Does traumatic brain injury increase the risk for venous thromboembolism in polytrauma patients?

Valle, Evan J.; Haren, Robert M. Van; Allen, Casey J.; Jouria, Jassin M.; Bullock, M. Ross; Schulman, Carl I.; Namias, Nicholas; Livingstone, Alan S.; Proctor, Kenneth G.

doi:10.1097/ta.0000000000000307

Cited by 23 publications

(16 citation statements)

References 16 publications

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“…Level I trauma centers in our study started chemoprophylaxis at a median time of 61.9 hours; however, evidence from studies using routine VTE screening show that a large proportion of trauma patients develop VTE before this time point. Valle et al 6 performed a prospective observational study on polytrauma patients with and without TBI and demonstrated that 30 per cent of VTE events were identified within the first two days of admission. Similarly, Skrifvar et al 5 reported that routine ultrasounds diagnosed VTE within three days in 29.4 per cent of 606 moderate to severe TBI patients.…”

Section: Discussionmentioning

confidence: 99%

“…4 Even with prophylaxis, VTE events are common in patients with traumatic brain injury (TBI), with an incidence of 20 to 54 per cent. [4][5][6] The high incidence of VTE in this patient population may be attributed to one or more of the following risk factors: inappropriate thrombosis caused by the systemic release of the tissue factor from the brain, prolonged immobility, and delayed chemoprophylaxis initiation. [7][8][9][10] The approach to preventing VTE after TBI with chemoprophylaxis has been debated because of concerns of worsening intracranial hemorrhage, particularly with severe TBI.…”

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confidence: 99%

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Chemoprophylaxis and Venous Thromboembolism in Traumatic Brain Injury at Different Trauma Centers

Yeates

Grigorian

Schubl

et al. 2020

The American Surgeon

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Patients with severe traumatic brain injury (TBI) are at an increased risk of venous thromboembolism (VTE). Because of concerns of worsening intracranial hemorrhage, clinicians are hesitant to start VTE chemoprophylaxis in this population. We hypothesized that ACS Level I trauma centers would be more aggressive with VTE chemoprophylaxis in adults with severe TBI than Level II centers. We also predicted that Level I centers would have a lower risk of VTE. We queried the Trauma Quality Improvement Program (2010–2016) database for patients with Abbreviated Injury Scale scores of 4 and 5 of the head and compared them based on treating the hospital trauma level. Of 204,895 patients with severe TBI, 143,818 (70.2%) were treated at Level I centers and 61,077 (29.8%) at Level II centers. The Level I cohort had a higher rate of VTE chemoprophylaxis use (43.2% vs 23.3%, P < 0.001) and a shorter median time to chemoprophylaxis (61.9 vs 85.9 hours, P < 0.001). Although Level I trauma centers started VTE chemoprophylaxis more often and earlier than Level II centers, there was no difference in the risk of VTE ( P = 0.414) after controlling for covariates. Future prospective studies are warranted to evaluate the timing, safety, and efficacy of early VTE chemoprophylaxis in severe TBI patients.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Chemoprophylaxis and Venous Thromboembolism in Traumatic Brain Injury at Different Trauma Centers

Yeates

Grigorian

Schubl

et al. 2020

The American Surgeon

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“…Although a recent report has raised doubts, 14 TBI is considered an independent risk factor for developing venous thromboembolic events (VTEs) following injury. Enoxaparin (ENX), a low-molecular-weight heparin, is the preferred agent for VTE prophylaxis in trauma but is often withheld in TBI patients fearing progression of intracranial hemorrhage from its anti-coagulant properties.…”

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confidence: 99%

Does enoxaparin interfere with HMGB1 signaling after TBI? A potential mechanism for reduced cerebral edema and neurologic recovery

Eisenstadt

Kumasaka³

et al. 2016

Journal of Trauma and Acute Care Surgery

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BACKGROUND Enoxaparin (ENX) has been shown to reduce cerebral edema and improve neurologic recovery after traumatic brain injury (TBI), through blunting of cerebral leukocyte (LEU) recruitment. High mobility group box 1 (HMGB1) protein may induce inflammation through LEU activation. We hypothesized that ENX after TBI reduces LEU-mediated edema through blockade of HMGB1 signaling. METHODS Twenty-three CD1 mice underwent severe TBI by controlled cortical impact and were randomized to one of four groups receiving either monoclonal antibody against HMGB1 (MAb) or isotype (Iso) and either ENX (1 mg/kg) or normal saline (NS): NS + Iso (n = 5), NS + MAb (n = 6), ENX + Iso (n = 6), ENX + MAb (n = 6). ENX or NS was administered 2, 8, 14, 23 and 32 hours after TBI. MAb or Iso (25 μg) was administered 2 hours after TBI. At 48 hours, cerebral intravital microscopy served to visualize live LEU interacting with endothelium and microvascular fluorescein isothiocyanate–albumin leakage. The Neurological Severity Score (NSS) graded neurologic recovery; wet-to-dry ratios determined cerebral/lung edema. Analysis of variance with Bonferroni correction was used for statistical analyses. RESULTS ENX and MAb similarly reduced in vivo pial LEU rolling without demonstrating additive effect. In vivo albumin leakage was greatest in vehicle-treated animals but decreased by 25% with either MAb or ENX but by 50% when both were combined. Controlled cortical impact–induced cerebral wet-to-dry ratios were reduced by MAb or ENX without additive effect. Postinjury lung water was reduced by ENX but not by MAb. Neurologic recovery at 24 hours and 48 hours was similarly improved with ENX, MAb, or both treatments combined. CONCLUSION Mirroring ENX, HMGB1 signaling blockade reduces LEU recruitment, cerebrovascular permeability, and cerebral edema following TBI. ENX further reduced lung edema indicating a multifaceted effect beyond HMGB1 blockade. Further study is needed to determine how ENX may play a role in blunting HMGB1 signaling in brain injury patients.

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“…Unterschiede zwischen Traumapatienten mit und ohne Schädel-Hirn-Trauma konnten nicht beobachtet werden [34]. Innerhalb der ersten 2-3 Tage traten 30% der Thrombosen auf, in der Folge wurde ein linearer Anstieg der kumulativen Häufigkeit bis zum mindestens 30.…”

Section: Caveunclassified

“…Innerhalb der ersten 2-3 Tage traten 30% der Thrombosen auf, in der Folge wurde ein linearer Anstieg der kumulativen Häufigkeit bis zum mindestens 30. Tag beobachtet [34].…”

Section: Caveunclassified

Intensivbehandlung des polytraumatisierten Patienten

Waydhas¹,

Hamsen²

2017

Orthopädie und Unfallchirurgie up2date

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Does traumatic brain injury increase the risk for venous thromboembolism in polytrauma patients?

Abstract: Epidemiologic study, level III.

Cited by 23 publications

References 16 publications

Chemoprophylaxis and Venous Thromboembolism in Traumatic Brain Injury at Different Trauma Centers

Chemoprophylaxis and Venous Thromboembolism in Traumatic Brain Injury at Different Trauma Centers

Does enoxaparin interfere with HMGB1 signaling after TBI? A potential mechanism for reduced cerebral edema and neurologic recovery

Intensivbehandlung des polytraumatisierten Patienten

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