49. Graham SM, Ballantyne GH. Cecal diverticulitis. A review of the American experience. Dis Colon

Rectum 1987;30(10):821–826.

50. Gouge TH, Coppa GF, Eng K, et al. Management of diverticulitis of the ascending colon. 10 years’

experience. Am J Surg 1983;145(3):387–391.

51. Hayward MW, Hayward C, Ennis WP, et al. A pilot evaluation of radiography of the acute

abdomen. Clin Radiol 1984;35(4):289–291.

52. Field S, Guy PJ, Upsdell SM, et al. The erect abdominal radiograph in the acute abdomen: should its

routine use be abandoned? Br Med J (Clin Res Ed) 1985;290(6486):1934–1936.

53. 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.

54. Rao PM, Rhea JT, Novelline RA, et al. Helical CT with only colonic contrast material for diagnosing

diverticulitis: prospective evaluation of 150 patients. AJR Am J Roentgenol 1998;170(6):1445–1449.

55. Rao PM, Rhea JT, Novelline RA. Helical CT of appendicitis and diverticulitis. Radiol Clin North Am

1999;37(5):895–910.

56. Ambrosetti P, Grossholz M, Becker C, et al. Computed tomography in acute left colonic

diverticulitis. Br J Surg 1997;84(4):532–534.

57. Sudakoff GS, Lundeen SJ, Otterson MF. Transrectal and transvaginal sonographic intervention of

infected pelvic fluid collections: a complete approach. Ultrasound Q 2005;21(3):175–185.

58. Lewis M. Bleeding colonic diverticula. J Clin Gastroenterol 2008;42(10):1156–1158.

59. McGuire HH Jr. Bleeding colonic diverticula. A reappraisal of natural history and management. Ann

Surg 1994;220(5):653–656.

60. Drapanas T, Pennington DG, Kappelman M, et al. Emergency subtotal colectomy: preferred

approach to management of massively bleeding diverticular disease. Ann Surg 1973;177(5):519–

526.

61. Rafferty J, Shellito P, Hyman NH, et al. Practice parameters for sigmoid diverticulitis. Dis Colon

Rectum 2006;49(7):939–944.

62. Ambrosetti P, Chautems R, Soravia C, et al. Long-term outcome of mesocolic and pelvic diverticular

abscesses of the left colon: a prospective study of 73 cases. Dis Colon Rectum 2005;48(4):787–791.

63. Chautems RC, Ambrosetti P, Ludwig A, et al. Long-term follow-up after first acute episode of

sigmoid diverticulitis: is surgery mandatory?: a prospective study of 118 patients. Dis Colon Rectum

2002;45(7):962–966.

64. Aydin HN, Remzi FH, Tekkis PP, et al. Hartmann’s reversal is associated with high postoperative

adverse events. Dis Colon Rectum 2005;48(11):2117–2126.

65. Constantinides VA, Heriot A, Remzi F, et al. Operative strategies for diverticular peritonitis: a

decision analysis between primary resection and anastomosis versus Hartmann’s procedures. Ann

Surg 2007;245(1):94–103.

66. Salem L, Flum DR. Primary anastomosis or Hartmann’s procedure for patients with diverticular

peritonitis? A systematic review. Dis Colon Rectum 2004;47(11):1953–1964.

67. Reissfelder C, Buhr HJ, Ritz JP. What is the optimal time of surgical intervention after an acute

attack of sigmoid diverticulitis: early or late elective laparoscopic resection? Dis Colon Rectum

2006;49(12):1842–1848.

68. Purkayastha S, Constantinides VA, Tekkis PP, et al. Laparoscopic vs. open surgery for diverticular

disease: a meta-analysis of nonrandomized studies. Dis Colon Rectum 2006;49(4):446–463.

69. Zingg U, Pasternak I, Guertler L, et al. Early vs. delayed elective laparoscopic-assisted colectomy in

sigmoid diverticulitis: timing of surgery in relation to the acute attack. Dis Colon Rectum

2007;50(11):1911–1917.

70. Lee SW, Yoo J, Dujovny N, et al. Laparoscopic vs. hand-assisted laparoscopic sigmoidectomy for

diverticulitis. Dis Colon Rectum 2006;49(4):464–469.

71. Parks TG. Natural history of diverticular disease of the colon. Clin Gastroenterol 1975;4(1):53–69.

72. Farmakis N, Tudor RG, Keighley MR. The 5-year natural history of complicated diverticular disease.

Br J Surg 1994;81(5):733–735.

73. Makela J, Vuolio S, Kiviniemi H, et al. Natural history of diverticular disease: when to operate? Dis

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Colon Rectum 1998;41(12):1523–1528.

74. Parks TG. Natural history of diverticular disease of the colon. A review of 521 cases. Br Med J

1969;4(5684):639–642.

75. Makela J, Kiviniemi H, Laitinen S. Prevalence of perforated sigmoid diverticulitis is increasing. Dis

Colon Rectum 2002;45(7):955–961.

76. Zaidi E, Daly B. CT and clinical features of acute diverticulitis in an urban U.S. population: rising

frequency in young, obese adults. AJR Am J Roentgenol 2006;187(3):689–694.

77. Pautrat K, Bretagnol F, Huten N, et al. Acute diverticulitis in very young patients: a frequent

surgical management. Dis Colon Rectum 2007;50(4):472–477.

78. Nelson RS, Velasco A, Mukesh BN. Management of diverticulitis in younger patients. Dis Colon

Rectum 2006;49(9):1341–1345.

79. Spivak H, Weinrauch S, Harvey JC, et al. Acute colonic diverticulitis in the young. Dis Colon Rectum

1997;40(5):570–574.

80. Guzzo J, Hyman N. Diverticulitis in young patients: is resection after a single attack always

warranted? Dis Colon Rectum 2004;47(7):1187–1190; discussion 1190–1191.

81. Vignati PV, Welch JP, Cohen JL. Long-term management of diverticulitis in young patients. Dis

Colon Rectum 1995;38(6):627–629.

82. Anaya DA, Flum DR. Risk of emergency colectomy and colostomy in patients with diverticular

disease. Arch Surg 2005;140(7):681–685.

83. West SD, Robinson EK, Delu AN, et al. Diverticulitis in the younger patient. Am J Surg

2003;186(6):743–746.

84. Sachar DB. Diverticulitis in immunosuppressed patients. J Clin Gastroenterol 2008;42(10):1154–

1155.

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Chapter 70

Anorectal Disorders

David J. Maron and Steven D. Wexner

Key Points

1 The most common manifestation of internal hemorrhoids is painless, bright red rectal bleeding

associated with bowel movements. A high-fiber diet supplemented with bulk-forming agents may

reduce symptoms of hemorrhoids and is ideal for first- and second-degree hemorrhoids.

