Several mechanisms may be responsible for persistent neuritic pain. Regeneration may have resulted in a local "short circuit" in which afferent fibers sustain a signal of pain despite the resolution of the initial pain stimulus. Sprouting nerve fibers may connect with their own trunks to create such a short circuit. When an aggregation of such fibers is palpable, it is referred to as a neuroma. A second mechanism of neuritic pain may occur when tissues that normally isolate pain fibers from other sensory fibers have broken down, allowing "crosstalk" (or ephaptic transmission) between the fibers, resulting in pain conduction (Devor, 1989).

Neuritis may occur as a result of direct physical trauma (such as cutting, stretching or contusion of a nerve) or may result from other injury such as viral inflammation (e.g., herpes zoster). Neuritis pain tends to be localized to the distribution of the involved nerve, although neuromae may refer to a distant point. The pain description associated with neuritic pain usually involves aching or burning and may involve extreme sensitivity to touch in the area of pain. If significant loss of afferent conduction persists, neuritis may be accompanied by deafferentation pain.

Deafferentation is generated in the central nervous system in response to the loss of afferent sensory information. The mechanism is not completely understood, but probably reflects changes in the sensitivity and signal processing of secondary or tertiary neurons (occurring at the spinal or thalamic levels) when the usual flow of afferent information no longer arrives for processing. As a colleague once noted, "If you can't hear the music, you turn up the volume‑‑and get a lot of static." The most familiar examples of deafferentation pain are post‑spinal cord injury pain and phantom limb pain following loss of an extremity. However, deafferentation pain may be a component of many pain syndromes related to nerve injury. Deafferentation pain often has two components: a baseline aching or burning pain experienced in an area of numbness, with superimposed fleeting, lancinating pains. Both sensations, or one or the other, may be present.

SYMPATHETICALLY MAINTAINED PAIN. The role of the sympathetic nervous system in the perpetuation of persistent pain syndromes is increasingly appreciated. The prototype of sympathetically maintained pain is reflex sympathetic dystrophy (RSD). Classic RSD occurs when, as an injury appears to be healing, the level of pain associated with the injury increases rather than decreases. Temperature and color fluctuations occur early; over time, the involved limb becomes cool, dusky, mildly swollen and with shiny skin and atrophic hair and nails. The pain is characterized as aching or burning and spreads beyond the initial site. The limb is hypersensitive to the touch and often is held in a splinted, immobilized position, eventually developing contractures. RSD may occur in response to any type of tissue injury and occasionally occurs spontaneously. RSD has been observed to occur more frequently in smokers than in nonsmokers. When associated with a nerve injury, the condition is called causalgia.

While full‑blown RSD and causalgia are seen less frequently today than in the past because of early diagnosis and treatment (sympathetic dysfunction currently is recognized as a component of many pain syndromes). The mechanisms of sympathetically mediated pain are debated but may involve a number of factors. When injury occurs, an acute sympathetic response is normal. This is the "fight or flight" response, which allows escape and provides decreased blood flow to the injured extremity to avoid exsanguination. For reasons that are unclear, in some chronic pain situations, this sympathetic response may persist locally beyond the time when it is adaptive and may become a primary source of pain. A high level of sympathetic outflow may alter receptor sensitivity because of decreased circulation, with accumulation of H + ion and increased levels of norepinephrine. When nerves are involved in the injury, efferent sympathetic fibers may directly stimulate afferent pain fibers due to loss of insulating tissue.

Clinically, a sympathetically maintained component of pain should be suspected when alterations of surface blood flow to a painful area are observed, associated alterations in temperature or skin color are noted, hypersensitivity to touch is present or global aching or burning pain that progresses away from an area of injury is described (Janig, 1990).

Pain‑Sustaining Mechanisms

Some addiction medicine specialists and pain clinicians have described a "syndrome of pain facilitation or disinhibition" as occurring in the presence of a chronic pain syndrome and concurrent active addictive disease. This putative syndrome is characterized by a diffuse anatomic

pattern of pain, a relatively constant level of pain and a lack of response to any intervention other than the administration of the chemical on which the individual is dependent (or sometimes other psychoactive and potentially dependence‑producing medications).

Addiction medicine specialists, working in drug and alcohol treatment centers, note that patients with active addiction and concurrent pain often believe that they are using alcohol, benzodiazepines, opiates or other drugs at least partially to reduce their pain. Patients often fear increased pain when the use of such chemicals is discontinued. Following addiction treatment, however, patients usually report that pain is unchanged or even reduced. Occasionally, pain actually is resolved; only rarely does it increase (unpublished, 1992; Finlayson et al, 1986). Physicians who specialize in pain management have observed similar improvement following detoxification from addictive drugs (Taylor et al, 1980). In addition to general reduction in pain, observed changes may include the emergence of a clearer anatomic focus or pattern of pain, more variability in the intensity of pain and an improvement in therapeutic responses to non‑pharmacologic approaches to pain treatment.

Brodner and Taub (1978) describe a series of individuals with chronic pain of non‑malignant origin whose pain improved following detoxification from opiates; they theorize that a subtle withdrawal syndrome occurring in the presence of opiates was responsible for maintaining the pain. Headaches that improve on discontinuation of both opiate and non‑opiate analgesics are well‑described in the literature (Rapoport, 1988; Kudrow, 1982; Blanchard et al, 1989). The persistence of such headaches in the presence of medications has been ascribed to a "rebound effect" that emerges between medication doses.

