You are in: eMedicine Specialties > Pediatrics: Surgery > General Surgery Necrotizing Enterocolitis: Surgical PerspectiveArticle Last Updated: Jan 4, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Robert K Minkes, MD, PhD, Staff Pediatric Surgeon, Houston Pediatric Surgeons, Texas Children's Hospital Robert K Minkes is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, and Phi Beta Kappa Coauthor(s): Li Ern Chen, MD, Staff Physician, Department of Surgery, Barnes Jewish Hospital, Washington University School of Medicine; Tapash K Palit, MD, Vascular Surgery Fellow, Department of Surgery, Arizona Heart Institute; Robert S Bloss, MD, Clinical Associate Professor of Surgery and Pediatrics, University of Texas Medical School; Clinical Assistant Professor, Department of Surgery, Baylor College of Medicine; Consulting Staff, Houston Pediatric Surgeons Editors: Diana Farmer, MD, Associate Professor, Departments of Clinical Surgery, Pediatrics, Obstetrics, Gynecology and Reproductive Services, Division of Pediatric Surgery and the Fetal Treatment Center, University of California at San Francisco; Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc; Andre Hebra, MD, Chief, Division of Pediatric Surgery, Medical University of South Carolina; H Biemann Othersen Jr, MD, Professor of Surgery and Pediatrics, Emeritus Head, Division of Pediatric Surgery, Medical University of South Carolina; Philip Glick, MD, MBA, Professor, Departments of Surgery, Pediatrics, and Gynecology and Obstetrics, Vice-Chairperson for Finance and Development, Department of Surgery, State University of New York at Buffalo Author and Editor Disclosure Synonyms and related keywords: necrotizing enterocolitis, NEC, newborn NEC, neonatal NEC, infectious enteritis, abdominal distension, bloody stools, pneumatosis intestinalis, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Staphylococcus aureus, Staphylococcus epidermidis, Clostridium perfringens, Pseudomonas aeruginosa, xanthine, theophylline, aminophylline, indomethacin, necrotic intestine, pneumoperitoneum, thrombocytopenia, sepsis, peritonitis, prematurity, ileal perforation, apnea, bradycardia INTRODUCTIONSection 2 of 12
  Necrotizing enterocolitis (NEC) is one of the most common reasons for surgical consultation in neonates and is the most common GI emergency in the neonatal population. As advances in neonatal intensive care have progressed over the last 30 years and as premature newborns are surviving long enough for the disease to develop, the incidence of NEC in neonatal intensive care units (NICUs) has increased. NEC remains one of the most challenging diseases confronted by pediatric surgeons and still carries a mortality rate of 30-50% when a perforation occurs. Despite advances in technology and recent clinical trials, NEC likely represents a spectrum of diseases with variable causes and manifestations, and surgical care must therefore be individualized. NEC typically occurs in the second to third week of life in the infant who is premature and has been formula fed. Although various clinical and radiographic signs and symptoms are used to make the diagnosis, the classic clinical triad consists of abdominal distension, bloody stools, and pneumatosis intestinalis. Occasionally, signs and symptoms include temperature instability, lethargy, or other nonspecific findings of sepsis. History of the ProcedureNumerous vague reports in 19th-century literature report describe infants who died from peritonitis in the first few weeks of life. The first half of the 20th century brought more reports of peritonitis with ileal perforation due to what was called infectious enteritis. In 1953, Scmid and Quaiser called this condition newborn NEC.1 The first clear report of NEC did not appear until 1964, when Berdon from the New York Babies Hospital described the clinical and radiographic findings of 21 infants with the disease.2 ProblemNEC is an acute inflammatory disease with a multifactorial and controversial pathogenesis. NEC occurs in newborns and is characterized by variable damage to the intestinal tract ranging from mucosal injury to full-thickness necrosis and perforation. FrequencyThe incidence of NEC is difficult to ascertain. Reports generally indicate an incidence of 1-3 cases per 1000 live births. The incidence among patients in NICU settings is reportedly 2-2.5%. However, this