**9. Management**

*Pediatric Surgery, Flowcharts and Clinical Algorithms*

**7.1 Differentiating medical and surgical NEC: use of biomarkers**

Pneumoperitoneum is not a very reliable clinical feature for surgical NEC and is

observed in less than half of all infants with intestinal perforation or necrosis [15, 39]. Clinical deterioration despite maximal medical therapy is considered a relative indication for surgical intervention. Research has been done to identify a dependable predictor for intestinal necrosis. The most commonly used biochemical markers for bowel necrosis among pediatric surgeons are platelet count (99%), C-reactive protein (CRP) concentration (90%), white blood cell count (83%), lactate levels (43%), fecal calprotectin 10%, and interleukin (IL)-6 or interleukin-8 10% [40]. Fecal calprotectin is a marker of intestinal inflammation and can differentiate between local Bell stage II and systemic Bell III NEC with 76% sensitivity and 92% specificity [41]. Fecal levels of another protein, S100A12, are noted to be higher in infants with suspected NEC who subsequently develop bowel perforation. Unremitting and relentlessly high CRP levels despite treatment may indicate advanced stage of NEC and bowel necrosis. IL-8 levels have been shown to be significantly elevated in patients developing surgical NEC compared to medically managed NEC [42]. The levels can also discriminate NEC totalis from focal and multifocal diseases and predict 60-day mortality [43]. Maximum concentration of CRP and duration of CRP elevation are increased in infants who developed intestinal strictures following NEC, while the negative predictive value of CRP levels <10 mg/dL for stricture development is 100% [44]. Intestinal fatty acid-binding protein (I-FABP), a marker of intestinal injury and progression to severe NEC, is located in mature enterocytes of small intestinal villi and is released into the blood stream after cell disruption and subsequently excreted into the urine. At onset of symptoms, I-FABP concentrations have been shown to be significantly higher in infants who later developed surgical NEC [45]. Other biomarkers being investigated for surgical NEC are serum amyloid A protein, liver fatty

acid-binding protein, urine peptides, and heart rate characteristic index.

Blood stream infection can present like NEC and must be ruled out. Sepsis and other conditions that can cause feeding intolerance, rectal bleeding, abdominal distension, gastric retention of feed, or intestinal perforation can be differentiated from NEC by the absence of radiologic evidence of pneumatosis intestinalis and the characteristic combination of rectal bleeding presenting as heme-positive or grossly bloody stools, abdominal distention, bilious vomiting, and gastric aspirates as seen in NEC. Spontaneous intestinal perforation is characterized by a single noninflammatory perforation that is typically located at the terminal ileum or colon. It occurs primarily in infants with birth weight <1000 g and is differentiated from NEC by the presence of less severe systemic signs and absence of pneumatosis intestinalis. Infectious enteritis may present with frequent, occasionally bloody stools with abdominal distension but no pneumatosis. Congenital anomalies of GIT, such as Hirschsprung disease, small bowel atresia, meconium ileus, and acquired conditions like volvulus and intussusception, present with intestinal obstruction and at times secondary enterocolitis. Abdominal radiography differentiates these conditions from NEC. Anal fissures can result in rectal bleeding and can be detected on pertinent thorough physical examination. Milk protein allergy-induced enterocolitis may present with heme-positive stools and other GI symptoms similar to NEC in preterm infants but no pneumatosis. Such patients respond to dietary modification by switching the formula to extensively hydrolyzed or amino acid-based ones and

**8. Differential diagnosis**

may have eosinophilia along with thrombocytosis.

**34**

The basic principles of management of NEC are bowel decompression and rest, antibiotics coverage, cardiorespiratory support, fluid resuscitation, provision of blood products, and surgical intervention if indicated. The management strategies according to Bell's staging are outlined in **Table 4**. Surgical consultation is obtained in all stages of NEC including stage 1. Total parenteral nutrition (TPN) should be provided during the period that the infant is nil by mouth.
