Diverticulitis

Back

Practice Essentials

Diverticular disease (diverticulosis, diverticulitis) is a general term that refers to the presence of diverticula, small pouches in the large intestinal (colonic) wall. These outpouchings arise when the inner layers of the colon push through weaknesses in the outer muscular layers.[1] Notably, diverticulosis can occur anywhere in the colon, but it is most common in the left colon (descending or sigmoid colon).

See Can't-Miss Gastrointestinal Diagnoses, a Critical Images slideshow, to help diagnose the potentially life-threatening conditions that present with gastrointestinal symptoms.

Signs and symptoms of diverticulitis

Diverticulitis arises when diverticula become inflamed or infected. The clinical presentation of diverticulitis depends on the location of the affected diverticulum, the severity of the inflammatory process, and the presence of complications. The usual initial symptoms are as follows:

On physical examination, the following may be found:

See Presentation for more detail.

Diagnosis of diverticulitis

The diagnosis of acute diverticulitis can usually be made on the basis of the history and physical examination findings, but laboratory tests may be of help when the diagnosis is in question, as follows:

Computed tomography (CT) scanning of the abdomen is considered the best imaging method to confirm the diagnosis. Sensitivity and specificity, especially with helical CT and colonic contrast medium, can be as high as 97%. Possible CT scan findings include the following:

Other tests and procedures are as follows:

See Workup for more detail.

Treatment of diverticulitis

The management of patients with diverticulitis depends on their presentation severity, presence of complications, and comorbid conditions.

Uncomplicated diverticulitis can be managed medically and in an ambulatory setting. Complicated disease requires a more aggressive approach that can often require urgent or elective surgery, and treatments that are specific to the complication itself (ie, abscess drainage).[2]

The modified Hinchey classification is based on CT scan findings and is used to categorize diverticulitis, as well as help to guide appropriate interventions.[3]

Antibiotics have been the mainstay of therapy for most patients with acute diverticulitis, but more recently, their necessity has been questioned, especially in mild, uncomplicated disease.[4]

Outpatient treatment of diverticulitis

Patients with clinically mild diverticulitis, typically with Hinchey stage 0 and Ia disease, are considered uncomplicated and can be treated with the following outpatient regimen[2, 5] :

The effectiveness of single- or multiple-agent antibiotic regimens for outpatient therapy are essentially the same when they provide both anaerobic and aerobic coverage.[6, 7]

Potential regimens include the following:

Indications for hospital admission include the following:

Inpatient treatment of diverticulitis

Patients with complicated diverticular disease fall under Modified Hinchey stage Ib II, III and IV. Individuals in Modified Hinchey stage Ib may require hospitalization and the following treatment regimen[2] :

Modified Hinchey stages II-IV require hospitalization, nothing by mouth, IV antibiotics, and percutaneous abscess drainage; surgical consultation and elective procedure for patients in stage II, and urgent surgical evaluation and resection for those in stage III and IV.

Monotherapy with beta-lactamase-inhibiting antibiotics or carbapenems is appropriate for patients who are moderately ill and require admission. Such antibiotics include piperacillin/tazobactam, ticarcillin/clavulanic acid, or ertapenem.[6] Monotherapy in severely ill patients, especially those who are immunocompromised includes meropenem, imipenem-cilastatin, piperacillin-tazobactam, or doripenem.

Multiple-drug regimens may consist of metronidazole and a third-generation cephalosporin or a fluoroquinolone, such as ceftriaxone, cefotaxime, ciprofloxacin, or levofloxacin. Multiple-drug regimens include cefepime plus metronidazole, as well as ceftazime plus metronidazole.

Pain management considerations are as follows:

Classic surgical indications include some features characteristic of Hinchey stage III or IV disease, such as the following:

See Treatment and Medication for more detail.

Background

Diverticular disease (diverticulosis, diverticulitis) is a general term that references the presence of diverticula, small pouches in the large intestinal (colonic) wall. These outpouchings arise when the inner layers of the colon push through weaknesses in the outer muscular layers.[1] Notably, diverticulosis can occur anywhere in the colon, but it is most common in the left colon (descending or sigmoid colon).

The cause of diverticulosis is unclear, but it has been associated with increased pressure from constipation or increasing abdominal girth in obesity. The classic high-fat and low-fiber diet of the Western culture may be a major contributor to the development of diverticulosis. The low-fiber diet is thought to predispose to diverticulosis owing to a slower fecal transit time and smaller stool weight. The highest prevalence of diverticular disease is in North America, where approximately 50% of the older adult population has diverticulosis, as compared to a 0.5% prevalence in the developing nations of Africa and Asia.[10]

Diverticular disease can be asymptomatic (diverticulosis) or involve acute or chronic, symptomatic inflammation of these pouches (diverticulitis). Although diverticulitis has been generally considered a disease of older adults, as many as 20% of patients with diverticulitis are younger than 50 years. In its chronic form, patients may have recurrent bouts of low-grade or overt diverticulitis.

For patient education resources, see Digestive Disorders Center, as well Diverticulitis (Diverticulosis) Symptoms and Diet and Abdominal Pain (Adults).

Pathophysiology

A diverticulum is a mucosal protrusion through the intestinal wall that occurs along natural areas of weakness. In the large intestine, there is only one complete muscular layer, the inner circular layer, whereas the small intestine and rectum have two muscular layers. The outer longitudinal muscular layer of the large intestine is arranged in three ribbons, the taeniae coli. Diverticula typically occur at sites where the vasa recta, or nutrient vessels in the wall of the colon, penetrate the circular layer, between the taeniae.[11]

Diverticula typically develop in rows along the mesenteric side of the antimesenteric taeniae coli; rarely, they penetrate through the taeniae. It is presumed that the diverticula occur along the mesentery due to the larger caliber of vessels producing a larger area of weakness in the circular muscle layer. As individuals age, the colonic wall collagen develops more cross-linking, leading to decreased elasticity and an increased risk of mucosal herniation. Thus, the stiffer colonic wall is more prone to submucosal tears, which, in turn, can contribute to herniation.[12]

Because the taeniae are shorter than the length of the colon, the colon develops saclike folds, the haustra.[13] As partially digested food, water, and digestive enzymes enter the large intestine in the form of chyme, colonic movement is triggered in the form of segmentation. Segmentation contractions occur as a result of the circular muscle layer, which results in slow mixing. This contrasts with peristalsis of the intestinal longitudinal muscles, which cause forward (caudal) progression of the luminal contents. It has been thought that the waves of high intestinal pressure during segmentation lead to muscular atrophy and herniation of the colon wall, which, in turn, form diverticula. This process may also explain why diverticulosis is more commonly found in the sigmoid colon, which has the smallest caliber and therefore receives the highest pressures in the large intestine.

Dietary habits may also be a significant contributing factor in the development of diverticulosis,[11] particularly given the global geographic distribution of this condition. Slow colonic transit time, heavy stool weight, and decreasing stool frequency (constipation) may contribute to diverticulum formation.[10] Studies to determine which dietary components have the largest effect on stool habits have shown that the standard Western diet (eg, high red meat content, low fiber, refined sugar) has a strong association with the incidence of diverticulosis. However, causation remains to be proven.

True diverticula contain all the layers of the gastrointestinal wall (mucosa, muscularis propria, and adventitia) (eg, Meckel diverticulum). False diverticula, or pseudo-diverticula do not contain the muscular layers or adventitia, only involving the submucosa and mucosa. Diverticula can occur anywhere in the gastrointestinal tract but are usually observed in the colon. As noted earlier, the sigmoid colon has the highest intraluminal pressures and is the most commonly affected site.

Diverticula found in the left colon (predominantly in the sigmoid) are usually false diverticula, and they are often seen in Western populations. Right-sided and cecal diverticula, however, are more frequently true diverticula; these are usually seen in people of Asian descent. Cecal diverticula are generally rare compared to those found in the left colon.[14]

Diverticulitis is defined as an inflammation of one or more diverticula. Its pathogenesis remains unclear. Fecal material or undigested food particles may collect in a diverticulum, causing obstruction. This obstruction may result in distention of the diverticula secondary to mucous secretion and overgrowth of normal colonic bacteria. Vascular compromise and subsequent microperforation or macroperforation then ensue. Alternatively, some investigators believe that increased intraluminal pressure[15] or inspissated food particles cause erosion of the diverticular wall, resulting in inflammation, focal necrosis, and perforation. Diverticulitis is frequently mild when pericolic fat and mesentery wall off a small perforation. However, larger perforations and more extensive disease lead to abscess formation and, rarely, intestinal rupture or peritonitis.

