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Karcutskie CA, Meizoso JP, Ray JJ, et al. Association of Mechanism of Injury With Risk for Venous Thromboembolism After Trauma. JAMA Surg. 2017;152(1):35–40. doi:10.1001/jamasurg.2016.3116
Does mechanism of injury influence the independent risk factors for venous thromboembolism after trauma?
This cohort study finds that, although the Greenfield Risk Assessment Profile accurately predicts venous thromboembolism after blunt and penetrating trauma, independent risk factors are different based on the mechanism of injury.
Risk assessment and prophylactic strategies for venous thromboembolism may improve if mechanism of injury is considered.
To date, no study has assessed whether the risk of venous thromboembolism (VTE) varies with blunt or penetrating trauma.
To test whether the mechanism of injury alters risk of VTE after trauma.
Design, Setting, and Participants
A retrospective database review was conducted of adults admitted to the intensive care unit of an American College of Surgeons–verified level I trauma center between August 1, 2011, and January 1, 2015, with blunt or penetrating injuries. Univariate and multivariable analyses identified independent predictors of VTE.
Main Outcomes and Measures
Differences in risk factors for VTE with blunt vs penetrating trauma.
In 813 patients with blunt trauma (mean [SD] age, 47  years) and 324 patients with penetrating trauma (mean [SD] age, 35  years), the rate of VTE was 9.1% overall (104 of 1137) and similar between groups (blunt trauma, 9% [n = 73] vs penetrating trauma, 9.6% [n = 31]; P = .76). In the blunt trauma group, more patients with VTE than without VTE had abnormal coagulation results (49.3% vs 35.7%; P = .02), femoral catheters (9.6% vs 3.9%; P = .03), repair and/or ligation of vascular injury (15.1% vs 5.4%; P = .001), complex leg fractures (34.2% vs 18.5%; P = .001), Glasgow Coma Scale score less than 8 (31.5% vs 10.7%; P < .001), 4 or more transfusions (51.4% vs 17.6%; P < .001), operation time longer than 2 hours (35.6% vs 16.4%; P < .001), and pelvic fractures (43.8% vs 21.4%; P < .001); patients with VTE also had higher mean (SD) Greenfield Risk Assessment Profile scores (13  vs 8 ; P ≤ .001). However, with multivariable analysis, only receiving 4 or more transfusions (odds ratio [OR], 3.47; 95% CI, 2.04-5.91), Glasgow Coma Scale score less than 8 (OR, 2.75; 95% CI, 1.53-4.94), and pelvic fracture (OR, 2.09; 95% CI, 1.23-3.55) predicted VTE, with an area under the receiver operator curve of 0.730. In the penetrating trauma group, more patients with VTE than without VTE had abnormal coagulation results (64.5% vs 44.4%; P = .03), femoral catheters (16.1% vs 5.5%; P = .02), repair and/or ligation of vascular injury (54.8% vs 25.3%; P < .001), 4 or more transfusions (74.2% vs 39.6%; P < .001), operation time longer than 2 hours (74.2% vs 50.5%; P = .01), Abbreviated Injury Score for the abdomen greater than 2 (64.5% vs 42.3%; P = .02), and were aged 40 to 59 years (41.9% vs 23.2%; P = .02); patients with VTE also had higher mean (SD) Greenfield Risk Assessment Profile scores (12  vs 7 ; P < .001). However, with multivariable analysis, only repair and/or ligation of vascular injury (OR, 3.32; 95% CI, 1.37-8.03), Abbreviated Injury Score for the abdomen greater than 2 (OR, 2.77; 95% CI, 1.19-6.45), and age 40 to 59 years (OR, 2.69; 95% CI, 1.19-6.08) predicted VTE, with an area under the receiver operator curve of 0.760.
Conclusions and Relevance
Although rates of VTE are the same in patients who experienced blunt and penetrating trauma, the independent risk factors for VTE are different based on mechanism of injury. This finding should be a consideration when contemplating prophylactic treatment protocols.
