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Diverticular disease of the colon: A conservative approach works best

The most effective treatment regimen is antibiotics, fluids, and bowel rest. When surgical intervention is indicated for diverticulitis, a single-stage elective procedure is the preferred method.

Michael T. Kelley, MS, PA-C, LCDR/MSC/USN

Michael Kelley is a physician assistant at the Naval Health Clinic, Charleston, South Carolina. He has indicated no relationships to disclose relating to the content of this article.

Diverticular disease of the colon (DDC) used to be extremely rare, but the introduction of milled grains and refined sugars to the diet in industrialized countries has increased its prevalence. DDC continues to be rare in rural areas of Africa, Asia, and the Americas, where diets have remained relatively unchanged over time. Longitudinal studies have shown that persons from these areas who migrate to westernized societies develop DDC at a similar rate as those who are native to westernized cultures.¹

Typically occurring in the fifth through seventh decades of life, DDC is often asymptomatic. When it has manifested itself, patients commonly present with left lower quadrant (LLQ) abdominal pain, fever, and leukocytosis. Changes in stool patterns, pneumaturia, fecaluria, and stool within the vagina are other potential signs. Initial treatment involves fluid resuscitation, antibiotics, and bowel rest. Complications or failure to respond to treatment usually indicates the need for surgical intervention. This article reviews the pathology, clinical manifestations, and current treatment options for DDC.

ETIOLOGY AND EPIDEMIOLOGY

Increased intraluminal pressures within the large intestine, specifically the descending and sigmoid colons, cause diverticula to form in the mucosal lining secondary to the increased propulsion needed to expel low-bulk stools (see Figure 1). Diverticula are outpouchings in the mucosal layers of the colon wall (see Figure 2). The outpouchings herniate through the colon musculature on the antimesenteric surface, into the pericolic fat of the mesocolon and/or the appendices epiploicae. A true diverticulum is an outpouching that penetrates through all layers of the colonic wall; these are rare and considered congenital. Outpouchings that penetrate only the mucosa and submucosa are more common. Diverticulitis occurs when the diverticula become inflamed, most often because of an entrapped fecalith.

Up to 30 million middle-aged and elderly persons in the United States have diverticulosis, defined as the presence of left-sided diverticula without inflammation. Up to one-third of the US population will have diverticulosis by age 50 years, and two-thirds will have the condition by age 80 years.^2-6 Diverticulitis will develop in 10% to 25% of persons with diverticulosis. Approximately 10% of persons younger than 40 years will develop diverticulosis, with 2% to 7% of cases developing into diverticulitis.^5,7 Diverticulosis is more prevalent in men within this younger age group, whereas prevalence is essentially equal between the sexes among older patients. Between 5% and 25% of older patients will experience a complication, and up to 200,000 patients will require hospitalization. Approximately 50% of all patients hospitalized for diverticulitis eventually require surgery.^5,7

Increased life expectancy is the most common factor to influence the prevalence of DDC. Total dietary fiber intake is consistently inversely related to prevalence of DDC.^8,9 Exercise has been inversely associated with the risk of DDC, but this has not been definitively proven.^7,10 Obesity was found to be a relative risk; however, alcohol and caffeine consumption and cigarette smoking do not increase the risk of DDC.¹¹ Consistent use of NSAIDs and acetaminophen increases the overall risk of symptomatic DDC, particularly those risks associated with bleeding.¹²

PATHOPHYSIOLOGY

Colonic peristalsis is the movement of contents through the colon via sequential, concentric contractions of circular (haustra coli) and longitudinal (taeniae coli) bands of musculature. Sequential contractions narrow the lumen of the bowel, increasing intraluminal pressure in that segment and propelling the stool toward evacuation. As a person ages, structural or inflammatory changes develop within the bowels, leading to progressive weakening of the musculature and connective tissues. The colonic musculature must exert significantly more pressure (up to 90 mm Hg in the sigmoid colon) in order to move fecal matter when there is no unabsorbable dietary fiber within the stool. With no bulky, fiber-filled stool to push, this pressure is directed onto the colon walls.^5,13,14 The colon wall is weakest where nutrient vessels from the mesenteric side of the colon travel between the muscular and mucosal layers, predisposing this area of the colon to herniation caused by the increased intraluminal pressure.

