58 – Is there a definite association between BMI and VTE?

58 – Is there a definite association between BMI and VTE?

Ana Torres, Emanuele Chisari, Jessica Morton, Emilio Romanini, Vitali Goriainov, Nicola Gallagher, Rajiv Kaila, Antonio J. Andrade, David Beverland.

Response/Recommendation: Extensive evidence confirms a definite association between unprovoked venous thromboembolism (VTE) and increasing body mass index (BMI). However, the evidence linking BMI to postoperative VTE is more equivocal.

Strength of Recommendation: Moderate.

Rationale: VTE is a multifactorial disease, resulting from the interaction of genetic and acquired risk factors. Multiple observational population-based studies demonstrate that obesity, as assessed by increased BMI, is an independent risk factor for increased risk of VTE in the nonsurgical patient1–4. This association between BMI and  VTE has been demonstrated to likely be causal in Mendelian randomization studies5,6. The World Health Organization (WHO) classifies BMI into underweight (BMI < 18.5 kg/m2), normal weight (BMI between 18.5 – 24.9 kg/m2), overweight (BMI between 25 – 29.9 kg/m2), Class 1 obese (BMI between 30 – 34.9 kg/m2), Class 2 obese (BMI between 35 – 39.9 kg/m2), and Class 3 obese (BMI ≥ 40 kg/m2)7. In clinical practice, obesity is typically defined as BMI > 30 kg/m2 8. With regards to orthopaedic surgery, conflicting evidence has been reported. The majority of studies have found that BMI > 30 kg/m2 correlates to a greater risk of VTE in both total hip arthroplasty (THA) and total knee arthroplasty (TKA)9–23. However, other studies have refuted these findings and have not detected and a correlation between high BMI and postoperative VTE24–29. In a systematic review and metanalysis, Zhang et al., found BMI > 30 kg/m2 to increase the risk of VTE in patients undergoing primary TKA and THA19. A larger metanalysis of 89 studies including 14’763,963 joint replacements found an increasing risk of VTE with increasing BMI, relative risks >25 kg/m2 vs < 25 kg/m2 1.40 (1.24-1.57), > 30 kg/m2 vs < 30 kg/m2 1.65 (1.23-2.22), and > 50 kg/m2 vs < 50 kg/m2 1.72 (1.10-2.67) [15]. In analysis of the American College of Surgeons – National Surgical Quality Improvement Program (ACS-NSQIP) database, Sloan et al., found elevated BMI did not increase the risk of deep venous thrombosis (DVT) in revision TKA or THA, however, in patients undergoing primary THA and TKA elevated BMI was associated with elevated risk of pulmonary embolism (PE)9. In a single-institution study of 26,391 primary and revision TJA Parvizi et al., found that elevated BMI (p<0.035) was an independent risk factor for symptomatic PE12.

Obesity, as reflected in increased BMI, has not only been proven as a risk factor for VTE in THA and TKA but also in patients undergoing several other areas of orthopaedic surgery. In total shoulder arthroplasty obesity has been found to be a risk factor for VTE30,31. Obesity is also an independent risk factor for increased incidence of VTE after hip arthroscopy32,33, as well as shoulder and knee arthroscopy34. Obese patients have also found to be at an increased risk of VTE following foot and ankle surgery35–37. Although in patients with chronic Achilles tendon ruptures, elevated BMI trended towards association with VTE but did not reach statistical significance38. The literature in spine surgery generally continues to support BMI as a risk factor for VTE39–44, although there is not a universal consensus45,46. In patients who underwent lumbar spine surgery, the risk for DVT was higher in overweight patients and increased for subsequent obesity classes39. This is supported by metanalysis performed by Jiang et al., who noted odds ratio [OR] of 3.15 (95% confidence interval [CI] 1.92-5.17) for increased risk of VTE in obese patients, being defined as BMI > 30 kg/m2 40.

The exact etiology of a possible correlation between obesity and increased risk of VTE remains unknown. Obese patients may be at increased risk for VTE secondary to longer operative times, lower postoperative mobility, and ineffectiveness of mechanical prophylaxis9. Obesity has been associated with inflammatory states that may contribute to increased thrombus formation and subsequent embolization3,47. Furthermore, obesity is associated with reduced fibrinolysis attributable to increased concentrations of type-1 plasminogen activator inhibitor (PAI-1), an inhibitor of endogenous fibrinolysis, shifting the balance between thrombosis and thrombolysis towards thrombosis48.

The association between BMI and VTE remains unproven. Obese patients are also at higher risk of bleeding and wound-related complications. Thus, the use of any thromboprophylaxis should be balanced against the increased risk for complications and bleeding in obese patients9,49.


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