Acute Pain Management and Acute Pain Services
Pamela E. Macintyre
David A. Scott
The International Association for the Study of Pain (IASP) defines pain in general as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (1). This highlights the influence of a variety of factors (affective and subjective) on the pain experience and the need to consider all relevant biopsychosocial (pathophysiologic, psychological, and social) factors when assessing and managing pain, whether that pain is acute or chronic.
Ready and Edwards (2) defined acute pain as “pain of recent onset and probably limited duration” and said that “it usually has an identifiable temporal and causal relationship to injury.” They characterized chronic pain as that which “commonly persists beyond the time of healing of an injury and frequently there may not be any clearly identifiable cause.” However, it is realized that acute pain and chronic pain are not separate entities but part of a pain continuum. This is reflected in the increasing overlap of therapies used in both acute and chronic pain settings.
Earlier chapters have already reviewed in detail the various drugs and techniques used for neuraxial and peripheral neural blockade in acute pain management (efficacy, side effects, complications, clinical applications, etc.). Therefore, this chapter only briefly mentions these topics, and instead concentrates on other aspects of acute pain management.
Analgesic techniques and drugs will be discussed briefly, especially those used for systemic rather than regional analgesia, and the importance of multimodal analgesia will be emphasized. However, the main focus will be on the consequences of and reasons for the continued undertreatment of acute pain, the very important issue of transition of acute to chronic (persistent) pain, preemptive and preventive analgesia, the organizational requirements needed to deliver safe and effective acute pain management (especially assessment and monitoring of patients), and the influence that patient variables (e.g., patient age, gender, and psychological factors) may have on some of the drugs and techniques used.
Undertreatment of Acute Pain
Evidence for Undertreatment
It is an unfortunate fact that 25% to 67% of patients (surgical and medical) in hospitals experience at least one episode of moderate to severe pain during their stay (3,4,5,6). Although these figures depend on the population surveyed, inadequate pain relief has been a consistent observation over the last 20 years, despite the significant improvements in the understanding of acute pain and advances in the sophistication of acute pain management options that have occurred over this time. This failure stems from a number of causes, as has been investigated by many professional organizations in addition to the Joint Council of American Hospital Organizations (JCAHO), the United States Department of Veteran Affairs (VA), and the Australian National Institute for Clinical Studies (NICS).
Consequences of Undertreatment
“Nobody ever died from pain after surgery” is an aphorism that is unfortunately frequently cited as a justification for avoiding the perceived complexities of acute pain management. In particular, this sort of statement reflects an attitude that acute pain is usually expected, short-lived, and, therefore, not a high priority. Yet, from a basic humanitarian point of view, the relief of pain and suffering is clearly important (7). It has also been believed for many years that the relief of acute pain would result in improved outcomes. Although this has been difficult to demonstrate until recently, these potential benefits formed one of the bases for the establishment of the first organized acute pain services (APS) in the 1980s.
In a retrospective review of esophagectomy patients, a lower incidence of cardiorespiratory complications and decreased mortality was associated with patients managed by an APS using epidural or parenteral opioid analgesia, compared with those receiving traditional as-required (p.r.n.) intramuscular opioids (8). Although such uncontrolled studies may be criticized on methodological grounds, an established body of evidence now supports the conclusion that effective pain relief can lead to improved clinical outcomes (see later and also Chapters 6 and 7). The effective management of acute postoperative pain has benefits relating to the facilitation of rehabilitation, and, therefore, recovery, by reducing stress responses that may impact the body in a number of ways and by reducing the incidence and intensity of long-term complications such as chronic pain.
It is not ethically possible to design studies to investigate the effects of inadequately treated pain, and, therefore, outcome data generally relate to comparisons of one analgesic technique with another. Often not detailed, however, are the outcomes in trials in which the primary analgesic technique has failed and, as a result, the patient may have experienced inadequate pain relief for a significant period of time. One such set of outcomes was reported in a trial by Bode et al. (9) in a study investigating the effect of regional anesthesia and analgesia versus general anesthesia on cardiovascular outcomes in high-risk vascular patients. Although no differences in cardiac outcomes were
observed between the two study groups, there were 32 failed regional anesthetics in 235 patients; these patients had nonsignificantly higher cardiac morbidity (failed regional, regional, general anesthesia: myocardial infarction 6.3%, 3.6%, 4.9%, respectively; cardiac failure 15.6%, 7.1%, 8.9%, respectively) and significantly higher mortality (9.4%, 2.7%, 1.5%, respectively; p = .03). In a case report describing a fatal postoperative in-stent thrombosis in a patient with coronary artery stents having a thoracotomy and lobectomy, inadequate postoperative pain relief was associated with severe tachycardia and hypertension prior to the event (10). The temporal association of the hemodynamic responses to the undertreated pain and subsequent fatal myocardial infarction highlights the importance of maintaining effective pain control and promptly intervening when necessary. In a retrospective review of a small number of patients (n = 43) following lung reduction surgery, an association was seen between inadequate analgesia and complications such as atrial fibrillation and respiratory failure (11).
observed between the two study groups, there were 32 failed regional anesthetics in 235 patients; these patients had nonsignificantly higher cardiac morbidity (failed regional, regional, general anesthesia: myocardial infarction 6.3%, 3.6%, 4.9%, respectively; cardiac failure 15.6%, 7.1%, 8.9%, respectively) and significantly higher mortality (9.4%, 2.7%, 1.5%, respectively; p = .03). In a case report describing a fatal postoperative in-stent thrombosis in a patient with coronary artery stents having a thoracotomy and lobectomy, inadequate postoperative pain relief was associated with severe tachycardia and hypertension prior to the event (10). The temporal association of the hemodynamic responses to the undertreated pain and subsequent fatal myocardial infarction highlights the importance of maintaining effective pain control and promptly intervening when necessary. In a retrospective review of a small number of patients (n = 43) following lung reduction surgery, an association was seen between inadequate analgesia and complications such as atrial fibrillation and respiratory failure (11).