Trauma patients are typically classified according to the mechanism of injury—blunt or penetrating. However, advanced trauma life support guidelines do not distinguish management based on the mechanism of injury.1 Several studies have found significantly different outcomes between patients who experienced blunt and penetrating trauma who were resuscitated to similar end points,2-5 even when severity of the injuries are closely matched.6-12
Venous thromboembolism (VTE) is a significant cause of late morbidity and mortality after trauma13 despite thromboprophylaxis.14-27 At least 2 models stratify risk of VTE specifically in trauma patients to guide surveillance and prophylaxis: the Trauma Embolic Scoring System28 and the Greenfield Risk Assessment Profile (RAP).18 To our knowledge, no study has assessed the differences in risk of VTE from the independent risk factors of blunt and penetrating trauma.
We stratified patients in the intensive care unit by either blunt or penetrating trauma mechanism, and then determined which RAP risk factors are associated with VTE. We hypothesized that the mechanism of injury alters the independent VTE risk factors.
This was a retrospective cohort study conducted at the Ryder Trauma Center in the University of Miami and Jackson Memorial Medical Center and was approved by the University of Miami Institutional Review Board with a waiver of informed consent. Adult patients sustaining blunt or penetrating trauma and admitted to the Ryder Trauma Center intensive care unit from August 1, 2011, to January 1, 2015, were included. Patients who were younger than 18 years, incarcerated, pregnant, or died less than 72 hours after admission were excluded.
Thirty percent of the population was concurrently enrolled in a prospective observational trial evaluating hypercoagulability and VTE in patients who have undergone traumatic injury. This group was deemed to be at high risk for VTE, using a RAP score of 10 or more, based on previous work.25,29 All high-risk patients enrolled in this concurrent study received weekly surveillance venous duplex ultrasonography (VDU) of the lower extremities, in addition to chemical and mechanical prophylaxis. Deep vein thrombosis was diagnosed with VDU. Pulmonary embolism was identified by computed tomography with angiography of the chest. The VDU protocols at our institution have been previously reported.30
Briefly, all VDUs were performed by certified ultrasonography technologists and interpreted by an attending radiologist. The deep venous systems of both lower extremities are examined from the inguinal ligament to the ankles using B-mode compression, color augmentation, and spectral Doppler ultrasound. Studies were considered positive if abnormalities were detected in a deep vein at any level, above or below the knee. In all patients, the RAP score (Table 1) was calculated prospectively by a trained research associate.
All statistical analyses were performed using SPSS Statistics, version 22.0 (IBM Corp). Categorical variables are expressed as frequency (percentage) and compared between groups using χ2 or Fisher exact test, as appropriate. Parametric data are expressed as mean (SD) and compared using t tests for 2 independent samples. Nonparametric data are expressed as median (interquartile range) and compared using the Mann-Whitney test. Variables demonstrating statistical significance on univariate analyses were entered into a multivariable logistic regression model. Odds ratios (ORs) and 95% CIs are reported. Area under the receiver operator curve (AUROC) was used to assess predictive values of models. P ≤ .05 was considered statistically significant for all results.
The study population comprised 1137 patients: 813 with blunt trauma and 324 with penetrating trauma. Patient demographics and injury characteristics are shown in Table 2.
Quiz Ref IDThere was no difference in rates of VTE, deep vein thrombosis, or pulmonary embolism based on mechanism of injury. In patients with blunt trauma, the overall VTE rate was 9% (n = 73), with a deep vein thrombosis rate of 6.6% (n = 54) and a pulmonary embolism rate of 2.7% (n = 22). In patients with penetrating trauma, the overall VTE rate was 9.6% (n = 31), with a deep vein thrombosis rate of 7.7% (n = 25) and a pulmonary embolism rate of 2.5% (n = 8).
In patients with blunt trauma, those with VTE had a worse mean (SD) Injury Severity Score (29  vs 21 ; P ≤ .001), admission heart rate (102  vs 95  beats/min; P = .03), admission systolic blood pressure (122  vs 135 ; P = .01), admission Glasgow Coma Scale score (11  vs 13 ; P ≤ .001), and base deficit (–4  vs –2 ; P = .007). As expected, mean (SD) RAP score (13  vs 8 ; P ≤ .001) and median (interquartile range) hospital length of stay (40 [22-78] vs 12 [7-26] days; P ≤ .001) were also higher in patients with VTE. Quiz Ref IDThere was no difference in time to first prophylaxis between patients with VTE and those without VTE.
