Feeding Intolerance in Preterm Infants

Feeding intolerance in preterm infants is the inability to digest enteral feeds, shown by gastric residuals, vomiting or abdominal distension that forces feeds to be reduced or stopped. There is no universal definition, and most cases reflect gut immaturity rather than disease.

It affects about a quarter to a half of very preterm infants, with the highest rate at gestations under 28 weeks. It delays full enteral feeding and prolongs parenteral nutrition, which raises the risk of sepsis and cholestasis.

Causes are immaturity, delayed introduction of feeds, rapid advancement, medications (opioids, caffeine), infection, necrotising enterocolitis, patent ductus arteriosus, anaemia, intestinal obstruction and electrolyte disturbance.

Pathophysiology.

Gastric emptying, small bowel motility, lactase activity and coordinated sucking and swallowing mature in the last trimester. Preterm infants have slow transit and a poorly coordinated migrating motor complex.

Gut hormone surges and mucosal growth depend on enteral stimulation, so withholding feeds worsens intolerance.

• Gastric residuals, regurgitation, vomiting, abdominal distension and delayed passage of stool.
• Apnoea, bradycardia or lethargy with feeds.
• Infant otherwise well in simple intolerance, with a soft abdomen.

Red flags.

• Bilious or blood stained vomit or aspirate.
• Rigid, tender, discoloured or rapidly distending abdomen, with absent bowel sounds.
• Blood in stool, temperature instability, apnoea, or shock.

• Clinical review of the abdomen, stool pattern, vital signs and feed history.
• Routine measurement of gastric residual is not advised. Large bilious residuals or those over a third to half of the previous feed with other signs need action.
• Full blood count, CRP, blood culture and gas when unwell. Abdominal radiograph (supine and lateral) when distension, bilious vomiting or blood in stool occurs, looking for pneumatosis, portal venous gas, perforation or obstruction.
• Abdominal ultrasound for bowel wall thickening, and contrast study for suspected malrotation.

Differential diagnosis. Necrotising enterocolitis, spontaneous intestinal perforation, sepsis, intestinal atresia or malrotation, Hirschsprung disease, meconium ileus or plug, metabolic disease and cow's milk protein intolerance.

• Exclude surgical disease and sepsis first. If necrotising enterocolitis is suspected, stop feeds and start the full medical and surgical regimen.
• In simple intolerance, avoid stopping feeds for long. Reduce volume or hold one or two feeds, then restart at the previous tolerated volume.
• Start trophic feeds of 10 to 20 mL/kg/day early, preferably with mother's own milk, then advance by 20 to 30 mL/kg/day as tolerated. Use donor milk when mother's milk is unavailable.
• Use continuous or slow bolus infusion over 30 to 60 minutes for infants who tolerate bolus feeds poorly, and place the infant prone or on the left side after feeds.
• Rectal stimulation or glycerol suppository to promote stool passage in delayed meconium passage.
• Prokinetic drugs have limited evidence. Erythromycin 3 mg/kg orally every 8 hours can be tried for up to 14 days under specialist direction, monitoring for QT prolongation and pyloric stenosis.
• Treat contributing factors: anaemia, infection, haemodynamically significant duct and constipation.

Monitoring. Daily weight, abdominal girth, stool, feed volumes, and the infant's response. Review urgently for any red flag.

Referral and escalation. Refer to paediatric surgery for bilious vomiting, signs of perforation or suspected obstruction.