rate widely varies by region, by institutions, and by year within the same institution. Cases tend to cluster, suggesting an environmental component to the pathophysiology. Nations with a lower rate of premature births than that in the United States generally have a lower rate of NEC as well. For example, a large study of NICUs in Japan identified a 0.3% incidence, which is significantly lower than that in similar patient populations in the United States.3 EtiologyNo specific etiology of NEC has been identified; multiple factors are believed to contribute to its development. The principal factors identified are prematurity and enteral feedings. Prematurity and feeding NEC is principally a disease of premature infants. Although approximately 5-25% of infants with NEC are born full term, studies have found a markedly decreased risk of NEC with increasing gestational age. This finding suggests that maturation of the GI system plays an important role in the development of NEC. The premature neonate has numerous physical and immunologic impairments that compromise intestinal integrity. Gastric acid and pepsin production are decreased during the first month of life. Pancreatic exocrine insufficiency is associated with low levels of enterokinase, the enzyme that converts trypsinogen to trypsin, which allows hydrolysis of intestinal toxins. Mucus secretion from immature goblet cells is decreased. Gut motility is impaired, and peristaltic activity is poorly coordinated. Finally, secretory immunoglobulin A (IgA) is deficient in the intestinal tract of premature infants not fed breast milk. The initiation of early enteral feedings is associated with NEC. Some series have reported decreased rates of NEC when feeding volumes are reduced. In a prospective randomized trial, Book et al found a significant increase in the development of NEC among preterm infants fed a hyperosmolar elemental formula compared with those fed a milk formula.4 Infectious organisms Infectious organisms are thought to play a key role in the development of NEC. Whether bacterial infection has a primary inciting role in NEC or whether an initial intestinal mucosal injury allows secondary bacterial invasion is unclear. Positive blood cultures are found in 30% of patients; the most commonly identified organisms are Escherichia coli and Klebsiella pneumoniae. Proteus mirabilis, Staphylococcus aureus, Staphylococcus epidermidis, Enterococcus species, Clostridium perfringens, and Pseudomonas aeruginosa have also been identified. E coli, Klebsiella species, Enterobacter cloacae, P aeruginosa, Salmonella species, S epidermidis, C perfringens, Clostridium difficile, and Clostridium butyricum commonly grow in stool cultures. Klebsiella species, E coli, S epidermidis, and yeast are most commonly identified on peritoneal cultures. Fungal infection is believed to be an opportunistic infection in the presence of an altered host intestinal defense system. The observation of an epidemic or cluster of cases in a short period in one nursery after sporadic cases support the key role of infectious organisms in NEC. Nursery personnel are known to experience acute GI illnesses in association with these outbreaks, and the institution of infection control measures has accordingly reduced the rates of NEC. Medications The use of numerous medications has been implicated as a risk factor for NEC. Xanthine derivatives, such as theophylline and aminophylline, slow gut motility and produce oxygen free radicals during their metabolism to uric acid. Indomethacin used to treat patent ductus arteriosus may cause splanchnic vasoconstriction leading to impaired intestinal integrity. Vitamin E used to treat retinopathy of prematurity is known to impair leukocyte function and has been associated with NEC. Experimental studies In animal models, cytokines, such as platelet-activating factor (PAF), induced intestinal injuries that were grossly and histologically similar to those seen in humans with NEC. In addition, an ischemic-reperfusion model of intestinal injury with reactive vasodilation after an initial ischemic insult was shown to elaborate oxygen free radicals in the intestinal mucosa. These free radicals are extremely toxic to cellular organelles and cell membranes. Pretreatment with free-radical scavengers significantly decreased the intestinal injury. PathophysiologyThe