Large bowel obstruction
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Large bowel obstruction (LBO) is often impressive on imaging, on account of the ability of the large bowel to massively distend. This condition requires prompt diagnosis and treatment.
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Large bowel obstructions are far less common than small bowel obstructions, accounting for only 20% of all bowel obstructions 4.
The classic presentation is with abdominal pain, distension, and failure of passage of flatus and stool. As dilatation of the colon increases, the risk of perforation also increases. Perforation may occur at the site of obstruction, or more proximally secondary to ischemic change, which may be implied by the presence of intramural gas or decreased mural enhancement. Signs of peritonism, sepsis, and shock may develop when perforation occurs.
The underlying etiology of large bowel obstructions is age-dependent, but in adulthood, the most common cause is colonic cancer (50-60%), typically in the sigmoid 1-4.
The second most common cause in adults is acute diverticulitis (involving the sigmoid colon). Together, obstructing tumors and acute diverticulitis account for 90% of all causes of large bowel obstruction. While adhesions are the leading cause of small bowel obstruction, for practical purposes, they do not tend to cause large bowel obstruction. Overall causes of large bowel obstruction include 4:
- colorectal carcinoma (most common, 50-60%)
- pelvic tumors; direct spread or metastatic disease
- colonic diverticulitis
- cecal volvulus (1-3%)
- cecal bascule
- sigmoid volvulus (3-8%)
- ischemic stricture (see ischemic colitis)
- fecal impaction/fecaloma (most common cause in debilitated elderly)
- hernias (uncommon) 5
- intussusception 7
Large bowel obstructions are characterized by colonic distension proximal to the obstruction, with collapse distally. In some cases, the point of obstruction and site of obstruction are not the same, with the point of obstruction located distal to the apparent cut-off point, e.g. an obstructing sigmoid tumor may present with an apparent cut-off at the splenic flexure.
In general the colon is considered dilated if it is over 6 cm in diameter, with the cecum having an upper limit of 9 cm 1. See the separate article on the 3-6-9 rule. A cecal diameter of 12 to 15 cm increases the risk for cecal rupture 7.
- colonic distension: gaseous secondary to gas-producing organisms in feces
- collapsed distal colon: very few or no air-fluid levels are found in the large bowel because water is reabsorbed 7
- small bowel dilatation, which depends on
- duration of obstruction
- incompetence of the ileocecal valve
- rectum has little or no air 7
In advanced cases one may see the stigmata of an ischemic colon, namely:
- intramural gas (pneumatosis coli)
- portal venous gas
- free intra-abdominal gas (pneumoperitoneum)
CT is currently the most widely used modality for assessment of large bowel obstructions and is not only able to confirm the diagnosis and localize the location of obstruction but in most instances also is able to identify the cause.
The large bowel will be distended with a thinned stretched wall but should enhance (unless ischemic). If the ileocecal valve is competent then the small bowel may be mostly collapsed.
It should be traced distally until a transition is found. The cause is often present at this point, although sometimes the obstructing lesion is distal to the apparent transition point.
Complications, such as those of ischemia or perforation, should be assessed for 5.
Imaging features will depend on the underlying cause and are thus discussed separately (see above).
Treatment and prognosis
Treatment depends on the underlying cause and presentation, but in all cases, resuscitation and correction of electrolyte imbalances should be carried out.
In patients who have signs of peritonitis clinically or features suggestive of perforation or necrosis then emergency laparotomy is required to avoid overwhelming sepsis 2. This is usually resection of the affected bowel and causative lesion, bring out the remaining proximal large bowel or small bowel (if cecum resected) as a colostomy/enterostomy, and oversewing the rectal stump (Hartmann procedure) with second operation weeks or months later to re-anastomose the bowel 2.
In patients without overt peritonitis, but evidence of an obstructing lesion (e.g. colorectal carcinoma) surgery is also carried out relatively expediently. Traditionally a three-stage operation,
- decompressive colostomy proximal to the obstruction
- resection of the lesion
was the primary mode of surgical treatment, although with advances in anastomosis technique single-stage procedures with primary anastomosis are more commonly performed 2.
In some patients, especially those not considered fit to have a general anesthetic, or who have extensive systemic disease, a self-expanding colonic stent may be used to decompress the colon 2.
When a clear transition point, especially when a causative lesion is identified, then there is little doubt in the diagnosis. The main problem occurs in patients where an abrupt transition point is not present, in which case a number of other possibilities should be entertained:
- no transition point
- often history contains cause for ileus (e.g. surgery)
small bowel obstruction
- a long duration of obstruction and/or incompetent ileocecal valve can lead to prominent small bowel dilatation, however, the absence of distension of the colon is usually a giveaway
- although no abrupt transition point is present, a less well-defined zone of caliber change is usually present, most frequently in the region of the splenic flexure 3
toxic megacolon secondary to Clostridioides difficile colitis
- C. difficile infection is usually preceded by antibiotic use or chemotherapy and is therefore usually encountered in unwell, hospitalized patients with significant co-morbidity
- bowel wall thickening usually a prominent feature
- usually, bowel wall is thickened but can be thinned and dilated
- absent or poor wall enhancement
- usually respects vascular territories
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