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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. Plain radiographs of the abdomen are useful by showing evidence of extraluminal gas (pneumatosis, portal venous gas or pneumoperitoneum) or an abnormal bowel gas pattern, particularly a persistently unaltered gas-filled dilated loop of bowel on serial radiographs (fixed loop). More recently ultrasonography has proven to be useful as it may detect signs and complications of NEC before they are evident on radiographs.
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, parenteral nutrition, and prompt antibiotic therapy. Monitoring is clinical, although serial supine and left lateral decubitus abdominal roentgenograms should be performed every 6 hours. Signs of radiographic worsening of NEC include dilated bowel loops, pneumatosis intestinalis, portal venous gas, and pneumoperitoneum. Where the disease is not halted through medical treatment alone, or when the bowel perforates, immediate emergency surgery to resect the dead bowel is required. This 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.
NEC has no definitive known cause. An infectious agent has been suspected, as cluster outbreaks in neonatal intensive care units (NICUs) have been seen, but no common organism has been idenitfied. A combination of intestinal flora, inherent weakness in the neonatal immune system, alterations in mesenteric blood flow and milk feeding may be factors. NEC is almost never seen in infants before oral feedings are initiated.
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. Longterm 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.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Necrotizing_enterocolitis". A list of authors is available in Wikipedia.|