pathogenesis of NEC most commonly begins with a premature GI tract. An impaired host intestinal defense system and immunologic immaturity combine to allow colonization of the GI tract by the bacterial flora present in the NICU. Antibiotics frequently administered to treat respiratory distress in the neonate depress the native flora, which provide some protection against pathologic organism overgrowth. Enteral feedings with formula provide a carbohydrate substrate for bacterial proliferation and confer none of the immunoglobulin protection that breast milk provides. Bacteria may violate the intestinal mucosa by migrating through the mucosa or through defects in mucosal continuity. The resulting inflammatory reaction elaborates cytokines and other mediators of cellular injury. This further injures the mucosa and may extend through to the deeper layers of the bowel wall. Progressive intestinal damage may occur as further bacterial invasion through the mucosal injury results in full-thickness necrosis and subsequent perforation. ClinicalThe clinical presentation of 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 distension 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. INDICATIONSSection 3 of 12
The principle indication for operative intervention is perforated or necrotic intestine. Infants with necrotic intestine are identified based on various clinical, laboratory, and radiologic findings. The most compelling predictor of intestinal necrosis indicating a need for operative intervention is pneumoperitoneum. Other relative indications for operative intervention are erythema in the abdominal wall, gas in the portal vein, and positive paracentesis. Note that evaluation by a pediatric surgeon early in the course of necrotizing enterocolitis is important to avoid any delay in operative intervention. The most common indication for operative treatment is pneumoperitoneum. Many infants may have isolated perforations or necrotic tissue that wall off the abdominal cavity and do not show free intraperitoneal air. Knowing whether these infants may benefit from early operative intervention is difficult. RELEVANT ANATOMYSection 4 of 12
Necrotizing enterocolitis (NEC) most commonly affects the terminal ileum and the proximal ascending colon. However, varying degrees of NEC can affect any segment of the small intestine or colon. The entire bowel may be involved and may be irreversibly damaged. CONTRAINDICATIONSSection 5 of 12
Contraindications to surgical intervention include patients with stage I or stage II disease, for whom nonoperative medical therapy is the treatment of choice. In addition, surgical intervention should be deferred in patients with more severe disease whose condition responds to initial medical management. Critically ill newborns with a relative contraindication to formal operative exploration may be treated with the placement of a peritoneal drain. Although this is typically a temporizing measure, these extremely ill infants may recover with drain placement alone and do not require exploratory laparotomy. However, peritoneal drain placement may be the treatment of choice for extremely small (<600 g) premature newborns. Such premature, critically ill infants cannot tolerate formal exploration, and drain placement may be preferred and definitive. Nevertheless, many infants whose condition is too unstable for formal exploration do not survive regardless of intervention. WORKUPSection 6 of 12
Lab Studies
Imaging Studies
Diagnostic Procedures
Histologic FindingsWith NEC, the areas most commonly affected are the terminal ileum and the proximal ascending colon. The pattern of disease may involve a single isolated area or multiple discontinuous lesions. The most common histologic findings are associated with mucosal injury. These include coagulation necrosis of the mucosa with active and chronic inflammation, mucosal ulceration, edema, hemorrhage, and pneumatosis of the submucosa. Advanced disease may result in full-thickness necrosis of the intestinal wall. Regenerative changes with epithelial regeneration, granulation tissue formation, and fibrosis are seen in as many as two thirds of patients. This indicates an inflammatory process lasting several days with concurrent areas of continuing injury and healing. StagingThe Bell system is the staging system most commonly used to describe NEC.
