Diverticulitis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun M.D., PhD.; Mohamed Moubarak, M.D. [2]; Ahmed Elsaiey, MBBCH [3] James Nasr[4]
Synonyms and keywords: Colonic diverticulitis, Diverticulitis of large intestine
Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2], Ahmed Elsaiey, MBBCH [3], James Nasr[4]
Overview
Diverticulitis is a common disease of the digestive tract that affects the colon. Diverticulitis develops from diverticulosis, which involves the formation of pouches (diverticula) on the outside of the colon. Diverticulitis results when one of these diverticula becomes inflamed, usually due to fecal trapping with bacterial translocation, microperforation, and altered gut microbiome and immune response.[1][2][3] Diverticulitis is classified as complicated or uncomplicated. In the United States the annual incidence of diverticulitis is around 180 per 100 000 people.[4] Among those with diverticulosis, only about 1% to 4% will develop diverticulitis in their lifetime.[5][6] The highest incidence occurs in patients older than 60, with rising incidence in adults younger than 50, particularly among men. Men are more commonly affected before age 50, while females are more commonly affected after age 50.[7] Risk factors include age, obesity, genetics, connective-tissue disorders, NSAIDs, steroids, opioids, hypertension, and type 2 diabetes.[8] Diverticulitis can cause many complications as abscess, perforation, peritonitis, and fistula formation. Symptoms of diverticulitis include left lower abdominal pain, fever, cramps, and constipation.[9] Common physical examination findings include tachycardia, fever, abdominal tenderness, guarding and rebound tenderness, and presence of a palpable mass.[10][11] Uncomplicated diverticulitis is managed with observation and pain management, with or without antibiotics.[12] Complicated diverticulitis is treated with intravenous antibiotics and, when indicated, percutaneous drainage or surgical resection.[13][14]
Historical Perspective
Diverticulitis was first described by Dr. Lavater in the 1700s. In the 18th century, Dr. Littre was the first person to describe the diverticular disease. Dr. Meckel gave a full description of the diverticulum in 1812.
Classification
Diverticulitis may be classified according to the 2014 guidelines by the German Societies of Gastroenterology (DGVS) and of Visceral Surgery (DGAV). They unanimously agreed on a classification system (Classification of Diverticular Disease (CDD)), that takes practical algorithms (symptomatic, asymptomatic, complicated, uncomplicated, acute, recurrent), ongoing surgical aspects (purulent versus fecal peritonitis), and contemporary diagnostic standards in clinical practice into account. As a result, this classification comprises the entire spectrum of diverticular disease. While the CDD system remains in use in some European centers, current U.S. guidance, including the 2025 JAMA review, primarily classifies diverticulitis as uncomplicated or complicated, with severity stratified using the modified Hinchey classification.[8]
Pathophysiology
Diverticula are sac-like protrusions of the mucosal and submucosa through weak points in the muscular wall, and occur more commonly in the sigmoid colon. Diverticulitis is the inflammation of a diverticulum. The first steps in the pathogenesis of diverticulitis are an increase in intraluminal pressure, change in intestinal motility, and bacterial colonization.[3] The inflammation is caused by histamine, tumor necrosis factor, and metalloproteinases, which have been found in diverticulitis patients’ tissue biopsies. Obstruction of the diverticula leads to bacterial colonization, which causes inflammation.
Causes
Common causes of diverticulitis include diverticulosis, and is believed to result from obstruction of a diverticulum by fecal material leading to bacterial translocation and mucosal inflammation, increased intraluminal pressure causing microperforation, and alterations in the gut microbiome and bile acids that disrupt the mucosal barrier and immune response.[1][2][3]
Differentiating Diverticulitis from Other Diseases
Diverticulitis must be differentiated from other diseases that cause lower abdominal pain and fever, such as appendicitis, inflammatory bowel disease, colon cancer, cystitis, and endometritis. Diverticulitis must be also differentiated from diseases causing peritonitis.
Epidemiology and Demographics
The lifetime risk of diverticulitis among individuals with diverticulosis is approximately 1% to 4%.[5][6] The highest incidence is in patients older than 60. Men are more commonly affected before age 50, while females are more commonly affected after age 50. The prevalence of diverticulitis has increased in developed countries.[7] In the United States, approximately 200,000 cases are admitted to the hospitals annually.[8] In Japan, more cases of right side diverticulitis have been reported than cases of left side diverticulitis.
Risk Factors
Risk factors for diverticulitis include older age, obesity, genetic predisposition, connective-tissue disorders (polycystic kidney disease, Marfan syndrome, and Ehlers-Danlos syndrome), hypertension, type 2 diabetes, and use of NSAIDs, corticosteroids, and opioids.[8]
Screening
There is insufficient evidence to recommend routine screening for diverticulitis.
Natural History, Complications, and Prognosis
Diverticulitis natural history is still being clarified. Diverticulitis can cause many complications that can be fatal in some cases. These complications include abscess, perforation, peritonitis, and fistula formation. Prognosis of diverticulitis is excellent; more than 90% of patients with uncomplicated diverticulitis improve with conservative management, and recurrence risk is lower than previously believed.[15]
Diagnosis
History and Symptoms
The most common symptoms of diverticulitis include left lower abdominal pain, fever, cramps, and constipation. A positive history of change in bowel habits is suggestive of diverticulitis. Less common symptoms include flatulence, nausea, and vomiting.[9]
Physical Examination
Patients with diverticulitis usually appear toxic due to pain. Common physical examination findings include tachycardia, fever, abdominal tenderness, guarding and rebound tenderness, and presence of a palpable mass. Diverticulitis diagnosis depends on taking a proper history, performing a physical examination, and imaging conifrmation. The known diagnostic criteria for diverticulitis include abdominal tenderness, especially in the left lower quadrant, and leukocytosis. CT scan findings help in disease confirmation.
