Monitoring is clinical, although serial supine and left lateral decubitus abdominal X-rays should be performed every six hours.As an infant recovers from NEC, feeds are gradually introduced. "Trophic feeds" or low-volume feeds (<20 ml/kg/day) are usually initiated first. How and what to feed are determined by the extent of bowel involved, the need for surgical intervention, and the infants clinical appearance.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 develop short bowel syndrome if extensive portions of the bowel must be removed.In the case of an infant whose bowel is left in discontinuity, the surgical creation of a mucous fistula or connection to the distal bowel may be helpful, as this allows for refeeding of ostomy output to the distal bowel. This refeeding process is believed to improve bowel adaptation and aid in advancement of feeds. Prognosis
Typical recovery from NEC if medical, nonsurgical 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.
The condition was first described between 1888 and 1891. 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 and failure to thrive, 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. Cause
The exact cause is unclear. Several risk factors have been implicated:

Maternal factors
Acid-suppressing medications
Chorioamnionitis
Cocaine abuse
In utero growth restriction
Increased body mass index
Intrahepatic cholestasis during pregnancy
Lack of prenatal steroids
Mode of delivery
Placental abruption
Pre-eclampsia
Smoking

Main risk factors
Low birth weight
Prematurity
Formula feeding (bovine based)
Intestinal dysbiosis

Other risk factors
Acute hypoxia
Antibiotic exposure
Blood transfusions
Cardiac anomalies
Neonatal anemia
Poor intestinal perfusion
Prolonged use of indomethacin for patent  ductus arteriosus closure

Diagnosis
Diagnosis is usually suspected clinically, but often requires the aid of diagnostic imaging, most commonly radiography, which can show the intestines and may show areas with death tissue or a bowel perforation.