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Reliable, easy-to-read patient information on common medical conditions β€” written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Diverticulosis

Introduction

Template:DiseaseDisorder infobox

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Synonyms and keywords: Diverticular disease; diverticulosis of colon; diverticulosis of large intestine

Overview

Overview

Overview

Diverticulosis is the condition of having diverticula in the colon which are outpocketings of the colonic mucosa and submucosa through weaknesses of muscle layers in the colon wall. These are more common in the sigmoid colon, which is a common place for increased pressure. This is uncommon before the age of 40 and increases in incidence after that age.[1] Diverticulosis may be asymptomatic or symptomatic.

Symptomatic Diverticular Diseases

Diverticular disease is defined as clinically significant and symptomatic diverticulosis due to diverticular bleeding, diverticulitis, segmental colitis associated with diverticula or symptomatic uncomplicated diverticular disease.

Historical Perspective

The Diverticulosis described as early as 17th century but, most of the information we now have is based on much of the work during the 20th century[2].

Classification

Diverticulosis may be asymptomatic or symptomatic. Diverticular diseases categorized as their symptoms to the[3]:

  • Diverticular bleeding
  • Diverticulitis
  • Segmental colitis associated with diverticula
  • Symptomatic uncomplicated diverticular disease

Pathpphysiology

The most important scenario behind the formation of Diverticula is, weakness in colon wall. Increased motility and increased level of VIP are another factors[4][5][6][7][8][9].

Diffrenetial Diagnosis

It depends on the Pathologic event that causes the symptomatic disease.It may lead to Lower GI Bleeding or diverticulitis. Either of this disorders has it’s own related differential diagnosis including: [10][11]: Colonic Ischemia,anorectal source of bleeding(hemorrhoids, anal fissures, rectal ulcers),neoplasia (polyps and cancers),Angiodysplasia,Postpolypectomy,Inflammatory bowel disease,Other colitis (infectious, antibiotic associated, colitis of unclear etiology),Small bowel/upper GI bleed

Epidemiology and Demographics

The prevalence of diverticulosis is age-dependent, increasing from less than 20 percent at age 40 to 60 percent by age 60.[12][13] Western and industrialized nations have prevalence rates of 5 to 45 percent, depending upon the method of diagnosis and age of the population. Approximately, 10% of the US population over the age of 40 and half over the age of 60 has diverticulosis. This disease is common in the US, Britain, Australia, Canada, and is uncommon in Asia and Africa. It is the most common cause for rectal bleeding in US adults over the age of 40 years.Approximately 95 percent of patients with diverticula have sigmoid diverticula.

Risk Factors

Risk factors for diverticulosis include low intake of dietary fiber, high intake of fat and red meat, and obesity[14][15][16].

Screening

There is insufficient evidence to recommend routine screening for diverticulosis.

natural history, complications and prognosis

Majority of patients with diverticula remain asymptomatic[17],it may progress to symptomatic disease based on the pathologic events that includes:Acute diverticulitis and Lower GI Bleeding Overall prognosis of Diverticulosis is excellent. Once the symptomatic disease occurs mortality rates vary depending on the presence of complications and patient comorbidities[18]. In patients with acute uncomplicated diverticulitis, conservative treatment is successful in 70 to 100 percent of patients and mortality is negligible[18].

History and Symptoms

The most common symptoms including[19]:Bleeding (variable amounts), Bloating, Abdominal pain/cramping after meals or otherwise often in the left lower abdomen, changes in bowel movements (diarrhea or constipation).

Physical examination

Diverticulosis will not cause any physical findings unless progress to symptomatic disease such as: Diverticulitis or Lower gastrointestinal bleeding.

CT scan findings

On contrast imaging of the gastrointestinal tract (e.g, computed tomography [CT]/magnetic resonance [MR] enterography), bowel diverticula appear as globular outpouchings[20].

Colonoscopy findings

Diverticula may be visualized as outpouchings of the wall that have the appearance of a blind sac[21].

Medical Therapy

Often no treatment is needed unless the symptomatic disease develops. If the patient develops the symptomatic disease(Lower GI Bleeding, Diverticulitis) one of medical therapy or surgical therapy based on the condition will be consider.

Primary Prevention

Dietary fiber and a vegetarian diet may reduce the incidence of symptomatic diverticular disease by decreasing intestinal inflammation and altering the intestinal microbiota.[15]. vigorous physical activity appears to reduce the risk of diverticulitis and diverticular bleeding.[22].