Long-term effects on the central nervous system (CNS) also need to be considered in the context of undertreated pain. A number of investigations now show evidence of an association between the intensity of acute pain with the development of persistent pain. For example, in a survey of 265 mastectomy patients, chronic pain in the breast area was significantly associated with intensity of postoperative pain (multivariate odds ratio [OR] 1.65; range, 1.16–2.35) (12). Similar studies in thoracic surgical patients support the link between acute pain intensity and persistent pain (13,14,15). Further examples are given later in the section discussing the transition of acute to chronic pain.
Overall, the increasing evidence that undertreated pain is associated with adverse clinical outcomes is supported by the wide range of clinical investigations comparing alternative analgesic techniques and associated improved clinical outcomes with improved quality of analgesia.
Reasons for Undertreatment
A number of reasons have been put forward in an attempt to explain the failure to provide consistently effective acute pain management in the hospital setting (16). This failure is despite the improvements gained by the now widespread adoption of some form of APS in most large hospitals. Many of these reasons parallel those barriers that are described for the provision of effective care for chronic pain sufferers, and can be divided into institutionally, clinician-, and patient-based factors (17).
At an institutional level, a key factor limiting the effectiveness of acute pain management is a lack of resource provision. Such resources include adequate and appropriate staffing, time and personnel to educate staff and patients and to carry out appropriate assessment and monitoring of patients, and the provision and use of proper guidelines and protocols for analgesic drugs and methods of drug administration. In addition, although APSs may be established, their structure may vary (e.g., anesthesiologist-based or nurse-based). Despite evidence for improved pain outcomes associated with an APS (18,19,20,21), the cost-effectiveness of the various APS structures is still not clear (8,19,22).
The diffuse nature of the problem is yet another factor limiting institutional awareness of the problem of undermanaged pain. Acute pain management is an element of care in all hospital settings, but particularly in the emergency department and postsurgical areas, including intensive care. As such, it crosses the boundaries of clinical specialty practice, as well as affecting clinicians at different levels (nurse aid, nurse, resident doctor, consultant, etc.). Without a clear focus for attention or an obvious economic driver, it falls upon clinicians to recognize the value of integrated pain management, to make a case for such integration, and to draw together the necessary resources. It was from these concerns that APSs were initially developed in the mid-1980s; however, the nature of the implementation of such services is still inconsistent and leaves room for improvement (19).
Cultural changes within institutions are necessary to overcome some of these administrative and organizational barriers. Clear lines of responsibility need to be established while remaining cognizant of the significant professional boundaries that exist.
Institution-wide changes cannot be implemented without appropriate audit and review, which surveys suggest is not consistently undertaken even by APSs (23). A salutatory example of the benefits of review, and the risks of an unbalanced strategy for pain management, was documented by Vila et al. (24). In response to the JCAHO call for improved pain assessment and intervention, an institution-wide algorithm-based strategy for titration of analgesia according to numerical pain scores was adopted. This resulted in lower pain scores but also an increased incidence of respiratory depression. The recommendations from this experience were to improve the awareness of increasing sedation as a predictor of opioid-induced CNS and respiratory depression, and promote the routine use of sedation scoring. This example emphasizes the need for an integrated approach to pain management, including the full cycle of implementation of carefully thought out strategies with appropriate education and training, followed by assessment and reporting of outcomes. Such reporting also has the advantage of raising the profile of pain management with the organization.
At a clinician level, there also exist many barriers to be overcome before a patient’s pain can be effectively managed. Over the years, a number of surveys have been done documenting the beliefs and attitudes of nurses and doctors regarding pain assessment and prescription of analgesic drugs. These consistently find that pain assessment is infrequent (16) and that it often underestimates pain compared with the patient’s own perceptions (25). With regard to prescribing, one of the most commonly held misconceptions is still that short-term opioid use in the treatment of acute pain poses an increased risk of addiction. This may be reinforced by “pseudo-addiction” (26) or pain behaviors that appear to be inappropriately drug-seeking when in fact they are an appropriate response to undertreated pain. No evidence supports these concerns (27). Another key reason for undertreatment of acute pain is the fear of overtreatment, leading to drug-related side effects and complications.
Drug administration practices are often outdated, both in the prescription of drug orders and their implementation. The factors just mentioned, relating to fear of overuse and addiction, often result in the prescription of doses that are inadequate or given too infrequently. In addition, p.r.n. drug orders must be used carefully to avoid reactive rather than proactive pain management. Conventional, intramuscular p.r.n. administration is known to be ineffective in controlling acute postoperative pain, with incidences of moderate to severe pain of 67% and severe pain of 29% reported in one review (5).
Clearly, circumstances arise in which breakthrough or incident pain may trigger an unexpected need for supplementation. In these cases, the cycle from need to response must be short, but this may not always be achievable in a busy ward environment. This situation is an example in which patient-controlled analgesia (PCA) provides more effective care than traditional p.r.n. approaches (5,28,29). Strategies for using p.r.n. or PCA
opioid analgesia proactively (i.e., in anticipation of mobilization, physiotherapy, etc.), coupled with appropriate regular (time-based) analgesic prescriptions are likely to be the most effective in providing acute pain relief.
opioid analgesia proactively (i.e., in anticipation of mobilization, physiotherapy, etc.), coupled with appropriate regular (time-based) analgesic prescriptions are likely to be the most effective in providing acute pain relief.
Education programs for medical and nursing staff are essential and should include the need for frequent and regular assessment of pain, the appropriate use of prescribed drugs, and the need to titrate pain relief for each patient. Clinicians also must be more aware of the options available for multimodal analgesic therapy. This includes a wide range of pharmacologic options, but also includes consideration of physical therapies and other strategies that may improve patient comfort. The use of multimodal analgesia, appropriate education and policies, frequent patient assessment, and appropriate titration, are all necessary components in preventing inadequate analgesia.