Laboratory Findings
Diverticulitis diagnosis starts by taking history precisely and performing a physical examination. Lab tests are important in excluding other causes of abdominal pain and any other gastrointestinal disease. These lab tests include CBC, CRP, urinalysis, and liver tests. Imaging procedures including CT scan and colonoscopy are important measures in diagnosing diverticulitis.[16][17]
CT scan
Contrast-enhanced CT scan is the diagnostic test of choice for diverticulitis. It confirms the diagnosis, evaluates for complications such as abscess, perforation, and obstruction, and can guide percutaneous abscess drainage when needed.[15] [18]
MRI
On abdominal MRI, diverticulitis is characterized by thickening of the colon wall, the presence of the diverticula, and exudates from the colon. It may also show the presence of multiple abscesses. MRI is a good imaging modality that can be used in the diagnosis of diverticulitis since it has the advantage that it doesn’t involve exposure to radiation and rules out other abdominal causes of acute abdomen.[19] However, MRI is not the best diagnostic procedure for diverticulitis; CT scan is preferred.[15]
Ultrasound
On abdominal ultrasonography, diverticulitis is characterized by abscess formation, hypoechoic pericolic fat, the presence of diverticula, and thickening of the colon segments. Extra diverticular exudates and fluids can be also observed. [20]
X-ray
On abdominal X-ray, diverticulitis is characterized by multiple air and fluid levels if there is an intestinal perforation. Chest X-ray should be done in patients with diverticulitis to investigate for pneumoperitoneum, which is a harbinger of a critical illness and will lead to a change in the management plan for the case. X-ray can be used if CT is not available and in uncomplicated cases.
Other imaging findings
There are no other specific imaging findings for diverticulitis. Other studies such as barium enema and colonoscopy are contraindicated in the acute phase of diverticulitis due to the risk of perforation.
Other diagnostic studies
There are no other specific diagnostic studies for diverticulitis. Other studies such as barium enema and colonoscopy are contraindicated in the acute phase of diverticulitis due to the risk of perforation.
Treatment
Medical Therapy
Uncomplicated diverticulitis is managed with observation and pain management, with or without antibiotics.[12] Complicated diverticulitis is treated with intravenous antibiotics and, when indicated, percutaneous drainage or surgical resection.[13][14]
Surgery
Surgery is not the first-line treatment option for patients with diverticulitis. Emergency or urgent surgery is usually reserved for patients complicated with peritonitis, who are unresponsive to treatment, who have intestinal obstruction, or with abscess formation. Elective surgery may be performed and it depends on many factors like the age of the patient, severity score, and persistence of symptoms.[12]
Prevention
Primary prevention of diverticulitis focuses on overall lifestyle improvements. Physical activity, and weight loss to achieve a BMI less than 25.0 may reduce diverticulitis incidence.[21] High-fiber diets have been associated with general bowel health, although they have not been shown to prevent diverticulosis or diverticulitis.[22]
References
- ↑ 1.0 1.1 Humes D, Simpson J, Spiller RC. Colonic diverticular disease. BMJ Clin Evid. 2007 Aug 15;2007:0405. PMID: 19454119; PMCID: PMC2943810.
- ↑ 2.0 2.1 von Rahden BH, Germer CT. Pathogenesis of colonic diverticular disease. Langenbecks Arch Surg. 2012 Oct;397(7):1025-33. doi: 10.1007/s00423-012-0961-5. Epub 2012 Jun 20. PMID: 22711236.
- ↑ 3.0 3.1 3.2 Strate LL, Morris AM. Epidemiology, Pathophysiology, and Treatment of Diverticulitis. Gastroenterology. 2019 Apr;156(5):1282-1298.e1. doi: 10.1053/j.gastro.2018.12.033. Epub 2019 Jan 17. PMID: 30660732; PMCID: PMC6716971.
- ↑ Bharucha AE, Parthasarathy G, Ditah I, Fletcher JG, Ewelukwa O, Pendlimari R, Yawn BP, Melton LJ, Schleck C, Zinsmeister AR. Temporal Trends in the Incidence and Natural History of Diverticulitis: A Population-Based Study. Am J Gastroenterol. 2015 Nov;110(11):1589-96. doi: 10.1038/ajg.2015.302. Epub 2015 Sep 29. PMID: 26416187; PMCID: PMC4676761.
- ↑ 5.0 5.1 Stollman N, Smalley W, Hirano I; AGA Institute Clinical Guidelines Committee. American Gastroenterological Association Institute guideline on the management of acute diverticulitis. Gastroenterology. 2015;149(7):1944-1949. doi:10. 1053/j.gastro.2015.10.003
- ↑ 6.0 6.1 Shahedi K, Fuller G, Bolus R, Cohen E, Vu M, Shah R, Agarwal N, Kaneshiro M, Atia M, Sheen V, Kurzbard N, van Oijen MG, Yen L, Hodgkins P, Erder MH, Spiegel B. Long-term risk of acute diverticulitis among patients with incidental diverticulosis found during colonoscopy. Clin Gastroenterol Hepatol. 2013 Dec;11(12):1609-13. doi: 10.1016/j.cgh.2013.06.020. Epub 2013 Jul 12. PMID: 23856358; PMCID: PMC5731451.
- ↑ 7.0 7.1 Long B, Werner J, Gottlieb M. Emergency medicine updates: Acute diverticulitis. Am J Emerg Med. 2024;76:1-6. doi:10.1016/j.ajem.2023.10.051.
