11.2 Common Pediatric & Neonatal Illnesses

Common Pediatric & Neonatal Illnesses: Diagnosis & Management

Neonatal Jaundice

Neonatal hyperbilirubinemia is common and requires a systematic approach to distinguish physiologic states from pathologic processes. The initial step is differentiating unconjugated (indirect) from conjugated (direct) hyperbilirubinemia. Conjugated hyperbilirubinemia (defined as direct bilirubin > 1.0 mg/dL if total bilirubin is < 5.0 mg/dL, or > 20% of the total bilirubin) is always pathologic.

• Conjugated Hyperbilirubinemia: Commonly caused by biliary atresia or neonatal hepatitis. Biliary atresia presents at 2–8 weeks of life with progressive jaundice, pale/acholic stools, dark urine, and hepatomegaly due to fibro-obliterative destruction of the extrahepatic biliary tree. Diagnostic workup includes abdominal ultrasound (absent/triangular cord sign), HIDA scan (demonstrating absent excretion), and gold-standard liver biopsy. Management is the surgical Kasai portoenterostomy; delay beyond 8 weeks of life significantly increases the risk of progression to cirrhosis requiring liver transplantation.
• Unconjugated Hyperbilirubinemia:
  • Physiologic Jaundice: Appears after 24 hours of life, peaks at 3–5 days, and resolves within 1–2 weeks. It results from transiently decreased UGT1A1 activity, short red blood cell lifespan, and increased enterohepatic circulation.
  • Breastfeeding Jaundice (Lactation Failure): Occurs in the first week of life due to insufficient milk intake, leading to dehydration, weight loss, and slow stooling, which increases enterohepatic bilirubin reabsorption. Treatment focuses on improving breastfeeding frequency (8–12 times/day) and hydration.
  • Breast Milk Jaundice: Occurs later (onset 3–5 days, peaking at 2 weeks) due to factors in breast milk (e.g., beta-glucuronidase) that increase bilirubin deconjugation and reabsorption. Bilirubin levels may remain elevated but are rarely dangerous, and breastfeeding should continue.
  • Hemolytic Disorders: Jaundice presenting within the first 24 hours of life, rapidly rising bilirubin (> 0.2 mg/dL/hour), or anemia/reticulocytosis suggest hemolysis (e.g., ABO incompatibility, Rh incompatibility, G6PD deficiency).
• Management: Hour-specific bilirubin nomograms guide phototherapy and exchange transfusion. Phototherapy converts unconjugated bilirubin into water-soluble photoisomers excreted in bile/urine. Exchange transfusion is indicated for severe hyperbilirubinemia at risk of kernicterus (bilirubin-induced neurological dysfunction, marked by lethargy, hypotonia, opisthotonus, or seizures) when phototherapy fails or levels exceed the threshold.

Febrile Seizures

Febrile seizures occur in children aged 6 months to 5 years in the setting of a fever (> 38.0°C or 100.4°F) without evidence of intracranial infection or metabolic derangement.

• Simple Febrile Seizures: Generalized tonic-clonic, last less than 15 minutes, and do not recur within a 24-hour period. Management consists of parental reassurance, antipyretics for comfort (acetaminophen or ibuprofen; note that antipyretics do not reduce the recurrence rate of febrile seizures), and evaluation of the source of the fever. Lumbar puncture is not routinely indicated unless meningeal signs are present, the child is under-immunized, or pre-treatment with antibiotics masks signs of meningitis.
• Complex Febrile Seizures: Focal onset, last 15 minutes or longer, or recur within 24 hours. These require a more detailed workup, observation, and potentially diagnostic evaluation (e.g., EEG, neuroimaging) if neurological abnormalities persist. Active seizures lasting > 5 minutes are treated with abortive therapy (IV lorazepam or rectal diazepam).

Acute Bronchiolitis

Acute bronchiolitis is a viral lower respiratory tract infection in infants and children < 2 years, most commonly caused by respiratory syncytial virus (RSV).

• Clinical Presentation: Starts with upper respiratory symptoms (rhinorrhea, congestion) followed by lower airway involvement (tachypnea, wheezing, crackles, retractions, and nasal flaring). Apnea is a risk, especially in infants < 2 months or premature infants.
• Diagnosis & Management: Diagnosis is clinical. Routine chest X-rays, viral swab panels, and laboratory tests are not recommended unless the child is critically ill or has an atypical presentation. Management is strictly supportive: maintaining hydration (oral or IV), nasal suctioning (especially before feeding), and supplemental oxygen if oxygen saturation is persistently < 90%. Bronchodilators (albuterol), epinephrine, systemic corticosteroids, and nebulized hypertonic saline are not routinely recommended, as clinical trials show they do not alter the course of the disease or decrease hospitalization rates.

