ISSN 2398-2969      

Intestine: rupture

icanis

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

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Treatment

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Outcomes

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Further Reading

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