References

  1. ↑ Comparato G, Pilotto A, FranzΓ¨ A, Franceschi M, Di Mario F (2007). “Diverticular disease in the elderly”. Digestive diseases (Basel, Switzerland). 25 (2): 151–9. doi:10.1159/000099480. PMIDΒ 17468551.
  2. ↑ Martel J, Raskin JB (2008). “History, incidence, and epidemiology of diverticulosis”. J. Clin. Gastroenterol. 42 (10): 1125–7. doi:10.1097/MCG.0b013e3181865f18. PMIDΒ 18936648.
  3. ↑ N. H. Stollman & J. B. Raskin (1999). “Diagnosis and management of diverticular disease of the colon in adults. Ad Hoc Practice Parameters Committee of the American College of Gastroenterology”. The American journal of gastroenterology. 94 (11): 3110–3121. doi:10.1111/j.1572-0241.1999.01501.x. PMIDΒ 10566700. Unknown parameter |month= ignored (help)
  4. ↑ Meyers MA, Volberg F, Katzen B, Alonso D, Abbott G (1973). “The angioarchitecture of colonic diverticula. Significance in bleeding diverticulosis”. Radiology. 108 (2): 249–61. doi:10.1148/108.2.249. PMIDΒ 4541643.
  5. ↑ MORSON BC (1963). “THE MUSCLE ABNORMALITY IN DIVERTICULAR DISEASE OF THE COLON”. Proc. R. Soc. Med. 56: 798–800. PMCΒ 1897181. PMIDΒ 14080071.
  6. ↑ Chia JG, Wilde CC, Ngoi SS, Goh PM, Ong CL (1991). “Trends of diverticular disease of the large bowel in a newly developed country”. Dis. Colon Rectum. 34 (6): 498–501. PMIDΒ 1645247.
  7. ↑ Trotman IF, Misiewicz JJ (1988). “Sigmoid motility in diverticular disease and the irritable bowel syndrome”. Gut. 29 (2): 218–22. PMCΒ 1433293. PMIDΒ 3345933.
  8. ↑ Bassotti G, Battaglia E, Spinozzi F, Pelli MA, Tonini M (2001). “Twenty-four hour recordings of colonic motility in patients with diverticular disease: evidence for abnormal motility and propulsive activity”. Dis. Colon Rectum. 44 (12): 1814–20. PMIDΒ 11742167.
  9. ↑ Milner P, Crowe R, Kamm MA, Lennard-Jones JE, Burnstock G (1990). “Vasoactive intestinal polypeptide levels in sigmoid colon in idiopathic constipation and diverticular disease”. Gastroenterology. 99 (3): 666–75. PMIDΒ 1696228.
  10. ↑ Strate LL (2005). “Lower GI bleeding: epidemiology and diagnosis”. Gastroenterol. Clin. North Am. 34 (4): 643–64. doi:10.1016/j.gtc.2005.08.007. PMIDΒ 16303575.
  11. ↑ Padidar AM, Jeffrey RB, Mindelzun RE, Dolph JF (1994). “Differentiating sigmoid diverticulitis from carcinoma on CT scans: mesenteric inflammation suggests diverticulitis”. AJR Am J Roentgenol. 163 (1): 81–3. doi:10.2214/ajr.163.1.8010253. PMIDΒ 8010253.
  12. ↑ Painter NS, Burkitt DP (1975). “Diverticular disease of the colon, a 20th century problem”. Clin Gastroenterol. 4 (1): 3–21. PMIDΒ 1109818.
  13. ↑ Peery AF, Barrett PR, Park D, Rogers AJ, Galanko JA, Martin CF, Sandler RS (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.
  14. ↑ Peery AF, Sandler RS, Ahnen DJ, Galanko JA, Holm AN, Shaukat A, Mott LA, Barry EL, Fried DA, Baron JA (2013). “Constipation and a low-fiber diet are not associated with diverticulosis”. Clin. Gastroenterol. Hepatol. 11 (12): 1622–7. doi:10.1016/j.cgh.2013.06.033. PMCΒ 3840096. PMIDΒ 23891924.
  15. ↑ 15.0 15.1 Aldoori WH, Giovannucci EL, Rimm EB, Wing AL, Trichopoulos DV, Willett WC (1994). “A prospective study of diet and the risk of symptomatic diverticular disease in men”. Am. J. Clin. Nutr. 60 (5): 757–64. PMIDΒ 7942584.
  16. ↑ Strate LL, Liu YL, Aldoori WH, Syngal S, Giovannucci EL (2009). “Obesity increases the risks of diverticulitis and diverticular bleeding”. Gastroenterology. 136 (1): 115–122.e1. doi:10.1053/j.gastro.2008.09.025. PMCΒ 2643271. PMIDΒ 18996378.
  17. ↑ Simpson J, Spiller R (2002). “Colonic diverticular disease”. Clin Evid (8): 436–44. PMIDΒ 12603892.
  18. ↑ 18.0 18.1 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. PMIDΒ 16741596.
  19. ↑ Simpson J, Spiller R (2002). “Colonic diverticular disease”. Clin Evid (7): 398–405. PMIDΒ 12230665.
  20. ↑ Vernava AM, Moore BA, Longo WE, Johnson FE (1997). “Lower gastrointestinal bleeding”. Dis. Colon Rectum. 40 (7): 846–58. PMIDΒ 9221865.
  21. ↑ Ghorai S, Ulbright TM, Rex DK (2003). “Endoscopic findings of diverticular inflammation in colonoscopy patients without clinical acute diverticulitis: prevalence and endoscopic spectrum”. Am. J. Gastroenterol. 98 (4): 802–6. doi:10.1111/j.1572-0241.2003.07383.x. PMIDΒ 12738459.
  22. ↑ Aldoori WH, Giovannucci EL, Rimm EB, Ascherio A, Stampfer MJ, Colditz GA, Wing AL, Trichopoulos DV, Willett WC (1995). “Prospective study of physical activity and the risk of symptomatic diverticular disease in men”. Gut. 36 (2): 276–82. PMCΒ 1382417. PMIDΒ 7883230.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Historical Perspective

Historical Perspective

Overview

In the 1700s, Alexis Littre was the first to describe diverticular diseases, where he reported “diverticular hernia” without explaining it. It was not until 1849 that Jean Cruveilheir, a French anatomist, was the first to describe in detail the diverticular herniations through the muscular wall of the colon. In 1907, the surgical management of dirverticulosis was first reported by William James Mayo, an American physician and surgeon. The association between intake of dietary fibers and prevention of diverticulosis was first made by Painter and Burkitt in 1971.

Historical Perspective

  • In the 1700s, Alexis Littre was the first to describe diverticular diseases, where he reported “diverticular hernia” without explaining it.[1]
  • In 1815, Fleischman was the first to coin the term duvertikel.[1]
  • In 1849, Jean Cruveilheir, a French anatomist, was the first to describe in detail the diverticular herniations through the muscular wall of the colon.[2]
  • In 1899, Ernst Graser, a British surgeon, described diverticulitis, and in 1904, Edwin Beer, an American surgeon, demonstrated the histological and clinical association between diverticulosis and diverticulitis.[3][4]
  • In 1907, the surgical management of dirverticulosis was first reported by William James Mayo, an American physician and surgeon.[5]
  • It was not until 1971 that Painter and Burkitt demonstrated the association between fiber intake and prevention of diverticulosis.[6]

