History
The clinical presentation of necrotizing enterocolitis (NEC) includes nonspecific aspects of the history, such as vomiting, diarrhea, feeding intolerance and high gastric residuals following feedings. More specific GI tract symptoms include abdominal distention and frank or occult blood in the stools.
With disease progression, abdominal tenderness, abdominal wall edema, erythema, crepitans, or palpable bowel loops indicating a fixed and dilated loop of bowel may develop. Systemic signs, such as apnea, bradycardia, lethargy, labile body temperature, hypoglycemia, and shock, are indicators of physiologic instability.
Epidemiologic studies demonstrate that demographics, risk factors, patient characteristics, and clinical course differ significantly between term and preterm infants with NEC.
Term baby
Compared with a preterm infant, a term baby with NEC presents at a younger age, with a reported median age of onset that ranges from 1-3 days of life in the immediate postnatal period but that may appear as late as age 1 month.
The term neonate who is immediately affected postnatally is usually systemically ill with other predisposing conditions, such as birth asphyxia, respiratory distress, congenital heart disease, or metabolic abnormalities, or has a history of abnormal fetal growth pattern.
Maternal risk factors that reduce fetal gut blood flow, such as placental insufficiency from acute disease (eg, pregnancy-induced hypertension), chronic disease (eg, diabetes), or maternal cocaine abuse, can increase the baby's risk for developing NEC.
Specific signs and symptoms that may be part of the history include bilious vomiting or gastric aspirates, abdominal distention, passage of blood per rectum, abdominal radiographs that reveal dilated loops of bowel, pneumatosis intestinalis, free abdominal air, and other signs of systemic infection, including shock and acidosis.
Premature baby
Premature babies are at risk for developing necrotizing enterocolitis for several weeks after birth, with the age of onset inversely related to gestational age at birth.
Premature infants with patent ductus arteriosus are at higher risk for developing NEC earlier in life, particularly if they are treated with indomethacin for pharmacologic closure. However, patients with persistent patent ductus arteriosus who ultimately required surgical ligation were found to have a higher NEC-associated mortality rate than did patients whose patent ductus arteriosus was successfully closed without surgery.
Patients are typically advancing on enteral feedings or may have achieved full-volume feeds when symptoms develop.
Increased incidence in the posttransfusion period has been reported in otherwise healthy premature babies who are feeding enterally and undergo blood transfusion for asymptomatic anemia of prematurity.
Presenting symptoms may include subtle signs of feeding intolerance that progress over several hours to a day, subtle systemic signs that may be reported enigmatically by the nursing staff as "acting different," and, in advanced disease, a fulminant systemic collapse and consumption coagulopathy.
Symptoms of feeding intolerance can include abdominal distention/tenderness, delayed gastric emptying as evidenced by increasing gastric residuals, and, occasionally, vomiting.
Systemic symptoms can insidiously progress to include nonspecific signs and symptoms, such as increased apnea and bradycardia, lethargy, and temperature instability, among the primary manifestation(s).
Patients with fulminant NEC present with profound apnea, rapid cardiovascular and hemodynamic collapse, and shock.
The baby's feeding history can help increase the index of suspicion for early NEC. Babies who are breastfed have a lower incidence of NEC than do formula-fed babies.
Rapid advancement of formula feeding has been associated with an increased risk of NEC. [21] However, multiple subsequent studies have failed to substantiate this finding.
Physical Examination
The pertinent physical findings in patients who develop necrotizing enterocolitis (NEC) can be primarily GI, primarily systemic, indolent, fulminant, or any combination of these. A high index of clinical suspicion is essential to minimize potentially significant morbidity or mortality.
GI signs can include any or all of the following:
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Increased abdominal girth
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Visible intestinal loops
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Obvious abdominal distention and decreased bowel sounds
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Change in stool pattern
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Hematochezia
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Palpable abdominal mass
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Erythema of the abdominal wall
Systemic signs can include any of the following:
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Respiratory failure
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Decreased peripheral perfusion
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Circulatory collapse
With insidious onset, the clinical signs may be mild, whereas patients with fulminant disease can present with severe clinical abnormalities.
If abdominal signs are present, surgical consultation may be advisable. Disease progression ranges from indolent to fulminant, and early and expeditious involvement of surgical colleagues can be helpful, especially if appropriate surgical care requires transfer to another facility.
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Normal (top) versus necrotic section of bowel. Photo courtesy of the Department of Pathology, Cornell University Medical College.
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Pneumatosis intestinalis. Photo courtesy of Loren G Yamamoto, MD, MPH, Kapiolani Medical Center for Women & Children, University of Hawaii, with permission.
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Pneumatosis intestinalis. Photo courtesy of Loren G Yamamoto, MD, MPH, Kapiolani Medical Center for Women & Children, University of Hawaii, with permission.
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Pneumatosis intestinalis. Photo courtesy of Loren G Yamamoto, MD, MPH, Kapiolani Medical Center for Women & Children, University of Hawaii, with permission.
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Pneumatosis intestinalis. Photo courtesy of Loren G Yamamoto, MD, MPH, Kapiolani Medical Center for Women & Children, University of Hawaii, with permission.
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Pneumoperitoneum. Photo courtesy of the Department of Pathology, Cornell University Medical College.
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Resected portion of necrotic bowel. Photo courtesy of the Department of Pathology, Cornell University Medical College.
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Micrograph of mucosal section showing transmural necrosis. Photo courtesy of the Department of Pathology, Cornell University Medical College.
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Histologic section of mucosal wall demonstrating pneumatosis. Photo courtesy of the Department of Pathology, Cornell University Medical College.
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Histologic section of bowel mucosa showing regeneration of normal cellular architecture. Photo courtesy of the Department of Pathology, Cornell University Medical College.
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Extensive pneumatosis intestinalis.
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Necrotizing enterocolitis totalis. Pneumatosis intestinalis and multiple areas of perforation were seen.
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Pneumatosis intestinalis.
