Pain Management for the Postoperative Cardiac Patient

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Chapter 31 Pain Management for the Postoperative Cardiac Patient

Adequate postoperative analgesia prevents unnecessary patient discomfort, may decrease morbidity, may decrease postoperative hospital length of stay, and thus may decrease cost. Because postoperative pain management has been deemed important, the American Society of Anesthesiologists has published practice guidelines regarding this topic.¹ Furthermore, in recognition of the need for improved pain management, the Joint Commission on Accreditation of Healthcare Organizations has developed new standards for the assessment and management of pain in accredited hospitals and other health care settings.² Patient satisfaction (no doubt linked to adequacy of postoperative analgesia) has become an essential element that influences clinical activity of not only anesthesiologists but also all health care professionals.

Achieving optimal pain relief after cardiac surgery is often difficult. Pain may be associated with many interventions, including sternotomy, thoracotomy, leg vein harvesting, pericardiotomy, and/or chest tube insertion, among others. Inadequate analgesia and/or an uninhibited stress response during the postoperative period may increase morbidity by causing adverse hemodynamic, metabolic, immunologic, and hemostatic alterations. Aggressive control of postoperative pain, associated with an attenuated stress response, may decrease morbidity and mortality in high-risk patients after noncardiac surgery and may also decrease morbidity and mortality in patients after cardiac surgery. Adequate postoperative analgesia may be attained via a wide variety of techniques (Table 31-1). Traditionally, analgesia after cardiac surgery has been obtained with intravenous opioids (specifically morphine). However, intravenous opioid use is associated with definite detrimental side effects (nausea/vomiting, pruritus, urinary retention, respiratory depression), and longer-acting opioids such as morphine may delay tracheal extubation during the immediate postoperative period via excessive sedation and/or respiratory depression. Thus, in the current era of early extubation (“fast-tracking”), cardiac anesthesiologists are exploring unique options other than traditional intravenous opioids for control of postoperative pain in patients after cardiac surgery.³ No single technique is clearly superior; each possesses distinct advantages and disadvantages. It is becoming increasingly clear that a multimodal approach/combined analgesic regimen (utilizing a variety of techniques) is likely the best way to approach postoperative pain (in all patients after surgery) to maximize analgesia and minimize side effects. When addressing postoperative analgesia in cardiac surgical patients, choice of technique (or techniques) is made only after a thorough analysis of the risk/benefit ratio of each technique in the specific patient in whom analgesia is desired.

Table 31-1 Techniques Available for Postoperative Analgesia

Local anesthetic infiltration

Nerve blocks

Opioids

Nonsteroidal anti-inflammatory agents

α-Adrenergic agents

Intrathecal techniques

Epidural techniques

Multimodal analgesia

PAIN AND CARDIAC SURGERY

Surgical or traumatic injury initiates changes in the peripheral and central nervous systems that must be addressed therapeutically to promote postoperative analgesia and, it is hoped, positively influence clinical outcome (Boxes 31-1 and 31-2). The physical processes of incision, traction, and cutting of tissues stimulate free nerve endings and a wide variety of specific nociceptors. Receptor activation and activity are further modified by the local release of chemical mediators of inflammation and sympathetic amines released via the perioperative surgical stress response. The perioperative surgical stress response peaks during the immediate postoperative period and exerts major effects on many physiologic processes. The potential clinical benefits of attenuating the perioperative surgical stress response (above and beyond simply attaining adequate clinical analgesia) have received much attention during the past decade and remain fairly controversial. However, it is clear that inadequate postoperative analgesia and/or an uninhibited perioperative surgical stress response has the potential to initiate pathophysiologic changes in all major organ systems, including the cardiovascular, pulmonary, gastrointestinal, renal, endocrine, immunologic, and/or central nervous systems, all of which may lead to substantial postoperative morbidity.

BOX 31-1 Pain and Cardiac Surgery

• Originates from many sources

• Most commonly originates from chest wall

• Preoperative expectations influence postoperative satisfaction

• Quality of postoperative analgesia may influence morbidity/mortality

BOX 31-2 Potential Clinical Benefits of Adequate Postoperative Analgesia

• Hemodynamic stability

• Metabolic stability

• Immunologic stability

• Hemostatic stability

• Stress response attenuation

• Decreased morbidity/mortality

Pain after cardiac surgery may be intense and originates from many sources, including the incision (e.g., sternotomy, thoracotomy), intraoperative tissue retraction and dissection, vascular cannulation sites, vein-harvesting sites, and chest tubes, among others. Patients in whom an internal mammary artery is surgically exposed and used as a bypass graft may have substantially more postoperative pain.

