Low fiber Diet Male Occlusion of foreign body to the appendix ↑ Intra luminal Pressure Vasocongestion ↓ Blood supply in the appendix ↓ Oxygen supply in the appendix Disruption of cell membrane of appendix Start of Inflammatory process
RLQ Abdominal pain, Vomiting
Inflammation of appendix
Rupture of appendix
Hyperthermia ↑ WBC
Release of fecal materials in the abdomical cavity
↓ Peristalsis
Secondary Peritonitis
Abdominal distention
Hypoactive bowel sounds
↑ Immune response Release of chemical mediators (macrophages, fibrin, blood cells)
Adhesions Intestinal obstruction Ischemia of the bowel wall
Necrosis of the intestine
Exploratory Lapatoromy
49 | Pathophysiology
Hypoalbuminemia
Delayed wound healing Disruption of anastamosis Anastamosis leak
Microcirculatory changes Poor perfusion of vital organ
Inability to utilize/remove metabolic waste
Decrease oxygen delivery ↓ Oxygen saturation
Subcellular and cellular injury Release of toxic products Down regulation of oxygen metabolism Failure of energy production acidosis
Major organ dysfunction acidosis
↓ Urine production ↑ Urine concentration Constipation
Septicemia DEATH
50 | Pathophysiology
Interpretation: The appendix is a small, finger-like appendage attached to the cecum just below the ileocecal valve. Because it empties into the colon inefficiently and its lumen is small, it is prone to becoming obstructed and vulnerable to infection. The factors that increases the risk of the pat ient of having appendicitis is that he is a male having episodes of constipation, and consuming a low fiber diet. These factors might contribute to the occlusion of foreign body to the appendix. Once occlusion happens, an increase in intra luminal pressure and vasocongestion occurs. This decreases the blood supply as well as oxygen supply in the appendix which will disrupt the cellular membrane and functions. Due to the d isruption of the cell membrane of appendix, inflammation of the appendix occurs as manifested by r ight lower quadrant abdominal pain and vomiting. Once rupture, the appendix releases fecal materials in the abdo minal cavity, which causes a decrease in peristaltic movement and seco ndary peritonitis. The release of fecal materials in the abdominal cavity causes a decrease in peristaltic movement due to increase gas and fluid content as evidence by abdominal distention and hypoactive bowel sounds. Secondary Peritonitis occurs as an inflammatory response of the periton eum secondary to rupture of underlying organs. Because peritoneum is particularly well adapted for producing an inflammatory response, hyperthermia, and increase white blood cell count is evident. Release of chemical mediato rs such as macrophages, fibrin, and blood cell adheres to structures (adhesions) to seal of the appendix and localized the 51 | Pathophysiology
infection. Localization is enhanced by sympathetic stimulation that limits intestinal motility and leads to obstruction of the intestines. Intestinal obstruction causes the bowe l wall to be ischemic. Ischemia leads to necrosis of the intestine. Surgical management such as exploratory laparotomy was done to remove the ruptured appendix and intestines. Resection and an astomosis of the distal ileus to prevent further necrosis of the intestine. Due to poo r compliance to medication and treatment course, hypoalbuminea occurs. Albumin is a protein responsible for wo und healing; a decrease will cause a delay in the pro cess of wound healing. Due to hypoalbuminea, a disruption in the anastomosis and leaking happens as evidence by yellowish abdominal secretions that lead to tertiary peritonitis. Tertiary peritonitis is an inflammation of the peritoneum after a surgical procedure to control secondary peritonitis. It leads to more serious complications because it affects other bodily functions and patient may die because of generalized septicemia. Tertiary peritonitis causes fluids to shift to the extravascular space as evidence by poor skin turgor and edema. It also causes vasodilation and an increase in cardiac contractility as evidence by increase pulse rate and delayed capillary refill. Decrease venous return and cardiac contractility and vasod ilation results to a low cardiac output. Hypotension and changes in the microcirculatory functions such as poor perfusion of vital organ happens. Major organ dysfunction, release of toxic product s, down regulation of oxygen metabolism, failure of energy production and ac idosis are subcellular and cellular injury that may result to septicemia and eventua lly the death of the patient.