It has been postulated that diverticulitis may also result from alterations in immune responses and in the intestinal bacteria, or gut microbiome.[16] As small tears develop in the colon and become inflamed/infected, diverticulitis results. The microbiome is a prominent area of focus in current research. Investigators hope to isolate and grow bacteria from stool samples of individuals with asymptomatic diverticulosis and those with acute diverticulitis. Should these bacterial populations statistically differ, it may help clinicians to understand which patients are at a greater risk of developing diverticulitis. It may also allow the treatment of such changes in microbiota and the prevention of complicated disease.

Fistula formation is a complication of diverticulitis. Fistulas to adjacent organs and the skin may develop, especially in the presence of an abscess. In men, colovesicular fistulas are the most common. In women, the uterus is interposed between the colon and the bladder, and this complication of fistula formation is only seen following a hysterectomy. The uterus precludes fistula formation from the sigmoid colon to the urinary bladder. However, colovaginal and colocutaneous fistulas can form, albeit uncommonly.

Recurrent attacks of diverticulitis can result in the formation of scar tissue, leading to narrowing and obstruction of the colonic lumen.

Epidemiology

United States data

Acute diverticulitis is the third most common inpatient gastrointestinal diagnosis in the United States, at an annual cost of $2.1 billion, and it is the most frequently listed gastrointestinal diagnosis in outpatient clinics and the emergency department.[5]

The prevalence of diverticulosis has been shown to be age dependent and ranges from less than 20% at age 40 years to 60% by age 60 years.[2] The prevalence of diverticulitis has been rising over the past several decades, affecting an estimated 180/100,000 persons per year.[17] ​

Previously, it was believed that around 15%-20% of patients with diverticulosis would develop diverticulitis; however, more recent findings have shown the numbers to be closer to 1%-4%.[18] Of those with incident disease, approximately 20% have one or more recurrent episodes within 10 years.[2]

Diverticulitis is also a leading indication for elective colectomy. This condition affects patients' quality of life beyond the period of acute illness.

International data

Diverticular disease occurs more frequently in Western countries but continues to increase worldwide. Why diverticular disease is less common in underdeveloped countries is unclear, but it is presumably secondary to lifestyle and dietary factors. For example, the prevalence of diverticulosis increased in Japan after its population adopted a more Western lifestyle.[19]

Diverticulitis involving the left colon typically affects false diverticula, which are also usually found in Western populations. Right-sided and cecal diverticulitis (involving true diverticula) are more prevalent in the Asian population, accounting for up to 75% of cases of diverticulitis in this group.[20]

Age- and sex-related demographics

The incidence of diverticular disease increases with age (>65% in those >85 years). Most patients with diverticulitis are older than 50 years; the mean age at presentation appears to be about 60 years. However, diverticulitis is increasingly being seen in younger persons.

Although a male preponderance was noted in early series, subsequent studies have suggested either an equal sex distribution or a female preponderance.[2]

In those younger than 50 years, diverticulitis is more common in men; a slight female preponderance exists between the ages of 50 and 70 years, and there is a marked female preponderance in those older than 70 years.[21]

Prognosis

The prognosis in patients with diverticulitis depends on the severity of the illness, the presence of complications, and the presence of any coexisting medical problems. Younger patients with diverticulitis may have more severe disease, possibly due to a delay in the diagnosis and treatment. Immunosuppressed patients have significantly higher morbidity and mortality due to sigmoid diverticulitis.[22]

Morbidity/mortality

Of the patients who have diverticulosis, 80%-85% remain asymptomatic. Approximately 5% develop diverticulitis; 15%-25% of those with diverticulitis develop complications that lead to surgical intervention. These complications include abscess formation, intestinal rupture, peritonitis, and fistula formation.

Diverticulitis may be a more severe illness in those who are immunocompromised, who have significant comorbid conditions, and in those taking anti-inflammatory medications. Note the following:

Many studies have demonstrated the significant association between obesity and the risk of developing diverticulitis. In a large prospective study of 47,228 male health professionals, men with a body mass index (BMI) of at least 30 kg/m2 had a higher relative risk of 1.78 for diverticulitis compared to men with a BMI of less than 21 kg/m2, after adjustment for other risk factors.[26]

Complications

Complications of diverticulitis may be more severe in immunocompromised patients (those infected with human immunodeficiency virus (HIV), organ transplant recipients, those on long-term corticosteroids). These patients are more likely to have perforation.[27]

Complications of diverticulitis include the following:

Abscess

Abscesses amenable to percutaneous drainage are larger than 4 cm.[28] Abscesses not amenable to percutaneous drainage are either too small (< 3 cm) or they are adjacent to important structures.[28] Patients who do not improve within 24 to 48 hours after drainage should be referred for surgery.

Patients with abscesses successfully treated with antibiotics or are percutaneously drained should also be referred for elective surgery because of a high rate of recurrence in this population.[27]

Perforation

Frank perforation is diagnosed by the presence of free air under the diaphragm, with or without extravasation of contrast medium or fluid, which can be complicated with life-threatening diffuse peritonitis.

Microperforation (or contained perforation) is only evident by the presence of air bubbles outside of the bowel wall on computed tomography (CT) imaging.

Obstruction

Surgical resection of the involved bowel segment is mandatory to rule out cancer.

Fistula

Diverticular fistulas rarely close spontaneously, and a resection of the affected bowel segment is generally required.

History

The clinical presentation of diverticulitis, in which diverticula become inflamed or infected, depends on the location of the affected diverticulum, the severity of the inflammatory process, and the presence of complications. Left lower quadrant pain is the most common presenting complaint and occurs in 70% of patients. The pain is often described as crampy and may be associated with a change in the bowel habit. Right-sided diverticulitis of the cecum or ascending colon may present with right lower quadrant pain, which may be confused for acute appendicitis. Even in simple, uncomplicated cases, patients may have fever and/or leukocytosis (an elevated white blood cell count). Symptoms of mild diverticulitis may be confused with overlapping symptoms of irritable bowel syndrome.

The usual initial symptoms of diverticulitis include the following:

Other signs and symptoms in diverticulitis may arise due to an increasing severity of inflammation and the development of complications. Feared complications of diverticulitis include, but are not limited to, abscess (infected collection of pus), perforation (full thickness tearing of the colon), and fistula (abnormal connection between two organs).

Note that immunosuppressed individuals, including those taking corticosteroids, and the elderly are more likely to have an atypical presentation, or may not be symptomatic at all.

A microperforation, most likely walled off by adjacent structures, may present with no systemic signs of illness or infection. However, the disease may progress from a localized and walled-off process to one with peridiverticular inflammatory phlegmon and localized abscess. Systemic signs of infection (eg, fever) then develop.

Diverticulitis can mimic other conditions

Because diverticula and, hence, diverticulitis can develop anywhere in the gastrointestinal tract, symptoms may mimic multiple conditions. Note the following:

Physical Examination

Diverticulitis can present with a range of physical findings, mirroring the severity of the inflammation and the presence of complications, including the following:

Simple and complicated diverticulitis

In simple diverticulitis, fever and localized abdominal tenderness in the area of the affected diverticula are common findings. Left lower quadrant tenderness is the most common physical finding, as most diverticula occur in the sigmoid colon.[15] Right lower quadrant tenderness, mimicking acute appendicitis, can occur in right-sided diverticulitis.

In complicated diverticulitis with abscess formation, a tender palpable mass may be noted. In fact, 20% of cases present with a palpable mass on abdominal, pelvic, or rectal examination. Peritonitis due to a free perforation results in generalized tenderness with rebound and guarding on abdominal examination. The abdomen may be distended and tympanic to percussion. Bowel sounds may be diminished or absent.

Elderly and immunocompromised patients

Elderly patients and individuals taking corticosteroids may have unremarkable findings on physical examination even in the presence of severe diverticulitis. Such patients must be evaluated with a high index of suspicion to avoid a delay in establishing the correct diagnosis.