2 Rubber band ligation is suitable for symptomatic first- and second- and some third-degree internal

hemorrhoids that do not respond to bulk-forming agents.

3 Hemorrhoidectomy is required in only a few patients with symptomatic hemorrhoids. It should be

considered when conservative therapy has failed, or when hemorrhoids are complicated by

associated pathology such as ulceration, fissures, fistulas, large hypertrophied anal papillae, or

extensive skin tags.

4 Anal fissure is an ischemic ulcer in the lower portion of the anal canal; its treatment, both medical

and surgical, involves relaxing the internal anal sphincter.

5 Anal fistula is a chronic form of perianal abscess, spontaneously or surgically drained, in which the

tract persists, with an internal opening at the dentate line and an external opening on the perianal

skin.

6 Rectal prolapse results from intussusception that extends beyond the anal verge. Fit patients are best

treated with transabdominal rectopexy. Patients with significant medical comorbidities are best

treated using a perineal approach.

7 Anal condylomata acuminata are caused by human papillomavirus, as are anal intraepithelial

neoplasia and anal cancers.

8 Palpable lesions of the anal canal are not hemorrhoids and may be cancers; examination under

anesthesia and biopsy allow for correct diagnosis.

ANATOMY AND PHYSIOLOGY

A detailed understanding of the anatomy and physiology of the rectum and anus is critical to accurate

diagnosis and management of anorectal disorders.

The Rectum

The rectum begins at the level of the sacral promontory and measures approximately 15 cm in length. It

descends along the curvature of the sacrum and passes through the levator ani muscles, where it

becomes the anal canal. Although the rectum develops from the hindgut in conjunction with the sigmoid

and left colon, it differs from the colon in that the outer muscular layer is continuous, characterized by

the merging of the three taenia bands. The rectum has three lateral curves whose infoldings form

submucosal folds in the lumen, known as the valves of Houston. Because of these curves, the rectum

may gain 5 cm in length when straightened during resection.

The posterior aspect of the rectum lacks peritoneum and is directly adherent to the mesorectum.

Anteriorly, the upper two-thirds of the rectum are covered by peritoneum; the lower third has no

peritoneal covering. The level of the anterior peritoneal reflection (also referred to as the pouch of

Douglas) is variable, but is usually 7 to 9 cm from the anal verge in men and 5 to 7 cm in women. The

mesorectum is covered with a thin layer of investing fascia (fascia propria), which is distinct from the

fascia overlying the sacrum. It is in this plane between these two fascial layers that a “total mesorectal

excision” for rectal cancer is performed. The endopelvic fascia that covers the sacrum posterior to the

rectum is also referred to as Waldeyer fascia; anteriorly, Denonvilliers fascia lies between the rectum

and the vagina in females and the seminal vesicles in males (Fig. 70-1).1

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Traditionally, elective colon resection was recommended for young people (age younger than 50 years)

after one documented episode of uncomplicated diverticulitis. This recommendation was based on the

belief that DD is more virulent in young patients. However, data are conflicting in this regard. There

have been reports of young patients increased risk of complicated disease at presentation, increased

frequency of recurrences (in the same time period as older patients, not as a function of longevity), and

higher risk of needing emergency surgery and colostomy. Recommendation for elective resection

following a single episode of uncomplicated diverticulitis in patients younger than 50 years of age was

motivated by an interest in avoiding a colostomy and avoiding major morbidity and mortality. In view

of conflicting data and adoption of technical strategies for avoiding end-colostomies in all patients,

Nelson et al. have suggested following the same guidelines that are used for older patients.63,77–83

10 Immunocompromised patients are more likely to fail medical management and must be watched

closely since the manifestations of failure may be more subtle than in immunocompetent patients.

Transplant patients, those on steroids or chemotherapy, diabetics, and dialysis patients are at risk.

Elective resection in anticipation of transplant is also considered in some patients with DD.

Interestingly, human immunodeficiency virus (HIV)-positive patients with normal CD4 counts appear to

behave as if they were immunologically normal with respect to the incidence of diverticulitis and its

clinical course. Since HIV infection has principally been an illness of younger people, most studies of

diverticulitis have not included a large number of HIV-positive patients.84 That may change as longevity

improves with current antiretroviral regimens.

SUMMARY

DD is common and includes a spectrum of presentations and anatomic locations, favoring the left colon

in Western societies. The etiology is likely multifactorial, with a low-residue diet being a common

factor. The CT scan has dramatically improved diagnostic accuracy and helped with treatment planning.

Treatment often parallels the Hinchey stage, particularly the modified Hinchey classification. Surgical

treatment has evolved to favor medical management and image-guided percutaneous drainage of

abscesses when feasible to convert surgical emergency–staged procedures into either single-stage

procedures or procedures with primary anastomosis and diverting loop stoma. The distinction of

1841

complicated DD and colon cancer can be difficult, but early contrast enema studies or colonoscopy can

be safely performed and are the most helpful diagnostic procedures in this setting. The indications for

elective resection following successful medical management of DD are being reconsidered, and it is

becoming clear that elective sigmoid resection for DD should be offered to avoid recurrent symptoms,

not primarily to avoid free perforation and the need for an emergent colostomy. Minimally invasive

surgery is state of the art, and the hand-assisted techniques are particularly useful for elective DD

resections.

References

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13. Gallagher JJ, Welch JP. Giant diverticular of the sigmoid colon: a review of differential diagnosis

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14. Beighton PH, Murdoch JL, Votteler T. Gastrointestinal complications of the Ehlers-Danlos

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15. Cook JM. Spontaneous perforation of the colon: report of two cases in a family exhibiting Marfan’s

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16. Wess L, Eastwood MA, Wess TJ, et al. Cross linking of collagen is increased in colonic

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17. Morson BC. The muscle abnormality in diverticular disease of the colon. Proc R Soc Med

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18. Whiteway J, Morson BC. Elastosis in diverticular disease of the sigmoid colon. Gut 1985;26(3):258–

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19. Painter NS, Truelove SC, Ardran GM, et al. Segmentation and the localization of intraluminal

pressures in the human colon, with special reference to the pathogenesis of colonic diverticula.

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20. Painter NS. The aetiology of diverticulosis of the colon with special reference to the action of

certain drugs on the behaviour of the colon. Ann R Coll Surg Engl 1964;34:98–119.

21. Taylor I, Duthie HL. Bran tablets and diverticular disease. Br Med J 1976;1(6016):988–990.

22. Snape WJ Jr, Carlson GM, Matarazzo SA, et al. Evidence that abnormal myoelectrical activity

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23. Bassotti G, Battaglia E, Spinozzi F, et al. Twenty-four hour recordings of colonic motility in patients

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2001;44(12):1814–1820.

