Glucagon-Like Peptide-1 Receptor Agonists Decrease Medical and Surgical Complications in Morbidly Obese Patients Undergoing Primary TKA

Background: Weight optimization methods in morbidly obese patients with a body mass index (BMI) of ≥40 kg/m 2 undergoing total knee arthroplasty (TKA) have shown mixed results. The purpose of this study was to evaluate the effect of perioperative use of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) in patients with a BMI of ≥40 kg/m 2 undergoing primary TKA. Methods: Using an administrative claims database, patients with morbid obesity undergoing primary TKA were stratified into GLP-1 RA use for 3 months before and after the surgical procedure (treatment group) and GLP-1 RA non-use (control group), and were matched on the basis of patient age, gender, diagnosis of type-2 diabetes mellitus, and Charlson Comorbidity Index (CCI). In addition, these groups were compared with a contemporaneous cohort of patients undergoing TKA with a BMI of 35.0 to 39.9 kg/m 2 . Outcomes including infection, complications, revision, and readmission were compared between the matched cohorts. Results: There were significant decreases in the rates of 90-day periprosthetic joint infection (PJI) (1.0% compared with 1.8%; p = 0.037), any medical complications (10.6% compared with 12.7%; p = 0.033), pulmonary embolism ( 0.05) between these groups. Compared with obese patients (BMI of 35.0 to 39.9 kg/m 2 ), patients who had a BMI of ≥40 kg/m 2 and were taking a GLP-1 RA did not have increased rates of infection or 90-day or 2-year complications (p > 0.05). Conclusions: GLP-1 RA administration for at least 90 days prior to and after primary TKA in patients with a BMI of ≥40 kg/m 2 was associated with reductions in the risks of 90-day PJI, any medical complications, and readmission. Additionally, the reduced complication rate that was achieved was similar to that of obese patients with a BMI of 35.0 to 39.9 kg/m 2 undergoing TKA. Randomized clinical trials are needed to define the true effect of these agents on clinical outcomes following TKA. Level of Evidence: Therapeutic Level III . See Instructions for Authors for a complete description of levels of evidence.