Necrotizing Enterocolitis

Necrotizing enterocolitis (NEC) is an acquired inflammatory disease affecting the gut of newborns, predominantly premature infants.
Incidence in infants weighing less than 1500 g is 10%.
It is the most common newborn surgical emergency and leading cause of infant morbidity and mortality in neonatal intensive care units (NICUs).¹

HISTORICAL BACKGROUND

Pathologic findings of intestinal perforation in neonates as the cause of death were first described in 1888.
Agerty in 1943 did the first report of successfully treated infant with localized ileal perforation.
In 1953 Schmid and Quaiser first used the term necrotizing enterocolitis.
In 1964 Berdon reported clinical and radiographic findings of 21 patients with NEC.

PATHOPHYSIOLOGY

NEC is rare in full-term infants and those who have never been fed.
Premature infants lack mature barrier defense owing to poorly developed mucosal cells; goblet cells produce scant amount of mucus; gastric, pancreatic, and intestinal secretions are reduced. Secretory IgA levels are low or absent.
Three components are essential in the development of NEC: presence of bacteria, injury to intestinal mucosa, and availability of metabolic substrate (enteral feedings).
Bacteria gain access to macrophages and dendritic cells of the innate immune system, which recognizes pathogenic bacteria toll-like receptors (TLRs). Based on the results of experiments in cell culture and in mice, it appears that NEC is a TLR4-driven process.

CLINICAL PRESENTATION

Several days after feeds are started, abdomen becomes distended and large amount of bilious gastric residual is produced.
Physical examination: distended abdomen, palpable bowel loops, and lethargy.
Erythema of the abdominal wall is ominous sign developing when underlying gangrene or perforation of the bowel is present. It occurs because thin abdominal wall and lack of subcutaneous fat allow the inflammatory reaction to produce cellulitis.

DIAGNOSIS

Laboratory Findings

Anemia, thrombocytopenia, neutropenia, and acidosis (resulting from hypovolemia and sepsis).
Levels of IL-6, IL-10, and C-reactive protein are increased. The highest levels of IL-10 were documented in the patients who did not survive.
Blood cultures are positive in 30% to 35% of patients and commonly grow Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Staphylococcus aureus, Staphylococcus epidermidis, enterococci, Clostridium perfringens, and Pseudomonas aeruginosa. Peritoneal cultures are most commonly positive for Klebsiella species, E. coli, coagulase-negative staphylococci, Enterobacter species, and yeast.

Imaging Findings

Abdominal X-ray (anteroposterior and left lateral decubitus views) is the current standard for diagnosing. Pneumatosis intestinalis (intramural gas) is the hallmark of NEC (Figure 26.1). Portal venous air is present in case of extensive intestinal injury, but it is not necessarily an indication for operation (Figure 26.2).
Abdominal ultrasound: evaluation of bowel wall thickness and echogenicity, free and focal fluid collections, peristalsis, and the presence or absence of bowel wall perfusion by using Doppler imaging.

Figure 26.1 Necrotizing enterocolitis. This schematic is a composite of the theories about factors thought to be involved in the pathogenesis of NEC. Large boxes denote the progression of this disease, whereas small boxes denote the factors thought to initiate or propagate the disease process. (Reprinted with permission from Alldredge BK, et al. Applied Therapeutics: The Clinical Use of Drugs. 10th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2013. Originally adapted from Crouse DT. Necrotizing enterocolitis. In: Pomerance JJ, Richardson CJ, eds. Neonatology for the Clinician. Norwalk, CT: Appleton & Lange; 1993:364.)

Only gold members can continue reading. Log In or Register to continue