References

  1. ↑ 1.0 1.1 Matrana MR, Margolin DA (2009). “Epidemiology and pathophysiology of diverticular disease”. Clin Colon Rectal Surg. 22 (3): 141–6. doi:10.1055/s-0029-1236157. PMCΒ 2780269. PMIDΒ 20676256.
  2. ↑ Cruveilhier, S (1849). “Traite de’anatomie pathologique”. Balliere et Cie. 1: 592–3. |access-date= requires |url= (help)
  3. ↑ Graser, E (1899). “Uber multiple faslsche darmdivetikelin der fleura sigmoida”. Munch Med Wochenschr. 46: 74. |access-date= requires |url= (help)
  4. ↑ Beer, E (1904). “Some pathological and clinical aspects of acquired (false) diverticula of the intestine”. Am J Med Sci. 128: 125–45. |access-date= requires |url= (help)
  5. ↑ Mayo, WJ; Wilson, LB; Griffin, HZ (1907). “Acquired diverticulitis of the large intestine”. Surg Gynecol Obstet. 5: 8–15. |access-date= requires |url= (help)
  6. ↑ Painter NS, Burkitt DP (1971). “Diverticular disease of the colon: a deficiency disease of Western civilization”. Br Med J. 2 (5759): 450–4. PMCΒ 1796198. PMIDΒ 4930390.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D.

Classification

Classification

Overview

Diverticulosis may be classified based on clinical manifestations into either symptomatic vs. asymptomatic.

Classification

Diverticulosis may be classified based on clinical manifestations into either symptomatic vs. asymptomatic.[1]

References

  1. ↑ Stollman NH, Raskin JB (1999). “Diagnosis and management of diverticular disease of the colon in adults. Ad Hoc Practice Parameters Committee of the American College of Gastroenterology”. Am. J. Gastroenterol. 94 (11): 3110–21. doi:10.1111/j.1572-0241.1999.01501.x. PMIDΒ 10566700.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Pathophysiology

Pathophysiology

Overview

The development of colonic diverticuli is the result of weakening in the muscular layer of the colonic wall. Additional factors that may be critical in the development of diverticulosis include increased motility and increased cooncentration of VIP.[1][2][3][4][5][6]

Pathogenesis

Weakening of Colonic Muscular Layer

  • The development of colonic diverticuli is the result of weakening in the muscular layer of the colonic wall.
  • The most common colonic sites of diverticula development are regions of muscular weakness, which correspond to locations where the vasa recta penetrate the circular muscle layer of the colon[7][1].
  • The development of diverticula in the sigmoid colon may be explained by Laplace’s law: pressure (P) is proportional to wall tension (T) and is inversely proportional to bowel radius (R), where k is a conversion factor (P = kT Γ· R). Since the sigmoid colon is the segment of the colon with the smallest diameter, it is the site of the highest pressure during segmentation of the colon.[8]
  • A typical colonic diverticulum is a “false” or pulsion diverticulum, in which the mucosa and submucosa herniate through the muscle layer, covered only by serosa (shown below).

Abnormal Colonic Motility

  • Abnormal colonic motility is an important predisposing factor in the development diverticula.
  • Patients with diverticulosis have exaggerated segmentation contractions in which segmental muscular contractions separate the lumen into chambers.
  • It is hypothesized that the increase in intraluminal pressure predisposes to herniation of mucosa and submucosa.[2][3][4][5]

Additional Factors

Pathogenesis of Complicated Diverticulosis

Diverticular bleeding

  • As a diverticulum herniates, the penetrating vessel responsible for the wall blood blood supply weakness and is draped over the dome of the diverticulum, separated only from the bowel lumen by mucosa.[7][1]
  • Over time, the vasa recta is exposed to injury along its luminal aspect, leading to eccentric intimal thickening and thinning of the media.
  • These changes may result in segmental weakness of the artery, predisposing to rupture into the lumen.[7][1]

Diverticulitis

The primary process is thought to be an erosion of the diverticular wall by increased intraluminal pressure or inspissated food particles.

References

  1. ↑ 1.0 1.1 1.2 1.3 Meyers MA, Volberg F, Katzen B, Alonso D, Abbott G (1973). “The angioarchitecture of colonic diverticula. Significance in bleeding diverticulosis”. Radiology. 108 (2): 249–61. doi:10.1148/108.2.249. PMIDΒ 4541643.
  2. ↑ 2.0 2.1 MORSON BC (1963). “THE MUSCLE ABNORMALITY IN DIVERTICULAR DISEASE OF THE COLON”. Proc. R. Soc. Med. 56: 798–800. PMCΒ 1897181. PMIDΒ 14080071.
  3. ↑ 3.0 3.1 Chia JG, Wilde CC, Ngoi SS, Goh PM, Ong CL (1991). “Trends of diverticular disease of the large bowel in a newly developed country”. Dis. Colon Rectum. 34 (6): 498–501. PMIDΒ 1645247.
  4. ↑ 4.0 4.1 Trotman IF, Misiewicz JJ (1988). “Sigmoid motility in diverticular disease and the irritable bowel syndrome”. Gut. 29 (2): 218–22. PMCΒ 1433293. PMIDΒ 3345933.
  5. ↑ 5.0 5.1 Bassotti G, Battaglia E, Spinozzi F, Pelli MA, Tonini M (2001). “Twenty-four hour recordings of colonic motility in patients with diverticular disease: evidence for abnormal motility and propulsive activity”. Dis. Colon Rectum. 44 (12): 1814–20. PMIDΒ 11742167.
  6. ↑ 6.0 6.1 Milner P, Crowe R, Kamm MA, Lennard-Jones JE, Burnstock G (1990). “Vasoactive intestinal polypeptide levels in sigmoid colon in idiopathic constipation and diverticular disease”. Gastroenterology. 99 (3): 666–75. PMIDΒ 1696228.
  7. ↑ 7.0 7.1 7.2 Meyers MA, Alonso DR, Baer JW (1976). “Pathogenesis of massively bleeding colonic diverticulosis: new observations”. AJR Am J Roentgenol. 127 (6): 901–8. doi:10.2214/ajr.127.6.901. PMIDΒ 1087123.
  8. ↑ PAINTER NS, TRUELOVE SC, ARDRAN GM, TUCKEY M (1965). “SEGMENTATION AND THE LOCALIZATION OF INTRALUMINAL PRESSURES IN THE HUMAN COLON, WITH SPECIAL REFERENCE TO THE PATHOGENESIS OF COLONIC DIVERTICULA”. Gastroenterology. 49: 169–77. PMIDΒ 14323727.
  9. ↑ Rege RV, Nahrwold DL (1989). “Diverticular disease”. Curr Probl Surg. 26 (3): 133–89. PMIDΒ 2651018.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Causes