- ↑ 8.0 8.1 8.2 8.3 Peery AF, Wilson GC, Crockett SD. Diverticulitis: A Review. JAMA. 2025;333(2):158-168. doi:10.1001/jama.2024.23427.
- ↑ 9.0 9.1 Longstreth GF, Iyer RL, Chu LH, Chen W, Yen LS, Hodgkins P, Kawatkar AA. Acute diverticulitis: demographic, clinical and laboratory features associated with computed tomography findings in 741 patients. Aliment Pharmacol Ther. 2012 Nov;36(9):886-94. doi: 10.1111/apt.12047. PMID: 22967027.
- ↑ Zaidi E, Daly B. CT and clinical features of acute diverticulitis in an urban U.S. population: rising frequency in young, obese adults. AJR Am J Roentgenol. 2006 Sep;187(3):689-94. doi: 10.2214/AJR.05.0033. PMID: 16928931.
- ↑ Al-Saadi H, Abdulrasool H, Murphy E. Evaluation of Clinical Assessment in Predicting Complicated Acute Diverticulitis. Cureus. 2023 Feb 6;15(2):e34709. doi: 10.7759/cureus.34709. PMID: 36777973; PMCID: PMC9907385.
- ↑ 12.0 12.1 12.2 Garfinkle R, Bennett RD, Dantu S, Gasior A, Hawkins AT, Holland J, Ore AS, Shaffer VO, Taylor JP, Sylla P, McLemore EC, Boutros M. SAGES white paper on antibiotic omission in the management of acute uncomplicated diverticulitis: why, when, who, and most importantly, how. Surg Endosc. 2025 Jun;39(6):3456-3465. doi: 10.1007/s00464-025-11738-w. Epub 2025 Apr 22. PMID: 40263135.
- ↑ 13.0 13.1 Gregersen R, Mortensen LQ, Burcharth J, Pommergaard HC, Rosenberg J. Treatment of patients with acute colonic diverticulitis complicated by abscess formation: A systematic review. Int J Surg. 2016 Nov;35:201-208. doi: 10.1016/j.ijsu.2016.10.006. Epub 2016 Oct 11. PMID: 27741423.
- ↑ 14.0 14.1 Garfinkle R, Kugler A, Pelsser V, Vasilevsky CA, Morin N, Gordon P, Feldman L, Boutros M. Diverticular Abscess Managed With Long-term Definitive Nonoperative Intent Is Safe. Dis Colon Rectum. 2016 Jul;59(7):648-55. doi: 10.1097/DCR.0000000000000624. PMID: 27270517.
- ↑ 15.0 15.1 15.2 Brown RF, Lopez K, Smith CB, Charles A. Diverticulitis: A Review. JAMA. Published online July 24, 2025. doi:10.1001/jama.2025.10234
- ↑ Rafferty J, Shellito P, Hyman NH, Buie WD, Standards Committee of American Society of Colon and Rectal Surgeons (2006). “Practice parameters for sigmoid diverticulitis”. Dis Colon Rectum. 49 (7): 939–44. doi:10.1007/s10350-006-0578-2. PMID 16741596.
- ↑ Käser SA, Fankhauser G, Glauser PM, Toia D, Maurer CA (2010). “Diagnostic value of inflammation markers in predicting perforation in acute sigmoid diverticulitis”. World J Surg. 34 (11): 2717–22. doi:10.1007/s00268-010-0726-7. PMID 20645093.
- ↑ Destigter KK, Keating DP. Imaging update: acute colonic diverticulitis. Clin Colon Rectal Surg. 2009 Aug;22(3):147-55. doi: 10.1055/s-0029-1236158. PMID: 20676257; PMCID: PMC2780264.
- ↑ Heverhagen JT, Sitter H, Zielke A, Klose KJ. Prospective evaluation of the value of magnetic resonance imaging in suspected acute sigmoid diverticulitis. Dis Colon Rectum. 2008 Dec;51(12):1810-5. doi: 10.1007/s10350-008-9330-4. Epub 2008 Apr 29. PMID: 18443876.
- ↑ Laméris W, van Randen A, Bipat S, Bossuyt PM, Boermeester MA, Stoker J. Graded compression ultrasonography and computed tomography in acute colonic diverticulitis: meta-analysis of test accuracy. Eur Radiol. 2008 Nov;18(11):2498-511. doi: 10.1007/s00330-008-1018-6. Epub 2008 Jun 4. PMID: 18523784.
- ↑ Liu PH, Cao Y, Keeley BR, Tam I, Wu K, Strate LL, Giovannucci EL, Chan AT. Adherence to a Healthy Lifestyle is Associated With a Lower Risk of Diverticulitis among Men. Am J Gastroenterol. 2017 Dec;112(12):1868-1876. doi: 10.1038/ajg.2017.398. Epub 2017 Nov 7. PMID: 29112202; PMCID: PMC5736501.
- ↑ Peery AF, Barrett PR, Park D, Rogers AJ, Galanko JA, Martin CF, Sandler RS. A high-fiber diet does not protect against asymptomatic diverticulosis. Gastroenterology. 2012 Feb;142(2):266-72.e1. doi: 10.1053/j.gastro.2011.10.035. Epub 2011 Nov 4. PMID: 22062360; PMCID: PMC3724216.
Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]
Overview
Diverticulitis was first described by Dr. Lavater. In the 18th century, Dr. Littre was the first person to describe diverticular disease. Dr. Meckel gave a full description of the diverticulum in 1812.
