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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 device to the patient’s bone. The resultant intramedullary hypertension (>500 mm Hg) can cause embolization of fat, bone marrow, cement, and air into the femoral venous channels. Residual methylmethacrylate monomer can produce vasodilation and a decrease in systemic vascular resistance.

Clinical Manifestations of Bone Cement Implantation

• Hypoxia: Increased pulmonary shunt

• Hypotension

• Dysrhythmias, including heart block and sinus arrest

• Pulmonary hypertension: Increased pulmonary vascular resistance

• Decreased cardiac output.

Strategies to Minimize the Effects of Bone Cement Implantation

• Increasing inspired oxygen concentration prior to cementing

• Maintaining euvolemia by monitoring central venous pressure

• Creating a vent hole in the distal femur to relieve intramedullary pressure

• Performing high-pressure lavage of the femoral shaft to remove debris (potential microemboli)

• Using an uncemented femoral component

Pneumatic Tourniquet

Pneumatic tourniquets provide a bloodless field that greatly facilitates surgery. Inflation pressure is usually set about 100 mm Hg over the patient’s baseline systolic blood pressure. Prolonged inflation (>2 hr) routinely leads to transient muscle dysfunction from ischemia but may produce rhabdomyolysis or permanent peripheral nerve injury.

Potential Problems Associated with Pneumatic Tourniquets

• Hemodynamic changes

• Arterial thromboembolism

• Pulmonary embolism

• Pain: The mechanism and neural pathways for the severe aching and burning sensation defy precise explanation. Tourniquet pain gradually becomes so severe over time that patients may require substantial supplemental analgesia, if not general anesthesia, despite a regional block that is adequate for surgical anesthesia.

• Metabolic derangements: Washout of accumulated metabolic wastes in the ischemic extremity increases PaCO₂, ETCO₂, and serum lactate and potassium levels. These metabolic alterations can cause an increase in minute ventilation in a spontaneously breathing patient and, rarely, dysrhythmias.

Fat Embolism Syndrome

Although some degree of fat embolism probably occurs in all cases of long-bone fracture, fat embolism syndrome is a less frequent but potentially fatal (10%–20% mortality) event that can complicate anesthetic management. Fat embolism syndrome classically presents within 72 hours after long-bone or pelvic fracture, with the triad of dyspnea, confusion, and petechiae.

Diagnosis

• The diagnosis of fat embolism syndrome is suggested by petechiae on the chest, upper extremities, axillae, and conjunctiva. Coagulation abnormalities such as thrombocytopenia or prolonged clotting times are occasionally present. Serum lipase activity may be elevated but does not predict disease severity.

• Pulmonary involvement typically progresses from mild hypoxia and a normal chest radiograph to severe hypoxia or respiratory failure with chest radiography findings of diffuse patchy pulmonary opacity.

Management

• Early stabilization of the fracture decreases the incidence of fat embolism syndrome and, in particular, reduces the risk of pulmonary complications.

• Supportive treatment consists of oxygen therapy with continuous positive airway pressure ventilation to prevent hypoxia. Systemic hypotension requires appropriate pressor support.

Deep Venous Thrombosis and Pulmonary Embolism

Deep venous thrombosis (DVT) and pulmonary embolism (PE) are serious causes of morbidity and mortality after major orthopedic operations on the pelvis and lower extremities. Additional risk factors include obesity, age older than 60 years, procedures lasting longer than 30 min, use of a tourniquet, lower extremity fracture, and immobilization for more than 4 days. Patients at highest risk are those undergoing hip surgery and knee replacement or major lower extremity trauma operations with published DVT rates of 40% to 80% without thromboprophylaxis.

Neuraxial anesthesia alone or combined with general anesthesia may reduce thromboembolic complications by several mechanisms:

• Sympathectomy-induced increases in lower extremity venous blood flow

• Systemic antiinflammatory effects of local anesthetics

• Decreased platelet reactivity

• Attenuated postoperative increases in factor VIII and von Willebrand factor

• Attenuated postoperative decreases in antithrombin III

• Alterations in stress hormone release

Related posts:

Intravenous Anesthetics Anesthesia for Patients with Cardiovascular Disease Anesthesia for Genitourinary Surgery Peripheral Nerve Blocks Anesthesia for Patients with Endocrine Disease Obstetric Anesthesia

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