The presence of fistulas

If a fistula forms, physical examination findings vary depending on the type of fistula. Colovesicular fistulas may present with urinary tract symptoms, such as suprapubic, flank, or costovertebral angle tenderness. Fecaluria or pneumaturia can also be observed. Female patients with colovaginal fistulas may present with a purulent vaginal discharge.

Laboratory Studies

The diagnosis of acute diverticulitis can usually be made on the basis of the history and physical examination. Laboratory tests may be helpful when the diagnosis is in question.

A hemogram may reveal leukocytosis and a left shift, indicating infection. However, the absence of leukocytosis does not rule out diverticulitis, as 20%-40% of patients have a normal white blood cell count. This is particularly true in patients who are immunocompromised, who are elderly, and who have less severe disease. A hemoglobin level is important when the patient reports hematochezia.

Measurement of blood chemistries may be helpful in the patient who is vomiting or has diarrhea to assess electrolyte abnormalities. Assess renal function prior to the administration of most intravenous contrast material.

Liver function tests and lipase levels may help to exclude other causes of abdominal pain.

If a colovesical fistula is suspected, a urinalysis may reveal red or white blood cells. However, inflammation and infection due to diverticulitis adjacent to the ureters or the bladder may be the source of these cells. A urine culture may confirm sterile pyuria due to inflammation versus polymicrobial infection in the case of a fistula.

Blood cultures should be obtained prior to the administration of empiric parenteral antimicrobial therapy in patients who are severely ill or in those with complicated disease.

A pregnancy test must be performed in any female of childbearing age who presents with abdominal pain to rule out ectopic pregnancy, as well as prior to radiologic studies and before administering certain antibiotics to protect a viable fetus.

Imaging Studies

Although the diagnosis of diverticulitis can be made on clinical grounds, a computed tomography (CT) scan of the abdomen is considered the best imaging method to confirm the diagnosis. The American College of Radiology (ACR) appropriateness criteria for left lower quadrant pain support this recommendation because of the specificity and sensitivity of CT scans, which allow for the diagnosis of the causes of left lower quadrant pain that resembles diverticulitis.[29]

Note the following:

Barium contrast enema is not the imaging modality of choice during an acute episode of abdominal pain and should only be considered in mild to moderate uncomplicated cases of diverticulitis when the diagnosis is in doubt, or for follow-up evaluation for suspected fistula.[29] A water-soluble contrast medium should be used, as leakage of barium into the peritoneum would be catastrophic.

Plain radiograph films are not helpful in making the diagnosis of diverticulitis. However, plain abdominal radiograph series with supine and upright films can demonstrate bowel obstruction or ileus. If free air is present, this can indicate bowel perforation.

Procedures

Endoscopy is not recommended in the acute setting given the risk of worsening diverticulitis and bowel perforation. After the diverticulitis has subsided, colonoscopy can be used to evaluate the extent of diverticulosis or to rule out a malignancy masquerading as a benign postinflammatory stricture.

Similarly, when findings on computed tomography scan demonstrate are suspicious for colonic carcinoma, colonoscopy is the imaging modality of choice.[29]

Staging

Several staging schemes have been proposed for diverticulitis based on the clinical findings, disease extent on imaging studies, and the presence of complications. The simplest method may be to differentiate among asymptomatic diverticulosis, uncomplicated diverticulitis, and complicated diverticulitis.

Clinical staging by Hinchey's classification is based on computed tomography findings and directed toward selection of the proper surgical procedure when diverticulitis is complicated, as follows:

Table. Modified Hinchey Classification Stage and Diverticulitis Category



View Table

See Table

Approach Considerations

The management of patients with diverticulitis depends on their presentation severity, presence of complications, and comorbid conditions. Therefore, there is no standard treatment in the medical management of diverticular disease, including diverticulitis.[4]

The initial approach involves determining whether the patient has complicated or uncomplicated disease.[2] Uncomplicated diverticulitis is defined as localized diverticular inflammation without complication, whereas complicated diverticulitis consists of inflammation associated with a complication such as abscess, fistula, obstruction, bleeding, or perforation.[30] Computed tomography (CT) imaging can confirm the diagnosis of diverticulitis and distinguish between both disease processes.

Uncomplicated diverticulitis can be managed medically and in an ambulatory setting, whereas complicated disease requires a more aggressive approach that can often require urgent or elective surgery, and treatments that are specific to the complication itself (eg, abscess drainage).[2] A gastroenterology consultation may be helpful, as can further assistance with surgical and interventional radiology consultations. The modified Hinchey classification is based on CT scan findings and is used to categorize diverticulitis as well as help to guide appropriate interventions.[3]

Emergency colectomy is performed when severe complications arise or when the patient's condition does not respond to medical treatment. Complications requiring surgical intervention include the following: purulent peritonitis, uncontrolled sepsis, fistula, and obstruction. In a retrospective study of over 3000 patients, about 20% of patients admitted for acute diverticulitis required emergency colectomy.

Elective resection of the involved bowel segment after three episodes of uncomplicated diverticulitis to prevent further attacks is generally recommended by consensus guidelines. In addition, earlier resection for younger patients with diverticulitis as well as for patients who are immunocompromised has been proposed. As most complicated diverticulitis occurs on the first presentation and data for elective resection have come from small retrospective studies, this recommendation remains controversial.

Successful percutaneous drainage of a diverticular abscess has not been associated with greater recurrence or more severe disease and does not necessitate elective colectomy.

Antibiotics are known to be the mainstay of therapy for most patients with acute diverticulitis, but recent studies have questioned their necessity, especially in mild, uncomplicated disease.[4, 31] It appears that antimicrobial use in acute uncomplicated diverticulitis increases patients' stay in the hospital without lowering the overall or individual complication rates.[32]

A 2012 Cochrane review showed no significant benefit of antibiotic therapy in the treatment of uncomplicated diverticulitis, however these data were based mostly on one well-done randomized controlled trial.[33] The 2015 American Gastroenterological Association (AGA) guidelines stated that clinicians must be selective in using antibiotics in patients in this subgroup of patients.[5]

Patients who have been successfully treated for acute diverticulitis should be reassessed in 6-8 weeks. Those who are symptom free at that time should undergo colonoscopy to rule out malignancy, if they have not had a recent, high-quality colonic examination.[5]

Medical Care

The treatment approach for diverticulitis can be broadly classified into either uncomplicated disease or complicated disease, and it takes into account a few other special considerations.[15] Acute uncomplicated diverticulitis is successfully treated in 70%-100% of patients with conservative management.[34, 35, 36] Patients who present to the emergency department with uncomplicated diverticulitis appear to be able to be safely discharged on oral antibiotics, provided computed tomography (CT) scan findings have been evaluated.[37] However, those whose CT scan findings reveal complicated disease should be admitted for inpatient management with surgical consultation.[37]

The American Gastroenterological Association (AGA) suggests selective, rather than routine, use of antibiotics in patients with acute uncomplicated diverticulitis.[5, 38] Some studies indicate that nonantibiotic management of acute uncomplicated diverticulitis is safe and feasible.[31, 39]

Acute diverticulitis tends to be more severe in very elderly people and in patients who are immunocompromised or who have debilitating comorbid conditions, such as diabetes and renal failure.

Outpatient treatment of diverticulitis

Patients with mild diverticulitis, typically with Modified Hinchey stage 0 and Ia disease, can be started on an outpatient treatment regimen. This consists of a clear liquid diet and 7-10 days of an oral (PO) broad-spectrum antimicrobial regimen that covers anaerobic microorganisms, such as Bacteroides fragilis and Peptostreptococcus and Clostridium organisms, as well as aerobic microorganisms, such as Escherichia coli and Klebsiella, Proteus, Streptococcus, and Enterobacter organisms. Single and multiple antibiotic regimens are equally effective as long as both groups of organisms are covered.[6, 7] According to the World Gastroenterology Organisation (WGO) 2007 practice guidelines for diverticular disease, such a regimen should result in improvement within 48-72 hours.[1]

Note the following:

Inpatient treatment of diverticulitis

Hospitalization is required in the presence of evidence of severe diverticulitis, such as systemic signs of infection or peritonitis. Patients who are unable to tolerate oral hydration, whose condition is refractory to outpatient therapy (ie, persistent or increasing fever, pain, or leukocytosis after 2-3 days), who are immunocompromised, or who have comorbidities may also require hospitalization. Patients' pain may be severe enough to require parenteral narcotic analgesia.

