Colostomy Closure

Large Bowel Obstruction and Pseudo-Obstruction

Large bowel obstruction can be classified as dynamic (mechanical) or adynamic (pseudo-obstruction). Mechanical obstruction is characterized by blockage of the large bowel (luminal, mural, or extramural), resulting in increased intestinal contractility as a physiologic response to relieve the obstruction. Pseudo-obstruction is characterized by the absence of intestinal contractility, often associated with decreased or absent motility of the small bowel and stomach.

Colorectal cancer is the single most common cause of large intestinal obstruction in the United States, whereas colonic volvulus is the more common cause in Russia, Eastern Europe, and Africa. Approximately 2% to 5% of patients with colorectal cancer in the United States present with complete obstruction. Intraluminal causes of colorectal obstruction include fecal impaction, inspissated barium, and foreign bodies. Intramural causes, in addition to carcinoma, include inflammation (e.g., diverticulitis, Crohn's disease, lymphogranuloma venereum, tuberculosis, schistosomiasis), Hirschsprung's disease (aganglionosis), ischemia, radiation, intussusception, and anastomotic stricture. Extraluminal causes include adhesions, the most common cause of small bowel obstruction, but rarely a cause of colonic obstruction, hernias, tumors in adjacent organs, abscesses, and volvulus.

The signs and symptoms of large bowel obstruction depend on the cause and location of the obstruction. Cancers arising in the rectum or left colon are more likely to obstruct than those arising in the more capacious proximal colon. Regardless of the cause of the blockage, the clinical manifestations of large bowel obstruction include the failure to pass stool and flatus associated with increasing abdominal distention and cramping abdominal pain.

The colon becomes distended as gas (approximately two thirds is swallowed air, and the remainder includes the products of bacterial fermentation), stool, and liquid accumulate proximal to the site of blockage. If the obstruction is the result of a segment of colon trapped by a hernia or by a volvulus, the blood supply can become compromised, or strangulated. The venous return is blocked initially, causing localized swelling that can, in turn, occlude the arterial supply with resultant ischemia that if uncorrected, can progress to necrosis or gangrene. The strangulation at first involves only the entrapped, or incarcerated, segment of bowel, but the colon proximal to that segment becomes progressively dilated because of the obstruction.

Another route to vascular compromise of the obstructed colon occurs if the bowel proximal to the point of obstruction distends to the extent that the intramural pressure within the intestinal wall exceeds the capillary pressure, depriving the bowel of adequate oxygenation. This route to ischemic necrosis can occur with mechanical obstruction and pseudo-obstruction.

A closed loop obstruction occurs when the proximal and distal parts of the bowel are occluded. A strangulated hernia or volvulus almost always leads to this condition. The more common form of closed loop obstruction, however, is seen when a cancer occludes the lumen of the colon in the presence of a competent ileocecal valve. In this situation, increasing colonic distention causes the pressure in the cecum to become so high that the vessels in the bowel wall are occluded, and necrosis and perforation can occur.

The treatment of large bowel obstruction obviously depends on the cause of the obstruction, and specific treatments are covered in the discussion of those entities (see later). However, some principles of diagnosis and treatment can be generalized. The obstruction needs to be relieved with some expediency before compromise of the blood supply results in ischemia and gangrene. The diagnosis should be established to guide appropriate treatment. History and physical examination provide important clues. The abdomen should be palpated for masses, the groins inspected for hernias, and a digital rectal examination performed to exclude rectal cancer. Plain films of the abdomen provide considerable information concerning the location of the obstruction and, in some situations, may be diagnostic of a volvulus. A CT scan may be helpful in revealing an inflammatory process, such as an abscess associated with diverticulitis. If a volvulus or distal sigmoid cancer is suspected, a water-soluble contrast enema may establish the diagnosis. Treatment options vary considerably, depending on the diagnosis, and it is helpful to establish the diagnosis before an operation to guide therapy properly. If the cause of the obstruction is a cancer of the distal or mid rectum, the preferred treatment is to relieve the obstruction by a loop colostomy and then treat the cancer with neoadjuvant chemoradiation, with the plan to resect the primary lesion at a later time. On the other hand, if the obstructing cancer is in the sigmoid colon, the surgical options include Hartmann's operation (sigmoidectomy with descending colostomy and closure of the rectal stump), sigmoidectomy with primary colorectal anastomosis (with or without intraoperative colonic lavage), and abdominal colectomy with ileorectal anastomosis.

Right-sided colonic obstruction, whether caused by cancer or the result of volvulus, is generally treated by resection and primary anastomosis of the ileum and transverse colon.

