The Effect of Intravenous Ondansetron on Reducing Hypotension Due to Bone Cement Syndrome in Total Knee Prosthesis Surgery

THE EFFECT OF INTRAVENOUS ONDANSETRON ON REDUCING HYPOTENSION DUE TO BONE CEMENT SYNDROME IN TOTAL KNEE PROSTHESIS SURGERY: A RANDOMIZED CONTROLLED THREE-BLIND STUDY

Bone cement implantation syndrome (BCIS) is a complication associated with the implantation of polymethylmethacrylate bone cement. Hypoxia, hypotension, and/or unexpected loss of consciousness often result from cementation, prosthetic placement, joint reduction, or tourniquet removal; It is a major cause of intraoperative and postoperative morbidity and mortality (1). Therefore, reducing the occurrence and severity of BCIS is an important issue.

Donaldson et al.; developed a classification system for BCIS severity. Grade 0: no hypotension/hypoxia, Grade 1: moderate hypoxia (SpO2 <94%) or hypotension [> 20% decrease in systolic blood pressure (SBP) from baseline], Grade 2: severe hypoxia (SpO2 <88%) or hypotension (SBP> 40% decrease in systolic blood pressure (SBP) from baseline) or unexpected loss of consciousness, Grade 3: cardiovascular collapse requiring cardiopulmonary resuscitation (1).

BCIS is mainly known for its association with hip hemiarthroplasty, total hip arthroplasty (TKA), and vertebroplasty, but is also seen during total knee arthroplasty (TKA). The incidence and associated mortality of BCIS has been investigated only in cemented hemiarthroplasty after displaced femoral neck fractures and in operations performed with cemented TCA and hemiarthroplasty in cancer patients (2,3). To our knowledge, the incidence associated with BCIS (compared to hemiarthroplasty or TKA), associated factors, and mortality for other hips, knee, or shoulder arthroplasty is not yet known. Little is known about the incidence, mortality risk, and factors associated with the development of BCIS during hip hemiarthroplasty and cemented arthroplasty procedures other than primary TKA. Rachid Rassir MD et al.; found that 26% of patients developed BCIS after arthroplasty and 6% of all patients experienced severe BCIS (4).

Severe BCIS (Grades 2 and 3) is more common in patients undergoing hip hemiarthroplasty and hip-knee revision arthroplasty, while less common in patients undergoing unicondylar knee arthroplasty and shoulder arthroplasty (4). The pathophysiology of BCIS is unclear. The first theories focused on circulating MMA monomers; however, recent evidence suggests an embolism-mediated model (1,5). Other additional theories focus on the role of histamine release, complement activation, and finally the multimodal possibilities of all these factors together (1,5). The origin of the embolism may be fat, bone marrow, cement, air, bone, or platelet aggregates. Embolism travels to the lungs, heart, and cerebral and coronary circulations (1,5,6). The main clinical problem is acute right ventricular failure due to pulmonary embolism. In addition, bone cement embolism can mechanically induce endothelial injury, which produces reflex vasoconstriction through the release of endothelial mediators. Embolic agents also directly increase PVR by increasing blood thrombin and tissue thromboplastin levels. It can cause a decrease in systemic vascular resistance (SVR) by promoting the release of mediators such as serotonin, thromboxane A2, platelet-activating factor, and adenosine diphosphate. Serotonin is the most prominent mediator released. It is a potent pulmonary vasoconstrictor, and causes dilation of peripheral arterioles. Together, increased PVR in the presence of reduced RV preload causes a marked decrease in cardiac output (CO). Hypotension worsens as CO is increasingly affected (7). Ondansetron, a 5-hydroxytryptamine 3 (5-HT3) receptor antagonist, has been given preoperatively and intraoperatively to block serotonin-induced pulmonary vasoconstriction (7).