The descending colon and sigmoid colon are the most common sites of diverticula. However, diet and culture can also impact colonic location of DDC. Right-sided DDC is more common in the Far East, whereas the sigmoid colon is involved in more than 95% of documented cases of DDC in western societies.^2,3,15 Diverticula in the upper portion of the descending colon generally form with short, wide necks. In contrast, diverticula in the sigmoid colon tend to form with long, narrow necks, creating a predisposition for fecaliths to become lodged in the diverticular neck (see Figure 3). Over time, stool trapped within the diverticula erode the diverticular wall or obstruct the orifice. Bacterial overgrowth, perforation, and/or leakage develop. Infections spread via abscess formation or fistulization to adjacent organs.^3-6,16-18

CLINICAL PRESENTATION AND DIAGNOSIS

Seventy percent of patients with diverticulitis present with left-sided abdominal pain, and up to 50% of them have had a previous episode.¹⁷ Onset is typically gradual and progresses to a severe, cramping pain in the LLQ. In addition to pain, the most frequent presenting complaint is constipation (50% of patients); however, diarrhea (25%-35%), nausea and vomiting (20%-62%), and urinary symptoms (10%-15%) also can occur. LLQ tenderness and a low-grade fever (lower than 102°F) are usually present. Nausea and vomiting indicate a possible intestinal obstruction. Palpable masses are present in 20% of patients and suggest presence of a contained abscess,¹⁷ whereas diffuse tenderness and/or peritoneal signs could indicate free leakage of abscess fluid into the peritoneal cavity.

Laboratory tests for diverticulitis typically demonstrate leukocytosis, usually exceeding 12,000/mL with a predominance of polymorphonuclear cells, and the ESR is greater than 30 mm/h. Forty-five percent of patients will have a normal WBC count, most often including patients who have a condition that causes immunosuppression.

Patients who complain of passing air or gas in the urine (pneumaturia) may have a colovesical fistula; however, the presence of mixed colonic flora, vegetable matter, and fecaluria is more suggestive of this type of fistula. Colovesical fistulae occur in up to 68% of patients.¹⁹ Presence of a fistula is determined by instilling a dye marker, such as methylene blue, into the rectum or bladder. If the patient has hematuria, culture and Gram’s stain also can determine if a colovesical fistula is present. Women may complain of a vaginal infection or fecal matter within the vagina.^5,18,19

Chest and abdominal plain films should be obtained. The presence of free air within the peritoneal cavity suggests perforation, whereas air/fluid within the bowel suggests an ileus; air in the bladder suggests a colovesical fistula. Contrast radiography is generally used only to confirm a questionable diagnosis. Contrast enema is contraindicated during active episodes of diverticulitis because barium can potentially leak through a perforation and exacerbate existing peritonitis. Water-soluble contrast is safer to use in the acute setting.

However, CT is notably superior to water-soluble contrast enema for sensitivity (95% vs 89%) as well as for ability to grade the severity of inflammation (26% vs 9%) when used to diagnose left-sided diverticulitis.²⁰ CT can reveal colonic wall thickening and pericolic fat inflammation. Fistulae and abscesses can also be evaluated; however, fistulae are difficult to see on CT when a contrast medium is not used. In patients with more complicated cases of diverticulitis, interventional radiology (CT/ultrasound [US]) is utilized to decompress acute abscess formations, allowing for surgical treatment in a more stable setting. CT and/or US allow the clinician to evaluate the soft tissues of the lower abdomen in real-time and at a lower cost than MRI.

Colonoscopy provides clear visualization of the diverticula, and tissue biopsy samples can be obtained. However, invasive endoscopic procedures should be performed only when no clinical signs of diverticulitis are present because of the risk of bowel perforation or abscess rupture.

DIFFERENTIAL DIAGNOSIS

Diverticulitis often mimics other GI pathology, such as inflammatory bowel disease (IBD) and appendicitis. It can also be confused with colon cancer, which can make the diagnosis of DDC challenging in older patients. In women, ectopic pregnancy; endometriosis; ovarian cysts; and ovarian, uterine, or cervical cancer must be considered as well.