24. Painter NS, Burkitt DP. Diverticular disease of the colon: a deficiency disease of Western

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25. Painter NS, Burkitt DP. Diverticular disease of the colon, a 20th century problem. Clin Gastroenterol

1975;4(1):3–21.

26. Korzenik JR. Diverticulitis: new frontiers for an old country: risk factors and pathogenesis. J Clin

Gastroenterol 2008;42(10):1128–1129.

27. Peery AF, Sandler RS, Ahnen DJ, et al. Constipation and a low-fiber diet are not associated with

diverticulosis. Clin Gastroenterol Hepatol 2013;11(12):1622–1627.

28. Korzenik JR. Case closed? Diverticulitis: epidemiology and fiber. J Clin Gastroenterol 2006;40(suppl

3):S112–S116.

29. Strate LL, Liu YL, Syngal S, et al. Nut, corn, and popcorn consumption and the incidence of

diverticular disease. JAMA 2008;300(8):907–914.

30. Milner P, Crowe R, Kamm MA, et al. Vasoactive intestinal polypeptide levels in sigmoid colon in

idiopathic constipation and diverticular disease. Gastroenterology 1990;99(3):666–675.

31. Yun AJ, Bazar KA, Lee PY. A new mechanism for diverticular diseases: aging-related vagal

withdrawal. Med Hypotheses 2005;64(2):252–255.

32. Costedio MM, Coates MD, Danielson AB, et al. Serotonin signaling in diverticular disease. J

Gastrointest Surg 2008;12(8):1439–1445.

33. Floch MH. A hypothesis: is diverticulitis a type of inflammatory bowel disease?J Clin Gastroenterol

2006;40(suppl 3):S121–S125.

34. Daniels L, Philipszoon LE, Boermeester MA. A hypothesis: Important role for gut microbiota in the

etiopathogenesis of diverticular disease. Dis Colon Rectum 2014;57(4):539–543.

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36. Hall JF. The microbiome and diverticulitis: a new target for medical therapy?Dis Colon Rectum

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37. Ghorai S, Ulbright TM, Rex DK. Endoscopic findings of diverticular inflammation in colonoscopy

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38. Cohen E, Fuller G, Bolus R, et al. Increased Risk for Irritable Bowel Syndrome After Acute

Diverticulitis. Clin Gastroenterol Hepatol 2013;11(12):1614–1619.

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41. Simpson J, Scholefield JH, Spiller RC. Origin of symptoms in diverticular disease. Br J Surg

2003;90(8):899–908.

42. Stead RH. Nerve remodelling during intestinal inflammation. Ann N Y Acad Sci 1992;664:443–455.

43. Brewer DB, Thompson H, Haynes IG, et al. Axonal damage in Crohn’s disease is frequent, but nonspecific. J Pathol 1990;161(4):301–311.

44. Hinchey EJ, Schaal PG, Richards GK. Treatment of perforated diverticular disease of the colon. Adv

Surg 1978;12:85–109.

45. Kaiser AM, Jiang JK, Lake JP, et al. The management of complicated diverticulitis and the role of

computed tomography. Am J Gastroenterol 2005;100(4):910–917.

46. Woods RJ, Lavery IC, Fazio VW, et al. Internal fistulas in diverticular disease. Dis Colon Rectum

1988;31(8):591–596.

47. Grissom R, Snyder TE. Colovaginal fistula secondary to diverticular disease. Dis Colon Rectum

1991;34(11):1043–1049.

48. Chintapalli KN, Esola CC, Chopra S, et al. Pericolic mesenteric lymph nodes: an aid in

distinguishing diverticulitis from cancer of the colon. AJR Am J Roentgenol 1997;169(5):1253–1255.

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approach was favored for many years because it is quick and simple and there is no chance of

anastomotic leak. However, 30% to 50% of patients treated in this way never undergo reversal of the

stoma, and when they do, the complication rate is high (major complications in 5% to 25%, anastomotic

leak in 2% to 30%).64,65

Algorithm 69-1. Diverticulitis Treatment based on Modified Hinchey Score (0–IV).

Despite these problems, this is still the procedure of choice in unstable patients. However, in the more

stable patient who requires an urgent operation because of generalized diverticular peritonitis on

presentation or failure of nonoperative management, the goal should be resection with primary

anastomosis and creation of a diverting stoma, usually a loop ileostomy. The anastomotic leak rate in

patients with free diverticular perforation who undergo a single-stage operation acutely is 13%.66 While

diverting ileostomy or colostomy upstream from a primary anastomosis does not prevent an

anastomotic leak, it lessens the consequences of a leak by diverting the fecal stream from the area,

preventing potentially devastating gross fecal soilage through the defect.

Obstruction

Complete obstruction from DD is unusual. Partial obstruction resulting from edema, spasm, and

inflammation is more common. The differential diagnosis includes cancer and inflammatory bowel

disease. Medical treatment and elective resection are usually successful. Rarely is the placement of a

colonic stent necessary, but it may be used to allow for bowel preparation before a single-stage

resection with primary anastomosis. A diverting stoma may be necessary to relieve obstruction and

enable completion of the workup and treatment before definitive resection. If perforation has resulted

from obstruction, even when the distinction between obstructive cancer and diverticular obstruction

cannot be made, the perforated segment should be resected and diverting end-colostomy performed. If

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this is a right-sided process in a relatively stable patient, primary anastomosis and diverting loop

ileostomy can be considered.

Fistula

The presence of a fistula usually obviates the need for an emergency operation because the abscess has

in effect spontaneously drained internally. A single-stage operation should be planned. The bladder side

of a colovesical fistula is usually disrupted bluntly at the time of colon resection. No repair of the

bladder is needed unless there is a visibly patent opening at the transected fistula tract site. A urinary

drainage catheter is left in place for 7 to 10 days after surgery.46 A cystogram can be done to verify

closure of the tract opening and can facilitate discharge without an indwelling catheter following

laparoscopic resection, which is often earlier than after open procedures. It is not necessary to leave a

pelvic drain at the time of resection. Likewise, fistula tract openings to the vaginal cuff do not require

closure. At most, omentum can be draped into the pelvis to separate the fresh colorectal anastomosis

from the opening on the vagina.

Giant Colonic Diverticulum

Treatment is surgical resection of the involved segment of colon. Planned electively, a single-stage

operation is indicated. Once perforated, the decision process parallels common diverticulitis, preference

being given to resection with primary anastomosis and diverting loop stoma in the stable patient.

MANAGEMENT

Operative Strategies

8 The most important advance in the surgical management of DD besides trying to convert staged,

emergency operations into elective, single-stage operations is the introduction of minimally invasive

surgical techniques. No matter what the approach, certain challenges face the surgeon operating for DD.