The withdrawal syndrome characteristic of a particular substance tends to evoke a physiological state opposite from the condition of intoxication with that substance. For example, the withdrawal from sedative‑hypnotic drugs such as alcohol, the benzodiazepines and barbiturates is characterized by a physiologic state of arousal, with documented increases in sympathetic arousal, increased neurological reflexes, and central nervous system arousal (involving anxiety, sleeplessness and irritability). Opiate withdrawal provokes a similar state, with additional symptoms such as abdominal cramping, muscle and bone pain, yawning and diarrhea. Stimulants such as cocaine and amphetamines have withdrawal states characterized by hypoarousal, manifested as exhaustion, depression, sleep disturbance and anhedonia. Physiologic changes associated with cocaine withdrawal (such as reduced sympathetic tone and hyporeflexia) are less well‑documented, although they sometimes are clinically observed.

Most individuals who abuse alcohol, cocaine, opiates or other street drugs do not maintain stable blood levels of their substances and therefore periodically enter states of withdrawal (if any degree of physical dependency is present), alternating with states of intoxication. Similarly, individuals prescribed opiates for treatment of pain or benzodiazepines for pain‑related sleep disturbance or anxiety, often are prescribed short‑acting medications that may cause them to enter a state of relative withdrawal alternating with a physiologic state adapted to the medication.

If the transition between alternating states of withdrawal and intoxication or physiologic adaptation does mediate a syndrome of pain disinhibition, several mechanisms may be active. These include sympathetic, myotonic, affective, sleep‑related and receptor mechanisms. As previously discussed, the sympathetic nervous system plays a role in the mediation of many types of pain through direct neurogenic mechanisms and through vascular flow changes. Addicted persons may have intermittently high levels of sympathetic arousal, either as a result of withdrawal (from alcohol and other sedatives and opiates) or due to direct sympathetic stimulation by the drugs abused (such as cocaine and other stimulants). Such sympathetic stimulation may alter nociceptive pathways and pain inhibitory mechanisms in ways that intensify the pain experience.

Similarly, withdrawal from alcohol, benzodiazepines, barbiturates and opiates‑‑or intoxication with cocaine and other stimulants‑‑may cause increased levels of muscle tension (Hall, 1990; Geari, 1987). Because muscle tension, spasm or restrictions are prominent features (either primary or secondary) of many pain syndromes, fluctuations in muscle tone may contribute to a more diffuse and/or intense pain experience.

Virtually all forms of addiction are associated with significant sleep disturbances in either the active use or withdrawal phases, or both. Sleep disturbance is a wellestablished exacerbating factor in chronic pain and may represent another mechanism by which addiction affects chronic pain. Significant affective changes are common in the presence of addictive disease, both in active use states and in withdrawal periods.

Depression and anxiety are both known to augment the experience of pain. Depressive symptoms are common in the presence of alcoholism, occurring in up to 60% of actively drinking alcoholics. Evidence suggests that depression is more frequently a sequela of alcoholism than an antecedent or coincidental occurrence. Depression is a prominent feature of chronic cocaine use and of some stages of cocaine withdrawal (Hall, 1990). A reciprocal relationship between depression and pain long has been recognized (Gallemore & Wilson, 1969; Ward, Bloom & Friedel, 1979). Similarly, the facilitation of pain by anxiety has been documented (Linton & Gotesam,1985). Anxiety is a common symptom both in acute alcoholism and in the presence of alcohol withdrawal (Schuckit, Irwin & Brown, 1989). Anxiety is a common manifestation of cocaine and other stimulant use; it has been described as a common feature of withdrawal from a wide spectrum of drugs, including cocaine, benzodiazepines and opiates (Emmet‑Oglesby, 1989). Depression and anxiety related to addiction may represent contributing factors in the maintenance or exacerbation of chronic pain in an addicted patient.

Changes in opiate receptors and in endogenous systems of pain inhibition may play a role in the observed pain facilitation or disinhibition in some individuals who are chronically dependent on opioids and/or other psychoactive drugs. Chronic use of opioids, alcohol, cocaine and other drugs has been reported to induce various changes in central opiate receptors and in norepinephrine, serotonin, dopamine and GABA availability, altering neuromodulation of brain reward mechanisms (Blum, 1989). Such receptor and neurotransmitter changes may affect modulation of nociception as well.

Several factors unrelated to withdrawal phenomena also may increase pain in the presence of addiction. Alcohol and other drug intoxication may mask pain that otherwise would appropriately signal irritation or injury, thus allowing an individual to overuse his or her body in a way that perpetuates an underlying physical problem associated with the persistent pain problem.

The functional changes associated with addiction may augment the general distress of chronic pain. Individuals with active addictive disease often cannot fulfill their usual work and domestic roles, frequently have dysfunctional relationships, suffer financial losses and may develop secondary physical discomforts and illnesses. These all may feed into the cycle of chronic pain causing escalation of pain, distress and disability. Finally, individuals who are addicted may simply be unable to comply with prescribed regimens for treatment of their pain syndrome because of periods of intoxication and/or recovery from intoxication.

Evaluation of pain in the individual with addictive disease must include careful delineation of each of the physical or nociceptive components of the pain syndrome, as well as identification of associated distresses that may act as perpetuating factors for pain. Treatment should address each of the identified physical causes of pain and each of the perpetuating factors.

Tools for the Management of Pain

Pain management tools generally fall into four categories: physical treatments, psychological interventions, anesthesia block procedures, and systemic medications. Effective pain treatment interventions vary according to the physiologic causes of pain, other symptoms and distresses associated with the pain and the context in which the pain occurs. It is important for the physician treating pain in persons with addictive disorders to have an appreciation of a variety of pain management approaches in order to plan treatment for individual patients. The reader is referred to a number of concise, yet detailed, guides to pain management for more information on treatment approaches (Panel, 1992; Abrams, 1990; Warfield, 1991; American Pain Society Committee on Acute and Cancer Pain, 1992; Ready & Edwards, 1992).

