10.3 Paediatric Abdominal Emergencies, Dehydration & Neonatal Jaundice

Paediatric Abdominal Emergencies, Dehydration & Neonatal Jaundice

Paediatric abdominal emergencies span a diverse spectrum of congenital anatomical anomalies, mechanical obstructions, and acute inflammatory conditions. Timely diagnosis is vital because clinical deterioration can occur swiftly, with dehydration and electrolyte collapse compounding surgical pathology. Concurrently, jaundice in the neonatal period requires immediate differentiation between physiological unconjugated hyperbilirubinaemia and life-threatening biliary atresia.

Paediatric Surgical Abdominal Emergencies

Three conditions dominate paediatric gastrointestinal emergencies: infantile hypertrophic pyloric stenosis, intussusception, and Hirschsprung's disease.

Infantile Hypertrophic Pyloric Stenosis (IHPS)

IHPS results from hypertrophy and hyperplasia of the circular smooth muscle fibres of the pyloric sphincter, creating functional gastric outlet obstruction.

• Metabolic Derangement: Persistent vomiting of gastric hydrochloric acid (HCl) causes severe hypochloraemic, hypokalaemic metabolic alkalosis.
• Paradoxical Aciduria Mechanism: As systemic dehydration worsens, secondary hyperaldosteronism stimulates renal sodium reabsorption in the distal nephron. To conserve sodium, the kidney excretes potassium. Once severe hypokalaemia ensues, the kidney is forced to secrete hydrogen ions (H⁺) into the urine instead of potassium, producing the paradoxical phenomenon of acidic urine in the face of systemic metabolic alkalosis.
• CRITICAL SURGICAL RULE: Pyloric stenosis is a MEDICAL RESUSCITATION EMERGENCY, not an immediate surgical emergency. An infant must never be taken to the operating theatre while metabolic alkalosis persists (venous bicarbonate > 30 mmol/L or chloride < 100 mmol/L), as alkalosis significantly increases the risk of life-threatening postoperative central apnoea under general anaesthesia. Resuscitate with IV 0.9% normal saline supplemented with 5% dextrose and 20–40 mmol/L potassium chloride until electrolytes, acid-base parameters, and hydration are entirely normalized.

Intussusception

Intussusception involves the invagination ("telescoping") of a proximal segment of bowel into an adjacent distal segment. In over 85% of cases, it is ileocolic.

• Aetiology: In infants under 2 years, it is usually idiopathic, secondary to lymphoid hyperplasia of Peyer's patches triggered by a viral illness (adenovirus, rotavirus). In older children (> 2 years), a pathological lead point must be suspected (Meckel's diverticulum, polyp, Henoch-Schönlein purpura haematoma, or intestinal lymphoma).
• First-Line Intervention: Radiological reduction via pneumatic (air) or hydrostatic contrast enema under fluoroscopic or ultrasound monitoring (success rate > 80%).
• Contraindications to Enema: Signs of generalized peritonitis, bowel perforation, shock, or frank intestinal necrosis. These cases require urgent resuscitation, intravenous antibiotics, and emergency exploratory laparotomy for manual reduction or bowel resection.

Assessment and Management of Paediatric Dehydration

Gastroenteritis is the primary cause of acute dehydration in children. Fluid depletion must be assessed methodically using objective clinical signs in accordance with NICE guideline CG84 (Diarrhoea and vomiting caused by gastroenteritis in under 5s); intravenous fluid prescribing in children follows NICE NG29 (Intravenous fluid therapy in children and young people in hospital).

Clinical Staging of Dehydration (NICE CG84)