Historical Perspective
- In 1589, Dr. Hildanus was the first physician to discover diverticular lesion in the colon.[1]
- In the 1700s, Alexis Littre was the first to describe diverticular diseases when he described a diverticular hernia.[2]
- In 1812, Dr. Meckel described the diverticulum now known as Meckel’s diverticulum.
- In 1902, Dr. Deetz provided a full description of infection of the diverticulum.
References
- ↑ MOSES WR (1947). “Meckel’s diverticulum; report of two unusual cases”. N Engl J Med. 237 (4): 118–22. doi:10.1056/NEJM194707242370403. PMID 20252118.
- ↑ Matrana, Marc; Margolin, David (2009). “Epidemiology and Pathophysiology of Diverticular Disease”. Clinics in Colon and Rectal Surgery. 22 (03): 141–146. doi:10.1055/s-0029-1236157. ISSN 1531-0043.
Classification
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omodamola Aje B.Sc, M.D. [2] James Nasr[3]
Overview
Diverticular diseases may be classified based on the presenting signs and symptoms according to the German guidelines that were published by the German Society of Gastroenterology (DGVS) and of Visceral Surgery (DGAV) in 2014. This aggreed upon classification system (Classification of Diverticular Disease (CDD), takes signs and symptoms, natural history (symptomatic, asymptomatic, complicated, uncomplicated, acute, recurrent), surgical aspects (purulent vs. fecal peritonitis), and clinically relevant diagnostic tests into account. As a result, this classification comprises the entire spectrum of diverticular disease. While the CDD system remains in use in some European centers, current U.S. guidance, including the 2025 JAMA review, primarily classifies diverticulitis as uncomplicated or complicated, with severity stratified using the modified Hinchey classification.[1]
Classification
The following table describes the classification of diverticular disease according to the German guidelines (in 2014) by the German Societies of Gastroenterology (DGVS) and of Visceral Surgery (DGAV).[2]
| Type | Subtype | Description | Features |
|---|---|---|---|
| Type 0
(Asymptomatic diverticulosis) |
Type 0 | None |
|
| Type 1
(Acute uncomplicated diverticulitis) |
Type 1a | Diverticulitis without peridiverticulitis |
|
| Type 1b | Diverticulitis with phlegmonous peridiverticulitis |
| |
| Type 2
(Acute complicated diverticulitis) |
Type 2a | Microabscess |
|
| Type 2b | Macro-abscess | ||
| Type 2c | Free perforation |
| |
| Type 2c1 | Purulent peritonitis | ||
| Type 2c2 | Fecal peritonitis | ||
| Type 3
Chronic diverticular disease (relapsing or persistent) |
Type 3a | Symptomatic uncomplicated diverticular disease (SUDD) |
|
| Type 3b | Relapsing diverticulitis without complications |
| |
| Type 3c | Relapsing diverticulitis with complications | ||
| Type 4
(Diverticular bleeding) |
Type 4 | Diverticular bleeding |
|
References
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2], Ahmed Elsaiey, MBBCH [3] James Nasr[4]
Overview
Diverticula are sac-like protrusions of the mucosal and submucosa through weak points in the muscular wall, and occur more commonly in the sigmoid colon. Diverticulitis is the inflammation of a diverticulum. The first steps in the pathogenesis of diverticulitis are an increase in intraluminal pressure, change in intestinal motility, and bacterial colonization.[1] The inflammation is caused by histamine, tumor necrosis factor, and metalloproteinases, which have been found in diverticulitis patients’ tissue biopsies. Obstruction of the diverticula leads to bacterial colonization, which causes inflammation.
Pathophysiology
Pathogenesis
The pathogenesis of diverticulitis is believed to be erosion of the wall of the diverticulum. It is worsened by an increase in intraluminal pressure or food remnants.
- Diverticula are protrusions of the mucosa and serosa intestinal layers and occur more often on the left side than the right side. Diverticulitis is the inflammation of this protrusion.
- Inflammation and focal necrosis ensue, resulting in perforation and inflammation.[2]
- The pathogenesis of diverticulitis includes three main processes, which are:
- Change in the intestinal motility
- Increase in the luminal pressure
- Secondary infection may be caused by colonic microbial flora[3]
- In vivo tests showed that adding chemicals to the colonic tissue can lead to diverticulitis. Neuro-alteration of the tissue was noticed during this test. It showed increased contractility and loss of relaxation.[4] This alteration in the muscle tissue due to inflammation leads to histological changes of the muscle and nerves.
- Inflammation in cases of diverticulitis is caused by histamine, tumor necrosis factor, and matrix metalloproteinases. These substances were detected in colonic tissue biopsies of diverticulitis patients.[5]
- The collection of feces and undigested food in the diverticula leads to diverticulum obstruction. This obstruction, by increasing intraluminal pressure, leads to diverticulum distension and collection of the bacteria that cause inflammation.
- The presence of lymphocytes and granulomas are predictive of chronic inflammation.
Gross Pathology
The gross pathology of diverticulitis includes features such as:[6][7]
- Corrugated – like cardboard
- Wall thickening (reactive)
- Located usually in the sigmoid colon
- May be found in the appendix
Microscopic Pathology
The possible histopathological findings of diverticulitis may include the following:
- Abscess at which neutrophils, lymphocytes, and fibrosis are observed.
- Sulfur granules with peripheral inflammatory cells.
- A brief video showing histopathological findings in patients with diverticulitis:
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References
- ↑ Strate LL, Morris AM. Epidemiology, Pathophysiology, and Treatment of Diverticulitis. Gastroenterology. 2019 Apr;156(5):1282-1298.e1. doi: 10.1053/j.gastro.2018.12.033. Epub 2019 Jan 17. PMID: 30660732; PMCID: PMC6716971.