Table 1. Equianalgesic Opioid Doses

DRUG	APPROXIMATE EQUIANALGESIC	APPROXIMATE EQUIANALGESIC
	ORAL DOSE	PARENTERAL DOSE
Opioid Agonists
Morphine	30 mg q 3-4 hour	10 mg q 3-4 hour
	(around-the-clock dosing)
	60 mg q 3-4 hour
	(single dose or intermittent dosing)
Codeine	130 mg q 3-4 hour	75 mg q 3-4 hour
Hydromorphone (Dilaudid)	7.5 mg q 3-4 hour	1.5 mg q 3-4 hour
Hydrocodone	30 mg q 3-4 hours	Not available
(in Lorcet, Lortab, Vicodin)
Levorphanol	4 mg q 6-8 hours	2 mg q 6-8 hours
(Levo-Dromoran)
Meperidine (Demerol)	300 mg q 2-3 hours	100 mg q 3 hours
Methadone (Dolophine, others)	20 mg q 6-8 hours	10 mg q 6-8 hours
Oxycodone	30 mg q 3-4 hours	Not available
(Roxicodone, also in Percocet,
Percodan, Tylox, others)
Oxymorphone (Numorphan)	Not available	1 mg q 3-4 hours
Opioid Agonist-Antagonists
and Partial Agonists
Buprenorphine (Buprenex)	Not available	0.3-0.4 mg q 6-8 hours
Butorphanol (Stadol)	Not available	2 mg q 3-4 hours
Nalbuphine (Nubain)	Not available	10 mg q 3-4 hours
Pentazocine (Talwin, others)	150 mg q 3-4 hours	60 mg q 304 hours
Note: Published tables vary in the	Caution: Recommended doses do not	Caution: Doses listed for patients
suggested doses that are equianalge-	apply to patients with renal or hepat-	with body weight less than 50 kg
sic to morphine. Clinical response	is insufficiency or other conditions	cannot be used as initial starting
is the criterion that must be applied	affecting drug metabolism and kinet-	doses in babies less than 6 months
for each patient; titration to clinical	ics.	of age. Consult the AHCPR Clini-
response is necessary. Because		cal Practice Guideline for Acute
there is not complete cross-tolerance	Source: Acute Pain Guidelines	Pain Management: Operative or
among these drugs, it usually is	Panel (1992). Acute Pain Manage-	Medical Procedures and Trauma
necessary to use a lower than equi-	ment: Operative or Medical Proce-	section on management of pain in
analgesic dose when changing	dures and Trauma. Rockville, MD,-	neonates for recommendations.
drugs, and to re-titrate the response.	U.S. Dept. of Health and Human
	Services.

PHYSICAL TREATMENT APPROACHES. Physical treatment approaches include the use of therapeutic heat and/or cold treatments, stimulation analgesia (most commonly, transcutaneous electrical nerve stimulation, or TENS), manual treatments such as massage, manipulation and stretch, and the use of orthotic devices such as splints and braces to protect, immobilize or position body parts to reduce pain (Lee, 1990). Exercise directed at stretching, strengthening and conditioning are important components of treatment of most myofascial and biomechanical pain syndromes. Physical approaches to the treatment of pain often are effective in both acute and chronic pain settings. Because many such approaches can be implemented by the individual who is in pain, they provide a sense of control to the individual and encourage self‑care, both of which are helpful for the individual with addictive disease.

ANESTHESIA BLOCK APPROACHES. Anesthesia procedures have a diverse role in the treatment of pain (Cousins & Bridenbaugh, 1990). Epidural infusions of local anesthetics or opioids may be used to provide continuous analgesia for postoperative, post‑traumatic or cancer pain, or for other acute medical pain such as kidney stones or acute pancreatitis. Regional nerve blocks with long‑acting anesthetics may provide prolonged analgesia for rib or other fractures, or for soft tissue trauma. Nerve blocks or triggerpoint injections may interrupt sustaining cycles of sympathetic or myofascial pain and resolve the symptoms. Steroid injections may resolve pain associated with the inflammatory process.

Such procedures generally can be used safely in individuals with addictive disease. Epidural opioids act locally in the spinal cord to provide analgesia. Depending on the type and dose of drug used, some drug may find its way into the CSF or systemic circulation. This is generally thought to be clinically unimportant in terms of central effects. However, in a recovering opioid addict, the use of epidural local anesthetic alone (without opioids), if it is effective, may be preferred by some clinicians to avoid concerns regarding stimulation of drug craving or other central effects.

PSYCHOLOGICAL TREATMENT APPROACHES. Psychological interventions may include introduction of the relaxation response to reduce muscular and psychic tension; cognitive restructuring and behavioral interventions to alter the individual's understanding of the pain and reduce the destructive responses to pain; psychotherapy to reduce interpersonal stresses and heal intrapsychic processes that may be contributing to the pain; and treatment of anxiety and depression. In the addicted patient, psychological interventions may directly address factors that drive addiction, as well as those that perpetuate pain. (Psychological approaches to pain treatment are addressed in Chapter 2 of this section.)

MEDICATIONS. In treating pain, medications may be used to directly reduce pain, or may be employed to manage distressing sequelae and perpetuating factors, such as sleep disturbance, anxiety or depression. When non‑medication treatment approaches are easily available and likely to be effective in treating pain in an individual with addictive disease, these may be preferred to medications, as their use does not reinforce drug‑taking as a solution to coping with discomfort. However, medications (both non‑opioids and opioids) can be effectively and safely used to control pain in patients with addictive disorders.

Although addicts are most likely to misuse medications that have the capacity to produce physical dependence and/or produce mood‑altering effects, physicians should be aware that many addicts have a propensity to misuse any medication. "If a little is good, more must be better" often is the perception. Therefore, it always is important to be explicit in providing instructions regarding medication use. Written instructions signed by the patient, with a copy included in the medical record, are recommended, particularly when opioid medications are prescribed. The potential short‑ and long‑term toxic effects should be explained at this time. Also, it is wise to decide in advance how lost or destroyed medications with be dealt with; this decision should be documented. Relevant pharmacologic aspects of specific medication groups used to treat pain are discussed in Section VIII, Chapter 3.