When all RAP factors were considered for predicting VTE in patients with blunt trauma, the AUROC was 0.745. The individual RAP factors are assessed for patients with blunt trauma in Table 3. More patients with VTE than without VTE had abnormal coagulation laboratory values (49.3% vs 35.7%; P = .02), femoral catheters (9.6% vs 3.9%; P = .03), 4 or more transfusions (51.4% vs 17.6%; P < .001), operation time longer than 2 hours (35.6% vs 16.4%; P < .001), repair and/or ligation of vascular injury (15.1% vs 5.4%; P = .001), Glasgow Coma Scale score less than 8 (31.5% vs 10.7%; P < .001), complex leg fractures (34.2% vs 18.5%; P = .001), and pelvic fractures (43.8% vs 21.4%; P < .001). Quiz Ref IDControlling for these factors in a multivariable logistic regression, independent predictors of VTE included receiving 4 or more transfusions (OR, 3.47; 95% CI, 2.04-5.91), Glasgow Coma Scale score less than 8 (OR, 2.75; 95% CI, 1.53-4.94), and pelvic fracture (OR, 2.09; 95% CI, 1.23-3.55) (Table 4). The AUROC for this reduced model was 0.730.
When all RAP factors were considered for predicting VTE in patients with penetrating trauma, the AUROC was 0.803. The individual RAP risk factors are assessed for patients with penetrating trauma in Table 5. More patients with VTE than without VTE had abnormal coagulation laboratory values (64.5% vs 44.4%; P = .03), femoral catheters (16.1% vs 5.5%; P = .02), 4 or more transfusions (74.2% vs 39.6%; P < .001), operation time longer than 2 hours (74.2% vs 50.5%; P = .01), repair and/or ligation of vascular injury (54.8% vs 25.3%; P < .001), and Abbreviated Injury Score for the abdomen greater than 2 (64.5% vs 42.3%; P = .02), and were aged 40 to 59 years (41.9% vs 23.2%; P = .02). Quiz Ref IDControlling for these factors in a multivariable logistic regression, independent predictors of VTE included repair and/or ligation of vascular injury (OR, 3.32; 95% CI, 1.37-8.03), Abbreviated Injury Score for the abdomen greater than 2 (OR, 2.77; 95% CI, 1.19-6.45), and age 40 to 59 years (OR, 2.69; 95% CI, 1.19-6.08) (Table 4). The AUROC for this reduced model was 0.760.
The results of this study affirm the validity of RAP for assessing overall risk of VTE in either blunt (AUROC = 0.745) or penetrating (AUROC = 0.803) trauma patients. Quiz Ref IDThe major new findings are that blunt vs penetrating injury mechanism influences the individual risk factors for VTE.
After blunt trauma, transfusion status, neurologic status, and pelvic fracture independently predict VTE. Transfusion status was the strongest predictor in this group. In contrast, after penetrating trauma, vascular injury, severe abdominal injury, and younger age independently predict VTE. These findings, in context with previous work, suggest that mechanism of injury may influence the body’s subsequent compensatory response, and that current scoring systems do not account for the differences between blunt vs penetrating trauma.
Several previous investigators have shown that blunt or penetrating injury mechanism influences mortality and/or acute renal failure outcomes even with the same resuscitation fluid.2-5 Martin et al6 showed that functional disability and severe disability for feeding, expression, or locomotion differed after blunt and penetrating carotid artery injuries even when the injuries were similar. George et al7 reported that the physiological pattern of premenopausal adult female sex hormones may provide a survival advantage in patients who underwent blunt trauma; however, the converse pattern prevails for those who underwent penetrating trauma. These findings all support a fundamental difference associated with mechanism of injury.
In 2008, the US Surgeon General published a call to action for prevention of VTE, underscoring its significance as a public health concern.13 Furthermore, many national agencies, including the Centers for Medicare & Medicaid Services,31 have placed VTE in a category of reasonably preventable hospital-acquired conditions. A study in 2012 showed that, in high-risk trauma patients with a RAP score of 10 or more, routine screening VDU identified a rate of VTE of 28%, with two-thirds of those being asymptomatic.25 In addition, there is evidence that a significant number of VTEs occur in low-risk patients with a RAP score less than 5,27 a population that both the Eastern Association for the Surgery of Trauma22 and the American College of Chest Physicians16 claim may be cost inefficient to screen with VDU. Thus, current assessment of risk for VTE is somewhat deficient.