Consider the following:

IV tigecycline is no longer recommended for patients with a severe penicillin allergy due to an increased mortality risk relative to other antimicrobials used to treat severe infections.[40] This higher all-cause mortality warranted a US Food and Drug Administration (FDA) Drug Safety Communication in September 2010, and the addition of a Black Box Warning to its prescribing information.[40] In September 2013, an additional warning was added to the Black Box Warning to indicate that the increased risk of death with IV tigecycline occurred both with FDA-approved uses and nonapproved uses.[41] Tigecycline is now reserved for use in situations when alternative treatments are not suitable.[41]

Dietary and activity considerations

Diet

In mild episodes of diverticulitis, a clear liquid diet is advised. Clinical improvement should occur within 2-3 days; the diet can then be advanced as tolerated. In episodes of moderate to severe acute diverticulitis, administer nothing by mouth (NPO).

Once the acute episode of diverticulitis has resolved, the patient may advance their diet as tolerated and then maintain a lifelong high-fiber diet. Colonoscopy or, alternatively, barium enema with flexible sigmoidoscopy should be obtained after resolution of an initial episode (typically 2-6 wk after recovery) to exclude other diagnoses, such as malignancy,[5, 29] ischemia, and inflammatory bowel disease.

An increasing number of studies have reported the efficacy of different regimens of anti-inflammatory agents, including mesalamine; nonabsorbable antibiotics such as rifaximin; and probiotics alone or in combination in the management of diverticulitis.[42, 43] The AGA does not recommend the use of mesalamine, and it suggests against the use of rifaximin or probiotics, following acute uncomplicated diverticulitis.[5]

In the first US double-blind, placebo-controlled trial of the anti-inflammatory agent mesalamine for diverticulitis, 117 patients randomly assigned within 7 days of documented acute diverticulitis to a once-daily regimen of either 2.4 g delayed-release mesalamine or placebo over 12 weeks, followed by a 9-month treatment-free period, demonstrated persistently lower global symptoms scores for 10 gastrointestinal symptoms on a 0-6 Likert scale in patients receiving mesalamine compared with the placebo group.[43] The rate of complete response was significantly higher with the use of mesalamine than placebo at 6 weeks and 52 weeks, whereas probiotics in combination with mesalamine did not provide additional efficacy.[43]

Studies imply a high-fiber diet will prevent progression of diverticulosis. However, after patients have become symptomatic, the benefit of fiber supplementation is less clear. Recommending patients to avoid seeds and nuts is less common, since it is currently thought that they may not play a significant role in the development of diverticulitis, as previously believed.

Long-term management probably includes a high-fiber, low-fat diet.

Activity

Normal activity is possible after resolution of the acute episode. Patients with diverticular disease should consider vigorous physical activity.[5]

Surgical Care

An estimated 15%-25% of patients who present with a first episode of acute diverticulitis have complicated disease that requires surgery. According to the World Gastroenterology Organisation (WGO) 2007 guidelines, 15%-30% of patients admitted for the management of diverticulitis will need surgery during their admission, with a surgical mortality of 18%.[1]

Classic surgical indications include some features characteristic of Hinchey stage III or IV disease, as follows:

Recurrent episodes of acute diverticulitis

Elective surgery was previously recommended in any patient who had two or more episodes of diverticulitis that were successfully treated medically; other data have since called this practice into question when the patient is otherwise healthy.

Perioperative considerations

Preoperative antibiotics should be administered to all patients. Single- and multiple-drug regimens, as discussed in Medical Care, are appropriate choices. However, for patients with more extensive contamination, a single-drug regimen (with either imipenem/cilastin or piperacillin/tazobactam) or a multiple-drug regimen (with ampicillin, gentamicin, and metronidazole) may be warranted for peritonitis. Bowel preparation is usually possible for nonemergent situations.

Emergent surgical approach

Guidelines from the 2006 American Society of Colon and Rectal Surgeons (ASCRS) recommend emergency surgery for patients with diffuse peritonitis and for those whose condition fails nonoperative management. Also, patients who are immunosuppressed or immunocompromised are at an increased risk of disease refractory to medical therapy or of bowel perforation, and they should be approached with a lower threshold for surgery.[44]

A two-stage surgical approach is generally the most common procedure performed for the emergency treatment of acute diverticulitis. Note the following:

Elective surgery

The decision to proceed with elective surgery, typically at least 6 weeks after recovery from acute diverticulitis, should be made on a case-by-case basis.[5] The 2015 American Gastroenterological Association (AGA) guidelines suggest against elective colonic resection in patients with an initial episode of acute uncomplicated diverticulitis.[5] As recommended by the 2007 World Gastroenterology Organisation (WGO) guidelines, this decision should include consideration of the age and medical condition of the patient, the frequency and severity of attacks, and the presence of any persistent symptoms after the acute episode.[5] Other appropriate indications for elective colectomy include an inability to exclude carcinoma, following an episode of complicated diverticulitis treated nonoperatively, or after percutaneous drainage of a diverticular abscess.[1]

Note the following:

Three-stage procedure

The classic three-stage surgical approach is rarely indicated at present because of its high associated morbidity and mortality. This procedure is considered only in critical situations in which resection cannot safely be performed. Consider the following:

Laparoscopy

Increasing experience with laparoscopic techniques for colon resection suggests that some of its advantages include less pain, a smaller scar, and shorter recovery time.[47] There is no change in early or late complications, and the cost and outcome are comparable to open procedures. The laparoscopic approach is best suited for patients in whom the episode of acute diverticulitis has resolved and in patients with Hinchey stage I or II disease.

Special considerations

Consider the following for some forms of complicated diverticulitis:

Prevention

A lifelong high-fiber diet for those with asymptomatic diverticular disease may reduce the incidence of diverticulitis and its complications. The 2015 American Gastroenterological Association (AGA) guidelines suggest a fiber-rich diet or fiber supplementation in individuals with a history of acute diverticulitis.[5] However, the guidelines are against routinely advising these patients to avoid the consumption of popcorn and nuts.

According to a large study in the United Kingdom, a high-fiber diet and a vegetarian diet were each significantly associated with a lower risk of diverticular disease-related hospital admission or death.[49]

Long-Term Monitoring

After recovering from acute diverticulitis, patients should have their colons examined to rule out malignancy. Current modalities include colonoscopy, barium enema, and computed tomography (CT) colonography (virtual colonoscopy).

Virtual colonoscopy may be helpful in evaluating diverticulitis in the elective setting. This procedure combines insufflation of the colon in conjunction with a CT scan to provide data that allow computer generation of a three-dimensional image. Although the technology is widely available in many centers, it is limited by the inability to sample suspicious lesions.

Biopsy of suspicious lesions or strictures can be performed during colonoscopy, which is advantageous.

Medical Society Guidelines

2015 American Gastroenterological Association (AGA) guidelines

The AGA recommendations on the treatment of diverticulitis include the following[5] :

2006 American Society of Colon and Rectal Surgeons (ASCRS) practice parameters

The ASCRS recommendations on the management of diverticulitis include the following[44] :

Medication Summary

Diverticulosis is treated with lifelong dietary modification. However, antibiotics have been the mainstay of therapy for most patients with acute diverticulitis, but more recently, their necessity has been questioned, especially in mild, uncomplicated disease.[4, 31] It appears that antimicrobial use in acute uncomplicated diverticulitis increases patients' stay in the hospital without lowering the overall or individual complication rates.[32] Other studies have shown that the effectiveness of single- or multiple-agent antibiotic regimens for outpatient therapy are essentially the same when they provide both anaerobic and aerobic coverage.[6, 7]

Empiric therapy requires broad-spectrum antibiotics effective against known enteric pathogens. For complicated cases of diverticulitis in hospitalized patients, carbapenems are the most effective empiric therapy because of increasing bacterial resistance to other regimens.

Potential regimens include the following:

Metronidazole (Flagyl, Medro)

Clinical Context:  Active against various anaerobic bacteria. Enters cell, binds DNA, and inhibits protein synthesis, causing cell death.

Ciprofloxacin (Cipro)

Clinical Context:  Bactericidal antibiotic that inhibits bacterial DNA synthesis. Used for infections due to E coli, K pneumoniae, E cloacae, P mirabilis, P vulgaris, P aeruginosa, H influenzae, M catarrhalis, S pneumoniae, S aureus (methicillin susceptible), S epidermidis, S pyogenes, Campylobacter jejuni, Shigella species, and Salmonella typhi.