Management of Acute Pain

Under treatment of pain has been shown to prolong hospitalizations and duration of disability. Undertreatment of acute pain is common in all patients (Morgan, 1985; Marks & Sacher, 1973), but may be more common in individuals perceived to have addictive disorders (Shine & Demas, 1984; Cohen, 1980). The reasons for this appear related to fears on the part of both patients and staff of causing or exacerbating addiction through the use of opioids (Shine & Demas, 1984). In fact, it seems more likely that undertreatment of pain in an individual with addictive disease will increase distress and anxiety and increase pain, thus presenting more potent risk factors for relapse than simple exposure to dependence‑producing medications.

Individuals with addictive disease often experience high levels of anxiety in association with the stress of trauma, illness or surgery. These may in turn affect how these persons experience pain. Identification and attention to their concerns may make pain management easier.

Physicians should inform patients with addictive disease who have acute pain that they are aware of the patients' addictive disease; further, they should reassure them that this will not be an obstacle to relief of pain. If a patient has an opioid addiction, the clinician should not consider opioid discontinuation until the acute pain situation is resolved (Table 2). If a patient is an actively drinking alcoholic or is dependent on other non‑opioid ‑drugs, withdrawal symptoms should be treated when they occur in the course of pain treatment (Table 3).

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Table 2. Acute Pain Treatment: Opioid Addicts

PROVIDE BASELINE OPIOID REQUIREMENTS Estimate average daily opioid dosage; Calculate equivalent dose of opioid to be used; Give baseline opioid at appropriate intervals; Remember: baseline doses do not provide analgesia for acute pain.

USE NON‑MEDICATION APPROACHES AND/OR NON

OPIOID ANALGESICS, IF EFFECTIVE, FOR PAIN

‑‑ Regional anesthesia or analgesia techniques;

‑‑ TENS, thermal treatments, other physical

approaches;

‑‑ NSAIDs, tricyclics, anticonvulsants, others as

indicated.

PROVIDE EFFECTIVE DOSES OF OPIOIDS, AS NEEDED

‑‑ Consider tolerance in determining doses and

frequency;

‑‑ Give on scheduled or continuous basis;

‑‑ Use PRN only for adjusting schedule;

‑‑ Taper analgesic doses when acute pain resolves.

TREAT ASSOCIATED SYMPTOMS AS INDICATED

‑‑ Sleep disturbances;

‑‑ Affective changes: anxiety, depression;

‑‑ Secondary physical problems.

ADDRESS ADDICTION

‑‑ Consider detoxification only when acute pain is

resolved;

‑‑ Address other addiction issues, as appropriate.

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Table 3. Treatment of Acute Pain:

Non‑Opioid Addicts

PROVIDE EFFECTIVE ANALGESIA

‑‑ Non‑medication intervention, if effective;

‑‑ Non‑opioid analgesics, if effective;

‑‑ Effective doses, when opioids are required;

Scheduled or continuous doses

PRNs only for adjustment of schedule

Taper to discontinue

TREAT WITHDRAWAL SYMPTOMS

EVALUATE AND TREAT ADDICTION

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Addiction counselling should be offered during treatment and may be initiated at any time as long as acute pain is adequately controlled. Pain relief should be provided in an effective and timely manner. Undertreatment of pain may create drug craving for pain‑relieving medications, as well as anxiety, frustration, anger and other feelings that tend to feed addiction (McCaffery & Vourakis, 1992).

When they are effective, easily available and safe, certain non‑medication approaches such as ice, TENS or regional anesthesia are preferred by some clinicians over systemic medications to provide relief of acute pain in individuals with addictive disease. When medications are indicated to relieve pain, those that are the least likely to produce physical dependency and have the least tendency to alter mood generally are preferred, but only if they are effective. While exposure to dependency producing or mood‑altering drugs is one component of the development of addiction or relapse to drug use, such exposure alone does not create addiction. When such drugs are needed to manage pain, they should be used effectively.

In the acute pain setting, opioids are the mainstay of treatment. However, they have a strong capacity to produce physical dependence and alter mood and may become the object of addiction in individuals with addictive disease. Nonetheless, they may be used effectively and safely in patients with addictive disease when indicated for pain control (Portenoy, 1990; Sees & Clark, 1993; Wesson, Ling & Smith, 1993).

When opioids or other potentially addictive medications are needed for the treatment of pain, they should be used in effective doses. Scheduled administration is preferred over PRN dosing in individuals who have active addictive disease or who are in recovery, if the pain is sustained rather than intermittent. This approach has several advantages:

The patient does not have to ask for medications, which in an addict may be interpreted as drug‑seeking behavior rather than a search for pain relief and thus may create friction between the patient and care providers. Delays in receiving medication are avoided, so more timely and effective pain relief is obtained and drug craving is avoided. Because the drug administration is time contingent rather than symptom contingent, reinforcement of the pain symptoms is minimized. PRN doses of medication should be provided initially, in addition to scheduled doses, for titration of medications to the required dosing level, then discontinued.

Intermittent, non‑scheduled medications are appropriate in the acute pain setting when an individual has little or no baseline pain, but has pain related to specific activities. In such cases, it often is recommended that opioids be prescribed prospectively, contingent with the activity, not contingent on the expression of pain. For example, a patient with post‑prandial biliary pain might be prescribed a short‑acting analgesic, with instructions to take it 30 minutes before meals. Or a burn patient might be prescribed such medications prior to bandage changes. This approach avoids a time lapse between the onset of pain and relief of pain and is less likely to reinforce the pain experience.