Inflammation distorts the anatomic planes. Dense fibrosis and adhesions impede sharp dissection and

make it difficult to get good traction and countertraction that enable dissection. Inflammatory adhesions

interfere with visualization and sometimes even palpation of anatomic structures.

Key concepts apply to both laparoscopic and open procedures. The goal is not to remove every

diverticulum but rather to resect the area of inflammation or complication. The proximal resection line

should be at soft, pliable bowel. The distal resection line must be at the top of the rectum demarcated

by splaying of the bunched longitudinal muscle fibers (taenia coli) into the continuous longitudinal,

outer layer of the rectal muscularis propria. The point of transection is almost never below the anterior

pelvic peritoneal reflection. The splenic flexure should almost always be mobilized to facilitate creation

of a tension-free colorectal anastomosis. The anastomotic site itself must be free from diverticula, which

can be difficult in the patient with dense, pandiverticulosis. Manual, pinch dissection (or “finger

fracture”) techniques are used to separate structures and divide areas of fibrosis and thick adhesions.

Dissection commences away from the focus of inflammation, usually proximal to it. The left ureter

should be identified as early as possible and before transecting major vessels or the colon. In the setting

of severe inflammation in the left lower quadrant or pelvis, it can be very helpful to mobilize and divide

the proximal bowel as an initial operative maneuver. Likewise, when dense inflammation makes the

standard, lateral-to-medial mobilization of the sigmoid difficult, a medial-to-lateral approach can

sometimes provide access to less inflamed tissues. While typically not needed, when a preoperative CT

scan shows dense inflammation in proximity to the left ureter, placement of ureteral stents can help

with ureteral identification and protection during dissection. Whether using open or laparoscopic

techniques, an elective operation should be deferred for 4 to 6 weeks after the last episode of

inflammation so that acute inflammatory changes do not interfere with either the dissection or the

construction of a safe colorectal anastomosis.67

There is growing experience with laparoscopic resection of even complicated DD. A meta-analysis

comparing laparoscopic to open diverticulitis resections concluded that the laparoscopic patients had

lower infection rates (overall and wound); decreased pulmonary, gastrointestinal, and cardiovascular

complications; and a shorter time to recovery of bowel function and hospital discharge. Although

studies in the meta-analysis included acute and chronic indications for surgery and complicated as well

as uncomplicated diverticulitis in both groups, the authors cautioned that the retrospective nature of the

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reviewed studies introduced selection bias.68 When laparoscopic resections for DD are performed early

(2 to 16 days after hospital admission), the conversion rates are higher than when surgery is delayed

(more than 6 weeks).69 Hand-assisted minimally invasive operations may offer significant benefit

compared to pure laparoscopic surgery for DD, showing lower conversion rates, shorter operative times,

and no compromise of the speedy recovery associated with fully laparoscopic operations.70

Elective Surgery

Several observations form the basis of recommendations for elective resection following episodes of

diverticulitis. Forty percent of diverticulitis patients admitted to the hospital will develop a

complication, 23% following a single episode and 58% following two episodes. Thirty to 45% of

patients hospitalized for diverticulitis will have another flare, usually within 5 years (90%). Among

patients hospitalized a second time, only 10% remain symptom-free.71–73 Mortality doubles with a

second flare. The classic indications for elective resection include two or more episodes of documented

diverticulitis, a single episode of complicated diverticulitis (modified Hinchey stage Ib or II), one

documented episode in an immunocompromised patient, one documented episode in a young patient

(40 to 50 years old), and an inability to exclude cancer as the cause of the signs and symptoms.

9 Practice parameters outlined by the American Society of Colon and Rectal Surgeons note that most

patients who present with complicated diverticulitis do so at their first episode, so operating on patients

with uncomplicated episodes of diverticulitis may not reduce the risk of emergency surgery and

mortality. “The age and medical condition of the patient, the frequency and severity of the attack(s),

and whether there are persistent symptoms after the acute episode” may be better determinants of

recommendation for elective resection.61 Complications develop often enough after successful medical

management of complicated diverticulitis to warrant recommending elective resection.56 Kaiser et al.45

reported that 41% of patients treated with percutaneous drainage of a diverticular abscess will later

develop severe sepsis.

It has been noted that the incidence of DD has steadily increased among young people, from 12% in

196974 to 20% in 199875 to 54% in a study of young and obese American patients in 2006.76

 

Ambrosetti et al. reported on 423 patients with acute diverticulitis on CT scan, categorizing them as

having either moderate disease or severe disease. Criteria for moderate disease included localized wall

thickening or inflammation of pericolic fat (modified Hinchey stage Ia; see Table 69-2). Severe disease

included the presence of extraluminal air or contrast (contained perforation) or abscess (modified

Hinchey stages Ib and II). Of the 42 patients who failed nonoperative management, 32 had severe

disease. Twenty percent of those patients who were initially successfully managed nonoperatively

developed secondary complications such as fistulas (median follow-up 46 months). They concluded that

the presence of severe disease at the index episode predicted failure of nonoperative management and

that there is a high risk of secondary complications after initial nonoperative management.56

Ultrasound. Abdominal ultrasound has been emphasized in the European literature and is attractive as

a strategy for limiting radiation exposure. However, its diagnostic limitations (user dependence,

interference from overlying bowel gas, and decreased accuracy in obese patients) have precluded its

widespread adoption in the United States. In skilled hands, it may have a role in image-guided

percutaneous drainage of abscesses.57

Contrast Enema Study (Barium Enema). Contrast enemas have been the “gold standard” test for the

presence and anatomic distribution of diverticula (Fig. 69-7). For reasons cited earlier, CT scan has

supplanted contrast enemas in the acute setting. However, they are better than CT for helping

distinguish colon cancer from diverticular obstruction, and contrast can also traverse narrowed areas of

the colon impassable by an endoscope. While caution must be used in the acute setting to avoid

perforation, these studies can be performed safely. Caveats are that contrast must be administered

gently, water-soluble contrast should be used, and a single contrast study is performed in unprepared

bowel to avoid the increased risk of perforation and fecal contamination with the administration of air.

In chronic DD, the contrast enema can demonstrate stricture, angulation, and segmentation-type

contractions. It can also be useful for the evaluation of fistulas.

Figure 69-7. Barium enema showing multiple diverticula of the colon.

6 Endoscopy. Like contrast enema studies, colonoscopy or flexible sigmoidoscopy can be used

judiciously in the acute setting. It is particularly helpful in distinguishing malignancy from DD and can

therefore help guide early management of acute presentations when malignancy as the cause of

symptoms is being considered.

Cystoscopy. Cystoscopy can help diagnose colovesical fistulas. Although the fistula tract is usually

difficult to see, focal hyperemia and inflammation may be noted. Symptoms of a colovesical fistula and

air in the uninstrumented bladder on CT scan are usually sufficient for diagnosis.

