Cemented Versus Noncemented Total Hip ArthroplastyEmbolism, Hemodynamics, and Intrapulmonary Shunting
MARK H. ERETH, M.D., JOSEPH G. WEBER, M.D., MARTIN D. ABEL, M.D., ROBERT L.LENNON, D.O., Department ofAnesthesiology; DAVID G. LEWALLEN, M.D., Department of Orthopedics; DUANE M. ILSTRUP, M.S., Section ofBiostatistics; KAI REHDER, M.D.,* Department ofAnesthesiology
Bone cement implantation syndrome is characterized by hypotension, hypoxemia, cardiac arrhythmias, cardiac arrest, or any combination of these complications. It may result from venous embolization that occurs in conjunction with intramedullary hypertension in the femur during insertion of the prosthesis in patients undergoing cemented total hip arthroplasty (THA). Intramedullary hypertension does not occur in patients undergoing noncemented THA. In this study, we sought to compare embolization between patients undergoing cemented and noncemented THA and to determine whether this state resulted in cardiorespiratory deterioration. In this prospective investigation of 35 patients undergoing elective THA, we used transesophageal echocardiography and invasive hemodynamic monitoring, and in 12 of them, we monitored distribution of pulmonary ventilation and perfusion intraoperatively. Embolization was significantly greater after insertion of the prosthesis in patients undergoing cemented than in those undergoing noncemented THA. Cemented THA was also associated with decreased cardiac output and increased pulmonary artery pressure and pulmonary vascular resistance. Increases in ventilation-perfusion mismatching, however, could not be demonstrated 30 minutes after insertion of the femoral prosthesis. Intraoperative monitoring for embolism may help physicians assess patients in whom cardiorespiratory function deteriorates during THA.
During insertion of the joint prosthesis in cemented total hip arthroplasty (THA), embolization of intramedullary fat, bone marrow, methyl methacrylate bone cement, or air can cause bone cement implantation syndrome.'? Embolization during THA results from high intramedullary pressure.v' Polymerization of methyl methacrylate cement produces an expanding exothermic interface between the cancellous bone of the femur and the prosthesis. The resultant intramedullary hypertension is as
*Emeritus staff. This study was supported in part by Grant HL 21584 from the National Institutes of Health, Public Health Service, and by the Mayo Foundation. Address reprint requests to Dr. M. H. Ereth, Department of Anesthesiology, Mayo Clinic, Rochester, MN 55905. Mayo Clin Proc 67:1066-1074,1992
great as 900 mm Hg in canine models and 575 mm Hg in humans.t" Insertion of noncemented prostheses, with no bone-cement interface, consistently results in intramedullary pressures of less than 100 mm Hg.4 ,5 Bone cement implantation syndrome has not been associated with noncemented methods. Venous embolism, as evidenced by a "snow flurry" detected with transesophageal echocardiography, occurs during cemented THA. 7-10 Air, fat, bone marrow, hematopoietic stem cells, endothelial cells, and other intramedullary debris are extruded into the femoral venous channels by the expanding and pressurized bone-cement interface and eventually embolize to the heart and lungs 6,9.11-13 or, in the case of paradoxical embolism, to the brain. In the bloodstream, such emboli may produce an intense and complex biochemical and physiologic response." In addition, local tissue mediators of coagulation or complement activation (or both) may be released because of trauma to tissue during implantation of a cemented pros-
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thesis. These materials may contribute to the development of bone cement implantation syndrome through their biochemical effects on vascular tone, coagulation, and myocardial contractility, as well as to the physical effects of impeding blood flow through pulmonary vessels.'>" Bone cement implantation syndrome is variable and may manifest with hypotension, hypoxemia, cardiac arrhythmias, cardiac arrest, or any combination of these problems or may cause sudden death.v" These complications frequently occur within minutes after implantation of the methyl methacrylate bone cement and the prosthetic component. Bone cement implantation syndrome contributes to morbidity and mortality in patients undergoing cemented THA. 3 The perioperative mortality associated with THA ranges from 0.02 to 6.6%.19-26 In a review of intraoperative mortality among 21,895 patients in whom a THA was performed during the past 20 years at our institution, we confirmed 19 intraoperative deaths due to bone cement implantation syndrome among 15,211 patients who underwent cemented hip arthroplasties but no intraoperative deaths among 6,684 patients who underwent noncemented hip arthroplasties (P
