Open access peer-reviewed chapter

Diverticular Disease

Written By

Can Konca, Suleyman Utku Celik and Cihangir Akyol

Submitted: May 24th, 2017 Reviewed: May 17th, 2018 Published: September 5th, 2018

DOI: 10.5772/intechopen.78763

Chapter metrics overview

992 Chapter Downloads

View Full Metrics

Abstract

Diverticulosis is a common problem, especially in industrialized countries. The main risk factors for the development of diverticular disease are physical inactivity and consumption of a low-fiber diet. Among the population with diverticulosis, only 10–25% of the patients develop diverticulitis. Computed tomography (CT) scans are very helpful for diagnosis and deciding the treatment strategy. Patients with acute diverticulitis usually have a good response to conservative therapy. However, some of the patients present with complications such as perforation, fistula, abscess, stricture, and obstruction. Depending on disease severity, they commonly require surgical or radiologic intervention. Despite lots of contradictory results on treatment approaches, recent guidelines tend to be less invasive than the ones in the past. As a result, less invasive treatment protocols, including nonsurgical follow-up, percutaneous drainage, minimally invasive surgery and resection with primary anastomosis, are more commonly used than the more invasive Hartmann procedure. In this chapter, we discuss the clinical characteristics, diagnostic workup and different treatment approaches in the management of diverticular diseases.

Keywords

  • diverticular diseases
  • diverticulitis
  • diverticulosis
  • epidemiology
  • management

1. Introduction

Diverticulosis is a common medical problem, most frequently in industrialized countries. It is defined as saccular outpouchings of the bowel wall and is usually located at the sigmoid colon. Diverticulosis is not a disease per se but a condition, and thus, it is usually asymptomatic. When these saccular outpouchings become obliterated, inflammation in bowel wall and hence diverticulitis develops. There are many types of diverticular disease with respect to its clinical presentation. Usually, it presents as a mild and medically treatable uncomplicated diverticulitis. However, complicated diverticulitis such as abscess, perforation, fistula or obstruction can be the first presentation as well. Diverticular hemorrhage is another complication of diverticulosis, but inflammation is not a factor in its pathophysiology and it is a different clinical condition apart from diverticulitis. As a result, diverticular hemorrhage will not be discussed in this chapter.

As its prevalence rises with industrialization, numerous efforts have been made to find the best treatment option. Although some debates are still ongoing, minimally invasive treatments become more common, and necessity of high morbidity-related procedures like the Hartmann procedure is more questionable nowadays.

Advertisement

2. Incidence

In Western countries, the prevalence depends on age. The incidence increases with age, and nearly 70% of the 80-year-old population has diverticulosis [1]. Among the population with diverticulosis, only 10–25% of the patients develop diverticulitis, 10–20% of those patients with diverticulitis will be hospitalized for treatment and surgical therapy will be reserved only for 20–50% of these patients [2].

The left-sided diverticular disease is more common in western countries; on the other hand, the right-sided diverticular disease is more common in eastern countries. In the United States, the localization of diverticular disease involves sigmoid and left colon in 95% of the patients, and 95% of the surgical candidates for diverticular disease have sigmoid colon diverticulosis [3].

Recent studies have estimated that symptomatic diverticulitis under the age of 65 tends to have a male predominance and have more severe CT findings. Additionally, diverticular bleeding is more common in men, whereas obstructions are more common in women [4, 5].

Advertisement

3. Pathophysiology and etiology

The saccular outpouching in diverticulosis is not a true diverticula. They do not contain all layers of the bowel wall; instead, they are formed by the herniation of mucosal and submucosal layers of the bowel wall through the muscular layer. Thus, they are called ‘false’ or ‘pulsion’ diverticula. Diverticular disease tends to occur at the weakest points of the colon wall where the vasa recta penetrate the circular muscle. As a result, diverticula are localized at each side of the mesenteric taenia and on the mesenteric border of the two antimesenteric taenias [6]. Also, the structure of the colon wall contains differences from normal colon wall such as thickened circular muscle, narrow lumen and shortened taenia [7]. Besides the structural changes in the colonic wall, alterations in colonic motility have a role in the development of diverticular disease. Increased colonic motility causes enhanced longitudinal haustral contractions and temporary isolation of a segment of colon, a process called segmentation. As a result, segmentation generates a pulsion force causing visible distension of the local diverticula [7].

Moreover, the imbalance of the neurotransmitter spectrum reported in diverticular disease involves both excitatory agents, such as acetylcholine and substance P, and inhibitory agents, such as nitric oxide and vasoactive intestinal polypeptide (VIP) released by enteric nerve cells [8, 9].

On microscopic examination, the structure of the taenia contains more elastin, which is increased over 200% compared to controls, and colonic collagen changes are similar to the ones that occur with aging [7, 8, 9]. These structural changes are similar to connective tissue disorders such as Marfan syndrome or Ehler-Danlos syndrome in which diverticulosis tends to occur earlier than the normal population [10].

The localization of the colonic segment of diverticular disease and complications, such as diverticulitis, microperforation and abscess, depends on the intraluminal pressure of the colonic segment. As a result, sigmoid colon is the most common localization for the disease since it has the highest intraluminal pressure and increased motility index with regard to its smaller diameter [3].

