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5.Debilitating disease that is not refractory to medical treatment

6.Fulminant colitis

7.Hemorrhage (rare)

8.Cancer (much less common than with UC)

b.Surgical considerations

1.A high recurrence rate (50% within 5 years) follows intestinal resection. The most likely site of recurrence is at the anastomosis from the previous operation.

2.A goal of surgery is to conserve bowel.

a.Wide margins of normal bowel are not required; only grossly involved bowel should be resected.

b.To conserve bowel, strictureplasty may sometimes be indicated to relieve obstruction (rather than intestinal resection).

3.Abdominal abscesses should be drained percutaneously prior to laparotomy.

4.Total proctocolectomy with ileostomy is required for severe rectal disease. Ileal pouch anal anastomosis is contraindicated because of the high incidence of anal disease and recurrent bowel disease in the pouch.

5.TPN and bowel rest for 7–10 days preoperatively will promote resolution of intra-abdominal inflammation and will reduce the risk of injury to adjacent, secondarily inflamed bowel.

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6.In most cases, the plan of surgery should be to resect the involved bowel and to fashion a primary anastomosis.

VIII Pseudomembranous Colitis (Antibiotic-associated Colitis)

A Epidemiology and clinical presentation

1.Acute diarrhea associated with the use of antibiotics

a.Clindamycin and ampicillin most often are implicated, but almost every antibiotic has been reported to be associated with this syndrome.

b.In 25% of cases, the antibiotic has been discontinued before the development of diarrhea.

2.This syndrome is common in hospitals and nursing homes.

a.Epidemics of the disease have been reported in these institutions.

b.This syndrome may occur after intestinal operations, especially after antibiotic bowel preparation.

3.Clostridium difficile has been shown to be the causative organism.

a.C. difficile elaborates two exotoxins.

b.Colonic inflammation is probably caused by the exotoxins.

c.Yellow plaques, or pseudomembranes, may cover the mucosa.

1.Pseudomembranes are composed of fibrin and cellular debris.

2.The absence of pseudomembranes does not rule out this syndrome.

B Pathogenesis

1. Antibiotics alter the normal colonic bacterial population.


2.C. difficile, an organism that is normally suppressed by colonic bacteria, emerges as a pathogen and causes mild diarrhea to severe life-threatening colitis.

CDiagnosis

1.A history of diarrhea after treatment with an antibiotic is suspicious.

2.Proctoscopy or colonoscopy may reveal pseudomembranes, which are virtually diagnostic if present.

3.A stool sample should be sent for C. difficile toxin titer.

DTreatment

1.The causative antibiotic should be stopped.

2.Metronidazole is the treatment of choice and may be given orally or intravenously. Oral vancomycin is also effective but is reserved for refractory or persistent cases. The daily cost for metronidazole treatment is less than $1 but is $200 for vancomycin.

3.Constipating agents (e.g., loperamide) should be avoided.

4.Cholestyramine may be administered to bind the toxin, but it may also inhibit the therapeutic antibiotic and therefore is seldom indicated.

5.Recurrence is common (25%) and requires retreatment. Metronidazole is again the agent of choice if the patient initially responded to it.

6.Abdominal colectomy with ileostomy has been required for rare cases of fulminant pseudomembranous colitis.

IX Ischemic Colitis

AEtiology

1.Points of communication between collateral arteries are theoretically at increased risk for ischemia. These points include the splenic flexure and the midsigmoid colon. However, any segment of the colon may be involved (rectal involvement is very rare).

2.Predisposing factors include:

a.Surgery, especially ligation of the inferior mesenteric artery during aortic surgery

b.Atherosclerosis, vasculitis, collagen vascular diseases

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c.Polycythemia vera

d.Congestive heart failure

e.Digitalis, oral contraceptives, antihypertensive medications, and vasopressors

f.Low-flow states (myocardial infarction, sepsis)

3.Three phases of ischemic colitis may be recognized.

a.Transient ischemia (mucosal involvement)

1.Symptoms are usually mild abdominal pain and passage of maroon-colored stool.

2.Barium enema may reveal “thumbprinting” (mucosal hemorrhage).

3.Colonoscopy reveals dusky, hemorrhagic mucosa.

b.Partial-thickness ischemia with late stricture. Symptoms are more severe and include abdominal tenderness,


fever, and leukocytosis.

c.Gangrenous ischemia. Symptoms of an acute abdomen are present with abdominal pain, peritonitis, and signs of sepsis.

BTreatment

1.Transient ischemia is treated symptomatically.

a.Hospitalization and observation are indicated until the severity of disease is determined.

b.Any causative factors should be corrected, if possible.

2.Partial-thickness ischemia

a.Close observation, intravenous fluids, and broad-spectrum antibiotics are usually required.

b.If a stricture develops and is asymptomatic, no treatment is required. Symptomatic strictures require resection.

3.Gangrenous ischemia

a.Emergency resection of nonviable bowel is required.

b.Anastomosis is not usually safe in such circumstances, thus a colostomy is required.

X Volvulus

AOverview

1.Volvulus is a twist or torsion of an organ on a pedicle.

2.Symptoms are produced by occluding the bowel lumen (obstruction) or occluding the blood supply (ischemia).

3.The incidence is low in the United States.

a.Diverticulitis and cancer are more common causes of colon obstruction.

b.Volvulus is the most common cause of colon obstruction in Africa.