Amoxicillin/clavulanate (Augmentin, Amoclan)

Clinical Context:  Amoxicillin inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins. The addition of clavulanate inhibits beta-lactamase–producing bacteria.

This agent is a good alternative antibiotic for patients allergic or intolerant to the macrolide class. It is usually well tolerated and provides good coverage to most infectious agents, but it is not effective against Mycoplasma and Legionella species. The half-life of an oral dosage form is 1-1.3 h. It has good tissue penetration but does not enter the cerebrospinal fluid.

For children >3 months, base the dosing protocol on amoxicillin content. Because of different amoxicillin/clavulanic acid ratios in 250-mg tab (250/125) vs 250-mg chewable tab (250/62.5), do not use 250-mg tab until child weighs >40 kg.

Sulfamethoxazole and Trimethoprim (Bactrim, Bactrim DS, Septra DS)

Clinical Context:  Inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid.

Antibacterial activity of TMP-SMZ includes the common urinary tract pathogens, except Pseudomonas aeruginosa.

Ceftriaxone (Rocephin)

Clinical Context:  Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin binding proteins. Exerts antimicrobial effect by interfering with the synthesis of peptidoglycan, a major structural component of bacterial cell wall. Bacteria eventually lyse due to the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested.

Highly stable in the presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately 33-67% of dose is excreted unchanged in urine, and the remainder is secreted in bile and ultimately in feces as microbiologically inactive compounds. Reversibly binds to human plasma proteins, and binding have been reported to decrease from 95% bound at plasma concentrations < 25 mcg/mL to 85% bound at 300 mcg/mL.

Cefotaxime (Claforan)

Clinical Context:  Third-generation cephalosporin with broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. Arrests bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins, which, in turn, inhibits bacterial growth. Used for septicemia and the treatment of gynecologic infections caused by susceptible organisms.

Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms.

Ceftolozane/tazobactam (Zerbaxa)

Clinical Context:  A cephalosporin antibiotic plus a beta-lactamase inhibitor. Indicated for use in combination with metronidazole for complicated intra-abdominal infections caused by Enterobacter cloacae, Escherichia coli, Klebsiella oxytoca, Klebsiella pneumoniae, Proteus mirabilis, Pseudomonas aeruginosa, Bacteroides fragilis, Streptococcus anginosus, Streptococcus constellatus, and Streptococcus salivarius. Dose must be adjusted for reduced CrCl.

Moxifloxacin (Avelox)

Clinical Context:  Moxifloxacin is the only fluoroquinolone that is FDA approved as monotherapy for the treatment of complicated intra-abdominal infections. Moxifloxacin, a broad-spectrum antibiotic, exhibits activity against Escherichia coli, Bacteroides fragilis, Streptococcus anginosus, Streptococcus constellatus, Enterococcus faecalis, Proteus mirabilis, Clostridium perfringens, Bacteroides thetaiotaomicron, or Peptostreptococcus species. Moxifloxacin is active against gram-positive organisms and anaerobes but is less active against Enterobacteriaceae and Pseudomonas species.

Levofloxacin (Levaquin)

Clinical Context:  For pseudomonal infections and infections due to multidrug resistant gram-negative organisms.

Ampicillin/Sulbactam (Unasyn)

Clinical Context:  Drug combination of beta-lactamase inhibitor with ampicillin. Interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication orally. Covers skin, enteric flora, and anaerobes. Not ideal for nosocomial pathogens.

Piperacillin and Tazobactam sodium (Zosyn)

Clinical Context:  Anti-pseudomonal penicillin plus beta-lactamase inhibitor. Inhibits biosynthesis of cell wall mucopeptide and is effective during the stage of active multiplication.

Ticarcillin and clavulanate potassium (Timentin)

Clinical Context:  Inhibits biosynthesis of cell wall mucopeptide and is effective during active replication.

Antipseudomonal penicillin and beta-lactamase inhibitor that provides coverage against most gram-positive and gram-negative bacteria and most anaerobes.

Meropenem (Merrem)

Clinical Context:  Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. Effective against most gram-positive and gram-negative bacteria. Has slightly increased activity against gram-negative organisms and slightly decreased activity against staphylococci and streptococci compared with imipenem. Drugs of this class are a good choice for empiric therapy of GI-based infections in hospitalized patients with complicated conditions.

Gentamicin

Clinical Context:  Aminoglycoside antibiotic used to cover gram-negative organisms.

Not the drug of choice (DOC). Consider if penicillins or other less toxic drugs are contraindicated, when clinically indicated, and in mixed infections caused by susceptible staphylococci and gram-negative organisms.

Dosing regimens are numerous; adjust dose based on CrCl and changes in volume of distribution. May be given IV/IM.

Imipenem and cilastatin (Primaxin)

Clinical Context:  Used for the treatment of multiple organism infections as in peritonitis when other agents are not appropriate.

Ampicillin

Clinical Context:  Broad-spectrum penicillin. Interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication orally.

Tigecycline (Tygacil)

Clinical Context:  Tetracycline-type antibiotic with broad coverage. NOTE: Tigecycline has a Black Box Warning. This agent was previously used in patients with a severe penicillin allergy, but owing to an increased risk of all-cause mortality, IV tigecycline is now reserved for use in situations when alternative treatments are not suitable. It is FDA approved for complicated intra-abdominal infections, as well as complicated skin and skin structure infections and community-acquired bacterial pneumonia.

Class Summary

Empiric antimicrobial therapy is essential and should cover all pathogens likely to cause diverticulitis.

What is diverticulitis?What are the symptoms of diverticulitis?Which physical findings indicate diverticulitis?Which lab tests may be useful in the diagnosis of diverticulitis?Which imaging methods are used to confirm the diagnosis of diverticulitis?What is the role of the Hinchey classification for diverticulitis?What is the treatment for mild diverticulitis?Which antibiotics are effective in the treatment of diverticulitis?What are the indications for hospital admission for diverticulitis?What is included in inpatient treatment of diverticulitis?When is antibiotic monotherapy indicated for the treatment of diverticulitis and which antibiotics are used?What are the possible multiple-drug therapies for diverticulitis?What should be considered when selecting medications for pain management in patients with diverticulitis?What are the surgical indications for diverticulitis?What is the spectrum of conditions included in diverticular disease?What are diverticula and how are they differentiated from pseudodiverticula (false diverticula)?What is the definition and pathogenesis of diverticulitis?What is the role of dietary habits in the development of diverticulitis?What is the pathophysiology of fistula formation in diverticulitis?How do recurrent attacks of diverticulitis affect the colon?What is the incidence of diverticulitis in the US?How does the global incidence of diverticulitis vary?Is there an age and/or gender predilection for diverticulitis?What is the prognosis of diverticulitis?How likely are patients with diverticulosis to develop diverticulitis?What is the morbidity and mortality of diverticulosis?Is obesity a risk factor for developing diverticulitis?What are the possible complications of diverticulitis?What is the most common presenting complaint of diverticulitis?What are the localized and systemic signs of diverticulitis?What are the physical findings of uncomplicated diverticulitis?What are the physical findings of complicated diverticulitis?What are the physical findings of diverticulitis in elderly or immunocompromised patients?What are the physical findings of diverticulitis in patients with a fistula?What are the differential diagnoses for Diverticulitis?How is the diagnosis of acute diverticulitis made?What is the role of hemogram in the diagnosis of diverticulitis?What is the role of blood chemistry testing in the diagnosis of diverticulitis?What is the role of liver function tests in the diagnosis of diverticulitis?What is the role of urinalysis and urine culture in the diagnosis of diverticulitis?When are blood cultures indicated in the management of diverticulitis?When is a pregnancy test indicated in the diagnosis of diverticulitis?What is the role of CT scanning in the diagnosis of diverticulitis?What is the role of barium contrast enema in the diagnosis of diverticulitis?What is the role of radiography in the diagnosis of diverticulitis?When are endoscopy and colonoscopy indicated in the diagnosis of diverticulitis?What is the basis used for staging diverticulitis?What is the clinical staging of diverticulitis using the Hinchey and modified Hinchey classifications?Which specialists may be consulted regarding the treatment and management of diverticulitis?Which complications of diverticulitis require surgical intervention?What are the guidelines for elective resection for the treatment of diverticulitis?Is percutaneous drainage of an abscess effective treatment for diverticulitis?Is conservative management an option for patients with acute uncomplicated diverticulitis?Which patients are at risk for a more severe course of acute diverticulitis?What are the treatment options for mild diverticulitis?When is hospitalization indicated in patients with diverticulitis and which treatment options should be considered?Which procedures should be performed once an initial acute episode of diverticulitis has resolved?Which anti-inflammatory agents are effective for the management of diverticulitis?When is a clear liquid diet indicated in patients with diverticulitis?When is oral administration contraindicated in patients with diverticulitis?What is the role of a high-fiber diet in patients with diverticulosis?Should activity be restricted in patients with diverticulitis?What is the likelihood that an initial episode of acute diverticulitis will require surgical intervention?What are the surgical indications for diverticulitis?When is elective surgery for diverticulitis indicated?What are perioperative considerations for diverticulitis?What are the ASCRS guidelines for emergency surgery for diverticulitis?Which surgical procedures are performed for the emergency treatment of acute diverticulitis?What are the AGA and WGO guidelines for elective surgery for diverticulitis?What is the three-stage surgical approach for diverticulitis?What are the surgical considerations for complicated diverticulitis?Does a high-fiber diet reduce the incidence of diverticulitis and its complications?What monitoring is required following an episode of acute diverticulitis?What is virtual colonoscopy and is it effective for evaluating diverticulitis?Which medications are used to treat diverticulitis?Which medications in the drug class Antibiotics are used in the treatment of Diverticulitis?