Advertisement

4. Risk factors

The main risk factors for the development of diverticular disease are physical inactivity and consumption of a low-fiber diet [11, 12, 13]. Fiber from fruits and vegetables has the most protective effect against diverticulosis development while higher consumption of red meat and fat increases the incidence [11, 14]. Thus, the incidence of diverticulosis increases with a Western-style diet [11, 15]. On the other side, diverticulosis is less common among vegetarians [16]. As the fiber intake increases, the stool becomes more bulky and lesser segmentation forms in the colon and diameter of the sigmoid colon increases. By that way, transportation of the stool becomes easier with lower intracolonic pressures obtained [3].

Other identified risk factors for the development of complicated diverticular disease are smoking (three times higher risk of developing complications), NSAID use, steroid use, renal failure, and organ transplantation [17, 18].

Several studies have been evaluated the role of age in diverticular disease and diverticulitis. The incidence of diverticular disease increases with age. At the age of 40, its incidence is 5%, whereas at the age of 80 the incidence rises up to 80% [19]. As the age gets older, diverticula are more proximally located and increased in number. On the other hand, diverticulitis at younger ages is more likely to develop complications [20, 21].

Recent studies demonstrated that obesity and higher body mass index are also associated with an increased incidence of diverticulitis, especially patients under the age of 40 years [21, 22, 23, 24]. Additionally, an association between increased cross-sectional visceral fat area and complicated diverticulitis had been demonstrated [25].

Advertisement

5. Signs and symptoms

The degree of inflammation and existing complications are the two main factors determining the clinical presentation of diverticular disease.

In acute diverticulitis, the most common complaint is abdominal pain. Since sigmoid colon is the most common localization of diverticulitis in adults, the pain is usually located in the left lower quadrant. Variable localizations can occur depending on the anatomy of the sigmoid colon such as right lower quadrant or suprapubic pain. Especially in Asian populations, cecal diverticulitis may present as right lower quadrant pain [26, 27, 28].

About 50% of the patients with acute diverticulitis have constipation, while 25–35% are accompanied by diarrhea [29].

The degree and radiation of pain vary according to the severity and extent of inflammation. Early in the presentation, a localized left lower quadrant sensitivity can be observed while acute abdomen due to peritoneal irritation develops after perforation. Dysuria and urinary urgency may occur as well due to the presence of inflammation which is in close proximity to the bladder [30]. The persistent abdominal pain can be based on increased pain-mediating neurotransmitters (e.g. galanin, neuropeptide K) and enteric nerve fiber remodeling most likely due to postinflammatory reactions—similar to irritable bowel syndrome [7].

Nausea and vomiting can be present due to peritoneal irritation or the development of complications such as bowel obstruction [30].

Advertisement

6. Laboratory findings

In patients with acute diverticulitis, inflammation-related leukocytosis and elevated C-reactive protein (CRP) may be detected. Nevertheless, in uncomplicated patients, leukocyte levels may remain within the normal range of up to 45% of patients [31]. Serum amylase levels may be increased in patients with perforation and colonic flora may contaminate urine cultures if colovesical fistula develops.

Advertisement

7. Imaging

Abdominal X-rays may detect subdiaphragmatic free air due to a perforation in patients with acute diverticulitis. However, direct X-rays have no diagnostic value in patients with uncomplicated diverticulitis.

Abdominal ultrasonography is a preferred method of imaging since it is cheap and noninvasive. However, it is an operator-dependent method and has an inferior sufficiency in the evaluation of luminal organs and ruling out other causes of abdominal pain. Hypoechoic peridiverticular inflammatory reaction, detection of a peridiverticular or mural abscess, thickening of the intestinal wall more than 4 mm in the area of abdominal sensitivity and presence of diverticula in other segments of bowel are among the ultrasonographic findings that support a diagnosis of acute diverticulitis [32].

CT is the most useful imaging technique for diagnosing acute diverticulitis with a sensitivity of 94% and a specificity of 99% [33]. Additionally, it allows assessment of the complications and other causes of abdominal pain. CT findings that support the diagnosis of acute diverticulitis are the presence of diverticula in the bowel, pericolic fat stranding, colonic wall thickening that is more than 4 mm and abscess formation (Figure 1) [34].

Figure 1.

Computed tomography scan demonstrates infiltration of the fat surrounding the sigmoid colon (small arrow) whose wall is thickened and irregular (big arrow).

It is a fast and reliable test and also serves as a guide for percutaneous drainage. It can also be used to determine the severity and extent of the disease. Ambrosetti et al. was first to classify the disease severity according to the CT findings [31]. They divided acute diverticulitis into two groups as mild and severe according to the CT findings (Table 1). Surgical intervention was more frequently needed in patients who had severe disease. Similarly, in people who had severe disease under the age of 50 years, recurrences and complications were more frequent [31]. According to another study, the markers of nonoperative treatment failure were defined as the presence of abscess formation or extraluminal air >5 mm in diameter [35].

Mild diverticulitisWall thickening (>5 mm)
Pericolic fat stranding
Severe diverticulitisMild diverticulitis findings and at least one of the followings:
  • Abscess

  • Extraluminal air

  • Extraluminal contrast

Table 1.

Ambrosetti CT criteria for diverticulitis severity.

