Surgery on the knee is often performed using regional anesthetic techniques. Neural structures may be blocked at the neuraxial (spinal, epidural), plexus (psoas compartment), or peripheral nerve (femoral, lateral femoral cutaneous, sciatic) level. Regional anesthetics offer several advantages over general anesthetics for these patients, including improved postoperative analgesia, decreased incidence of nausea and vomiting, less respiratory and cardiac depression, improved perfusion via sympathetic block, reduced blood loss, and decreased risk of thromboembolism.³³ The regional technique and the local anesthetic solution used depend on a variety of factors, including duration of surgery, degree of sensory and motor block desired, and length of postoperative analgesia. Surgical anesthesia for operative procedures on the knee in which a tourniquet will be used requires blockade of all four nerves (femoral, lateral femoral cutaneous, obturator, and sciatic nerves) innervating the leg. Although it is possible to perform major knee surgery under peripheral nerve block, more often a single-injection femoral or lumbar plexus (psoas compartment) block is combined with a spinal or general anesthetic. Spinal anesthesia can be accomplished with hyperbaric or isobaric solutions, although the latter are favored by most orthopedic anesthesiologists. Injection of hyperbaric solutions often results in a higher level of sensory and motor blockade than needed for the surgical procedure, with subsequent earlier offset of anesthesia. Epidural blockade offers the advantage of a continuous catheter technique that can be continued into the postoperative period. Patients with an absolute contraindication to regional anesthesia (patient refusal, infection at the site of needle placement, systemic anticoagulation) are candidates for general anesthesia. Thus, although knee surgery may be performed under general or regional anesthesia, the ability to provide superior postoperative analgesia, rapid postoperative rehabilitation, and reduced cost of medical care may result from thoughtfully implemented regional anesthetic and analgesic techniques.

Monitoring Requirements

Patients undergoing knee surgery of any type require standard monitoring, including electrocardiography, noninvasive blood pressure assessment, and pulse oximetry, regardless of anesthetic technique. Many revision procedures are lengthy and are associated with significant blood loss. Placement of an arterial cannula and a urinary catheter will facilitate fluid management and allow intraoperative measurement of hemoglobin and clotting parameters.

Blood Loss and Pneumatic Tourniquet Inflation

The use of intraoperative tourniquets decreases intraoperative blood loss. However, postoperative drainage averages 500 to 1000 mL per knee (resulting in a decrease in hemoglobin level of 1 to 2 g/dL). Thus, postoperative monitoring of blood loss and hemodynamic parameters is necessary for patient considered at high risk for excessive bleeding or cardiovascular complications.

Tourniquets are often used to minimize blood loss and provide a bloodless operating field. Appropriate selection of tourniquet cuff size and inflation pressure is paramount in reducing the risk of neuromuscular injury related to tourniquet ischemia. The cuff should be large enough to comfortably encircle the limb to ensure circumferentially uniform pressure. The width of the inflated cuff should be more than half the limb diameter.

Damage to underlying vessels, nerves, and muscles has been reported following tourniquet inflation.²⁰ Injury is a function of both inflation pressure and duration of inflation.^27,⁴² Direct pressure from the cuff is more damaging distally than the ischemia.^35,⁴² Arterial spasm, venous thrombosis, and nerve injury are demonstrable after several hours. Clinical examination, electromyography, and effluent blood analysis all show completely reversible changes for inflation of 1 to 2 hours, which is the basis for the recommendation of this period as the safe duration for tourniquet use; longer inflation times are associated with prolonged or irreversible changes in neurologic and/or muscular function.^22,²⁵

Transient systemic metabolic acidosis and increased arterial carbon dioxide levels have been demonstrated after tourniquet deflation and do not cause deleterious effects in healthy patients. Prolonged inflation or the simultaneous release of bilateral tourniquets may produce clinically significant acidosis. Tourniquet release has also been associated with cerebral embolic phenomena.¹¹

When a pneumatic tourniquet is used with regional anesthetic techniques, some patients complain of dull, aching pain or become restless, even though seemingly adequate analgesia has been provided for the operation itself. Patient discomfort usually appears approximately 45 minutes after the tourniquet is inflated and becomes more intense with time. No satisfactory explanation for its genesis has been found. The definitive treatment for tourniquet pain is release of the tourniquet. Relief of pain is prompt and complete. During surgery, however, opioids and hypnotics are usually effective.