Causes

Overview

Diverticula are thought to be caused by an increased pressure within the lumen of the colon. Increased intra-colonic pressure secondary to constipation may result in weaknesses in the colon walls giving way to diverticula. Other causes may include high-pressure colonic spasm, which may be due to dehydration or low-fiber diets. Fiber causes stools to retain more water and to become easier to pass during a bowel movement.

Common Causes

Causes by Organ System

Cardiovascular No underlying causes
Chemical/Poisoning No underlying causes
Dental No underlying causes
Dermatologic No underlying causes
Drug Side Effect No underlying causes
Ear Nose Throat No underlying causes
Endocrine No underlying causes
Environmental No underlying causes
Gastroenterologic Low-fiber diet, Constipation, Colonic wall weakness, Frequent straining, Increased intra colonic pressure
Genetic No underlying causes
Hematologic No underlying causes
Iatrogenic No underlying causes
Infectious Disease No underlying causes
Musculoskeletal/Orthopedic No underlying causes
Neurologic No underlying causes
Nutritional/Metabolic Low-fiber diet, Processed food use
Obstetric/Gynecologic No underlying causes
Oncologic No underlying causes
Ophthalmologic No underlying causes
Overdose/Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary No underlying causes
Renal/Electrolyte No underlying causes
Rheumatology/Immunology/Allergy No underlying causes
Sexual No underlying causes
Trauma No underlying causes
Urologic No underlying causes
Miscellaneous Lack of exercise

Causes in Alphabetical Order

  • Colonic wall weakness
  • Constipation
  • Frequent straining
  • Increased intra colonic pressure
  • Lack of exercise
  • Low-fiber diet
  • Olderage
  • Processed food use.

References

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Differentiating Diverticulosis from other Diseases

Differentiating Diverticulosis from other Diseases

Overview

Diverticulosis must be differentiated from other diseases that cause abdominal discomfort, bloating, and occasional bleeding, such as other diverticular diseases (diverticulitis and diverticular bleed), as well as other GI diseases, such as acute pancreatitis, colon cancer, colitis, inflammatory bowel disease, bowel obstruction, volvulus, and appendicitis.

Differential Diagnosis

Differential diagnosis of diverticulosis includes the following:[1]

Diseases Clinical manifestations Para-clinical findings Gold standard
Symptoms
Lab Findings Imaging Histopathology
Bowel frequency Blood in stool Abdominal pain Tenesmus Other symptoms Anemia Colonoscopy CT scan Other diagnostic study
Diverticular diseases[2][3][4] ↑ or ↓ +/- +

RLQ

– –
  • Not recommended
 Barium enema
  • Circumferential narrowing
  • Spiculated contour
  • Tapered margins
  • N/A
 CT scan
Hemorrhoids[5] ↓ + + –
  • Perianal Itching
  • Pain with defecation
  • Painful-hard lump in anus
 + Anoscopy
  • Protruding mass from the anus
  • N/A
 DRE
  • N/A
 Clinical
Anal fissure[6] – + + – +/- Anoscopy
  • Anal wall laceration
  • N/A
  • N/A
  • N/A
 Clinical
Infectious colitis[7] ↑ + + – –
  • N/A
 Stool analysis

Stool cultures

  • N/A
 Stool culture
Irritable bowel syndrome[8] ↑ ↓ + + + –
  • Not recommended
  • N/A
 Diagnosis of exclusion
  • N/A
 Clinical diagnosis (Rome criteria)
Strangulated hernia ↓ – +

RLQ

– –
  • N/A
 Ultrasound:
  • N/A
 Ultrasound
Bowel endometriosis[9] ↑ or ↓ + +

Pelvic

+ +
  • N/A
  • N/A
 Transvaginal ultrasound
  • Heterogeneous, hypoechoic, spiculated mass

T1-weighted or fat-suppression T1-weighted MRIs

  • N/A
 Transvaginal ultrasound
Appendicitis[10] ↑ – +

RLQ

– –
  • N/A

Ultrasound

  • Aperistaltic, noncompressible, dilated appendix (>6 mm)
  • Appendicolith
  • Echogenic prominent pericaecal fat
  • Periappendiceal fluid collection
  • N/A
 CT scan
Colorectal carcinoma (Adenocarcinoma)[11] ↑ or ↓ + +/- + + PET scans

Barium enema

Biopsy, genetic testing, and histopathological analysis
Peutz-Jeghers syndrome
[12][13][14][15][16] 		↑ or ↓ + + – + Barium enema

MRI

Genetic testing for STK11 and colonoscopy
Carcinoids
[17][18][19][20][21] 		↑ +/- + – +
  • Well-defined single/multiple lesions
  • Round/ovoid in shape
  • Variable in size between 2-5 cm
 PET scan (11C-5-hydroxytryptophan, 11C-5-HTP)

MRI

Ki-67 index

  • Solid/spongy nests of cells accentuated by neatly outlined luminal spaces
 Biopsy and histopathological analysis
Juvenile Polyposis Coli[22][23][24][25][26] ↑ + + – + Barium study

Stool DNA test

Diagnose if any of the following positive:

Diagnostic criteria fulfilment
Gastrointestinal Stromal Tumors (GIST)[27][28][29][30][31] – +/- – – +/- Benign

Malignant GIST with metastasis:

