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The editors would like to acknowledge that this chapter is abridged from a chapter originally written by Drs. Edward R. Mariano and Jody C. Leng.


Bone Cement

Bone cement, polymethylmethacrylate, is frequently required for joint arthroplasties. The cement interdigitates within the interstices of cancellous bone and strongly binds the prosthetic implant to the patient’s bone. Mixing polymerized methylmethacrylate powder with liquid methylmethacrylate monomer causes polymerization and cross-linking of the polymer chains. This exothermic reaction leads to hardening of the cement and expansion against the prosthetic components. The resultant intramedullary hypertension (>500 mm Hg) can cause embolization of fat, bone marrow, cement, and air into venous channels. Systemic absorption of residual methyl methacrylate monomer can produce vasodilation and a decrease in systemic vascular resistance. The release of tissue thromboplastin may trigger platelet aggregation, embolic microthrombus formation, and cardiovascular instability as a result of the circulation of vasoactive substances. Nevertheless, most patients experience no adverse response to the application of bone cement.

The clinical manifestations of bone cement implantation syndrome include hypoxia (increased pulmonary shunt), hypotension, arrhythmias (including heart block and sinus arrest), pulmonary hypertension (increased pulmonary vascular resistance), and decreased cardiac output. Emboli frequently occur during the insertion of a femoral prosthesis for hip arthroplasty. Treatment strategies for this complication include increasing inspired oxygen concentration prior to cementing, monitoring to maintain euvolemia and adequate blood pressure, creating a vent hole in the distal femur to relieve intramedullary pressure, performing high-pressure lavage of the femoral shaft to remove potentially microembolic debris, or using a femoral component that does not require cement.

Pneumatic Tourniquets

Use of a pneumatic tourniquet on an extremity creates a bloodless field that may facilitate surgery. However, tourniquets can produce potential problems of their own, including hemodynamic changes, pain, metabolic alterations, arterial thromboembolism, and pulmonary embolism. Inflation pressure is usually set approximately 100 mm Hg higher than the patient’s baseline systolic blood pressure. Prolonged inflation (>2 h) can lead to muscle ischemia and may produce rhabdomyolysis or contribute to perioperative neuropathy. Tourniquet inflation has also been associated with increases in body temperature in pediatric patients undergoing lower extremity surgery.

Awake patients predictably experience tourniquet pain with inflation pressures of 100 mm Hg above systolic blood pressure for more than a few minutes. During a regional anesthetic, tourniquet pain may gradually become so severe in some patients over time that they may require substantial supplemental intravenous analgesia, if not general anesthesia, despite the fact that the block is adequate to “cover” the surgical incision. Even during general anesthesia, the noxious stimulus of tourniquet compression often manifests as a gradually increasing mean arterial blood pressure beginning approximately 1 h after cuff inflation. Signs of progressive sympathetic activation include marked hypertension, tachycardia, and diaphoresis.

Cuff deflation invariably and immediately relieves tourniquet pain ...

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