Diverticulosis

From Wikipedia, the free encyclopedia
  (Redirected from Diverticular disease)
Jump to: navigation, search
Not to be confused with Diverticulitis.
Diverticulosis
Classification and external resources
Diverticulosis 2.jpg
Diverticulosis as seen endoscopically
ICD-10 K57
ICD-9 562.00
OMIM 223320
DiseasesDB 3871
eMedicine med/3102
MeSH D004240

Diverticulosis, also known as "diverticular disease", 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]

Signs and symptoms[edit]

Diverticulosis can present with painless rectal bleeding as bright red blood per rectum. Cramps and tenderness may also occur in the affected areas.[citation needed]

Most people with colonic diverticulosis are unaware of this structural change. When symptoms do appear in a person over 40 years of age it is important to obtain medical advice and exclude more dangerous conditions such as cancer of the colon or rectum.[2][3][4][5]

The clinical forms of colonic diverticulosis are:

Uncomplicated diverticulosis[edit]

Some patients with diverticulosis complain of symptoms such as cramping, bloating, flatulence, and irregular defecation. However, it is unclear if these symptoms are attributable to the underlying diverticulosis or to coexistent irritable bowel syndrome.[6]

Complicated colonic diverticulosis[edit]

This is very uncommon but highly dangerous. The diverticula may bleed, either rapidly (causing bleeding through the rectum) or slowly (causing anemia). The diverticula can become infected and develop abscesses, or even perforate. These are serious complications and medical care is needed. Infected diverticula and development of abscesses merits the term diverticulitis. First time bleeding from the rectum, especially in individuals aged over age 40, could be due to colon cancer, colonic polyps and inflammatory bowel disease rather than diverticulosis and requires clinical investigation.[7][8][9]

Risk factors[edit]

  1. increasing age
  2. constipation
  3. a diet that is low in dietary fiber (contradicted by the latest study)[10]
  4. connective tissue disorders (such as Marfan syndrome and Ehlers Danlos Syndrome) that may cause weakness in the colon wall
  5. hereditary or genetic predisposition[11]
Whole slide of a transverse section of left colon with diverticulosis

The exact etiology of colonic diverticulosis has yet to be fully clarified and many of the claims are only anecdotal.[12][13] The modern emphasis on the value of fiber in the diet began with Cleave.[14] A strong case was made by Neil Painter[15] and Adam Smith[16] that a deficiency of dietary fiber is the cause of diverticular disease. They argued that the colonic muscles needed to contract strongly in order to transmit and expel the small stool associated with a fiber deficient diet. The increased pressure within the segmented section of bowel over years gave rise to herniation at the vulnerable point where blood vessels enter the colonic wall.

However, the U.S. National Institutes of Health (NIH) considers the fiber theory "unproven."[17] Furthermore, a February, 2012 study in the journal Gastroenterology found that "A high-fiber diet and increased frequency of bowel movements are associated with greater, rather than lower, prevalence of diverticulosis."[10] The study involved 2,104 participants, 30–80 years old, who underwent outpatient colonoscopies from 1998 to 2010 and were interviewed regarding diet and physical activity.

Denis Burkitt suggested that the mechanical properties of the colon may be different in the African and the European subjects. He theorized that because Africans eat a diet containing more fiber than Europeans and use the natural squatting position for defecation, they pass bulky stools without straining, and hence rarely if ever develop colonic diverticulosis.[18]

Change in the strength of the colonic wall with age may be an aetiological factor.[19] Connective tissue is a significant contributor to the strength of the colonic wall. The mechanical properties of connective tissue depend on a wide variety of factors, the type of tissue and its age, the nature of the intramolecular and intermolecular covalent cross links and the quantity of the glycosaminoglycans associated with the collagen fibrils. The submucosa of the colon is composed almost entirely of collagen, both type I and type III. Several layers of collagen fibres make up the submucosa of the human colon. The collagen fibril diameters and fibril counts are different between the left and right colon and change with age and in colonic diverticulosis,.[20][21] The implication is that changes normally associated with ageing are more pronounced in colonic diverticulosis.[22] Iwasaki found that the tensile strength of the Japanese colon obtained at postmortem declined with age.[23] Similarly the mechanical properties of the colon are stronger in African than European subjects.[22] However, this race-based claim is contradicted by the virtually identical incidence of diverticular disease in black and white Americans.[24]

