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Total-Hip Replacement

Background

Anesthetic management of total-hip replacement varies according to the complexity of the surgery, complications that may arise during the surgery, and the medical status of the patient. Complex procedures such as those involving acetabular bone grafting, insertion of a long-stem femoral prosthesis,[57] removal of a prosthesis, revision surgery, or surgery in patients with acetabular protrusion (which entails a risk of entering the pelvic cavity or iliac vessels, or both) complicate the management of the anesthetic.

Anesthetic Management
Monitoring

Because most candidates for total-hip replacement have only a limited ability to exercise, their cardiopulmonary function can be difficult to assess. This often-elderly population frequently has underlying systemic diseases. Fluid administration must be carefully managed during this type of extensive surgery. There is an increased likelihood of developing hypoxemia or pulmonary edema, or both, because of pulmonary endothelial injury from fat or bone marrow emboli[58] and from ventilation-perfusion mismatching (see "Positioning" and Table 61-3 and Table 61-4 ). It is therefore reasonable to use invasive hemodynamic monitoring perioperatively in the elderly or medically compromised patient undergoing total-hip replacement, especially when this involves complex or revision surgery.

Blood Loss

Extensive studies during and after total-hip replacement show that use of hypotensive or regional (epidural or spinal) anesthesia reduces the blood loss by 30% to 50%.[59] [60] Lowering intraoperative mean arterial pressure to 50 mm Hg reduces intraoperative blood loss more effectively than a mean arterial pressure of 60 mm Hg, although overall blood loss was not significantly different.[61] Caution must be exercised when using a hypotensive epidural technique, and the anesthesiologist must be constantly alert to signs of hypovolemia.[62] [63]

Blood loss during total-hip replacement is significantly greater during revision surgery. In these patients, several modalities to reduce the risk of homologous transfusion should be used, including preoperative donation of autologous blood, induced hypotension, preoperative use of erythropoietin,[64] [65] or hemodilution. Cell savers can be used if blood loss is expected to be greater than 1 L, but in cases of infection, the use of these devices is contraindicated. With the use of hypotensive epidural anesthesia, intraoperative blood losses of more than 300 mL are unusual, limiting the need for the cell saver or antifibrinolytic agents.

Positioning

Most total-hip replacements are performed with the patient in the lateral decubitus position. This creates a potential ventilation-perfusion mismatch with resultant hypoxemia, a problem that appears most often in patients with underlying lung disease. The lateral decubitus position also can create neurovascular problems, because the dependent shoulder presses on the axillary artery and brachial plexus [66] and the anterior stabilizing post compresses the femoral triangle.[33] These problems can be minimized by placing an inflatable axillary roll beneath the upper thorax and by careful positioning of the anterior stabilizing post at the dependent groin. Inflatable axillary roles help reduce dependent shoulder discomfort when surgery is performed in the lateral decubitus position under regional anesthesia.[67] Patients who are given hypotensive anesthesia may be at greater risk for neurovascular injury, because less extrinsic pressure is required to compress a less tense vessel. [28] Continuous surveillance of the patients positioning throughout the case is necessary to avoid preventable injury.

Cement Fixation

The quality of the cement-bone interface is improved if there is no blood covering the cancellous bone as the cement is applied. Hypotensive anesthesia has been


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TABLE 61-5 -- Suggested management of major orthopedic procedures
Procedure Average Duration (hr) Range of Blood Loss (units) Suggested Monitoring Procedure or Special Techniques
Total hip 1–4 1–6 Autologous blood donation



Arterial cannula



Central venous pressure (optional)



Foley catheter (optional)



Epidural catheter (optional for postoperative pain treatment)



Induced hypotension



Cell Saver (revision)



Psoas compartment/lumbar plexus block (for postoperative analgesia)
Total knee 1.5–3 0–2 (with tourniquet) Autologous blood donation



Arterial cannula



Foley catheter (optional)



Epidural catheter (for postoperative analgesia)



Femoral nerve block (for postoperative analgesia)
Major spinal surgery 3–8 1–10 Autologous blood donation



