|Classification and external resources|
Radiograph of an infant with necrotizing enterocolitis
Necrotizing enterocolitis (NEC) is a medical condition primarily seen in premature infants, where portions of the bowel undergo necrosis (tissue death). It occurs postnatally (i.e., is not seen in stillborn infants) and is the second most common cause of morbidity in premature infants, causing 386 deaths in the United States in 2011, down from 472 in 2010.
Signs and symptoms
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). 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.
The diagnosis is usually suspected clinically but often requires the aid of diagnostic imaging modalities, most commonly radiography. Specific radiographic signs of NEC are associated with specific Bell's stages of the disease:
Bell's stage 1/Suspected disease:
- Mild systemic disease (apnoea, bradycardia, temperature instability)
- Mild intestinal signs (abdominal distention, gastric residuals, bloody stools)
- Non-specific or normal radiological signs
Bell's stage 2/Definite disease:
- Mild to moderate systemic signs
- Additional intestinal signs (absent bowel sounds, abdominal tenderness)
- Specific radiologic signs (pneumatosis intestinalis or portal venous air)
- Laboratory changes (metabolic acidosis, thrombocytopaenia)
Bell's stage 3/Advanced disease:
- Severe systemic illness (hypotension)
- Additional intestinal signs (striking abdominal distention, peritonitis)
- Severe radiologic signs (pneumoperitoneum)
- Additional laboratory changes (metabolic and respiratory acidosis, disseminated intravascular coagulation)
More recently ultrasonography has proven to be useful as it may detect signs and complications of NEC before they are evident on radiographs, specifically in cases that involve a paucity of bowel gas, a gasless abdomen, or a sentinel loop. Diagnosis is ultimately made in 5–10% of very low-birth-weight infants (<1,500g). It is not known, however, whether some underlying pathology contributes to premature birth and low birth weight.
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, and prompt antibiotic therapy. Monitoring is clinical, although serial supine and left lateral decubitus abdominal roentgenograms should be performed every six 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 from 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. In a 2012 policy statement, the American Academy of Pediatrics recommended feeding preterm infants human milk, finding "significant short- and long-term beneficial effects," including lower rates of NEC. 
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.)
Neonatologists at the University of Iowa reported on the importance of providing small amounts of trophic oral feeds of human milk starting as soon as possible, 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. 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.
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Typical recovery from NEC if medical, non-surgical treatment succeeds, includes 10–14 days or more without oral intake and then demonstrated ability to resume feedings and gain weight. Recovery from NEC alone may be compromised by co-morbid conditions that frequently accompany prematurity. Long-term complications of medical NEC include bowel obstruction and anemia.
Despite a significant mortality risk, long-term prognosis for infants undergoing NEC surgery is improving, with survival rates of 70–80%. "Surgical NEC" survivors are at-risk for complications including short bowel syndrome and neurodevelopmental disability.
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