Clinical ReviewVenous thromboembolism in trauma patients: A review*
Section snippets
Incidence
The first reports of PE and DVT after trauma were from autopsy studies. In 1934, McCartney2 documented that in 1604 trauma autopsies, PE was the cause of death in 61 patients (3.8%). In another necropsy study of trauma patients in 1961, Sevitt and Gallagher3 found a 65% incidence of DVT and a 20.3% incidence of PE. In a medical examiner report of 950 fatal injuries, Fitts et al4 found that PE was the cause of death in 143 patients (15%). In a 1976 autopsy study, Coon5 found that 14.3% of the
Pathophysiology
In 1856, Virchow11 described a triad of conditions associated with the development of venous thrombosis. These included intimal injury, stasis, and hypercoagulability. All 3 conditions are frequently seen in the trauma patient soon after injury. Intimal injury may be present as a result of direct tissue destruction of venous blood vessel walls from the inciting traumatic event. Stasis may occur as a result of paralysis, immobilization, or decreased blood flow caused by hemorrhagic shock.
Risk factors for venous thromboembolism
Several studies have demonstrated high-risk factors for the development of VTE in trauma patients. Knudson et al6 showed that 4 variables were strongly associated with the occurrence of thromboembolic complications: older age (49 ± 23 versus 36 ± 17 years), days immobilized (23 ± 15 versus 10 ± 13 days), transfusions received (11 ± 12 versus 3 ± 5 U packed red cells), and a prolonged initial partial thromboplastin time (39 ± 28 versus 26 ± 5 seconds). Shackford et al7 observed that patients
Deep vein thrombosis
There are several diagnostic modalities used to detect DVT in trauma patients. These include physical examination, venography, impedance plethysmography, and ultrasound. Impedance plethysmography, although widely used in the past, will not be discussed here because it is a rarely used diagnostic modality, replaced primarily by ultrasound.
The most readily available and easiest to perform diagnostic modality to detect DVT in trauma patients is physical examination. Unfortunately, it is the least
Standard prophylaxis
SCH and VCB are the 2 prophylactic agents most commonly used in trauma patients. Heparin is a mucopolysaccharide of 6000 to 30,000 d that occurs naturally in the mast tissue cells of the lung, liver, and intestine. Its anticoagulant properties, thought to be the result of its strong electronegative charge, allow it to combine with many different proteins, including those of the coagulation cascade. Heparin works by combining with antithrombin III and forming a complex that inactivates
Investigational prophylaxis
Low-molecular-weight heparins (LMWH) are distillates of unfractionated heparin (UFH) of molecular weight 4000 to 5000 d (compared with 6 to 30,000 d for UFH). One effect of the smaller molecular weight is a longer plasma half-life resulting from fewer interactions with cells, platelets, and plasma proteins. Below a molecular weight of about 5.6 d, the LMWH tend to lose anti-IIa activity (and hence an inability to be reliably monitored with activated partial thromboplastin time).48 They do
Complications
The most common complication related to pharmacologic prophylaxis with heparin is bleeding. This is of paramount concern in trauma patients with multi-system injuries who are at especially high risk for serious fatal complications from bleeding diathesis. Brathwaite et al76 retrospectively reviewed the outcome of 70 “low-risk” trauma patients who were treated with anticoagulation for VTE. Complications developed in 36% of the patients, some of which were life threatening (3 subdural hematomas,
Decision analysis on prophylactic measures after trauma
The decision on which prophylactic measure to use on each patient is not always easy and not always based on irrefutable data in the literature. As such, venous thromboprophylaxis is still a relatively inexact science. Despite these limitations, a few practical guidelines may prove useful in the decision analysis based on our management protocols at our institution (University of Vermont College of Medicine).
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A patient who is not considered at high risk (as previously discussed) and is
Future directions
During the past 5 years, several factors have been discovered that contribute to thrombosis in the role of coagulation abnormalities. It has now been demonstrated that resistance to activated protein C (first described in 1993)86 caused by a mutation in clotting factor V (factor V Leiden) is prevalent in up to 5% of the general population.87, 88 Likewise, hypercoagulable abnormalities such as high levels of factor VIII (up to 11% of the general population)89 or hyperhomocystinemia (up to 5% of
Summary
VTE is a problem that continues to plague trauma patients. Many of Virchow's triad (intimal injury, stasis, hypercoagulability) may already be present in the trauma patient with the time of their injury and may explain why there is a 7% to 12%6, 7 incidence of DVT and a 2% to 3%9 incidence of PE, despite adequate prophylaxis in recent studies. The highest-risk injuries appear to be those with spine fracture or spinal cord injury,4, 8 head injury,1, 2 lower-extremity fracture,1, 7, 8 and pelvic
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2023, Journal of Surgical ResearchAdmission thrombelastography does not guide dose adjustment of enoxaparin in trauma patients
2020, Surgery Open ScienceCitation Excerpt :Venous thromboembolism (VTE) is a significant source of morbidity and mortality in traumatically injured patients [1]. The interplay of Virchow's triad (ie, hemostasis or alteration of blood flow, endothelial injury, hypercoagulability) is often the underlying mechanism that results in development of VTE [2]. Derangements in clotting factors can occur, which produce a hypercoagulable response contributing to the formation of a thrombus [3–5].
Post-TBI splenectomy may exacerbate coagulopathy and platelet activation in a murine model
2020, Thrombosis Research
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Reprint requests: Frederick Rogers, MD, Fletcher Allen Health Care, Department of Surgery, 111 Colchester Ave, FL 466, Burlington, VT 05401.