Definition: Serious intestinal inflammation and injury thought to be secondary to bowel ischemia, immaturity, and infection. Occurs principally in infants who have been fed. Show
Risk factors: Prematurity, asphyxia, African American race, hypotension, polycythemia–hyperviscosity syndrome, umbilical vessel catheterization, exchange transfusion, bacterial and viral pathogens, enteral feeds, PDA, congestive heart failure, cyanotic heart disease, RDS, intrauterine cocaine exposure. 3.Clinical findings: SeeTable EC 18.B. a.Systemic: Temperature instability, apnea, bradycardia, metabolic acidosis, hypotension, disseminated intravascular coagulopathy. b.Intestinal: Blood in stool, absent bowel sounds, and/or abdominal tenderness or mass. Elevated pregavage residuals in the absence of other clinical symptoms rarely raise a suspicion of NEC. c.Radiologic: Ileus, intestinal pneumatosis, portal vein gas, ascites, pneumoperitoneum (seeChapter 26). 4.Management: Nothing by mouth, NG tube decompression, maintain adequate hydration and perfusion, broad spectrum antibiotics for 7 to 10 days based on hospital antibiogram, surgical consultation. Surgery is performed for signs of perforation or necrotic bowel. 5.Minimizing risk of NEC: a.Several studies link the use of probiotics and a decreased risk of NEC.24 However, variations among formulations of probiotics, dosing, and lack of long-term studies on outcome have prevented the standard use of probiotics in the NICU.25 b.There have been additional studies on supplements including L-arginine and lactoferrin.26-28 Data remains insufficient to support a practice recommendation.29 c.The exclusive use of human milk, including donor breast milk, has been shown to decrease the risk of NEC and associated mortality.30 View chapter on ClinicalKey Necrotizing EnterocolitisEsther Jacobowitz Israel, Claudio Morera, in Encyclopedia of Gastroenterology, 2004 EpidemiologyNecrotizing enterocolitis (NEC) is an almost exclusively newborn disease. The incidence is 1 to 3 in 1000 live births and the prevalence is 1 to 5% of all infants in neonatal intensive care unit, especially premature infants. There is no seasonal, geographic, or gender disparity. The age at onset of NEC is inversely related to birth weight and gestational age. Immature infants, particularly low-birth-weight (LBW) babies, are at prolonged risk as they can develop NEC as late as 10 weeks of age. Infants weighing less than 1000 g are particularly vulnerable. Advances in neonatal intensive care have improved survival of premature infants beyond the first days of life. This situation has been accompanied by a further increase in NEC-associated infant mortality, from 11.5 deaths per 100,000 live births in the presurfactant era to 12.3 in the postsurfactant era. Nevertheless, 10 to 35% of affected neonates are full-term infants with different risk factors than those found in premature infants (Table I). TABLE I. Risk Factors for Necrotizing Enterocolitis PrematureFull-termLower gestational ageCyanotic: congenital heart diseaseFeedingPolycythemiaExchange transfusionsPerinatal asphyxiaSmall for gestational ageUmbilical cathetersMaternal preeclampsiaAntenatal cocaine View chapterPurchase book Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B0123868602004998 Paediatric Abdominal ImagingAndreas Adam CBE, MB, BS(Hons), PhD, PhD (hon caus), DSc (hon caus), FRCP, FRCR, FRCS, FFRRCSI(Hon), FRANZCR(Hon), FACR(Hon), FMedSci, in Grainger & Allison's Diagnostic Radiology, 2021 Necrotising EnterocolitisThe precise aetiology of NEC remains unknown. In the past, the term NEC has been used as an umbrella term for any pre-term infant presenting with abdominal distension and complications including pneumoperitoneum and pneumatosis. It is now accepted that NEC is not a single disease entity but a multifactorial condition associated with a variety of risk factors and outcomes. Animal studies have identified a receptor within the gut mucosa implicated in the pathophysiology of NEC. TLR4 has been shown to increase ischaemia within the gut mucosa in response to pathogenic bacteria. Risk factors for NEC include hypoxia/ischaemia (which is the cause of so-called ‘term-NEC’ in babies with congenital cardiac disease), prematurity, delayed enteric feeding, exposure to abnormal gut pathogens (owing to prolonged antibiotic use), enteric pathogens (implicated in ‘cluster-NEC’ seen during infectious outbreaks on neonatal units), multiple blood transfusions and early cow's milk protein allergies. Many of these risk factors are additive, and some result in more severe forms of disease such as those associated with multiple blood transfusions. There