Persistent pain after cardiac surgery, although rare, can be problematic.⁴ The cause of persistent pain after sternotomy is multifactorial, yet tissue destruction, intercostal nerve trauma, scar formation, rib fractures, sternal infection, stainless-steel wire sutures, and/or costochondral separation may all play roles. Such chronic pain is often localized to the arms, shoulders, or legs. Postoperative brachial plexus neuropathies may also occur and have been attributed to rib fracture fragments, internal mammary artery dissection, suboptimal positioning of patients during surgery, and/or central venous catheter placement. Postoperative neuralgia of the saphenous nerve has also been reported after harvesting of saphenous veins for coronary artery bypass grafting (CABG). Younger patients appear to be at higher risk for developing chronic, long-lasting pain. The correlation of severity of acute postoperative pain and development of chronic pain syndromes has been suggested (patients requiring more postoperative analgesics may be more likely to develop chronic pain), yet the causative relationship is still vague.

Patient satisfaction with quality of postoperative analgesia is as much related to the comparison between anticipated and experienced pain as it is to the actual level of pain experienced. Satisfaction is related to a situation that is better than predicted, dissatisfaction to one that is worse than expected. Patients undergoing cardiac surgery remain concerned regarding the adequacy of postoperative pain relief and tend to preoperatively expect a greater amount of postoperative pain than that which is actually experienced. Because of these unique preoperative expectations, patients after cardiac surgery who receive only moderate analgesia postoperatively will likely still be satisfied with their pain control. Thus, patients may experience pain of mode-rate intensity after cardiac surgery yet still express very high satisfaction levels.

POTENTIAL CLINICAL BENEFITS OF ADEQUATE POSTOPERATIVE ANALGESIA

Inadequate analgesia (coupled with an uninhibited stress response) during the postoperative period may lead to many adverse hemodynamic (tachycardia, hypertension, vasoconstriction), metabolic (increased catabolism), immunologic (impaired immune response), and hemostatic (platelet activation) alterations. In patients undergoing cardiac surgery, perioperative myocardial ischemia (diagnosed by electrocardiography and/or transesophageal echocardiography) is most commonly observed during the immediate postoperative period and appears to be related to outcome. Intraoperatively, initiation of CPB causes substantial increases in stress response hormones (e.g., norepinephrine, epinephrine) that persist into the immediate postoperative period and may contribute to myocardial ischemia observed during this time. Furthermore, postoperative myocardial ischemia may be aggravated by cardiac sympathetic nerve activation, which disrupts the balance between coronary blood flow and myocardial oxygen demand. Thus, during the pivotal immediate postoperative period after cardiac surgery, adequate analgesia (coupled with stress-response attenuation) may potentially decrease morbidity and enhance health-related quality of life.⁵

TECHNIQUES AVAILABLE FOR POSTOPERATIVE ANALGESIA

Local Anesthetic Infiltration

Pain after cardiac surgery is often related to median sternotomy (peaking during the first 2 postoperative days). One method that may hold promise is continuous infusion of local anesthetic (Box 31-3). In a prospective, randomized, placebo-controlled, double-blind clinical trial, White and associates⁶ studied 36 patients undergoing cardiac surgery. Intraoperative management was standardized. All patients had two indwelling infusion catheters placed at the median sternotomy incision site at the end of surgery (one in the subfascial plane above the sternum, one above the fascia in the subcutaneous tissue). Patients received 0.25% bupivacaine (n = 12), 0.5% bupivacaine (n = 12), or normal saline (n = 12) via a constant rate infusion through the catheter (4 mL/hr) for 48 hours after surgery. Average times to tracheal extubation were similar in the three groups (5 to 6 hours). Compared with the control group (normal saline), there was a statistically significant reduction in verbal rating scale pain scores and patient-controlled analgesia (PCA) using intravenous morphine in the 0.5% bupivacaine group. Patient satisfaction with their pain management was also improved in the 0.5% bupivacaine group (vs. control). However, there were no significant differences in PCA morphine use between the 0.25% bupivacaine and control groups. Although tracheal extubation time and the duration of the intensive care unit (ICU) stay (30 hours vs. 34 hours, respectively) were not significantly altered, time to ambulation (1 day vs. 2 days, respectively) and duration of hospital stay (4.2 days vs. 5.7 days, respectively) were lower in the 0.5% bupivacaine group than in the control group.

BOX 31-3 Local Anesthetic Infiltration

• Advantage: Simple, reliable analgesia

• Disadvantage: Tissue necrosis?

The management of postoperative pain with continuous direct infusion of local anesthetic into the surgical wound has been described following a wide variety of surgeries other than cardiac (inguinal hernia repair, upper abdominal surgery, laparoscopic nephrectomy, cholecystectomy, knee arthroplasty, shoulder surgery, and gynecologic operative laparoscopy). The infusion pump systems used for anesthetic wound perfusion are regulated by the U.S. Food and Drug Administration (FDA) as medical devices. Thus, adverse events involving these infusion pump systems during direct local anesthetic infusion into surgical wounds are reported to this organization. Complications encountered with these infusion pump systems reported to the FDA include tissue necrosis, surgical wound infection, and cellulitis after orthopedic, gastrointestinal, podiatric, and other surgeries. None of these reported adverse events has involved patients undergoing cardiac surgery.