1837

TREATMENT

Symptomatic Diverticulosis

Fiber supplements and increased dietary fiber (goal 25 to 30 g/d) constitute the cornerstone of

symptomatic diverticulosis treatment once diverticular stricture has been ruled out as the cause of

symptoms. Stricture is an indication for elective segmental colectomy, typically a sigmoid colectomy to

remove the area of stricture and the most dense region of diverticula.

Hemorrhagic Diverticular Disease

Diverticular hemorrhage stops spontaneously in more than 90% of patients; of these, 75% will not bleed

again.58 Patients who have a second episode of diverticular hemorrhage should undergo hemicolectomy

of the involved portion of colon59 after localizing the site of hemorrhage endoscopically with a tagged

red blood cell scan or with angiography, because these patients are likely to bleed again. If the site of

bleeding cannot be determined definitively as left or right sided, a subtotal colectomy is the procedure

of choice.60

Diverticulitis

7 The treatment of diverticulitis typically parallels the Hinchey classification (Algorithm 69-1)44:

Stage I, confined pericolic abscess: antibiotics and bowel rest

Stage II, pelvic or retroperitoneal abscess: percutaneous abscess drainage

Stage III, purulent peritonitis: resuscitation and urgent operation

Stage IV, feculent peritonitis: resuscitation and urgent operation

Stage I diverticulitis is mild when patients can tolerate a diet, have no systemic symptoms (no fever,

tachycardia, hypotension), and have no substantial peritoneal signs. The CT scan shows either minor

pericolic fat stranding or wall thickening in the presence of diverticulosis. Outpatient management is

usually appropriate for these patients. Broad-spectrum oral antibiotics are prescribed for 7 to 10 days,

and patients start a clear liquid diet, advancing to a solid diet as symptoms resolve. If this is a first

episode of presumed diverticulitis, an elective confirmatory study with either barium enema or

colonoscopy is planned after inflammation has subsided. Progression of symptoms on this regimen

warrants hospital admission and repeat CT scan may be necessary. The vast majority (70% to 100%) of

patients with uncomplicated diverticulitis will recover without operative intervention. Although nearly

a third will relapse, long-term fiber supplementation appears to reduce this risk.61

Severe stage I inflammation is indicated by intolerance of diet, possible nausea and vomiting, fever,

chills, and peritoneal signs on examination, which are often focal. The CT scan may show a phlegmon or

contained pericolic abscess. These patients are admitted to the hospital for parenteral broad-spectrum

antibiotics. They are placed on bowel rest, intravenous fluids are administered, and if nausea and

vomiting are major symptoms, a nasogastric tube may be placed. Analgesia is provided but limited to

enable evaluation of symptom progression. In addition, since narcotics are known to cause strong,

nonpropulsive sigmoid colon contractions, their use in patients with diverticulitis should be minimized.

Small (<2 cm) pericolic abscesses may resolve with intravenous antibiotics; larger contained abscesses

will likely require percutaneous drainage with CT (or possibly ultrasound) guidance.61,62 If a smaller

abscess is treated initially with antibiotics only but symptoms fail to improve, percutaneous drainage

should be considered. Progression of symptoms despite percutaneous drainage of an abscess usually

indicates the need for surgery. Historically, 10% to 25% of patients requiring hospitalization for

treatment of diverticulitis will not improve or will worsen with medical management alone; overall,

30% of hospitalized patients will require an operation. Those patients who recover from an initial

episode of complicated diverticulitis (contained perforation or abscess) should be considered for singlestage, elective segmental colectomy after the resolution of acute inflammation.63 As will be discussed

further, minimally invasive surgical techniques are increasingly being used with good outcomes in these

patients.

Patients who fail nonoperative management of diverticulitis or who present with purulent or feculent

peritonitis require operative treatment. The goal of surgery in these patients – especially if they are

toxic, developing multisystem organ failure, or hemodynamically unstable – is to resect the perforation

and make a stoma. This defines a Hartmann procedure, in which the offending segment of colon is

resected, a proximal stoma is constructed, and the distal colon and/or rectum are closed and left in the

pelvis. The distal remaining segment of colon and rectum is referred to as a Hartmann pouch. This

1838

 

to avoid confusing diverticulitis-associated colitis with inflammatory bowel disease. Probiotics and

nonsteroidal anti-inflammatory medications are being explored as potentially protective agents.26,39,40

Diagnosis

Noninflammatory Diverticular Disease

Most patients with diverticulosis noted on barium study, colonoscopy, or abdominal CT scan are

asymptomatic. In patients who have vague, crampy, left lower quadrant pain in the absence of fever,

leukocytosis, or CT findings of focal inflammation, other causes of pain must also be considered.

Additional symptoms reported may include nausea, flatulence, bloating, and change of bowel habit. The

differential diagnosis includes colonic adenocarcinoma, constipation, inflammatory bowel disease, and

IBS. There are no peritoneal signs on examination, the rectal examination is unrevealing, and

proctoscopy shows no inflammation. Postinflammatory neurogenic alteration has been postulated as a

cause of visceral hypersensitivity.41–43 Nonspecific, mild mucosal inflammation and muscle spasm may

also contribute. There is considerable overlap with IBS. In addition to high-fiber modification of the diet

and bulk-forming agents such as psyllium or flaxseed, anticholinergics, analgesics, and antibiotics can be

prescribed to manage symptoms.

Hemorrhagic Diverticular Disease. Like bleeding from colonic angiodysplasia, diverticular

hemorrhage is classically asymptomatic until presentation with lower gastrointestinal hemorrhage that

can be massive. This differs from hemorrhage from inflammatory bowel disease or ischemic colitis

where there are typically symptoms before bleeding begins. A foregut source of bleeding must be

excluded by nasoenteric recovery of bilious, nonbloody aspirate or upper endoscopy. Likewise, an

anorectal source of bleeding must be excluded by examination. Localization of lower gastrointestinal

hemorrhage of any cause is necessary to help guide appropriate colon resection should that be required.

Although most cases of diverticular hemorrhage are self-limited, recurrence or failure of bleeding to

stop spontaneously determines the need for resection. Colonoscopy, tagged red blood cell scan, or, if

bleeding is brisk enough, angiography is used to localize bleeding (Fig. 69-4).

Giant Colonic Diverticula. Symptoms and signs of giant colonic diverticula may be noninflammatory

(pain, bloating, nausea, vomiting, diarrhea, abdominal tenderness and mass) or inflammatory, resulting

from perforation (pain, leukocytosis, fever, localized or generalized peritonitis).13

Inflammatory Diverticular Disease

The constellation of inflammatory signs and symptoms corresponds to the spectrum of inflammatory

complications of DD. The Hinchey classification44 categorized the severity of acute diverticulitis and has

been modified to reflect refinements of diagnosis enabled by improved CT scan quality (Table 69-2).45

The modified classification also includes manifestations of chronic inflammation such as fistula

formation and stricture/obstruction.