- ↑ Rege RV, Nahrwold DL (1989). “Diverticular disease”. Curr Probl Surg. 26 (3): 133–89. PMID 2651018.
- ↑ Morris AM, Regenbogen SE, Hardiman KM, Hendren S (2014). “Sigmoid diverticulitis: a systematic review”. JAMA. 311 (3): 287–97. doi:10.1001/jama.2013.282025. PMID 24430321.
- ↑ Guagnini F, Valenti M, Mukenge S, Matias I, Bianchetti A, Di Palo S; et al. (2006). “Neural contractions in colonic strips from patients with diverticular disease: role of endocannabinoids and substance P.” Gut. 55 (7): 946–53. doi:10.1136/gut.2005.076372. PMC 1856307. PMID 16423891.
- ↑ Tursi A, Elisei W, Brandimarte G, Giorgetti GM, Inchingolo CD, Nenna R; et al. (2012). “Mucosal expression of basic fibroblastic growth factor, Syndecan 1 and tumor necrosis factor-alpha in diverticular disease of the colon: a case-control study”. Neurogastroenterol Motil. 24 (9): 836-e396. doi:10.1111/j.1365-2982.2012.01946.x. PMID 22680042.
- ↑ Nicholson BD, Hyland R, Rembacken BJ, Denyer M, Hull MA, Tolan DJ (2011). “Colonoscopy for colonic wall thickening at computed tomography: a worthwhile pursuit?”. Surg Endosc. 25 (8): 2586–91. doi:10.1007/s00464-011-1591-7. PMID 21359889.
- ↑ Sohn TJ, Chang YS, Kang JH, Kim DH, Lee TS, Han JK, Kim SH, Hong YO (2013). “Clinical characteristics of acute appendiceal diverticulitis”. J Korean Surg Soc. 84 (1): 33–7. doi:10.4174/jkss.2013.84.1.33. PMC 3539107. PMID 23323233.
Causes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Ogheneochuko Ajari, MB.BS, MS [3] James Nasr[4]
Overview
Common causes of diverticulitis include diverticulosis, and is believed to result from obstruction of a diverticulum by fecal material leading to bacterial translocation and mucosal inflammation, increased intraluminal pressure causing microperforation, and alterations in the gut microbiome and bile acids that disrupt the mucosal barrier and immune response.[1][2][3]
Causes
Common Causes
Common causes of diverticulitis include the following:[4]
- Obstruction by fecal material
- Increased luminal pressure
- Alterations in the gut microbiome
- Diverticulosis
- Toclizumab
Causes by Organ System
| Cardiovascular | No underlying causes |
| Chemical / poisoning | No underlying causes |
| Dermatologic | No underlying causes |
| Drug Side Effect | Toclizumab |
| Ear Nose Throat | No underlying causes |
| Endocrine | No underlying causes |
| Environmental | No underlying causes |
| Gastroenterologic | Obstruction, Increased luminal pressure, alteration in gut microbiome, diverticulosis |
| Genetic | No underlying causes |
| Hematologic | No underlying causes |
| Iatrogenic | No underlying causes |
| Infectious Disease | No underlying causes |
| Musculoskeletal / Ortho | No underlying causes |
| Neurologic | No underlying causes |
| Nutritional / Metabolic | Lack of exercise, abdominal distension, constipation |
| Obstetric/Gynecologic | No underlying causes |
| Oncologic | No underlying causes |
| Opthalmologic | No underlying causes |
| Overdose / Toxicity | No underlying causes |
| Psychiatric | No underlying causes |
| Pulmonary | No underlying causes |
| Renal / Electrolyte | No underlying causes |
| Rheum / Immune / Allergy | No underlying causes |
| Sexual | No underlying causes |
| Trauma | No underlying causes |
| Urologic | No underlying causes |
| Dental | No underlying causes |
| Miscellaneous | No underlying causes |
References
- ↑ Humes D, Simpson J, Spiller RC. Colonic diverticular disease. BMJ Clin Evid. 2007 Aug 15;2007:0405. PMID: 19454119; PMCID: PMC2943810.
- ↑ von Rahden BH, Germer CT. Pathogenesis of colonic diverticular disease. Langenbecks Arch Surg. 2012 Oct;397(7):1025-33. doi: 10.1007/s00423-012-0961-5. Epub 2012 Jun 20. PMID: 22711236.
- ↑ Strate LL, Morris AM. Epidemiology, Pathophysiology, and Treatment of Diverticulitis. Gastroenterology. 2019 Apr;156(5):1282-1298.e1. doi: 10.1053/j.gastro.2018.12.033. Epub 2019 Jan 17. PMID: 30660732; PMCID: PMC6716971.
- ↑ Bugiantella W, Rondelli F, Longaroni M, Mariani E, Sanguinetti A, Avenia N (2015). “Left colon acute diverticulitis: an update on diagnosis, treatment and prevention”. Int J Surg. 13: 157–64. doi:10.1016/j.ijsu.2014.12.012. PMID 25497007.
Differentiating Diverticulitis from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2],Seyedmahdi Pahlavani, M.D. [3], Omodamola Aje B.Sc, M.D. [4], Ahmed Elsaiey, MBBCH [5]
Overview
Diverticulitis must be differentiated from other diseases that cause lower abdominal pain and fever like appendicitis, inflammatory bowel disease, colon cancer, cystitis, and endometritis. Diverticulitis must be also differentiated from diseases causing peritonitis.
Differentiating Diverticulitis from other Diseases
Diverticulitis must be differentiated from other diseases that cause lower abdominal pain and fever. Diverticulitis must be also differentiated from diseases causing peritonitis.