Endoscopic ultrasonography

Benign:

Malignant GIST:

Endoscopic ultrasound

biopsy and histopathological analysis

Hamartoma[34] ↑ + + +
  • N/A
 –
  • Large polypoid mass
 Biopsy Biopsy
Colorectal Lymphoma[35][36] – +/- + – +
  • Polypoid or ulcerated mass, intramural lesion, aphthous ulcer, stricture, extraluminal mass, or diffuse, multiple polypoid lesions
 Double-contrast enema

Biopsy

Biopsy
Kaposi’s sarcoma[37] ↑ + + – +
  • N/A
 Serology

Biopsy

Biopsy
Arteriovenous malformation[38] – + – –
  • N/A
 +
  • Bright red, flat lesions
  • Rarely, polypoid
  • N/A
  • N/A
 Accidental finding
Ulcerative colitis[39] ↑ + +

LLQ

+ +
  • N/A
  • N/A
 Endoscopic biopsy
Crohn’s disease[39] ↑ + +

RLQ

+ +
  • N/A
  • N/A
 Endoscopic biopsy

References

  1. ↑ Strate LL (2005). “Lower GI bleeding: epidemiology and diagnosis”. Gastroenterol. Clin. North Am. 34 (4): 643–64. doi:10.1016/j.gtc.2005.08.007. PMIDΒ 16303575.
  2. ↑ Shen SH, Chen JD, Tiu CM, Chou YH, Chiang JH, Chang CY, Lee CH (September 2005). “Differentiating colonic diverticulitis from colon cancer: the value of computed tomography in the emergency setting”. J Chin Med Assoc. 68 (9): 411–8. doi:10.1016/S1726-4901(09)70156-X. PMIDΒ 16187597.
  3. ↑ Shen, Shu-Huei; Chen, Jen-Dar; Tiu, Chui-Mei; Chou, Yi-Hong; Chiang, Jen-Huei; Chang, Cheng-Yen; Lee, Chen-Hsen (2005). “Differentiating Colonic Diverticulitis from Colon Cancer: The Value of Computed Tomography in the Emergency Setting”. Journal of the Chinese Medical Association. 68 (9): 411–418. doi:10.1016/S1726-4901(09)70156-X. ISSNΒ 1726-4901.
  4. ↑ Sheiman, Laura; Levine, Marc S.; Levin, Alicia A.; Hogan, Jonathan; Rubesin, Stephen E.; Furth, Emma E.; Laufer, Igor (2008). “Chronic Diverticulitis: Clinical, Radiographic, and Pathologic Findings”. American Journal of Roentgenology. 191 (2): 522–528. doi:10.2214/AJR.07.3597. ISSNΒ 0361-803X.
  5. ↑ Jacobs, Danny; Solomon, Caren G. (2014). “Hemorrhoids”. New England Journal of Medicine. 371 (10): 944–951. doi:10.1056/NEJMcp1204188. ISSNΒ 0028-4793.
  6. ↑ Schlichtemeier S, Engel A (2016). “Anal fissure”. Aust Prescr. 39 (1): 14–7. doi:10.18773/austprescr.2016.007. PMCΒ 4816871. PMIDΒ 27041801.
  7. ↑ DuPont HL (January 2012). “Approach to the patient with infectious colitis”. Curr. Opin. Gastroenterol. 28 (1): 39–46. doi:10.1097/MOG.0b013e32834d3208. PMIDΒ 22080825.
  8. ↑ IwaΕ„czak B, IwaΕ„czak F (August 2017). “[Functional gastrointestinal disorders in children and adolescents. The Rome IV criteria]”. Pol. Merkur. Lekarski (in Polish). 43 (254): 75–82. PMIDΒ 28875974.
  9. ↑ Wolthuis AM, Meuleman C, Tomassetti C, D’Hooghe T, de Buck van Overstraeten A, D’Hoore A (November 2014). “Bowel endometriosis: colorectal surgeon’s perspective in a multidisciplinary surgical team”. World J. Gastroenterol. 20 (42): 15616–23. doi:10.3748/wjg.v20.i42.15616. PMCΒ 4229526. PMIDΒ 25400445.
  10. ↑ Choi D, Park H, Lee YR, Kook SH, Kim SK, Kwag HJ, Chung EC (2003). “The most useful findings for diagnosing acute appendicitis on contrast-enhanced helical CT”. Acta Radiol. 44 (6): 574–82. PMIDΒ 14616200.
  11. ↑ Secco GB, Fardelli R, Campora E, Lapertosa G, Gentile R, Zoli S, Prior C (1994). “Primary mucinous adenocarcinomas and signet-ring cell carcinomas of colon and rectum”. Oncology. 51 (1): 30–4. doi:10.1159/000227306. PMIDΒ 8265100.
  12. ↑ Zhong ME, Niu BZ, Ji WY, Wu B (June 2016). “Laparoscopic restorative proctocolectomy with ileal pouch-anal anastomosis for Peutz-Jeghers syndrome with synchronous rectal cancer”. World J. Gastroenterol. 22 (22): 5293–6. doi:10.3748/wjg.v22.i22.5293. PMIDΒ 27298573.
  13. ↑ Kopacova, Marcela; Tacheci, Ilja; Rejchrt, Stanislav; Bures, Jan (2009). “Peutz-Jeghers syndrome: Diagnostic and therapeuticapproach”. World Journal of Gastroenterology. 15 (43): 5397. doi:10.3748/wjg.15.5397. ISSNΒ 1007-9327.
  14. ↑ Giardiello, F; Trimbath, J (2006). “Peutz-Jeghers Syndrome and Management Recommendations”. Clinical Gastroenterology and Hepatology. 4 (4): 408–415. doi:10.1016/j.cgh.2005.11.005. ISSNΒ 1542-3565.
  15. ↑ Beggs, A. D.; Latchford, A. R.; Vasen, H. F. A.; Moslein, G.; Alonso, A.; Aretz, S.; Bertario, L.; Blanco, I.; Bulow, S.; Burn, J.; Capella, G.; Colas, C.; Friedl, W.; Moller, P.; Hes, F. J.; Jarvinen, H.; Mecklin, J.-P.; Nagengast, F. M.; Parc, Y.; Phillips, R. K. S.; Hyer, W.; Ponz de Leon, M.; Renkonen-Sinisalo, L.; Sampson, J. R.; Stormorken, A.; Tejpar, S.; Thomas, H. J. W.; Wijnen, J. T.; Clark, S. K.; Hodgson, S. V. (2010). “Peutz-Jeghers syndrome: a systematic review and recommendations for management”. Gut. 59 (7): 975–986. doi:10.1136/gut.2009.198499. ISSNΒ 0017-5749.
  16. ↑ Kopacova, Marcela; Tacheci, Ilja; Rejchrt, Stanislav; Bures, Jan (2009). “Peutz-Jeghers syndrome: Diagnostic and therapeuticapproach”. World Journal of Gastroenterology. 15 (43): 5397. doi:10.3748/wjg.15.5397. ISSNΒ 1007-9327.
  17. ↑ Chung TP, Hunt SR (May 2006). “Carcinoid and neuroendocrine tumors of the colon and rectum”. Clin Colon Rectal Surg. 19 (2): 45–8. doi:10.1055/s-2006-942343. PMCΒ 2780103. PMIDΒ 20011309.
  18. ↑ Diagnostics: Biochemical Markers, Imaging, and Approach. National cancer institute. http://www.cancer.gov/types/gi-carcinoid-tumors/hp/gi-carcinoid-treatment-pdq