A modified Hinchey classification system was defined by the addition of preoperative CT findings to the parameters of Hinchey classification used in the evaluation of acute diverticulitis (Table 2) [36, 37, 38]. In the modified system, stage I was divided into stage Ia characterized by the presence of pericolic inflammation and phlegmon and stage Ib with pericolic abscess (Figure 2). While BT can provide sufficient discrimination in stages 0, I and II, it is insufficient in distinguishing stages III and IV, which are purulent and feculent peritonitis, respectively [36].

StageFindings
0
Ia
Ib
II
III
IV
Mild clinical diverticulitis
Confined pericolic inflammation phlegmon
Confined pericolic abscess within sigmoid mesocolon
Pelvic, distant intraperitoneal abscess
Generalized purulent peritonitis
Feculent peritonitis

Table 2.

Modified Hinchey classification system for acute diverticulitis.

Figure 2.

Coronal view of the inflamed sigmoid colon with characteristic findings of diverticular abscess.

Another method that can be used for diagnosis is MRI. However, it is slower, more expensive and less accessible than CT and thus still not routinely used. It may be useful in situations where CT is insufficient such as colovesical or colovaginal fistulas.

Advertisement

8. Differential diagnosis

The differential diagnosis of acute diverticulitis includes other causes of lower abdominal pain. Colorectal cancer; acute appendicitis; inflammatory bowel disease; infectious colitis; ischemic colitis; bowel obstruction; irritable bowel syndrome; gynecologic causes like tubo-ovarian abscess, ectopic pregnancy and ovarian torsion and urologic causes like urolithiasis, cystitis and pyelonephritis should be excluded before establishing the diagnosis of acute diverticulitis. Many of these entities can be ruled out by history, physical examination, laboratory studies and imaging.

Colorectal cancer (CRC) is probably the most important and challenging condition in the diagnostic evaluation since it can mimic the clinical features and CT findings of acute diverticulitis such as bowel wall thickening. The findings that are suggestive for acute diverticulitis, in that case, are the presence of pericolonic and mesenteric inflammation, colonic segment involvement of more than 10 cm and absence of metastatic mesenteric lymph nodes [39, 40]. In almost 10–20% of the cases, CRC and acute diverticulitis differentiation cannot be clearly established and endoscopic evaluation needs to be scheduled after the resolution of inflammatory process [41].

Advertisement

9. Role of endoscopy

In acute diverticulitis, endoscopic evaluation of the colon is not recommended because of the risk of free perforation [42]. But in order to exclude underlying malignancy, colonoscopic evaluation is recommended after at least 6 weeks from the resolution of clinical findings (Figure 3) [42, 43, 44]. The incidence of finding CRC after an acute diverticulitis episode is between 2.8 and 3.4% [45, 46].

Figure 3.

Endoscopic visualization of diverticulosis.

Advertisement

10. Treatment of acute diverticulitis

In acute diverticulitis, treatment protocol depends on the severity of the disease. Generally, mild diverticulitis can be treated in outpatient settings. On the other hand, complicated diverticulitis usually requires hospitalization and surgical intervention.

10.1. Treatment of uncomplicated diverticulitis

In mild cases without fever and marked peritonitis, outpatient treatment is recommended [47]. Routine antibiotic usage is still contradictory in the guidelines [47, 48, 49, 50]. If antibiotic treatment is planned, the coverage of the therapy should include Gram-negative rods, Gram-positive rods and especially the anaerobic flora of the colon [47, 51]. Most common microorganisms are Escherichia coliand Bacteroides fragilis[52, 53]. There is no clear recommendation for dietary restriction for outpatient treatment. A diet rich in fiber (20–30 g/daily) is recommended for the patients with diverticulosis to lower the risk of developing diverticulitis [11, 54]. Recent studies demonstrated that combination of mesalamine use with antibiotics lowers symptom severity and prevents disease recurrence [55, 56, 57]. Probiotic use is another topic under investigation in the management of acute diverticulitis [58, 59, 60].

Patients with fever, immunosuppression, sepsis, severe abdominal pain or diffuse peritonitis, those who failed outpatient treatment and intolerant of oral intake, and those with significant comorbidities or older age should be treated as an inpatient. Restriction of oral intake until the resolution of the symptoms and intravenous antibiotics are recommended [61, 62, 63].

Traditional teaching for the treatment of recurrent uncomplicated diverticulitis used to be planning an elective operation after the second acute episode [64]. But recent studies showed that in patients followed up with a nonoperative management protocol for uncomplicated diverticulitis, only 5.5% of them required emergency operations [65, 66]. As a result, waiting until third or even fourth episode before deciding for an elective operation has been defined as a more cost-effective management plan with less morbidity [47, 67]. Also, it is found that the probability of surgery after the first hospitalized attack was the same after three attacks [66].

Today, it is thought that after a conservatively managed episode, diverticular disease usually follows a rather benign clinical course and that complications develop mostly at first presentation [33]. Therefore, elective sigmoid resections should be restricted for use in treating complicated disease, such as symptomatic stenosis, fistulas to an adjacent organ or recurrent diverticular bleeding [33, 64, 65, 66].