The strength of the colon decreases with age in all parts of the colon, except the ascending colon. The fall in tensile strength with age is due to a decrease in the integrity of connective tissue.[25] Cross linkage of collagen is increased in colonic diverticulosis. The mucosal layer is possibly more elastic and it is likely that the stiffer external layers break and allow the elastic mucosa to herniate through forming a diverticulum. Collagen has intermolecular and intramolecular cross links which stabilise and give strength to the tissue in which it is located. Accumulation of covalently linked sugar molecules and related increasing cross linking products are found in a variety of tissues with ageing, skin, vascular tissue, the cordae tendinae of heart valves and the colon.[26] This reduces the strength and pliability of the collagen. Colonic diverticulosis increases in frequency with age.[27] There is a reduction in the strength of the colonic mucosa with age, and that increased contractions in the descending and sigmoid colon secondary to an insufficient fibre content of the diet cause protrusion through this weakened wall. Colonic diverticulosis is in general a benign condition of the bowel which uncommonly becomes symptomatic and even less commonly becomes a truly clinical complicated problem.

Diagnosis[edit]

In cases of asymptomatic diverticulosis, the diagnosis is usually made as an incidental finding on other investigations.

While a good history is often sufficient to form a diagnosis of diverticulosis or diverticulitis, it is important to confirm the diagnosis and rule out other pathology (notably colorectal cancer) and complications.

Investigations

  • Plain Abdominal X-ray may show signs of a thickened wall, ileus, constipation, small bowel obstruction or free air in the case of perforation. Plain X-rays are insufficient to diagnose diverticular disease.
  • Contrast CT is the investigation of choice in acute episodes of diverticulitis and where complications exist.
  • Colonoscopy will show the diverticulum and rule out malignancy. A colonoscopy should be performed 4–6 weeks after an acute episode.
  • Barium enema is inferior to colonoscopy in terms of image quality and is usually only performed if the patient has strictures or an excessively tortuous sigmoid colon where colonoscopy is difficult or dangerous.
  • MRI provides a clear picture of the soft tissue of the abdomen, however its expense often outweighs the benefits when compared to contrast CT or colonoscopy.
  • There is no blood test for diverticulosis.

It is important to note that both barium enema and colonoscopy are contraindicated during acute episodes of diverticulitis, as the barium may leak out into the abdominal cavity, and colonoscopy can cause perforations of the bowel wall.

Management[edit]

Many patients with diverticulosis have minimal to no symptoms, and do not require any specific treatment. A high-fiber diet and fiber supplements are advisable to prevent constipation.[28] [29] The American Dietetic Association recommends 20-35 grams each day. Wheat bran has much to commend it as this has been shown to reduce intra colonic pressure.[30][31] Ispaghula is also effective at 1-2 grams a day.

The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) says foods such as nuts, popcorn hulls, sunflower seeds, pumpkin seeds, caraway seeds, and sesame seeds have traditionally been labeled as problem foods for people with this condition; however, no scientific data exists to prove this hypothesis. The seeds in tomatoes, zucchini, cucumbers, strawberries, raspberries, and poppy seeds, are not considered harmful by the NIDDK.

Some doctors also recommend avoidance of fried foods, nuts, corn, and seeds to prevent complications of diverticulosis. Whether these diet restrictions are beneficial is uncertain; recent studies have stated that nuts and popcorn do not contribute positively or negatively to patients with diverticulosis or diverticular complications.[32][33]

Colonic stimulants should be avoided. Treatments, like some colon cleansers, that cause hard stools, constipation, and straining, are not recommended.

Complicated diverticulosis requires treatment of the complication. These complications are often grouped under a single diagnosis of diverticulitis and require skilled medical care of the infection, bleeding and perforation which may include intensive antibiotic treatment, intravenous fluids and surgery. Complications are more common in patients who are taking NSAIDS or aspirin. As diverticulosis occurs in an older population such complications are serious events.

Complications[edit]

Infection of a diverticulum can result in diverticulitis. This occurs in 10%-25% of people with diverticulosis. Tears in the colon leading to bleeding or perforations may occur; intestinal obstruction may occur (constipation or diarrhea does not rule this possibility out); and peritonitis, abscess formation, retroperitoneal fibrosis, sepsis, and fistula formation are also possible occurrences. Rarely, an enterolith may form.

Low fiber, constipation and use of stimulant laxatives increase the risk of bleeding, as does a history of diverticulitis.