is an inverse relationship between birth weight, gestational age and the development of NEC. As above, those term infants prone to hypoxia and ischaemia are also at risk of NEC. NEC usually presents in the second week of life, following the commencement of enteral feeds. This is thought to be secondary to relative ischaemia in the postprandial period. Initially superficial, the inflammatory process in NEC can extend to become transmural. Diffuse or discrete involvement of the bowel can occur, with the most commonly affected sites being the terminal ileum and colon. The clinical symptoms and signs are non-specific to begin with and include feeding intolerance, lethargy, hypoglycaemia, temperature instability, bradycardia, oxygen desaturation, increased gastric aspirates and gastric distension. Disease progression leads to vomiting, diarrhoea (often with the passage of blood or mucus in the stool) and, eventually, to shock. There are four important radiographic features of NEC that are often quoted. One of the earliest features of NEC is a non-specific global dilatation of bowel loops. On serial radiographs, attention should be paid to the presence of persistent dilatation of specific bowel loops, the so-called ‘fixed loop’. Pneumatosis intestinalis or intramural gas can be seen in many conditions (Table 71.3). In the context of NEC, more extensive pneumatosis correlates with increased severity. Portal venous gas is seen as branching linear lucencies over the liver that radiate from the region of the porta hepatis to the periphery of both lobes. It develops in approximately 30% of cases and, when seen, it is poor prognostic indicator (Fig. 71.10). Perhaps the most important feature is free gas. One-third of children with NEC will perforate, most commonly in the ileocaecal region. The radiologist should be aware of another phenomenon known as neonatal spontaneous intestinal perforation (SIP). This occurs in low birth weight infants without demonstrable cause and is most common in the terminal ileum. It is a different entity to NEC and the prognosis is much better than perforation caused by NEC. In many cases, a single anteroposterior (AP) abdominal radiograph is sufficient to make the diagnosis of perforation. Where clinical suspicion is high and the AP radiograph is inconclusive, a lateral view is obtained. There is no consensus as to the optimal technique. The supine, cross-table lateral view is useful to detect small amounts of free intraperitoneal air, typically as triangles of gas between bowel loops or over the dome of the liver. There is no need to reposition the infant when the image is taken. Alternatively, a lateral decubitus radiograph may be used, which requires the child to be repositioned on their left side for several minutes to allow air to collect over the liver surface on the right side of the abdomen. View chapter on ClinicalKey Necrotizing enterocolitisPamela A. Zachar MD, in Berman's Pediatric Decision Making (Fifth Edition), 2011 A. Necrotizing enterocolitis (NEC) can be a devastating and fatal disease in neonates, but early recognition and aggressive management can limit morbidity and mortality. Most infants (90%) who experience development of NEC are born prematurely. Age at onset is inversely related to gestational age at birth; thus, NEC presents in the convalescent stage of a preterm infant’s course but usually within 2 or 3 days of birth in a term infant. The risk remains high in preterm infants until they reach 35 to 36 weeks of age. B.Proven risk factors for NEC include prematurity, formula feeding, maternal cocaine use, and histamine-2 receptor blocker therapy. Other factors that have been associated with NEC include presence of a patent ductus arteriosus, intrauterine growth retardation, perinatal asphyxia, and ethnicity, with black infants being at particularly high risk. C.Many aspects of infant feeding have been investigated as risk factors for the development of NEC. Breast-feeding is the only factor that has been clearly shown to reduce the risk for the development of NEC. No specific feeding regimen has been proved to prevent NEC, but most experts recommend cautious rates of feeding advancement in premature infants. D.Early presenting signs of NEC include abdominal distension, feeding intolerance with increased gastric residuals, emesis, grossly bloody stools, and, less often, diarrhea. Infants may exhibit nonspecific systemic symptoms such as lethargy, temperature instability, and an increase in apnea and bradycardia. Common physical examination findings include abdominal distension, tenderness, mass, and, in severe cases, discoloration of the abdominal