10.2. Treatment of complicated diverticular disease

Complications of diverticulitis are perforation, fistula, abscess, stricture and obstruction. Depending on disease severity, they usually require surgical or radiologic intervention. While parenteral antibiotics and bowel rest could be adequate for the treatment of mild cases, exploratory laparotomy could be needed for patients with severe clinical findings [65].

10.3. Diverticular abscess

In acute diverticulitis, diverticular abscess occurs between 16 and 56% of the patients and can be localized in pericolic, pelvic, hepatic or retroperitoneal areas [38, 68]. CT is the most effective tool for diagnosis since it can identify the size, localization, and surrounding structures that preclude percutaneous drainage (Figure 4). The size of the abscess is essential for the treatment plan, as abscesses less than 4 cm usually resolve with parenteral antibiotics. On the other hand, larger abscesses require percutaneous drainage or surgical drainage if they are not suitable for percutaneous access (Figure 5) [38, 63, 69]. Transabdominal route is the preferred method for percutaneous drainage if possible [70]. But percutaneous drainage is amenable in 20–30% of diverticular abscesses with a 20–30% failure rate [71]. In multilocular and complex abscesses, the failure rate is higher than simple unilocular abscesses [70].

Figure 4.

Computed tomography revealed a modified Hinchey stage II diverticulitis.

Figure 5.

A management for diverticular abscess.

Percutaneous drainage does not negate the need for surgery, but in 60–80% of the patients, surgery can be performed in a single stage and electively [47, 72]. Traditionally, patients with diverticular abscess referred for surgery because of the high risk of recurrent sepsis [37]. With recent studies showing asymptomatic follow-up of the patients treated with successful percutaneous or surgical drainage, the need for elective surgery becomes questionable [38, 73, 74]. As a result, recent guidelines do not recommend routine elective resections after successful nonsurgical treatment of diverticular abscess [47]. On the other hand, symptomatic or immunocompromised patients should be referred for elective surgery [47, 72].

10.4. Perforated diverticulitis

Only 1–2% of the patients with acute diverticulitis presents with free perforation. There are two types of perforation in acute diverticulitis: purulent peritonitis and feculent peritonitis. The differential diagnosis of these conditions is difficult with CT and often requires exploratory laparoscopy or laparotomy. Usually, patients have a fever, acute abdominal findings on examination and significant leukocytosis. Free perforation of acute diverticulitis usually occurs on the first attack and presents with abdominal distention with diffuse tenderness, rigidity and rebound tenderness. The condition can lead to sepsis and septic shock if not treated with a rapid intervention and the mortality rates approach 20% [75, 76].

The goal of the treatment is to eliminate the septic focus. Traditionally, the Hartmann procedure was the choice of treatment, but it has a high morbidity and mortality rate and requires a second major abdominal surgery for reversal colostomy. Studies have shown that nearly one-third of the patients could not undergo the second reversal operation and have permanent colostomy, especially in the elderly population [77]. As a result, resection with primary anastomosis has been studied as an alternative method for the treatment of perforated diverticulitis. Several studies have shown superior results with that procedure compared to the Hartmann procedure depending on the patient’s condition [76, 78]. Recent guidelines recommend open or laparoscopic resection with primary anastomosis in hemodynamically stable patients [47]. The factors affecting the choice of treatment are hemodynamic instability, the severity of diffuse peritonitis, ischemia or edema of the bowel at the anastomotic segment, immunocompromised state and malnutrition.

Recent studies investigated laparoscopic lavage for the definitive treatment of Hinchey III diverticulitis and considered it as a safe approach for selected patients [47, 79]. On the other hand, there are conflicting results in the literature against laparoscopic lavage [80, 81, 82]. Further trials will be needed for the standardization of this technique.

10.5. Fistulas

Approximately 2% of the patients with acute diverticulitis will develop fistula formation to the adjacent structures [83]. Fistula formation is a result of spontaneous rupture and decompression of an abscess to an adjacent structure like urinary bladder, vagina, colon, small intestine, uterus or abdominal wall and skin. They usually do not require emergency surgery. Colovesical fistula can be seen in 65% of the cases and is the most common type of fistula [84, 85, 86]. Because of the anatomic blockage of uterus and vagina in women, colovesical fistulas are more common in men. Patients with colovesical fistulas present with polymicrobial urinary infections, pneumaturia, and fecaluria. Air or contrast in the bladder can be seen on CT scans. Cystoscopy and colonoscopy should be done in those patients to exclude bladder or colon cancer involvement.

In women who have undergone prior hysterectomy, colovaginal fistulas are more common. Fecal vaginal discharge and passage of air per vagina can be seen in these patients.

Surgery is indicated when fistula formation diagnosed. Resection of the colonic segment and suture repair of the affected structure with interpositioning of the omentum between anastomosis and the repair site is the treatment of choice [87, 88].

10.6. Diverticular stricture/obstruction

Recurrent attacks of diverticulitis can lead to sigmoid stricture and less commonly obstruction. Because obstructing colon cancer is far more common than diverticular stricture, the differential diagnosis should be focused to exclude malignancy.

The treatment plan depends on the severity of the obstruction. Patients with partial obstruction can be treated in elective settings; on the other hand, patients with complete obstruction will require emergency surgery. Options for surgery include the Hartmann procedure, resection and primary anastomosis with or without on-table lavage [89, 90].

