The Possible Pathophysiological Outcomes and Mechanisms of Tourniquet-Induced Ischemia-Reperfusion Injury during Total Knee Arthroplasty.

Prangmalee Leurcharusmee,Passakorn Sawaddiruk,Nipon Chattipakorn,Siriporn C Chattipakorn,Yodying Punjasawadwong

doi:10.1155/2018/8087598

Prangmalee Leurcharusmee, Passakorn Sawaddiruk + Show 3 more

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https://doi.org/10.1155/2018/8087598

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Abstract

Ischemia and reperfusion (I/R) injury induced by tourniquet (TQ) application leads to the release of both oxygen free radicals and inflammatory cytokines. The skeletal muscle I/R may contribute to local skeletal muscle and remote organ damage affecting outcomes after total knee arthroplasty (TKA). The aim of the study is to summarize the current findings associated with I/R injury following TKA using a thigh TQ, which include cellular alterations and protective therapeutic interventions. The PubMed database was searched using the keywords “ischemia reperfusion injury,” “oxidative stress,” “tourniquet,” and “knee arthroplasty.” The search was limited to research articles published in the English language. Twenty-eight clinical studies were included in this qualitative review. Skeletal muscle I/R reduces protein synthesis, increases protein degradation, and upregulates genes in cell stress pathways. The I/R of the lower extremity elevates local and systemic oxidative stress as well as inflammatory reactions and impairs renal function. Propofol reduces oxidative injury in this I/R model. Ischemic preconditioning (IPC) and vitamin C may prevent oxygen free radical production. However, a high dose of N-acetylcysteine possibly induces kidney injury. In summary, TQ-related I/R during TKA leads to muscle protein metabolism alteration, endothelial dysfunction, oxidative stress, inflammatory response, and renal function disturbance. Propofol, IPC, and vitamin C show protective effects on oxidative and inflammatory markers. However, a relationship between biochemical parameters and postoperative clinical outcomes has not been validated.

Highlights

Total knee arthroplasty (TKA) is a surgical treatment aiming at improving the mobility and quality of life of patients suffering from advanced knee osteoarthritis
Use of a TQ during TKA resulted in skeletal muscle Ischemia and reperfusion (I/R) injury to localized skeletal muscle, systemic circulation, and distant organs
During I/R, genes related to the cell stress pathways are upregulated in skeletal muscle cells without evidence of mitochondrial dysfunction

Summary

Introduction

Total knee arthroplasty (TKA) is a surgical treatment aiming at improving the mobility and quality of life of patients suffering from advanced knee osteoarthritis. The prevalence of this procedure has substantially increased in the past decade and is expected to continue [1, 2]. Muscle atrophy following a use of intraoperative thigh tourniquet (TQ) results in early postoperative deficits in quadriceps strength and subsequently impaired TKA rehabilitation. Limb exsanguination followed by TQ inflation transiently increases central blood volume and systemic vascular resistance, induces a hypercoagulable state, and activates fibrinolytic activity. The use of a TQ is considered a risk factor for thromboembolism [5]. The incidence of deep vein thrombosis and pulmonary thromboembolism after TKA was found to be similar regardless of the use of the TQ [6]

Objectives

Conclusion