Venous thromboembolism in coagulopathic surgical intensive care unit patients: is there a benefit from chemical prophylaxis?

Division of Trauma and Critical Care, Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA.
The Journal of trauma (Impact Factor: 2.35). 06/2011; 70(6):1398-400. DOI: 10.1097/TA.0b013e318217868d
Source: PubMed

ABSTRACT Coagulation abnormalities in critically ill surgical patients cause confusion in administration of venous thromboembolism (VTE) prophylaxis. Pharmaceutical VTE prophylaxis is often withheld because of presumed increased risk for bleeding and assumption that these patients would not benefit from it. Coagulopathic critically ill surgical patients are at risk for VTE and should be treated with chemical prophylaxis.
A retrospective review was performed of all coagulopathic patients (international normalized ration >1.5 or platelets <100,000 per μL) admitted for at least 72 hours to the surgical intensive care units of a tertiary care center between January 2008 and January 2009. Patients were divided into two groups based on providing (group 1) or withholding (group 2) chemical prophylaxis. The incidence of VTE was then compared between the two groups.
A total of 513 patients were included in the study: 241 patients in group 1 and 272 patients in group 2. The overall incidence of VTE was 16.4%. The incidence of VTE in the patients who received chemical prophylaxis was 17.0%, whereas the incidence in patients without chemical prophylaxis was 15.8% (p = 0.72).
Coagulopathic critically ill surgical patients remain at significant risk for VTE. Unfortunately, chemical VTE prophylaxis does not seem to decrease this risk. Further research is warranted to investigate the nature of this increased risk of VTE and the reason chemical VTE prophylaxis has no benefit.

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    ABSTRACT: Venous thromboembolic (VTE) disease has a high incidence following trauma, but debate remains regarding optimal prophylaxis. Thrombelastography (TEG) has been suggested to be optimal in guiding prophylaxis. Thus, we designed a phase II randomized controlled trial to test the hypothesis that TEG-guided prophylaxis with escalating low-molecular weight heparin (LMWH), followed by antiplatelet therapy would reduce VTE incidence. Surgical intensive care unit trauma patients (n = 50) were randomized to receive 5,000 IU of LMWH daily (control) or to TEG-guided prophylaxis, up to 5,000 IU twice daily with the addition of aspirin, and were followed up for 5 days. In vitro studies were also conducted in which apheresis platelets were added to blood from healthy volunteers (n = 10). Control (n = 25) and TEG-guided prophylaxis (n = 25) groups were similar in age, body mass index, Injury Severity Score, and male sex. Fibrinogen levels and platelet counts did not differ, and increased LMWH did not affect clot strength between the control and study groups. The correlation of clot strength (G value) with fibrinogen was stronger on Days 1 and 2 but was superseded by platelet count on Days 3, 4, and 5. There was also a trend in increased platelet contribution to clot strength in patients receiving increased LMWH. In vitro studies demonstrated apheresis platelets significantly increased clot strength (7.19 ± 0.35 to 10.34 ± 0.29), as well as thrombus generation (713.86 ± 12.19 to 814.42 ± 7.97) and fibrin production (274.03 ± 15.82 to 427.95 ± 16.58). Increased LMWH seemed to increase platelet contribution to clot strength early in the study but failed to affect the overall rise clot strength. Over time, platelet count had the strongest correlation with clot strength, and in vitro studies demonstrated that increased platelet counts increase fibrin production and thrombus generation. In sum, these data suggest an important role for antiplatelet therapy in VTE prophylaxis following trauma, particularly after 48 hours. Therapeutic study, level III.
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