About Us Physicians Education Members Patient and Public Corporate Partners DCR Research Foundation
Home > Physicians > Education > Core Subjects > Diverticultis
Print

Diverticultis

Janice Rafferty, MD
Associate Professor
Chief, Division of C & R Surgery
University of Cincinnati Surgeons, Inc.
Cincinnati, OH

Etiology

The majority of colonic diverticular change in the western world is acquired. It was essentially a curiosity before the 20th century, being first described in a medical text by Telling in 1920. Its development in economically developed Western civilization is attributed to a lack of dietary fiber, where roller milling removes up to 2/3 of the fiber content of flour in refined foods. Some prospective studies suggest a relationship between restricted physical activity and development of diverticular change. Acquired diverticuli are actually pulsion or pseudodiverticuli, the result of herniation of the mucosa and muscularis mucosa through the colon wall near the taenaie where blood vessels penetrate. Congenital diverticula, on the other hand, are true diverticula involving all layers of the colonic wall, tending to be single and right sided. The sigmoid colon is the most common site of pulsion diverticuli, and is involved in 95% of cases. Thirty-five percent of patients also have more proximal disease. It is estimated that 30% of the population has acquired diverticular change by the age of 60 years, while almost 60% of those 80 years and older are affected. Diverticula are rare below the pelvic peritoneal reflection. Right-sided diverticulosis is rare in Western countries but is the predominant pattern in Asian populations.

The cause of pseudodiverticular change appears to be related to increased intraluminal pressure exerted by hard firm narrow stool on a thickened colon wall with decreased elasticity. Segmentation of isolated portions of the colon results in unduly high pressure in the lumen, resulting in mucosal herniation. Insoluble fiber is known to increase the wet weight of stool, increasing stool caliber and decreasing pressure exerted on the wall of the colon. Gear et al found that vegetarians consume on average 4.5 grams of fiber per day, and have a 12% incidence of diverticulosis, versus non-vegetarians who consume less than half the amount of indigestible fiber. They have a 33% incidence of diverticular change. Transit time is also thought to be a contributing factor, since those who consume a diet high in insoluble fiber have a transit time twice as fast as those on a traditional western diet.

There is no clear evidence supporting a link between diverticulosis and obesity, cardiovascular disease, anismus, IBD, or colorectal malignancy. There does appear to be a relationship between the incidence of uncomplicated diverticulosis and irritable bowel syndrome. In both conditions, there is an exaggerated response to neostigmine and food intake; in addition, both respond favorably to regulation of transit time, stool weight and intracolonic pressure promoted by a high fiber diet.

Uncomplicated diverticulitis

Symptomatic uncomplicated diverticulitis is the result of occlusion of a diverticulum, which results in inflammation and microperforation. Extent of symptoms is related to involvement of adjacent structures, including small bowel, omentum, fallopian tube, bladder and abdominal wall. Complaints often include pain in the left iliac fossa, and a change in bowel habit- either obstipation, diarrhea, or mucus. Other symptoms may be distension, right lower quadrant pain, and urgency. Urinary frequency suggests the inflammatory mass is abutting the bladder. Pain is occasionally moderated by passage of stool or flatus. Nausea and vomiting may accompany the ileus that can accompany localized diverticulitis. A peridiverticular abscess is expected to elicit localized peritonitis on physical exam. An elevated fever and white blood cell count can be expected. Plain abdominal films may show an ileus.

Complicated diverticulitis

Complications of diverticulitis include obstruction, fistula, abscess, hemorrhage, and free perforation causing either purulent or feculent peritonitis.

Complete colonic obstruction due to a diverticular stricture is uncommon. A more frequent cause of colonic obstruction is malignancy, which should be ruled out with endoscopic exam. Obstruction of small bowel adherent to an inflammatory mass of the colon is a more common obstructive complication associated with diverticulitis.

Fistula to bladder, vagina, small bowel, ureter, and skin are reported complications of diverticulitis. Colovaginal fistula most often involves the posterior vaginal fornix in a woman who has had a hysterectomy. Enteroenteric fistulae may be asymptomatic, though some complain of diarrhea. Fistulas to the urinary tract can cause dysuria, frequency, pneumaturia and fecaluria.

Abdominal or pelvic abscess can result from perforation of an inflamed occluded diverticulum. The abscess may be walled off by adjacent structures, or limited to the mesentery or retroperitoneum. Abscess is the result of over 30% of complicated diverticultis.