The clinical manifestations of IBD include abdominal pain, fever, hematochezia, constipation and/or diarrhea, and possible abdominal masses. Signs of Crohn’s disease are segmental colonic wall thickening and potential abscess/fistula formations seen on CT. Endoscopic and/or histologic examination can provide a definitive diagnosis. Sigmoidoscopy and/or colonoscopy will show inflammation, “cobblestoned” colonic mucosa, and ulcerations in patients with IBD (see Figure 4 and Figure 5). In DDC, the colonic mucosa will most often appear normal around the inflamed divertic-ula^21-25 (see Figure 6). DDC spares the colorectal area, whereas inflammatory changes to the colorectal region are present in IBD.

Colorectal cancer and DDC occur predominantly in older persons. Up to 24% of colorectal cancers are located in the sigmoid colon.²⁶ Perforation, obstruction, and fistula formation are common to both conditions; if the patient has bleeding and unexplained weight loss, however, this raises suspicion of colon cancer.²⁷

One study found that patients who had diverticulitis had an increased risk of left-sided colon cancer, compared with patients who had diverticulosis with no clinical signs of diverticulitis.²⁸ In another study, males with extensive diverticular disease (EDD) had no relative risk for colorectal neoplasia; however, females with EDD had increased risk for both neoplasia and advanced neoplasia in the proximal/distal colon.²⁹ Evaluation for colorectal carcinoma in patients with EDD should be considered when symptoms resolve. Carcinoma of the bladder, prostate, ovaries, and uterus should also be considered.

An elevated WBC count, fever, and LLQ pain can be signs of appendicitis. Right-sided diverticulitis or a redundant sigmoid colon residing in the right lower quadrant can confuse the diagnosis. CT can be invaluable in making a diagnosis of either atypical appendicitis or diverticulitis.

NONINVASIVE TREATMENT

Fiber therapy adds bulk to the stool and slows the progression of DDC. Ten to 25 g of fiber daily is recommended for normal bowel function. Treatment of mild diverticulitis, defined as not requiring hospitalization, consists of close monitoring, a clear liquid diet, and oral antibiotics. This regimen is only for patients with normal functional status, minimal to no indication of systemic infection, and minimal pain.

Patients with acute diverticulitis may require hospitalization. Initially, the patient is to have nothing by mouth. Antispasmodics and analgesics can be administered to rest the bowels. IV fluid resuscitation, antibiotics, and rest will allow for a thorough evaluation of the patient in the first 48 to 72 hours. Initial antibiotic therapy should provide broad-spectrum coverage for normal intestinal flora.³⁰ Ampicillin (2 g IV every 4-6 hours), amoxicillin/clavulanate (1,000 mg twice a day), trimethoprim/sulfamethoxazole (160/800 mg twice a day), ciprofloxacin (750 mg twice a day), or levofloxacin (750 mg/d) are recommended coverage for aerobic organisms. Metronidazole (500 mg IV every 6 hours or 1 g twice a day) or clindamycin (450-900 mg IV every 8 hours) provides adequate broad-spectrum coverage for anaerobic organisms. Rifaximin (800 mg/d) plus mesalazine (2.4 g/d) for 10 days followed by mesalazine (1.6 g/d) alone for 8 weeks is proven highly effective against uncomplicated diverticulitis.^31,32

Diverticulitis typically begins to subside within 3 to 7 days. Initially, the patient is given a liquid diet and progresses to eating solid foods as tolerated. After discharge, the patient continues a gradual progression to a high-fiber diet (25-35 g/d) with continued outpatient care.⁵ Some clinicians recommend eliminating foods such as nuts, corn, and various seeds. Approximately one-third of patients who are free of symptoms with no complications after the first episode will remain asymptomatic. Only about 10% of patients who experience a second episode that is severe enough to warrant hospitalization will remain completely symptom free.

