An intraluminal model of necrotizing enterocolitis in the developing neonatal piglet

The most common risk factors for the development of necrotizing enterocolitis (NEC) are prematurity and enteral feeding. Most models of NEC involve ischemic insult resulting in generalized necrosis, different from the classical ileocecal predilection of NEC. This anatomic predisposition is explained by dysmotility of immature gut, leading to bacterial overgrowth in the terminal ileum and colon. Infant formula containing lactose as the sole carbohydrate source overwhelms partially developed lactase activity, allowing enteric bacteria to ferment excess carbohydrate to short-chain fatty acids, decreasing intraluminal gut pH and predisposing to mucosal injury. Impaired clearance of intraluminal contents exacerbates this effect. In the present study the authors used a model of NEC, originally developed in rabbits and based on analysis of intestinal contents of NEC babies, modified and adapted here to neonatal piglets, the gastrointestinal tract of which more closely resembles the human neonate.

Piglets < 3 days old and 2 weeks old were laparotomized. Loops created from the distal ileum to the proximal colon were injected with isoosmolar acidified casein solution or 0.9% saline. Segments were harvested 3 hours later, sectioned for H&E, and graded from 0 (intact villi) to 4 (transmural necrosis).

Acidified casein-induced damage included areas of necrosis, submucosal edema, inflammatory cell infiltrate, and lymphatic distension. In younger animals, lesions were more pronounced (3.25 +/- 0.13 for the < 3-day-old v 2.43 +/- 0.14 for the 2-week-old piglets; P < .005).

The authors believe that this piglet NEC model most closely approximates human NEC because it incorporates two of the most common risk factors: dysmotility (by creating intestinal loops) and enteral feeding (by intraluminal injection of acidified casein).