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| Diverticula Disease |
| Etiology: Increased intraluminal colonic pressure congenital weakness of colon wall at points of entrance of nutrient arteries Acquired weakness of colon wall as with increased elastin formation with age, or connective tissue abnormalities associated with diseases such as Marfan1s or Scleroderma |
| Pathogenesis: Chronic or recurrent increase in intraluminal colonic pressure causes herniation of the mucosa through the colon wall in an area of potential weakness where the penetrating nutrient arteries enter the muscularis propria |
| Epidemiology: A disease of the U.S. and other developed countries where processed food has replaced cereal fiber A disease of the population above age 40, increasing with age Diverticulosis in the younger population is often associated with connective tissue disorders The incidence of diverticulosis is increasing in Western countries and in populations with a change to processed food |
| General Gross Description: Diverticuli are most common in the sigmoid colon, but may be found along the entire length of the colon. They are concentrated along the course of the Taenia Coli On the serosal surface, non-inflamed diverticuli (diverticulosis) appear as small saccular protuberances less than 1.0cm with thin compressible walls if empty of fecal contents or firm is filled with fecal matter Their color is the same as the serosa of the adjoining bowel Transverse section of the diverticular sacs will reveal a thin wall with the lumen being empty or containing fecal matter which may be soft or quite desiccated and firm. A fortunate cut will demonstrate a thin tract leading from the sac to the lumen of the colon where the adjoining mucosa will appear entirely normal The mucosa is usually studded with small(When inflamed(diverticulitis), they are most commonly seen at the stage of diverticular abscess formation The serosal surface is erythematous, may contain exudate over the region of abscess formation, and the pericolic fat is firm Transverse section will usually reveal an area of necrotic tissue or a pocket of pus, with the surrounding tissue being firm secondary to organization The mucosa is generally normal with openings to numerous non inflamed diverticuli noted |
| General Microscopic Description: Diverticuli are acquired protrusions of the mucosa through the colonic wall and contain a lining of normal colonic mucosa which may be compressed by inspissated fecal matter, an attenuated muscularis mucosa and submucosa. Muscularis propria is never seen A thin track lined by normal colonic mucosa leads from the sac to the lumen where normal colonic mucosa is seen Inflamed diverticuli contain inspissated fecal material and begin with accumulation of polys followed by necrosis of the mucosal lining.When symptomatic the inflammation has spread into the serosa and pericolic tissue, and when seen surgically a diverticular abscess has usually formed When removed surgically we usually see fibroblastic organization of the pericolic tissue If the colon is removed because of massive bleeding due to diverticula disease, and you are able to find the involved diverticulum, it is usually not inflamed and partially destroyed by the hemorrhage |
| Clinical Correlations: While the prevalence of diverticulosis is high, only 20% of afflicted people are ever symptomatic The most common symptom is colicky left lower quadrant pain thought to be due to acute increase in intraluminal pressure The most common complication is diverticulitis which is accompanied by left lower pain, fever and often tenderness. Presence of a palpable mass indicates abscess formation. Other bowel symptoms are usually present but are variable Minor blood loss commonly occurs in diverticula disease, but severe acute blood loss occurs in 3-5% of afflicted people. It is the most common cause of massive lower GI hemorrhage Recurrent episodes of diverticulitis may lead to extensive focal scarring and signs of obstruction Most people with diverticulosis are asymptomatic or have mild disease and overall only 1% will require hospitalization |
| References: Cotran RS, Kumar V, Robbins SL. Robbins Pathologic Basis of Disease, 5th edition. W.B. Saunders. Philadelphia, 1994, pp.806-808 Sleisenger MH and Fordtran JS. Gastrointestinal Disease 5th edition vol 2, W.B.Saunders Philadelphia, 1993 pp.1347- |