wall (erythema or a bluish cast). Severe cases may be accompanied by signs of shock, such as diminished pulses and perfusion, tachycardia, and hypotension. When disseminated intravascular coagulation (DIC) is present, oozing from the umbilical stump or puncture sites may occur. E.Initial laboratory evaluation should include complete blood count (CBC) with differential, blood chemistries and blood gases, and cultures of blood and urine. Common findings include leukopenia or leukocytosis and thrombocytopenia, glucose instability, metabolic acidosis, and electrolyte abnormalities. Other tests such as lumbar puncture, stool studies, and coagulation profiles may be considered based on the clinical scenario. F.Radiologic imaging is essential to the diagnosis of NEC. Abdominal radiography should include anteroposterior and left lateral decubitus or cross-table lateral views, because a single view is inadequate to detect the subtle signs of perforation (pneumoperitoneum). Early x-ray findings may include intestinal dilatation, thickened intestinal walls, and air–fluid levels. Other findings more specific to NEC include intramural air (pneumatosis intestinalis), portal venous air, and pneumoperitoneum. A fixed or persistent dilated loop of bowel that remains unchanged for 24 to 36 hours often represents a necrotic intestinal loop. G.NEC may be indolent or fulminant. At presentation, patients can be stratified into groups based on the modified Bell stages of disease. Stage I (suspected NEC) includes infants with mild systemic symptoms, nonspecific abdominal symptoms, and radiographs either normal or with mild ileus. Stage II (mild-to-moderate definite NEC) includes infants with mild-to-moderate systemic symptoms that can include mild acidosis and thrombocytopenia, more prominent abdominal distension, and tenderness. In stage II, radiographs show pneumatosis. Stage III (advanced NEC) includes infants who are severely ill with respiratory failure, signs of shock and/or DIC, and those with evidence of perforation. H.NEC stage I can represent either the earliest stages of a process that would have developed into more serious disease without treatment, or it can represent other, more benign, clinical entities. Initial treatment should be the same regardless of the stage at presentation. Differential diagnosis for NEC stage I includes septicemia, slow intestinal motility and simple feeding intolerance, milk allergy, and intestinal infections including rotavirus. I.Initial treatment includes discontinuation of feeding, placement of large-bore orogastric or nasogastric tube (OG/NG) to suction, and initiation of antibiotic therapy with intravenous antibiotics. Choice of antibiotics will depend on the resistance patterns and common flora of the nursery, but will most likely include either ampicillin or vancomycin and an aminoglycoside or cephalosporin (Table 1). J.In general, radiographs should be repeated every 6 to 8 hours, and blood gases, blood counts, and electrolytes should be followed at least every 12 to 24 hours until the condition stabilizes. K.In a clinically stable infant with NEC stage I, measurement of serial C-reactive protein (CRP) levels can aid in the differentiation of true NEC from other entities. One recent study demonstrated that following a serum CRP level every 12 hours for three measurements was a strong marker for absence of NEC when all three levels were normal. L.Consultation with a neonatologist should begin when the diagnosis of NEC is strongly suspected. In general, when NEC stage II or III is confirmed, consultation with pediatric surgery should also be initiated. These cases should be managed at a center where pediatric surgery is immediately available. M.Very severely ill patients should receive ventilatory assistance before respiratory failure ensues. Apnea, respiratory acidosis, and hypoxemia are specific indicators for assisted ventilation. Intestinal capillary leak may deplete circulating fluid volume and protein, and DIC and gastrointestinal hemorrhage may lead to significant blood loss. Maintenance fluids should be provided at 100% to 150% of baseline with additional crystalloid and packed red blood cells as indicated. DIC and significant thrombocytopenia should be treated with fresh frozen plasma and platelet transfusions. N.If intestinal perforation is suspected, addition of clindamycin or metronidazole to antibiotic coverage should be considered. (Refer to most recent edition of The Harriet Lane Handbook for recommended dosing based on age and weight.) Although many experts recommend coverage for anaerobic pathogens, one small, randomized, controlled trial using