TREATMENTSection 7 of 12
Medical therapyThe mainstay of treatment for patients with stage I or II necrotizing enterocolitis (NEC) is nonoperative management (see Necrotizing Enterocolitis). The initial course of treatment consists of stopping enteral feedings, performing nasogastric decompression, and initiating broad-spectrum antibiotics. Historically, antibiotic coverage has consisted of ampicillin, gentamicin, and either clindamycin or metronidazole, although the specific regimen used should be tailored to the most common nosocomial organisms found in the particular NICU. Authors in some series propose the use of enteral aminoglycosides for the treatment of NEC, but several prospective trials have shown no efficacy for this treatment. In addition, a strong index of suspicion for fungal septicemia must be maintained, especially in the infant with a deteriorating condition and negative bacterial cultures. Patients with stage I disease with improving signs and symptoms and negative workup results may usually resume feedings in 7-10 days. Once feedings resume, stools may be monitored for reducing substances and occult blood, and feedings should be stopped if a test for either becomes positive. Patients with stage II NEC are typically treated for 10 days. During this time, a central venous catheter should be inserted, and total parenteral nutrition supplying 120 kcal/kg/d should be administered. Prolonged central venous access is associated with line infection, and blood cultures should be drawn through the central line if suspicion of infection exists. Clinical improvement after this time should be marked by a benign abdominal examination, normal WBC and platelet counts, and an absence of acidosis. If clinical improvement occurs, the patient is slowly fed small amounts of clear fluids, and then dilute formula, with careful monitoring for distension, emesis, and other signs of NEC. Feedings are slowly advanced over 7-10 days; large-volume feedings or highly concentrated formulas should be avoided. Patients with stage III NEC and those who do not demonstrate clinical improvement may need intense supportive care, including ventilatory support, aggressive resuscitation, and the initiation of vasopressors. These patients require urgent surgical evaluation. Surgical therapyThe underlying principle in the operative management of NEC is to identify neonates with a necrotic intestine. However, recognition of intestinal necrosis and the decision to operate can be difficult. A pneumoperitoneum is the most commonly accepted absolute indication for operative intervention in NEC. In a comparison of multiple indicators of intestinal necrosis, Kosloske found that the best were pneumoperitoneum, portal-vein gas, and a positive paracentesis.5 Good indicators were a fixed dilated loop of bowel, erythema of the abdominal wall, and a palpable abdominal mass. Severe pneumatosis in all 4 quadrants is a fair indicator, but pneumatosis alone is not an indication for operation because more than 50% of infants with NEC and pneumatosis are treated successfully with nonoperative treatment. Infants who have pneumoperitoneum during nonoperative treatment should undergo surgery if they are physiologically stable. If they are unstable, a peritoneal drainage catheter should be placed. Bowel necrosis eventually develops in more than 75% of infants with portal-vein gas. This suggests that operative intervention should be considered when portal-vein gas is identified. Although prolonged nasogastric decompression can produce abdominal radiographs with a paucity of bowel gas suggesting ascites, a gasless abdomen often indicates ascites. This finding can be confirmed with ultrasonography and paracentesis. A positive paracentesis is a good indicator of intestinal gangrene. A fixed dilated loop of bowel is a relatively unusual finding seen in 4-43% of patients with NEC and may indicate an area of necrosis. Because of this, many surgeons use this as a relative indication for surgery. Approximately 60% of these patients undergo surgery. Surgery is generally indicated in the medically treated patient whose clinical condition deteriorates. The signs of deterioration include worsening abdominal examination findings, signs of peritonitis, worsening and intractable acidosis, persistent thrombocytopenia, rising leukocytosis or worsening leukopenia, and hemodynamic instability. Surgery should ideally be performed at the time of impending intestinal perforation, but this is rarely accomplished. After perforation occurs, peritoneal contamination ensues with subsequent intra-abdominal abscess formation. In theory, operation before perforation may decrease the intra-abdominal inflammatory response and shorten the length of required bowel resection by preventing ischemic and necrotic extension to other areas of intestine. Perforation is not always recognized when it occurs, especially if the area of necrosis is