Nerve Blocks

With the increasing popularity of minimally invasive cardiac surgery, which utilizes nonsternotomy incisions (minithoracotomy), the use of nerve blocks for the management of postoperative pain has increased as well (Box 31-4).⁷ Thoracotomy incisions (transverse anterolateral minithoracotomy, vertical anterolateral minithoracotomy), owing to costal cartilage trauma tissue damage to ribs, muscles, or peripheral nerves, may induce more intense postoperative pain than that resulting from median sternotomy. Adequate analgesia after thoracotomy is important because pain is a key component in alteration of lung function after thoracic surgery. Uncontrolled pain causes a reduction in respiratory mechanics, reduced mobility, and increases in hormonal and metabolic activity. Perioperative deterioration in respiratory mechanics may lead to pulmonary complications and hypoxemia, which may in turn lead to myocardial ischemia/infarction, cerebrovascular accidents, thromboembolism, and delayed wound healing, leading to increased morbidity and prolonged hospital stay. Various analgesic techniques have been developed to treat postoperative thoracotomy pain. The most commonly used techniques include intercostal nerve blocks, intrapleural administration of local anesthetics, and thoracic paravertebral blocks. Intrathecal techniques and epidural techniques are also very effective in controlling post-thoracotomy pain.

BOX 31-4 Nerve Blocks

• Advantage: Simple, long-lasting analgesia

• Disadvantage: Unreliable?

Intercostal nerve block has been used extensively for analgesia after thoracic surgery. Intercostal nerve blocks can be performed either intraoperatively or postoperatively and usually provide sufficient analgesia lasting 6 to 12 hours (depending on amount and type of local anesthetic used) and may need to be repeated if additional analgesia is required. Local anesthetics may be administered as a single treatment under direct vision, before chest closure, as a single preoperative percutaneous injection, as multiple percutaneous serial injections, or via an indwelling intercostal catheter. Blockade of intercostal nerves interrupts C-fiber afferent transmission of impulses to the spinal cord. A single intercostal injection of a long-acting local anesthetic can provide pain relief and improve pulmonary function in patients after thoracic surgery for up to 6 hours. To achieve longer duration of analgesia, a continuous extrapleural intercostal nerve block technique may be used in which a catheter is placed percutaneously into an extrapleural pocket by the surgeon. A continuous intercostal catheter allows frequent dosing or infusions of local anesthetic agents and avoids multiple needle injections. Various clinical studies have confirmed the analgesic efficacy of this technique, and the technique compares favorably with thoracic epidural analgesic techniques. A major concern associated with intercostal nerve block is the potentially high amount of local anesthetic systemic absorption, yet multiple clinical studies involving patients undergoing thoracic surgery have documented safe blood levels with standard techniques. Clinical investigations involving patients undergoing thoracic surgery indicate that intercostal nerve blockade by intermittent or continuous infusion of 0.5% bupivacaine with epinephrine is an effective method, as is continuous infusion of 0.25% bupivacaine through indwelling intercostal catheters for supplementing systemic intravenous opioid analgesia for post-thoracotomy pain.

Intrapleural administration of local anesthetics initiates analgesia via mechanisms that remain incompletely understood. However, the mechanism of action of extrapleural regional anesthesia seems to depend primarily on diffusion of the local anesthetic into the paravertebral region. Local anesthetic agents then affect not only the ventral nerve root but also afferent fibers of the posterior primary ramus. Posterior ligaments of the posterior primary ramus innervate posterior spinal muscles and skin and are traumatized during posterolateral thoracotomy. Intrapleural administration of local anesthetic agent to this region through a catheter inserted in the extrapleural space thus creates an anesthetic region in the skin. The depth and width of the anesthetic region depend on diffusion of the local anesthetic agent in the extrapleural space.

Thoracic paravertebral block involves injection of local anesthetic adjacent to the thoracic vertebrae close to where the spinal nerves emerge from the intervertebral foramina (Fig. 31-1). Thoracic paravertebral block, compared with thoracic epidural analgesic techniques, appears to provide equivalent analgesia, is technically easier, and may harbor less risk. Several different techniques exist for successful thoracic paravertebral block and have been extensively reviewed.⁸ The classic technique, most commonly used, involves eliciting loss of resistance. Injection of local anesthetic results in ipsilateral somatic and sympathetic nerve blockade in multiple contiguous thoracic dermatomes above and below the site of injection (along with possible suppression of the neuroendocrine stress response to surgery). These blocks may be effective in alleviating acute and chronic pain of unilateral origin from the chest and/or abdomen. Bilateral use of thoracic paravertebral block has also been described. Continuous thoracic paravertebral infusion of local anesthetic via a catheter placed under direct vision at thoracotomy is also a safe, simple, and effective method of providing analgesia after thoracotomy. It is usually used in conjunction with adjunct intravenous medications (opioid or other analgesics) to provide optimum relief after thoracotomy.