Pseudo-obstruction of the colon, also called Ogilvie's syndrome , after its description by Sir William Heneage Ogilvie in 1948, describes the condition of distention of the colon, with signs and symptoms of colonic obstruction, in the absence of an actual physical cause of the obstruction. Ogilvie described two patients with clinical features of colonic obstruction, despite a normal barium enema. Both patients underwent laparotomy for the condition; neither had mechanical obstruction, but both had unsuspected malignant disease involving the area of the celiac axis and semilunar ganglion. The cause of the dilation was attributed to the malignant infiltration of the sympathetic ganglia. Subsequently, there have been numerous descriptions of cases of colonic distention in the absence of mechanical obstruction and without malignant involvement of the visceral autonomic nerves. Very few cases of pseudo-obstruction have malignant infiltration of the autonomic nerves as the cause; in fact, the exact pathogenesis of the syndrome remains unknown, and it has been associated with a heterogeneous group of conditions.

Primary pseudo-obstruction is a motility disorder that is a familial visceral myopathy (hollow visceral myopathy syndrome) or a diffuse motility disorder involving the autonomic innervation of the intestinal wall. The latter may be modified by a disturbance of intestinal hormones or may be principally caused by disordered autonomic innervation.

Secondary pseudo-obstruction is more common and has been associated with neuroleptic medications, opiates, severe metabolic illness, myxedema, diabetes mellitus, uremia, hyperparathyroidism, lupus, scleroderma, Parkinson's disease, and traumatic retroperitoneal hematomas. One mechanism thought to play a role in the pathogenesis is sympathetic overactivity overriding the parasympathetic system. Indirect support for this theory has been derived from the success in treating the syndrome with neostigmine, a parasympathomimetic agent. Further support comes from reports of immediate resolution of the syndrome after administration of an epidural anesthetic that provides sympathetic blockade.

Pseudo-obstruction may present in an acute or chronic form. The acute variety usually affects patients with chronic renal, respiratory, cerebral, or cardiovascular disease. It generally involves only the colon, whereas the chronic form affects other parts of the GI tract, usually presents as bouts of subacute and partial intestinal obstruction, and tends to recur periodically.

Acute colonic pseudo-obstruction should be suspected when a medically ill patient suddenly develops abdominal distention. The abdomen is tympanitic, usually nontender, and bowel sounds are generally present. Plain abdominal radiographs reveal a distended colon, with the right and transverse segments tending to be most dramatically affected. The radiologic appearance is one of large bowel obstruction.

The most useful investigation is a water-soluble contrast enema, which should be performed in all patients in whom the diagnosis is suspected, provided their condition is stable enough to warrant the procedure ( Figure 30-1-1 ). The contrast enema can reliably differentiate between mechanical obstruction and pseudo-obstruction, a differentiation that is essential to guide appropriate therapy.

Colonoscopy is an alternative diagnostic investigation for pseudo-obstruction and has the attractive advantage that it can be used for treatment. However, colonoscopy runs the risk of distending the proximal colon even more, with insufflation of more air and, at present, the water-soluble contrast enema is generally the preferred initial test.

When the diagnosis of acute pseudo-obstruction is suspected, treatment should accompany the diagnostic evaluation. Initial treatment includes nasogastric decompression, replacement of extracellular fluid deficits, and correction of electrolyte abnormalities. All medications that inhibit bowel motility, such as opiates, should be discontinued. Patient response is monitored by serial abdominal examinations and radiography. Most patients improve with this regimen. Until the mid-1990s, the treatment generally used when the colonic distention failed to resolve with supportive measures was colonoscopic decompression. Although this approach was usually successful, it required skilled personnel and equipment and carried the risk for colonic perforation from instrument trauma and insufflation. In addition, the procedure often had to be repeated because of recurrence of the colonic distention.

Sympathetic blockade by epidural anesthesia has been shown to relieve colonic pseudo-obstruction successfully. However, at present, the trend has been to treat this condition with neostigmine, a parasympathomimetic agent. It is obviously imperative that mechanical obstruction be excluded by water-soluble contrast enema or colonoscopy before the administration of neostigmine because the subsequent high pressures generated in the colon against a distal obstruction could cause colonic perforation.

Neostigmine enhances parasympathetic activity by competing with acetylcholine for acetylcholinesterase binding sites. In the treatment of colonic pseudo-obstruction, 2.5 mg of neostigmine is given IV over 3 minutes. The resolution of the condition is indicated within less than 10 minutes of administration of the drug by the passage of stool and flatus by the patient. The recurrence rates following the administration of neostigmine appear to be far lower than those associated with colonoscopic decompression, with satisfactory decompression being achieved in approximately 90% of patients after a single administration of the medication.

A significant side effect of neostigmine is bradycardia, and all patients must be monitored by telemetry during administration of the drug. Atropine must be immediately available; patients with significant cardiac disease or asthma are not candidates for this treatment.

If treatment with neostigmine, an epidural anesthetic, or colonoscopic decompression is not successful, or if signs of peritonitis or intestinal perforation occur, laparotomy is required. In the absence of perforation or ischemia, a loop colostomy is indicated to vent the proximal and distal colon. Any areas of perforation or ischemia must be resected, which usually requires right colectomy, ileostomy and mucous fistula.

Complications of Colostomy Closure