SURGICAL TREATMENT

Overall, approximately 20% of patients with diverticulitis will require surgical intervention. Table 1 lists the recommended indications for surgery from the American Society of Colon and Rectal Surgeons.³³ Table 2 defines the four stages of the most commonly used grading system for diverticulitis with perforation.³⁴

The optimal intervention is a single-stage procedure performed 6 to 8 weeks after resolution of an acute episode. Complicated abscesses are treated with IV antibiotics and CT/US-guided percutaneous drainage before urgent surgery is attempted. If the patient responds favorably, elective single-stage intervention can be performed at a later date.^35-37

The single-stage procedure is a resection of the diseased bowel and primary anastomosis of the remaining colon. Patients with disease that does not respond to therapy or worsens within the first 48 to 72 hours and patients with peritonitis or nonresponsive diverticulitis with abscesses may require urgent surgery. Urgent surgical intervention is performed in two stages. First, resection of the involved segment of colon is followed by diversion of the fecal stream via a proximal colostomy. The distal bowel is managed with a mucous fistula or Hartmann’s pouch until the acute inflammation and infection resolve, usually within 3 to 6 months (see Figure 7). Then a colostomy reversal and anastomosis of the remaining bowel is performed.³⁸ Recurrence rates after resection vary from 7% to 15%.^15,39

Despite advances in medical knowledge and technology, certain risks remain. Since the 1980s, postoperative mortality from urgent surgery remains at 12% to 36%.⁴⁰ Advancing age, obesity, and other comorbid conditions are associated with increased mortality in elective surgery for DDC. Pessaux and colleagues reported overall mortality and morbidity rates of 1.2% and 24.9%, respectively, but found that age older than 75 years and obesity were statistically significant risk factors for increased mortality.⁴¹ Obesity also plays a role in postoperative infections. In a review of 45 patients who developed postoperative infections, 44.4% required ongoing wound care after discharge.⁴² Within this study, 54% of the patients had a body mass index (BMI) higher than 25 kg/m², and 23% had a BMI higher than 30 kg/m².⁴²

Morbidity is more significant in patients who undergo two-stage surgeries. Half the patients who underwent a two-stage procedure, with the Hartmann’s pouch, never regained intestinal continuity; 25% had recurrent pain and inflammation; and approximately 10% had recurrent diverticulitis.⁴⁰ Patients who underwent primary resection had shorter hospital stays (15 vs 24 days) and lower rates of postoperative peritonitis (2% vs 25%) compared to patients who underwent secondary resection.⁴³

Recent studies support delaying surgery and using nonsurgical management even, contrary to current guidelines, in younger patients with recurrent diverticulitis.^44-47 Symptomatic patients with CT-confirmed abscess can be effectively managed with antibiotics, CT-guided percutaneous drainage, and bowel rest. Conservative measures are proven to cost 80% less than inpatient treatment, result in 2% fewer colostomies, and cause fewer deaths compared with elective resection.⁴⁰

CONCLUSION

DDC has become more prevalent as diets have become more refined. The resultant lack of dietary fiber is the most commonly implicated factor for the increased incidence of DDC. LLQ pain, tenderness to palpation, fever, and leukocytosis are common signs and symptoms of the disease. Recurrent attacks, especially those requiring hospitalization, are an ominous sign. Primary medical treatment includes rest, IV fluid resuscitation, and antibiotics; however, nonresponsive diverticulitis requires surgical intervention. JAAPA

DRUGS MENTIONED

Acetaminophen
Amoxicillin/clavulanate (Augmentin)
Ampicillin (Principen)
Ciprofloxacin (Cipro, Proquin)
Clindamycin (Cleocin)
Levofloxacin (Levaquin)
Mesalazine
Metronidazole (Flagyl)
Rifaximin (Xifaxan)
Trimethoprim/sulfamethoxazole (Bactrim, Septra, Sulfatrim)