The RAP is an accepted tool for trauma patients and is routinely used in our institution for risk stratification. Developed in 1997 by Greenfield et al,18 it was intended to identify patients who would best benefit from chemical prophylaxis. It compiled a set of several factors that were known to increase risk of VTE among patients who have sustained traumatic injury. Each factor was assigned a weight that influences the overall risk. A RAP score greater than 5 was deemed high risk. To our knowledge, no study to date has questioned whether mechanism of injury influences the individual VTE risk factors identified by Greenfield et al.18
Our results show that independent predictors of VTE after blunt trauma included transfusion status, neurologic status, and pelvic fracture, whereas after penetrating trauma, the independent predictors were severe abdominal injury, vascular injury, and younger age. Because of these differences, it is logical to question whether the weights for the individual risk factors should be altered to reflect the mechanism of injury. An adjustment based on this finding may allow the RAP to further identify cases of VTE that are currently classified as low risk with the current scoring system. In addition, any changes based on mechanism of injury could aid in the development of appropriate prophylactic protocols.
The results and interpretations of our study must be considered with the context of several limitations. First, this is a retrospective study; therefore, cause and effect cannot be established. Second, there is no obvious biological mechanism to explain the difference between the 2 injury mechanisms. Although we are able to identify the differences between our 2 cohorts, we are unable to identify the exact cause. Third, the diagnosis of VTE differed based on whether the patient was high risk or low risk. Patients with a RAP score of 10 or more were prescreened on admission and received weekly VDU, allowing for discovery of asymptomatic VTE, thereby introducing surveillance bias to our sample. For patients with a RAP score of less than 10, there was no screening protocol and VTEs were only studied and identified if they were symptomatic. Thus, the overall rate of VTE in the low-risk patients may be an underestimate.
Rates of VTE are the same in blunt or penetrating trauma patients, but the independent risk factors for VTE are different based on mechanism of injury; this finding should be considered when contemplating thromboprophylaxis strategies. Factors that increase risk of VTE in patients with blunt trauma are blood transfusions, decreased neurologic status, and pelvic fracture. Factors that increase risk in patients with penetrating trauma are vascular injury, severe abdominal injury, and age 40 to 59 years. We believe these findings show an inherent difference in risk of VTE that is dependent on mechanism of injury. With this evidence, it is possible to further investigate whether an adjusted RAP incorporating mechanism of injury could capture missed VTE in the patient population currently classified as low risk and better guide prophylactic efforts.
Corresponding Author: Kenneth G. Proctor, PhD, Ryder Trauma Center, Divisions of Trauma, Surgical Critical Care, and Burns, DeWitt Daughtry Family Department of Surgery, University of Miami Leonard M. Miller School of Medicine, 1800 NW 10th Ave, Ste T-215 (Box D40), Miami, FL 33136 (email@example.com).
Accepted for Publication: June 1, 2016.
Published Online: September 28, 2016. doi:10.1001/jamasurg.2016.3116
Author Contributions: Dr Proctor had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Karcutskie, Meizoso, Namias, Proctor.
Acquisition, analysis, or interpretation of data: Karcutskie, Meizoso, Ray, Horkan, Ruiz, Schulman, Proctor.
Drafting of the manuscript: Karcutskie, Proctor.
Critical revision of the manuscript for important intellectual content: All authors.
Statistical analysis: Karcutskie, Meizoso, Ray, Proctor.
Administrative, technical, or material support: Horkan, Ruiz, Schulman, Proctor.
Study supervision: Namias, Proctor.
Conflict of Interest Disclosures: None reported.
Funding/Support: This study was supported in part by grants from the Naval Medical Research Center, and the US Army Medical Research and Material Command.
Role of the Funder/Sponsor: The Naval Medical Research Center and the US Army Medical Research and Material Command partially supported the design and conduct of the study. They had no role in the collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.
Previous Presentation: This paper was presented at the 2016 Annual Meeting of the Association of VA Surgeons; April 10, 2016; Virginia Beach, Virginia.
Additional Contributions: Ronald J. Manning, ARNP, MSPH, University of Miami, assisted with compliance and adherence to institutional review board regulatory procedures. He received no financial compensation. We thank the nurses and staff of the Ryder Trauma Center Trauma Resuscitation Unit and Trauma Intensive Care Unit.
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