Author

Elie M Ghoulam, MD, MS, Resident Physician, Department of Internal Medicine, St Louis University School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Danisa M Clarrett, MD, MS, Fellow, Division of Gastroenterology and Hepatology, St Louis University School of Medicine

Disclosure: Nothing to disclose.

Elizabeth V Marsicano, MD, Assistant Professor of Internal Medicine, Associate Program Director of Gastroenterology, Director of Clinical Operations, Division of Gastroenterology and Hepatology, St Louis University School of Medicine

Disclosure: Nothing to disclose.

Specialty Editors

Marc D Basson, MD, PhD, MBA, FACS, Senior Associate Dean for Medicine and Research, Professor of Surgery, Pathology, and Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD, Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Duminda B Suraweera, MD, Resident Physician, Department of Medicine, Olive View–UCLA Medical Center

Disclosure: Nothing to disclose.

Kamyar Shahedi, MD, Clinical Instructor, Olive View-UCLA Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Disclosure: Nothing to disclose.

Stanley K Dea, MD, Chief of Endoscopy, Acting Chief of Gastroenterology, Consulting Gastroenterologist Olive View-University of California at Los Angeles Medical Center; Director of Enteral Feeding, West Los Angeles Veterans Affairs Medical Center; Director of Endoscopic Training, University of California at Los Angeles Affiliated Training Program in Gastroenterology

Disclosure: Nothing to disclose.

Yuvrajsinh Narendrasinh Chudasama, MD, Staff Physician, Department of Internal Medicine, Olive View-UCLA Medical Center; Assistant Clinical Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine

Disclosure: Nothing to disclose.

Acknowledgements

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

David Greenwald, MD Associate Professor of Clinical Medicine, Fellowship Program Director, Department of Medicine, Division of Gastroenterology, Montefiore Medical Center, Albert Einstein College of Medicine

David Greenwald, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, and New York Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Norvin Perez, MD Medical Director, Juneau Urgent and Family Care

Norvin Perez, MD is a member of the following medical societies: American College of Emergency Physicians and American Medical Association

Disclosure: Nothing to disclose.

Waqar A Qureshi, MD Associate Professor of Medicine, Chief of Endoscopy, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine and Veterans Affairs Medical Center

Waqar A Qureshi, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Ahmed Sherif, MD Staff Physician, Department of Internal Medicine, Montefiore Medical Center

