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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTczMzg4LW92ZXJ2aWV3\nDrugs & Diseases > Gastroenterology\nAuthor: Elie M Ghoulam, MD, MS; Chief Editor: BS Anand, MD more...\nSections Diverticulitis\nDiverticular 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).\nSee Can't-Miss Gastrointestinal Diagnoses, a Critical Images slideshow, to help diagnose the potentially life-threatening conditions that present with gastrointestinal symptoms.\nSigns and symptoms of diverticulitis\nDiverticulitis 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:\nAbdominal pain (most commonly in the left lower quadrant)\nConstipation or obstipation\nOn physical examination, the following may be found:\nLocalized abdominal tenderness\nAbdominal distention\nTympanic abdomen to percussion\nA tender mass (abscess formation)\nHypo- or hyperactive bowel sounds\nAbsent bowel sounds (perforation)\nGeneralized abdominal pain with rebound and guarding (perforation)\nUrinary tract findings (colovesicular/colovaginal fistula) include suprapubic, flank, costovertebral tenderness; pneumaturia (air in urine); fecaluria (stool in urine); purulent vaginal discharge\nSee Presentation for more detail.\nDiagnosis of diverticulitis\nThe 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:\nThe white blood cell count may show leukocytosis and a left shift, but it may be normal in immunocompromised, elderly, or less severely ill patients.\nA hemoglobin level is important in patients who report hematochezia.\nElectrolyte assays may be helpful in the patient who is vomiting or has diarrhea.\nAssess renal function prior to the administration of most intravenous contrast material.\nLiver enzyme and lipase levels may help to exclude other causes of abdominal pain.\nUrinalysis may reveal red or white blood cells in patients with a colovesicular fistula or with diverticulitis adjacent to the ureters or the bladder.\nA urine culture may distinguish sterile pyuria due to inflammation from polymicrobial infection due to a fistula.\nObtain blood cultures prior to the administration of empiric parenteral antimicrobial therapy in patients who are severely ill or in those with complicated disease.\nPerform a pregnancy test in any female of childbearing age with abdominal pain.\nComputed 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:\nPericolic fat stranding due to inflammation\nColonic diverticula\nBowel wall thickening\nSoft-tissue inflammatory masses\nPhlegmon\nOther tests and procedures are as follows:\nContrast enema, using water-soluble medium, may be an option in mild-to-moderate uncomplicated cases of diverticulitis.\nA plain abdominal radiographic series with supine and upright films can demonstrate bowel obstruction or ileus; the presence of free air can indicate bowel perforation.\nTreatment of diverticulitis\nThe management of patients with diverticulitis depends on their presentation severity, presence of complications, and comorbid conditions.\nUncomplicated 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]\nThe modified Hinchey classification is based on CT scan findings and is used to categorize diverticulitis, as well as help to guide appropriate interventions. [3]\nAntibiotics 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]\nOutpatient treatment of diverticulitis\nPatients 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] :\nClear liquid diet for 2-3 days; advancement to low fiber as tolerated\n7-10 days of oral (PO) broad-spectrum antimicrobial therapy on a case-by case basis\nAcetaminophen and antispasmodics for pain\nThe 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]\nPotential regimens include the following:\nCiprofloxacin plus metronidazole\nTrimethoprim-sulfamethoxazole plus metronidazole\nAmoxicillin-clavulanate\nMoxifloxacin (for patients intolerant of both metronidazole and beta-lactam agents)\nIndications for hospital admission include the following:\nEvidence of severe diverticulitis (ie, systemic signs of infection or peritonitis)\nInability to tolerate oral hydration\nFailure of outpatient therapy (ie, persistent or increasing fever, pain, or leukocytosis after 2-3 days) [8]\nImmune-compromise or significant comorbidities\nPain severe enough to require parenteral narcotic analgesia\nInpatient treatment of diverticulitis\nPatients 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] :\nClear liquid diet; advancement to low fiber as tolerated\nIntravenous (IV) or PO antibiotics\nElective surgical resection\nAbscess >4 cm: Drain percutaneously\nAbscess < 3 cm: Antibiotics typically resolve\nModified 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.\nMonotherapy 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.\nMultiple-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.\nPain management considerations are as follows:\nMorphine is preferred, despite theoretical risk of affecting bowel tone and sphincters.\nMeperidine is associated with adverse effects.\nNonsteroidal anti-inflammatory drugs and corticosteroids have been associated with a greater risk of colonic perforation. [2]\nAcetaminophen and antispasmodics such as dicyclomine are first-line agents for managing pain and cramping in mild to moderate disease. [5]\nClassic surgical indications include some features characteristic of Hinchey stage III or IV disease, such as the following:\nFree-air perforation with fecal peritonitis\nSuppurative peritonitis secondary to a ruptured abscess\nUncontrolled sepsis\nAbdominal or pelvic abscess (unless CT scan-guided aspiration is possible)\nFistula formation\nIntestinal obstruction\nFailing medical therapy\nImmunocompromised status [9]\nSee Treatment and Medication for more detail.\nDiverticular 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).\nThe 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]\nDiverticular 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.\nFor patient education resources, see Digestive Disorders Center, as well Diverticulitis (Diverticulosis) Symptoms and Diet and Abdominal Pain (Adults).\nA 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]\nDiverticula 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]\nBecause 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.\nDietary 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.\nTrue 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.\nDiverticula 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]\nDiverticulitis 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.\nIt 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.\nFistula 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.\nRecurrent attacks of diverticulitis can result in the formation of scar tissue, leading to narrowing and obstruction of the colonic lumen.