Differentiating diverticulitis from diseases causing lower abdominal pain and fever
Diverticulitis must be differentiated from other diseases that cause lower abdominal pain and fever like appendicitis, inflammatory bowel disease, colon cancer, cystitis, and endometritis.[1][2][3][4][5][6]
| Diseases | Symptoms | Signs | Diagnosis | Other Features | |||||
|---|---|---|---|---|---|---|---|---|---|
| Location of abdominal pain | Bowel habits | Rebound tenderness | Guarding | Genitourinary signs | Lab findings | Imaging | |||
| GI diseases | Diverticulitis | Left lower quadrant (LLQ) | Constipation
or |
– | + | + |
|
||
| Appendicitis | LLQ / RRQ | Constipation | + | + | – |
|
|||
| Inflammatory bowel disease | LLQ | Bloody diarrhea | – | – | – |
| |||
| Colon carcinoma | LLQ | Constipation | – | – | – |
|
|||
| Strangulated hernia | LLQ | – | – | – | – |
|
|||
| Gentiourinary diseases | Cystitis | LLQ | – | + | – |
|
|
||
| Prostatitis | LLQ
Groin pain |
– | – | – |
|
|
|||
| Pelvic inflammatory disease | Bilateral | – | – | – |
|
||||
| Gynecological diseases | Endometritis | LLQ | – | + | – | + |
|
|
|
| Salpingitis | LLQ/ RLQ | +/- | +/- |
|
|||||
Differentiating diverticulitis from diseases causing peritonitis
The following table differentiates diverticulitis from other diseases causing peritonitis:
| Classification of acute abdomen based
on etiology |
Presentation | Clinical findings | Diagnosis | Comments | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Fever | Rigors and Chills | Abdominal Pain | Jaundice | Hypotension | Guarding | Rebound Tenderness | Bowel sounds | Lab Findings | Imaging | ||||
| Common causes of | Spontaneous bacterial peritonitis | + | Diffuse | − | − | − | − | Hypoactive |
|
Ultrasound for evaluation of liver cirrhosis | – | ||
| Perforated gastric and duodenal ulcer | + | Diffuse | − | + | + | + | N | Air under diaphragm in upright chest x- ray (CXR) | Upper GI endoscopy for diagnosis | ||||
| Acute suppurative cholangitis | + | + | RUQ | + | + | + | + | ± | |||||
| Acute cholangitis | + | − | RUQ | + | − | − | − | N | Abnormal LFT | Ultrasound shows biliary dilatation | Biliary drainage (ERCP) + intravenous (IV) antibiotics | ||
| Acute cholecystitis | + | RUQ | + | − | − | Hypoactive | Ultrasound shows gallstone and evidence of inflammation | Murphy’s sign | |||||
| Acute pancreatitis | + | Epigastric | ± | − | − | N | Increased amylase / lipase | Ultrasound shows evidence of inflammation | Pain radiation to back | ||||
| Acute appendicitis | + | RLQ | − | + | + | Hypoactive | Leukocytosis | Ultrasound shows evidence of inflammation | Nausea & vomiting, decreased appetite | ||||
| Acute diverticulitis | + | LLQ | ± | + | − | Hypoactive | Leukocytosis | CT scan and ultrasound shows evidence of inflammation | |||||
| Hollow Viscous Obstruction | Small intestine obstruction | − | Diffuse | − | + | ± | Hyperactive then absent | Leukocytosis | Abdominal X ray | Nausea & vomiting associated with constipation, abdominal distention | |||
| Gall stone disease/Cholelithiasis | ± | − | |||||||||||
| Volvulus | – | Diffuse | – | + | – | Hypoactive | Leukocytosis | CT scan and abdominal X ray | Nausea & vomiting associated with constipation, abdominal distention | ||||
| Biliary colic | – | RUQ | + | – | – | N | Increased bilirubin and alkaline phosphatase | Ultrasound | Nausea & vomiting | ||||
| Renal colic | – | Flank pain | – | – | – | N | Hematuria | CT scan and ultrasound | Colicky abdominal pain associated with nausea & vomiting | ||||
| Vascular Disorders | Ischemic causes | Mesenteric ischemia | ± | Periumbilical | – | – | – | Hyperactive | Leukocytosis and lactic acidosis | CT scan | Nausea & vomiting, normal physical examination | ||
| Acute ischemic colitis | ± | Diffuse | – | + | + | Hyperactive then absent | Leukocytosis | CT scan | Nausea & vomiting | ||||
| Hemorrhagic causes | Ruptured abdominal aortic aneurysm | – | Diffuse | – | – | – | N | Normal | CT scan | Unstable hemodynamics | |||
| Intra-abdominal or retroperitoneal hemorrhage | – | Diffuse | – | – | – | N | Anemia | CT scan | History of trauma | ||||
| Gynaecological Causes | Fallopian tube | Acute salpingitis | + | LLQ/ RLQ | − | ± | ± | N | Leukocytosis | Pelvic ultrasound | Vaginal discharge | ||
| Ovarian cyst complications and endometrial disease | Torsion of the cyst | – | RLQ / LLQ | – | ± | ± | N | Increased ESR and CRP | Ultrasound | Sudden onset sever pain with nausea and vomiting | |||
| Endometriosis | – | RLQ/LLQ | – | +/- | +/- | N | Normal | Laproscopy | Menstrual-associated symptoms, pelvic | ||||
| Cyst rupture | – | RLQ / LLQ | – | +/- | +/- | N | Increased ESR and CRP | Ultrasound | Sudden onset sever pain with nausea and vomiting | ||||
| Pregnancy | Ruptured ectopic pregnancy | – | RLQ / LLQ | – | – | – | N | Positive pregnancy test | Ultrasound | History of missed period and vaginal bleeding | |||
| Functional | Irritable bowel syndrome | – | Diffuse | – | – | – | – | N |
|
– |
| ||
References
- ↑ Laurell H, Hansson LE, Gunnarsson U (2007). “Acute diverticulitis–clinical presentation and differential diagnostics”. Colorectal Dis. 9 (6): 496–501, discussion 501-2. doi:10.1111/j.1463-1318.2006.01162.x. PMID 17573742.
