Acute intestinal infarction (acute mesenteric ischemia)

Acute intestinal infarction (acute mesenteric ischemia)

    * Introduction
    * Causes
    * Signs and symptoms
    * Diagnosis
    * Treatment
Acute mesenteric ischemia is interruption of blood flow through the intestinal embolism, thrombosis or blood pressure, leading to release of mediators of inflammation and infarction.
Initial manifestations of severe pain and physical signs are minimal. Diarrhea, vomiting and sometimes fever are common. Abdominal distention, intestinal bleeding and pain in case of diffuse peritonitis, defense, severe dehydration and shock peritoneum are late manifestations of intestinal infarction.
Myocardial untreated leads to death within a few days or several hours in mild forms extensive injuries. Causes of death can be toxic and septic shock and shock hipovolemicc loop necrotic perforation or peritonitis.
Treatment is only surgical intervention is the only measure that may allow survival. The absence of surgery is allowed only if the state prohibits cardiocirculatorie laparotomy or if the patient is able preterminala. Preoperative intensive training is required which will combat shock, central venous infusion, electrolyte rebalancing. The prognosis is unfavorable, the mortality was 35%. If bowel resection affects over 50% of its length is over 75% mortality. Venous infarction has a better prognosis, but in case of failure of anticoagulant therapy for three months before recurrence increased to over 25%. In large bowel resections, the prognosis is affected by nutrition, resection bearable maximum of 75% in length, if preserved ileocaecal valve.
Pathogenesis
Blood perfusion failure may result from arterial occlusion by embolism or thrombosis, the venous system or process occlusive thrombosis: vasospasm or low cardiac output.
Embolism includes 50% of cases of infarction, arterial thrombosis 25%, cardiac output decreased 20% and 10% venous thrombosis. Hemorrhagic infarction is venous occlusion in both pathological condition or blood pressure. Lesion severity is inversely proportional to the mesenteric blood flow and is influenced by the number of branches, systemic pressure, ischemic, and collateral circulation.
Lesions in the affected portion of intestine can range from reversible ischemia until transmural myocardial necrosis and perforation. They are complicated by vasospasm reagent. Aretriala failure cause tissue hypoxia and muscle spasm of the bowel, leading to intestinal emptying by vomiting and diarrhea. At this stage abdominal tenderness is usually present producing classic signs of visceral pain disproportionate to physical examination.
Mucosal barrier is disrupted by ischemia and persist as bacteria, toxins and vasoactive substances are released into the bloodstream. This process causes death by sepsis, heart failure or organ failure. As the damage worsens hypoxia, edema and intestinal wall becomes cyanotic. Intestinal fluids are released into the peritoneal cavity. Intestinal necrosis occurs within 8-12 hours after onset of clinical symptoms. Embolic infarction is caused by cardiac emboli usually home. Vascular occlusion is the sudden so that patients do not develop compensatory collateral pressure. CAE superior mesenteric artery is embolization due May succeptibila the narrow angle of detachment of the aorta.
Thrombotic infarction is a complication of atherosclerosis terdiva visceral. Symptoms develop two or three arteries blocked, celiac and superior mesenteric are often involved.