\nUnited States data\nAcute 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]\nThe 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] ​\nPreviously, 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]\nDiverticulitis is also a leading indication for elective colectomy. This condition affects patients' quality of life beyond the period of acute illness.\nInternational data\nDiverticular 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]\nDiverticulitis 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]\nAge- and sex-related demographics\nThe 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.\nAlthough a male preponderance was noted in early series, subsequent studies have suggested either an equal sex distribution or a female preponderance. [2]\nIn 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]\nThe 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]\nMorbidity/mortality\nOf 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.\nDiverticulitis 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:\nAfter a first occurrence of acute diverticulitis, the 5-year recurrence rate is 20%. [23]\nPatients with diverticulitis who are managed conservatively (ie, do not undergo surgery) have a recurrence rate of 20%-35%.\nIn a study of 252 patients, a 47% recurrence rate was reported after 7 years. [24] The rate of surgery in these patients was 8% at 7 years and rose to 14% by 13 years. Recurrence after surgical resection ranged from 1% to 3%. The mortality from complications in patients with recurrent disease in the study was 1%.\nAnother study of 337 patients hospitalized for complicated diverticulitis revealed an association of perforation and mortality in those without a prior history of diverticulitis. [25] Of those patients with complicated diverticulitis, 53% presented with a first event.\nThese morbidity and mortality data, as well as the recurrence rates, are based on a retrospective review of relatively short-term data.\nMany 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]\nComplications 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]\nComplications of diverticulitis include the following:\nAbscess: Most common complication of diverticulitis\nIntestinal fistula, perforation, or obstruction\nGeneralized peritonitis\nStricture disease\nAbscesses 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.\nPatients 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]\nFrank 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.\nMicroperforation (or contained perforation) is only evident by the presence of air bubbles outside of the bowel wall on computed tomography (CT) imaging.\nSurgical resection of the involved bowel segment is mandatory to rule out cancer.\nDiverticular fistulas rarely close spontaneously, and a resection of the affected bowel segment is generally required.\n[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.\nSwanson SM, Strate LL. Acute colonic diverticulitis. Ann Intern Med. 2018 May 1. 168(9):ITC65-80. [Medline]. [Full Text].\nWasvary H, Turfah F, Kadro O, Beauregard W. 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Modified Hinchey Classification Stage and Diverticulitis Category\nModified Hinchey Classification Stage\nClinically mild diverticulitis, or diverticula with colonic wall thickening on CT\nColonic reaction with inflammatory reaction in the pericolic fat (phlegmon)\nPericolic or mesenteric abscess\nIntra-abdominal abscess, pelvic or retroperitoneal abscess\nGeneralized purulent peritonitis\nGeneralized fecal peritonitis\nElie M Ghoulam, MD, MS Resident Physician, Department of Internal Medicine, St Louis University School of Medicine\nDanisa M Clarrett, MD, MS Fellow, Division of Gastroenterology and Hepatology, St Louis University School of Medicine\nDanisa M Clarrett, MD, MS is a member of the following medical societies: American College of Gastroenterology, American Medical Association, Student National Medical Association\nElizabeth 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\nElizabeth V Marsicano, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Neurogastroenterology and Motility Society\nMarc 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\nMarc D Basson, MD, PhD, MBA, FACS is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Gastroenterological Association, Phi Beta Kappa, Sigma Xi\nBS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine\nBS 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, American Society for Gastrointestinal Endoscopy\nStanley 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\nStanley K Dea, MD is a member of the following medical societies: American Society for Gastrointestinal Endoscopy, Southern California Society of Gastroenterology\nYuvrajsinh 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\nYuvrajsinh Narendrasinh Chudasama, MD is a member of the following medical societies: American College of Physicians, American Medical Association\nKamyar Shahedi, MD Clinical Instructor, Olive View-UCLA Medical Center, University of California, Los Angeles, David Geffen School of Medicine\nKamyar Shahedi, MD is a member of the following medical societies: American College of Physicians, American Medical Association, California Medical Association\nDuminda B Suraweera, MD Resident Physician, Department of Medicine, Olive View–UCLA Medical Center\nDuminda B Suraweera, MD is a member of the following medical societies: American College of Physicians\nBS 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\nDavid Greenwald, MD Associate Professor of Clinical Medicine, Fellowship Program Director, Department of Medicine, Division of Gastroenterology, Montefiore Medical Center, Albert Einstein College of Medicine\nDavid 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\nNorvin Perez, MD Medical Director, Juneau Urgent and Family Care\nNorvin Perez, MD is a member of the following medical societies: American College of Emergency Physicians and American Medical Association\nWaqar 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\nWaqar 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\nAhmed Sherif, MD Staff Physician, Department of Internal Medicine, Montefiore Medical Center\nencoded search term (Diverticulitis) and Diverticulitis\nSmall Intestinal Diverticulosis\nFast Five Quiz: How Much Do You Know About Diverticulitis?\nImaging in Diverticulitis of the Colon\nLower Gastrointestinal Bleeding\nA 60-Year-Old Man With Intense Left-Sided Abdominal Pain\nClinical Trends for October 2016\nDiverticular Disease: The Old, the New, and the Ever-Changing View\nColonic Diverticula Are Not Associated With Mucosal Inflammation or Chronic Gastrointestinal Symptoms\nLymphogranuloma Venereum Proctitis Can Mimic IBD\nCan't-Miss Gastrointestinal Diagnoses\nJournal Article Diverticular Disease: The Old, the New, and the Ever-Changing View\nDiseases & Conditions Diverticulitis\nDiseases & Conditions Imaging in Diverticulitis of the Colon\nDiseases & Conditions Small Intestinal Diverticulosis"