REFERENCES

	1.	Stollman NH, Raskin JB. Diverticular disease. In: DiMarino AJ Jr, Benjamin SB, eds. Gastrointestinal Disease: An Endoscopic Approach. Thorofare, NJ: Slack, Inc; 2002:859-879.
	2.	Ertan A. Colonic diverticulitis. Recognizing and managing its presentations and complications. Postgrad Med. 1990;88(3);67-72, 77.
	3.	Arnell TD, Stabile BE. Acute colonic diverticulitis. Probl Gen Surg. 2002;19(1):109-120.
	4.	West AB, Losada M. The pathology of diverticulosis coli. J Clin Gastroenterol. 2004;38(suppl 1):S11-S16.
	5.	Floch MH, Bina I. The natural history of diverticulitis: fact and theory. J Clin Gastroenterol. 2004;38(suppl 1):S2-S7.
	6.	Ye H, Losada M, West AB. Diverticulosis coli: update on a “Western” disease. Adv Anat Pathol. 2005;12(2):74-80.
	7.	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(2):276-282.
	8.	Aldoori WH, Giovannucci EL, Rimm EB, et al. A prospective study of diet and the risk of symptomatic diverticular disease in men. Am J Clin Nutr. 1994;60(5):757-764.
	9.	Aldoori WH, Giovannucci EL, Rockett HR, et al. A prospective study of dietary fiber types and symptomatic diverticular disease in men. J Nutr. 1998;128(4):714-719.
	10.	Peters HP, De Vries WR, Vanberge-Henegouwen GP, Akkermans LM. Potential benefits and hazards of physical activity and exercise on the gastrointestinal tract. Gut. 2001;48(3):435-439.
	11.	Aldoori WH, Giovannucci EL, Rimm EB, et al. A prospective study of alcohol, smoking, caffeine, and the risk of symptomatic diverticular disease in men. Ann Epidemiol. 1995;5(3):221-228.
	12.	Aldoori WH, Giovannucci EL, Rimm EB, et al. Use of acetaminophen and nonsteroidal anti-inflammatory drugs: a prospective study and the risk of symptomatic diverticular disease in men. Arch Fam Med. 1998;7(3):255-260.
	13.	Simmang CL, Shires GT III. Diverticular disease of the colon. In: Feldman M, Friedman LS, Sleisenger MH, Scharschmidt BF, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 7th ed. Philadelphia, PA: Saunders; 2002:2100-2112.
	14.	Beitz JM. Diverticulosis and diverticulitis: spectrum of a modern malady. J Wound Ostomy Continence Nurs. 2004;31(2):75-82.
	15.	Schoetz DJ Jr. Uncomplicated diverticulitis. Indications for surgery and surgical management. Surg Clin North Am. 1993;73(5):965-974.
	16.	Freeman SR, McNally PR. Diverticulitis. Med Clin North Am. 1993;77(5):1149-1167.
	17.	Bogardus ST Jr. What do we know about diverticular disease? A brief overview. J Clin Gastroenterol. 2006;40(suppl 3):S108-S111.
	18.	Rothenberger DA, Wiltz O. Surgery for complicated diverticulitis. Surg Clin North Am. 1993;73(5):975-992.
	19.	Pontari MA, McMillen MA, Garvey RH, Ballantyne GH. Diagnosis and treatment of enterovesical fistulae. Am Surg. 1992;58(4):258-263.
	20.	Ambrosetti P, Jenny A, Becker C, et al. Acute left colonic diverticulitis—compared performance of computed tomography and water-soluble contrast enema: prospective evaluation of 420 patients. Dis Colon Rectum. 2000;43(10):1363-1367.
	21.	Peppercorn MA. The overlap of inflammatory bowel disease and diverticular disease. J Clin Gastroenterol. 2004;38(suppl 1):S8-S10.
	22.	Gledhill A, Dixon MF. Crohn’s-like reaction in diverticular disease. Gut. 1998;42(3):392-395.
	23.	Jani N, Finkelstein S, Blumberg D, Regueiro M. Segmental colitis associated with diverticulosis. Dig Dis Sci. 2002;47(5):1175-1181.
	24.	Fearnhead NS, Mortensen NJ. Clinical features and differential diagnosis of diverticular disease. Best Pract Res Clin Gastroenterol. 2002;16(4):577-593.
	25.	Shapiro PA, Peppercorn MA, Antonioli DA, et al. Chron’s disease in the elderly. Am J Gastroenterol. 1981;76(2):132-137.