When scheduled medications are required on an outpatient basis in individuals with addictive disease, it is helpful to give specific times for drug administration (as at 7:00 a.m., 3:00 p.m. and 11:00 p.m.) rather than indicating that a drug should be taken three times a day or every eight hours. This reduces the potential for confusion over dosing and possible resultant misuse. If an individual has difficulty controlling medication use but needs opioids for pain relief, it may be helpful to have a trusted other, such as spouse or friend, dispense the medications, either by the dose or by limited‑time intervals such as one or two days. Daily dispensing also may be arranged through a visiting nursing or pharmacy.

The individual in pain should be included in the decision‑making process regarding dosing and scheduling. This provides the patient with a sense of control and allays anxiety over whether the pain will be adequately treated. It also may give the physician valuable insights in designing an effective treatment regimen. Addicted patients and patients with therapeutic drug dependence often are experts on the drug doses they require to meet their basic dependence needs and the additional levels required to treat their acute pain. Occasionally such consultation will result in prescription of doses beyond that needed for analgesia; if patients become obviously intoxicated or sedated with prescribed doses, medications should be titrated to avoid the observed side effects while continuing to provide analgesia.

Long‑acting opioids such as methadone, levodromoran and sustained‑release morphine tend to cause less of a "high" or "rush" than do short‑acting medications such as hydromorphone and oxycodone and therefore are less likely to be abused. When sustained use of oral opioids is required over a period of several days, an equianalgesic dose of along‑acting opioid may be preferable to a short‑acting medication. Onset of action is slower with long‑acting opioids, however, and initiation of opioid treatment with short‑acting oral agents to achieve rapid relief of pain usually is most effective.

Opioids should be tapered when their use is discontinued in an individual with addictive disease. This usually avoids withdrawal symptoms, which can include craving and pain and which may lead to requests for continued opioids or to self‑administration of street drugs or alcohol to attenuate symptoms.

Patient‑controlled analgesia (PCA) can be successfully used in individuals with addictive disease, but such use is controversial. Because PCA, if used optimally, provides a stable analgesic blood level of opioids, its use usually results in more uniform pain relief at a lower total dose of medications (Hill et al, 1990) and without peaks (which may cause sedation or intoxication) and valleys (which may result in pain, anxiety and drug craving). As with scheduled dosing, the use of PCA eliminates the need for the patient to requests opioids for pain relief and thus avoids potential staff/patient conflicts, which can arise when addicts request opioids. Thus, from certain perspectives, PCA is ideal for use with addicts.

On the other hand, because PCA requires selfadministration, it may create ambivalence in recovering persons and in patients with active addiction problems, who have difficulty limiting their administration of opioids to levels that provide analgesia without intoxication. The latter problem may be managed to some degree through the physician's control of the incremental dose size and frequency and the total dose available over a period of time. In theory, PCA may reinforce pain through the pairing of pain with self‑administration of opioids and thus may make cessation of analgesic doses of opioids difficult. In practice, however, these issues rarely arise. As with all pain control options, the use of PCA for control of acute pain in individuals with addiction problems should be considered on a case‑by‑case basis, with attention given to the patient's preferences and the staff's comfort.

Pain treatment that does not confuse, stress or frustrate staff and/or patient is important. For example, if an epidural infusion of local anesthetic is available for management of post‑thoracotomy pain in a recovering opiate addict, but the floor nurses are unfamiliar with management of such catheters, the overall needs of that patient probably will be better met with scheduled doses of opiates.

Individuals who are on methadone maintenance or who are physically dependent on either therapeutically prescribed or street opioids must have their baseline opioid requirements met and additional pain treatment provided (Wesson, Ling & Smith, 1993; Hill et al, 1990). The average baseline daily dose of opiate should be determined and either the same drug provided at the determined dose or an equianalgesic dose of an alternative opioid calculated and provided in appropriately scheduled doses (see Table 1 for an analgesic equivalence chart) (Panel, 1992). In practice, one‑half to three‑quarters of the calculated equianalgesic dose often is provided, since there appears to be incomplete cross‑tolerance between opioids and an opioid to which the individual has not been regularly exposed may be relatively more potent for that individual than one s/he has been using regularly (Foley, 1991).

For example, a patient who has been using methadone 80 mg per day is admitted to the hospital with acute pancreatitis and placed on NPO. Intramuscular methadone is not available in this hospital. The medication available is morphine sulfate. As shown in the opioid equivalence chart, 20 mg PO methadone is equal to 10 mg IV or IM MS04, the MS04 dose that is equivalent to 80 mg methadone would be 40 mg MS04 IV or IM per day. Because the patient is naive to morphine, somewhere between 20 and 30 milligrams likely would meet the patient's baseline requirements. Since MS04 is a 4‑6 hour medication and the patient is physically dependent on opioids, the MS04 should be given in divided doses at four hour intervals, 5‑6 mg every four hours. Alternatively, one might provide a continuous infusion of 1 mg per hour or 24 mg per 24 hours. This meets only the patient's baseline opioid needs.

The baseline dose of opioid to which the patient is habituated should not be expected to provide any relief of acute pain, and so the patient must be provided additional treatment for pain. If non‑opioid pain treatment such as regional analgesia, NSAIDS, TENS or ice are effective, they may be used to control pain. Their use may negate the need for opioids or lower the dose required for effective analgesia. When opioids are required for analgesia (which is most often the case in an acute pain setting), it is important to recognize that an opioid‑dependent patient may require larger and more frequent doses to achieve analgesia because of tolerance. Using our example above, since some tolerance to analgesic effects of MS04 is likely, these doses should be relatively high. Doses of 10‑15 mg every four to five hours in addition to the baseline dose of MS04 is an appropriate initial regimen (adjusted as indicated). Patient‑controlled analgesia with a background continuous infusion equal to the baseline opioid dose is another option.