11. Prognosis

Among patients with diverticulosis, only 4% will develop acute diverticulitis and 15% of these patients will require surgical treatment [91, 92]. Although the incidence is as low as 16% below 45 years of age, it has been proposed that younger individuals have the more severe disease but require lesser surgical intervention [31].

Mortality rates of the patients with peritonitis vary between 0 and 36% depending on the patients’ characteristics. On the other hand, elective colectomy has a low rate of mortality rate around 1% [93]. The anastomotic leakage rate is also higher in Hinchey III or IV diverticulitis (8–22%) than elective colectomy (1–3%) [76, 93, 94, 95]. On the other hand, Hartmann reversal rates are between 20 and 50% depending on the patients’ comorbidities and condition [96, 97, 98].

Recurrent diverticulitis or its symptoms develop at a rate of 3–13% after elective resection [99, 100]. The most important determinant is the level of the anastomosis [100]. When anastomosis is established with the distal sigmoid colon, the incidence of recurrence is 12.5% while the incidence is 6.7% for the anastomosis with the proximal rectum [101]. Thus, resection of the sigmoid colon entirely and anastomosis to the proximal rectum is recommended. It is not necessary to resect all the diverticular segments more proximal than sigmoid colon but the proximal resection margin should be soft pliable bowel [63].

Immunocompromised patients usually present with severe and complicated disease. Studies have shown that approximately 40% of them had free perforation and emergency surgery required in 60% of the patients. As a result, they have higher postoperative morbidity and mortality rates as 65 and 40% accordingly [102, 103, 104].

12. Conclusion

Diverticular disease is a common condition in developed countries. In order to lower the rising incidence, population-based dietary modifications should be considered. Recent treatment guideline recommendations are focused on less invasive and elective solutions. As a result, a shift to nonsurgical follow-up or elective minimally invasive surgery from high morbidity-related Hartmann procedure should be done whenever possible, depending on the patients’ condition, to achieve lesser morbidity and mortality rates.

Conflict of interest

The authors declare that they have no conflict of interest.