Infection of a diverticulum often occurs as a result of stool collecting in a diverticulum.

More than 10% of the U.S. population over the age of 40 and 50% over the age of 60 has diverticulosis. This disease is common in the U.S., Britain, Australia, Canada, and is uncommon in Asia and Africa.[1][34] Large-mouth diverticula are associated with scleroderma.

Financial impact[edit]

"The complications of diverticulosis cause considerable morbidity in the United States; health care expenditures for this disorder are estimated to be $2.5 billion per year."[10]

See also[edit]

References[edit]

  1. ^ a b Comparato G, Pilotto A, Franzè A, Franceschi M, Di Mario F (2007). "Diverticular disease in the elderly". Digestive diseases (Basel, Switzerland) 25 (2): 151–9. doi:10.1159/000099480. PMID 17468551. 
  2. ^ Shepherd NA (1992) Diverticular disease. In Oxford Textbook of Pathology, pp. 1256-1258 [J O'D McGee, PG Isaacson and NA Wright, editors]. Oxford: Oxford University Press.
  3. ^ Christensen J (1991) Gross and microscopic anatomy of the large intestine. In The Large Intestine Physiology, Pathophysiology and Disease, pp. 13-35 [SF Phillips, JH Pemberton and RG Shorter, editors]. New York: Raven Press.
  4. ^ West, AB (2008). "The pathology of diverticulitis". J Clin Gastroenterol 42 (10): 1137–8. doi:10.1097/MCG.0b013e3181862a9f. PMID 18936652. 
  5. ^ Drummond, H (1916). "Sacculi of the large intestine with special reference to their relation to the blood vessels of the bowel wall". British Journal of Surgery 4 (15): 407–413. doi:10.1002/bjs.1800041505. 
  6. ^ "Clinical manifestations and diagnosis of colonic diverticular disease". Literature review. 
  7. ^ Eastwood MA (1987) Diverticular disease. In the Oxford Textbook of Medicine, 2nd ed., pp. 12.133-12.137 [DJ Weatherall, JGG Ledingham and DA Warrell, editors). Oxford: Oxford University Press.
  8. ^ Stollman, N; Raskin, JB. (2004). "Diverticular disease of the colon". Lancet 363 (9409): 631–9. doi:10.1016/S0140-6736(04)15597-9. PMID 14987890. 
  9. ^ Touzios, JG; Dozois, EJ (2009). "Diverticulosis and acute diverticulitis". Gastroenterol Clin North Am. 38 (3): 513–25. doi:10.1016/j.gtc.2009.06.004. PMID 19699411. 
  10. ^ a b c Anne F. Peery, Patrick R. Barrett, Doyun Park, Albert J. Rogers, Joseph A. Galanko, Christopher F. Martin, Robert S. Sandler. A High-Fiber Diet Does Not Protect Against Asymptomatic Diverticulosis. Gastroenterology, February, 2012
  11. ^ American College of Gastroenterology - "Diverticulosis and Diverticulitis" - http://patients.gi.org/topics/diverticulosis-and-diverticulitis/
  12. ^ Commane, DM; Arasaradnam, RP; Mills, S; Mathers, JC; Bradburn, M. (2009). "Diet, ageing and genetic factors in the pathogenesis of diverticular disease". World J Gastroenterol 15 (20): 2479–88. doi:10.3748/wjg.15.2479. PMC 2686906. PMID 19468998. 
  13. ^ Raskin, M; Raskin, JB (2008). "History, incidence, and epidemiology of diverticulosis". J Clin Gastroenterol 42 (10): 1125–7. doi:10.1097/MCG.0b013e3181865f18. PMID 18936648. 
  14. ^ Cleave TL 1974 The Saccharine disease Wright Bristol
  15. ^ Painter NS (1975) Diverticular disease of the colon. Heinemann Medical Books
  16. ^ Smith AN (1991) Diverticular disease of the colon in The Large Intestine ed Phillips SF, Pemberton JH and Shorter RG Raven Press pp549-578
  17. ^ "Understanding Diverticulosis and Diverticulitis - NIH MedicinePlus". Nlm.nih.gov. 2012-08-27. Retrieved 2013-10-04. 
  18. ^ Burkitt DP & Trowell HC, editors (1975) Refined Carbohydrate Foods and Disease. Some Implications of Dietary Fibre. London: Academic Press
