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PATHOPHYSIOLOGY:

Characterized by inflammation of segments of the GI tract, mot frequently in the sigmoid colon. The inflammation involves all layers of the bowel wall. The areas of involvement are usually discontinuous with segments of normal bowel occurring between diseased portions. The outpouches of mucosa appear as slit-like openings from the mucosa surface of an opened bowel. The diverticula from at weak points in the color wall, usually where arteries penetrate the tunica muscularis to nourish the mucosal layer. The colonic mucosa herniates through the smooth muscle layer. A common associated finding is thickening of the circular and longitudinal (teniae coli) muscles surrounding the diverticula. Hypertrophy and contraction of these muscles increases intraluminal pressure and degree of herniation. Habitual consumption of a low-residue diet reduces fecal bulk, thus reducing the diameter of the colon. Wall pressure increases as the diameter of cylindrical structure decreases so pressure within the narrow lumen can rupture the diverticula possibly leading to abscess formation or peritonitis.
SIGNS & SYMPTOMS:

S&S depend on the site of involvement and the extent of the disease process. Onset is usually insidious with non-specific complaints of: non-bloody diarrhea, fatigue, abdominal pain, fever, weight loss, malnutrition, dehydration, electrolyte imbalances, anemia, increased peristalsis, flatulence and pain. Diverticula with an obstructed opening become inflamed or abscessed. The patient may develop fever, leukocytosis, and tenderness of the LLQ. RLQ pain and severe complications, such as hemorrhage, peritonitis, bowel obstruction, and fistula formation are rare.