Question 1#

Regarding normal physiological changes in the neonate, which ONE of the following is INCORRECT?

A. A neonate will lose approximately 10% of its birth weight in the first week of life

Answer: D: A neonate will lose about 10% of birth weight in the first week of life; this is a combination of initial osmotic diuresis post birth, passage of meconium, as well as initial slow introduction of breast or bottle feeding. Birth weight is usually regained at 10–14 days. General weight gain is 30 g per day or 1% of birth weight per day. Poor weight gain is an important indicator of a chronic organic process such as congenital heart disease, metabolic disease, malabsorption and chronic infection.

The average intake is 60–90 mL per feed or 10 minutes per breast every 2–3 hours. Breastfed infants need to feed more often (1.5 to every 2 hours) because breast milk is easier to digest and leaves the stomach sooner than formula. Ten wet nappies per day are usual, with 1 stool per day to 1 stool per week for breastfed babies.

The heart rate in a newborn is often elevated to 180–200 bpm in settings of stress but this is usually a variable sinus tachycardia. Normal BP is 60–90 systolic and normal saturation is between 94–100%.

Reference:

1. Mody AP, Silverman BK. Problems in the early neonatal period. In: Fleisher GR, Ludwig S, editors. Textbook of pediatric emergency medicine. 6th ed. Philadelphia: Lippincott Williams & Wilkins; 2011. p. 902–1010.

Question 2#

Regarding jaundice in the newborn period, which ONE of the following is TRUE?

A. Breastmilk jaundice is a common complication in the first 24–48 hours of neonatal life

Answer: C: The following is a useful guide in determining the causes of jaundice classified by time of onset:

• First 24 hours: jaundice within 24 hours is probably pathological It may be due to erythroblastosis fetalis, concealed haemorrhage, sepsis or congenital infections, including syphilis, cytomegalovirus, rubella and toxoplasmosis. Haemolysis (e.g. G6PD-deficiency or ABO incompatability) is suggested by a rapid rise in serum bilirubin concentration (>0.5 mg/dL/hr), anaemia, pallor, indirect (unconjugated) hyperbilirubinaemia, reticulocytosis, hepatosplenomegaly, and a positive family history.
• First few days: usually physiologic Early-onset breastfeeding jaundice and Crigler-Najjar syndrome are seen initially on the second or third day. Crigler-Najjar syndrome is a familial non-haemolytic icterus syndrome with a uniformly poor prognosis and ongoing kernicterus risk throughout life. Jaundice appearing after the third day and within the first week may suggest bacterial sepsis or urinary tract infection; it may also be due to other infections, notably syphilis, toxoplasmosis, cytomegalovirus, and enterovirus.
• After week 1 Wide differential including breast milk jaundice, septicaemia, congenital atresia or paucity of the bile ducts, hepatitis, galactosemia, hypothyroidism, cystic fibrosis, and congenital haemolytic anaemia crisesrelated to red blood cell morphology and enzyme deficiencies.
• Persistent jaundice during the first month of life includes hepatitis, cytomegalic inclusion disease, syphilis, toxoplasmosis, familial non-haemolytic icterus, congenital atresia of the bile ducts and galactosemia.

Rarely, physiologic jaundice may be prolonged for several weeks, as in infants with hypothyroidism or pyloric stenosis.

References:

1. Ambalavanan N, Carlo WA. Jaundice and hyperbilirubinemia in the newborn. In: Kliegman RM, Behrman RE, Jenson HB, et al, editors. Nelson textbook of pediatrics. 19th ed. Philadelphia: Saunders Elsevier; 2011. p. 600–12.
2. Bhutani VK, Johnson LH, Sivieri EM. Predictive ability of a predischarge hour-specific serum bilirubin for subsequent significant hyperbilirubinemia in healthy term and near-term newborns. Pediatrics 1999;103:6–14.
3. Bhutani VK, Johnson LH, Keren R. Diagnosis and management of hyperbilirubinemia in the term neonate: for a safer first week. Pediatr Clin North Am 2004;51:843–61.

Question 3#

Regarding neonatal sepsis and meningitis, which ONE of the following is INCORRECT?

A. Neonatal meningitis is commonly caused by GBS, Escherichia coli, Listeria monocytogenes, Streptococcus pneumoniae, other streptococci and non-typable Haemophilus influenzae

Answer: D: The most common bacterial causes of neonatal meningitis are GBS, E. coli and L. monocytogenes. S. pneumoniae, other streptococci, non-typable H. influenzae, both coagulase-positive and coagulase-negative staphylococci, Klebsiella, Enterobacter, Pseudomonas, Treponema pallidum (syphilis) and Mycobacterium tuberculosis may also produce meningitis. 

