Diet-induced obesity prevents the development of acute traumatic coagulopathy

McCully, Belinda H.; Dean, Rondi K.; McCully, Sean P.; Schreiber, Martin A.

doi:10.1097/ta.0000000000000461

Cited by 7 publications

(14 citation statements)

References 24 publications

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“…Previous work has shown that in animal models of trauma and human cohorts, obesity prevents prolongation of clot initiation, enhances fibrin cross-linking, and promotes clot strength following hemorrhagic shock. (12, 33) Several studies have also shown an interaction with obesity and platelet activity due to alterations in several pathways that invoke platelet activation. (34) Leptin, a signaling hormone produced by adipocytes has been shown to enhance platelet aggregation, promoting thrombosis.…”

Section: Discussionmentioning

confidence: 99%

Obesity is associated with postinjury hypercoagulability

Samuels

Moore

Coleman

et al. 2019

J Trauma Acute Care Surg

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Background: Obesity is linked to hypercoagulability with an increased risk of venous thromboembolic events (VTE) in the uninjured population. Therefore, we hypothesize that obesity (Body Mass Index (BMI) ≥30 kg/m2) is associated with a hypercoagulable state postinjury characterized by increased clot strength and resistance to fibrinolysis. Methods: Our prospective Trauma Activation Protocol database includes all trauma activations patients for whom a rapid thrombelastography (TEG) is obtained within 60 minutes postinjury prior to any transfusions. The dataset was then stratified by BMI and subjects with BMI ≥ 30 kg/m2 were compared to those with BMI<30 kg/m2). The following TEG measurements were obtained: activated clotting time (ACT), clot formation rate (angle), maximum clot strength (MA), and % clot lysis 30 min after MA (LY30, %). Fibrinolysis shutdown (SD) was defined as LY30 < 0.6% and hyperfibrinolysis (HF) as LY30 > 7.6%. Continuous variables are expressed as median (IQR). Results: Overall, 687 patients were included of whom 161 (23%) had BMI ≥ 30kg/m2 (BMI30). The BMI30 group was older, had a lower proportion of males and of blunt trauma, and were less severely injured. After adjustment for confounders, BMI30 was independently associated with lower odds of MA<55mm (OR 0.28; 95% CI 0.130.60) and of HF (OR 0.31; 95% CI 0.10–0.97) and higher odds of SD (OR 1.82; 95% CI 1.09–3.05). No independent association was observed with angle<650 (OR 0.57 95% CI 0.30–1.05). While VTEs were more frequent among BMI30 patients (5.0 vs 3.3%), this did not reach significance after confounding adjustment (p=0.11). Conclusion: Obesity was protective against diminished clot strength and hyperfibrinolysis, and obesity was associated with an increased risk of fibrinolytic shutdown in severely injured patients. These findings suggest a relative hypercoagulability. Although no difference in VTEs was noted in this study, these findings may explain the higher rate of VTEs reported in other studies.

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Section: Discussionmentioning

confidence: 99%

Obesity is associated with postinjury hypercoagulability

Samuels

Moore

Coleman

et al. 2019

J Trauma Acute Care Surg

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“…In our prior trial, 13 with higher observed VTE rates, BMI ranged from 30.6 to 32.8. In a rat obesity model, McCully et al 32 demonstrated that obese rats do not develop the acute coagulopathy of trauma after hemorrhagic shock and are hypercoagulable at baseline. Other authors 21 suggest that obesity decreases the effectiveness of enoxaparin prophylaxis.…”

Section: Discussionmentioning

confidence: 99%

Thrombelastography-Based Dosing of Enoxaparin for Thromboprophylaxis in Trauma and Surgical Patients

et al. 2016

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“…Venous thromboembolism can be a major cause of organ failure after hemorrhage, and the risk of developing this complication is increased in obese trauma patients (68). For example, in Sprague-Dawley rats subjected to an uncontrolled hemorrhage (54), those fed a high-fat diet remained in a hypercoagulable state as compared to those fed a normal diet, which may play a role increasing the risk of thromboembolism. Characterized by insulin resistance and a hypercoagulable state, obese animals could be used to determine the impacts of stress hyperglycemia and thromboembolism on outcomes following hemorrhage.…”

Section: Obesity and Animal Models Of Critical Illnessmentioning

confidence: 99%

Obesity and Critical Illness

Mittwede

Clemmer

Bergin

et al. 2016

Shock

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Critical illness is a major cause of morbidity and mortality around the world. While obesity is often detrimental in the context of trauma, it is paradoxically associated with improved outcomes in some septic patients. The reasons for these disparate outcomes are not well understood. A number of animal models have been used to study the obese response to various forms of critical illness. Just as there have been many animal models that have attempted to mimic clinical conditions, there are many clinical scenarios that can occur in the highly heterogeneous critically ill patient population that occupies hospitals and intensive care units. This poses a formidable challenge for clinicians and researchers attempting to understand the mechanisms of disease and develop appropriate therapies and treatment algorithms for specific subsets of patients, including the obese. The development of new, and the modification of existing animal models is important in order to bring effective treatments to a wide range of patients. Not only do experimental variables need to be matched as closely as possible to clinical scenarios, but animal models with pre-existing comorbid conditions need to be studied. This review briefly summarizes animal models of hemorrhage, blunt trauma, traumatic brain injury, and sepsis. It also discusses what has been learned through the use of obese models to study the pathophysiology of critical illness in light of what has been demonstrated in the clinical literature.

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Diet-induced obesity prevents the development of acute traumatic coagulopathy

Abstract: Obesity prevents the development of ATC following hemorrhage shock. Complications associated with obesity following hemorrhagic shock may be attributed to the preserved hypercoagulable state.

Cited by 7 publications

References 24 publications

Obesity is associated with postinjury hypercoagulability

Obesity is associated with postinjury hypercoagulability

Thrombelastography-Based Dosing of Enoxaparin for Thromboprophylaxis in Trauma and Surgical Patients

Obesity and Critical Illness

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