ba necrotizing enterocolitis

7/31/2019 BA Necrotizing Enterocolitis

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Dr. Andreas Andri L.TJ.


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It is an acquired rather than a congenital disease

Its clinical spectrum varies :Mild abdominal distentionIleusOccult blood in the stoolsPneumatosis coli to one with fulminant sepsis

Shock from widespread intestinal necrosis

It has become the single most common surgical emergency in newborns

It is the major cause of death among neonates who undergo sur-gical procedures

Rossier et al first used the term necrotizing enterocolitis in 1959


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Pathogenesis

Three main factors which create the setting in which NEC occurs :Ichemic damage to the intestineBacterial colonizationSubstrate

Intestinal ischemia

Vasospasm ( diving reflex or selective mesenteric ischemia, umbilical artery catheterization, hypothermia)

Thrombosis ( exchange transfusion, polycythemia)Low flow states ( hypotension, patent ductus arteriosus, asphyxia, respiratory dis-

tress syndrome)

Bacterial colonization

The presence of hydrogen gas within the lumen and cysts of pneumatosis intestinalissupports the role of bacteria, since the only source of hydrogen gas in humans is bac-terial fermentation


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Substrate

Ninety to ninety-five percent of infants in whom NEC develops have been fedcommercial formula .

The formula serves as a substrate for bacterial proliferation.

Direct intestinal mucosal injury may be caused by the high osmolarity of formulas orby 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 Bacterial Colonization

Immature Intestine

Unfed Infant Full Term Infant

NEC

Pathogenesis of necrotizing enterocolitis


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


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Cultures are obtained of theblood, urine, csf, and in some cases, peritoneal fluid.

BGA, WBC, HCT,Plate counts, Electrolytes, Coagulation studies


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Medical Treatment

As soon as the diagnosis of NEC is suspected all oral feedingsare discontinued, and orogastric tube is passed to decompress thegastrointestinal 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-negativeorganisms ( Enteral antibiotics are not indicated)

Parenteral nutrition is provided to supply the infant with 110 to 150kcal/kg/day


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Bowel rest and antibiotics are continued for 10 to 14 days after theresolution of pneumatosis

Feedings are commenced with dilute, lactose-free formula of lowosmolarity

The feedings are slowly increased in concentration and volume as the

enteral nutrition is reduced


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Surgical Treatment Koloske et al evaluated 10 clinical radiologic and laboratory criteria for surgery

Pneumoperitoneum valid indications forPositive paracentesis sugeryErythema of the abdominal wallFixed abdominal mass

Persistently dilated intestinal loop on serial radiographs

Clinical deterioration not reliable indicator of Abdominal tenderness intestinal ganggrene (Lower gastrointestinal bleeding need for surgery )

AscitesSevere thrombocytopenia

Pneumoperitoneum is the only absolute indication for surgery


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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


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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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ba necrotizing enterocolitis

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