Finally, many patient factors may limit effective acute pain management. In chronic pain, as in acute pain settings, patients may be reluctant to report pain for fear of being judged a “complainer” or a “bad patient” (30). In addition, without appropriate education, patients often feel that they are “supposed” to have significant pain and that it is, therefore, inevitable. These attitudes are strongly affected by individual cultural and social characteristics, and may be aggravated by communication difficulties posed by language or cognitive barriers. Fear of addiction to opioids is also a concern for some patients. Wherever possible, preoperative education regarding the importance of pain reporting and providing an explanation of ways this can be achieved is an important first step in improving the effectiveness of pain assessment and hence pain treatment (31). Finally, specific characteristics of the patients themselves (discussed in more detail later) may affect their management, such as prior pain experience, adverse drug reactions, opioid tolerance, age, culture, gender, and genetics, as well as psychological factors.
The implementation of some sort of APS structure is not enough on its own to address the problems of undertreatment of acute pain. Overall, to overcome the barriers described and to improve the management of acute pain, education strategies need to be developed and underpinned by widespread institutional support with respect to both principles and also practice, in terms of resources. Quality improvement and risk management strategies also need to be implemented (32). It is only through a unified approach throughout the hospital system that the goals of effective pain management will be achieved (33). The Australian and New Zealand College of Anaesthetists (ANZCA) Faculty of Pain Medicine has developed a Statement of Rights to Pain Management (34) that is directed at these issues. These patient rights include (in abbreviated form):
Education about effective pain management options
Appropriate assessment and management of pain
Regular recording of assessment results to facilitate ongoing care
Care from health professionals with appropriate training and experience
Appropriate effective pain management strategies supported by appropriate policies and procedures
Transition from Acute to Chronic Pain
Persistent Pain Syndromes
Chronic or persistent pain (pain lasting more than 3 months after the expected resolution of the cause) has long been regarded as a separate entity from acute pain, with significantly different clinical characteristics. Acute pain may be described by patients as sharp, localized, and often triggered by movement if it is somatic in origin, or dull, aching, and nauseating if it is visceral in origin. Persistent pain, especially if neuropathic in origin, may be described as stabbing, burning, and not clearly associated with a trigger action. Other characteristics of neuropathic pain include sensory deficits, paresthesiae, hyperalgesia, and allodynia.
Neuropathic pain—pain resulting from injury to or disorder of the nervous system—has traditionally been placed in the “chronic pain” category of pain syndromes, and often clinicians involved in the management of postoperative pain have ignored or overlooked the possibility of neuropathic pain being a significant component of acute pain. Yet, by simply observing most surgical procedures, it is clear that damage to peripheral nerves is unavoidable although usually inadvertent. It is now known from laboratory research that behavioral signs of neuropathic pain may appear within hours of nerve injury and persist for weeks to months thereafter.
This has several implications for the clinician. The first and most obvious is that the acute pain experienced by patients postoperatively or after an injury may comprise elements of both nociceptive (“normal” acute pain) and neuropathic pain, and that these pain types may respond to different treatment strategies. The second is that there may be different surgical techniques or analgesic approaches that can be implemented during surgery to minimize the risk of neuropathic pain postoperatively. Finally, the incidence of long-term chronic or persistent pain disorders following surgical procedures may be reduced by perioperative interventions designed to avoid or treat acute neuropathic pain.
The association between surgical procedures and persistent pain was highlighted in the early 1990s by a survey of pain clinics in northern Britain (35) and by studies investigating postthoracotomy pain (13,15). In the survey of chronic pain clinics (35), over 20% of patients associated the onset of their persistent pain with a surgical procedure. This has been confirmed by other authors, especially with respect to neuropathic pain (36,37,38). The incidence of persistent pain as a long-term consequence following surgery is especially high after certain procedures, such as surgery involving the chest wall (thoracotomy, mastectomy, and midline sternotomy for cardiac surgery). This may be related to the likelihood of surgical trauma to one or more branches of the intercostal nerves supplying sensation to these regions.
Other procedures with a strong association include herniorrhaphy, knee joint procedures, and limb amputation (37,39,40) (Table 43-1).
Factors Associated with an Increased Risk of Persistent Pain
Some of the risk factors shown to be associated with an increased incidence of persistent pain are listed in Table 43-2. It is important to note that not all patients develop persistent pain syndromes despite having technically similar surgical procedures. This implies that other factors are involved that increase the likelihood of developing a long-term problem. Although not exhaustive, these factors include preexisting pain, postoperative pain intensity, psychological factors, concurrent neurologic injury, genetic factors, and gender. Some of these factors may impact on the intensity of postoperative pain (e.g., female gender) (41) and the incidence of chronic pain (e.g., depression)
(12), whereas others may increase the likelihood of nerve injury or impaired healing (e.g., radiotherapy or chemotherapy).
(12), whereas others may increase the likelihood of nerve injury or impaired healing (e.g., radiotherapy or chemotherapy).
Table 43-1 Estimated incidence of chronic postoperative pain and disability after selected surgical procedures | ||||||||||||||||||
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Preexisting Pain
Preexisting pain has been recognized as a factor associated with postoperative phantom pain since the publication by Bach (42) citing the beneficial effects of preoperative pain control before lower limb amputation. In a small trial of 25 patients with painful lower limbs, 11 patients received epidural analgesia for 3 days prior to amputation. The incidence of phantom limb pain at 6 months was significantly reduced (none in the pretreatment group and five in the control group), and this continued as a trend to 1 year. Although criticized for its size and other uncontrolled factors, this study has been widely cited as being a clinical example of the effectiveness of “preemptive analgesia.” However, preemptive analgesia (discussed later) is more specifically the prevention of central sensitization by using an analgesic technique prior to and during the time of nociceptive input. Nonetheless, the presence of preexisting pain induces some degree of CNS hyperexcitability or sensitization, and this certainly contributes to postsurgical pain (43).
Table 43-2 Factors contributing to the development of persistent postsurgical pain | |
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A further example is provided in a prospective study of 346 patients undergoing abdominal surgery, in whom moderate to severe preoperative pain was significantly associated with an increased severity of postoperative pain (OR 2.96; 95% confidence interval [CI]; 1.32–6.60) (41). In the same study, the presence of a chronic pain condition was also linked to an increase in postoperative pain (OR 1.75; 95% CI; 1.03–2.98).