Clinical investigations

Clinical history and physical exam are often sufficient to direct initial therapy. Useful initial supporting tests include CBC, urinalysis, and abdominal films. Other radiographic studies are particularly useful in the evaluation of a patient with diverticulitis. Computed tomography of the abdomen and pelvis is the examination of choice in the acute setting. Accuracy is enhanced if oral, IV and rectal contrast are used. This exam can demonstrate the extent of complicated disease, and point toward therapeutic options as well. Phlegmon, abscess, adjacent organ involvement, fistula, and distant septic complications can be seen on CT.

Occasionally CT scan is not available. In this setting, a gently administered water-soluble contrast enema is useful. Findings associated with diverticulitis include presence of smooth stenosis and spasm with intact mucosa and surrounding diverticulosis. Strictures in diverticulitis are usually longer and more regular than in carcinoma. Fistula and abscess may be seen with this test as well. Bowel wall edema can be remarkable.

Cystogram is occasionally useful to confirm bullous edema associated with a colovesical fistula, although CT is the diagnostic test of choice. Ultrasound exam of the inflammatory mass can help distinguish phlegmon from abscess if CT is not available. Findings are easily obscured by overlying small bowel distension. Endoscopic exam has limited use in the acute setting, and may actually exacerbate complications. Some authors find endoscopic exam to be superior to radiographic exam.

Treatment

Uncomplicated diverticulitis

Certain patients with uncomplicated diverticulitis may be managed in the outpatient setting, provided that they do not demonstrate advanced disease such as high fever, shaking chills, signs of local peritonitis, or symptoms of intestinal obstruction. Patients must be able to take fluids and tolerate an oral antibiotic regimen, such as amoxicillin or cipro/flagyl. Those unable to tolerate oral intake due to ileus or signs of less mild disease will require hospitalization, intravenous fluids, and IV antibiotics. Subsequent studies, such as colonoscopy or contrast enema, must be planned to confirm the diagnosis following resolution of acute inflammation. . Most patients, about 85%, recover completely with medical therapy. Diverticulitis will eventually recur in about one third, often within the first year after the initial episode. Unless the symptoms are mild, patients should avoid oral intake until it becomes obvious that urgent surgical or radiologic intervention will not be necessary.

Complicated diverticultis

Approximately 15% of patients with diverticulitis will develop abscess, either within the mesenteric leaves or in the pelvis. For these patients, hospitalization and intravenous antibiotics are indicated. Abscesses less than 2cm in diameter may resolve without intervention. Patients with larger abscesses should be considered candidates for percutaneous catheter drainage, as long as an appropriate "window" for catheter placement can be located. This approach allows temporization of the acute situation and avoidance of the need for a stoma. Staged resection should be planned 6-8 weeks later when inflammation has resolved. If symptoms of sepsis do not resolve within about 48-72 hours of drainage, surgical intervention is indicated.

The historically advocated three-stage approach to complicated diverticulitis is no longer advised, due to unacceptable morbidity and mortality associated with non-resection of the inflamed segment of colon and lack of sepsis control. When at all possible, the inflamed segment of colon and associated abscess should be resected. The proximal extent of bowel resection is determined by palpation, not by extent of diverticular change (which may be pancolonic). The segment to be resected should be hypertrophic with a thickened muscular wall. The distal extent of resection should not be the peritoneal reflection (which has a variable location), but the top of the rectum where the taenaei coli splay out onto the anterior wall. Adjacent structures adherent to the inflammatory mass- small bowel, ureters, bladder and vagina- should be bluntly dissected off. Only ureteral repair is necessary if a fistula is present. Bladder drainage for 7-14 days will allow healing without repair, and closure of the vaginal cuff is not mandated. Small bowel resection is rarely necessary.

Anastomosis is reserved for those patients with Hinchey stage I or II disease, and certain patients with purulent peritonitis (Hinchey stage III). In general anastomosis is performed in the elective setting, following a mechanical bowel preparation. Occasionally anastomosis can be performed in the emergent setting, provided the patient is stable and blood loss is minimal. In this case intra-operative colonic lavage is an option, as is a "protective" loop ileostomy.

The operation of choice for toxic patients or those with gross fecal contamination is a Hartmann’s procedure, with construction of an end-descending colostomy after resection of the perforated inflamed segment. The rectal stump can be closed or brought out as a mucus fistula. Mortality rate for the primary procedure should be less than 5%. Unfortunately almost a third of those who have a Hartmann’s procedure never have the stoma closed.

