NECROTIZING ENTEROCOLITIS
Overview
Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in the neonatal period. Involving ischemic necrosis of the bowel wall, or intestinal mucosa, gas-producing enteric organisms invade the mucosal lining of the intestine (pneumatosis intestinalis) potentially resulting in focal or widespread bowel perforation.
NEC occurs in one to three per 1,000 live births and occurs predominantly in preterm infants, with an incidence of approximately 6% to 7% in very-low-birth-weight (VLBW) infants (birth weight less than 1,500 g; Stoll et al., 2015). Secondary disease is most often seen in full-term infants with comorbid conditions, including birth asphyxia, trisomy 21, congenital heart disease, rotavirus infection, and Hirschsprung’s disease. In neonatal intensive care units (NICUs) alone, NEC occurs in 1% to 5% of patients, accounting for nearly 20% of NICU costs annually (Gephart, McGrath, Effken, & Halpern, 2012). The overall incidence in the United States is approximately 3,000 infants annually with 1,000 infants succumbing to the disease.
Variations in the severity of this disorder occur, but all cases result in substantial short- and long-term morbidity in survivors. Morbidity and mortality rates associated with NEC have not improved in decades despite other substantial advances in neonatal care. The average mortality from NEC is 20% to 30%, with mortality as high as 50% for those infants requiring surgical intervention (Fitzgibbons et al., 2009). Characterized by host intestinal immaturity and multifactorial influences, reduction in the incidence and severity of NEC has focused on the identification and elimination of risk factors.
Background
The Centers for Disease Control and Prevention (CDC) defines NEC as a condition occurring in infants less than or equal to 1 year of age and meeting one of the two criteria: (a) at least one clinical sign (bilious aspirate, vomiting, abdominal distension, or occult/gross blood in stools without rectal fissure) and one imaging test finding (pneumatosis intestinalis, portal venous gas, or pneumoperitoneum or (b) one surgical finding (surgical evidence of extensive bowel necrosis, more than 2 cm of bowel affected, or surgical evidence of pneumatosis intestinalis with or without intestinal perforation; CDC, 2018).
Although the pathogenesis of NEC is complex and multifactorial, three major risk factors have been implicated in its development: prematurity, bacterial colonization of the gut, and formula feeding (Hackam, Afrazi, Good, & Sodhi, 2013). NEC is characterized by inflammation and initiated by impaired mesenteric perfusion with loss of mucosal integrity followed by necrosis. Disrupted, abnormal 203colonization of the intestine, mucosal barrier dysfunction, and an exaggerated, immune response contribute to the potential devastating consequences of the disease. Subsequent perforation of the bowel may occur at any location, allowing free air to migrate beyond the intestinal lumen to the peritoneum or venous portal system, progressing to peritonitis, sepsis, and death. The terminal ileum and colon are often affected, and, in its most severe form, the entire intestine may be involved.
Clinical manifestations vary and can be insidious or catastrophic in the presentation. Commonly, the infant who presents with NEC has been thriving and suddenly presents with clinical instability. Symptoms are typically nonspecific and suggestive of general instability, including temperature instability, apnea and bradycardia, hypotension, thrombocytopenia, abdominal tenderness or distension, abdominal wall erythema or discoloration, gastric residuals, absent bowel sounds, emesis, or blood in the stool.
Although NEC may occur as late as 3 months of age in VLBW infants, it typically presents in the second or third week of life. The greatest single risk factor for NEC is prematurity, with the rate of NEC decreasing after 32 weeks postmenstrual age. The majority of patients have received enteral feedings before diagnosis. Additional risk factors for the development of NEC include immaturity of the host immunologic system, luminal factors, intestinal epithelial barrier, and gut motility. Bacterial overgrowth in the context of low gastric–hydrogen ion output in the neonate contributes to the colonization of enteric pathogens (Carrion & Egan, 1990).
Effective treatment depends on a multisystem approach, including bowel rest, gastric decompression, supportive hydration, and correction of hypotension, hyponatremia, and metabolic acidosis. Antibiotic surveillance is warranted for potential overwhelming sepsis, with concurrent antifungal therapy if bowel perforation is suspected. Surgical consultation should be initiated when NEC is suspected and there are concerning findings of fixed dilated loops of bowel or evidence of pneumoperitoneum (free peritoneal air or portal venous gas) present on abdominal radiographs. Surgical management may include placement of a peritoneal drain or laparotomy with bowel resection for the removal of necrotic bowel.
Clinical Aspects
ASSESSMENT
NEC is a progressive disease necessitating serial laboratory testing, radiographic surveillance, and keen clinical assessment. The most significant single predictor of outcome following NEC is gestational age. When controlled for gestational age, whether or not the infant needs surgery is predictive of outcome; however, mortality and morbidity are highest in those infants requiring surgical intervention (Henry & Moss, 2008). There are also poorer long-term developmental outcomes in infants requiring surgical intervention versus medical management of NEC.
204NURSING INTERVENTIONS, MANAGEMENT, AND IMPLICATIONS
Nursing care focuses on surveillance for NEC in populations at risk, with early recognition of clinical symptoms, serial clinical assessments, and preparation for surgery or transport to a tertiary care center. A high index of suspicion in any infant meeting the identified risk factors during the prenatal, intrapartum, or postpartum course should prompt intensive surveillance of signs and symptoms; serial radiographs, measurement of abdominal girth, analysis of blood pressure, intake, output, and acid–base balance are important indicators of severity of disease. Optimal outcome following the diagnosis of NEC rests on early recognition, treatment, and access to a tertiary care center when progressive disease or bowel perforation is suspected.
Research has identified strategies to reduce the incidence of NEC. Prenatal strategies for prevention include maternal administration of antenatal corticosteroids (ANCS). A Cochrane review has suggested that maternal treatment with a single course of antenatal steroids reduced NEC by 46% (Brownfoot, Gagliardi, Bain, Middleton, & Crowther, 2013).
The use of human milk has been shown to be protective against NEC in multiple randomized controlled trials. Donor breast milk for enteral feedings is protective when maternal breast milk is not available (Quigley & McGuire, 2014). Nursing support of maternal breast feeding or pumping of breast milk is influential in the prevention of NEC, especially in preterm infants.
Standardized, unit-specific feeding protocols guiding slow advancement of feeding volume and caloric density, avoidance of hypertonic formulas and medications, and prompt treatment of polycythemia are additional preventive measures suggested in the literature, although with less scientific rigor. In a recent meta-analysis (Morgan, Young, & McGuire, 2015), the slow advancement of enteral feedings delays the establishment of full enteral feedings but did not show a statistically significant effect on the risk of NEC in very preterm or VLBW infants.
Ibuprofen treatment as an alternative to indomethacin for closure of a patent ductus arteriosus, which is a common complication in very preterm infants, has been associated with a reduction in the incidence of NEC (Ohlsson, Walia, & Shah, 2015). Also of note, probiotics have been cited as having a protective effect in the prevention of NEC in premature infants, and in the reduction of severity as well as the mortality (Neu, 2014). Ongoing research is focused on the safest preparation and administration of probiotics.
Summary
Early recognition and aggressive treatment of this disorder have improved clinical outcomes, yet NEC accounts for substantial long-term morbidity and mortality, especially in VLBW infants. Effective preventive strategies include the feeding of breast milk and the use of standardized feeding guidelines. Nurses play a critical role in recognizing signs and symptoms of NEC to facilitate early diagnosis and treatment in infants at highest risk, and in encouraging mothers to provide breast milk.
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