clindamycin showed an increase in bowel strictures. O.Surgical indications include pneumoperitoneum, presence of a fixed loop on serial radiographs, and clinical deterioration despite maximal medical management. Other relative indications include portal venous air, abdominal wall erythema, abdominal mass, unremitting metabolic acidosis, and hyperkalemia or severe DIC. Paracentesis has been shown to be useful at predicting presence of bowel necrosis. Primary peritoneal drainage may be considered rather than open laparotomy, although studies have not conclusively demonstrated which approach is superior. P.Infants diagnosed with NEC stage II or beyond should be treated with antibiotics and kept NPO for 7 to 14 days. NEC stage I may be treated with shorter courses of antibiotics depending on clinical course and rate of resolution of symptoms. Parenteral nutrition should be initiated promptly by peripheral vein. After 24 hours of antibiotic therapy, central line placement should be considered. Q.Once treatment is complete, enteral feedings can be introduced with unfortified breast milk or formula. Volume and strength should be increased slowly while tapering parenteral nutrition. A contrast study is indicated if signs of intestinal obstruction develop during refeeding, because strictures are not an uncommon sequela of NEC. View chapterPurchase book Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780323054058001686 Necrotizing EnterocolitisIn Imaging in Pediatrics, 2018 KEY FACTSTerminology• Necrotizing enterocolitis (NEC): Life-threatening condition of neonatal GI tract characterized by inflammation, ischemia, & translocation of bacteria into bowel wall Imaging• Diagnosis based on clinical & imaging findings •Mainstay of imaging for suspected NEC: Radiography ○Findings range from nonspecific (paucity of bowel gas) to suggestive (thickened, dilated bowel loops) to diagnostic [pneumatosis, portal venous gas (PVG), & free peritoneal gas] ○Duke Abdominal Assessment Scale for radiographs –Standard lexicon for reporting NEC findings –Strong intraobserver & interobserver agreement –↑ scores correlate with need for surgery •Ultrasound excellent adjunct ○Radiographically occult necrosis requiring surgery suggested by absent vascularity + ↓ peristalsis ○Additional findings include focal fluid collections, echogenic ascites, ↑ bowel wall echogenicity, intramural gas, bowel wall thickening or thinning, PVG, & free air •Contrast enema not used acutely; useful to localize strictures after treatment of acute episode Clinical Issues• Most common in very low birth weight (< 1,500 g) premature infants 2-3 weeks after delivery ○10% in term infants (usually with underlying diseases) •Typical history: Feeding intolerance with emesis, ↑ gastric residuals, bloody stools ○Other frequent clinical findings include abdominal distention &/or discoloration, apnea & bradycardia, lethargy, temperature instability •Treatment: IV nutrition + antibiotics ± surgery •Overall mortality 10-50% ○Death secondary to sepsis from bowel perforation •Delayed bowel strictures in 10-20% of survivors View chapterPurchase book Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780323477789500982 Necrotizing EnterocolitisRobert M. Insoft, in Essence of Anesthesia Practice (Third Edition), 2011 Assessment pointsSystemEffectAssessment by HxPETestCARDIOShock Key Reference: Henry MW, Moss RL. Necrotizing enterocolitis. Annu Rev Med. 2009;60:111–124. Perioperative ImplicationsPreoperative Preparation• Most neonates may be treated medically with fluid resuscitation, antibiotics, ventilatory support, and hyperalimentation. •Surgery indicated for pneumoperitoneum from intestinal wall perforation, intestinal gangrene (detected by abd paracentesis), and presence of portal vein gas. Other indications incl clinical deterioration, abd wall erythema, and an unresolved ileus. •D/C enteral feeds and insert NG tube connected to suction for intestinal decompression. •Therapeutic goals incl normalization of vital signs, ensuring adequate oxygenation and ventilation (e.g., tracheal intubation, mechanical ventilation, adequate perfusion) •Vigorous fluid resuscitation to keep up with third space losses from peritonitis and sepsis •Correct metabolic acidosis—achieved through fluid resuscitation •Inotropic agents such as dopamine and do-butamine may be required to optimize cardiac output •Correct coagulopathy with FFP, plts, and packed RBCs •Administer broad-spectrum antibiotics, with anaerobic coverage highly considered as well Monitoring• Routine plus glucose and electrolytes Induction/Maintenance• Potent anesthetic agents are poorly tolerated. •Carefully titrated