An investigation into the cellular-level adverse effects of tourniquet use on the infrapatellar fat pad in primary total knee arthroplasty: A prospective randomized study

Abstract

Objective: This study aimed to examine the cellular-level adverse effects of tourniquet use on the infrapatellar fat pad (IPFP) in patients undergoing primary total knee arthroplasty (TKA).

Methods: Infrapatellar fat pad samples were collected in a prospective, randomized design to compare 2 groups of primary TKA patients with a tourniquet (T) and without a tourniquet (NT). The study included 80 knees of 58 patients with a mean age of 65.91 ± 9.04 years. The authors collected 3 samples from the T group (after exposure to the fat pad "t1," just before deflating the tourniquet "t2," just before fascia closure "t3") and 2 samples from the NT group (t1 and t3) for each patient. BAX, Bcl-2, and HIF-1α staining showed the extent of cellular hypoxia and apoptosis in IPFP cells, whereas the oxidative stress index (OSI) was determined using a biochemical method. The Knee Injury and Osteoarthritis Outcome Score (KOOS), Knee Society Score (KSS), and Kujala score were used as clinical outcome measures.

Results: The mean HIF-1α, BAX/Bcl-2, and OSI scores across all time points were significantly higher in the T group than in the NT group (p<0.001) (d=1.16, 2.9, and 0.9, respectively). The mean BAX/Bcl-2 (P=.030) and HIF-1α (P < .001) scores significantly peaked at t2 in the T group (d=-1.2 and -3.9, respectively). The OSI had higher levels at t1 (P=.011) and t3 (P=.073) (d=0.2 and 0.1, respectively) than at t2 in the T group. The third-month postoperative follow-up revealed that the mean KOOS, KSS, and Kujala score improved significantly compared to the baseline preoperative values (P < .001); however, there was no difference between the T and NT groups regarding the maximum and total knee range of motion or clinical outcome scores.

Conclusion: Evidence from this study has shown that tourniquet use during primary TKA may be associated with significantly increased cellular hypoxia, oxidative stress, and apoptosis in the IPFP.

Level of evidence: Level I, Therapeutic study.