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Diverticular disease: diverticulitis, bleeding, and fistula

DEFINITION Diverticula of the intestinal tract are pockets or protrusions deriving from the lumen and extending through the wall of the gut. Diverticula that are enclosed by all layers of the bowel (serosa, muscle, and mucosa) are called true; those that lack muscle as a component of the sac are termed false. True diverticula are usually congenital, while false diverticula are acquired and usually secondary to pulsion forces within the gut. Diverticula may arise in both the small and large bowel, but this discussion will be limited to colonic diverticula. Diverticula of the colon are generally multiple and, in the absence of inflammation, are collectively described as diverticulosis. In the presence of inflammation, the condition is termed diverticulitis. While this distinction is clear when the colon is examined surgically or histologically, symptoms of colonic dysfunction due to diverticulosis sometimes mimic those of diverticulitis. Thus, clinical distinction between the two conditions is often blurred. The term diverticular disease of the colon may be applied to all stages of the disease from diverticulosis and its complications. PATHOPHYSIOLOGY The pathophysiology of diverticular disease is complex, involving abnormalities of anatomy and neuromuscular function, physical principles of pressure relationships within cylinders and spheres, the virulence of mixed bacterial flora of the colon, and inflammatory processes within the peritoneal cavity and in the retroperitoneal space. In the sigmoid, where the lumen of the gut is small, muscular tension generates maximum pressures within the lumen of the bowel. These high pressures promote the extrusion of diverticula through weak areas in the gut wall: points of blood vessel penetration and the intermuscular spaces between circular smooth muscle fasicles in
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the inter-tineal intervals. Diets low in fibre do not distend the sigmoid and appear to promote these changes. Life-long low-residue diets in rats and rabbits produce diverticulosis of the colon, and broad-based population studies also seem to indicate a protective effect of high fibre diets on diverticular disease in man. Dietary factors may therefore play a significant role in the development and progression of diverticular disease of the colon. The mixed and virulent bacterial flora of the colon may include E. coli, Pseudomonas, Serratia, Enterobacter, Citrobacter, Bacteroides, Enterococci, and Clostridia, most of which are facultative or obligate anaerobes. Depending upon the degree of extraluminal spread of these bacteria there may be localized inflammation with tissue necrosis, general peritonitis, or septicaemia with septic shock.

INCIDENCE The true incidence of colon diverticular disease is unknown and varies in different countries, depending upon factors such as genetic predisposition, diet, and age of the population. Among Western countries diverticular disease is uncommon before the age of 40; about 5 per cent of the population are estimated to have the disease by age 50 and approximately 70 per cent by age 85. In one large series, 94.6 per cent of cases of colonic diverticular disease were located in the sigmoid, while the descending colon was affected in 0.7 per cent; transverse colon, 1.0 per cent; ascending colon, 2.2 per cent; and caecum 1.5 per cent. CLINICAL FEATURES The clinical manifestations of diverticular disease cover a broad spectrum. Many patients remain asymptomatic for long periods. The most frequent early symptoms are those of functional colonic disturbance distension, cramps, diarrhoea or constipation, and local pain in the left lower abdomen. Concomitant bacterial inflammation
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(diverticulitis) may be associated with increased pain, left lower abdominal tenderness, palpable mass, fever, dysuria, urinary frequency and, occasionally, pneumaturia. General peritonitis and septicaemia signify more serious infection or perforation of a diverticulum. Rarely, the disease may present as septicaemia with pylephlebitis and gas in the portal venous system, or as a retroperitoneal infection dissecting upward to present as pneumomediastinum. More commonly, retroperitoneal infection tracks into the scrotum on either side, into the abdominal wall, the perineum, or into the left upper thigh. Attachment of small bowel loops to the inflammatory process in the colon may result in small bowel obstruction or development of a fistula into the small bowel. In females, diverticulitis may be associated with creation of fistulae into the fallopian tubes, uterus, or vagina, as well as into the urinary bladder. Diverticular disease presenting as massive rectal haemorrhage is usually seen in patients who have diffuse diverticular disease throughout the colon. Rarely, diverticular disease may present with acute colon obstruction or with a tender, palpable mass due to a giant diverticulum of the sigmoid. COMPLICATIONS The complications of diverticular disease include sepsis, fistula (usually as a result of healed sepsis), bleeding, obstruction, and intractable painful disturbance of bowel function. Septic complications of diverticular disease include localized inflammation within the bowel wall or mesentery, localized pelvic abscess, perforation with diffuse bacterial and/or feculent peritonitis, adherence to adjacent visceral or peritoneal surfaces, septicaemia, and septic shock. Sepsis is the indication for surgery in approximately 35 per cent of patients requiring operative treatment of colonic diverticular disease. Fistulae form as the result of spontaneous drainage of an abscess into an adjacent viscus or to the external surface of the body. A channel communicating with the
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lumen of the bowel is thus created. Because of inflammation and continuing faecal contamination, fistulae rarely heal spontaneously; about 5 per cent of all operations required for diverticular disease involve treatment of fistulae. Bleeding is intermittent and slight in approximately 10 per cent of patients with diverticular disease: this must be distinguished from bleeding caused by adenocarcinoma of the colon. Acute, massive haemorrhage from diverticular disease is of greater significance: this is not due to diverticulitis, and generally occurs in individuals with diffuse diverticulosis affecting the colon. Erosion of a small blood vessel by inspissated faeces in the diverticulum has been suggested as a cause for massive haemorrhage. An alternative mechanism may be traction and tearing of the relatively inelastic vessels when the diverticulum stretches during peristaltic contraction. Massive bleeding is the indication for surgery in approximately 10 per cent of patients requiring operative treatment of diverticular disease. Colon obstruction secondary to diverticular disease may be partial and chronic or complete and acute. The acute presentation may be accompanied by concurrent small bowel obstruction, and should always be suspected. Operations for obstruction are somewhat less frequent than those required for massive bleeding, about 9 per cent of cases. Patients with intractable disturbance of bowel function (distension, cramps, diarrhoea, or constipation) and persistent pain may require surgical treatment even in the absence of the more defined complications listed above. These patients require careful clinical evaluation and judgment, and comprise about 25 per cent of those undergoing surgery for diverticular disease.