The risk does not just apply to patients having surgery. For example, higher levels of pain in patients with acute herpes zoster are associated with a higher incidence and severity of postherpetic neuralgia (44).
Nerve Injury
Nerve injury resulting from the site and extent of surgery is an important factor in the development of neuropathic pain (40) and may present in the early perioperative period (37). This has clinical implications for acute pain management because neuropathic pain is often less responsive to opioid analgesics, thus reinforcing the need for a multimodal analgesic strategy.
At the site of nerve injury, an inflammatory response is initiated by local factors and also by mediators that are conducted down the injured axon. The local neuronal membrane characteristics alter, so that there is a lowered threshold for depolarization with the expression of low-threshold sodium (Na+) channels at the site of injury (45,46). In normal nerve regrowth, this may be seen in the Tinel sign, in which the progress of the axon down the peripheral nerve sheath can be determined by tapping on the course of the nerve until the patient reports a tingling sensation. Unsuccessful attempts at nerve regrowth may result in local neuroma formation with local hypersensitivity. Neuropathic pain results from a constant stream of afferent discharge to the CNS, coupled with central neural responses to axonal injury, causing nerve growth factor and other cytokines to be expressed in the dorsal root ganglion and the dorsal horn of the spinal cord. New, nonconventional connections form that do not have the same presynaptic inhibitory opioid receptor responses as the conventional nociceptive pathways (47). This impacts on possible therapeutic options.
Postoperative Pain
Evidence for the role of neuropathic pain and altered neuronal excitability in early postoperative pain comes from the clinical characteristics of patients’ pain and clinical trials (48). The characteristics of neuropathic pain, including sensory changes, dysesthesia, and allodynia, can be elicited by asking patients about the character of their pain and not simply relying on unidimensional pain scores.
Studies using low doses of intravenous (IV) lidocaine have shown a reduction in postoperative analgesic requirements well beyond the expected pharmacologic effect of the drug (49). The plasma levels attained with these regimens have been demonstrated to be effective in blocking low-threshold Na+ channels, such as those occurring at the site of nerve injury (46,50). Acting at a central site, the antineuropathic drug gabapentin is effective in reducing perioperative analgesic requirements
(51,52), also reinforcing the role of neuropathic pain as a component of acute postoperative pain.
(51,52), also reinforcing the role of neuropathic pain as a component of acute postoperative pain.
As noted earlier, the intensity of postoperative pain is associated with the development of persistent pain. Although this could be attributed solely to the extent of tissue trauma, a number of studies have shown that, for identical surgical procedures, the severity of postoperative pain is a factor in influencing chronic pain outcomes. In a retrospective study of 509 breast surgery patients, both the type of operation (e.g., with or without axillary dissection) and the severity of postoperative pain were associated with the presence of chronic breast pain (53). In both retrospective and prospective surveys of thoracotomy patients, early postoperative pain has been significantly associated with persistent pain (13,15). Two studies comparing different types of analgesia following thoracotomy also demonstrated this effect (14,54). Taken together, convincing evidence suggests that the modification of pain intensity in the immediate postoperative period can influence the incidence of longer-term persistent pain syndromes.
Phantom pain is a characteristic form of postamputation pain that can vary in intensity from mild discomfort to excruciating pain. Although most frequently associated with limb amputation, it may also occur with resection of other parts of the body, including breast and teeth. Phantom limb sensation occurs in a majority of amputees and diminishes over months to years. Phantom pain occurs in up to 80% of patients, and 1 year later, may still persist in up to two-thirds of these (55). Phantom pain is probably a form of “pain memory,” and is likely to be a manifestation of central sensitization prior to or during the amputation, and cortical reorganization following the event (56). It has many similarities with other forms of neuropathic pain.
Radiotherapy and Chemotherapy
Radiotherapy has been identified as an independent risk factor in the development of chronic postmastectomy pain (53) and the intensity of that pain (57), possibly because of the effect on the healing of injured chest wall nerves or the development of fibrotic scar tissue. Chemotherapeutic agents such as vincristine have long been known to be associated with painful peripheral neuropathies, and recent laboratory evidence suggests that this mechanism is different from that of traumatic neuropathic pain (58). Thus, it is likely that the combination of the neurologic insults of chemotherapy with surgical nerve trauma may have at least an additive effect on neuropathic pain outcomes.
Prevention Strategies
The key objectives in preventing or reducing the transition from acute to chronic pain are to (a) modify risk factors wherever possible and (b) provide the current best practice as far as preventive therapies are concerned. As already noted, the etiologic mechanisms of postsurgical neuropathic pain remain incompletely characterized, and it is unclear why the same injury will cause neuropathic pain in some individuals but not others. This finding even extends to the laboratory where, despite carefully controlled circumstances, some animals will manifest allodynia following nerve injury and others will not. Thus, it is not surprising that evidence for precise recommendations is still limited.
Surgical strategies that minimize nerve injury and decrease the extent of tissue damage should result in an improvement in outcomes. Perioperative pain is decreased by the use of minimally invasive surgical techniques such as video-assisted thoracic surgery (VATS) and laparoscopic cholecystectomy. Although this would be expected to translate into reduced persistent pain problems, the results have been modest. A retrospective review of 343 patients reported a 30% incidence of persistent pain in the months following VATS thoracotomy, compared with a 44% incidence in those having open procedures (59). There was no difference at 12 months. This may reflect the difficulty in avoiding injury to intercostal nerves even after minimal-access procedures. Laparoscopic cholecystectomy has also been associated with mixed long-term outcomes compared with open surgery. This may be due in part to more complex issues relating to the source of pain being from the gallbladder bed or biliary tract (60). Nonetheless, on the basis of reduced acute pain intensity alone, modification of surgical techniques should be encouraged.