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References

  1. [Guideline] Murphy T, Hunt RH, Fried M, Krabshuis JH. WGO Practice Guidelines. Diverticular disease. World Gastroenterology Organisation (WGO). Available at http://www.worldgastroenterology.org/diverticular-disease.html. 2007; Accessed: June 10, 2011.
  2. Swanson SM, Strate LL. Acute colonic diverticulitis. Ann Intern Med. 2018 May 1. 168(9):ITC65-80. [View Abstract]
  3. Wasvary H, Turfah F, Kadro O, Beauregard W. Same hospitalization resection for acute diverticulitis. Am Surg. 1999 Jul. 65(7):632-5; discussion 636. [View Abstract]
  4. Cuomo R, Cargiolli M, Cassarano S, Carabotti M, Annibale B. Treatment of diverticular disease, targeting symptoms or underlying mechanisms. Curr Opin Pharmacol. 2018 Oct 3. 43:124-31. [View Abstract]
  5. [Guideline] Stollman N, Smalley W, Hirano I, AGA Institute Clinical Guidelines Committee. American Gastroenterological Association Institute Guideline on the Management of Acute Diverticulitis. Gastroenterology. 2015 Dec. 149(7):1944-9. [View Abstract]
  6. [Guideline] Solomkin JS, Mazuski JE, Bradley JS, et al. Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America. Surg Infect (Larchmt). 2010 Feb. 11(1):79-109. [View Abstract]
  7. Gilbert DN, Chambers HF, Eliopoulos GM, et al. The Sanford Guide to Antimicrobial Therapy. 47th ed. Sperryville, VA: Antimicrobial Therapy, Inc; 2017.
  8. [Guideline] Feingold D, Steele SR, Lee S, et al. Practice parameters for the treatment of sigmoid diverticulitis. Dis Colon Rectum. 2014 Mar. 57(3):284-94. [View Abstract]
  9. Regenbogen SE, Hardiman KM, Hendren S, Morris AM. Surgery for diverticulitis in the 21st century: a systematic review. JAMA Surg. 2014 Mar. 149(3):292-303. [View Abstract]
  10. Hobson KG, Roberts PL. Etiology and pathophysiology of diverticular disease. Clin Colon Rectal Surg. 2004 Aug. 17(3):147-53. [View Abstract]
  11. Matrana MR, Margolin DA. Epidemiology and pathophysiology of diverticular disease. Clin Colon Rectal Surg. 2009 Aug. 22(3):141-6. [View Abstract]
  12. Hughes LE. Postmortem survey of diverticular disease of the colon. II. The muscular abnormality of the sigmoid colon. Gut. 1969 May. 10(5):344-51. [View Abstract]
  13. Morson BC. The muscle abnormality in diverticular disease of the colon. Proc R Soc Med. 1963 Sep. 56:798-800. [View Abstract]
  14. Karatepe O, Gulcicek OB, Adas G, et al. Cecal diverticulitis mimicking acute appendicitis: a report of 4 cases. World J Emerg Surg. 2008 Apr 21. 3:16. [View Abstract]
  15. [Guideline] Floch MH, Longo WE. United States guidelines for diverticulitis treatment. J Clin Gastroenterol. 2016 Oct. 50 suppl 1:S53-6. [View Abstract]
  16. Barbara G, Scaioli E, Barbaro MR, et al. Gut microbiota, metabolome and immune signatures in patients with uncomplicated diverticular disease. Gut. 2017 Jul. 66(7):1252-61. [View Abstract]
  17. Bharucha AE, Parthasarathy G, Ditah I, et al. Temporal trends in the incidence and natural history of diverticulitis: a population-based study. Am J Gastroenterol. 2015 Nov. 110(11):1589-96. [View Abstract]
  18. Shahedi K, Fuller G, Bolus R, et al. Long-term risk of acute diverticulitis among patients with incidental diverticulosis found during colonoscopy. Clin Gastroenterol Hepatol. 2013 Dec. 11(12):1609-13. [View Abstract]
  19. Sugihara K, Muto T, Morioka Y, Asano A, Yamamoto T. Diverticular disease of the colon in Japan. A review of 615 cases. Dis Colon Rectum. 1984 Aug. 27(8):531-7. [View Abstract]
  20. Elisei W, Brandimarte G, Tursi A. Management of diverticulosis: what's new?. Minerva Med. 2017 Oct. 108(5):448-63. [View Abstract]
  21. Strate LL, Modi R, Cohen E, Spiegel BM. Diverticular disease as a chronic illness: evolving epidemiologic and clinical insights. Am J Gastroenterol. 2012 Oct. 107(10):1486-93. [View Abstract]
  22. Brandl A, Kratzer T, Kafka-Ritsch R, et al. Diverticulitis in immunosuppressed patients: a fatal outcome requiring a new approach?. Can J Surg. 2016 Aug. 59(4):254-61. [View Abstract]
  23. Peery AF. Recent advances in diverticular disease. Curr Gastroenterol Rep. 2016 Jul. 18(7):37. [View Abstract]
  24. Mueller MH, Glatzle J, Kasparek MS, et al. Long-term outcome of conservative treatment in patients with diverticulitis of the sigmoid colon. Eur J Gastroenterol Hepatol. 2005 Jun. 17(6):649-54. [View Abstract]
  25. Chapman J, Davies M, Wolff B, et al. Complicated diverticulitis: is it time to rethink the rules?. Ann Surg. 2005 Oct. 242(4):576-81; discussion 581-3. [View Abstract]
  26. Strate LL, Liu YL, Aldoori WH, Syngal S, Giovannucci EL. Obesity increases the risks of diverticulitis and diverticular bleeding. Gastroenterology. 2009 Jan. 136 (1):115-22.e1. [View Abstract]
  27. Jacobs DO. Clinical practice. Diverticulitis. N Engl J Med. 2007 Nov 15. 357(20):2057-66. [View Abstract]
  28. Siewert B, Tye G, Kruskal J, et al. Impact of CT-guided drainage in the treatment of diverticular abscesses: size matters. AJR Am J Roentgenol. 2006 Mar. 186(3):680-6. [View Abstract]
  29. [Guideline] American College of Radiology. ACR appropriateness criteria: left lower quadrant pain - suspected diverticulitis. Available at https://acsearch.acr.org/docs/69356/Narrative/. 1996; reviewed 2014; Accessed: 2016.
  30. Wilkins T, Embry K, George R. Diagnosis and management of acute diverticulitis. Am Fam Physician. 2013 May 1. 87(9):612-20. [View Abstract]
  31. Boermeester MA, Humes DJ, Velmahos GC, Soreide K. Contemporary review of risk-stratified management in acute uncomplicated and complicated diverticulitis. World J Surg. 2016 Oct. 40(10):2537-45. [View Abstract]
  32. Gottlieb M, Shah N, Yu B. Can acute uncomplicated diverticulitis be safely treated without antibiotics?. Ann Emerg Med. 2019 Jun. 73(6):e75-e76. [View Abstract]
  33. Shabanzadeh DM, Wille-Jorgensen P. Antibiotics for uncomplicated diverticulitis. Cochrane Database Syst Rev. 2012 Nov 14. 11:CD009092. [View Abstract]
  34. Ricciardi R, Baxter NN, Read TE, Marcello PW, Hall J, Roberts PL. Is the decline in the surgical treatment for diverticulitis associated with an increase in complicated diverticulitis?. Dis Colon Rectum. 2009 Sep. 52(9):1558-63. [View Abstract]
  35. Alonso S, Pera M, Pares D, et al. Outpatient treatment of patients with uncomplicated acute diverticulitis. Colorectal Dis. 2010 Oct. 12(10 online):e278-82. [View Abstract]
  36. Sanchez-Velazquez P, Grande L, Pera M. Outpatient treatment of uncomplicated diverticulitis: a systematic review. Eur J Gastroenterol Hepatol. 2016 Jun. 28(6):622-7. [View Abstract]
  37. Sirany AE, Gaertner WB, Madoff RD, Kwaan MR. Diverticulitis diagnosed in the emergency room: is it safe to discharge home?. J Am Coll Surg. 2017 Jul. 225(1):21-5. [View Abstract]
  38. Peery AF, Stollman N. Antibiotics for acute uncomplicated diverticulitis: time for a paradigm change?. Gastroenterology. 2015 Dec. 149(7):1650-1. [View Abstract]
  39. Brochmann ND, Schultz JK, Jakobsen GS, Oresland T. Management of acute uncomplicated diverticulitis without antibiotics: a single-centre cohort study. Colorectal Dis. 2016 Nov. 18(11):1101-7. [View Abstract]
  40. US Food and Drug Administration. FDA Drug Safety Communication: Increased risk of death with Tygacil (tigecycline) compared to other antibiotics used to treat similar infections. Available at https://www.fda.gov/Drugs/DrugSafety/ucm224370.htm. September 1, 2010; Accessed: September 7, 2010.
  41. US Food and Drug Administration. FDA Drug Safety Communication: FDA warns of increased risk of death with IV antibacterial Tygacil (tigecycline) and approves new Boxed Warning. Available at https://www.fda.gov/Drugs/DrugSafety/ucm369580.htm. September 27, 2013; Accessed: October 9, 2013.
  42. Trivedi CD, Das KM, NDSG. Emerging therapies for diverticular disease of the colon. J Clin Gastroenterol. 2008 Nov-Dec. 42(10):1145-51. [View Abstract]
  43. Stollman N, Magowan S, Shanahan F, Quigley EM, DIVA Investigator Group. A randomized controlled study of mesalamine after acute diverticulitis: results of the DIVA trial. J Clin Gastroenterol. 2013 Aug. 47(7):621-9. [View Abstract]
  44. [Guideline] Rafferty J, Shellito P, Hyman NH, Buie WD, Standards Committee of American Society of Colon and Rectal Surgeons. Practice parameters for sigmoid diverticulitis. Dis Colon Rectum. 2006 Jul. 49(7):939-44. [View Abstract]
  45. Riansuwan W, Hull TL, Millan MM, Hammel JP. Nonreversal of Hartmann's procedure for diverticulitis: derivation of a scoring system to predict nonreversal. Dis Colon Rectum. 2009 Aug. 52(8):1400-8. [View Abstract]
  46. Fleming FJ, Gillen P. Reversal of Hartmann's procedure following acute diverticulitis: is timing everything?. Int J Colorectal Dis. 2009 Oct. 24(10):1219-25. [View Abstract]