Postoperative Analgesia

Patients undergoing total joint arthroplasty experience significant postoperative pain. Failure to provide adequate analgesia impedes aggressive physical therapy and rehabilitation, which are critical to maintaining joint range of motion; this potentially delays hospital dismissal. Traditionally, postoperative analgesia following total joint replacement was provided by intravenous patient-controlled analgesia (PCA) or by epidural analgesia. Each technique has distinct advantages and disadvantages. For example, opioids do not consistently provide adequate pain relief and often cause sedation, constipation, nausea/vomiting, and pruritus. Epidural infusions containing local anesthetics (with or without an opioid) provide superior analgesia but are associated with hypotension, urinary retention, motor block limiting ambulation, and spinal hematoma secondary to anticoagulation. Single-dose and continuous peripheral nerve techniques that block the lumbar plexus (fascia iliaca, femurs, psoas compartment blocks) with/without sciatic nerve blockade have been used in this patient population.^1,^5,^17,⁴⁷ Several studies have reported that unilateral peripheral block provided a quality of analgesia and surgical outcomes similar to those of continuous epidural analgesia, but with fewer side effects.^5,⁴⁷ This suggests that continuous peripheral techniques may be the optimal analgesic method following total joint arthroplasty.

Multimodal Analgesia

Multimodal analgesia represents a multidisciplinary approach to pain management, with the aim of maximizing positive aspects of treatment while limiting associated side effects. Because many of the negative side effects of analgesic therapy are opioid related (and dose dependent), limiting perioperative opioid use is a major principle of multimodal analgesia. The use of peripheral or neuraxial regional anesthetic techniques and a combination of opioid and nonopioid analgesic agents for breakthrough pain results in superior pain control, attenuation of the stress response, and decreased opioid requirements.

Systemic Analgesics

Opioid Analgesics

Adequate analgesia achieved with systemic opioids is frequently associated with side effects, including sedation, nausea, and pruritus. However, despite these well-defined side effects, opioid analgesics remain an integral component of postoperative pain relief. Systemic opioids may be administered by intravenous, intramuscular, and oral routes. Current analgesic regimens typically provide intravenous PCA for 24 to 48 hours postoperatively, with subsequent conversion to oral agents. The PCA device may be programmed for several variables, including bolus dose, lockout interval, and background infusion (Table 74-1). The optimal bolus dose is determined by the relative potency of the opioid; insufficient dosing results in inadequate analgesia, whereas excessive dosing increases the potential for side effects, including respiratory depression. Likewise, the lockout interval is based on the onset of analgesic effects; a lockout interval that is too short allows the patient to self-administer additional medication before achieving the full analgesic effect (and may result in accumulation/overdose of the opioid). A prolonged lockout interval will not allow adequate analgesia. The optimal bolus dose and lockout interval are not known, but ranges have been determined. Varying the settings within these ranges appears to have little effect on analgesia or side effects. Although most PCA devices allow the addition of a background infusion, routine use in adult opioid-naive patients is not recommended. However, background opioid infusion may have a role in opioid-tolerant patients. Because of variation in patient pain tolerance, PCA dosing regimens may have to be adjusted to maximize the benefits and to minimize the incidence of side effects.

Table 74-1 Intravenous Opioids for Patient-Controlled Analgesia

Adverse effects of opioid administration can cause serious complications in patients undergoing major orthopedic procedures. In a systematic review, Wheeler and associates ⁵⁵ reported gastrointestinal side effects (nausea, vomiting, ileus) in 37%, cognitive effects (somnolence and dizziness) in 34%, pruritus in 15%, urinary retention in 16%, and respiratory depression in 2% of patients receiving PCA opioid analgesia.

Oral opioids (Table 74-2) are available in immediate-release and controlled-release formulations. Although immediate-release oral opioids are effective in relieving moderate to severe pain, they must be administered as often as every 4 hours. When these medications are prescribed as needed (prn), delayed administration may be followed by increased pain. Furthermore, interruption of the dosing schedule, particularly during the night, may lead to an increase in the patient’s pain. The adverse effects of oral opioid administration are considerably fewer than those associated with intravenous administration, and they are mainly gastrointestinal in nature.⁵⁵

Table 74-2 Oral Analgesics

A controlled-release formulation of oxycodone (OxyContin) is available and has been shown to provide therapeutic opioid concentrations and sustained pain relief over an extended period.

