Necrotizing enterocolitis (NEC), characterized by inflammatory necrosis of the bowel, is the most common surgical emergency in neonates. The incidence of NEC is around 1–5 in every 1000 live births in the United States and the mortality rate ranges from 15% to 30%. Micropreemies are at particularly high risk for developing NEC, with an incidence of 5%–15% in infants with a birth weight <1500 g (Table 141-1).
TABLE 141-1Stages of Necrotizing Enterocolitis ||Download (.pdf) TABLE 141-1 Stages of Necrotizing Enterocolitis
|Stage ||Clinical ||Gastrointestinal ||Radiologic |
|I (suspected) ||Apnea, bradycardia, lethargy, temperature instability ||Abdominal distention, bloody stool, gastric residual ||Intestinal dilation, ileus |
|IIA (definite) ||– ||Absent bowel sound, grossly bloody stool ||Pneumatosis intestinalis |
|IIB (definite) ||Metabolic acidosis, thrombocytopenia ||Abdominal wall edema and tenderness ||Portal venous gas |
|IIIA (advanced) ||Hypotension, respiratory and metabolic acidosis, disseminated intravascular coagulation (DIC), neutropenia ||Peritonitis, erythema, induration ||Ascites |
|IIIB (advanced) ||Shock ||– ||Pneumoperitoneum |
The exact cause of NEC is as of yet unknown, but multiple factors have been implicated. It is thought that intestinal ischemia contributes to the development of NEC, because reperfusion of the bowel following ischemic injury can cause vascular congestion and hemorrhage. Numerous pathogenic organisms have been connected to outbreaks of NEC. Because microorganisms can proliferate in milk present in the gut of infants, enteral milk feedings have also been implicated as a risk factor.
More than 90% of infants with NEC are premature, often with a gestational age of fewer than 32 weeks. Other risk factors include hypotension, respiratory distress syndrome, patent ductus arteriosus, and apnea. Congenital heart disease and perinatal hypoxia are the greatest risk factors for NEC in full-term infants.
The earliest symptoms of NEC are nonspecific such as poor feeding, vomiting, lethargy, temperature instability, apnea, and bradycardia. Abdominal distention, intestinal dilation, and ileus with edematous bowel are often observed. Pneumatosis intestinalis or portal venous air are significant factors in confirming diagnosis and are often accompanied by metabolic and hematologic abnormalities including thrombocytopenia, coagulopathies, anemia, and hyperglycemia. In the severe stages of NEC, infants may present with intestinal necrosis or perforation and respiratory instability. Morbidity includes short gut syndrome and sepsis.
Medical treatment of NEC includes discontinuation of enteral feedings, decompression of the abdomen, intravenous (IV) fluids, and broad-spectrum antibiotics. Packed red blood cells (PRBC) and platelets are transfused as needed. Laboratory studies should be obtained, including blood count, platelet count, and acid–base studies. Dopamine may be used to increase intestinal perfusion.
In 20%–40% of patients, clinical symptoms of NEC may persist or worsen and require surgical intervention. Indications for surgery include persistent metabolic acidosis, intestinal obstruction, or perforation. Surgical procedures involve either peritoneal drainage at the bedside or exploratory laparotomy.