localized and the contamination is contained. These perforations may heal on their own, or they may be a source of ongoing infection or intestinal obstruction. A perforation may also form a spontaneous fistula through the skin or umbilicus. Preoperative detailsAfter the decision to proceed with surgery is made, the patient's general physiologic condition should be optimized. Provide vigorous fluid replacement, correct any clinically significant anemia or coagulopathy, and ensure adequate urine output of at least 1 mL/kg/h. To minimize heat loss, place the infant on a heated air pad, and a warmed operating room and warmed intravenous and irrigation fluids should be used. The use of heated and humidified oxygen and anesthetic gases may further minimize heat loss. Blood products should be available during surgery. Intraoperative detailsThe abdomen can be entered via a right transverse incision just below the umbilicus by using electrocautery to ensure hemostasis. This incision provides adequate exposure away from a frequently large liver and decreases the risk of retractor injury to the liver. Care must be taken at the time of entry into the peritoneal cavity to avoid injury to dilated loops of intestine. If any free intraperitoneal fluid is identified, samples may be taken for aerobic, anaerobic and fungal culture. Bloody peritoneal fluid in seen in necrosis and brown turbid fluid is found in perforation. The abdominal cavity is then systematically inspected for evidence of necrosis and perforation. Particular attention is paid to the right lower quadrant because the terminal ileum and proximal ascending colon are most commonly involved. The guiding principle of surgery for NEC is to resect only perforated and unquestionably necrotic intestine and to make every effort to preserve the ileocecal valve. White or gray bowel indicates ischemic necrosis. Hemorrhagic or edematous areas of bowel may represent areas of mucosal ischemia and injury but do not necessarily indicate nonviable bowel. Saccular protrusions of bowel wall have undergone mucosal, submucosal, and muscularis necrosis and are covered only by a layer of serosa. These are areas of impending intestinal perforation. Palpation may also be helpful because resilient pliable bowel is typically viable, and lax and boggy bowel that indents on palpation is often necrotic. If the viability of remaining bowel is significantly questionable, a second-look operation can be performed in 24-48 hours to assess the viability of the remaining intestine. If a single area of bowel is resected, a proximal ostomy and distal mucus fistula are created. The viability of the bowel at the cut margins can be ascertained by whether the cut edges bleed. The enterostomy and mucus fistula are brought out at opposite ends of the incision, with the serosa sutured to the abdominal wall fascia with interrupted sutures. About 2 cm of bowel is left to protrude above the abdominal wall, and the end of the ostomy is not matured. If ostomy viability is in question postoperatively, the ends of the intestine may be excised and observed for adequate bleeding. Primary anastomosis is not generally advocated because of the risk of ischemia at the anastomosis, leading to increased incidence of leakage, stricture, fistula, or breakdown. However, intestinal resection with primary anastomosis may be safely performed in select cases. Patients must demonstrate a clearly demarcated small segment of injured bowel with normal-appearing residual intestine and be in good general condition with no evidence of sepsis, coagulopathy, or physiologic compromise. If multiple segments of intestine are involved because of necrosis or perforation, a decision must be made regarding the course of action. Historically, the individual segments of affected intestine are resected, and multiple ostomies are created. However, a number of other surgical options have been proposed. A single proximal stoma may be created and the distal bowel segments anastomosed in continuity, thus avoiding multiple stomas. Moore proposes a technique of patch, drain, and wait, which involves transverse single-layer repair of bowel perforations (patch), placement of 2 Penrose drains in the lower quadrants (drain), and the initiation of long-term parenteral nutrition (wait); however, this technique is not widely advocated. The thin, distended bowel wall holds suture poorly, and the abdominal cavity does not drain freely with open gravity drainage. In addition, this technique does not address the source of intra-abdominal sepsis because necrotic bowel is not resected. In a small series, Vaughn describes a different technique of clip and drop-back.6 The unquestionably necrotic segments of intestine are resected and the transected ends are stapled closed. A second-look operation is performed in 48-72 hours when the clips are removed, and reanastomosis is performed without any ostomies. NEC totalis occurs