References

  1. 1. Everhart JE, Ruhl CE. Burden of digestive diseases in the United States. Part II: Lower gastrointestinal diseases. Gastroenterology. 2009;136(3):741-754
  2. 2. Somasekar K, Foster ME, Haray PN. The natural history diverticular disease: Is there a role for elective colectomy? Journal of the Royal College of Surgeons of Edinburgh. 2002;47(2):481-482, 484
  3. 3. Bogardus ST Jr. What do we know about diverticular disease? A brief overview. Journal of Clinical Gastroenterology. 2006;40(Suppl 3):S108-S111
  4. 4. Hall JF et al. Colonic diverticulitis: Does age predict severity of disease on CT imaging? Diseases of the Colon and Rectum. 2010;53(2):121-125
  5. 5. McConnell EJ, Tessier DJ, Wolff BG. Population-based incidence of complicated diverticular disease of the sigmoid colon based on gender and age. Diseases of the Colon and Rectum. 2003;46(8):1110-1114
  6. 6. Parks TG. Natural history of diverticular disease of the colon. A review of 521 cases. British Medical Journal. 1969;4(5684):639-642
  7. 7. Hobson KG, Roberts PL. Etiology and pathophysiology of diverticular disease. Clinics in Colon and Rectal Surgery. 2004;17(3):147-153
  8. 8. Stumpf M et al. Increased distribution of collagen type III and reduced expression of matrix metalloproteinase 1 in patients with diverticular disease. International Journal of Colorectal Disease. 2001;16(5):271-275
  9. 9. Whiteway J, Morson BC. Elastosis in diverticular disease of the sigmoid colon. Gut. 1985;26(3):258-266
  10. 10. Wess L et al. Cross linking of collagen is increased in colonic diverticulosis. Gut. 1995;37(1):91-94
  11. 11. Aldoori WH et al. A prospective study of diet and the risk of symptomatic diverticular disease in men. The American Journal of Clinical Nutrition. 1994;60(5):757-764
  12. 12. Aldoori WH et al. Prospective study of physical activity and the risk of symptomatic diverticular disease in men. Gut. 1995;36(2):276-282
  13. 13. Aldoori WH et al. A prospective study of dietary fiber types and symptomatic diverticular disease in men. The Journal of Nutrition. 1998;128(4):714-719
  14. 14. Manousos O et al. Diet and other factors in the aetiology of diverticulosis: An epidemiological study in Greece. Gut. 1985;26(6):544-549
  15. 15. Kiguli-Malwadde E, Kasozi H. Diverticular disease of the colon in Kampala, Uganda. African Health Sciences. 2002;2(1):29-32
  16. 16. Nair P, Mayberry JF. Vegetarianism, dietary fibre and gastro-intestinal disease. Digestive Diseases. 1994;12(3):177-185
  17. 17. Hwang SS et al. Diverticulitis in transplant patients and patients on chronic corticosteroid therapy: A systematic review. Diseases of the Colon and Rectum. 2010;53(12):1699-1707
  18. 18. Papagrigoriadis S et al. Smoking may be associated with complications in diverticular disease. The British Journal of Surgery. 1999;86(7):923-926
  19. 19. Kaushik M et al. Minimally invasive management of complicated diverticular disease: Current status and review of literature. Digestive Diseases and Sciences. 2016;61(3):663-672
  20. 20. Ouriel K, Schwartz SI. Diverticular disease in the young patient. Surgery, Gynecology & Obstetrics. 1983;156(1):1-5
  21. 21. Schauer PR et al. Virulent diverticular disease in young obese men. American Journal of Surgery. 1992;164(5):443-446; discussion 446-448
  22. 22. Aldoori WH et al. A prospective study of alcohol, smoking, caffeine, and the risk of symptomatic diverticular disease in men. Annals of Epidemiology. 1995;5(3):221-228
  23. 23. Dobbins C et al. The relationship of obesity to the complications of diverticular disease. Colorectal Disease. 2006;8(1):37-40
  24. 24. Rosemar A, Angeras U, Rosengren A. Body mass index and diverticular disease: A 28-year follow-up study in men. Diseases of the Colon and Rectum. 2008;51(4):450-455
  25. 25. Jeong JH et al. Correlation between complicated diverticulitis and visceral fat. Journal of Korean Medical Science. 2011;26(10):1339-1343
  26. 26. Jacobs DO. Clinical practice. Diverticulitis. The New England Journal of Medicine. 2007;357(20):2057-2066
  27. 27. Sugihara K et al. Diverticular disease of the colon in Japan. A review of 615 cases. Diseases of the Colon and Rectum. 1984;27(8):531-537
  28. 28. Markham NI, Li AK. Diverticulitis of the right colon--experience from Hong Kong. Gut. 1992;33(4):547-549
  29. 29. Konvolinka CW. Acute diverticulitis under age forty. American Journal of Surgery. 1994;167(6):562-565
  30. 30. Feuerstein JD, Falchuk KR. Diverticulosis and diverticulitis. Mayo Clinic Proceedings. 2016;91(8):1094-1104
  31. 31. Ambrosetti P et al. Acute left colonic diverticulitis: A prospective analysis of 226 consecutive cases. Surgery. 1994;115(5):546-550
  32. 32. Maconi G, Carmagnola S, Guzowski T. Intestinal ultrasonography in the diagnosis and management of colonic diverticular disease. Journal of Clinical Gastroenterology. 2016;50(Suppl 1):S20-S22
  33. 33. Lameris W et al. Graded compression ultrasonography and computed tomography in acute colonic diverticulitis: Meta-analysis of test accuracy. European Radiology. 2008;18(11):2498-2511
  34. 34. Hulnick DH et al. Computed tomography in the evaluation of diverticulitis. Radiology. 1984;152(2):491-495
  35. 35. Poletti PA et al. Acute left colonic diverticulitis: Can CT findings be used to predict recurrence? AJR. American Journal of Roentgenology. 2004;182(5):1159-1165
  36. 36. Baker ME. Imaging and interventional techniques in acute left-sided diverticulitis. Journal of Gastrointestinal Surgery. 2008;12(8):1314-1317
  37. 37. Kaiser AM et al. The management of complicated diverticulitis and the role of computed tomography. The American Journal of Gastroenterology. 2005;100(4):910-917
