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Dr. Andreas Andri L.TJ.

It is an acquired rather than a congenital disease Its clinical spectrum varies : Mild abdominal distention Ileus Occult blood in the stools Pneumatosis coli to one with fulminant sepsis Shock from widespread intestinal necrosis It has become the single most common surgical emergency in new borns It is the major cause of death among neonates who undergo surgical procedures Rossier et al first used the term necrotizing enterocolitis in 1959

Pathogenesis

Three main factors which create the setting in which NEC occurs : Ichemic damage to the intestine Bacterial colonization Substrate Intestinal ischemia
Vasospasm ( diving reflex or selective mesenteric ischemia, umbilical artery catheteri zation, hypothermia) Thrombosis ( exchange transfusion, polycythemia) Low flow states ( hypotension, patent ductus arteriosus, asphyxia, respiratory distress syndrome)

Bacterial colonization
The presence of hydrogen gas within the lumen and cysts of pneumatosis intestinalis supports the role of bacteria, since the only source of hydrogen gas in humans is bacterial fermentation

Substrate
Ninety to ninety-five percent of infants in whom NEC develops have been fed commercial formula. The formula serves as a substrate for bacterial proliferation.

Direct intestinal mucosal injury may be caused by the high osmolarity of formulas or by a feeding schedule that is advanced too rapidly

Barlow et al. showed that fresh breast milk was protective against the development of NEC experimentally. Intestinal Ischemia Carbohydrate Substrate Immature Intestine Unfed Infant Full Term Infant Bacterial Colonization

NEC Pathogenesis of necrotizing enterocolitis

Diagnosis

NEC occuring in the first day of life is rare and is usually found in larger, full term infants who have respiratory distress or who have receive exchange transfusion for polycytemia The initial findings are : abdominal distention with increased gastric aspirate that may be clear, bloody, or bilious. Localized abdominal erythema and induration, with marked abdominal tenderness are signs of associated peritonitis The advanced disease, there is marked abdominal distention, bilious emesis, rapid deterioration, and shock The differential diagnosis icludes: midgut volvulus, sepsis with paralytic ileus, and Hirschprungs disease

Abdominal roentgenogram (not only for the initial diagnosis, but also to evaluate the results of therapy) Pneumatosis intestinalis or bubles of subserosal air identified on plain abdominal rontgenograms are essential for the diagnosis

Cultures are obtained of the blood, urine, csf, and in some cases, peritoneal fluid. BGA, WBC, HCT,Plate counts, Electrolytes, Coagulation studies

Medical Treatment

As soon as the diagnosis of NEC is suspected all oral feedings are discontinued, and orogastric tube is passed to decompress the gastrointestinal tract IV fluid, coloid, and blood are given to maintain a urine output of 1.5 to 2.0 ml/kg/hour Intubation and assisted ventilation ( are required because of lethargy, sepsis, and massive abdominal distention) Systemic antibiotics to cover for both gram positive and gram-negative organisms ( Enteral antibiotics are not indicated) Parenteral nutrition is provided to supply the infant with 110 to 150 kcal/kg/day

Bowel rest and antibiotics are continued for 10 to 14 days after the resolution of pneumatosis
Feedings are commenced with dilute, lactose-free formula of low osmolarity The feedings are slowly increased in concentration and volume as the enteral nutrition is reduced

Surgical Treatment

Koloske et al evaluated 10 clinical radiologic and laboratory criteria for surgery Pneumoperitoneum Positive paracentesis Erythema of the abdominal wall Fixed abdominal mass Persistently dilated intestinal loop on serial radiographs valid indications for sugery

Clinical deterioration Abdominal tenderness Lower gastrointestinal bleeding Ascites Severe thrombocytopenia

not reliable indicator of intestinal ganggrene ( need for surgery )

Pneumoperitoneum is the only absolute indication for surgery

The abdomen is entered through a supraumbilical transverse incision The standard surgical treatment of NEC is resection of all necrotic intestine, exteriorization of the viable ends, and preservation of as much potentially viable bowel as possible to prevent development of the short gut syndrome In infants with localized NEC, perforated and ganggrenous bowel is resected using multiple segmental resections as necessary to preserve intestinal length Harberg et al recommended resection with primary anastomosis in all infants operated on for NEC

Before closure, the abdominal cavity os copiously lavaged with warm saline and antibiotic solution Oral feedings are resumed when normal gastrointestinal function returns but not sooner than 7 days after surgery.

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