Symptoms of acute diverticulitis include steady, left lower-quadrant abdominal pain; fever; change in

bowel habits (constipation or diarrhea); anorexia; nausea; vomiting; bloating; and urinary tract

symptoms such as urinary frequency or retention. Examination will reveal left lower-quadrant

tenderness that may be appreciable only with deep palpation in stage 0 inflammation. In stage I or II

inflammation, focal peritoneal signs in the left lower quadrant are likely, and there may be a tender

mass. Digital rectal examination may also reveal pelvic tenderness or a tender mass in the cul-de-sac.

Generalized peritoneal signs would be expected for stage III or IV inflammation. Dehydration with

earlier stages or evolving sepsis with later stages may cause tachycardia and hypotension. Leukocytosis

is more likely with advancing stage of inflammation. The differential diagnosis includes perforated

colon cancer, acute appendicitis, perforated peptic ulcer, acute ischemic colitis, pancreatitis, and flare of

Crohn disease or ulcerative colitis. Normal serum amylase and lipase help exclude a diagnosis of

pancreatitis. Imaging studies and endoscopy help to distinguish diverticulitis from the other diagnoses.

However, active inflammation or contained perforation may limit the utility of rectal contrast CT,

barium enema studies, and endoscopy in the acute setting. Distinguishing perforated colon cancer from

DD can be especially challenging, even in the operating room.

Diverticular fistula formation represents internal drainage of an abscess (or external drainage in the

case of colocutaneous fistulas). Approximately half of diverticular fistulas are colovesical fistulas.

Women with colovesical or colovaginal fistulas have usually had a hysterectomy.46,47 Urinary tract

infection symptoms, pneumaturia, and fecaluria are common complaints. Recurrent urinary tract

1834

infection in elderly men should raise concern for the presence of a colovesical fistula, which is often

secondary to DD. Passage of feces or flatus from the vagina is a characteristic symptom of a colovaginal

fistula. Colocutaneous fistulas are a rare complication of DD.

Figure 69-4. Superior mesenteric arteriogram from a patient with bleeding from a right colon diverticulum. A: Early radiograph

with contrast material outlining the diverticulum (arrow). B: Late radiograph demonstrating overflow of contrast material into the

colonic lumen(arrow).

Thirteen percent of large-bowel obstructions are due to DD. The concurrent incidence of colon

carcinoma in 7% of patients with symptomatic sigmoid DD confounds diagnosis and treatment.48 CT

scan is not as reliable for distinguishing these diagnoses as colonoscopy or contrast enema studies.

Right-sided diverticulitis frequently is confused with appendicitis, and misdiagnosis is common. The

duration of symptoms is usually longer than appendicitis. Patients are usually older than those with

appendicitis (late 30s or 40s) but younger than patients with typical left-sided diverticulosis (over 50

years of age).49,50

CLASSIFICATION

Table 69-2 Modified Hinchey Classification

1835

Figure 69-5. Sigmoid diverticulitis with pericolic abscess(arrows).

Imaging and Diagnostic Studies for Diverticular Disease

Plain Radiographs. While seldom useful in the diagnosis of uncomplicated diverticulitis, a three-way

abdominal series that includes an upright chest radiograph, an abdominal flat plate, and a left lateral

decubitus view is useful for demonstrating free air. An ileus pattern or soft tissue mass may also be

detected.51,52

5 Computed Tomography Scan. CT scanning has revolutionized the diagnosis of acute diverticulitis

and, sometimes, by way of percutaneous abscess drainage, its treatment. The accuracy of CT scans in

the acute setting is central to the trend toward converting what formerly were surgical emergencies into

elective, often single-stage operations. Intravenous and water-soluble oral and rectal enteric contrast

should be administered. Water-soluble contrast is used to avoid barium peritonitis that may result if

barium leaks from a perforated diverticulum into the peritoneal cavity.

A CT scan can reveal the presence and extent of diverticulosis, but its real strength is characterizing

extracolonic inflammatory change. Signs of inflammation include colon wall thickening, pericolic fat

stranding, or phlegmon formation. Pericolic abscess size and location can be detected (Fig. 69-5).

Perforation is evidenced by free air; contained perforation may be identified by loculated extraluminal

pericolic air. CT more accurately demonstrates diverticular abscesses and severity of inflammation than

contrast enema studies.53 Air in the bladder or contrast in the vagina may indicate the presence of a

fistula (Fig. 69-6).

Figure 69-6. A: Computed tomography scan demonstrating air in the urinary bladder (arrow) in the presence of a colovesical

fistula secondary to diverticulitis. B: Air in the urinary bladder (small arrow) in association with a paravesical inflammatory mass

(large arrow). (Reproduced with permission from Sarr MG, Fishman EK, Goldman SM. Enterovesical fistula. Surg Gynecol

Obstet1987;164(1):41–48.)

Rao et al.54 reported a misdiagnosis rate of up to 67% for diverticulitis in patients with abdominal

pain managed without CT imaging. An alternate diagnosis is suggested by CT scan in 45% to 58% of

cases when diverticulitis is not found, including small-bowel obstruction, acute cholecystitis,

appendicitis, gynecologic disease, and primary epiploic appengitis.55 Correct preoperative diagnosis of

right-sided diverticulitis has also been enhanced by CT scanning.

Not only is CT useful for improving diagnostic accuracy, but also findings can predict failure of

medical management or risk of secondary complications following medical management.

1836

 

studies of the colon wall showed thinning of the circular muscle associated with early diverticula. Gaps

in the circular muscle were observed with larger diverticula.7

Figure 69-1. Cross section of the colon illustrating the relation of diverticula to the blood vessels penetrating the circular muscle

layer, the taeniae, and the appendices epiploicae.

Figure 69-2. Postevacuation film of barium enema, demonstrating a giant colonic diverticulum (arrows) partially filled with

barium. (Reproduced with permission from McNutt R, Schmitt D, Schulte W. Giant colonic diverticula. Dis Colon 1988;31:625.)

