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In the patients with trauma, DIC is a predictor of ARDS, multiple organ dysfunction syndrome, and death. TNF-alpha and IL-1 beta might be one of the causes of DIC, while plasminogen activator inhibitor-1 may be one of the aggravating factors of ARDS and multiple organ dysfunction syndrome. Plasminogen activator inhibitor-1 is a good predictor of death for posttrauma DIC patients.

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A retrospective study was conducted on 53 patients who suffered severe trauma to determine the severity of intravascular hemolysis, the variations of renal function after trauma, and the effects of transfusion and haptoglobin therapy on these factors. Serum total haptoglobin, total hemoglobin, and urine free hemoglobin were measured 0, 1, 3, and 5 days after the trauma and renal tubular function was evaluated by the urinary N-acetyl-beta-D-glucosaminidase (NAG) index. Patients were divided into two groups depending on whether or not haptoglobin was given: group A (n = 34) did not receive haptoglobin, and group B (n = 19) was administered 4,421 +/- 245 U haptoglobin based on clinical indications. The total transfusion volumes were 3,477 +/- 594 ml and 10,146 +/- 1,794 ml, in groups A and B, respectively (P < 0.01). In group A, total haptoglobin was remarkably decreased to 69.4 +/- 11.6 mg/dl on day 0, but recovered to within the normal range on day 3, while the total hemoglobin was increased and the urine hemoglobin was positive in 61.8% of the patients. In group B, decreases in total haptoglobin and increases in total hemoglobin were more remarkable, and 84.2% had a positive urine hemoglobin. On day 5, groups A and B had NAG indices of 18.8 +/- 3.3 and 133.6 +/- 33.8 U/L/creatinine respectively (P < 0.01). These findings led us to conclude that trauma caused hemolysis and that the administration of 4,000 U haptoglobin did not improve either the severity of hemolysis or the deteriorated renal tubular function caused by massive transfusion.

Accompanying cardiopulmonary arrest and resuscitation, neutrophils are activated and elastase is released. Elevated elastase level is associated with poorer prognosis. Urinastatin can suppress the release of elastase, when utilized at the dose described in this study, did not improve the clinical outcomes of patients who had suffered an out-of-hospital cardiac arrest.