Treatment of recurrent diverticulitis

About 50% of recurrences requiring hospital admission will develop in the first year after the initial attack; 90% will develop within 5 years. A high-fiber diet may reduce the risk of recurrence, although the data supporting this concept are difficult to interpret. With each recurrence of acute uncomplicated diverticulitis, patients become less likely to respond to medical therapy, with success decreasing from 70% to 85% after the first attack to only 6% after the third. Furthermore, after a second episode of diverticulitis, most patients will have persistent symptoms, and as many as 50% will experience complications. This observation underlies the basis for the recommendation that patients with more than two episodes of uncomplicated acute diverticulitis be considered for elective surgery. Patients with acute complicated diverticulitis should be considered for interval sigmoid resection even if complete resolution of the attack can be accomplished by antibiotics combined, when indicated, with percutaneous catheter drainage; recurrent complications developed in about 85% of such patients in one series as opposed to only 3% of those initially managed by resection.

Acute diverticulitis in patients less than 40 years of age is uncommon and evidence that it is aggressive is largely anecdotal. Surgery during the first admission for diverticulitis is in fact more common in the elderly than the young. Elective surgery for young patients after their first attack of acute diverticulitis, therefore, should only be recommended after careful consideration since the natural history is not been clearly understood.

Bibliography

  1. Painter N, Burkitt D. Diverticular disease of the colon: A deficiency disease of Western civilization. BMJ 1971; 1:450-454.
  2. Aldoori WH, Giovannucci EL, Rimm EB, et al. Prospective study of physical activity and the risk of symptomatic diverticular disease in men. Gut 1995; 36:276-282.
  3. Gear JS, Ware A, Fursdon P, et al. Symptomless diverticular disease and intake of dietary fiber. Lancet 1979; 1:511-514
  4. Havia T, Mauner R. The irritable colon syndrome. A follow-up study with special reference to the development of diverticula. Acta Chir Scand 1971;137: 569-572.
  5. Hunt RH, Waye JD. Colonoscopy, 1981; London, Chapman and Hall.
  6. Wong WD, Wexner SD, Lowry A, et al. Practice parameters for sigmoid diverticulitis. The Standards Task Force American Society of Colon and Rectal Surgeons. Dis Colon Rectum. 2000; 43(3):290-297.
  7. Sarin S, Boulos PB. Evaluation of current surgical management of acute inflammatory diverticular disease. Ann R Coll Surg Engl 1991; 73:278-282.
  8. Piardi T, Ferrari Bravo A, Giampaoli F, et al. Deferred elective colonic resection in complicated acute diverticulitis. Chir Ital 2003; 55(2):153-160.
  9. Ambrosetti P, Robert J, Witzig JA, et al. Incidence, outcome, and proposed management of isolated abscesses complicating acute left-sided colonic diverticulitis. A prospective study of 140 patients. Dis Colon Rectum 1992; 35:1072-1076.
  10. Stabile BE, Puccio E, vanSonnenberg E, et al. Preoperative percutaneous drainage of diverticular abscesses. Am J Surg 1990; 159:99-104.
  11. Belmonte C, Klas JV, Perez JJ, et al. The Hartmann procedure. First choice or last resort in diverticular disease? Arch Surg 1996; 131:612-617.
  12. Bell G, Panton O. Hartmann resection for perforated sigmoid diverticulitis. A retrospective study of the Vancouver General Hospital. Dis Colon Rectum 1984; 27:253-256.
  13. Eisenstat T, Rubin R, Salvati E. Surgical management of diverticulitis. The role of the Hartmann procedure. Dis Colon Rectum 1983; 26:429-432.
  14. Sarin S, Boulos PB: Long-term outcome of patients presenting with acute complications of diverticular disease. Ann R Coil Surg Engl 76:117-120, 1994.
  15. Parks T: Natural history of diverticular disease of the colon. Clin GastroenteroI4:53-69, 1975.
  16. Colcock B: Diverticular disease. Proven surgical management. Clin GastroenteroI4:99-119, 1975.
  17. Hyland JM, Taylor I: Does a high fibre diet prevent the compli- cations of diverticular disease? Br J Surg 67:77-79, 1980.
  18. Leahy AL, Ellis RM, Quill DS, Peel AL: High fibre diet in symptomatic diverticular disease of the colon. Ann R CoIl Surg EngI67:173-174,1985.