  38. 38. Stocchi L. Current indications and role of surgery in the management of sigmoid diverticulitis. World Journal of Gastroenterology. 2010;16(7):804-817
  39. 39. Padidar AM et al. Differentiating sigmoid diverticulitis from carcinoma on CT scans: Mesenteric inflammation suggests diverticulitis. AJR. American Journal of Roentgenology. 1994;163(1):81-83
  40. 40. Chintapalli KN et al. Diverticulitis versus colon cancer: Differentiation with helical CT findings. Radiology. 1999;210(2):429-435
  41. 41. Balthazar EJ et al. Limitations in the CT diagnosis of acute diverticulitis: Comparison of CT, contrast enema, and pathologic findings in 16 patients. AJR. American Journal of Roentgenology. 1990;154(2):281-285
  42. 42. Lahat A et al. Role of colonoscopy in patients with persistent acute diverticulitis. World Journal of Gastroenterology. 2008;14(17):2763-2766
  43. 43. Mortensen LQ et al. An 18-year Nationwide Cohort Study on the association between diverticulitis and colon cancer. Annals of Surgery. 2017;265(5):954-959
  44. 44. Sharma PV et al. Systematic review and meta-analysis of the role of routine colonic evaluation after radiologically confirmed acute diverticulitis. Annals of Surgery. 2014;259(2):263-272
  45. 45. van de Wall BJ et al. Endoscopic evaluation of the colon after an episode of diverticulitis: A call for a more selective approach. International Journal of Colorectal Disease. 2012;27(9):1145-1150
  46. 46. Lau KC et al. Is colonoscopy still mandatory after a CT diagnosis of left-sided diverticulitis: Can colorectal cancer be confidently excluded? Diseases of the Colon and Rectum. 2011;54(10):1265-1270
  47. 47. Vennix S et al. Systematic review of evidence and consensus on diverticulitis: An analysis of national and international guidelines. Colorectal Disease. 2014;16(11):866-878
  48. 48. Hjern F et al. Conservative treatment of acute colonic diverticulitis: Are antibiotics always mandatory? Scandinavian Journal of Gastroenterology. 2007;42(1):41-47
  49. 49. de Korte N et al. Use of antibiotics in uncomplicated diverticulitis. The British Journal of Surgery. 2011;98(6):761-767
  50. 50. Chabok A et al. Randomized clinical trial of antibiotics in acute uncomplicated diverticulitis. The British Journal of Surgery. 2012;99(4):532-539
  51. 51. Byrnes MC, Mazuski JE. Antimicrobial therapy for acute colonic diverticulitis. Surgical Infections. 2009;10(2):143-154
  52. 52. Kellum JM et al. Randomized, prospective comparison of cefoxitin and gentamicin-clindamycin in the treatment of acute colonic diverticulitis. Clinical Therapeutics. 1992;14(3):376-384
  53. 53. Ribas Y et al. Prospective randomized clinical trial assessing the efficacy of a short course of intravenously administered amoxicillin plus clavulanic acid followed by oral antibiotic in patients with uncomplicated acute diverticulitis. International Journal of Colorectal Disease. 2010;25(11):1363-1370
  54. 54. Strate LL et al. Nut, corn, and popcorn consumption and the incidence of diverticular disease. JAMA. 2008;300(8):907-914
  55. 55. Di Mario F et al. Efficacy of mesalazine in the treatment of symptomatic diverticular disease. Digestive Diseases and Sciences. 2005;50(3):581-586
  56. 56. Tursi A, Brandimarte G, Daffina R. Long-term treatment with mesalazine and rifaximin versus rifaximin alone for patients with recurrent attacks of acute diverticulitis of colon. Digestive and Liver Disease. 2002;34(7):510-515
  57. 57. Carter F et al. Mesalamine (5-ASA) for the prevention of recurrent diverticulitis. Cochrane Database of Systematic Reviews. 2017;10:CD009839
  58. 58. Giaccari S et al. Long-term treatment with rifaximin and lactobacilli in post-diverticulitic stenoses of the colon. Rivista Europea per le Scienze Mediche e Farmacologiche. 1993;15(1):29-34
  59. 59. Trivedi CD, Das KM, Ndsg.Emerging therapies for diverticular disease of the colon. Journal of Clinical Gastroenterology. 2008;42(10):1145-1151
  60. 60. Ojetti V et al. The use of probiotics in different phases of diverticular disease. Reviews on Recent Clinical Trials. 2018;13(2):89-96
  61. 61. Alonso S et al. Outpatient treatment of patients with uncomplicated acute diverticulitis. Colorectal Disease. 2010;12(10 Online):e278-e282
  62. 62. Etzioni DA et al. Outpatient treatment of acute diverticulitis: Rates and predictors of failure. Diseases of the Colon and Rectum. 2010;53(6):861-865
  63. 63. Feingold D et al. Practice parameters for the treatment of sigmoid diverticulitis. Diseases of the Colon and Rectum. 2014;57(3):284-294
  64. 64. Rafferty J et al. Practice parameters for sigmoid diverticulitis. Diseases of the Colon and Rectum. 2006;49(7):939-944
  65. 65. Anaya DA, Flum DR. Risk of emergency colectomy and colostomy in patients with diverticular disease. Archives of Surgery. 2005;140(7):681-685
  66. 66. Chautems RC et al. Long-term follow-up after first acute episode of sigmoid diverticulitis: Is surgery mandatory? A prospective study of 118 patients. Diseases of the Colon and Rectum. 2002;45(7):962-966
  67. 67. Richards RJ, Hammitt JK. Timing of prophylactic surgery in prevention of diverticulitis recurrence: A cost-effectiveness analysis. Digestive Diseases and Sciences. 2002;47(9):1903-1908
  68. 68. Ambrosetti P et al. Prognostic factors from computed tomography in acute left colonic diverticulitis. The British Journal of Surgery. 1992;79(2):117-119
  69. 69. Siewert B et al. Impact of CT-guided drainage in the treatment of diverticular abscesses: Size matters. AJR. American Journal of Roentgenology. 2006;186(3):680-686
  70. 70. Golfieri R, Cappelli A. Computed tomography-guided percutaneous abscess drainage in coloproctology: Review of the literature. Techniques in Coloproctology. 2007;11(3):197-208