Tramadol (Ultram) is a centrally acting analgesic that is structurally related to morphine and codeine (but is not truly an opioid). Its analgesic effect occurs through binding to the opioid receptors and blocking of reuptake of both norepinephrine and serotonin. Tramadol has gained popularity because of the low incidence of adverse effects, specifically, respiratory depression, constipation, and abuse potential. Thus, tramadol may be used as an alternative to opioids in a multimodal approach to postoperative pain, especially in patients who are intolerant to opioid analgesics.

Nonopioid Analgesics (Acetaminophen and Nonsteroidal Anti-Inflammatory Drugs)

The addition of nonopioid analgesics reduces opioid use, improves analgesia, and decreases opioid-related side effects. The multimodal effect is maximized through selection of analgesics that have complementary sites of action. For example, acetaminophen acts predominantly centrally, and other nonsteroidal anti-inflammatory drugs (NSAIDs) exert their effects peripherally.

The mechanism of analgesic action of acetaminophen has not been fully determined. Acetaminophen may act predominantly by inhibiting prostaglandin synthesis in the central nervous system. Acetaminophen has very few adverse effects and is an important addition to the multimodal postoperative pain regimen, although the total daily dose must be limited to less than 4000 mg. It is also important to note that many oral analgesics are an opioid–acetaminophen combination. In these preparations, the total dose of opioid will be restricted by the acetaminophen ingested.

NSAIDs have a mechanism of action through the cyclooxygenase (COX) enzymatic pathway; they ultimately block two individual prostaglandin pathways. The COX-1 pathway is involved in prostaglandin E₂–mediated gastric mucosal protection and thromboxane effects on coagulation. The inducible COX-2 pathway is mainly involved in the generation of prostaglandins included in the modulation of pain and fever, but it has no effect on platelet function or on the coagulation system. In general, NSAIDs block the COX-1 and COX-2 pathways. Traditionally, NSAIDs have been viewed as peripherally acting agents. However, a central analgesic effect may be attained through inhibition of spinal COX.

The introduction of specific COX-2 inhibitors represented a breakthrough in the treatment of pain and inflammation. However, despite their efficacy, two (rofecoxib [Vioxx]; valdecoxib [Bextra]) of three COX-2 inhibitors were voluntarily removed from general use because of an increased relative risk for confirmed cardiovascular events, such as heart attack and stroke, after 18 months of treatment. Celecoxib (Celebrex) is currently the only COX-2 inhibitor available in the United States, although the Food and Drug Administration (FDA) has requested that safety information be included regarding potential cardiovascular and gastrointestinal risks for all selective and nonselective NSAIDs except aspirin.¹⁴

Although numerous NSAIDs have been used in the perioperative management of pain, ketorolac is the only NSAID that can be given parenterally. An intravenous dose of ketorolac 10 to 30 mg was found to have similar efficacy to 10 to 12 mg of intravenous morphine. In surgical patients, ketorolac reduces opioid consumption by 36%. Because of the potential for serious side effects, ketorolac should be used for 5 days or less in the adult population with moderate to severe acute pain.⁴⁸

Major side effects limiting NSAID use for postoperative pain control (renal failure, platelet dysfunction, and gastric ulcers or bleeding) are related to nonspecific inhibition of the COX-1 enzyme.⁴⁸ Advantages of COX-2 inhibitors include lack of platelet inhibition and a decreased incidence of gastrointestinal effects. All NSAIDs have the potential to cause serious renal impairment. Inhibition of the COX enzyme may have only minor effects in the healthy kidney but unfortunately can lead to serious side effects in elderly patients or those with a low-volume condition (blood loss, dehydration, cirrhosis, or heart failure). Therefore, NSAIDs should be used cautiously in patients with underlying renal dysfunction, specifically in the setting of volume depletion due to blood loss.⁴⁸ Similar to COX-2 inhibitors, NSAIDs interfere with the inhibitory COX-1 effects of aspirin on platelet activity and may counter the cardioprotective effects.⁷

The effects of NSAIDs on bone formation and healing are of concern to the orthopedic population. Although the data are conflicting, evidence from animal studies indicates that COX-2 inhibitors may inhibit bone healing.¹⁵ Thus, adverse effects of COX-2 inhibitors must be weighed against their benefits. Until definitive human trials are performed, it is reasonable to be cautious regarding the use of COX-2 inhibitors, especially when bone healing is critical.

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