Structured Abstract
Background
Though obese patients have high thrombosis rates following injury, the role of obesity in coagulation after trauma remains unknown. We hypothesized that BMI is independently associated with increased measures of hypercoagulability longitudinally after injury.
Methods
Data were prospectively collected for 377 consecutive highest-level trauma activation patients with a body mass index (BMI) ≥ 18.5 kg/m2. Standard coagulation measures, citrated kaolin and functional fibrinogen thromboelastography (TEG), and clotting factors were measured at 0-120h. BMI categories were defined as normal weight (18.5-24.99 kg/m2), overweight (25-29.99 kg/m2), and obese (≥ 30 kg/m2).
Results
The 377 patients were mostly male (81%) and bluntly injured (61%), with median BMI of 25.8 kg/m2. 42% were normal weight (median BMI 22.5 kg/m2). There were no differences in age, gender, ISS or base deficit between groups. There were no differences in admission INR/PTT or factors II, V, VII, VIII, X, ATIII, or protein C. However, obese patients had higher admission platelet counts (303 vs. 269 × 109/L, p=0.004), lower D-dimer (1.88 vs. 4.00 ug/mL, p=0.004), and a trend toward higher factor IX (134 vs. 119 % activity, p=0.042) than normal weight patients. Measured by TEG, clot strength (MA) and functional fibrinogen level (FLEV) were also higher on admission for obese patients (MA 65.7 vs. 63.4 mm, p=0.016; FLEV 407 vs. 351 mg/dL, p=0.008). In multiple linear regression, the relationship of BMI to clot strength, FLEV, and FIX persisted through 24h. Similarly, the relationship of BMI and platelet count persisted through 120h (all p<0.05). In multiple logistic regression, for every 5kg/m2 increase in BMI, there was an 85% increase in odds of thromboembolic complication (OR 1.85, CI 1.13-3.08, p=0.017).
Conclusion
Obese trauma patients are hypercoagulable compared to their similarly-injured normal weight counterparts, which persists longitudinally after injury. The significance of this hypercoagulability requires elucidation for guidance of anticoagulation in this at-risk group.
Level of Evidence
Level III; prognostic