Optimizing postoperative analgesia using multimodal techniques remains the most significant contribution that clinicians can make. Recognition of the potentially opioid-resistant components of neuropathic pain in postoperative patients justifies consideration of drugs that have been shown to be effective in treating neuropathic pain, in addition to conventional analgesics in high-risk patients (40). A number of potentially useful drugs are already being used, such as nonsteroidal anti-inflammatory drugs (NSAIDs). In addition to their peripheral anti-inflammatory effect, which may also reduce inflammation at sites of nerve injury, there is evidence for cyclooxygenase (COX)-2–mediated mechanisms involved in central hypersensitivity at a spinal cord level. Tramadol may also be of benefit in neuropathic pain, possibly because of its nonopioid effects (61). Ketamine should be considered in the perioperative setting for high-risk patients because it is well tolerated in low doses, is morphine sparing (62), and is effective in the treatment of certain types of neuropathic pain (63).
Regional analgesic techniques should be encouraged. Epidural local anesthetics and/or opioids result in better analgesia after abdominal surgery than do parenteral opioids (64). Evidence from thoracic surgery and lower limb amputation suggests that regional techniques are associated with lower incidences of persistent pain (14) and severe phantom pain (65).
Obata et al. (54) compared 28 patients in whom epidural analgesia was commenced before surgery with 30 patients in whom epidural analgesia was started immediately postoperatively; both regimens were continued for 72 hours after surgery. Pain relief was significantly better in the preoperative epidural group; the incidence of chronic pain at 6 months was 33%, compared with 67% in the postoperative group. Similarly, Senturk et al. (14) allocated 86 thoracotomy patients to receive preoperative epidural analgesia lasting 48 hours, postoperative epidural analgesia lasting 48 hours, or IV PCA morphine only. The incidence of chronic pain at 6 months was 45%, 63%, and 78%, respectively, and chronic pain was associated with postoperative pain on day 2.
A number of investigations have attempted to identify factors that could be modified to reduce or prevent phantom pain. The early series published by Bach (referred to earlier [42]), suggested that strategies that allow the CNS to “unwind” or desensitize prior to amputation may result in a lower incidence and severity of phantom or neuropathic pain (47). Over the succeeding decades, many approaches have been tried to prevent the onset of phantom pain, including regional analgesia (66), sympathetic interruption (67), ketamine (63,68,69), and anticonvulsants (e.g., gabapentin) (70,71). Evidence to guide therapy is limited, despite the large number of reports published, because many are uncontrolled case series or clinical trials that were small or poorly controlled (72).
However, perioperative regional anesthesia and analgesia may offer some advantage. Gehling et al. (65) conducted a closer examination of published studies, looking at regional anesthesia and phantom limb pain after amputation using more graded end-points. It was concluded that a definite benefit accrues when regional techniques are used in these patients, particularly in diminishing the intensity of phantom limb pain.
Cyclooxygenase (COX)-2 inhibitors may also reduce the incidence of chronic pain after surgery. Celecoxib given perioperatively reduced pain scores and the incidence of chronic donor site pain after spinal fusion (73).
The decision to use other drugs with known efficacy in the treatment of established neuropathic pain, such as amitriptyline, venlafaxine, gabapentin, pregabalin, and lidocaine, in an attempt to reduce the risk of chronic pain, must be based on individual clinical assessment of the likely benefit versus tolerability and side effects (46,47,74,75).
Amitriptyline, given in the early stages of acute herpes zoster, has been shown to reduce the risk of chronic postherpetic neuralgia (76). It has also been reported that venlafaxine, given prior to surgery, reduced the incidence of chronic pain after breast surgery (77), although other investigators have not shown the same result (78). However, although antidepressants may have a role, their side effects may not always be well tolerated (79).
Gabapentinoids are being increasingly used for neuropathic pain and have recently been recommended as second- or third-line therapy (80). The mechanism of action of gabapentin is, despite its name, unrelated to γ-aminobutyric acid (GABA) receptors or metabolism, and is more likely to be a direct modulator of neuronal calcium channels. A meta-analysis of placebo-controlled randomized studies showed a positive effect of gabapentin in diabetic neuropathy and postherpetic neuralgia, and uncontrolled studies also suggest a benefit in other painful neuropathic conditions (81). The role of gabapentin in acute pain is not well defined, although it has been shown to be opioid-sparing, and may have long-term benefits. In a study of mastectomy patients, 66 patients received mexiletine (a Na+ channel blocker), gabapentin, or placebo for 10 days, starting preoperatively (78). Pain scores were reduced from day 2 to 6 in both active treatment groups. At 6 months, analgesic use was lower, and there was no difference in throbbing or aching nociceptive pain, although the incidence of neuropathic (burning) pain was significantly lower (5% in each of mexiletine and gabapentin groups versus 25% in the placebo group). However, in a study involving lower limb amputation, gabapentin given immediately postoperatively and continued for 30 days did not reduce the intensity or incidence of postamputation stump or phantom pain (71).
It is clear that acute pain management and chronic pain issues are interlinked. It is, therefore, important that all clinicians know about the potential benefits of effective analgesia in reducing the incidence and intensity of persistent pain, including phantom pain and other neuropathic pain. Although not all techniques have an established evidence base, the use of regional anesthesia and analgesic techniques, ketamine, and possibly antidepressants and anticonvulsants should be considered in selected patients.
Preemptive and Preventive Analgesia
The concept of preemptive analgesia was first proposed by Crile in 1913, a surgeon who advocated the use of nerve blocks to supplement general anesthesia to prevent painful wound scars (82). This was an important conceptual step, because it integrated both the notion of preventing pain before it occurred, and the possibility that acute events could influence long-term pain. Identification of neurophysiologic mechanisms stimulated modern clinical interest when laboratory research demonstrated a reduction in central hypersensitivity and plasticity (“wind-up”) when analgesic drugs were administered prior to the imposition of a nociceptive stimulus (83).