Alcoholics who are withdrawing while in acute pain should be treated with benzodiazepines or other medications to smooth withdrawal. Sometimes withdrawal symptoms such as sleeplessness, anxiety, or increases in blood pressure and pulse are misidentified by both patient and staff as reflecting pain. This may lead to rapidly increasingly doses of opioids, often without relief of symptoms. The prescription of appropriate doses of benzodiazepines to attenuate withdrawal usually results in improved pain control at lower doses of analgesics.

Recovering persons often benefit from increasing their recovery activities during times of stress, such as hospitalization, trauma and pain. Many clinicians and

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Table 4. When Pain Persists

Beyond Expected Healing

STEP 1: SEARCH FOR PHYSICAL CAUSES

Delayed healing; Undetected trauma; Disuse phenomena (muscle spasm, edema, contractures, etc.) Neuropathic pain (neuritis, neuroma, deafferentation) Sympathetic pain (RSD, causalgia).

STEP 2: IDENTIFY AND ADDRESS POSSIBLE PAINSUSTAINING FACTORS Sleep disturbances; Anxiety; Depression; Secondary gain factors.

STEP 3: CONSIDER PHYSICAL DEPENDENCE ON MEDICATIONS ‑‑ Adjust taper to avoid withdrawal; Calculate 24 hour opioid use Give in scheduled parenteral doses, or switch to equianalgesic doses of long‑acting oral opiate Taper at time‑contingent, not symptomcontingent, intervals Treat withdrawal symptoms, if needed. Treat pain with non‑opioid modalities; Treat associated symptoms with non‑dependence producing medications or non‑medication approaches.

STEP 4: CONSIDER POSSIBILITY OF ADDICTION ‑‑ Obtain evaluation by addictionist, if possible; ‑‑ Taper as for physical dependence; ‑‑ Institute recovery program, if needed.

STEP 5: MANAGE PAIN AS A CHRONIC PAIN PROBLEM.

individuals in recovery believe that exposure to opioids, sedative‑hypnotics or anesthetics‑‑even if these were not the patient's drugs of choice‑‑may lead to relapse. However, the distress of inadequately treated physical pain may represent a greater risk factor for relapse. Effective pain treatment by whatever means, coupled with an active recovery program, are likely the best supports for continued recovery.

When there is doubt regarding whether a patient is in pain or is requesting drugs because of addiction, it is more medically appropriate to err on the side of giving adequate pain relief. Physical dependence on opioids is reversible. Addiction is treatable. It is acceptable to be deceived from time to time if it means providing effective pain relief to the majority of patients who truly need it.

WHEN PAIN PERSISTS DESPITE APPARENT HEALING.

When a patient continues to complain of pain and to need pain medications despite expected and apparent healing from surgery, trauma, illness or other pain‑provoking pathology, several explanations should be considered (Table 4).

First, the patient may have an undetected physical problem, either related to the original painful problem or to a separate process. A thorough search for such a cause should be undertaken. The search should include a review of somatic causes of pain, such as abscess or undetected fracture, as well as less common and often overlooked neurogenic causes of pain. These may include neuroma formation at a site of injury, sympathetically maintained pain or reflex sympathetic dystrophy, and deafferentation pain (loss of sensory innervation to an area associated with centrally mediated pain).

Second, the patient may be physically dependent on analgesic medications and may be experiencing pain related to withdrawal as the medication is discontinued. Withdrawal may mediate pain through a variety of mechanisms, including alterations in sympathetic arousal, changes in muscle tone and alterations in opiate and other receptor function (Savage, 1993). A gradual taper of medications over several days usually avoids this rebound pain phenomenon. The ideal goal when tapering an individual who is physically dependent on medications should be to provide stable but decreasing blood levels of opioid so as to prevent intermittent withdrawal. In practice, this usually can be only approximated. A patient on IM or IV medications may be switched to equipotent doses of oral medications (refer to the analgesic equivalency chart) and then tapered. If a patient is on a shortacting opioid such as hydrocodone (Percocet), the taper may be easier if the patient is switched to an equivalent dose of a long‑acting opiate such as methadone, levodromoran or MSContin.

If increased discomfort occurs during the course of medication taper, the patient should be re‑reviewed for an undetected physical origin of pain. If none is found, the taper should be continued. Non‑opioid alternatives (such as TENS, NSAIDs or block therapy) should be provided to attenuate discomfort during withdrawal of medications. In most cases, increases in discomfort will be transient during and immediately following discontinuation of medications. If pain persists and no physical cause can be identified, treatment should be as for chronic pain.

Third, the individual may be using the medication to obtain relief of symptoms other than pain, such as anxiety or depression. Opioids may in fact provide some shortterm relief of such distress, but more specific treatments will be more effective and will allow tapering of pain medications. Patients who complain of increased pain on withdrawal of opioid medications should be assessed for anxiety, depressive symptoms and other psychological distresses that may be opioid‑responsive. More effective interventions should be undertaken when such symptoms are identified.

Finally, the individual may have developed an addiction to the medication. This is less common than the first three possibilities when treating a general hospital population, although it is a relatively more frequent occurrence in the population treated by addiction medicine specialists. Addiction in the context of pain treatment may be suggested by a number of behaviors. These include: unwillingness to consider a gradual taper of medications; reports of no subjective pain relief whatsoever by any interventions other than opioids; the use of drugs in a manner that elicits persistent side effects of somnolence, sedation or euphoria; failure to obtain analgesia with appropriate doses of oral, long‑acting analgesics, with a strong preference for short‑acting high‑dose analgesics; "running out" of medications before the prescribed time; and repeated reports of "loss" of medications (Sees & Clark, 1993; Wesson, Ling & Smith, 1993).

If addiction is suspected, the patient's drug and alcohol history should be thoroughly reviewed. If the patient is in recovery, he or she should be reengaged in the recovery system or recovery‑oriented activities initiated. If the individual had an active chemical dependency problem at the time of onset of the acutely painful injury or illness, addiction treatment should be initiated. If the person has no history of addictive disorder, consideration of possibilities one, two and three should be rereviewed and further evaluation by an addiction specialist obtained. (An accurate history of substance use may be difficult to obtain.) It is rare, but not unheard of, for addiction to be initiated through therapeutic use of medications.