Figure 31-1 Anatomy of the thoracic paravertebral space (A) and sagittal section through the thoracic paravertebral space showing a needle that has been advanced above the transverse process (B).

(From Karmakar MK: Thoracic paravertebral block [review article]. Anesthesiology 95:771, 2001.)

Opioids

Beginning in the 1960s, large doses of intravenous opioids have been administered to patients undergoing cardiac surgery (Box 31-5). Because even very large amounts of intravenous opioids do not initiate “complete anesthesia” (unconsciousness, muscle relaxation, suppression of reflex responses to noxious surgical stimuli), other intravenous/inhalation agents must be administered during the intraoperative period. Analgesia is the best known and most extensively investigated opioid effect, yet opioids are also involved in a diverse array of other physiologic functions, including control of pituitary and adrenal medulla hormone release and activity, control of cardiovascular and gastrointestinal function, and the regulation of respiration, mood, appetite, thirst, cell growth, and the immune system. A number of well-known and potential side effects of opioids (nausea and vomiting, pruritus, urinary retention, respiratory depression) may limit postoperative recovery when opioids are used for postoperative analgesia.

BOX 31-5 Opioids

• Advantage:

• Time-tested, reliable analgesia

• Disadvantages:

• Pruritus

• Nausea and vomiting

• Urinary retention

• Respiratory depression

The classic pharmacologic effect of opioids is analgesia, and these drugs have traditionally been the initial choice when a potent postoperative analgesic is required. Two anatomically distinct sites exist for opioid receptor–mediated analgesia: supraspinal and spinal. Systemically administered opioids produce analgesia at both sites. Supraspinally, the μ₁-receptor is primarily involved in analgesia whereas the μ₂-receptor is the one predominantly involved in the spinal modulation of nociceptive processing. κ-Receptors are important in mediating spinal and supraspinal analgesia as well. δ-Ligands may have a modulatory rather than a primary analgesic role. All three types of opioid receptors (μ, κ, and δ) have been demonstrated in peripheral terminals of sensory nerves. Activation of these receptors seems to require an inflammatory reaction because locally applied opioids do not produce analgesia in healthy tissue. The inflammatory process may also activate previously inactive opioid receptors.

Morphine is the prototype opioid agonist with which all opioids are compared. Morphine is perhaps the most popular analgesic used in patients after cardiac surgery. Many semisynthetic derivatives are made by simple modifications of the morphine molecule. Morphine is poorly lipid soluble and binds approximately 35% to plasma proteins, particularly albumin. Morphine is primarily metabolized in the liver, principally by conjugation to water-soluble glucuronides. The liver is the predominant site for morphine biotransformation, although extrahepatic metabolism also occurs in the kidney, brain, and possibly gut. Extrahepatic clearance accounts for approximately 30% of the total body clearance. The terminal elimination half-life of morphine is 2 to 3 hours. In patients with liver cirrhosis, morphine pharmacokinetics are variable, probably reflecting the variability of liver disease in patients. Morphine’s terminal elimination half-life in patients with renal disease is comparable to that of normal patients. While morphine is perhaps the most popular intravenous analgesic used in patients after cardiac surgery, other synthetically derived opioids have been developed and may be utilized as well. These include fentanyl, alfentanil, sufentanil, and remifentanil.

Patient-Controlled Analgesia

When intravenous opioids are used for controlling postoperative pain (most commonly morphine and fentanyl), PCA technology is generally used. Essentials in the successful use of PCA technology include “loading” the patient with intravenous opioids to the point of patient comfort before initiating PCA, ensuring that the patient wants to control analgesic treatment, using an appropriate PCA dose and lockout interval, and considering the use of a basal rate infusion. Focused guidance of PCA dosing by a dedicated acute pain service, compared with surgeon-directed PCA, may result in more effective analgesia with fewer side effects.

