Chapter 72 Necrotizing Enterocolitis (Case 31)
Patient Care
Clinical Thinking
• Radiographic evaluation of the abdomen requires two views (anteroposterior and left lateral decubitus or cross table lateral) to evaluate bowel gas pattern and presence of intraperitoneal air. A prone view may be helpful in assessing for air-fluid levels.
• Medical therapy for NEC typically consists of bowel rest, intestinal decompression, and broad-spectrum antibiotic therapy.
History
• Evaluate the maternal risk factors: Antenatal history of decreased placental perfusion, intrauterine growth restriction, maternal diabetes, hypermagnesemia, and administration of dexamethasone.
• Evaluate the neonatal risk factors: Degree of prematurity, postnatal age, comorbid conditions that might compromise intestinal perfusion or overall hemodynamic status (i.e., resuscitation at birth, patent ductus arteriosus, gastrointestinal malformation), and feeding regimen.
• Assess for symptoms of feeding intolerance: Evidence of delayed gastric emptying such as increased gastric residuals, abdominal distention, and evidence of occult or grossly bloody stools.
Physical Examination
• Signs of intestinal ileus: Abdominal distention, decreased bowel sounds, and palpable bowel loops.
• Signs of peritonitis: Abdominal distention, tenderness, palpable mass, and erythema or discoloration of the abdominal wall.
Tests for Consideration
• Complete blood count (CBC) with differential: To assess for leukopenia, leukocytosis, neutropenia, and thrombocytopenia $110
• Coagulation profile, including prothrombin time, activated partial thromboplastin time, fibrinogen, and fibrin split products: To monitor for a consumptive coagulopathy $300
• Cultures of the blood, urine, and cerebrospinal fluid (CSF): To document bacterial infection $135 each
Clinical Entities: Medical Knowledge
| Necrotizing Enterocolitis | |
|---|---|
| Pϕ | NEC is a severe inflammatory disease of the gastrointestinal tract that predominantly affects premature infants and has multifactorial pathogenesis. It results from a complex interaction of factors related to abnormal bacterial colonization, intestinal ischemia, reperfusion injury with activation of a proinflammatory cascade, and intestinal mucosal immaturity. The majority of cases are sporadic, but outbreaks may occur in nurseries. The incidence varies inversely with birth weight and gestational age, and infants less than 1000 grams at birth and less than 28 weeks’ gestation appear to be the most susceptible. The average age of onset is inversely related to gestational age. At the time of presentation, infants typically are advancing on enteral feedings or may have achieved full-volume feedings. |
| TP | Infants can present with increased gastric residuals, emesis, mild abdominal distention, decreased bowel sounds, or hematochezia, as well as systemic signs such as apnea, bradycardia, temperature instability, or lethargy. Physical examination may reveal increasing abdominal girth, visible intestinal loops, abdominal tenderness, palpable mass in the right lower quadrant, abdominal wall erythema secondary to necrotic loops adjacent to the abdominal wall, or abdominal discoloration from intraperitoneal meconium visible through the abdominal wall. Major systemic signs such as worsening respiratory failure, acidosis, decreased peripheral perfusion, shock, cardiovascular collapse, and bleeding diathesis can occur. |
| Dx | Radiographic imaging that includes two views is essential for diagnosing NEC and should be performed every 6 to 8 hours during the first 48 to 72 hours of disease to evaluate for pneumatosis intestinalis and pneumoperitoneum. Portal venous gas may be visible as thin, linear branching areas of radiolucency overlying the liver. The greatest risk for perforation is in the first 24 to 48 hours. A fixed dilated bowel loop that remains unchanged over serial radiographs may be a sign of intestinal ischemia or infarction. Metabolic derangements, including hyponatremia from fluid shifts, glucose instability, and metabolic acidosis, are commonly seen. Either leukocytosis or leucopenia as well as thrombocytopenia are often present. |
| Tx | The typical approach consists of bowel rest, intestinal decompression, systemic antibiotics, and parenteral nutrition. Broad-spectrum antibiotic coverage consisting of vancomycin, gentamicin, and metronidazole can be used. However, antimicrobial choices should be guided by local resistance patterns. Correction of electrolyte abnormalities, metabolic acidosis, and coagulopathy can be necessary. Arterial blood gas monitoring, ventilatory support necessitating intubation and fluid resuscitation with normal saline or colloid and pressor support may also be required. If surgical intervention is required, exploratory laparotomy usually involves resection of necrotic bowel and exteriorization of viable ends as an enterostomy and mucous fistula to allow for continued bowel decompression. Alternatively, primary peritoneal drainage can be considered in cases of perforated NEC in unstable or very low-birth-weight infants. See Nelson Essentials 63. |
| Meconium Obstruction of Prematurity |
|---|
| See Chapter 63, Delayed Meconium Passage. |
| Sepsis with Ileus |
|---|
| See Chapter 77, Neonatal Sepsis. |
| Spontaneous Intestinal Perforation | |
|---|---|