Croup (Laryngotracheobronchitis)

Croup is an upper airway infection typically caused by parainfluenza virus in children aged 6 months to 3 years.

• Clinical Presentation: Characterized by a barking cough, hoarseness, and inspiratory stridor due to subglottic narrowing. An anteroposterior neck X-ray may show the classic "steeple sign" (subglottic narrowing), but imaging is not required for diagnosis.
• Management: Guided by croup severity (Westley Croup Score).
  • Mild Croup (no stridor at rest): Managed out-of-hospital with a single dose of oral dexamethasone (0.15–0.6 mg/kg).
  • Moderate-to-Severe Croup (stridor at rest, retractions): Requires nebulized racemic epinephrine (which rapidly decreases airway edema via alpha-1 constriction) plus dexamethasone. These patients must be observed for at least 3–4 hours after epinephrine administration for a rebound effect (return of stridor). If stridor recurs or respiratory distress persists, they require hospitalization.

Pediatric Asthma Exacerbations

Pediatric asthma is characterized by reversible airway obstruction, airway inflammation, and hyperresponsiveness.

• Acute Exacerbation Management: Includes repeated doses of inhaled short-acting beta-agonists (SABA; e.g., albuterol) and inhaled anticholinergics (e.g., ipratropium bromide) for moderate-to-severe distress. Systemic corticosteroids (oral prednisolone or IV methylprednisolone) are indicated for all moderate-to-severe exacerbations and those not fully responding to initial SABA.
• Severe/Refractory Cases: Intravenous magnesium sulfate (a bronchodilator acting via calcium-channel antagonism) is administered for severe exacerbations unresponsive to initial therapies. High-flow nasal cannula or non-invasive positive pressure ventilation (BiPAP) is utilized for impending respiratory failure. Intubation is a last resort due to the high risk of barotrauma and air trapping.

Common Childhood Exanthems

• Measles (Rubeola): Caused by the measles virus. Prodrome of high fever, cough, coryza, and conjunctivitis. Koplik spots (small bluish-white spots on buccal mucosa) are pathognomonic. The rash is an erythematous maculopapular eruption starting on the face and spreading cranio-caudally. Treatment is supportive; Vitamin A supplementation is recommended as it decreases mortality and morbidity.
• Rubella (German Measles): Mild illness with low-grade fever, maculopapular rash starting on the face and spreading down, and prominent postauricular, suboccipital, and posterior cervical lymphadenopathy. Polyarthritis can occur, especially in adolescent girls. Exposure in pregnancy risks Congenital Rubella Syndrome (cataracts, patent ductus arteriosus, sensorineural hearing loss, "blueberry muffin" rash).
• Roseola Infantum (Exanthem Subitum): Caused by human herpesvirus 6 (HHV-6). Typically presents in children < 2 years with a high fever (often > 40°C) lasting 3–5 days, which resolves abruptly, followed by the appearance of a rose-pink maculopapular rash starting on the trunk and spreading to the extremities. High fever increases the risk of simple febrile seizures.
• Erythema Infectiosum (Fifth Disease): Caused by parvovirus B19. Presents with mild prodrome followed by a bright red rash on the cheeks ("slapped-cheek" appearance) and a reticular, lacy rash on the trunk and extremities. High-risk populations include pregnant patients (risk of hydrops fetalis) and patients with chronic hemolytic anemias (e.g., sickle cell disease), in whom infection can precipitate an aplastic crisis (marked by reticulocytopenia).
• Varicella-Zoster (Chickenpox): Presents with fever, malaise, and a highly pruritic rash that progresses from macules to papules to vesicles on an erythematous base ("dewdrops on a rose petal"). Lesions appear in crops, resulting in lesions at different stages of evolution.
• Hand-Foot-and-Mouth Disease: Caused by coxsackievirus A16 or enterovirus 71. Presents with painful oral vesicles/ulcers (herpangina) and maculopapular or vesicular lesions on the palms, soles, and buttocks. Management is supportive.
• Scarlet Fever: Complication of group A streptococcal pharyngitis. Characterized by fever, sore throat, strawberry tongue, and a diffuse erythematous rash with a "sandpaper" texture that is accentuated in flexural creases (Pastia's lines). Treated with penicillin or amoxicillin to prevent acute rheumatic fever.