Nonsteroidal Anti-inflammatory Agents

The NSAIDs, in contrast to the opioids’ central nervous system mechanism of action, mainly exert their analgesic, antipyretic, and anti-inflammatory effects peripherally by interfering with prostaglandin synthesis after tissue injury (Box 31-6).⁹ NSAIDs inhibit cyclooxygenase (COX), the enzyme responsible for the conversion of arachidonic acid to prostaglandin. Combining NSAIDs with traditional intravenous opioids may allow a patient to achieve an adequate level of analgesia with fewer side effects than if a similar level of analgesia was obtained with intravenous opioids alone. Numerous clinical investigations reveal the potential value (opioid-sparing effects) of NSAIDs when combined with traditional intravenous opioids during the postoperative period after noncardiac surgery. In fact, the administration of NSAIDs is one of the most common nonopioid analgesic techniques currently used for postoperative pain management. The efficacy of NSAIDs for postoperative pain has been repeatedly demonstrated in many analgesic clinical trials. Unlike opioids, which preferentially reduce spontaneous postoperative pain, NSAIDs have comparable efficacy for both spontaneous and movement-evoked pain, the latter of which may be more important in causing postoperative physiologic impairment. Certainly, NSAIDs reduce postoperative opioid consumption and accelerate postoperative recovery and represent an integral component of balanced postoperative analgesic regimens after noncardiac surgery. However, little is known regarding NSAID use in the management of pain after cardiac surgery. It is likely that concerns regarding NSAID side effects, including alterations in the gastric mucosal barrier, renal tubular function, and inhibition of platelet aggregation, have made clinicians reluctant to use NSAIDs in patients undergoing cardiac surgery. Other rare side effects of NSAIDs (from COX inhibition) include hepatocellular injury, asthma exacerbation, anaphylactoid reactions, tinnitus, and urticaria. Despite these fears, a small number of clinical investigations seem to indicate that NSAIDs may provide analgesia in patients after cardiac surgery without untoward effects (e.g., gastrointestinal ulceration, renal dysfunction, excessive bleeding).

NSAIDs are not a homogeneous group and vary considerably in analgesic efficacy as a result of differences in pharmacodynamic and pharmacokinetic parameters. NSAIDs are nonspecific inhibitors of COX, which is the rate-limiting enzyme involved in the synthesis of prostaglandins. A major scientific discovery revealed that COX exists in multiple forms. Most important, a constitutive form is present in normal conditions in healthy cells (COX-1) and an inducible form (COX-2) exists that is the major isozyme induced by and associated with inflammation. Simplistically, COX-1 is ubiquitously and constitutively expressed and has a homeostatic role in platelet aggregation, gastrointestinal mucosal integrity, and renal function, whereas COX-2 is inducible and expressed mainly at sites of injury (and kidney and brain) and mediates pain and inflammation. NSAIDs are nonspecific inhibitors of both forms of COX yet vary in their ratio of COX-1 to COX-2 inhibition. Recent molecular studies distinguishing between constitutive COX-1 and inflammation-inducible COX-2 enzymes have led to the exciting hypothesis that the therapeutic and adverse effects of NSAIDs could be uncoupled (Fig. 31-2).¹⁰

Figure 31-2 Cyclooxygenase pathways. Recent molecular studies distinguishing between COX-1 and COX-2 enzymes have led to the exciting hypothesis that the therapeutic and adverse effects of the nonspecific inhibitors (NSAIDs) could be uncoupled.

Rights were not granted to include this figure in electronic media. Please refer to the printed book.

(From Gajraj NM: Cyclooxygenase-2 inhibitors [review article]. Anesth Analg 96:1720, 2003.)

α₂-Adrenergic Agonists

The α₂-adrenergic agonists provide analgesia, sedation, and sympatholysis (Box 31-7). The potential perioperative analgesic benefits of α₂-agonists, when administered to patients undergoing cardiac surgery, were demonstrated almost 20 years ago. Most of the clinical investigations regarding perioperative use of this class of drugs remain focused on exploiting the sedative effects and beneficial cardiovascular effects (decreasing hypertension and tachycardia) associated with their use. α₂-Adrenergic agonists have been used perioperatively in patients undergoing cardiac surgery, yet the focus of such clinical investigations has been on the intraoperative period and the potential for enhanced postoperative hemodynamic stability, potentially leading to reduced postoperative myocardial ischemia (not specifically at enhanced postoperative analgesia).

BOX 31-7 α₂-Adrenergic Agonists

• Advantage:

• Cardiovascular stability?

• Disadvantages:

• Sedation

• Hypotension

Intrathecal and Epidural Techniques

It is clear from numerous clinical investigations that intrathecal and/or epidural techniques (using opioids and/or local anesthetics) initiate reliable postoperative analgesia in patients after cardiac surgery (Boxes 31-8 and 31-9). Additional potential advantages of using intrathecal and/or epidural techniques in patients undergoing cardiac surgery include stress-response attenuation and thoracic cardiac sympathectomy.

Intrathecal Techniques

Most clinical investigators have used intrathecal morphine in hopes of providing prolonged postoperative analgesia. Some clinical investigators have used intrathecal fentanyl, sufentanil, and/or local anesthetics for intraoperative anesthesia and analgesia (with stress response attenuation) and/or thoracic cardiac sympathectomy. An anonymous survey of members of the Society of Cardiovascular Anesthesiologists indicates that almost 8% of practicing anesthesiologists incorporate intrathecal techniques into their anesthetic management of adults undergoing cardiac surgery.¹¹ Of these anesthesiologists, 75% practice in the United States, 72% perform the intrathecal injection before induction of anesthesia, 97% use morphine, 13% use fentanyl, 2% use sufentanil, 10% use lidocaine, and 3% use tetracaine.