TORCHES infections (agents that cross the placenta; Toxoplasmosis gondii, rubella, CMV, herpes, syphilis) may be asymptomatic at birth or may have mild symptoms to multisystem involvement. Clinical signs that raise suspicion of an intrauterine infection (and help distinguish these infections from acute bacterial infections that occur during labour and delivery) include intrauterine growth restriction, microcephaly/hydrocephalus, intracranial calcifications, chorioretinitis, cataracts, myocarditis, pneumonia, hepatosplenomegaly, direct hyperbilirubinaemia, anaemia, thrombocytopenia, hydrops fetalis, and skin manifestations. Encephalitis is commonly caused by CMV, enteroviruses, herpes simplex virus (HSV), rubella, toxoplasmosis and treponemal organisms. Adverse late outcomes include sensorineural hearing loss, visual disturbances (including blindness), seizures and neurodevelopmental abnormalities.

Neonates with bacterial sepsis may have nonspecific signs and symptoms or focal signs of infection. Integrated Management of Childhood Illness (IMCI) criteria for bacterial sepsis include convulsions, respiratory rate >60 breaths/min, severe chest indrawing, nasal flaring, grunting, bulging fontanel pus draining from the ear, redness around the umbilicus extending to the skin, temperature >37.7°C (or feels hot) or <35.5°C (or feels cold), lethargic or unconscious, reduced movements, not able to feed, not attaching to the breast, no suckling at all, crepitations, cyanosis and a reduced digital capillary refill time. The initial manifestation may involve only one system, such as apnoea alone or tachypnoea with retractions or tachycardia, or it may be an acute catastrophic manifestation with multiorgan dysfunction. Redness of the umbilicus suggests omphalitis – a neonatal infection where the umbilical stump is colonised by bacteria from the maternal genital tract or the environment. Infection may remain localised or may spread to the abdominal wall, the peritoneum, the umbilical or portal vessels, or the liver. Abdominal wall cellulitis or necrotising fasciitis with associated sepsis and a high mortality rate may develop in infants with omphalitis. Prompt diagnosis and treatment are necessary to avoid serious complications.

Normal, uninfected infants 0–4 weeks of age may have the following elevated CSF findings: protein 0.84 ± 0.45 g/L, glucose 2.5 mmol/L ± 0.5 mmol/L, leukocyte count 11 ± 10 per mm³ with the 90th percentile being 22, proportion of polymorphonuclear leukocytes is 2.2 ± 3.8% with the 90th percentile being 6. Newborn CSF is often xanthochromic because of the frequent elevation of bilirubin and protein levels in this age group. Normal opening pressure ranges from 10 to 100 mm H₂ O in young children, 60 to 200 mm H₂ O after eight years of age, and up to 250 mm H₂ O in obese patients. Elevated CSF protein values and leukocyte counts and hypoglycorrhachia may develop in preterm infants after intraventricular haemorrhage. Many noninfectious processes, like certain inflammatory disorders, seizures and malignancy, as well as nonpyogenic congenital infections (toxoplasmosis, CMV, HSV, syphilis producing an aseptic meningitis), can also produce alterations in CSF protein value and leukocyte count. Hypoglycorrhacia (low glucose level in CSF) is also caused by chemical meningitis, inflammatory conditions, subarachnoid haemorrhage and hypoglycemia. Elevated levels of glucose in the blood is the only cause of having an elevated CSF glucose level. There is no pathologic process that causes CSF glucose levels to be elevated.

References:

1. Prober CG, Dyner L. Central nervous system infections. In: Kliegman RM, Behrman RE, Jenson HB, et al, editors. Nelson textbook of pediatrics. 19th edn. Philadelphia: Saunders Elsevier; 2011. p. 2086–98.
2. Stoll BJ. Infections of the neonatal infant. In: Kliegman RM, Behrman RE, Jenson HB, et al, editors. Nelson textbook of pediatrics. 19th edn. Philadelphia: Saunders Elsevier; 2011. p. 629–48.
3. Vergnano S, Sharland M, Kazembe P, et al. Neonatal sepsis: an international perspective. Arch Dis Child Fetal Neonatal Ed 2005;90:F220–4.
4. Seehusen DA, Reeves MM. Cerebrospinal fluid analysis. Am Fam Physician 2003;68(6):1103–9.
5. World Health Organization. Handbook : IMCI integrated management of childhood illness. Online. Available: http://whqlibdoc.who.int/publications/2005/9241546441. pdf

Question 4#

A 10-day-old neonate presents to the emergency department (ED) with cardiorespiratory collapse.

Which ONE of the following conditions is unlikely to be the underlying aetiology?