Arterial cannula



Central venous pressure



Foley catheter



Induced hypotension



Evoked potential monitoring



Wake-up test



Low dose ketamine infusion



Acute normovolemic hemodilution



Intraoperative autologous salvage (Cell Saver)
Major allograft surgery 2–8 2–10 Autologous blood donation



Arterial cannula



Central venous pressure



Foley catheter



Induced hypotension and/or hemodilution



Epidural catheter (for postoperative analgesia)
Major pelvic resection 2–8 2–10 Autologous blood donation



Arterial cannula



Central venous pressure



Foley catheter



Induced hypotension and/or hemodilution



Epidural catheter (for postoperative analgesia)



Evoked potential monitoring

shown radiographically to improve the quality of cement bone fixation[68] because it reduces bleeding from bone.[61]

Intraoperative Hypotension

Profound hypotension immediately after insertion of cemented femoral prostheses has resulted in cardiac arrest and death.[57] [69] [70] [71] These events are not seen with noncemented prostheses. This is now uncommon during elective primary total-hip replacement but not uncommon in certain high-risk groups ( Table 61-6 ). It seems likely that hypotension is related in some way to the use of cement ( Fig. 61-3 ). Two possible explanations are that hypotension may be caused by direct vasodilation or cardiac depression from methylmethacrylate or that it may be caused by the forced entry of air, fat, or bone marrow into the venous system, with resultant pulmonary emboli.[69] Large, echogenic emboli have been described after insertion of femoral prostheses; this supports the concept that the circulatory collapse is embolic[72] rather than from a toxic effect of the methylmethacrylate. Attempts to minimize this complication have included the use of a plug in the femoral shaft to limit the distal spread of cement in the femur,[73] venting of entrapped air, waiting for cement to
TABLE 61-6 -- Patients at risk for acute hypotension or cardiac arrest during total-joint replacement
Long-stem, cemented, primary total-hip replacement
  Metastatic cancer[76] [285]
  Removal of hardware after intertrochanteric hip fracture [57]
  Spiral fracture of femur[57]
Revision of long-stem, cemented femoral component
  Cemented prosthesis to distal femur
  Fracture below femoral component
Cemented, long-femoral-stem total-knee replacement[101] [102]


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Figure 61-3 Status of an 85-year-old woman who underwent primary total-hip replacement with a Richard screw with a long side plate. She had a history of chronic obstructive lung disease and osteoporosis. Pulmonary and radial artery pressures were stable until a 200-mm cemented femoral component was inserted (point A). One minute after impaction of the femoral component, pulmonary artery pressure increased acutely (point C), and arterial pressure decreased to 30 mm Hg. Epinephrine (25 µg) was injected through the distal port of the pulmonary artery catheter (point D). This resulted in a rapid restoration of arterial pressure, transient tachycardia, and stabilization of the pulmonary artery pressure. The hip was relocated at point B, which resulted in no change in pulmonary artery pressure. (Adapted from Sharrock NE: Anesthesia. In Rubash HE (ed): The Adult Hip. Philadelphia, Lippincott-Raven Publishers, 1998, pp 615–624.)

become more viscous before its insertion, and vacuum drainage in the proximal femur. [74] [75] These maneuvers minimize the disruption of bone marrow in the distal femur, thereby preventing catastrophic fat or bone marrow pulmonary embolism. Embolization can also be reduced by carefully lavaging the femoral canal.[76] In contrast, in the high-risk group, extensive reaming of the femur occurs, disrupting more bone marrow; and with pressurization with cement, significant marrow is forced into the circulation. This can be seen with transesophageal echocardiography[69] [72] [74] [75] [76] [77] ( Fig. 61-4 ).