In contrast to typical pseudodiverticula, giant colonic diverticula almost always arise from the

antimesenteric border of the colon. They are assumed to be a complication of ordinary colonic

diverticulosis, possibly developing after inflammatory narrowing of the neck of a pseudodiverticulum

causes a ball-valve mechanism that entraps gas in the diverticulum, causing it to enlarge (Fig. 69-2).13

The observation of colonic diverticula in young patients with connective tissue disorders such as

Marfan disease and Ehlers–Danlos syndrome raises the question of whether connective tissue genetic

derangements play a role in diverticulosis development.14,15 Ordinary senescent connective tissue

change may be a factor as well. Cross-linkage of collagen fibrils in the colon wall increases with age,

rising markedly after age 40, and appears to decrease compliance of the colon wall. In comparison with

age-matched controls, this cross-linkage is exaggerated in patients with diverticulosis.16

Thickening of the colon wall in diverticulosis was originally attributed to muscle hypertrophy.12,17

This was disproven by histologic studies, but increased elastin deposition in the taeniae coli of patients

with uncomplicated diverticulosis has been shown. The taeniae are shortened as a result, causing the

circular muscle to be accordioned in the two intertaenial zones, the same areas where pseudodiverticula

more commonly form.18 The functional significance of this is not known, but it has been speculated that

muscle contractions may be stronger in these areas.

Motility Factors

1831

Four unusual colonic motility patterns have been observed in the setting of diverticulosis: segmentation,

high-pressure waves, slow-wave motility pattern, and disorganized propulsive activity.

Segmentation

Painter et al.19 used cineradiography and manometry to study colonic motility and reported that when

simultaneous haustral contractions occur in the same segment of colon, high pressure is generated in the

intervening bowel, causing ballooning of the colon wall and distention of diverticula (Fig. 69-3).

Figure 69-3. The role of segmentation in colonic physiology. A: Interhaustral ring contraction (“segmentation”) leads to increased

luminal pressure when there is simultaneous segment wall contraction. B: Relaxation of an interhaustral ring allows passage of

colon contents from the high-pressure segment to a neighboring low-pressure segment. C: Resistance to colon content flow can be

imposed by interhaustral ring contraction that functions as a baffle. Resultant interruption of flow can also significantly increase

luminal pressure in that segment. D: Diverticula always arise from the segment wall between interhaustral rings and never at the

rings.

High-Pressure Waves

High-pressure waves are independent of normal peristalsis and have an amplitude of 10 mm Hg in

normal patients but have higher amplitude (up to 90 mm Hg) and longer duration in patients with

diverticulosis.20

Slow-Wave Motility Pattern

The normal slow-wave pattern in the colon is altered in DD.21,22

Disorganized Propulsive Activity

High-amplitude propulsive contractions occurred more frequently and were more likely to be

disorganized in patients with DD than normal subjects. Retropulsive contractions occurred more

frequently in segments of colon with diverticulosis.23

Diet

Decreased dietary fiber is the most consistent factor associated with the high incidence of diverticulosis

in Western populations. Painter and Burkitt first elucidated this connection after noting the striking

disparity in incidence between British society and sub-Saharan populations. They measured colon transit

time and stool weights in over 1,000 individuals in the United Kingdom and sub-Saharan Africa. The rise

in the incidence of DD coincident with the rise in refined food products in diets in the West was also

noted.24 Painter and Burkitt25 also reported improvement of DD symptoms in patients who increased

dietary fiber and recrudescence of symptoms once fiber intake decreased again. There is now a rising

1832

incidence of diverticulosis among previously low-risk populations in concert with changes to a Westernstyle diet as a consequence of economic development or immigration. Japanese immigrants to the

United States acquire diverticulosis risk comparable to other Westerners, although the right-sided

predominance of diverticulosis seen among Asians persists.5,26 The exact protective mechanism of stool

bulk is not understood. Evidence that contradicts the role of low-fiber diet or constipation as

contributing factors to DD is provided by a study of 2813 patients enrolled in a vitamin D and colon

polyp colonoscopy study. Five hundred and thirty-nine patients aged 45 to 75 who had the incidental

colonoscopic finding of diverticulosis without antecedent history of it were compared to 1569 controls.

The control group had a higher self-reported history of less frequent or lumpy stools, and there was no

difference in dietary fiber intake. However, inaccuracies of bowel and diet habit self-reports, the

evaluation of individuals with asymptomatic diverticulosis versus symptomatic DD, and the imperfect

sensitivity of colonoscopy for detection of diverticulosis should be considered in the interpretation of

these findings.27

While the focus on dietary fiber has emphasized insoluble fiber, soluble fiber may also be of value.

Soluble fiber is processed by intestinal flora, which may in turn affect diverticulosis.26,28 Finally, despite

the long-held admonition to avoid eating nuts and seeds, there is no evidence to support this

recommendation.29

Other Factors

Other neurologic and chemical mediators of colonic motility may play a role in pseudodiverticula

genesis. Vasoactive intestinal peptide levels are increased in the bowel wall of patients with

diverticulosis.30 Age-related vagal attrition has been postulated to contribute to colonic smooth muscle

dysmotility.31 Alterations of serotonin expression and function are noted after resolution of acute

diverticulitis and may contribute to lasting symptoms.32

Emerging Concepts

Two observations have focused interest in the possibility of a primary inflammatory etiology of

diverticulitis. One is that a subset of patients with uncomplicated diverticulitis are unresponsive to

antibiotic therapy as would be expected in the case of a smoldering, focal bowel-wall infection due to

diverticular sepsis or microperforation (see below). The other is that anti-inflammatory medications

appear to reduce flares of diverticulitis in some patients. Shifts in the microbiome have also been

detected in other lower gastrointestinal system disorders including colon cancer and IBD.33–36 Subtle

peridiverticular inflammatory changes have been noted in some patients with asymptomatic DD.37

Whether diverticulosis results from or causes inflammation and whether progression to diverticulitis

likewise results from or causes inflammation is an open question. Similar questions have existed

regarding an interrelation between IBS and DD. A longitudinal study of administrative and clinical data

from the Veterans’ Association found the hazard ratio for developing IBS after an episode of

diverticulitis was 4.7 compared to controls even though the study group of older males (mean age 62

years) is generally a lower risk group for IBS.38 Whether these “new IBS” cases should actually be

regarded as segmental diverticulitis that could be managed by resection as opposed to a pan-colonic

phenomenon has not been demonstrated.

Pathogenesis of Diverticulitis

4 The process by which a subset of people with diverticulosis develop diverticulitis has yet to be

explained. Overwhelming inflammatory changes that develop with perforation or other complications of

diverticulitis likely obscure subtle histologic details that might explain the pathogenesis of the disease.