Fluid Replacement Protocols

1. Management of Clinical Shock:
   • Immediate intravenous access (or intraosseous needle if IV access fails within 90 seconds).
   • Administer an immediate bolus of 10 mL/kg 0.9% normal saline (or 20 mL/kg in older children) over 10 to 15 minutes.
   • Re-evaluate ABCDE immediately. If signs of shock persist, repeat a second 10 mL/kg bolus and seek immediate senior paediatric or PICU assistance.
2. Management of Clinical Dehydration (Without Shock):
   • First-line therapy is Oral Rehydration Salt (ORS) solution: 50 mL/kg administered over 4 hours, given frequently in small volumes (e.g., 5 mL by syringe every 2–5 minutes).
   • If the child vomits persistently, consider an oral dose of ondansetron (if child > 6 months) or administer ORS via a nasogastric tube.
3. Intravenous Maintenance & Deficit Therapy:
   • Indicated if ORS fails, if there is persistent vomiting despite ondansetron, or if intestinal ileus occurs.
   • Deficit Volume: Calculate as % dehydration × weight (kg) × 10 mL (e.g., 5% dehydration in a 10 kg infant = 500 mL) replaced steadily over 24 to 48 hours.
   • Holliday-Segar Daily Maintenance Rule:
     • First 10 kg: 100 mL/kg/day
     • Next 10 kg (10–20 kg): 50 mL/kg/day
     • Each kg above 20 kg: 20 mL/kg/day
   • Fluid Composition: Isotonic crystalloids (e.g., 0.9% normal saline with 5% glucose and potassium chloride). Never use hypotonic fluids (e.g., 0.18% saline) due to the risk of acute hyponatraemic encephalopathy and brain herniation.

Neonatal Jaundice: Physiological vs Pathological

Jaundice affects up to 60% of term infants and 80% of preterm infants in the first week of life due to physiological polycythaemia, shortened erythrocyte lifespan (80 days vs 120 days), and developmental immaturity of hepatic uridine diphosphate glucuronosyltransferase (UGT1A1).

Temporal Classification of Neonatal Jaundice

• Jaundice Presenting < 24 Hours of Life: ALWAYS PATHOLOGICAL.
  • Causes: Haemolytic disease of the newborn (ABO incompatibility, Rhesus isoimmunisation), red cell enzyme defects (G6PD deficiency, pyruvate kinase deficiency), red cell membrane defects (hereditary spherocytosis), or congenital intrauterine infections (TORCH: Toxoplasma, Rubella, CMV, Herpes).
  • Investigations: Urgent total and conjugated serum bilirubin, maternal and neonatal blood group, Direct Antiglobulin Test (DAT / Coombs test), full blood count, and blood film.
• Physiological Jaundice (Onset > 24 Hours to 14 Days):
  • Typically appears on day 2–3, peaks on day 4–5, and completely resolves by day 10–14 in term infants (day 21 in preterm).
  • Predominantly unconjugated hyperbilirubinaemia.
  • Breast milk jaundice: A benign form of unconjugated jaundice in healthy, thriving, breastfed infants that may persist for up to 3 to 12 weeks. Caused by beta-glucuronidase in maternal breast milk increasing intestinal deconjugation and enterohepatic bilirubin circulation.
• Prolonged Jaundice (> 14 Days in Term; > 21 Days in Preterm):
  • Mandatory evaluation: Total AND conjugated (direct) bilirubin, liver function tests, thyroid function tests (screening for congenital hypothyroidism), and clean catch urine microscopy and culture.

Biliary Atresia: The Critical Time-Sensitive Surgical Emergency

• Pathology: Idiopathic progressive inflammatory obliterative cholangiopathy resulting in complete fibro-obliteration of the extrahepatic biliary tree, leading to biliary cirrhosis and hepatic failure.
• Cardinal Features: Persistent jaundice beyond 14 days of life, acholic (pale, clay-coloured, or chalky) stools, and dark tea-coloured urine that stains nappies yellow.
• Laboratory Hallmark: Conjugated hyperbilirubinaemia, defined as conjugated bilirubin > 25 µmol/L (or > 20% of total bilirubin).
• Definitive Treatment: Urgent Kasai portoenterostomy (hepatoportoenterostomy) to restore bile flow from the porta hepatis into a Roux-en-Y jejunal loop. Outcomes are best when it is performed early, ideally before about 8 weeks (60 days) of age; bile drainage is restored in roughly half to two-thirds of infants, and later surgery means more progression to biliary cirrhosis and a greater need for liver transplantation.

Mesenteric Adenitis

Inflammation of the mesenteric lymph nodes, often after a viral upper respiratory tract infection, causing right iliac fossa pain and fever in children that can mimic appendicitis. Ultrasound may show enlarged mesenteric nodes with a normal appendix. It is a diagnosis of exclusion: safety-net carefully and re-examine, because appendicitis can still develop.