  19. ↑ Rindi G, Falconi M, Klersy C, Albarello L, Boninsegna L, Buchler MW, Capella C, Caplin M, Couvelard A, Doglioni C, Delle Fave G, Fischer L, Fusai G, de Herder WW, Jann H, Komminoth P, de Krijger RR, La Rosa S, Luong TV, Pape U, Perren A, Ruszniewski P, Scarpa A, Schmitt A, Solcia E, Wiedenmann B (May 2012). “TNM staging of neoplasms of the endocrine pancreas: results from a large international cohort study”. J. Natl. Cancer Inst. 104 (10): 764–77. doi:10.1093/jnci/djs208. PMIDΒ 22525418.
  20. ↑ Fang C, Wang W, Zhang Y, Feng X, Sun J, Zeng Y, Chen Y, Li Y, Chen M, Zhou Z, Chen J (June 2017). “Clinicopathologic characteristics and prognosis of gastroenteropancreatic neuroendocrine neoplasms: a multicenter study in South China”. Chin J Cancer. 36 (1): 51. doi:10.1186/s40880-017-0218-3. PMCΒ 5480192. PMIDΒ 28637502.
  21. ↑ Signs and symptoms of carcinoid syndrome. National Cancer Institute. http://www.cancer.gov/types/gi-carcinoid-tumors/patient/gi-carcinoid-treatment-pdq
  22. ↑ Grotsky HW, Rickert RR, Smith WD, Newsome JF (March 1982). “Familial juvenile polyposis coli. A clinical and pathologic study of a large kindred”. Gastroenterology. 82 (3): 494–501. PMIDΒ 7054044.
  23. ↑ Brosens LA, Langeveld D, van Hattem WA, Giardiello FM, Offerhaus GJ (November 2011). “Juvenile polyposis syndrome”. World J. Gastroenterol. 17 (44): 4839–44. doi:10.3748/wjg.v17.i44.4839. PMCΒ 3235625. PMIDΒ 22171123.
  24. ↑ Latchford AR, Neale K, Phillips RK, Clark SK (October 2012). “Juvenile polyposis syndrome: a study of genotype, phenotype, and long-term outcome”. Dis. Colon Rectum. 55 (10): 1038–43. doi:10.1097/DCR.0b013e31826278b3. PMIDΒ 22965402.
  25. ↑ Latchford AR, Neale K, Phillips RK, Clark SK (October 2012). “Juvenile polyposis syndrome: a study of genotype, phenotype, and long-term outcome”. Dis. Colon Rectum. 55 (10): 1038–43. doi:10.1097/DCR.0b013e31826278b3. PMIDΒ 22965402.
  26. ↑ Latchford AR, Neale K, Phillips RK, Clark SK (October 2012). “Juvenile polyposis syndrome: a study of genotype, phenotype, and long-term outcome”. Dis. Colon Rectum. 55 (10): 1038–43. doi:10.1097/DCR.0b013e31826278b3. PMIDΒ 22965402.
  27. ↑ Niazi AK, Kaley K, Saif MW (May 2014). “Gastrointestinal stromal tumor of colon: a case report and review of literature”. Anticancer Res. 34 (5): 2547–50. PMIDΒ 24778074.
  28. ↑ Niazi AK, Kaley K, Saif MW (May 2014). “Gastrointestinal stromal tumor of colon: a case report and review of literature”. Anticancer Res. 34 (5): 2547–50. PMIDΒ 24778074.
  29. ↑ Medeiros F, Corless CL, Duensing A, Hornick JL, Oliveira AM, Heinrich MC, Fletcher JA, Fletcher CD (July 2004). “KIT-negative gastrointestinal stromal tumors: proof of concept and therapeutic implications”. Am. J. Surg. Pathol. 28 (7): 889–94. PMIDΒ 15223958.
  30. ↑ Kamiyama Y, Aihara R, Nakabayashi T, Mochiki E, Asao T, Kuwano H, Oriuchi N, Endo K (November 2005). “18F-fluorodeoxyglucose positron emission tomography: useful technique for predicting malignant potential of gastrointestinal stromal tumors”. World J Surg. 29 (11): 1429–35. doi:10.1007/s00268-005-0045-6. PMIDΒ 16222452.
  31. ↑ Miettinen M, Sobin LH, Lasota J (January 2005). “Gastrointestinal stromal tumors of the stomach: a clinicopathologic, immunohistochemical, and molecular genetic study of 1765 cases with long-term follow-up”. Am. J. Surg. Pathol. 29 (1): 52–68. PMIDΒ 15613856.
  32. ↑ Fletcher CD, Berman JJ, Corless C, Gorstein F, Lasota J, Longley BJ, Miettinen M, O’Leary TJ, Remotti H, Rubin BP, Shmookler B, Sobin LH, Weiss SW (April 2002). “Diagnosis of gastrointestinal stromal tumors: a consensus approach”. Int. J. Surg. Pathol. 10 (2): 81–9. doi:10.1177/106689690201000201. PMIDΒ 12075401.
  33. ↑ Fletcher CD, Berman JJ, Corless C, Gorstein F, Lasota J, Longley BJ, Miettinen M, O’Leary TJ, Remotti H, Rubin BP, Shmookler B, Sobin LH, Weiss SW (April 2002). “Diagnosis of gastrointestinal stromal tumors: a consensus approach”. Int. J. Surg. Pathol. 10 (2): 81–9. doi:10.1177/106689690201000201. PMIDΒ 12075401.
  34. ↑ Cauchin E, Touchefeu Y, Matysiak-Budnik T (September 2015). “Hamartomatous Tumors in the Gastrointestinal Tract”. Gastrointest Tumors. 2 (2): 65–74. doi:10.1159/000437175. PMCΒ 4668787. PMIDΒ 26672891.
  35. ↑ Quayle FJ, Lowney JK (May 2006). “Colorectal lymphoma”. Clin Colon Rectal Surg. 19 (2): 49–53. doi:10.1055/s-2006-942344. PMCΒ 2780105. PMIDΒ 20011310.
  36. ↑ Quayle, Frank; Lowney, Jennifer (2006). “Colorectal Lymphoma”. Clinics in Colon and Rectal Surgery. 19 (2): 049–053. doi:10.1055/s-2006-942344. ISSNΒ 1531-0043.
  37. ↑ Arora M, Goldberg EM (July 2010). “Kaposi sarcoma involving the gastrointestinal tract”. Gastroenterol Hepatol (N Y). 6 (7): 459–62. PMCΒ 2933764. PMIDΒ 20827371.
  38. ↑ Lee HH, Kwon HM, Gil S, Kim YS, Cho M, Seo KJ, Chae HS, Cho YS (2017). “Endoscopic resection of asymptomatic, colonic, polypoid arteriovenous malformations: Two case reports and a literature review”. Saudi J Gastroenterol. 23 (1): 67–70. doi:10.4103/1319-3767.199111. PMCΒ 5329980. PMIDΒ 28139503.
  39. ↑ 39.0 39.1 Fakhoury M, Negrulj R, Mooranian A, Al-Salami H (2014). “Inflammatory bowel disease: clinical aspects and treatments”. J Inflamm Res. 7: 113–20. doi:10.2147/JIR.S65979. PMCΒ 4106026. PMIDΒ 25075198.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Trusha Tank, M.D.[2], Seyedmahdi Pahlavani, M.D. [3]