Traditionally, it has been postulated that mechanical obstruction by food or fecal material of a

diverticulum leads to bacterial proliferation, gas, and toxin production in the occluded diverticulum,

causing diverticulitis. However, the largely extracolonic manifestations of diverticulitis (phlegmon,

abscess, and free perforation) suggest micro- or macroperforation as the inciting event, possibly as a

kind of diverticular “blow-out” secondary to segmentation-type contractions or high-pressure waves. In

recent years (and perhaps with the rising number of patients undergoing screening colonoscopy),

peridiverticular inflammation has been identified, often in asymptomatic patients. Diverticulitisassociated colitis is of unrecognized clinical significance, partly because so many patients with these

findings are asymptomatic and partly because the findings are not uniformly evident in patients

requiring surgical therapy for diverticulitis. It has been suggested that low-grade inflammation could

alter bowel motility and thereby contribute to diverticular perforation risk. Endoscopists are cautioned

1833

 

Chapter 69

Diverticular Disease

Lauren A. Kosinski, Kirk Ludwig, and Mary F. Otterson

Key Points

1 Diverticulosis and its complications are common in Western societies.

2 Sigmoid and left colon involvement predominate in non-Asian industrialized nations; the rectum is

spared.

3 Lack of dietary fiber, colonic anatomy, and disordered colonic motility are likely contributors to the

development of diverticulosis.

4 New data suggest that uncomplicated diverticulitis may be an inflammatory rather than an infectious

process.

5 Computed tomography (CT) imaging markedly improves diagnostic accuracy and treatment

planning.

6 Early, judicious use of contrast enema studies or colonoscopy can safely help distinguish diverticular

stricture from cancer.

7 Antibiotic therapy, bowel rest, and percutaneous drainage of diverticular abscesses can often convert

surgical emergencies into elective operations.

8 Bowel resection with primary anastomosis and temporary, diverting loop stoma is favored in acute

cases when possible; single-stage operations are preferred for elective cases.

9 Early enthusiasm for emergency laparoscopic washout and repair of diverticular perforations has not

been supported by prospective, randomized trials.

10 Criteria for elective colon resection for diverticulitis are evolving and trending toward more

restrictive indications.

Diverticular disease (DD) is one of the most common problems treated by surgeons, and management

strategies have evolved significantly in the last 15 years. A short time ago, virtually all cases of acute

diverticulitis were treated as surgical emergencies. Patients routinely underwent staged procedures and

were taken to the operating room for sigmoid colectomy and temporary end-colostomy within hours of

admission. Surgical and radiologic innovations have introduced less invasive options for managing even

complex disease. Surgery, when necessary, is often performed electively or semi-electively.

Key among recent major shifts in the diagnosis and management of DD are (a) strategies for

converting diverticular surgical emergencies into single-stage, elective operations with avoidance of a

colostomy; (b) utilization of computed tomography (CT) imaging for diagnosis and CT-guided

percutaneous drainage of diverticular abscesses; (c) reconsideration of indications for elective surgery;

and (d) emergence of laparoscopic surgical techniques as state-of-the-art approaches for DD. Fear that

younger patients with diverticulitis or older patients with a single episode of diverticulitis were at

increased risk of perforated diverticulitis and colostomy construction has been allayed by data that show

no increased risk. These data and recognition that even elective resection for DD may have higher

complication and colostomy rates than elective colon cancer resections

1 have fueled concern that the

cure might be worse than the disease and are shaping more stringent guidelines for elective resection.

CLASSIFICATION

1 Diverticulosis refers to the presence, whether symptomatic or asymptomatic, of colonic diverticula. In

common medical usage, this refers to the presence of pseudodiverticula in which mucosa and submucosa

have herniated through the circular layer of the muscularis propria, a very common acquired condition

in Western societies. True diverticula are rare. DD refers to the broad range of symptoms and findings

associated with diverticulosis and includes diverticulitis, an inflammatory and often infectious process.

1829

Inflammation can be acute or chronic. Acute inflammation can present with a pericolonic phlegmon,

colon perforation leading to focal abscess formation, or generalized purulent or fecal peritonitis. Acute

and chronic inflammation can result in fistula formation between the involved bowel segment and the

bladder, vagina, or skin. With chronic or recurrent inflammation, scarring of the involved segment can

cause bowel wall thickening, dysmotility, and stricture, which may present as altered bowel habit or

even frank obstruction.

ANATOMY

2 Colonic diverticula are pulsion diverticula that occur in predictable sites on the bowel wall. Likewise,

the pattern of segmental involvement of the colon and its progression are predictable. The sigmoid

colon is at highest risk and is affected in 95% of patients. Involvement is isolated to the sigmoid colon

in 30% to 60% of cases. Total colonic involvement occurs in 7% to 10% of cases.2 The rectum is almost

always spared. This segmental pattern of involvement is not observed in Asia, where 70% of

pseudodiverticula are isolated to the right colon and cecum. The reason for this discrepancy is not

known. Right colon pseudodiverticula are more likely to be solitary and tend to originate near the

ileocecal valve.3,4 When true colonic diverticula develop, they are also more likely to be right sided;

however, they are still much less common than pseudodiverticula of the right colon.

INCIDENCE

Diverticulosis is rare in nonindustrialized, less affluent societies. The French surgeon Alexis Littre is

credited with first describing diverticulosis in 1700, but it was not until the mid-1800s that there were

reports in the medical literature about the disease process and its treatment.5 The prevalence of

diverticulosis increased after the industrial revolution and through this century. Even before 1940, it

was recognized infrequently; retrospective reviews of colon radiographs and pathologic specimens

record an incidence of 5% to 10%.6 An incidence of 46% in people 51 years of age and older was

reported by Hughes from postmortem studies in 200 cadavers (Table 69-1).7 Incidence as a function of

gender varies by study, some studies citing an increased incidence among men and others finding a

higher incidence among women. It may be that the spectrum of complications and the age at which they

develop are gender specific. The majority of people with diverticulosis remain asymptomatic; only 15%

to 30% will go on to develop symptomatic disease.8 Of these, only 30% will require operative

treatment.9 In the United States in 1998, 2.2 million cases of DD were treated at an estimated cost of $2

billion.10 In 2005, DD was the primary diagnosis in 307,000 hospital discharges and accounted for 1.6

million inpatient days of care.11

Table 69-1 Incidence of Diverticulosis in Western Society

ETIOLOGY

3 Neither the etiology of diverticulosis nor factors causing progression to symptomatic disease have

been rigorously defined, but lack of dietary fiber, colonic dysmotility, and colonic structural

abnormalities and age-related changes have all been implicated. There may be an association between

irritable bowel syndrome (IBS) and diverticulitis, the microbiome may be a mediator in diverticular

inflammation, and idiopathic inflammation may also contribute to the DD spectrum.

Structural/Anatomic Factors

In the colon, the outer, longitudinal layer of the muscularis propria is condensed in three longitudinal

bands called the taeniae coli. One of these runs along the mesenteric aspect of the colon; the other two

are antimesenteric in location (Fig. 69-1). Mesenteric blood vessels encircle the colon and penetrate the

circular muscle in the intertaenial areas between the mesenteric taenia and the two antimesenteric

taeniae. Pseudodiverticula develop at areas where these vessels pass through muscle.12 Postmortem

1830

 

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