Echogenic material is observed with reaming the femur, after insertion of the cemented femoral component,[69] [72] [76] [77] and with relocation of the hip joint.[78] Large emboli may be observed in the right side of the heart, obstructing the right ventricular outflow tract and leading to right-sided heart failure, hypotension, and cardiac arrest. Small emboli traverse the right side of the heart and embolize to the lung. These may increase pulmonary artery pressure and intrapulmonary shunt but are less likely to cause intraoperative cardiac arrest. In patients with a patent foramen ovale, emboli may pass into the systemic circulation, causing myocardial infarction or stroke. [76] Although patent foramen ovale is common, severe systemic manifestations of fat emboli are uncommon after total-hip replacement, even though most patients have evidence of fat embolization during surgery. Fat may also pass through the pulmonary circulation, contributing to systemic manifestation of fat embolism after surgery.[79] Whether this contributes to acute delirium or persistent decline in cognitive function is unclear.[80] [81] [82] [83]

Hypotension may occur with impaction of the femoral component or after relocation of the hip joint (see Fig. 61-3 ). With impaction of the femoral component, the embolic material can be forced directly into the venous system. Obstruction of the femoral vein occurs during insertion of the femoral component, and fat or bone marrow is usually retained in the femoral vein until the hip joint is relocated. As soon as the obstruction of the vein is relieved, the emboli pass toward the right side of the heart. This process can be monitored with trans-esophageal echocardiography or by using oximetric pulmonary artery catheters[84] ( Fig. 61-5 ). An acute decline in mixed venous oxygen saturation occurs in conjunction with a rise in pulmonary artery pressure with release of an obstructed femoral vein containing embolic material.

Effective treatment for the acute hypotension is intravenous epinephrine (4 to 50 µg) as soon as the hypotension is observed.[57] The dose depends on the degree of hypotension. In the high-risk group, epinephrine (10 to 20 µg) is injected through the distal port of a pulmonary artery catheter the moment any reduction in arterial pressure is detected after impaction of the long-stem, cemented femoral component. If cardiac arrest occurs, much larger doses of epinephrine will be needed to resuscitate the patient.

Hypoxia has been described immediately after insertion of a cemented femoral prosthesis and for up to 5 days into the postoperative period. In the event of hypoxemia, the physician must first ascertain whether it has a specific cause, such as atelectasis of the dependent lung, hypoventilation, or fluid overload. Even with no


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Figure 61-4 Right atrium during echocardiography. A, Multiple, small emboli in the right atrium. B, A large embolus (7 cm long), which is probably a cast of the femoral vein. (Adapted from Christie J, Burnett R, Potts HR, et al: Echocardiography of transatrial embolism during cemented and uncemented hemiarthroplasty of the hip. J Bone Joint Surg Br 76:409–412, 1994.)


Figure 61-5 Pulmonary artery oxygen saturation (SVO2 ) during total-hip replacement is recorded from an oximetric pulmonary artery catheter (American Edwards, Baxter Healthcare Corporation, Irvine, CA). Notice the acute fall in pulmonary artery oxygen saturation after relocation of the hip at minute 62 after trial reduction (T) with 8 minutes of potential venous occlusion and minute 74 after final reduction (F) with 12 minutes of potential venous occlusion. (Adapted from Sharrock NE, Go G, Harpel PC, et al: The John Charnley Award. Thrombogenesis during total hip arthroplasty. Clin Orthop 319:16–27, 1995.)


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specific cause, hypoxemia may persist for some days after hip surgery.[85] It may be a result of the embolic effects of femoral shaft cement or fat embolism. [86] Pulmonary emboli with cement or bone marrow increase pulmonary artery pressures in dogs[87] and humans,[84] but it is unclear whether this is directly responsible for the hypoxemia observed. Postoperative management should include nasal oxygen, pulse oximetry (for several days if necessary),[58] judicious use of narcotics to provide analgesia but avoid hypoventilation or airway obstruction, appropriate fluid management, and diuresis. Hypoxia and fluid overload may further increase pulmonary pressures and increase the likelihood of pulmonary edema or right-sided heart failure. Postoperative hypoxia is more common in patients who snore.[88]

Postoperative Pain Management

Postoperative pain management may be accomplished by multiple modalities. Use of the epidural catheter for patient-controlled epidural analgesia is extremely effective and easy if the catheter has been properly placed for surgery. Addition of a lumbar plexus block (placed easily with a nerve stimulator at the time of surgery) significantly improves pain scores and decreases postoperative narcotic requirements.[89]

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