Introduction

• Intestinal rupture is a life-threatening condition requiring emergency stabilization and treatment (surgery).
• Cause:
  • Sequel to obstruction by foreign body, ruptured neoplasm, eg lymphoma, adrenocarcinoma, leiomyoma, torsion or intussusception.
  • As a result of penetrating trauma, eg gunshot.
  • Complication after bowel surgery, especially after anastomotic procedures.
  • Rarely secondary to hyperacidity caused by mast cell tumor/gastrinoma.
• Acid-base, electrolyte and hydration status are usually abnormal.
• Septic complications and peritonitis are likely to have begun prior to treatment.
• Signs: depression/collapse, abdominal pain, dehydration, vomiting, tachypnea.
• Diagnosis: history, radiography, abdominocentesis, hematology, biochemistry, ultrasonography.
• Treatment: surgical resection and anastomosis, abdominal lavage.
• Prognosis: guarded.

Pathogenesis

Etiology

• Bacterial contamination of the peritoneal space with enteric species, usually a mixed population of gram-positive and negative aerobes and anaerobes.

Pathophysiology

• Leakage of bowel contents into the abdomen → bacterial contamination and initiates the severe pathophysiological disturbances characteristic of generalized peritonitis. These are rapidly life-threatening.
• A marked peritoneal inflammatory response results in fluid, electrolytes and plasma proteins being lost into the peritoneal space.
• Hypovolemic shock ensues Shock.
• Systemic absorption of bacterial toxins and disseminated intravascular coagulation Disseminated intravascular coagulation are later, and frequently fatal, complications.

• Following a breach in bowel mucosa, vasoactive immunomodulating subtances, eg serotonin are released in response to the presence of activated macrophages and by triggering of the complement cascade system.
• A marked inflammatory response is initiated in the peritoneum in an attempt to control and contain contamination by phagocytosis of bacterial contaminants.
• Fluid and plasma proteins from the systemic circulation diffuse into the abdomen across the reactive peritoneal surfaces.
• Omentum adheres to the damaged areas of bowel and also contributes to the initial inflammatory events via its generous vascular and lymphatic supply.
• In generalized peritonitis following major bowel leaks, such mechanisms are insufficient to control the situation and a profound series of decompensatory events follow:
  • Severe fluid and electrolyte imbalances result.
  • Acid-base imbalances occur: metabolic acidosis, in conjunction with hyperkalemia, is a common finding.
• Sepsis, from the systemic absorption of bacteria and their toxins through damaged vascular endothelium, often results in hypoglycemia Hypoglycemia.
• Hemoconcentration and disseminated intravascular coagulation (DIC) Disseminated intravascular coagulation is a later finding, associated with systemic distribution of toxins and bacteria. This carries a grave prognosis.
• Death due to cardiac dysrhythmias Heart: dysrhythmia and metabolic crisis secondary to sepsis and disseminated intravascular coagulation occurs in the untreated case.

Timecourse

• Rapidly progressive and fatal.

  Intestinal rupture is a surgical emergency.

Diagnosis

Treatment

Outcomes