Epidemiology and Demographics

Epidemiology and Demographics

Overview

The prevalence of diverticulosis is age-dependent. The prevalence increases from fewer than 20% at age 40 to approximately 60% by age 60. At young age (<50 years), males are more commonly affected with diverticulosis than females, but there is a female preponderance after the age of 40-50 years. Caucasian individuals are at higher risk of developing diverticulosis compared with Asian and non-African Black individuals. Diverticulosis is more commonly diagnosed in developed countries than in developing countries.

Epidemiology and Demographics

Age

  • The prevalence of diverticulosis is age-dependent.
  • The prevalence increases from fewer than 20% at age 40 to approximately 60% by age 60.[1][2]

Gender

  • At young age (<50 years), males are more commonly affected with diverticulosis than females.
  • At older age, women are more frequently affected with diverticulosis than males.[3]

Race

  • There is a slight racial predilection to the development of diverticulosis.
  • Caucasian individuals are at higher risk of developing diverticulosis compared with Asian and non-African Black individuals.[4]

Developed Countries

  • In patients above the age of 40 years, the incidence of diverticulosis in the USA is approximately 10,000 per 100,000 individuals.
  • Diverticulosis is frequently diagnosed in the US, Britain, Australia, and Canada.
  • The majority of cases in developed countries are sigmoid-diverticulosis.

Developing Countries

  • Diverticulosis is less commonly diagnosed in developing countries compared with developed countries.
  • In Asia, the rate of right-sided diverticulosis is more common than in the developed countries, but sigmoid diverticlosis remains the most common location for diverticulosis.[5]

References

  1. ↑ Painter NS, Burkitt DP (1975). “Diverticular disease of the colon, a 20th century problem”. Clin Gastroenterol. 4 (1): 3–21. PMIDΒ 1109818.
  2. ↑ Peery AF, Barrett PR, Park D, Rogers AJ, Galanko JA, Martin CF, Sandler RS (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.
  3. ↑ Warner E, Crighton EJ, Moineddin R, Mamdani M, Upshur R (2007). “Fourteen-year study of hospital admissions for diverticular disease in Ontario”. Can. J. Gastroenterol. 21 (2): 97–9. PMCΒ 2657668. PMIDΒ 17299613.
  4. ↑ Golder M, Ster IC, Babu P, Sharma A, Bayat M, Farah A (2011). “Demographic determinants of risk, colon distribution and density scores of diverticular disease”. World J. Gastroenterol. 17 (8): 1009–17. doi:10.3748/wjg.v17.i8.1009. PMCΒ 3057143. PMIDΒ 21448352.
  5. ↑ Wang FW, Chuang HY, Tu MS, King TM, Wang JH, Hsu CW, Hsu PI, Chen WC (2015). “Prevalence and risk factors of asymptomatic colorectal diverticulosis in Taiwan”. BMC Gastroenterol. 15: 40. doi:10.1186/s12876-015-0267-5. PMCΒ 4383068. PMIDΒ 25888375.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Risk Factors

Risk Factors

Overview

Risk factors in the development of diverticulosis include advanced age, chronic constipation, connective tissue diseases (such as Marfan syndrome or Ehlers Danlos syndrome), low dietary fiber intake, high intake of fat and red meat, and obesity.

