Any weakness or defect in the wall of the peritoneal cavity may permit protrusion of a serosa-lined pouch of peritoneum called a hernia sac. Acquired hernias most commonly occur anteriorly, through the inguinal and femoral canals or umbilicus, or at sites of surgical scars. These are of concern because of visceral protrusion (external herniation). This is particularly true of inguinal hernias, which tend to have narrow orifices and large sacs. Small bowel loops herniate most often, but portions of omentum or large bowel also protrude, and any of these may become entrapped. Pressure at the neck of the pouch may impair venous drainage, leading to stasis and edema. These changes increase the bulk of the herniated loop, leading to permanent entrapment, or incarceration, and over time, arterial and venous compromise, or strangulation, can result in infarction.
Intussusception isthemostcommoncauseofintestinalobstructioninchildrenyoungerthan2yearsofageandcanusuallybetreatedbybariumenemaorairenema.
Hirschsprung disease istheresultofdefectiveneuralcrestcellmigrationfromcecumtorectum.Itgivesrisetofunctionalobstruction.
Abdominal herniation mayoccurthroughanyweaknessordefectinthewalloftheperitonealcavity,includinginguinalandfemoralcanals,umbilicus,andsitesofsurgicalscarring.
The largest portion of the gastrointestinal tract is supplied by the celiac, superior mesenteric, and inferior mesenteric arteries. As they approach the intestinal wall, the superior and inferior mesenteric arteries fan out to form the mesenteric arcades. Interconnections between arcades, as well as collateral supplies from the proximal celiac and distal pudendal and iliac circulations make it possible for the small intestine and colon to tolerate slowly progressive loss of the blood supply from one artery. By contrast, acute compromise of any major vessel can lead to infarction of several meters of intestine.
Ischemic damage to the bowel can range from mucosal infarction, extending no deeper than the muscularis mucosa; to mural infarction of mucosa and submucosa; to transmural infarction involving all three layers of the wall. While mucosal or mural infarctions often are secondary to acute or chronic hypoperfusion, transmural infarction is generally caused by acute vascular obstruction. Important causes of acute arterial obstruction include severe atherosclerosis (which is often prominent at the origin of mesenteric vessels), aortic aneurysm, hypercoagulable states, oral contraceptive use, and embolization of cardiac vegetations or aortic atheromas. Intestinal hypo-perfusion can also be associated with cardiac failure, shock, dehydration, or vasoconstrictive drugs. Systemic vasculitides also may damage intestinal arteries. While mesenteric venous thrombosis can lead to ischemic disease, it is uncommon. Other causes include invasive neoplasms, cirrhosis, portal hypertension, trauma, or abdominal masses that compress the portal drainage.
The severity of vascular compromise, time frame during which it develops, and vessels affected are the major variables that determine severity of ischemic bowel disease. Intestinal responses to ischemia occur in two phases. The initial hypoxic injury occurs at the onset of vascular compromise and, although some damage occurs, intestinal epithelial cells are relatively resistant to transient hypoxia. The second phase, reperfusion injury, is initiated by restoration of the blood supply and associated with the greatest damage. While the underlying mechanisms of reperfusion injury are incompletely understood, they involve free radical production, neutrophil infiltration, and inflammatory mediators such as complement and cytokines. Two aspects of intestinal vascular anatomy also contribute to the distribution of ischemic damage: