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|Metabolic acidosis
Affects about 5% of infants with birthweight < 1,500 g and typically is characterized by abdominal distension, bloody stools and pneumatosis intestinalis and bile stained vomiting
About
- Affects premature neonates
- Can lead to bowel perforation and peritonitis and septic shock
- Mortality can be 20-30%
Aetiology
- Immaturity of intestinal mucosa
- Intestinal ischaemia/reperfusion injury, infection, and immature immune response.
- Inflammatory mediators (e.g., PAF, TNF, cytokines) that precipitate intestinal injury.
Risks
- Low birth weight, Very premature, Formulae feeds
- Congenital heart disease
- Enteral feeds, bacterial overgrowth
- Polycythaemia
- Patent ductus arteriosus (PDA, decreased systemic output due to left-right shunt)
- Indomethacin (decreased intestinal perfusion through inhibition of cyclo-oxygenase)
- Steroids, when given in conjunction with indomethacin
- Umbilical arterial catheter (UAC) with tip at or above inferior mesenteric artery
- Umbilical venous catheter (UVC) with tip in portal system (especially with exchange
transfusion)
- Cocaine exposure in utero
- Respiratory Distress Syndrome
Clinical
- Difficult feeding or vomiting
- Unwell, green bile vomit, swollen tender abdomen
- Absent bowel sounds, blood in stools
- Perforation - rigid abdomen, moribund, tenderness
- Abdomen Distension, Mass, Abdominal wall oedema
- Ascites, Crepitus, Inflammatory hydrocele.
Investigations
- FBC, WCC elevated WCC, elevated CRP high lactate, low platelets
- Coag: DIC
- U&E: AKI and low Na
- Blood gas: Metabolic acidosis
- AXR: bowel wall oedema, gas in bowel wall, free gas, gas in portal veins. The best way to demonstrate free air is to do a right-side-up lateral decubitus view which may show air over the right lobe of the liver. Free air can be diagnosed on a supine film (visible falciform ligament, “double contrast" effect of air on both sides of the bowel wall, liver shadow darker centrally than peripherally). Lack of free air does not exclude perforation.
Staging Bell's Criteria
- Stage 1. Suspected NEC: gastric residuals, abdominal distension, occult or gross blood
in stool, x-ray normal to mild distension, temperature instability, apnoea, bradycardia
- Stage 2. Definite NEC: mild to moderate systemic illness, absent bowel sounds,
abdominal tenderness, pneumatosis intestinalis or portal venous gas, metabolic
acidosis, ? platelets
- Stage 3. Advanced NEC: severely ill, marked distension, signs of peritonitis,
hypotension, metabolic & respiratory acidosis, DIC, pneumoperitoneum if bowel
perforation present
Management
- Resuscitation: may need to include circulatory support, correction of acid/base status, intubation and ventilation, platelet transfusion, WBC transfusion etc. Most infants with established NEC with require analgesia with morphine infusion.
- All babies with suspected or proven NEC should be commenced on 10 days:Nil by mouth, IV feeding, Antibiotics, NBM and NG tube and IV fluids and TPN and Antibiotics
- Urgent surgical referral and may need bowel resection. Assessment of the need for, and timing of, surgery may be difficult. Free air is usually an indication for surgery although in very small babies (eg <1000g) surgery may be avoided and a peritoneal drain inserted instead. Dead bowel is usually manifested by an abdominal mass, erythema and persisting acidosis/thrombocytopaenia/hyponatraemia. Surgical treatment will comprise excision of any dead gut with either primary anastomosis or stoma formation [or open and close with relook at 48 hours if all gut affected]. Extensive bowel resection may result in short bowel syndrome and long term TPN.
- If NEC develops in a baby with PDA, begin medical management and consider urgent operative closure of PDA. Do not give indomethacin to an infant with
suspected or definite NEC.
Complications
- Peritonitis
- Sepsis and death
- Strictures
- Short bowel syndrome
References