  71. 71. Soumian S et al. Management of Hinchey II diverticulitis. World Journal of Gastro-enterology. 2008;14(47):7163-7169
  72. 72. Lamb MN, Kaiser AM. Elective resection versus observation after nonoperative management of complicated diverticulitis with abscess: A systematic review and meta-analysis. Diseases of the Colon and Rectum. 2014;57(12):1430-1440
  73. 73. Garfinkle R et al. Diverticular abscess managed with long-term definitive nonoperative intent is safe. Diseases of the Colon and Rectum. 2016;59(7):648-655
  74. 74. Franklin ME Jr et al. Is laparoscopic surgery applicable to complicated colonic diverticular disease? Surgical Endoscopy. 1997;11(10):1021-1025
  75. 75. Constantinides VA et al. Primary resection with anastomosis vs. Hartmann's procedure in nonelective surgery for acute colonic diverticulitis: A systematic review. Diseases of the Colon and Rectum. 2006;49(7):966-981
  76. 76. Salem L, Flum DR. Primary anastomosis or Hartmann's procedure for patients with diverticular peritonitis? A systematic review. Diseases of the Colon and Rectum. 2004;47(11):1953-1964
  77. 77. Macias LH et al. Diverticulitis: Truly minimally invasive management. The American Surgeon. 2004;70(10):932-935
  78. 78. Abbas S. Resection and primary anastomosis in acute complicated diverticulitis, a systematic review of the literature. International Journal of Colorectal Disease. 2007;22(4):351-357
  79. 79. Myers E et al. Laparoscopic peritoneal lavage for generalized peritonitis due to perforated diverticulitis. The British Journal of Surgery. 2008;95(1):97-101
  80. 80. Angenete E et al. Laparoscopic lavage is feasible and safe for the treatment of perforated diverticulitis with purulent peritonitis: The first results from the randomized controlled trial DILALA. Annals of Surgery. 2016;263(1):117-122
  81. 81. Schultz JK et al. Laparoscopic lavage vs primary resection for acute perforated diverticulitis: The SCANDIV randomized clinical trial. JAMA. 2015;314(13):1364-1375
  82. 82. Vennix S et al. Laparoscopic peritoneal lavage or sigmoidectomy for perforated diverticulitis with purulent peritonitis: A multicentre, parallel-group, randomised, open-label trial. Lancet. 2015;386(10000):1269-1277
  83. 83. Young-Fadok TM et al. Colonic diverticular disease. Current Problems in Surgery. 2000;37(7):457-514
  84. 84. Woods RJ et al. Internal fistulas in diverticular disease. Diseases of the Colon and Rectum. 1988;31(8):591-596
  85. 85. Melchior S et al. Diagnosis and surgical management of colovesical fistulas due to sigmoid diverticulitis. The Journal of Urology. 2009;182(3):978-982
  86. 86. Bahadursingh AM, Longo WE. Colovaginal fistulas. Etiology and management. The Journal of Reproductive Medicine. 2003;48(7):489-495
  87. 87. Rothenberger DA, Wiltz O. Surgery for complicated diverticulitis. The Surgical Clinics of North America. 1993;73(5):975-992
  88. 88. Mileski WJ et al. One-stage resection and anastomosis in the management of colovesical fistula. American Journal of Surgery. 1987;153(1):75-79
  89. 89. Murray JJ et al. Intraoperative colonic lavage and primary anastomosis in nonelective colon resection. Diseases of the Colon and Rectum. 1991;34(7):527-531
  90. 90. Horesh N et al. Changing paradigms in the management of diverticulitis. International Journal of Surgery. 2016;33(Pt A):146-150
  91. 91. Shahedi K et al. Long-term risk of acute diverticulitis among patients with incidental diverticulosis found during colonoscopy. Clinical Gastroenterology and Hepatology. 2013;11(12):1609-1613
  92. 92. Morris AM et al. Sigmoid diverticulitis: A systematic review. JAMA. 2014;311(3):287-297
  93. 93. Landen S, Nafteux P. Primary anastomosis and diverting colostomy in diffuse diverticular peritonitis. Acta Chirurgica Belgica. 2002;102(1):24-29
  94. 94. Peppas G et al. Outcomes after medical and surgical treatment of diverticulitis: A systematic review of the available evidence. Journal of Gastroenterology and Hepatology. 2007;22(9):1360-1368
  95. 95. Richter S et al. One-stage sigmoid colon resection for perforated sigmoid diverticulitis (Hinchey stages III and IV). World Journal of Surgery. 2006;30(6):1027-1032
  96. 96. Boland E et al. Hartmann's colostomy reversal: Outcome of patients undergoing surgery with the intention of eliminating fecal diversion. The American Surgeon. 2007;73(7):664-667. discussion 668
  97. 97. Aydin HN et al. Hartmann's reversal is associated with high postoperative adverse events. Diseases of the Colon and Rectum. 2005;48(11):2117-2126
  98. 98. Maggard MA et al. What proportion of patients with an ostomy (for diverticulitis) get reversed? The American Surgeon. 2004;70(10):928-931
  99. 99. Munson KD et al. Diverticulitis. A comprehensive follow-up. Diseases of the Colon and Rectum. 1996;39(3):318-322
  100. 100. Thaler K et al. Determinants of recurrence after sigmoid resection for uncomplicated diverticulitis. Diseases of the Colon and Rectum. 2003;46(3):385-388
  101. 101. Benn PL, Wolff BG, Ilstrup DM. Level of anastomosis and recurrent colonic diverticulitis. American Journal of Surgery. 1986;151(2):269-271
  102. 102. Lederman ED et al. Complicated diverticulitis following renal transplantation. Diseases of the Colon and Rectum. 1998;41(5):613-618
  103. 103. Tyau ES et al. Acute diverticulitis. A complicated problem in the immunocompromised patient. Archives of Surgery. 1991;126(7):855-858. discussion 858-859
  104. 104. Perkins JD et al. Acute diverticulitis. Comparison of treatment in immunocompromised and nonimmunocompromised patients. American Journal of Surgery. 1984;148(6):745-748

Written By

Can Konca, Suleyman Utku Celik and Cihangir Akyol

Submitted: May 24th, 2017 Reviewed: May 17th, 2018 Published: September 5th, 2018