A. Urea cycle disorder

Answer: C: Substance abuse during pregnancy results in poor maternal nutrition, acute withdrawal shortly after birth, and long-term effects on physical growth and neuro-development. Heroin and methadone are the drugs most frequently associated with withdrawal. Manifestations of withdrawal usually begin within the first 48 hours; rarely, symptoms may appear as late as 4–6 weeks of age. Tremors and hyper-irritability are the most prominent symptoms. Other signs include wakefulness, hyperacusis, hypertonicity, tachypnoea, diarrhoea, vomiting, high-pitched cry, fist sucking, poor feeding with weight loss (disorganized sucking) and fever. The diagnosis is generally established from the history and clinical findings. Meconium testing is more accurate than neonatal urine drug testing.

The usual cause of neonatal collapse presenting to the ED is sepsis. A careful consideration of potential differentials should be born in mind:

1- Cardiac:

• Congenital: hypoplastic left heart syndrome, other structural disease, persistent pulmonary hypertension of the newborn (PPHN)
• Acquired: myocarditis, hypovolemic or cardiogenic shock, PPHN

2-  Gastrointestinal:

• Necrotizing enterocolitis
• Spontaneous gastrointestinal perforation
• Structural abnormalities

3- Haematologic:

• Neonatal purpura fulminans
• Immune-mediated thrombocytopenia
• Immune-mediated neutropenia
• Severe anaemia
• Malignancies (congenital leukaemia)
• Hereditary clotting disorders

4- Metabolic:

• Hypoglycaemia Adrenal disorders: adrenal haemorrhage, adrenal insufficiency, congenital adrenal hyperplasia
• Inborn errors of metabolism: organic acidurias, lactic acidoses, urea cycle disorders, galactosemia

5- Neurologic:

• Intracranial haemorrhage: spontaneous, due to child abuse
• Hypoxic-ischemic encephalopathy
• Neonatal seizures
• Infant botulism

6- Respiratory:

• Respiratory distress syndrome
• Aspiration pneumonia: amniotic fluid, meconium or gastric contents
• Lung hypoplasia
• Tracheoesophageal fistula
• Transient tachypnea of the newborn

References:

1. Stoll BJ. Infections of the neonatal infant. In: Kliegman RM, Behrman RE, Jenson HB, et al, editors. Nelson textbook of pediatrics. 19th edn. Philadelphia: Saunders Elsevier; 2011. p. 629–48.
2. Stoll BJ, Klegman RM. Substance abuse and neonatal abstinence (withdrawal). In: Kliegman RM, Behrman RE, Jenson HB, et al, editors. Nelson textbook of pediatrics. 19th ed. Philadelphia: Saunders Elsevier; 2011. p. 579–99.

 

 

 

Question 5#

Which ONE of the following criteria is included in the definition of systemic inflammatory response syndrome (SIRS) in neonates and children?

A. A white cell count (WCC) >12,000/µL or <4,000/µL, or >10% bands

Answer: D: In neonates and paediatric patients, SIRS manifests as temperature instability, respiratory dysfunction (altered gas exchange, hypoxaemia, acute respiratory distress syndrome), cardiac dysfunction (tachycardia, delayed capillary refill, hypotension) and perfusion abnormalities (oliguria, metabolic acidosis). Increased vascular permeability results in capillary leak into peripheral tissues and the lungs, with resultant pulmonary and peripheral oedema. Disseminated intravascular coagulation (DIC) results in the more severely affected cases. The cascade of escalating tissue injury may lead to multisystem organ failure and death.

To make the diagnosis of SIRS, the presence of at least two of the following four criteria, one of which must be abnormal temperature or leukocyte count, must be present:

• Core temperature of >38.5°C or <36°C
• Tachycardia, defined as a mean heart rate
• >2 SD above normal for age in the absence of external stimulus, chronic drugs, or painful stimuli; or
• Otherwise unexplained persistent elevation over a 0.5- to 4-hour time period; or
• For children <1 year old: bradycardia, defined as a mean heart rate <10th percentile for age in the absence of external vagal stimulus, betablocker drugs, or congenital heart disease, or
• Otherwise unexplained persistent depression over a 0.5-hour time period
• Mean respiratory rate >2 SD above normal for age or mechanical ventilation for an acute process not related to underlying neuromuscular disease or the receipt of general anaesthesia
• Leukocyte count elevated or depressed for age (not secondary to chemotherapy-induced leukopenia) or >10% immature neutrophils

References:

1. Adams-Chapman I, Stoll BJ. Systemic inflammatory response syndrome. Semin Pediatr Infect Dis 2001;12:5–16.
2. Goldstein B, Giroir B, Randolph A, et al. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in paediatrics. Pediatric Critical Care Medicine 2005;6(1):2–8.