The mid 1990s saw the emergence of fast-track cardiac surgery, with the goal being tracheal extubation in the immediate postoperative period. Chaney and associates in 1997 ¹² were the first to study the potential clinical benefits of intrathecal morphine when used in patients undergoing cardiac surgery and early tracheal extubation. They prospectively randomized 40 patients to receive either intrathecal morphine (10 μg/kg) or intrathecal placebo before induction of anesthesia for elective CABG. Intraoperative anesthetic management was standardized (intravenous fentanyl, 20 μg/kg, and intravenous midazolam, 10 mg) and postoperatively all patients received intravenous morphine via PCA exclusively. Of the patients who were tracheally extubated during the immediate postoperative period, the mean time from ICU arrival to tracheal extubation was significantly (P = .02) prolonged in patients who received intrathecal morphine (10.9 ± 4.4 hours) compared with placebo controls (7.6 ± 2.5 hours). Three patients who received intrathecal morphine had tracheal extubation substantially delayed (12 to 24 hours) because of prolonged ventilatory depression (likely secondary to intrathecal morphine). Although the mean postoperative intravenous morphine use for 48 hours was less in patients who received intrathecal morphine (42.8 mg) compared with patients who received intrathecal placebo (55.0 mg), the difference between groups was not statistically significant. No clinical differences existed between groups regarding postoperative morbidity, mortality, or duration of postoperative hospital stay (approximately 9 days in each group).

These somewhat discouraging findings (absence of enhanced analgesia, prolongation of tracheal extubation time) stimulated the same group of investigators in 1999 to try again, this time decreasing the amount of intraoperative intravenous fentanyl patients received (hoping to decrease fentanyl’s effect on augmenting postoperative respiratory depression associated with intrathecal morphine).¹³ Forty patients were prospectively randomized to receive either intrathecal morphine (10 μg/kg) or intrathecal placebo before induction of anesthesia for elective CABG. Intraoperative anesthetic management was standardized (intravenous fentanyl, 10 μg/kg, and intravenous midazolam, 200 μg/kg) and all patients postoperatively received intravenous morphine exclusively via PCA. Of the patients tracheally extubated during the immediate postoperative period, mean time to tracheal extubation was similar in patients who received intrathecal morphine (6.8 ± 2.8 hours) compared with intrathecal placebo patients (6.5 ± 3.2 hours). However, once again, four patients who received intrathecal morphine had tracheal extubation substantially delayed (14, 14, 18, and 19 hours) because of prolonged respiratory depression (likely secondary to intrathecal morphine). The mean postoperative intravenous morphine use during the immediate postoperative period was actually higher in patients receiving intrathecal morphine (49.8 mg) compared with patients receiving intrathecal placebo (36.2 mg), yet the difference between groups was not statistically significant. No clinical differences existed between groups regarding postoperative morbidity, mortality, or duration of postoperative hospital stay (approximately 6 days in each group). Thus, Chaney and associates, from their three prospective, randomized, double-blind, placebo-controlled clinical investigations in the late 1990s involving 140 healthy adults undergoing elective CABG, concluded that although intrathecal morphine certainly can initiate reliable postoperative analgesia, its use in the setting of fast-track cardiac surgery and early tracheal extubation may be detrimental by potentially delaying tracheal extubation in the immediate postoperative period.

Epidural Techniques

Most clinical investigators have used thoracic epidural local anesthetics in hopes of providing perioperative stress response attenuation and/or perioperative thoracic cardiac sympathectomy. Some clinical investigators have used thoracic epidural opioids to provide intraoperative and/or postoperative analgesia. An anonymous survey of members of the Society of Cardiovascular Anesthesiologists indicates that 7% of practicing anesthesiologists incorporate thoracic epidural techniques into their anesthetic management of adults undergoing cardiac surgery.¹¹ Of these anesthesiologists, 58% practice in the United States. Regarding the timing of epidural instrumentation, 40% perform instrumentation before induction of general anesthesia, 12% perform instrumentation after induction of general anesthesia, 33% perform instrumentation at the end of surgery, and 15% perform instrumentation on the first postoperative day.

Numerous clinical studies further attest to the ability of thoracic epidural anesthesia and analgesia with local anesthetics and/or opioids to induce substantial postoperative analgesia in patients after cardiac surgery (Table 31-2).

Table 31-2 Reports of Epidural Anesthesia and Analgesia for Cardiac Surgery

Many clinical investigations have proven that thoracic epidural anesthesia with local anesthetics also significantly attenuates the perioperative stress response in patients undergoing cardiac surgery. Patients randomized to receive intermittent boluses of thoracic epidural bupivacaine intraoperatively followed by continuous infusion postoperatively exhibited significantly decreased blood levels of norepinephrine and epinephrine perioperatively when compared with patients managed similarly without thoracic epidural catheters.