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Physical signs of colon diverticular disease vary according to the stage. Abdominal distension, tenderness, a palpable and tender lower abdominal mass, and normal peristaltic sounds are often observed. Fever may or may not be present. Patients with diffuse peritonitis may have diffuse abdominal tenderness, spasm, and rebound tenderness, and they are usually febrile. Rectal examination may reveal high rectal tenderness or a mass; it may also be normal. Endoscopy has limited value in the diagnosis of acute diverticulitis, although rigid sigmoidoscopy may identify tenderness and fixation at the rectosigmoid junction. Colonoscopy is useful in identifying associated colitis, polyps, or adenocarcinoma, but spasm of the sigmoid may limit the effectiveness of the examination. Patients suffering from massive haemorrhage are not suitable candidates for colonoscopic study. Radiographic examination is the main diagnostic technique in colonic diverticular disease. In patients with chronic or subacute symptoms, a barium enema examination may confirm the presence of diverticula, provide evidence for or against the diagnosis of diverticulitis, and help to exclude the presence of adenocarcinoma or other associated disease of the bowel. MANAGEMENT OF UNCOMPLICATED COLON DIVERTICULAR DISEASE Uncomplicated diverticular disease can be managed by dietary manipulation, including provision of supplementary dietary fibre, stool softeners, and anticholinergic drugs to inhibit peristaltic cramps. High fibre intake results in a larger, softer stool which distends the colon and undergoes more rapid transit through the gut. The extra force is optimally provided by a diet rich in fruit, vegetables, and whole grain cereals, with generous water intake. Supplementary bulk may be supplied with 10 to 20 g of wheat bran daily.
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TREATMENT OF COMPLICATIONS OF COLON DIVERTICULAR DISEASE Septic complications Patients with acute diverticulitis should be treated by restriction of oral intake and by intravenous administration of fluids and antibiotics with a broad spectrum of activity against enteric pathogens. Many patients treated in this manner will improve rapidly, with resolution of the signs of local inflammation and ileus within a few days. Patients who remain febrile and tender and exhibit evidence of systemic illness after 12 to 24 h of treatment as outlined above should be re-examined: fever, leucocytosis and abdominal or rectal tenderness or mass are highly suggestive of a pericolic or pelvic abscess. Ultrasonography or repeat CT scan are useful for confirmation but on clinical grounds, such a patient is a candidate for surgical exploration.

If the abscess is wholly contained within the bowel wall and mesentery and can be extirpated with a segmental resection, and if the (unprepared) bowel is relatively empty and free of inflammation, a one-stage resection and end-to-end anastomosis may be considered. Such patients are uncommon, and a safer course is to resect the inflamed segment of bowel, close the distal resected end (usually rectum), and pull the proximal resected end through the abdominal wall as a colostomy. The most serious septic complication of diverticular disease is free perforation of the colon with bacterial or faecal peritonitis. The majority of patients presenting with this clinical picture have coexisting severe illnesses, and many are immunosuppressed. As soon as the patient is haemodynamically stable resection of the perforated bowel segment, rectal turn-in and end-colostomy of the descending colon should be performed. All pus and debris should be irrigated from the peritoneal cavity. If there

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is gross contamination, delayed primary closure of skin and subcutaneous fascia decreases the risk of wound sepsis. Massive colonic bleeding Massive bleeding is the indication for approximately 9 per cent of operations for colon diverticular disease. Patients with this presentation often have diffuse diverticulosis and usually do not have associated diverticulitis with pain and tenderness as localizing markers. Endoscopy is not generally helpful in such cases and it is better to proceed promptly with selective angiography of the superior and inferior mesenteric arteries. When the bleeding site is identified, a segmental resection with end-to-end anastomosis is the operation of choice. If the site cannot be located, subtotal colectomy with ileorectal anastomosis should be performed as an emergency procedure. Since there is no time for preoperative preparation of the bowel, these patients should receive broad-spectrum antibiotics intravenously pre- and postoperatively, as well as appropriate blood replacement. The expected mortality rate in this group of patients is approximately 10 per cent. Obstruction Obstruction in colonic diverticular disease may be chronic, due to postinfection scarring as well as to muscular narrowing of the sigmoid. Acute obstruction is usually associated with active diverticulitis or associated abscess and may be accompanied by obstruction of adherent small bowel loops. Acute colonic obstruction is usually superimposed on acute diverticulitis and, as described, is frequently associated with abscess or small bowel adhesions. These seriously ill patients require nasogastric suction, broad-spectrum triple antibiotics, intravenous fluids, and prompt surgical intervention. The optimum operative procedure in these patients is lysis of the small bowel adhesions, drainage of
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abscesses, resection of the inflamed strictured segment, rectal turn-in, and enddescending colostomy. Bowel continuity should be restored at a second procedure after an interval of 3 months. Colon obstruction is the indication for about 8 per cent of operations for diverticular disease, and the mortality rate is about 2 per cent. Acute obstruction occurs in one in eight of such patients.

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