This appeared to be confirmed by small-scale clinical studies such as that by Bach (42), showing a reduction in postamputation phantom limb pain with preoperative epidural analgesia. However, over the following two decades, clinical studies in acute surgical pain have frequently failed to show a significant or sustained reduction in postoperative analgesic requirements or postoperative pain, despite preincisional analgesia (84). In addition, until recently, there have been relatively few studies of chronic pain. This failure to confirm the neurophysiologic evidence is due to a number of factors, including the definition of preemptive analgesia, but it does not invalidate the underlying principles (85,86). In support of this perspective, a recent meta-analysis of a large number of clinical studies (87) has concluded that preemptive analgesia is effective in certain clinical circumstances.
The terminology relating to preemptive analgesia is frequently misunderstood. Common use of the concept is that the commencement of an analgesic strategy prior to surgery will result in profoundly decreased pain or analgesic requirements following the procedure, in comparison with initiation of pain relief once the stimulus has begun. Although this is to some extent true, preemptive analgesia actually refers to a process initiated prior to an acute nociceptive stimulus (the surgery or injury) that prevents CNS sensitization (central hypersensitivity).
To be most effective, preemptive analgesia strategies must interact at all sites of nociceptive input into the spinal cord: Thus, wound infiltration with local anesthetics will not block inputs from deeper structures, and epidural analgesia may not block all relevant dermatomes or autonomic nociceptive pathways. Importantly, the period of intense nociceptive input may continue well into the postprocedural period and be heightened by peripheral hypersensitivity (including inflammatory processes). Thus, the treatment used should extend in time to cover this stimulus as well (86). To achieve this level of control of central sensitization is very difficult in clinical practice, which explains why the treatment effect seen in many studies is small or absent despite encouraging laboratory work.
Seeking out strategies for preemptive analgesia has a broader justification because of the significant growth in recognition of persistent or chronic pain following surgical procedures (40). Central sensitization at the time of surgery may contribute to both the degree of acute postoperative pain and the likelihood of chronic neuropathic pain. Because the terminology associated with preemptive analgesia has often been confused, many investigators were not assessing changes in central hypersensitivity itself but rather looking for surrogate end-points such as analgesic requirements. In support of this approach, more recent studies have shown evidence that preemptive analgesia reduces acute and chronic pain after thoracotomy (14) and major abdominal surgery (88).
There are many studies, which by design, have potentially modified the sensitization process without demonstrating true “preemptive” analgesia. In these situations, the administration of a treatment strategy (drug/nerve block/wound infiltration) could be deemed to have had a “preventive” analgesic effect if the outcome outlasted the known effect-site activity. Thus, preventive analgesia (86) is demonstrated when a treatment or agent results in a reduction in analgesic consumption or pain
scores beyond the expected pharmacotherapeutic duration of action of the treatment. Preventive analgesic effects relating to acute pain outcomes have been demonstrated in a recent meta-analysis by Ong et al. (87).
scores beyond the expected pharmacotherapeutic duration of action of the treatment. Preventive analgesic effects relating to acute pain outcomes have been demonstrated in a recent meta-analysis by Ong et al. (87).
Thus, the impact of both preemptive analgesia and preventive analgesia can be ascertained from properly designed clinical investigations. For preemptive analgesic strategies to show benefits in hypersensitivity reduction and decreased chronic pain, they must attenuate a significant degree of nociceptive afferent input, and they must be maintained for sufficient duration—that is, into the postoperative period. Preventive analgesia is also a valuable concept, because even if hyperalgesia is not fully attenuated, the outcomes of reduced opioid requirements and decreased pain intensity are beneficial in themselves.
Assessment and Monitoring
Patients with acute pain must be assessed at frequent intervals to optimize analgesia and detect and manage side effects or complications at an early stage (89). Infrequent or inadequate assessment may contribute to the undertreatment of pain and poor clinical outcomes. Such assessments need to be undertaken using clearly described criteria and tools and need to include a pain history, measurement of pain intensity and functional impact of the pain, and monitoring of relevant vital signs, including sedation scoring for those receiving opioids. The results should be documented in a standardized fashion.
Wherever possible, a proper pain history and patient education should be done prior to elective surgery (90). At this time, the opportunity also exists to develop a pain management plan with the patient, advise on expectations and concerns, and discuss pain measurement tools and the importance of communicating pain experiences openly with his or her clinical caregivers (90).
Strategies should be in place to manage deviations from expected parameters. Although a deterioration in pain scores may indicate a need for increasing or modifying analgesic therapy, a significant unexpected increase in pain may be due to the onset of a new clinical condition (e.g., perforated viscus or compartment syndrome) and should be evaluated accordingly. Likewise, aggressive pain management without appropriate clinical monitoring may lead to an increase in adverse outcomes (24).
All of this must be undertaken within the context of the patient’s situation; that is, within the history of the acute pain event, history of past and ongoing long-term pain experiences, and with full knowledge of current analgesic and medical history. This may not be achievable in some circumstances (e.g., severe trauma) or in patients with poor communication abilities, including those with dementia.
Pain History
In acute pain, the pain history is important even if the clinical situation is clearly defined and the expectations are for a relatively rapid recovery. Although in some circumstances clinical priorities may dictate a need for a rapid pain control (e.g., in the emergency department), an exploration of the patient’s pain history, both acute and chronic, is important for the provision of effective and safe pain relief.
The key objectives of the pain history in patients with acute pain are:
Establish communication and rapport with the patient.
Understand the context of the current condition.
Learn the location, character, and intensity of the pain being experienced.
Establish the functional impact of the pain on the patient’s activity.
Identify all current drug therapies and the indications for their use.
Identify drug contraindications, adverse reactions, or “allergies” that might affect analgesic options.
Determine underlying chronic pain issues and treatments.
Learn about previous relevant acute pain episodes and how they responded to treatment.
The last two items are important in maximizing the effectiveness of treatment and also in interpreting pain intensity measurements.
The pain description provides the most valuable information used to guide treatment. Whenever possible, a detailed description of the patient’s pain should be made, guided by descriptors similar to those used in assessing chronic pain. These descriptors can be obtained reasonably quickly and include:
Site
Intensity: The subjective pain score or rating, measured at rest and with movement/activity
Character: Stabbing, burning, shooting, aching, etc.