A relatively large clinical investigation highlights the potential clinical benefits of thoracic epidural anesthesia in cardiac surgical patients. Scott and associates ¹⁴ prospectively randomized (nonblinded) 420 patients undergoing elective CABG to receive either thoracic epidural anesthesia (bupivacaine/clonidine) and general anesthesia or general anesthesia alone (control group). The two groups received similar intraoperative anesthetic techniques. In thoracic epidural anesthesia patients, the thoracic epidural infusion was continued for 96 hours after surgery (titrated according to need). In control patients, target-controlled infusion alfentanil was used for the first 24 postoperative hours, then followed by PCA morphine for the next 48 hours. Postoperatively, striking clinical differences were observed between the two groups. Postoperative incidence of supraventricular arrhythmia, lower respiratory tract infection, renal failure, and acute confusion were all significantly lower in patients receiving thoracic epidural anesthesia compared with control patients.

In contrast to the encouraging findings of the clinical investigation by Scott and associates, other prospective, randomized, nonblinded clinical investigations reveal that using thoracic epidural anesthesia techniques in patients undergoing cardiac surgery may not offer substantial clinical benefits.¹⁵ In 2002, Priestley and associates prospectively randomized 100 patients undergoing elective CABG to receive either thoracic epidural anesthesia (ropivacaine/fentanyl) and general anesthesia or general anesthesia alone (control group). The two groups received quite different intraoperative anesthetic techniques. Postoperatively, thoracic epidural anesthesia patients received epidural ropivacaine/fentanyl for 48 hours (supplemental analgesics available if needed), whereas control patients received nurse-administered intravenous morphine, followed by PCA morphine. Patients receiving thoracic epidural anesthesia were extubated sooner than controls (3.2 vs. 6.7 hours, respectively; P < .001), yet this difference may have been secondary to the different amounts of intraoperative intravenous opioid administered to the two groups (intraoperative intravenous anesthetic technique not standardized). Postoperative pain scores at rest were significantly lower in patients receiving thoracic epidural anesthesia only on postoperative days 0 and 1 (equivalent on days 2 and 3). Postoperative pain scores during coughing were significantly lower in patients receiving thoracic epidural anesthesia only on postoperative day 0 (equivalent on days 1, 2, and 3). There were no significant differences between the two groups in postoperative oxygen saturation on room air, chest radiograph changes, or spirometry. Furthermore, no clinical differences were detected between the two groups regarding postoperative mobilization goals, atrial fibrillation, postoperative hospital discharge eligibility, or actual postoperative hospital discharge.

All clinical reports involving utilization of intrathecal and thoracic epidural anesthesia and analgesia techniques for cardiac surgery involve small numbers of patients and few (if any) are well designed. There are no blinded, placebo-controlled clinical studies involving thoracic epidural anesthesia and analgesia. Furthermore, none of the existing clinical studies involving intrathecal and thoracic epidural anesthesia and analgesia techniques for cardiac surgery uses clinical outcome as a primary endpoint. Thus, there are clear deficiencies in the literature that prohibit definitive analysis of the risk/benefit ratio of intrathecal and thoracic epidural anesthesia and analgesia techniques as applied to patients undergoing cardiac surgery.

A 2004 meta-analysis by Liu and associates ¹⁶ assessed effects of perioperative central neuraxial analgesia on outcome after CABG. These authors, via MEDLINE and other databases, searched for randomized controlled trials in patients undergoing CABG with CPB. Fifteen trials enrolling 1178 patients were included for thoracic epidural anesthesia analysis, and 17 trials enrolling 668 patients were included for intrathecal analysis. Thoracic epidural techniques did not affect the incidences of mortality or myocardial infarction yet reduced risk of arrhythmias (atrial fibrillation and tachycardia), reduced risk of pulmonary complications (pneumonia and atelectasis), reduced time to tracheal extubation, and reduced analog pain scores. Intrathecal techniques did not affect incidences of mortality, myocardial infarction, arrhythmias, or time to tracheal extubation and only modestly decreased systemic morphine utilization and pain scores (while increasing incidence of pruritus). These authors conclude that central neuraxial analgesia does not affect rates of mortality or myocardial infarction after CABG yet is associated with improvements in faster time to tracheal extubation, decreased pulmonary complications and cardiac arrhythmias, and reduced pain scores. However, the authors also note that the majority of potential clinical benefits offered by central neuraxial analgesia (earlier extubation, decreased arrhythmias, enhanced analgesia) may be reduced and/or eliminated with changing cardiac anesthesia practice using fast-track techniques, use of β-adrenergic blockers or amiodarone, and/or use of NSAIDs or COX-2 inhibitors. These authors also note that the risk of spinal hematoma (addressed later in this chapter) due to central neuraxial analgesia in patients undergoing full anticoagulation for CPB remains uncertain.