when less than 25% of the intestinal length is found to be viable at the time of operation; this finding results in a number of grim treatment options. Simple closure of the abdomen is supported by findings that show a 42-100% mortality rate in patients with pan-involvement. Massive resection with excision of the ileocecal valve requires at least 20 cm of residual bowel for any hope of adequate enteral nutrition. Patients with a decreased bowel length require permanent parenteral nutrition. Martin and Neblett describe a technique of enterostomy diversion proximal to the involved bowel without bowel resection.7 This technique may facilitate bowel healing by allowing bowel decompression, reducing intestinal bacterial load, and decreasing metabolic demand. After intestinal resection, the length of remaining viable bowel should be sequentially measured along the antimesenteric border of the intestine and recorded. Neonates who are extremely ill and unable to tolerate surgery may be treated by means of peritoneal drainage in a technique described by Ein et al.8 A right lower quadrant incision is made at the bedside under local anesthesia, and a Penrose drain is inserted. The initial intent of this procedure was to temporize surgical treatment, and, indeed, some infants survived with this procedure alone and did not require subsequent laparotomy. Although laparotomy, resection, and enterostomy form the standard operative tenets of surgery for NEC, peritoneal drainage is a valuable adjunct in treatment of the physiologically unstable neonate weighing less than 1000 g and in many institutions is used as the primary procedure of choice. Postoperative detailsAfter undergoing an operation for NEC, infants should continue to receive intravenous antibiotics and total parenteral nutrition for at least 2 weeks. Supportive care, including ventilatory support, fluid and electrolyte monitoring and replacement, and correction of anemia and coagulopathy, should continue. During surgery infants with NEC often develop a coagulopathy which continues after surgery and can be difficult to manage. Blood can fill the abdominal cavity rapidly and create a compartment syndrome which requires drainage. Any infants with continued clinical deterioration must be evaluated for residual intestinal gangrene and possibly repeat surgical exploration. Infants who improve postoperatively should not resume enteral feedings for at least 10-14 days. Follow-upTiming of enterostomy closure to restore intestinal continuity is the principal follow-up issue for infants who are surgically treated for NEC. This procedure is generally performed 1-2 months after the original operation, depending on weight gain and ostomy output, among other factors. The argument against early ostomy closure is the difficulty of operating in a peritoneal cavity replete with adhesions and resolving inflammation; the ideal time is approximately 8 weeks. If goal enteral feeds can be accomplished there is some benefit in discharging home and performing a reanastamosis after several months. This gives the infant a chance to grow and better tolerate an additional laparotomy. Abnormally high ostomy output may indicate a need for early ostomy closure. A patient with a high jejunostomy may have substantial loss of fluid and electrolytes, with consequences such as failure to thrive and peristomal skin injury. These patients may benefit from early ostomy closure with attendant colonic water absorption. However, infants with a high ostomy and extensive ileal resection who undergo ostomy closure may have considerable secretory diarrhea after the colon comes in contact with unabsorbed bile salts. They may require treatment with a bile salt–binding agent, such as cholestyramine. Sodium chloride supplementation (1-3 mcg/kg/d) has been recommended to optimize growth in infants with small-bowel stomas. All patients who have any remaining large intestine after an initial operation for NEC must be examined with contrast-enhanced enema of the colon to identify any areas of stricture before the ostomy is closed. If any such areas are present, they are resected when the enterostomy is closed. In addition, some advocate a screening contrast enema study approximately 30 days after recovery in infants who were nonoperatively treated for NEC. Symptomatic colonic strictures require treatment, whereas asymptomatic strictures may be observed. COMPLICATIONSSection 8 of 12