narcotic and muscle relaxant technique is satisfactory. •N2O is usually avoided because of its potential for causing bowel distention. •Fluid resuscitation (lactated Ringer's, 5% albumin, and sometimes packed RBCs) is actively carried out during surgical procedure. Postoperative Period• Closely monitor in NICU for ongoing fluid requirements as third space loss continues. •Prolonged TPN is often required. •Stricture formation leading to partial or total bowel obstruction is a common complication in both medically and surgically treated neonates. •Short-bowel syndrome can occur, leading to long-term complications. Anticipated Problems/Concerns• Hypovolemia and bowel ischemia •Acidosis, shock, and death View chapterPurchase book Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9781437717204002326 Necrotizing EnterocolitisStephen S. Kim, Craig T. Albanese, in Pediatric Surgery (Sixth Edition), 2006 HISTORYIn 1888, Paltauf223 described five patients who died of overwhelming peritonitis, the cause being suggestive of NEC in three of them. Despite this report, many credit Generisch88 with publishing the first report of NEC in 1891, but on careful review of his description of the findings, it almost certainly was a case of meconium peritonitis rather than NEC. In 1939, Thelander289 reported 16 cases of perforation of the stomach, 30 of the duodenum, and 39 of the small and large intestines. Many of the patients who had intestinal perforations probably had NEC. The first report of a successfully treated infant with a localized ileal perforation as a result of NEC is attributed to Agerty et al.2 in 1943. In 1953, Schmid and Quaiser264 first used the term necrotizing enterocolitis. In 1959, Rossier and colleagues249 described 15 infants, 14 of whom died of “ulcerative-necrotic enterocolitis of the premature.” In 1964, Berdon et al.22 reported the clinical and radiographic findings of 21 patients with NEC. A year later, Mizrahi et al.195 reported 18 cases of NEC in premature infants. The incidence of NEC in the New York Babies' Hospital nursery between 1953 and 1963 was 0.9%, but the disease caused 2.3% of all nursery deaths. In 1975, Santulli et al.257 hypothesized that development of the disease had three essential components: injury to the intestinal mucosa, the presence of bacteria, and the availability of a metabolic substrate. During the 1960s, treatment of NEC was early surgery. By 1970 it was recognized that with early diagnosis, most patients could be managed without surgery. In 1978, Bell et al.21 published a severity-based classification scheme that was helpful in selecting therapy and allowing comparison of outcomes. In 1979, the International Classification of Diseases established a code for death from NEC, thereby allowing more precise epidemiologic and outcome analyses. Read full chapterView PDFDownload book Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780323028424500954 Necrotizing EnterocolitisKanecia Zimmerman, Daniel K. BenjaminJr., in Principles and Practice of Pediatric Infectious Diseases (Fifth Edition), 2018 Prognosis and ComplicationsNEC is associated with significant mortality. In a multicenter cohort study of 1722 extremely low–birth weight infants, the incidence of death among those with NEC was twice that of infants who did not develop NEC (P < 0.01). The death rate did not change substantially over the 12-year period (1998–2009). What are signs of NEC in babies?A baby with necrotizing enterocolitis might have these symptoms:. a swollen, red, or tender belly.. trouble feeding.. food staying in the stomach longer than expected.. constipation.. diarrhea and/or dark or bloody stools (poop). being less active or lethargic.. a low or unstable body temperature.. green vomit (containing bile). Which manifestation suggests that an infant is developing necrotizing enterocolitis NEC )?Initial manifestations are feeding difficulties and bloody or bilious gastric residuals (after feedings) followed by bilious emesis, abdominal distention, and/or gross blood in stool.
When is necrotizing enterocolitis suspected in a newborn?Although necrotizing enterocolitis usually occurs in babies between three and 12 days after birth, late onset may occur many weeks after birth. Each baby experiences the necrotizing enterocolitis symptoms differently, which may include: Abdominal distention (swelling) Bloody stools.
Which clinical findings are associated with necrotizing enterocolitis?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 gastrointestinal tract symptoms include abdominal distention and frank or occult blood in the stools.
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