  47. Rink AD, John-Enzenauer K, Haaf F, Straub E, Nagelschmidt M, Vestweber KH. Laparoscopic-assisted or laparoscopic-facilitated sigmoidectomy for diverticular disease? A prospective randomized trial on postoperative pain and analgesic consumption. Dis Colon Rectum. 2009 Oct. 52(10):1738-45. [View Abstract]
  48. Cirocchi R, Nascimbeni R, Binda GA, et al. Surgical treatment of acute complicated diverticulitis in the elderly. Minerva Chir. 2018 Oct 9. 14(1):[View Abstract]
  49. Crowe FL, Appleby PN, Allen NE, Key TJ. Diet and risk of diverticular disease in Oxford cohort of European Prospective Investigation into Cancer and Nutrition (EPIC): prospective study of British vegetarians and non-vegetarians. BMJ. 2011 Jul 19. 343:d4131. [View Abstract]
  50. Shahedi K, Fuller G, Bolus R, et al. Progression from incidental diverticulosis to acute diverticulitis [abstract 847]. Gastroenterology. 2012 May. 142(5) suppl 1:S-144.
  51. Lahat A, Avidan B, Sakhnini E, Katz L, Fidder HH, Meir SB. Acute diverticulitis: a decade of prospective follow-up. J Clin Gastroenterol. 2013 May-Jun. 47(5):415-9. [View Abstract]
  52. Deery SE, Hodin RA. Management of diverticulitis in 2017. J Gastrointest Surg. 2017 Oct. 21(10):1732-41. [View Abstract]
  53. Ambrosetti P, Robert JH, Witzig JA, et al. Acute left colonic diverticulitis in young patients. J Am Coll Surg. 1994 Aug. 179(2):156-60. [View Abstract]
  54. Bahadursingh AM, Virgo KS, Kaminski DL, Longo WE. Spectrum of disease and outcome of complicated diverticular disease. Am J Surg. 2003 Dec. 186(6):696-701. [View Abstract]
  55. Bordeianou L, Hodin R. Controversies in the surgical management of sigmoid diverticulitis. J Gastrointest Surg. 2007 Apr. 11(4):542-8. [View Abstract]
  56. Broderick-Villa G, Burchette RJ, Collins JC, Abbas MA, Haigh PI. Hospitalization for acute diverticulitis does not mandate routine elective colectomy. Arch Surg. 2005 Jun. 140(6):576-81; discussion 581-3. [View Abstract]
  57. Caterino JM, Emond JA, Camargo CA Jr. Inappropriate medication administration to the acutely ill elderly: a nationwide emergency department study, 1992-2000. J Am Geriatr Soc. 2004 Nov. 52(11):1847-55. [View Abstract]
  58. Dominguez EP, Sweeney JF, Choi YU. Diagnosis and management of diverticulitis and appendicitis. Gastroenterol Clin North Am. 2006 Jun. 35(2):367-91. [View Abstract]
  59. Evans JP, Cooper J, Roediger WE. Diverticular colitis - therapeutic and aetiological considerations. Colorectal Dis. 2002 May. 4(3):208-12. [View Abstract]
  60. Ferzoco LB, Raptopoulos V, Silen W. Acute diverticulitis. N Engl J Med. 1998 May 21. 338(21):1521-6. [View Abstract]
  61. Floch MH, White JA. Management of diverticular disease is changing. World J Gastroenterol. 2006 May 28. 12(20):3225-8. [View Abstract]
  62. Freeman SR. Diverticulitis. In: McNally PR, ed. GI/Liver Secrets. Philadelphia, PA: Hanley & Belfus; 1996. 332-8.
  63. Hackethal V. Diverticulitis surgery often avoidable, new standard needed. January 16, 2014. Medscape Medical News. Available at http://www.medscape.com/viewarticle/819310. Accessed: January 20, 2014.
  64. Isselbacher KJ, Epstein A. Diverticular disease. In: Fauci E, Braunwald E, Isselbacher KJ, et al, eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998. 1648-9.
  65. Janes SE, Meagher A, Frizelle FA. Management of diverticulitis. BMJ. 2006 Feb 4. 332(7536):271-5. [View Abstract]
  66. Kornitzer BS, Manace LC, Fischberg DJ, Leipzig RM. Prevalence of meperidine use in older surgical patients. Arch Surg. 2006 Jan. 141(1):76-81. [View Abstract]
  67. Marinella MA, Mustafa M. Acute diverticulitis in patients 40 years of age and younger. Am J Emerg Med. 2000 Mar. 18(2):140-2. [View Abstract]
  68. McCarthy DW, Bumpers HL, Hoover EL. Etiology of diverticular disease with classic illustrations. J Natl Med Assoc. 1996 Jun. 88(6):389-90. [View Abstract]
  69. Miura S, Kodaira S, Shatari T, Nishioka M, Hosoda Y, Hisa TK. Recent trends in diverticulosis of the right colon in Japan: retrospective review in a regional hospital. Dis Colon Rectum. 2000 Oct. 43(10):1383-9. [View Abstract]
  70. Novak JS, Tobias J, Barkin JS. Nonsurgical management of acute jejunal diverticulitis: a review. Am J Gastroenterol. 1997 Oct. 92(10):1929-31. [View Abstract]
  71. [Guideline] Oliver G, Lowry A, Vernava A, et al. Practice parameters for antibiotic prophylaxis--supporting documentation. The Standards Task Force. The American Society of Colon and Rectal Surgeons. Dis Colon Rectum. 2000 Sep. 43(9):1194-200. [View Abstract]
  72. Parks TG. Natural history of diverticular disease of the colon. Clin Gastroenterol. 1975 Jan. 4(1):53-69. [View Abstract]
  73. Patel DG, Thomson WG. Diverticulitis and diverticular hemorrhage. In: Brandt LJ, ed. Clinical Practice of Gastroenterology. Philadelphia, PA: Churchill Livingstone; 1999. Vol 1: 727-32.
  74. Pemberton JH, Armstrong DN, Dietzen CD. Diverticulitis. In: Yamada T, Alpers DH, Owyang C, et al, eds. Textbook of Gastroenterology. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1995. 1876-88.
  75. Poletti PA, Platon A, Rutschmann O, et al. Acute left colonic diverticulitis: can CT findings be used to predict recurrence?. AJR Am J Roentgenol. 2004 May. 182(5):1159-65. [View Abstract]
  76. [Guideline] Rafferty J, Shellito P, Hyman NH, Buie WD, Standards Committee of American Society of Colon and Rectal Surgeons. Practice parameters for sigmoid diverticulitis. Dis Colon Rectum. 2006 Jul. 49(7):939-44. [View Abstract]
  77. Rampton DS. Diverticular colitis: diagnosis and management. Colorectal Dis. 2001 May. 3(3):149-53. [View Abstract]
  78. 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 Jun. 170(6):1445-9. [View Abstract]
  79. Rege RV, Nahrwold DL. Diverticular disease. Curr Probl Surg. 1989 Mar. 26(3):133-89. [View Abstract]
  80. Regenbogen SE, Hardiman KM, Hendren S, Morris AM. Surgery for diverticulitis in the 21st century: a systematic review. JAMA Surg. 2014 Mar. 149(3):292-303. [View Abstract]
  81. Ripolles T, Agramunt M, Martinez MJ, Costa S, Gomez-Abril SA, Richart J. The role of ultrasound in the diagnosis, management and evolutive prognosis of acute left-sided colonic diverticulitis: a review of 208 patients. Eur Radiol. 2003 Dec. 13(12):2587-95. [View Abstract]
  82. Schoetz DJ Jr. Uncomplicated diverticulitis. Indications for surgery and surgical management. Surg Clin North Am. 1993 Oct. 73(5):965-74. [View Abstract]
  83. Schreyer AG, Furst A, Agha A, et al. Magnetic resonance imaging based colonography for diagnosis and assessment of diverticulosis and diverticulitis. Int J Colorectal Dis. 2004 Sep. 19(5):474-80. [View Abstract]
  84. Silverman ME, Shih RD, Allegra J. Morphine induces less nausea than meperidine when administered parenterally. J Emerg Med. 2004 Oct. 27(3):241-3. [View Abstract]
  85. Wu JS, Baker ME. Recognizing and managing acute diverticulitis for the internist. Cleve Clin J Med. 2005 Jul. 72(7):620-7. [View Abstract]
  86. Yacoe ME, Jeffrey RB Jr. Sonography of appendicitis and diverticulitis. Radiol Clin North Am. 1994 Sep. 32(5):899-912. [View Abstract]
  87. Harvey J, Roberts PL, Schoetz DJ, et al. Do appendicitis and diverticulitis share a common pathological link?. Dis Colon Rectum. 2016 Jul. 59(7):656-61. [View Abstract]
  88. Wright GP, Flermoen SL, Robinett DM, Charney KN, Chung MH. Surgeon specialization impacts the management but not outcomes of acute complicated diverticulitis. Am J Surg. 2016 Jun. 211(6):1035-40. [View Abstract]
  89. Mali JP, Mentula PJ, Leppäniemi AK, Sallinen VJ. Symptomatic treatment for uncomplicated acute diverticulitis: a prospective cohort study. Dis Colon Rectum. 2016 Jun. 59(6):529-34. [View Abstract]
  90. Weizman AV, Nguyen GC. Diverticular disease: epidemiology and management. Can J Gastroenterol. 2011 Jul. 25(7):385-9. [View Abstract]
  91. Wheat CL, Strate LL. Trends in hospitalization for diverticulitis and diverticular bleeding in the United States from 2000 to 2010. Clin Gastroenterol Hepatol. 2016 Jan. 14(1):96-103.e1. [View Abstract]
  92. Carabotti M, Annibale B. Mesalamine (5-ASA) for the prevention of recurrent diverticulitis (Review). Tech Coloproctol. 2019 Jun. 23(6):597-9. [View Abstract]
  93. Halim H, Askari A, Nunn R, Hollingshead J. Primary resection anastomosis versus Hartmann's procedure in Hinchey III and IV diverticulitis. World J Emerg Surg. 2019. 14:32. [View Abstract]
Modified Hinchey Classification StageCategory
0Clinically mild diverticulitis, or diverticula with colonic wall thickening on CTUncomplicated
IaColonic reaction with inflammatory reaction in the pericolic fat (phlegmon)Uncomplicated
IbPericolic or mesenteric abscessComplicated
IIIntra-abdominal abscess, pelvic or retroperitoneal abscessComplicated
IIIGeneralized purulent peritonitisComplicated
IVGeneralized fecal peritonitisComplicated