Risk Factors

Risk factors in the development of diverticulosis include the following:[1]

  • Advanced age
  • Chronic constipation
  • Connective tissue disorders
  • Low fiber diet
  • The role of fiber in the development of diverticulosis remains unclear. ALthough classically low fiber diet has been associated with development of diverticulosis, results from newer studies are conflicting.[2] However, dietary fiber and a vegetarian diet may reduce the incidence of symptomatic diverticular disease by decreasing intestinal inflammation and altering the intestinal microbiota.[3][4]
  • High fiber and red meat diet
  • The risk of diverticulosis may be significantly increased with diets that are high in total fat or red meat compared with fat and red meat-rich diets.[3]
  • Obesity

References

  1. ↑ Strate LL, Liu YL, Aldoori WH, Syngal S, Giovannucci EL (2009). “Obesity increases the risks of diverticulitis and diverticular bleeding”. Gastroenterology. 136 (1): 115–122.e1. doi:10.1053/j.gastro.2008.09.025. PMCΒ 2643271. PMIDΒ 18996378.
  2. ↑ Peery AF, Sandler RS, Ahnen DJ, Galanko JA, Holm AN, Shaukat A, Mott LA, Barry EL, Fried DA, Baron JA (2013). “Constipation and a low-fiber diet are not associated with diverticulosis”. Clin. Gastroenterol. Hepatol. 11 (12): 1622–7. doi:10.1016/j.cgh.2013.06.033. PMCΒ 3840096. PMIDΒ 23891924.
  3. ↑ 3.0 3.1 Aldoori WH, Giovannucci EL, Rimm EB, Wing AL, Trichopoulos DV, Willett WC (1994). “A prospective study of diet and the risk of symptomatic diverticular disease in men”. Am. J. Clin. Nutr. 60 (5): 757–64. PMIDΒ 7942584.
  4. ↑ Painter NS, Burkitt DP (1971). “Diverticular disease of the colon: a deficiency disease of Western civilization”. Br Med J. 2 (5759): 450–4. PMCΒ 1796198. PMIDΒ 4930390.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Screening

Screening

Overview

Screening for diverticulosis is not recommended in the general population.

Screening

Screening for diverticulosis is not recommended in the general population.

References

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Overview

Diverticulosis generally develops among elderly patients (> 65 years), but it is not uncommon to be diagnosed among 40-50 years old individuals. Patients with diverticulosis are usually asymptomatic, and without development of complications, the majority of patients are not diagnosed. A minority of patients develop complications of diverticulosis. Common complications of diverticulosis include diverticular bleeding, diverticulitis, abscess or fistula formation, or perforation. Overall, the prognosis of diverticulosis is excellent. The prognosis may vary based on development of complications and patient co-morbidities.

Natural History

  • Diverticulosis generally develops among elderly patients (> 65 years), but it is not uncommon to be diagnosed among 40-50 years old individuals.
  • Patients with diverticulosis are usually asymptomatic, and without development of complications, the majority of patients are not diagnosed.[1]
  • Only 15-20% of patients with diverticulosis report symptoms that are not related to complications of the disease, such as abdominal discomfort.
  • A minority (15% to 25%) of patients develop complications of diverticulosis (commonly diverticular bleeding, diverticulitis, abscess or fistula formation, or perforation).[2][3]

Complications

Common complications associated with diverticulosis include:[2][3][4][5]

Prognosis

  • Overall, the prognosis of diverticulosis is excellent.
  • Once patients are symptomatic, mortality rates vary depending on the presence of complications and patient comorbidities.[9]. In patients with acute uncomplicated diverticulitis, conservative treatment is successful in 70 to 100 percent of patients and mortality is negligible[9].

References

  1. ↑ 1.0 1.1 Simpson J, Spiller R (2002). “Colonic diverticular disease”. Clin Evid (8): 436–44. PMIDΒ 12603892.
  2. ↑ 2.0 2.1 Parks TG (1969). “Natural history of diverticular disease of the colon. A review of 521 cases”. Br Med J. 4 (5684): 639–42. PMCΒ 1630185. PMIDΒ 5359917.
  3. ↑ 3.0 3.1 Strate LL (2005). “Lower GI bleeding: epidemiology and diagnosis”. Gastroenterol. Clin. North Am. 34 (4): 643–64. doi:10.1016/j.gtc.2005.08.007. PMIDΒ 16303575.
  4. ↑ 4.0 4.1 Meyers MA, Alonso DR, Gray GF, Baer JW (1976). “Pathogenesis of bleeding colonic diverticulosis”. Gastroenterology. 71 (4): 577–83. PMIDΒ 1085269.
  5. ↑ 5.0 5.1 Casarella WJ, Kanter IE, Seaman WB (1972). “Right-sided colonic diverticula as a cause of acute rectal hemorrhage”. N. Engl. J. Med. 286 (9): 450–3. doi:10.1056/NEJM197203022860902. PMIDΒ 4536683.
  6. ↑ Gore S, Shepherd NA, Wilkinson SP (1992). “Endoscopic crescentic fold disease of the sigmoid colon: the clinical and histopathological spectrum of a distinctive endoscopic appearance”. Int J Colorectal Dis. 7 (2): 76–81. PMIDΒ 1613298.
  7. ↑ Makapugay LM, Dean PJ (1996). “Diverticular disease-associated chronic colitis”. Am. J. Surg. Pathol. 20 (1): 94–102. PMIDΒ 8540614.
  8. ↑ Ludeman L, Shepherd NA (2002). “What is diverticular colitis?”. Pathology. 34 (6): 568–72. PMIDΒ 12555996.
  9. ↑ 9.0 9.1 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. PMIDΒ 16741596.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D.

Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | CT | Endoscopy | Other Imaging Findings | Other diagnostic studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

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