Risk of Necrotizing Enterocolitis (Nec) for Premature Baby
NECROTIZING ENTEROCOLITIS (NEC) is the most common acquired gastrointestinal emergency in the preterm low birth weight newborn. It is a result of an insult to the immature gut, characterized by varying degrees of mucosal or transmural necrosis. Mostly affects premature infants, NEC involves infection and inflammation that causes destruction of the bowel (intestine) or part of the bowel.
Babies with NEC may have a tender or tense abdomen, need more oxygen or higher ventilator settings, have blood in their bowel movements, or exhibit signs of apnea. An X-ray of the abdomen confirms the diagnosis. Necrotizing enterocolitis (NEC) is a serious intestinal illness in babies.
- "necrotizing" means damage and death of cells
- "entero" refers to the intestine
- "colitis" means inflammation of the colon (lower part of the intestine)
Premature babies have body systems that are more immature. As a result, they may have difficulty with blood and oxygen circulation, digestion, and fighting infection, thus, increasing their chances of developing NEC.In the most serious cases, this condition can be life-threatening.
As if the birth of a premature baby isn't stressful enough, there are a number of diseases premature babies can experience within the first weeks of life. Necrotizing enterocolitis (NEC) is one of them.Although NEC may develop in low-risk newborns, most cases occur in premature babies. NEC is more common in babies weighing less than 1,500 grams (3 pounds, 4 ounces).
NEC is an acute intestinal necrosis syndrome of unknown etiology and prematurity is the single greatest risk factor. The causes are not well defined and may be resulting from complex interactions between mucosal injury secondary to a variety of factors, including ischemia (splanchnic vesoconstriction), luminal substrate (high osmolar, formula, large volume, rapid enteral feeding), infection and inflammatory mediators (cytokines, endotoxins, platelet activating factor), and poor host protective mechanisms in response to injury.
Those with a higher risk for this condition include:
- Premature infants
- Infants who are fed concentrated formulas
- Infants in a nursery where an outbreak has occurred
- Infants who have received blood exchange transfusions
No single factor has been established as the cause of NEC. It is now thought that NEC is the result of a combination of several factors. The two consistent findings are prematurity and feedings. The premature intestine reacts abnormally and develops an acute inflammatory response to feedings leading to intestinal necrosis (death). Some postnatal issues including heart abnormalities, obstruction of circulation in the bowel, infection or gastroschisis are also associated with NEC. Others are:
- Early onset of feed with hyperosmolar milk.
- Perinatal asphyxia.
- Umbilical vessel catheterization.
Pathogenesis of the disease is multifactorial, related to previous intestinal ischemia, bacterial or viral infection and immunologic immaturity of the gut.
Onset usually occurs in the first 2 weeks. Meconium is passed normally, and the first signs are abdominal distension with gastric retention. Other signs include vomiting or increased gastric residuals, bloody stool, abdominal tenderness, temperature instability, apnea and bradycardia.
Clinical manifestations: A triad of abdominal distension, blood in stool and gastric residuals should be suspected of necrotizing enterocolitis. The clinical features are variable, and the signs and symptoms may not be specific. The infant may develop feeding intolerance with retention of feeding, abdominal distension, temperature instability and lethargy.
Apnea may be a prominent feature. Bilious vomiting, acidosis and DIC may be present. There may be ileus, abdominal wall erythema, abnormal mass ,ascites and bloody stool.Pneumatosis intestinalis in abdominal x-ray is the hallmark of diagnosis. Besides, the x-ray may reveal bowel wall edema, intestinal dilatation, portal or hepatic venous air, pneumoperitonium.
The differential diagnosis includes- feeding intolerance, infectious enterocolitis, pneumonia and sepsis, acute abdomen due to any surgical cause.
Treatment /Management :
This includes immediate medical management and surgical intervention if indicated.
A. Medical Treatment :
- Cessation of feeding.Nothing per oral with gastrointestinal decompression.
- Decompression of gut by nasogastric tube.In case of bleeding diathesis- exchange transfusion or specific factor replacement is necessary.
- Maintenance of oxygenation.In case of shock- maintain blood pressure and urine output with fluids, fresh/ frozen plasma, whole blood; and dopamine, steroids.
- IV fluid to replace third-space GIT losses.Supportive care- maintains adequate hematocrit, PH, PO2, PCO2, and electrolyte
- balance and mechanical ventilation.
- Nutrition: Once stabilized begin IV alimentation followed by slow gradual introduction of enteral feeding.
- Broad spectrum antibiotics e.g. a combination which cover gram positive and negative organisms including anaerobic organism such as ampicillin,gentamycin and metronidazole, the regimen may changed later according to the culture results.
- Fresh blood transfusion.In case of bleeding diathesis- exchange transfusion or specific factor
- replacement is necessary.
- Close monitoring of vital signs, laboratory data (Blood gas, WBC count. Platelet count and X-ray).
B. Surgical treatment :
Necrotic bowel is removed and if the infant is in good condition primary anastomosis can be carried out, but if the infant's condition is parlous during the laparotomy, excise affected bowel, defunction with a proximal ostomy and do a repeat operation some week later to replace the bowel in continuity.
Two surgical procedures, one invasive and the other much less so, for premature infants with intestinal perforation due to necrotizing enterocolitis (NEC) produce virtually identical results, according to a Yale School of Medicine study published today in the New England Journal of Medicine.
The standard surgical procedure in such cases has been a laparotomy with resection of all necrotic intestine and intestinal diversion. This approach derives from experience in adults, in whom it would be considered unthinkable to leave necrotic
intestine in place.