The condition is typically seen in premature infants, and the timing of its onset is generally inversely proportional to the gestational age of the baby at birth, i.e. the earlier a baby is born, the later signs of NEC are typically seen.^[3] Initial symptoms include feeding intolerance, increased gastric residuals, abdominal distension and bloody stools. Symptoms may progress rapidly to abdominal discoloration with intestinal perforation and peritonitis and systemic hypotension requiring intensive medical support.

Diagnosis

The diagnosis is usually suspected clinically but often requires the aid of diagnostic imaging modalities. Radiographic signs of NEC include dilated bowel loops, paucity of gas, a "fixed loop" (unaltered gas-filled loop of bowel), pneumatosis intestinalis, portal venous gas, and pneumoperitoneum (extraluminal or "free air" outside the bowel within the abdomen). The pathognomonic finding on plain films is pneumatosis intestinalis.^[4] More recently ultrasonography has proven to be useful as it may detect signs and complications of NEC before they are evident on radiographs. Diagnosis is ultimately made in 5–10% of very low-birth-weight infants (<1,500g).^[5] However, it is not known whether some underlying pathology contributes to premature birth and low birth weight.

The clinical features are divided into 3 stages:

Stage 1 — Apnea, bradycardia, lethargy, abdominal distension and vomiting.

Stage 2 — Pneumatosis intestinalis and the above features.

Stage 3 — Low blood pressure, bradycardia, acidosis, disseminated intravascular coagulation (DIC) and anuria.

Treatment

Treatment consists primarily of supportive care including providing bowel rest by stopping enteral feeds, gastric decompression with intermittent suction, fluid repletion to correct electrolyte abnormalities and third space losses, support for blood pressure, parenteral nutrition,^[6] and prompt antibiotic therapy. Monitoring is clinical, although serial supine and left lateral decubitus abdominal roentgenograms should be performed every 6 hours. Where the disease is not halted through medical treatment alone, or when the bowel perforates, immediate emergency surgery to resect the dead bowel is generally required, although abdominal drains may be placed in very unstable infants as a temporizing measure. Surgery may require a colostomy, which may be able to be reversed at a later time. Some children may suffer later as a result of short bowel syndrome if extensive portions of the bowel had to be removed.

Once a child is born prematurely, thought must be given to decreasing the risk for developing NEC. Toward that aim, the methods of providing hyperalimentation and oral feeds are both important. The American Academy of Pediatrics, in a 2012 policy statement, recommended feeding preterm infants human milk, finding "significant short- and long-term beneficial effects," including lower rates of NEC. ^[7]

A study by researchers in Peoria, IL, published in Pediatrics in 2008, demonstrated that using a higher rate of lipid (fats and/or oils) infusion for very low birth weight infants in the first week of life resulted in zero infants developing NEC in the experimental group, compared with 14% with NEC in the control group (They started the experimental group at 2 g/kg/d of 20% IVFE and increased within two days to 3 g/kg/d; Amino acids were started at 3 g/kg/d and increased to 3.5).^[8]

Neonatologists at the University of Iowa NICU reported on the importance of providing small amounts of trophic oral feeds of human milk starting ASAP, while the infant is being primarily fed intravenously, in order to prime the immature gut to mature and become ready to receive greater oral intake.^[9] Human milk from a milk bank or donor can be used if mother's milk is unavailable. The gut mucosal cells do not get enough nourishment from arterial blood supply to stay healthy, especially in very premature infants, where the blood supply is limited due to immature development of the capillaries, so nutrients from the lumen of the gut are needed.