	26.	Cohn KH, Weimar JA, Fani K, DeSoto-LaPaix F. Adenocarcinoma arising within a colonic diverticulum: report of two cases and review of the literature. Surgery. 1993;113(2):223-226.
	27.	Stollman NH, Raskin JB. Diverticular disease of the colon. J Clin Gastroenterol. 1999;29(3):241-252.
	28.	Stefánsson T, Ekbom A, Sparèn P, Påhlman L. Association between sigmoid diverticulitis and left-sided colon cancer: a nested, population-based, case control study. Scand J Gastroenterol. 2004;39(8):743-747.
	29.	Kieff BJ, Eckert GJ, Imperiale TF. Is diverticulosis associated with colorectal neoplasia? A cross-sectional colonoscopic study. Am J Gastroenterol. 2004;99(10):2007-2011.
	30.	Brook I, Frazier EH. Aerobic and anaerobic microbiology in intra-abdominal infections associated with diverticulitis. J Med Microbiol. 2000;49(9):827-830.
	31.	Brandimarte G, Tursi A. Rifaximin plus mesalazine followed by mesalazine alone is highly effective in obtaining remission of symptomatic uncomplicated diverticular disease. Med Sci Monit. 2004;10(5):PI70-PI73.
	32.	Floch MH, White JA. Management of diverticular disease is changing. World J Gastroenterol. 2006;12(20):3225-3228.
	33.	Practice parameters for sigmoid diverticulitis. The Standards Task Force, American Society of Colon and Rectal Surgeons. Surg Laparosc Endosc Percutan Tech. 2000;10(3):142-148.
	34.	Hinchey EJ, Schaal PG, Richards GK. Treatment of perforated diverticular disease of the colon. Adv Surg. 1978;12:85-109.
	35.	Salem L, Veenstra DL, Sullivan SD, Flum DR. The timing of elective colectomy in diverticulitis: a decision analysis. J Am Coll Surg. 2004;199(6):904-912.
	36.	Mäkelä J, Vuolio S, Kiviniemi H, Laitinen S. Natural history of diverticular disease: when to operate? Dis Colon Rectum. 1998;41(12):1523-1528.
	37.	Bruce CJ, Coller JA, Murray JJ, et al. Laparoscopic resection for diverticular disease. Dis Colon Rectum. 1996;39(suppl 10):S1-S6.
	38.	Desai DC, Brennan EJ Jr, Reilly JF, Smink RD Jr. The utility of the Hartmann procedure. Am J Surg. 1998;175(2):152-154.
	39.	Thaler K, Weiss EG, Nogueras JJ, et al. Recurrence rates at minimum 5-year follow-up: laparoscopic versus open sigmoid resection for uncomplicated diverticulitis. Surg Laparosc Endosc Percutan Tech. 2003;13(5):325-327.
	40.	Janes SE, Meagher A, Frizelle FA. Management of diverticulitis. BMJ. 2006;332(7536):271-275.
	41.	Pessaux P, Muscari F, Ouellet JF, et al. Risk factors for mortality and morbidity after elective sigmoid resection for diverticultis: prospective multicenter multivariate analysis of 582 patients. World J Surg. 2004;28(1):92-96.
	42.	Smith RL, Bohl JK, McElearney ST, et al. Wound infection after elective colorectal resection. Ann Surg. 2004;239(5):599-607.
	43.	Zeitoun G, Laurent A, Rouffet F, et al. Multicentre, randomized clinical trial of primary versus secondary sigmoid resection in generalized peritonitis complicating sigmoid diverticultis. Br J Surg. 2000;87(10):1366-1374.
	44.	Anaya DA, Flum DR. Risk of emergency colectomy and colostomy in patients with diverticular disease. Arch Surg. 2005;140(7):681-685.
	45.	Broderick-Villa G, Burchette RJ, Collins JC, et al. Hospitalization for acute diverticulitis does not mandate routine elective colectomy. Arch Surg. 2005;140(6):576-583.
	46.	Chapman JR, Dozois EJ, Wolff BG, et al. Diverticulitis: a progressive disease? Do multiple recurrences predict less favorable outcomes? Ann Surg. 2006;243(6):876-830.
	47.	Bordeianou L, Hodin R. Controversies in the surgical management of sigmoid diverticulitis. J Gastrointest Surg. 2007;11(4):542-548.