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Comparing clinical predictors of deep venous thrombosis versus pulmonary embolus after severe injury: A new paradigm for posttraumatic venous thromboembolism?

Brakenridge, Scott C. MD, MSCS; Henley, Steven S. MS; Kashner, T. Michael PhD, JD, MPH; Golden, Richard M. PhD; Paik, Dae-Hyun PhD; Phelan, Herb A. MD, MSCS; Cohen, Mitchell J. MD; Sperry, Jason L. MD, MPH; Moore, Ernest E. MD; Minei, Joseph P. MD; Maier, Ronald V. MD; Cuschieri, Joseph MD; The Inflammation and the Host Response to Injury Investigators

Journal of Trauma and Acute Care Surgery:
doi: 10.1097/TA.0b013e31828cc9a0
AAST 2012 Plenary Papers
Abstract

BACKGROUND: The traditional paradigm is that deep venous thrombosis (DVT) and pulmonary embolus (PE) are different temporal phases of a single disease process, most often labeled as the composite end point venous thromboembolism (VTE). However, we theorize that after severe blunt injury, DVT and PE may represent independent thrombotic entities rather than different stages of a single pathophysiologic process and therefore exhibit different clinical risk factor profiles.

METHODS: We examined a large, multicenter prospective cohort of severely injured blunt trauma patients to compare clinical risk factors for DVT and PE, including indicators of injury severity, shock, resuscitation parameters, comorbidities, and VTE prophylaxis. Independent risk factors for each outcome were determined by cross-validated logistic regression modeling using advanced exhaustive model search procedures.

RESULTS: The study cohort consisted of 1,822 severely injured blunt trauma patients (median Injury Severity Score [ISS], 33; median base deficit, −9.5). Incidence of DVT and PE were 5.1% and 3.9%, respectively. Only 9 (5.7%) of 73 patients with a PE were also diagnosed with DVT. Independent risk factors associated with DVT include prophylaxis initiation within 48 hours (odds ratio [OR], 0.57; 95% confidence interval [CI], 0.36–0.90) and thoracic Abbreviated Injury Scale (AIS) score of 3 or greater (OR, 1.82; 95% CI, 1.12–2.95), while independent risk factors for PE were serum lactate of greater than 5 (OR, 2.33; 95% CI, 1.43–3.79) and male sex (OR, 2.12; 95% CI, 1.17–3.84). Both DVT and PE exhibited differing risk factor profiles from the classic composite end point of VTE.

CONCLUSION: DVT and PE exhibit differing risk factor profiles following severe injury. Clinical risk factors for diagnosis of DVT after severe blunt trauma include the inability to initiate prompt pharmacologic prophylaxis and severe thoracic injury, which may represent overall injury burden. In contrast, risk factors for PE are male sex and physiologic evidence of severe shock. We hypothesize that postinjury DVT and PE may represent a broad spectrum of pathologic thrombotic processes as opposed to the current conventional wisdom of peripheral thrombosis and subsequent embolus.

LEVEL OF EVIDENCE: Prognostic study, level III.

Author Information

From the Harborview Medical Center (S.C.B., R.V.M., J.C.), University of Washington, Seattle, Washington; Martingale Research Corporation (S.S.H., D.-H.P.), Plano; University of Texas at Dallas (R.M.G.), Richardson; and Division of Burn/Trauma/Critical Care (H.A.P., J.P.M.), University of Texas Southwestern Medical Center, Dallas, Texas; School of Medicine (S.S.H., T.M.K.), Loma Linda University; and Center for Advanced Statistics in Education (T.M.K.), VA Medical Center, Loma Linda; and University of California San Francisco (M.J.C.), San Francisco, California; Division of General Surgery and Trauma (J.L.S.), University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania; and Denver Health Medical Center (E.E.M.), University of Colorado Health Sciences Center, Denver, Colorado.

Submitted: September 6, 2012, Revised: February 7, 2013, Accepted: February 7, 2013.

This study was presented at the annual meeting of the American Association for the Surgery of Trauma, September 12–15, 2012, in Kauai, Hawaii.

This article does not necessarily reflect the views or opinions of the National Institutes of Health or the National Cancer Institute.

Address for reprints: Scott Brakenridge, MD, MSCS, University of Washington, Harborview Medical Center, Box 359796, 325 Ninth Ave, Seattle, WA 98104-2499; email: sbrakenr@u.washington.edu.

© 2013 Lippincott Williams & Wilkins, Inc.