Pathophysiology of Bowel Obstruction


All events that occur after the pathophysiology of bowel obstruction. The main pathophysiological changes in bowel obstruction is the intestinal lumen is clogged, it became a place of bacterial growth resulting in the accumulation of gases and liquids (70% of the gas that is ingested). Gas and fluid accumulation can occur in the proximal or distal intestine. When accumulation occurs in the distal region resulted in an increase in intra-abdominal pressure and intra lumen. This can increase the occurrence of increased capillary permeability and extravasation of water and electrolytes in the peritoneal. is the same, regardless of whether the obstruction is caused by mechanical or non-mechanical causes. The main difference is the paralytic obstruction inhibited peristalsis from the beginning, whereas the mechanical obstruction peristaltic first amplified, then intermittent, and eventually disappear. Approximately 6-8 liters of fluid excreted into the gastrointestinal tract every day. Most of the liquid is absorbed before approaching the colon. With increased permeability and extravasation cause fluid retention in the intestine and peritoneal cavity resulting in a decline in circulation and blood volume. Gas and fluid accumulation in the proximal intestine leads to the disturbance causing abdominal distension. Be pressure on mesenteric vein oxygenation resulting in the failure of the intestinal wall so that blood flow to the intestine decreased, there was ischemic and then necrotic bowel. In the necrotic bowel increased capillary permeability and release of bacteria and toxins resulting in perforation. With the perforais will cause the bacteria will get into the circulation, causing sepsis and peritonitis.


Another problem arising from abdominal distension is a decrease in bowel function and increase secretion resulting in accumulation in intra lumen which will progressively lead to retrograde peristaltic resulting in loss of fluid and electrolytes. If this is not addressed, can lead to hypovolemic shock. Losing excess fluid and electrolyte result in a decrease in cardiac output so that the blood being pumped can not meet the needs of the entire body, causing tissue perfusion disorders of the brain, and kidney cells. Decreased perfusion in the cell leads to anaerobic metabolism will increase lactic acid and causes metabolic acidosis. If they occur in the brain causes brain tissue hypoxia, ischemia and infarction. In the event of the kidneys to stimulate the exchange of sodium and hydrogen in the proximal tubule and the release of aldosterone, stimulates the secretion of hydrogen in the distal part of the nephron resulting in increased reabsorption of HCO 3 - and a decrease in the ability of the kidneys to dispose of HCO3. This will cause metabolic alkalosis. (Price & Wilson, 2007)

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