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Содержание Idiopathic Intestinal Pseudo-Obstruction

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Idiopathic Intestinal Pseudo-Obstruction

Most patients with gaseous distention of the intestine have either mechanical intestinal obstruction or paralytic ileus. In most patients with ileus, the disorder can be readily ascribed to peritonitis, metabolic disturbances, or drugs. Idiopathic intestinal pseudo-obstruction is a chronic illness characterized by symptoms of recurrent intestinal obstruction without demonstrable mechanical occlusion of the bowel. Patients with this disease have impaired motor response to intestinal distention, but the duodenal and colonic slow waves may be normal. Some patients have aperistalsis of the esophagus, with failure of the lower esophageal sphincter to relax. Heredity plays a role in this disorder. The symptoms of intestinal pseudo-obstruction include cramping abdominal pain, vomiting, distention, diarrhea, and sometimes steatorrhea. Physical examination reveals abdominal distention. Intestinal pseudo-obstruction is distinguished from mechanical intestinal obstruction by the absence of the radiographic findings of mechanical obstruction. Surgical treatment for this condition should be avoided. Intravenous hyperalimentation may help manage these patients.

PATHOGENESIS

Simple Mechanical Small Intestinal Obstruction

Mechanical obstruction of the small intestine causes accumulation of fluid and gas proximal to the obstruction, producing distention of the intestine. Ingested fluid, digestive secretions, and intestinal gas initiate the distention. As mentioned earlier, large volumes of saliva, gastric secretion, bile, and pancreatic juice enter the gut daily. The stomach has a very small capacity for absorbing fluid, so most alimentary fluid is absorbed by the small intestine.

Peristalsis normally propels intestinal gas aborally for expulsion from the rectum as flatus. Gas accumulating in the intestine proximal to an obstruction originates from swallowed air, carbon dioxide from neutralization of bicarbonate, and organic gases from bacterial fermentation. Swallowed air is the most important source of gas in intestinal obstruction because its nitrogen content is very high, and the intestinal mucosa cannot absorb nitrogen. As a result, intestinal gas is predominantly (70%) nitrogen. The large amount of carbon dioxide produced in the lumen of the gut is readily absorbed and therefore contributes little to the distention.

One of the most important events during simple mechanical small bowel obstruction is loss of water and electrolytes from the body, caused mainly by intestinal distention. First, reflex vomiting may result from intestinal distention. In addition, intestinal distention is self-perpetuating in the obstructed small bowel, because distention increases intestinal secretion. Experiments on dogs show that intestinal distention initially causes decreased absorption (decreased lumen-to-blood flux of water) in the obstructed segment, but not in the intestine distal to the obstruction. 31 This phenomenon increases the accumulation of fluid in the bowel proximal to the obstruction, perhaps further accentuating dehydration and causing further intestinal distention, which proceeds proximally. Increased secretion in the obstructed bowel occurs in humans.

The metabolic effects of fluid loss in simple mechanical obstruction of the small bowel depend on the site and the duration of the obstruction. Proximal obstruction of the small bowel causes relatively greater vomiting and less intestinal distention than distal obstruction. Proximal obstruction causes losses of water, Na+, Cl-, H+, and K+, producing dehydration with hypochloremia, hypokalemia, and metabolic alkalosis. Distal obstruction of the small bowel may entail loss of large quantities of fluid into the bowel; however, the abnormalities of serum electrolyte values are usually less dramatic, probably because less hydrochloric acid is lost.

Oliguria, azotemia, and hemoconcentration can accompany dehydration. If dehydration persists, circulatory changes such as tachycardia, low central venous pressure, and reduced cardiac output may cause hypotension and hypovolemic shock. Other sequelae of intestinal distention include increased intra-abdominal pressure, decreased venous return from the legs, and elevation of the diaphragm sufficient to impair ventilation.

Rapid proliferation of intestinal bacteria occurs during intestinal obstruction. Normally the small intestine contains few bacteria and may be almost sterile. There may be several causes for the sparse bacterial population of the small intestine, but normal peristalsis and the interdigestive migrating myoelectrical complex (MMC), with continued aboral progression of luminal content, minimize the small intestinal flora. During small intestinal stasis, whatever the cause, intraluminal bacteria proliferate rapidly, especially in intestinal obstruction. The small intestinal contents thus become feculent during obstruction because of large quantities of bacteria. Normally the colon, an organ that functions as a reservoir, contains large numbers of bacteria.

The bacteria in the small intestine probably contribute little to the ill effects of simple mechanical small intestinal obstruction, although recent studies show that bacterial translocation may occur in the distended viable small intestine.

Strangulation Obstruction

Strangulation occurs when the circulation to the obstructed intestine becomes impaired. Substantial increased intraluminal pressure impairs the bowel's circulation. Occlusion of the bowel lumen at two points along its length produces closed-loop obstruction. This type of obstruction may proceed more rapidly to strangulation than simple obstruction. Pressure necrosis can develop if the obstructed distending bowel is held by unyielding adhesive bands or hernial rings. The deformity or twisting of the mesentery, as in volvulus or intussusception, can occlude the mesenteric vessels. In strangulation obstruction, the patient may suffer all the ill effects of simple obstruction in addition to the effects of strangulation. Strangulation causes loss of blood and plasma into the strangulated segment. Predominant venous vascular obstruction may produce greater loss of blood or plasma than predominant arterial vascular obstruction. This loss of blood and plasma causes shock, particularly if the patient is already dehydrated. If strangulation produces gangrene, peritonitis and its sequelae occur. Rupture or perforation of a strangulated segment is possible and is a devastating complication.

In addition to the loss of blood and plasma, another important factor in strangulation obstruction is the toxic material from the strangulated loop. The luminal fluid from a strangulated intestinal loop and the bloody, malodorous peritoneal fluid are lethal when administered to normal animals. Bacteria and necrotic tissue appear to be necessary for the development of the toxic fluid. Apparently, this lethal fluid forms in the lumen of the strangulated intestine and passes through the injured intestinal wall. The peritoneum absorbs the toxic material, producing systemic effects.