 50% chance of normal development; but those with intraventricular haemorrhage have less than 10% chance of normal development. In contrast those with primary subarachnoid bleed have 90% chance of normal development.
  1. Differentiation of cephalhaematoma, caput succidaneum subgaleal haematoma.
In caput succidaneum bleeding is just beneath the skin, in cephalhaematoma it is beneath the periosteum while in subgaleal type it is just below epicranial aponeurosis. Caput is soft, pitting crosses suture line; subgaleal form is firm and floctuant and also crosses suture line whereas cephalhaematoma is firm tense and does not cross suture line. Both subgaleal and cephalhaematoma may increase after birth but only former is associated with marked blood loss.