- ↑ Hardin, M. Acute Appendicitis: Review and Update. Am Fam Physician”.1999, Nov 1;60(7):2027-2034
- ↑ Hanauer SB (1996). “Inflammatory bowel disease”. N Engl J Med. 334 (13): 841–8. doi:10.1056/NEJM199603283341307. PMID 8596552.
- ↑ Cystitis-acute. MedlinePlus.https://www.nlm.nih.gov/medlineplus/ency/article/000526.htm Accessed on February 9, 2016
- ↑ Prostatitis – bacterial. NLM Medline Plus 2016. https://www.nlm.nih.gov/medlineplus/ency/article/000519.htm. Accessed on March 2, 2016
- ↑ Ford GW, Decker CF (2016). “Pelvic inflammatory disease”. Dis Mon. 62 (8): 301–5. doi:10.1016/j.disamonth.2016.03.015. PMID 27107781.
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2] James Nasr[3]
Overview
The lifetime risk of diverticulitis among individuals with diverticulosis is approximately 1% to 4%.[1][2] The highest incidence is in patients older than 60. Men are more commonly affected before age 50, while females are more commonly affected after age 50. The prevalence of diverticulitis has increased in developed countries.[3] In the United States, approximately 200,000 cases are admitted to the hospitals annually.[4] In Japan, more cases of right side diverticulitis have been reported than cases of left side diverticulitis.
Epidemiology and Demographics
Prevalence
The prevalence of diverticulitis is well below 1% at age 40 and between 0.4% and 2% at age 60. [5]
Age
- The prevalence of diverticulitis increases with age.
- The mean age at admission for acute diverticulitis is 63 years.[6]
Gender
- Men under 50 are more often affected by diverticulitis than women of the same age.
- Men are more commonly affected before age 50, while females are more commonly affected after age 50. [3]
Race
- There is no racial predilection for diverticulitis.
Developed countries
- The prevalence and incidence of diverticulitis have significantly increased in developed countries that consume a lot of Westernized food that is poor in fiber.
- In the United States, about 200,000 cases of diverticulitis are admitted to hospitals annually.[4]
- In Japan, there has been an increase in the prevalence of right-sided diverticulosis similar to the increase in left-sided diverticula in Westernized countries.[7][8]
References
- ↑ Stollman N, Smalley W, Hirano I; AGA Institute Clinical Guidelines Committee. American Gastroenterological Association Institute guideline on the management of acute diverticulitis. Gastroenterology. 2015;149(7):1944-1949. doi:10. 1053/j.gastro.2015.10.003
- ↑ Shahedi K, Fuller G, Bolus R, Cohen E, Vu M, Shah R, Agarwal N, Kaneshiro M, Atia M, Sheen V, Kurzbard N, van Oijen MG, Yen L, Hodgkins P, Erder MH, Spiegel B. Long-term risk of acute diverticulitis among patients with incidental diverticulosis found during colonoscopy. Clin Gastroenterol Hepatol. 2013 Dec;11(12):1609-13. doi: 10.1016/j.cgh.2013.06.020. Epub 2013 Jul 12. PMID: 23856358; PMCID: PMC5731451.
- ↑ 3.0 3.1 Long B, Werner J, Gottlieb M. Emergency medicine updates: Acute diverticulitis. Am J Emerg Med. 2024;76:1-6. doi:10.1016/j.ajem.2023.10.051.
- ↑ 4.0 4.1 Peery AF, Wilson GC, Crockett SD. Diverticulitis: A Review. JAMA. 2025;333(2):158-168. doi:10.1001/jama.2024.23427.
- ↑ Brown RF, Lopez K, Smith CB, Charles A. Diverticulitis: A Review. JAMA. Published online July 24, 2025. doi:10.1001/jama.2025.10234
- ↑ Peery AF, Barrett PR, Park D, Rogers AJ, Galanko JA, Martin CF; et al. (2012). “A high-fiber diet does not protect against asymptomatic diverticulosis”. Gastroenterology. 142 (2): 266–72.e1. doi:10.1053/j.gastro.2011.10.035. PMC 3724216. PMID 22062360.
- ↑ Sugihara K, Muto T, Morioka Y, Asano A, Yamamoto T (1984). “Diverticular disease of the colon in Japan. A review of 615 cases”. Dis Colon Rectum. 27 (8): 531–7. PMID 6468190.
- ↑ Miura S, Kodaira S, Shatari T, Nishioka M, Hosoda Y, Hisa TK (2000). “Recent trends in diverticulosis of the right colon in Japan: retrospective review in a regional hospital”. Dis Colon Rectum. 43 (10): 1383–9. PMID 11052515.
Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2] James Nasr[3]
Overview
Risk factors for diverticulitis include older age, obesity, genetic predisposition, connective-tissue disorders (polycystic kidney disease, Marfan syndrome, and Ehlers-Danlos syndrome), hypertension, type 2 diabetes, and use of NSAIDs, corticosteroids, and opioids.[1]
Risk Factors
Risk factors for the recurrence of diverticulitis
Recurrence of diverticulitis has been reported to occur in 20% of patients with previous episodes of diverticulitis.[2] Risk factors for diverticulitis include the following:[3][4]
- Diverticulosis itself is a risk factor for recurrence
- Multiple diverticula
- Older age
- Obesity
- Genetic predisposition
- Polycystic kidney disease
- Marfan syndrome
- Ehlers-Danlos syndrome
- Hypertension
- Family history of diverticulitis
- Having a large portion of infected colon
- NSAIDs
- Corticosteroids
- Opioids
References
- ↑ Peery AF, Wilson GC, Crockett SD. Diverticulitis: A Review. JAMA. 2025;333(2):158-168. doi:10.1001/jama.2024.23427.
- ↑ Peery AF (2016). “Recent Advances in Diverticular Disease”. Curr Gastroenterol Rep. 18 (7): 37. doi:10.1007/s11894-016-0513-1. PMID 27241190.
- ↑ Levy MJ, Osterkamp RL, Glauninger K, Strate LL. Diverticulosis morphology is associated with risk of diverticulitis. Eur J Gastroenterol Hepatol. 2024 Apr 1;36(4):382-386. doi: 10.1097/MEG.0000000000002717. Epub 2024 Feb 28. PMID: 38417057; PMCID: PMC10914328.
- ↑ Peery AF, Shaukat A, Strate LL. AGA Clinical Practice Update on Medical Management of Colonic Diverticulitis: Expert Review. Gastroenterology. 2021 Feb;160(3):906-911.e1. doi: 10.1053/j.gastro.2020.09.059. Epub 2020 Dec 3. PMID: 33279517; PMCID: PMC7878331.
Screening
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
There is insufficient evidence to recommend routine screening for diverticulitis.
Screening
There is insufficient evidence to recommend routine screening for diverticulitis.
References
Natural History, Complications and Prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2] James Nasr[3]
Overview
Diverticulitis natural history is still being clarified. Diverticulitis can cause many complications that can be fatal in some cases. These complications include abscess, perforation, peritonitis, and fistula formation. Prognosis of diverticulitis is excellent; more than 90% of patients with uncomplicated diverticulitis improve with conservative management, and recurrence risk is lower than previously believed.[1]
Natural History
The natural history of diverticulitis is still not well understood. However, some studies have shown the disease to take a benign course with a low incidence of complications if left untreated.[2][3]
Complications
In complicated diverticulitis, bacteria may subsequently infect the outside of the colon if an inflamed diverticulum bursts open. If the infection spreads to the lining of the abdominal cavity (peritoneum), this can cause potentially fatal peritonitis. Sometimes, inflamed diverticula can cause narrowing of the bowel, causing an obstruction. Also, the affected part of the colon could adhere to the bladder or other adjacent organs, causing a fistula. These complications always require treatment to prevent them from progressing and causing serious illness.[4]
Abscess
- Abscess formation may take place in cases of diverticulitis.[5]
- The abscess can be detected by CT scan and can be resolved with antibiotics. If the abscess persists, cutaneous drainage is recommended.
Perforation and peritonitis
- Perforation can lead to secondary peritonitis due to chemical irrigation by feces.[6]
- This is rare but may be fatal.
Fistula
- Fistula formation is another complication of acute diverticulitis. It occurs between the colon and its adjacent structures, especially the bladder forming the colovesical fistula.
- Genitourinary manifestations may present as dysuria.[7]
Prognosis
In patients with acute uncomplicated diverticulitis, conservative treatment is successful in 70 to 100 percent of patients and mortality is negligible.[8]
References
- ↑ Brown RF, Lopez K, Smith CB, Charles A. Diverticulitis: A Review. JAMA. Published online July 24, 2025. doi:10.1001/jama.2025.10234
- ↑ Salem TA, Molloy RG, O’Dwyer PJ (2007). “Prospective, five-year follow-up study of patients with symptomatic uncomplicated diverticular disease”. Dis Colon Rectum. 50 (9): 1460–4. doi:10.1007/s10350-007-0226-5. PMID 17431721. Review in: J Fam Pract. 2007 Dec;56(12):992
- ↑ Floch MH, Bina I (2004). “The natural history of diverticulitis: fact and theory”. J Clin Gastroenterol. 38 (5 Suppl 1): S2–7. PMID 15115921.
- ↑ Morris AM, Regenbogen SE, Hardiman KM, Hendren S (2014). “Sigmoid diverticulitis: a systematic review”. JAMA. 311 (3): 287–97. doi:10.1001/jama.2013.282025. PMID 24430321.
- ↑ Bahadursingh AM, Virgo KS, Kaminski DL, Longo WE (2003). “Spectrum of disease and outcome of complicated diverticular disease”. Am J Surg. 186 (6): 696–701. PMID 14672782.
- ↑ Nagorney DM, Adson MA, Pemberton JH (1985). “Sigmoid diverticulitis with perforation and generalized peritonitis”. Dis Colon Rectum. 28 (2): 71–5. PMID 3971809.
- ↑ Woods RJ, Lavery IC, Fazio VW, Jagelman DG, Weakley FL (1988). “Internal fistulas in diverticular disease”. Dis Colon Rectum. 31 (8): 591–6. PMID 3402284.
- ↑ Rafferty J, Shellito P, Hyman NH, Buie WD (2006). “Practice parameters for sigmoid diverticulitis”. Dis. Colon Rectum. 49 (7): 939–44. doi:10.1007/s10350-006-0578-2. PMID 16741596.
Diagnosis
Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | CT | MRI | Ultrasound | X Ray | Other Imaging Findings | Other Diagnostic Studies
Treatment
Treatment
Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-effectiveness of therapy | Future or Investigational Therapies
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