  19. ^ Eastwood MA (1998) Structure and function of the colon. In Encyclopedia of Human Nutrition, pp. 945-953 [MJ Sadler, JJ Strain and B Caballero, editors). San Diego, CA: Academic Press.
  20. ^ Thomson, HG; Busuttil, A; Eastwood, MA; Smith, AN; Elton, RA (1987). "Submucosal collagen changes in the normal colon and in diverticular disease". International Journal of Colorectal Disease 2 (4): 208–213. doi:10.1007/BF01649507. PMID 3694019. 
  21. ^ Parry, D. A. D.; Barnes, G. R. G.; Craig, A. S. (1978). "A Comparison of the Size Distribution of Collagen Fibrils in Connective Tissues as a Function of Age and a Possible Relation between Fibril Size Distribution and Mechanical Properties". Proceedings of the Royal Society B 203 (1152): 305–321. doi:10.1098/rspb.1978.0107. JSTOR 77531. PMID 33395. 
  22. ^ a b Flint, MH; Craig, AS; Reilly, HC; Gillard, GC; Parry, DAD (1984). "Collagen fibril diameters and glycosaminoglycan content of skins - indices of tissue maturity and function". Connective Tissue Research 13 (1): 69–81. doi:10.3109/03008208409152144. PMID 6242397. 
  23. ^ Iwasaki, cited by Yamade, M.A.B.A. Strength of biological materials; Baltimore, Williams and Watkins, 1970).
  24. ^ Burkitt DP (1981). "Hiatus hernia: is it preventable?". Am. J. Clin. Nutr. 34 (3): 428–31. PMID 6259926. 
  25. ^ Watter, D.A.K.; Smith, A.N.; Eastwood, M.A.; Anderson, K.C.; Elton, R.A.; Mugerwa, J.W. (1985). "Mechanical properties of the colon: comparison of the features of the African and European colon in vitro". Gut 26 (4): 384–392. doi:10.1136/gut.26.4.384. PMC 1432523. PMID 3920126. 
  26. ^ Wess, L; Eastwood, MA; Wess, TJ; Busuttil, A; Miller, A (1995). "Cross linkage of collagen is increased in colonic diverticulosis". Gut 37 (1): 91–94. doi:10.1136/gut.37.1.91. PMC 1382775. PMID 7672689. 
  27. ^ Eastwood, M. "Colonic diverticula". Proceedings of the Nutrition Society 2003 Symposium on Dietary fibre in Health and disease. General Aspects of dietary fibre 62: 1–249. 
  28. ^ 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". The American journal of clinical nutrition 60 (5): 757–64. PMID 7942584. 
  29. ^ Gear, JS; Ware, A; Fursdon, P; Mann, JI; Nolan, DJ; Brodribb, AJ; Vessey, MP (1979). "Symptomless diverticular disease and intake of dietary fibre". Lancet 1 (8115): 511–4. doi:10.1016/S0140-6736(79)90942-5. PMID 85104. 
  30. ^ Marlett, JA; McBurney, MI; Slavin, JL; American Dietetic, Association (2002). "Position of the American Dietetic Association: health implications of dietary fiber". Journal of the American Dietetic Association 102 (7): 993–1000. doi:10.1016/S0002-8223(02)90228-2. PMID 12146567. 
  31. ^ Eglash, A; Lane, CH; Schneider, DM (2006). "Clinical inquiries. What is the most beneficial diet for patients with diverticulosis?". The Journal of family practice 55 (9): 813–5. PMID 16948968. 
  32. ^ Strate, LL; Liu, YL; Syngal, S; Aldoori, WH; Giovannucci, EL (2008). "Nut, Corn, and Popcorn Consumption and the Incidence of Diverticular Disease". JAMA 300 (8): 907–914. doi:10.1001/jama.300.8.907. PMC 2643269. PMID 18728264. 
  33. ^ "Eating Nuts, Popcorn Not Linked With Higher Risk of Diverticulosis". Newswise. 21 August 2008. Retrieved 26 August 2008. 
  34. ^ Manousos, O; Day, NE; Tzonou, A; Papadimitriou, C; Kapetanakis, A; Polychronopoulou-Trichopoulou, A; Trichopoulos, D (1985). "Diet and other factors in the aetiology of diverticulosis: an epidemiological study in Greece". Gut 26 (6): 544–9. doi:10.1136/gut.26.6.544. PMC 1432747. PMID 3924745. 

External links[edit]