장 폐색 II: 병태생리학

When a blockage forms in the intestinal lumen, the proximal intestine accumulates air and fluid, causing distention. This distention triggers stronger contractions as the gut attempts to overcome the obstruction, resulting in colicky abdominal pain, nausea, and vomiting that reduce fluid and food intake.

Sustained distention increases pressure within intestinal walls, impeding venous return and causing bowel wall edema. If pressure continues unrelieved, arterial blood flow becomes compromised, reducing oxygen supply and leading to ischemia, which can progress to tissue death and bowel perforation.

Bowel perforation is the spillage of intestinal contents rich in bacteria and digestive enzymes into the sterile peritoneal cavity. This causes peritonitis, an inflammatory response, and bacteria from stagnant bowel contents can enter the bloodstream, potentially leading to sepsis, a severe systemic inflammatory condition.

The distended intestine compresses the diaphragm, hindering lung expansion and potentially leading to reduced respiratory effort, atelectasis, and pneumonia. This respiratory compromise occurs as the accumulated gas and fluid in the bowel segment proximal to the obstruction creates significant abdominal distension.

Significant losses of water, potassium, sodium, and chloride occur due to vomiting and fluid shifts into the bowel. Early or high obstructions cause metabolic alkalosis, while lower obstructions may cause metabolic acidosis from lactic acid and starvation, leading to ketosis from reduced nutrient absorption.

Ongoing fluid loss results in dehydration and hypovolemia, decreasing blood volume and cardiac output. This leads to hemoconcentration, lower central venous pressure, and tachycardia, and in advanced stages, shock may develop, threatening vital organs and potentially resulting in multi-organ failure.

The obstructed intestine secretes exudate that leaks from capillaries into the bowel lumen, worsening intraluminal pressure and causing significant fluid buildup. This increased pressure within the intestinal wall further impedes venous return and contributes to bowel wall edema and potential ischemic complications.