Etiology

• Foreign bodies Intestine: linear foreign bodies.
• Tumors (lymphosarcoma, annular adenocarcinoma).
• Intussusception Intussusception.
• Strictures due to trauma or prior surgery.
• Abscesses.
• Congenital defects.
• Adhesions.

Pathophysiology

• Obstruction interferes with passage of luminal contents along the intestine.
• Distention of bowel occurs proximal to obstruction with fluid and/or gas and food.

• Foreign bodies may cause damage which varies according to their shape and size:
• • Laceration.
  • Obstruction.
  • Pressure necrosis.
  • Perforation.

Proximal obstruction

• High intramural pressure → compromised blood supply → possible shunting away from intestinal capillaries to arteriovenous anastomoses → hypoxia to the bowel, loss of viability and increased permeability to toxins, including endotoxins.
• Duodenum is more sensitive to circulatory changes associated with distension.

Obstruction proximal at pylorus

• Hydrogen ion loss → metabolic alkalosis often with hypokalemia.

Obstruction below the pancreatic and biliary ducts

• Vomiting and loss of absorption of fluid collecting proximal to the obstruction → rapid and severe losses with significant amount of bicarbonate ion → dehydration and/or hypovolemic shock → metabolic acidosis.

Distal obstruction

• Fluid and electrolyte losses less severe but significant in chronic cases.
• Less severe distension of intestinal wall → circulation of affected gut unimpeded.

Strangulation

• Partial or total obstruction of venous drainage and an intact arterial supply → intramural sequestration of blood and eventually bowel wall edema.
• Distended bowel proximal to the strangulation filled with gas and fluid containing a significant amount of blood → non-viable and necrotic bowel wall → transmural migration of toxins and bacteria → hypovolemia, endotoxic shock and death.

Timecourse

• Hours to days for acute obstruction.
• Partial or intermittent obstructions may show signs over weeks to months.