If addiction is suspected, medication should be tapered as described above. The use of alternative methods for addressing pain will be of particular importance. Simultaneously, addiction treatment also should be undertaken.

Unless an underlying physical cause is identified, pain often resolves or improves following discontinuation of medications and treatment of addiction. If it does not, the patient should be treated for chronic pain.

Chronic Pain of Non‑Malignant Origin

The treatment of chronic pain in individuals with addictive disease differs little from the treatment of such pain in individuals without addictive disease. The goals of chronic pain treatment are reduction of pain; improvement in associated symptoms such as sleep disturbance, depression and anxiety; restoration of function; and reduction of dependence on medications. These goals typically are approached through non‑pharmacologic means (Table 5).

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Table 5. Treatment of Chronic Pain: All Addicts

ADDRESS ADDICTION

‑‑ Detoxify or stabilize medications;

‑‑ Introduce recovery program.

DEFINE PHYSICAL COMPONENTS OF PAIN

‑‑ Treat with non‑medication approaches;

‑‑ Use non‑dependence producing medications if

medications are needed.

DEFINE PAIN SUSTAINING FACTORS

‑‑ Treat with non‑medication approaches;

‑‑ Use non‑dependence producing medications if

medications are needed.

ADDRESS FUNCTIONAL STATUS

‑‑ Encourage increased physical, social and

productive activity.

Addictive disease should be identified and addressed early in the treatment of chronic pain. Although some patients with pain and co‑existing addictive disease initially believe their chemical dependence is a product of their pain, in fact most patients find that their pain and associated symptoms are improved or at least unchanged following treatment of addiction. The sequelae of addiction often include perpetuating factors for pain, such as sleep disturbance, anxiety or depressive symptoms, changes in muscle and sympathetic tone, and dysfunction in usual life roles (Savage, 1993). When treatment of addiction produces improvement in these factors, pain often resolves or improves (Finlayson, Maruta & Morse, 1986; Finlayson et al, 1986; Brodner & Taub, 1978). When it does not, the chronic pain should be addressed in the same manner as for per‑sons without addictive disease.

Addiction treatment generally includes detoxification from dependence‑producing medications and introduction of a recovery program. This eliminates the pain‑generating or reinforcing factors inherent in physical dependence. Occasionally, however, a patient's pain symptoms may make withdrawal of medications early in treatment impossible. In such cases, stabilization of the medications to avoid abrupt changes in blood levels (which in turn may avoid intermittent emergence of withdrawal phenomena; Savage, 1993; Brodner & Taub, 1978), may be the best option. For example, an alcoholic patient who is taking large doses of hydrocodone (Percocet) for back pain and who is disabled by the back pain when the hydrocodone is tapered, may do best if switched to a long‑acting opioid such as sustained release morphine or methadone for pain early in treatment and then tapered slowly from that medication as the pain treatment progresses. Rarely, it may be appropriate to continue longacting opioids indefinitely.

Assessment of the patient with chronic pain must include a history of the onset of pain, treatments to date and responses to treatment, a clear description of the quality and temporal nature of the pain, and identification of factors that ameliorate or exacerbate the pain. Assessment must be made of the way the pain has affected the individual's life, including its effect on relationships, work and domestic roles and pleasurable recreational activities. Factors known to increase or sustain pain‑such as depression, anxiety, sleep disturbance, social isolation and inactivity‑‑must be identified. A list of all factors potentially contributing to the pain and to the patient's resulting distress should be generated and a plan for addressing each component of the problem developed. Interventions that address only the physical components are unlikely to resolve the pain.

Physical approaches such as stretching, exercise, applications of cold or heat, peripheral electrical stimulation, manual treatments and anesthesia procedures such as nerve blocks and trigger points are used to reduce physical symptoms. Behavioral interventions such as relaxation training, introduction of pacing of activities to minimize pain and changes in behavioral responses to pain are used to reduce the experience of pain and associated symptoms such as anxiety. Often a multidisciplinary team of pain specialists may be involved, although many of these approaches to pain management are interventions that easily can be introduced by a primary care physician.

The use of opioids for the treatment of chronic pain of non‑cancer origin is becoming an increasingly accepted option when other treatments fail to provide relief (Portenoy, 1990; Schug, Merry & Acland, 1991; Zenz, Strunnph & Tryba, 1992). Most proponents of long‑term opioid therapy for chronic non‑cancer pain view a history of addiction as a relative contraindication to the implementation of such therapy because of the problems persons with addictive disorders often experience in controlling their use of potentially intoxicating medications. However, for selected patients with severe, chronic non‑cancer pain and a concurrent history of addictive disease, there may be no other realistic treatment option. If long‑term opioid therapy provides subjective pain relief, an improved level of function, and better quality of life, and does not result in adverse consequences, signs of loss of control over medication use or return to alcohol or street drug use, many clinicians believe that it represents appropriate pain treatment. Such patients often gravitate to methadone maintenance clinics because no other clinicians are willing to provide them with therapeutic opioids for pain control (Members, 1992). In fact, although federal law prohibits the prescription of opioids to maintain addiction or prevent withdrawal, the law does not prohibit longterm prescription of opioids to persons with addictive disorders for the relief of pain (Joranson, Cleeland & Weisman, 1991; Clark, 1993).

If long‑term opioid therapy for treatment of chronic non‑cancer pain in an individual with a history of addiction is thought to be indicated, a team approach and a highly structured program is recommended. Ideally, the team should include an addiction medicine specialist, the patient's primary care physician and a pain specialist. A written contract should be developed with the patient that specifies the prescriber, the pharmacy to be used, the dose and schedule of medications, recovery activities expected, and the circumstances under which treatment will be continued or discontinued. A team physician should meet regularly with the patient to assess the therapeutic efficacy of the medication in terms of pain control and to monitor for addictive use of the medications. Progressive tolerance to the therapeutic effects of the medication or addictive use generally dictate discontinuation.