B

Sigmoid volvulus accounts for more than 80% of cases of colonic volvulus. Patients with this condition are often from nursing homes or mental institutions. Sigmoid volvulus is most common in men, and it occurs more often in blacks. The average age of a patient with this condition is 60 years.

1.Etiology. Several predisposing conditions are required:

a.A long, freely movable sigmoid colon

b.An ample, freely mobile sigmoid mesentery

c.A point of fixation about which the colon can twist (a loop of bowel with the limbs lying close together)

2.Pathogenesis. The sigmoid colon usually twists counterclockwise around the axis of the mesentery. This torsion about the mesentery is accompanied by an axial torsion of the bowel wall. The combined torsions of the mesentery and bowel cause obstruction of the colon lumen.

3.Diagnosis

a.History usually indicates increasing abdominal distention, discomfort, and obstipation.

b.Physical examination reveals abdominal distention and tympany.

c.Abdominal radiographs usually show a massively distended loop of bowel, with both ends in the pelvis and the


bow near the diaphragm (i.e., bent inner tube sign).

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d.Barium enema reveals the pathognomonic obstructing twist (i.e., ace of spades or bird's beak deformity).

4.Treatment

a.Sigmoidoscopic decompression is indicated for nonstrangulated sigmoid volvulus. This procedure should be terminated if necrotic mucosa is observed or if the volvulus cannot be reduced by gently inserting a rubber tube through the sigmoidoscope past the point of torsion. If the tube successfully reduces the volvulus, it should be left in the sigmoid and taped to the skin of the thigh to prevent immediate recurrence.

b.Sigmoidectomy with colostomy (Hartmann's operation) is indicated if decompression cannot be achieved or if there is gangrenous bowel.

c.Elective sigmoidectomy with colorectal anastomosis is recommended after the bowel has been decompressed and prepared as usual for colonic resection.

C

Cecal volvulus occurs much less frequently than sigmoid volvulus. It occurs most commonly in women, and patients are often younger than 40 years.

1.Etiology. A congenital anatomic anomaly is required for cecal volvulus.

a.Incomplete peritoneal fixation of the right colon is required for the cecum and right colon to have the mobility to form a volvulus.

b.Other contributing factors may include:

1.Cancer of the distal colon

2.Midgut nonrotation

3.Adhesions from previous surgery

2.Pathogenesis. The cecum and ascending colon usually twist clockwise. Bowel and vascular obstruction occur in a manner similar to that described for sigmoid volvulus.

3.Diagnosis

a.History usually indicates increasing abdominal pain. Diarrhea may have occurred initially. Obstipation follows.

b.Physical examination reveals abdominal distention and tympany. Rebound tenderness suggests gangrenous bowel.

c.Abdominal radiographs reveal a large, distended cecum that may occupy the left upper quadrant.

d.Barium enema reveals the ace of spades or bird's beak deformity.

4.Treatment

a.Right colectomy with ileotransverse colonic anastomosis is generally indicated if the bowel is viable.

b.Colonoscopic decompression has been successfully performed, but right colectomy is still indicated to prevent recurrence.

c.Cecopexy is an alternative to right colectomy, but recurrence rates have been high in some reports.

XI Dysfunction of the Anorectum

A

Incontinence is the inability to control elimination of rectal contents.


1.Etiology

a.Mechanical defects of the anal sphincter

1.Episiotomy injuries

2.Previous anal fistulotomies

3.Anorectal trauma (impalement injuries)

b.Neurogenic causes

1.Pudendal nerve injury due to prolonged labor

2.Pudendal nerve injury due to perineal descent

3.Systemic neurologic disease (multiple sclerosis)

c.Systemic disease

1.Scleroderma

2.Diabetes

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d.Causes unrelated to the anal sphincter

1.Severe diarrhea

2.Severe proctitis with decreased rectal capacity

3.Fecal impaction with overflow incontinence

4.Large rectal tumors

2.Evaluation. History and anorectal examination often suffice to establish the diagnosis.

a.Anterior sphincter defect and patulous anus after midline episiotomy may be confirmed by a thorough examination and, if necessary, endorectal ultrasound of the anal musculature.

b.Physiologic evaluation may be helpful if the cause of incontinence is not obvious.

1.Anal manometry can document the resting pressure, squeeze pressure, sphincter length, and minimal sensory volume of the rectum.

2.Pudendal nerve terminal motor latency can be tested to determine if the cause of incontinence is neurogenic in nature.

3.Surgical treatment

a.Sphincter defects, such as those caused by obstetric injuries, may be corrected by anal sphincter repair with excellent results.

b.More extensive loss of the anal sphincter may be treated by gracilis muscle transposition, which mobilizes the gracilis muscle to encircle the anus or by implantation of an artificial anal sphincter device.

c.Colostomy may be required for severe sphincter injuries or for neurogenic or systemic causes of incontinence.

B Obstructed defecation (pelvic floor–outlet obstruction)

1.Anal stenosis may be caused by circumferential hemorrhoidectomy (Whitehead deformity), trauma, or radiation. It may result in the inability to evacuate formed stool, with resultant abdominal bloating, intestinal dilatation, and discomfort. Treatment generally entails repeated dilation or advancing full-thickness pedicles of skin to the anal canal.

2.Nonrelaxation of the puborectalis is a functional disorder characterized by the inability to relax the puborectalis muscle at the time of defecation.

a.Symptoms include the need for digital maneuvers to eliminate stool, pelvic pain, a sense of incomplete