The most common complication after necrotizing enterocolitis (NEC) is intestinal stricture. It occurs when an area of intestinal ischemia heals with resultant fibrosis and scar formation that impinges on the diameter of the lumen. The most common site of stricture is the left colon, followed by the terminal ileum. Intestinal stricture is most common in infants treated nonoperatively because infants treated operatively should have undergone contrast enema before closure of the ostomy, and any area of stricture should have been resected when the ostomy was closed. Intestinal stricture should be suspected in any infant who receives nonoperative treatment for NEC and who fails to thrive and/or has bloody stools or bowel obstruction. Intestinal malabsorption is caused by loss of bowel length with decreased absorptive surface area, vitamin B-12 deficiency, bile salt deficiency, bacterial overgrowth, and intestinal hypermotility. Short gut syndrome is the most serious postoperative complication, occurring in as many as 23% of patients after intestinal resection. Cholestatic liver disease is a multifactorial condition caused by prolonged fasting and total parenteral nutrition. It is characterized by hepatomegaly and elevated aminotransferase and direct bilirubin levels. The treatment is initiating enteral feedings as early as possible to stimulate bile flow. Recurrent NEC is an uncommon complication that can occur after either operative or nonoperative management. It is seen in only 4-6% of patients with NEC. Recurrent NEC has not been associated with the method of managing the initial episode, the timing of enteral feedings, or the site of initial disease. Infants who survive NEC are at increased risk for neurodevelopmental disorders. As many as 50% of infants who survive NEC have some abnormality in intelligence and motor skills. However, the incidence of non–GI sequelae in matched cohorts with and without NEC are similar, implying that neurodevelopmental problems may be a function of underlying prematurity rather than of NEC itself. OUTCOME AND PROGNOSISSection 9 of 12
With improved supportive intensive care, including ventilatory management, anesthetic techniques, and total parenteral nutrition, the survival of infants with necrotizing enterocolitis (NEC) has steadily improved over the last 40 years. Although the mortality rate remains high, some series have reported a 70-80% survival rate in infants surgically treated for NEC. The improved prognosis is most notable in critically ill neonates who are younger than 28 weeks' gestational age and who weigh less than 1000 g. These neonates are still at significantly increased risk for paninvolvement and are more likely than other premature infants to require surgery. The improvement in treatment efficacy of infants with NEC is underscored by noting that if patients with pan-involvement are excluded, the survival in surgically treated infants with NEC is 95%. However, comparison between reported series is difficult because of wide variations in patient populations, extent of disease, coexisting conditions, and severity categorization between centers. FUTURE AND CONTROVERSIESSection 10 of 12
Efforts to reduce the incidence of necrotizing enterocolitis (NEC) may target infection control in the newborn nursery, augmentation of premature host defenses, stimulation of GI tract maturation, inhibition of inflammatory mediators, and reduction of enteric bacterial load. Enteral IgA is deficient in the premature GI system, and oral IgA supplementation reduces the incidence of NEC in rat models. In addition, a series in human infants found that those receiving an oral immunoglobulin G (IgG)–IgA preparation were significantly less likely to develop NEC than control subjects. The administration of prenatal glucocorticoids to mothers for fetal pulmonary maturation significantly reduces the incidence of NEC. In addition, postnatal treatment decreases the incidence of NEC, although not as effectively as prenatal treatment. In laboratory models PAF antagonists reduced bowel injury. However, their role in the prevention and treatment of NEC in humans has not been well established. Nonabsorbable oral antibiotics have been used in attempts to reduce the intestinal bacterial load and presumably inhibit the progression of NEC. However, several investigators found no significant difference in outcome between infants receiving oral antibiotics and control subjects. Although the incidence of NEC has not decreased in recent years, advances in treatment have improved the survival rates of infants with NEC. The survival rate of patients who are treated with surgery and do not demonstrate paninvolvement now surpasses 90%. Although no difference in 90-day survival was observed, follow-up data on the multicenter randomized clinical trial comparing laparotomy with primary peritoneal drainage may give insight as to which treatment has better longer term outcomes.9 In cases of neonates with relative indications for surgery, the development of minimally invasive instrumentation may allow routine laparoscopic exploration. Developments in equipment miniaturization may reduce the number of formal exploratory laparotomies necessary in this select group of patients. MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
Necrotizing Enterocolitis: Surgical Perspective excerpt Article Last Updated: Jan 4, 2008 | ||||||||||||||||||||||||||
