Disseminated intravascular coagulation can cause multiple organ failure including adult respiratory distress syndrome by obstruction of visceral microcirculation by microclots. It was reasoned that if a clot causes vascular obstruction, lysing the clot by a plasminogen activator would be of value.

Adult↗

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Endotoxemic shock.

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Blood Pressure↗

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Trauma, sepsis, and disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) was first observed clinically in a case of sepsis following severe trauma. It was postulated that the observed clotting defect and bleeding were due to the using up of clotting factors in an episode of intravascular clotting. It was also postulated that the multiple organ failure observed was due to obstruction of the microcirculation of the organs by microclots. Evidence for this process was worked out in many animal studies. It was then postulated that if these microclots could be lysed before organ necrosis was produced, organ failure could be prevented. This prevention was shown to be possible in animals. It was then tried in humans using plasminogen activators, and the approach was found to be effective. Using a low dose of plasminogen activator over a 24-hour period caused no changes in the coagulation profile or bleeding.

Adult↗

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Fibrinolytic agents: a new approach to the treatment of adult respiratory distress syndrome.

Nineteen patients suffering from adult respiratory distress syndrome (ARDS) secondary to trauma or sepsis, or both, failed to respond to treatment with mechanical ventilation with oxygen and positive end-expiratory pressure. On the premise that ARDS may be caused by the microclots of disseminated intravascular coagulation obstructing the pulmonary microcirculation, the patients were treated with either streptokinase or urokinase. Eighteen patients responded with significant improvement in PaO 2 value. No bleeding occurred and clotting parameters remained normal.

Adolescent↗

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Blood clotting problems in acute care.

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Blood Coagulation Disorders↗

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Comparison of bacterial translocation during traumatic shock and hemorrhagic shock in rats.

UNLABELLED: Traumatic shock has been classified as a kind of hypovolemic shock similar to hemorrhagic shock. Since bacterial translocation has been observed in shock, this study investigated the difference in bacterial translocation during traumatic shock and hemorrhagic shock, and considered this effect on lung injury during sepsis. METHODS: Forty-eight male or female Sprague-Dawley rats were divided into 2 groups, hemorrhagic shock and traumatic shock. Bacterial translocation, endotoxin, and blood gas were evaluated. Alterations of the lungs morphologically and functionally were observed. RESULTS: Traumatic shock induced more bacterial translocation and endotoxemia from the gut. Blood gas analysis shows a more severe disorder in traumatic shock than in hemorrhagic shock. Pathological morphologic changes of lungs were more severe in traumatic shock than in hemorrhagic shock. CONCLUSIONS: Traumatic shock cause more bacterial translocation and endotoxemia which subsequently caused serial pathological alterations in lung morphologically and functionally than pure hemorrhagic shock does. These results suggest that this trauma activates more severe mechanism to damage lungs.

Animals↗

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The effect of heparinization on intra-abdominal infection and acute pulmonary failure.

UNLABELLED: Acute severe purulent peritonitis is still a very life-threatening disease condition. The primary cause of death is multiple organ failure (MOF) where acute respiratory distress syndrome (ARDS) is the initial trigger. Studies have shown that heparin has a cytoprotective effect and stimulates an increase in cardiopulmonary function systematically. METHODS: Twenty-one Sprauge Dawley rats were used as an animal model by puncturing the distal wall of intestine and ligating the appendix without interfering with the continuity of intestinal tract. In the formal experiments, 100 rats were divided into two groups and equal amounts of distilled water was given intraperitoneally. Total mortality and early mortality rate were recorded. Abdominal autopsies and blood gas analyses were performed and lung tissue samples were taken for light and electronic microscope analyses. RESULTS: The mortality rate was not statistically significant. But early death rate, the average survival times and the rate of abscess formation were significantly lower in the heparin treated group. The histological study of the experimental specimen showed that in the control group, the incidence of ARDS was higher and there was a more severe ARDS-like change, especially polymorphonuclear neutrophil leukocytes infiltration into alveolar and interstitial spaces. Blood gas analysis demonstrated the beneficial aspects of heparin administration. CONCLUSIONS: Heparin can increase the early survival rate and increase the survival time of rats with experimental acute severe purulent peritonitis, and proves to be beneficial in preventing infection induced lung injury during sepsis. We conclude that the effect of heparin on the survival rate is related to less pulmonary function deterioration, thereby preventing ARDS and the triggering of MOF.

Acute Disease↗