Radiation
Aggravating or relieving factors
Associated symptoms: Nausea/vomiting, light headedness, etc.
For example, patients following thoracic surgery often have significant pain, but there may be multiple components. The wound itself may be acutely painful, especially if there has been surgical rib resection; there may be muscle spasm and pain in the chest wall as a reflex response to the pain or secondary to rib retraction or costochondral pain; and there may be referred pain from diaphragmatic irritation by the chest drains. The therapeutic strategies and expected time course for resolution of each of these components differs significantly, and management of any one element only will lead to incomplete treatment of the patient’s pain.
Pain Intensity Measurement
The IASP definition of pain emphasizes that it is a subjective experience; that it can be affected profoundly by other factors in the environment, such as anxiety and depression; and that its expression is related to the social and cultural background of the individual. Importantly, acute pain, like chronic pain, is not unidimensional and may not be effectively categorized by one measurable index. Many scales have been developed in an attempt to record the perceived level of pain (pain intensity scores) or to assess the degree of pain relief (analgesia scores). A number of these have direct application in a controlled research environment, whereas others have less reliability or are less complex but are simpler to apply and hence more useful on a day-to-day clinical basis.
Intensity is the subjective component of pain and is measured and recorded using one or more scales or tools. Tools for measuring pain intensity should be meaningful to the patient and clinician. A ranked scale is important to assess the response over time and to changes in therapy. It is most helpful if all scales can be recorded in a similar way on the patient’s observation chart, the most commonly used system for documentation being a numeric index from 0 to 10 (which is, therefore,
an 11-point scale). This index can be used to describe the result from a range of pain intensity tools.
an 11-point scale). This index can be used to describe the result from a range of pain intensity tools.
A summary of the types of tools and scales used is shown in Table 43-3 (91,92,93,94,95,96,97,98,99,100,101,102,103,104,105). The optimal measurement tool or scale may change from time to time because of the circumstances of the patient (e.g., sedation, confusion, etc.). Pain intensity should be assessed and recorded both at rest, and with movement that is relevant to the patient’s condition. However, these measures do not necessarily give the clinician a clear idea of the impact that the pain is having on limiting physical activity or rehabilitation. For this to be done, a functional activity assessment must be made.
Many scales are available for pain assessment in children (106). Children at different ages and with differing abilities will need appropriate tools for assessment, including parent’s or caregiver’s opinion and the response to analgesia. In the absence of demonstrated superiority of any one tool, it is important for an institution to adopt a consistent multidimensional approach to pain measurement and reporting. Refer to Chapter 47 for more details.
Pain assessment in patients with dementia presents a challenge because of the limited communication abilities of the sufferers. As with children, behavioral tools have proved effective, as has the use of reports from family members or personal caregivers. A number of projects have evaluated systems for use in dementia including the PAINAD (107) and Abbey scales (108). Although many of these are too time-consuming for frequent use (they lend themselves to the assessment of persistent pain), elements are applicable to acute pain, such as the modified FLACC scale (Table 43-3).
A limited and consistent set of tools should be established throughout the institution. This will improve care, because clinical staff moving from one area to another will have immediate familiarity with assessments and will know what responses might be necessary. In addition, patients can be educated about how to report their pain and even choose those tools they feel suit them best. An appropriate selection for an adult hospital might be a visual analog scale (VAS; with slide rulers provided), a numerical rating scale (NRS; with consistent wording used), a faces scale, and a behavioral tool (such as FLACC) when needed. All scores should be graded on a 0 to 10 scale for charting, and all patient observation charts throughout the institution should have a specific entry line for pain scoring. Clearly, if a patient does not have a painful condition then pain scoring need only be done once per shift, but otherwise assessments may need to be hourly or as required.
Functional Assessment
The functional impact of the patient’s pain can be assessed by history and if possible, direct observation. Pain management can only be considered to be fully effective if it both relieves the patient’s suffering and enables appropriate physical function. Without being able to undertake relevant activities, which in most cases involve rehabilitation, recovery from an underlying injury or surgery may be impaired (109). Pain also impacts on other aspects of function, such as the ability to sleep, and this should also be assessed.
One method for scoring functional impact is the Functional Activity Scale (FAS), which was developed as part of a pain management toolkit project in Australia (110). The activity to be used for assessing the FAS score must be determined on an individual basis: Coughing may be an appropriate activity target following abdominal surgery, whereas tolerance of physiotherapy and joint mobilization may be appropriate following knee surgery, or the ability to tolerate a lighted room for patients with migraine headaches. The FAS score is a simple three-level ranked categorical score designed to be applied at the bedside. Its fundamental purpose is to assess whether the patient can undertake appropriate activity at his or her current level of pain control, and to act as a trigger for intervention should this not be the case. This differs from, but is related to, pain intensity scoring with movement. It comprises both objective and subjective components in that the clinician asks the patient if he is able to perform the activity and gains the pain intensity score at the time. The patient is asked to perform the activity, or is taken through the activity in the case of structured physiotherapy (joint mobilization) or nurse-assisted care (e.g., ambulation, turning in bed). The ability to complete the activity is then assessed using the FAS, as detailed in Table 43-4.
A FAS score of A represents optimal pain control; B represents an adequate functional outcome, but further pain relief is required for comfort; and C represents inadequate pain control or unacceptable complications of pain control (motor block from neuraxial analgesia, nausea or sedation from opioids, etc.). The score of A needs to be determined relative to the patient’s pre-acute baseline function (which may already have limitations, as from severe arthritis). The FAS score is simple and flexible but requires staff education to be consistently applied; it has not yet been validated in large clinical trials (in part because there exists no “gold standard” for reference).
Overall, it is well recognized that clinical recovery depends on effective rehabilitation. This can be best achieved by careful patient questioning, combined with the use of selected tools to measure pain intensity and functional capacity, linked to appropriate guidelines for intervention should pain relief be inadequate (see example in Table 43-5). Finally, when reassessing patients during treatment for acute pain, it is important to remember that the patient’s current condition may well have altered since the last visit, even if only recent. Ambulation or physiotherapy, changes in drug therapy, side effects of drug treatment (e.g., nausea), the effects of altered sleep patterns, and even relationships with caregivers may all impact on the current situation.