| Pϕ | SIP is a spontaneous, focal intestinal perforation may arise from regional ischemia to the mucosa that spreads into the deeper layers of the affected intestine eventually resulting in transmural involvement. Perforations are sharply demarcated lesions without gross necrosis and localized to the antimesenteric side of the terminal ileum. In comparison with NEC, SIP occurs more frequently in extremely premature infants and typically presents during the first 2 weeks following birth. |
| TP | Affected infants appear clinically well despite a sudden onset of abdominal distention. A bluish discoloration of the abdominal wall suggests the presence of an intestinal perforation. |
| Dx | Abdominal radiographs may initially show a normal bowel gas pattern or transient bowel distension. Subsequent radiographs may demonstrate a paucity of bowel gas or a gasless abdomen. Pneumatosis intestinalis is not typically observed. Once intestinal perforation occurs, a pneumoperitoneum may be observed. Laboratory studies are often not helpful in differentiating this disease from NEC. |
| Tx | Supportive measures including bowel rest, intestinal decompression, and broad-spectrum antibiotic therapy. Surgical management consists of primary peritoneal drainage or laparotomy. See Nelson Essentials 63. |
| Intestinal Malrotation With Midgut Volvulus | |
|---|---|
| Pϕ | Malrotation results from a failure of the gastrointestinal tract to complete its normal rotation as it returns to the abdominal cavity at 8 to 10 weeks gestation. Normal mesenteric attachments are absent, so the midgut is attached to the posterior abdominal wall only at the duodenum and at the proximal colon. Abnormal peritoneal bands called Ladd bands form between the colon and the duodenum, which can lead to duodenal obstruction. In addition, unfixed bowel may twist around its mesentery, resulting in ischemia of the bowel supplied by the superior mesenteric artery. |
| TP | Infants present with symptoms of a high intestinal obstruction such as sudden onset of bilious vomiting, abdominal distention, and hematochezia. As the obstruction progresses, the abdomen becomes more distended, firm, and tender, consistent with developing peritonitis. |
| Dx | Upper gastrointestinal series is the definitive study to document position of the duodenojejunal junction and assess for evidence of volvulus. Malrotation is present if the duodenojejunal junction is displaced to the right of midline or inferior to the level of the pylorus. Midgut volvulus is present if the duodenum appears dilated and fluid filled with a “corkscrew” appearance of the distal duodenum and proximal jejunum as it spirals downward into the right or mid-upper abdomen. Contrast enema may demonstrate an abnormal position of cecum to the right or upper abdomen but may not be helpful because the cecal position is highly variable. Ultrasonography may reveal a “whirlpool sign” of bowel twisting around its mesentery. |
| Tx | Volvulus is a gastrointestinal emergency that requires immediate surgical intervention. The Ladd procedure is performed, which consists of volvulus reduction, resection of grossly necrotic bowel followed by primary anastomosis or enterostomy, lysis of peritoneal bands, replacement of the bowel in a malrotated position, and appendectomy. In cases of extreme necrosis, a second-look laparotomy may be performed 12 to 36 hours after the initial surgery to assess intestinal viability. See Nelson Essentials 129. |
| Hirschsprung Disease | |
|---|---|
| Pϕ | Intestinal dysmotility and functional distal intestinal obstruction occurs as a result of congenital agenesis of ganglion cells in the myenteric and submucosal plexuses secondary to a failure of neural crest cell migration. The aganglionic segment causes a lack of propagation of peristalsis and absent relaxation of the internal anal sphincter. The length of affected bowel influences the severity of observed dysmotility. |
| TP | Infants present with a history of delay in meconium passage within the first 48 hours of life. Other symptoms include infrequent passage of stool, feeding intolerance, bilious vomiting, and abdominal distention. Presentation may be delayed in the preterm infant whose enteral feeds are initiated beyond the immediate neonatal period. |
| Dx | Abdominal radiograph typically shows dilated intestinal loops with air-fluid levels in the colon. Contrast enema characteristically demonstrates a funnel-shaped transition zone between the narrowed aganglionic distal bowel and the markedly dilated normally ganglionated, proximal bowel. However, a distinct transition zone may not always be readily apparent. In cases of total aganglionosis, the enema shows reduced caliber of the entire colon, no clear transition zone, and contrast refluxed into the distended ileum. Retention of contrast in the colon for more than 24 hours following the procedure is also suggestive of disease. Definitive diagnosis is established by rectal biopsy that reveals an absence of ganglion cells in the submucosal layer and acetylcholinesterase staining of the submucosa, which identifies abnormal nerve hypertrophy. A suction biopsy of the rectal mucosa and submucosa is typically performed at bedside. |
| Tx | Initial management consists of gastric decompression by placement of a Replogle tube and repeated rectal irrigation. The definitive surgical intervention is resection of aganglionic segment with pull-through of the normal innervated bowel down to the anus. (See Chapter 35, Constipation.) See Nelson Essentials 126. |
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