Cancer Pain

Treatment of cancer‑related pain in the patient with addictive disease is similar to that in the person without addictive disease. The comfort of the patient should be the primary goal. Opioids never should be withheld when they are needed to achieve pain relief because of concerns regarding the development or perpetuation of addiction.

Mild cancer‑related pain may respond to treatment with NSAIDs. Bone pain due to metastases (even when severe) may be most effectively relieved with NSAIDs. Because NSAIDs and opioids act by different pharmacologic mechanisms and therefore have additive analgesic effects, it is generally recommended that when opioids are required, they be added to NSAID therapy rather than replace it, unless indications for discontinuation of NSAIDs are present (such as gastropathy or hemorrhage) or they have provided no relief (APS, 1989).

Most cancer patients require the use of opioids at some stage in the disease process. Opioids should be used as aggressively as required to effectively manage pain. Scheduled doses of long‑acting oral opioids generally are recommended in order to provide stable blood levels for effective pain control. Additional doses of medication should be made available for intermittent treatment of incidental or activity‑related pain as required. The doses should be titrated to achieve the optimum effect.

Most increases in opioid dose requirements in individuals with cancer pain are thought to be related to advancing disease rather than to opioid tolerance. However, persons with a history of chronic opiate use may develop rapidly increasing dose requirements reflecting their tolerance to the analgesic effects of the medications.

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Table 6. Treatment of Cancer Pain: All Addicts

PROVIDE EFFECTIVE ANALGESIA BY ANY MEANS

NECESSARY

‑‑ Opioids;

‑‑ Non‑opioid analgesics;

‑‑ Physical treatments;

‑‑ Anesthesia techniques, neuro ablation.

IDENTIFY AND ADDRESS NON‑PAIN DISTRESSES

BE AWARE THAT ADDICTS MAY USE OPIOIDS TO

TREAT NON‑PAIN DISTRESSES (GRIEF, FEAR, RAGE,

ANXIETY, DEPRESSION)

‑‑ If this occurs, introduce more specific and

effective treatments.

ENCOURAGE RECOVERY‑RELATED ACTIVITIES FOR SUPPORT, ESPECIALLY IF ACTIVE IN THE PAST.

Because tolerance to side effects such as respiratory depression occur more rapidly than tolerance to the analgesic effects, these should not generally represent a limiting factor in achieving analgesia. However, persistent sedation or other central effects may be a problem in some patients, particularly when high doses are required. Constipation may be a persistent side‑effect and should be prospectively avoided through the prescription of both a bowel stimulant (because opioids decrease bowel motility) and a stool softener (because slowed motility dries the stool).

There is no ceiling to the analgesic effects of pure agonist opioids, so there is no highest possible dose. Pain usually can be managed with oral opioids. If oral agents are not feasible because of absorption problems or vomiting, parenteral treatment may be indicated (in which case, continuous infusions are preferred to intermittent dosing). An attempt to titrate infusion to therapeutic effect without sedation or other central effects should be made. PCA may be a helpful adjunct to a continuous infusion. IV access may be difficult in individuals with a history of IV drug dependence; for these patients, continuous subcutaneous infusions may be more feasible. Transcutaneous administration of fentanyl via patch also may be effective.

Cancer often is accompanied by significant distress such as fear, grief over impending losses, depression, anger and spiritual conflict. Because persons with addictive disorders have a tendency to use drugs to relieve distressing feelings, cancer patients with addictive disease may be more at risk than others to use therapeutically prescribed opioids in an attempt to relieve such distresses. Most physicians would have no issue with such use of opioids to relieve symptoms in the setting of cancerrelated pain, if they were effective. However, sometimes such use results in increased distress and greater experience of pain despite massive doses of opioids. Effective non‑pharmacologic and pharmacologic means of addressing these distresses are available and should be employed to provide relief. For individuals in recovery from chemical dependency, the recovery system may provide meaningful support (McCaffery & Vourakis, 1992).

Regional anesthetic techniques such as continuous intra‑spinal infusions may provide effective ongoing relief for many types of cancer pain (Cousins & Bridenbaugh, 1990). Neuroablative procedures such as celiac plexus block for pancreatic cancer pain or nerve root blocks for pain localized to a specific dermatome also may be helpful in difficult cancer pain situations, particular for individuals with limited life expectancy (Table 6).

Summary

Pain is a complex, highly individual experience that often has multiple components. The presence of addictive disease in a patient with pain must be considered in both the evaluation and treatment plan. The evaluation of pain must include careful identification of the nociceptive components of pain and of associated distresses such as sleep disturbance, anxiety, depression, alterations in usual roles and drug dependence. Successful treatment of pain in the addicted person must address each of the nociceptive components of pain, as well as distressing associated symptoms that may serve to perpetuate the pain.

Effective management of acute pain, chronic nonmalignant pain and cancer pain can be achieved in persons with addictive disease if both physician and patient recognize the presence of the addictive disease process and address the issues it raises. Clear and honest communication with the patient is important. Treatment of pain must address both its physical origins and associated distressing symptoms. The treatment plan must be specifically tailored to the type of pain and the nature and stage of the patient's addictive disease. A team approach that involves an addiction medicine specialist, a primary care physician and a pain medicine specialist often is valuable in successful treatment of pain in the patient with concurrent addictive disease.

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Basic Pain Concepts

Classes of Pain

Physical Mechanisms of Pain

Tools for the Management of Pain

Management of Acute Pain

Chronic Pain of Non‑Malignant Origin

Cancer Pain

Summary