Monitoring for Side Effects and Complications
Provision of safe and effective acute pain management includes regular evaluation of the patient to detect and limit any side effects or complications. Although the regular assessment of heart rate, blood pressure, and respiratory rate is well-established practice, the widespread use of parenteral opioids requires routine and frequent assessment of sedation, as this almost always precedes respiratory depression (24,111). All assessments should be documented, and patient observation charts throughout the institution should contain a specific place for recording sedation scores as well as the “routine” observations in addition to pain scoring.
Little benefit is provided to the patient if the regular assessments for pain and side effects are not coupled with clearly defined trigger levels for intervention (Table 43-5). Such interventions may be as straightforward as the alteration of analgesia dosing, ranging through consultation with senior or more experienced clinicians, to resuscitation (e.g., oxygen, naloxone etc.).
The side effects and complications that are most common or important for consideration are listed in Table 43-6. This list has been drawn from a number of sources (112,113).
Table 43-3 Unidimensional Pain Intensity Measures | ||||||||||||||||||||||||||||
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Table 43-4 Functional Activity Scores | ||||||
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Nausea and Vomiting
Nausea and vomiting, although usually a minor adverse effect, is a significant source of patient dissatisfaction (114). In some circumstances, it can compromise surgical outcome (e.g., abdominal or chest wall flap reconstruction). An evidence-based strategy should be in place to manage perioperative nausea and vomiting (115).
Opioid exposure is a common cause of nausea and vomiting, and there is a known correlation between the risk of nausea and vomiting and increasing opioid dose (116,117,118). Risk factors other than opioids have been identified (119); nausea and vomiting may also occur without any postoperative opioid use (120). Intrathecal opioids are associated with a high incidence of nausea and vomiting, but this may not be dose-related (121). The use of multimodal analgesia results in a decreased need for opioids, which is associated with a decreased incidence of nausea and vomiting as well as sedation (62,117).
Table 43-5 Reportable observation guide | |||||||||||||||||||||||||||||||||||||||||||||
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In the review by Dolin and Cashman, the incidence of nausea was reported to be higher with PCA than following intramuscular/subcutaneous opioid analgesia (Table 43-6), but there was no difference in the incidence of vomiting (112). It is possible that this difference could be related to opioid dose. The much higher number of patients reporting moderate to severe or severe pain with intramuscular analgesia (5) would suggest that lower opioid doses were used in these patients.
Pruritus
Pruritus is a common opioid-related side effect, but its mechanism is not yet fully understood. The role of histamine remains unclear, as pruritus may occur after the administration of opioids that do not release histamine. The fact that drugs such as naloxone (a μ-receptor antagonist) can reverse opioid-related pruritus suggests that a μ-receptor–mediated mechanism may be in play (123).
Sedation
The importance of monitoring for opioid-induced CNS depression cannot be overstated. Significant sedation or respiratory depression occurring in patients receiving parenteral
opioids may lead to significant morbidity. The assumption that respiratory rate monitoring will effectively detect opioid-induced respiratory depression is flawed (24,111), and sedation scoring should be employed on a routine basis in addition to the other core clinical observations.
opioids may lead to significant morbidity. The assumption that respiratory rate monitoring will effectively detect opioid-induced respiratory depression is flawed (24,111), and sedation scoring should be employed on a routine basis in addition to the other core clinical observations.
Table 43-6 Adverse outcomes associated with acute pain management | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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The need to use sedation as an indicator of respiratory depression rather than rely on a decrease in respiratory rate is unfortunately commonly still not recognized. Cashman and Dolin (112,113) reported the incidences of sedation and respiratory depression (Table 43-6) in different papers; respiratory depression was defined in a number of ways by the authors of the various studies included in these reviews, none of which included an assessment of sedation.
The biggest weakness of sedation scoring is for patients who are assumed to be asleep, and who, therefore, may not be disturbed by clinical staff. At these times, patients should be noted to rouse slightly when clinical observations are made (e.g., pulse or blood pressure), and if they do not do so, then the stimulus should be increased until they respond. A suitable sedation scoring system is based on a scale from 0 to 3 (Table 43-7). The aim is for a sedation score of 0 or 1. A higher sedation score should require clinical intervention (reassessment, escalation of care, etc.).
Table 43-7 Example of a sedation scoring system | ||||||||||
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Complications Associated with Neuraxial Analgesia
A list of potential complications associated with neuraxial analgesia is listed in Table 43-8 (124,125,126,127,128,129,130,131,132), but more detail is given in other chapters of this book.
Patients receiving neuraxial infusions (i.e., epidural or subarachnoid) need regular assessment of motor and sensory block and body temperature, and inspection of the catheter insertion
site. Any unexpected progression of motor block, or the failure of it to resolve, should be considered suspicious and justifies an escalation of clinical care and thorough assessment of the patient. Ideally, low doses of local anesthetic should be used in epidural infusions, so that even if the catheter is placed at a lumbar spinal levels, the likelihood of motor block is low. Motor block is most frequently evaluated using the Bromage score (133). This scale is widely used and validated, and it is easy to train clinical staff in its use. It does not replace formal neurologic assessment should neurologic deficit be suspected.
site. Any unexpected progression of motor block, or the failure of it to resolve, should be considered suspicious and justifies an escalation of clinical care and thorough assessment of the patient. Ideally, low doses of local anesthetic should be used in epidural infusions, so that even if the catheter is placed at a lumbar spinal levels, the likelihood of motor block is low. Motor block is most frequently evaluated using the Bromage score (133). This scale is widely used and validated, and it is easy to train clinical staff in its use. It does not replace formal neurologic assessment should neurologic deficit be suspected.
Table 43-8 Adverse outcomes associated with perineural and epidural infusions | ||||||||||||||||||
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