Management of an NEC case is dependent on the stage of the disease based on Bell ’ s staging criteria (see Table 2). Generally, NEC is managed medically, surgically or in combination. Infants with vague symptoms such as apnea and bradycardia, abdominal distention and gastric residuals are often in mild stages of NEC and can be managed medically without further compromise to the bowel (Carter, 2007, p. 378). Medical management is aimed at treating the disease process once it has occurred and limiting the progression of disease.
Medical management of NEC is directed at preventing further injury to the bowel (Carter, 2007, p. 378, Thompson & Bizarro, 2008, p. 1232). Protocols vary between institutions, but most include stopping enteral feedings and initiating hyperalimentation for 10-14 days to allow for bowel rest and recovery, replacing gastric secretions, and preventing fluid and electrolyte imbalances. Respiratory and cardiovascular support including intubation and inotrope therapy are also required. Furthermore, serial kidney-ureter-bladder films are used to monitor for changes in bowel status (Carter, 2007, p.
378). According to Thompson and Bizarro (2008), a definite diagnosis of NEC – Stage ? 2A – usually call for pareneteral antibacterials for 7-14 days with bowel rest. In detail, earlier stages (stage ? IIIA) require bowel rest, parenteral antibacterials to limit bacterial invasion and translocation. The preterm is kept on nothing per orem [NPO] with total parenteral nutrition [TPN] for nutritional support. It is also crucial to evaluate systemic infection via sampling of the blood, urine and cerebrospinal fluid, if possible, for culture.
Antibacterial coverage is usually aimed at aerobic and anaerobic enteric species, and may include ampicillin or vancomycin for coverage of Gram-positive species; an aminoglycoside, such as gentamicin, or a third-generation cephalosporin, such as cefotaxime, for coverage of Gram-negative aerobes; and metronidazole or clindamycin for coverage of anaerobic organisms (p. 1232). Table 3 (from Thompson and Bizarro, 2008) lists some antibacterials used in the treatment of NEC.
Additional management includes clinical monitoring, cardiopulmonary support when needed, routine radiographic evaluation of disease progression (abdominal radiographs every 4-8 hours). Ultrasound may be used to evaluate/diagnose and may be able to detect pneumatosis intestinalis, portal venous gas, intraperitoneal gas, abnormal calibre of the bowel wall and lack of perfusion to the bowel. Vigilant monitoring of lab values is also a must and interventions may include transfusion of packed RBC to improve oxygen carrying capacity, and platelet and fresh frozen plasma transfusions to lessen the risk of hemorrhage (Thompson and Bizarro, 2008, p.
1232). However, 20–60% of neonates with NEC will require some type of surgical intervention (Thompson and Bizarro, 2008, p. 1232). Surgical intervention is indicated when the infant’s bowel has perforated, if there is evidence of necrotic bowel (such as fixed bowel loops, metabolic acidosis, disseminated intravascular coagulation, or septic shock), or if the infant’s condition worsens despite persistent medical management (Carter, 2007, p. 378). The goal for surgical treatment of NEC is to remove all necrotic bowel and preserve as much bowel length as possible (Yeo, 2006, p.
48). Decision is usually affected instability, size and tolerance to procedure and anesthesia based on the knowledge that up to 50% of ELBW NEC may die (Thompson and Bizarro, 2008, p. 1233). For neonates with intestinal perforation, laparotomy is performed with resection of the necrosed portion of intestine and an ostomy. Some may elect to perform resection and primary anastomosis. In some situations, a second laparotomy may be performed to re-evaluate areas of intestine with questionable viability.
This ‘second look’ may occur at 24–48 hours after the initial procedure to verify that perfusion is adequate or to determine if that area has succumbed to necrosis and needs to be resected. The bowel may then be re-anastomozed several weeks after recovery (Thompson and Bizarro, 2008, p. 1233). Several known surgical techniques/methods are a) “patch, drain, and wait”; b) “clip and drop back”; and c) bowel transplantation (Yeo, 2006, p. 48-49). NEC however can be prevented.
Preventive measures may include administration of maternal antenatal corticosteroids for threatened preterm delivery which has been shown to decrease the incidence of NEC. This is due to a mechanism similar to fetal lung maturation with administration of corticosteroids. Apparently the GI tract also matures under the influences of exogenous corticosteroids and this results in increased intestinal barrier strength which lowers translocation of bacteria and bacterial endotoxins. The anti-inflammatory properties of corticosteroids also exert protective effects.
Maternal antenatal corticosteroids for threatened preterm labor has now become a standard therapy (Thompson and Bizarro, 2008, p. 1233). Another preventive measure is the administration of trophic feedings. Trophic feedings – aka non-nutritive or priming feedings are initiated to stimulate peristalsis of the GI tract, induce appropriate enzymatic activity for digestion. The introduction of non-nutritive feedings for some period of time prior to advancement is often utilized and may be beneficial in preventing NEC (Thompson and Bizarro, 2008, p. 1233).
Thirdly, studies have found that feeding with breast milk – which contains maternal IgA, epidermal growth factor, PAF acetylhydrolase (which inactivates PAF), prebiotic elements (which favour the replication of commensal GI bacteria) and anti-inflammatory cytokines such as interleukin-10 – combine to facilitate digestion and replication of protective bacteria and provides protection to the mucosal barrier of the GI tract.
Findings indicate that NEC is 6 times more common in formula fed neonates compared to breast fed alone (Thompson and Bizarro, 2008, p. 1234). Fourth, probiotics – oral supplements containing microbes usually indigenous to the healthy human body – are thought to provide benefits via enhancing the IgA mucosal response, improving the mucosal protective barrier, increasing the production of anti-inflammatory cytokines, decreasing intestinal wall permeability and competitively excluding pathogenic microbes in the GI tract (Thompson and Bizarro, 2008, p. 1234).
Introduction of probiotics apparently has the following benefits: normalization of intestinal microflora, reduction of intestinal permeability, increased mucosal barrier function, protection of the gut from pathogens, decreased inflammatory processes, increased anti-inflammatory cytokines, improved enteral nutrition, and reduced infection rates (Yeo, 2006, p. 47).
Probiotics have been advocated for prevention or treatment of a variety of disorders including rotavirus infection, antibiotic-associated diarrhea, and traveler’s diarrhea (Bell, 2004, p. 173). On the other hand, prebiotics –compounds that selectively increase the population of existing commensal GI bacteria – were found to acts as substrates preferentially utilized by commensal bacterial to proliferate (Thompson and Bizarro, 2008, p. 1236).