RISK OF HEMATOMA FORMATION

Intrathecal or epidural instrumentation entails risk, the most feared complication being epidural hematoma formation. The estimated incidence of hematoma formation is approximately 1:220,000 after intrathecal instrumentation. Hematoma formation is more common (approximately 1:150,000) after epidural instrumentation because larger needles are used, catheters are inserted, and the venous plexus in the epidural space is prominent. Furthermore, hematoma formation does not occur exclusively during epidural catheter insertion; almost half of all cases develop after catheter removal.

Risk is increased when intrathecal or epidural instrumentation is performed before systemic heparinization, and hematoma formation has occurred in patients when diagnostic or therapeutic lumbar puncture has been followed by systemic heparinization. When lumbar puncture is followed by systemic heparinization, concurrent use of aspirin, difficult or traumatic instrumentation, and administration of intravenous heparin within 1 hour of instrumentation increase the risk of hematoma formation. However, by observing certain precautions, intrathecal or epidural instrumentation can be performed safely in patients who will subsequently receive intravenous heparin. By delaying surgery 24 hours in the event of a traumatic tap, by delaying heparinization 60 minutes after catheter insertion, and by maintaining tight perioperative control of anticoagulation, more than 4000 intrathecal or epidural catheterizations were performed safely in patients undergoing peripheral vascular surgery who received intravenous heparin after catheter insertion. A retrospective review involving 912 patients further indicates that epidural catheterization before systemic heparinization for peripheral vascular surgery is safe. However, the magnitude of anticoagulation in these two studies (activated partial thromboplastin time of approximately 100 seconds and activated clotting time approximately twice the baseline value) involving patients undergoing peripheral vascular surgery was substantially less than the degree of anticoagulation required in patients subjected to CPB.

Most clinical studies investigating the use of intrathecal or epidural anesthesia and analgesia techniques in patients undergoing cardiac surgery include precautions to decrease risk of hematoma formation. Some used the technique only after the demonstration of laboratory evidence of normal coagulation parameters, delayed surgery 24 hours in the event of traumatic tap, or required that the time from instrumentation to systemic heparinization exceed 60 minutes. While most clinicians investigating use of epidural anesthesia and analgesia techniques in patients undergoing cardiac surgery insert catheters the day before scheduled surgery, investigators have performed instrumentation on the same day of surgery. Institutional practice (same-day admit surgery) may eliminate the option of epidural catheter insertion on the day before scheduled surgery.

Although most investigators agree that risk of hematoma is likely increased when intrathecal or epidural instrumentation is performed in patients before systemic heparinization required for CPB, the absolute degree of increased risk is somewhat controversial; some believe the risk may be as high as 0.35%. An extensive mathematical analysis by Ho and associates ¹⁷ of the approximately 10,840 intrathecal injections in patients subjected to systemic heparinization required for CPB (without a single episode of hematoma formation) reported in the literature as of the year 2000 estimated that the minimum risk of hematoma formation was 1:220,000 and the maximum risk of hematoma formation was 1:3600 (95% confidence level); however, the maximum risk may be as high as 1:2400 (99% confidence level). Similarly, of the approximately 4583 epidural instrumentations in patients subjected to systemic heparinization required for CPB (without a single episode of hematoma formation) reported in the literature as of the year 2000, the minimum risk of hematoma formation was 1:150,000 and the maximum risk of hematoma formation was 1:1500 (95% confidence level); however, the maximum risk may be as high as 1:1000 (99% confidence level).

Certain precautions, however, may decrease the risk. The technique should not be used in a patient with known coagulopathy from any cause. Surgery should be delayed 24 hours in the event of a traumatic tap, and time from instrumentation to systemic heparinization should exceed 60 minutes. Additionally, systemic heparin effect and reversal should be tightly controlled (smallest amount of heparin used for the shortest duration compatible with therapeutic objectives) and patients should be closely monitored postoperatively for signs and symptoms of hematoma formation. An obvious economic disadvantage of intrathecal or epidural instrumentation in patients before cardiac surgery is the possible delay in surgery in the event of a traumatic tap. However, one study involving more than 4000 intrathecal or epidural catheterizations via a 17-gauge Tuohy needle indicates that the incidence of traumatic tap (blood freely aspirated) is rare (<0.10%).

Use of regional anesthetic techniques in patients undergoing cardiac surgery, while seemingly increasing in popularity, remains extremely controversial, prompting numerous editorials by recognized experts in the field of cardiac anesthesia.¹⁸ One of the main reasons such controversy exists (and likely will continue for some time) is that the numerous clinical investigations regarding this topic are suboptimally designed and use a wide array of disparate techniques, preventing clinically useful conclusions on which all can agree.