MARK H. ERETH, M.D., JOSEPH G. WEBER, M.D., MARTIN D. ABEL, M.D., ROBERT L.LENNON, D.O., Department ofAnesthesiology; DAVID G. LEWALLEN, M.D., Department of Orthopedics; DUANE M. ILSTRUP, M.S., Section ofBiostatistics; KAI REHDER, M.D.,* Department ofAnesthesiology
Bone cement implantation syndrome is characterized by hypotension, hypoxemia, cardiac arrhythmias, cardiac arrest, or any combination of these complications. It may result from venous embolization that occurs in conjunction with intramedullary hypertension in the femur during insertion of the prosthesis in patients undergoing cemented total hip arthroplasty (THA). Intramedullary hypertension does not occur in patients undergoing noncemented THA. In this study, we sought to compare embolization between patients undergoing cemented and noncemented THA and to determine whether this state resulted in cardiorespiratory deterioration. In this prospective investigation of 35 patients undergoing elective THA, we used transesophageal echocardiography and invasive hemodynamic monitoring, and in 12 of them, we monitored distribution of pulmonary ventilation and perfusion intraoperatively. Embolization was significantly greater after insertion of the prosthesis in patients undergoing cemented than in those undergoing noncemented THA. Cemented THA was also associated with decreased cardiac output and increased pulmonary artery pressure and pulmonary vascular resistance. Increases in ventilation-perfusion mismatching, however, could not be demonstrated 30 minutes after insertion of the femoral prosthesis. Intraoperative monitoring for embolism may help physicians assess patients in whom cardiorespiratory function deteriorates during THA.
During insertion of the joint prosthesis in cemented total hip arthroplasty (THA), embolization of intramedullary fat, bone marrow, methyl methacrylate bone cement, or air can cause bone cement implantation syndrome.'? Embolization during THA results from high intramedullary pressure.v' Polymerization of methyl methacrylate cement produces an expanding exothermic interface between the cancellous bone of the femur and the prosthesis. The resultant intramedullary hypertension is as
*Emeritus staff. This study was supported in part by Grant HL 21584 from the National Institutes of Health, Public Health Service, and by the Mayo Foundation. Address reprint requests to Dr. M. H. Ereth, Department of Anesthesiology, Mayo Clinic, Rochester, MN 55905. Mayo Clin Proc 67:1066-1074,1992
great as 900 mm Hg in canine models and 575 mm Hg in humans.t" Insertion of noncemented prostheses, with no bone-cement interface, consistently results in intramedullary pressures of less than 100 mm Hg.4 ,5 Bone cement implantation syndrome has not been associated with noncemented methods. Venous embolism, as evidenced by a "snow flurry" detected with transesophageal echocardiography, occurs during cemented THA. 7-10 Air, fat, bone marrow, hematopoietic stem cells, endothelial cells, and other intramedullary debris are extruded into the femoral venous channels by the expanding and pressurized bone-cement interface and eventually embolize to the heart and lungs 6,9.11-13 or, in the case of paradoxical embolism, to the brain. In the bloodstream, such emboli may produce an intense and complex biochemical and physiologic response." In addition, local tissue mediators of coagulation or complement activation (or both) may be released because of trauma to tissue during implantation of a cemented pros-
1066
Mayo Clio Proc, November 1992, Vol 67
thesis. These materials may contribute to the development of bone cement implantation syndrome through their biochemical effects on vascular tone, coagulation, and myocardial contractility, as well as to the physical effects of impeding blood flow through pulmonary vessels.'>" Bone cement implantation syndrome is variable and may manifest with hypotension, hypoxemia, cardiac arrhythmias, cardiac arrest, or any combination of these problems or may cause sudden death.v" These complications frequently occur within minutes after implantation of the methyl methacrylate bone cement and the prosthetic component. Bone cement implantation syndrome contributes to morbidity and mortality in patients undergoing cemented THA. 3 The perioperative mortality associated with THA ranges from 0.02 to 6.6%.19-26 In a review of intraoperative mortality among 21,895 patients in whom a THA was performed during the past 20 years at our institution, we confirmed 19 intraoperative deaths due to bone cement implantation syndrome among 15,211 patients who underwent cemented hip arthroplasties but no intraoperative deaths among 6,684 patients who underwent noncemented hip arthroplasties (P
