Intestinal Obstruction II: Pathophysiology

Intestinal obstruction triggers a series of physiological responses, starting with gas and fluid accumulation in the bowel segment proximal to the obstruction, leading to distension. This distended intestine compresses the diaphragm, hindering lung expansion and potentially leading to reduced respiratory effort, atelectasis, and pneumonia.

To overcome the blockage, the gut intensifies contractions, causing colicky abdominal pain, nausea, and vomiting, which reduces fluid and food intake and impairs nutrient absorption, leading to ketosis from starvation. Increased pressure within the intestinal wall can obstruct venous return, leading to bowel wall edema. If untreated, arterial blood flow may decrease, leading to ischemia and, eventually, bowel perforation.

As damage progresses, the intestinal wall becomes more permeable, allowing fluids and toxins to leak into the peritoneal cavity, which can trigger fever and peritonitis. Bacteria from stagnant bowel contents can enter the bloodstream, leading to sepsis, a severe inflammatory response.

Fluid and electrolyte imbalances also occur, with significant losses of water, potassium, sodium, and chloride due to vomiting and shifts into the bowel. Early or high obstructions can lead to metabolic alkalosis, while lower obstructions may cause metabolic acidosis from lactic acid and starvation.

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