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Dealing with pain 

Dealing with pain
Chapter:
Dealing with pain
Author(s):

Henry McQuay

DOI:
10.1093/med/9780199204854.003.03001

May 31, 2012: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.

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Essentials

Pain is complex—it is too simple to view pain transmission as a hard-wired, line-labelled system, because that cannot explain complexities such as phantom limb pain. The crucial mechanistic distinction for clinical practice is between normal (nociceptive) and nerve damage (neuropathic) pain.

Types of analgesics—conventional analgesics, from paracetamol through to morphine, work well in nociceptive pain and less well in neuropathic pain. Unconventional analgesics, antidepressants, and antiepileptic drugs work well in neuropathic and less well in nociceptive pain.

Treating pain—most pains are dynamic rather than static, hence patients need to be able to deal with mild through to severe pain. In both nociceptive and neuropathic pain a three-stage algorithm provides a framework for both patient and prescriber. For nociceptive pain: (1) mild pain—paracetamol (acetaminophen); (2) moderate pain—add (not substitute) weak opioid or non-steroidal anti-inflammatory drug; (3) severe pain—add (not substitute) strong opioid. For neuropathic pain: (1) mild pain—antidepressant; (2) moderate pain—add (not substitute) antiepileptic, e.g. gabapentin, pregabalin; (3) severe pain—add (not substitute) opioid.

Difficult pain—patients with complex pains, or with pain and complex needs, may need multidisciplinary approaches to untangle their pain, disability, and distress: tackling the elements singly is unlikely to succeed. There is no convincing evidence of the analgesic effectiveness of complementary approaches, but it is important to acknowledge that these interventions may make people feel better, although they rarely obviate the need for effective analgesia.

Pain sensation and transmission

The easiest way to think of pain in the nervous system is the idea of pain receptors and nerve cables dedicated to the transmission of pain signals; a hard-wired, line-labelled system. For most acute pain and chronic nociceptive pain, this simple idea works well. ‘Nociceptive’ here means pain caused by trauma as opposed to neuropathic pain that arises from nerve damage. The concept of specific cables whose transmission can be blocked is reinforced by everyday observations, e.g. the ability to perform surgery painlessly by using a local anaesthetic block. But the inadequacy of this simple explanation is exposed in chronic pain, particularly associated with nervous system damage. The return of pain after an initially successful cordotomy and the phenomenon of phantom limb pain are two examples. In a hard-wired, line-labelled system, the pain should not recur after the cordotomy and amputees should not feel pain in the absent foot or hand because the receptors and the cables are no longer there. The ability of the nervous system to rewire, known as plasticity, is recognized in the return of pain after destructive procedures, and the concept of ‘pain memory’ in the spinal cord and brain has to be invoked to explain phantom pain. Such phenomena mean that the simple view of a hard-wired, line-labelled system does not explain all kinds of pain.

Many treatments or interventions are used to treat both acute and chronic pain. Chronic pain, not surprisingly, is more convoluted, because its origins may be more complicated and because the nervous system can behave strangely if damaged or bombarded continuously by pain messages. The concept of plasticity has led to the adoption of some interventions and the rejection of others. Long-term destructive measures, such as cutting the nerves thought to carry a particular pain message, are going out of fashion. The reasoning is that the nervous system will ‘rewire’, the pain will re-emerge, and may well be more difficult to manage than it was in the first place. Better drug control of difficult pains has also reduced the necessity for destructive procedures.

Pain signals can be amplified or dampened by endogenous influences such as mood or endorphins, or exogenous factors such as drugs given or the circumstances of the injury. The classic damping-down scenario is the injured soldier who continues to get himself out of battle, despite a shattered leg. Conversely, a stubbed toe when you are tired and miserable is immeasurably more painful than the same injury on a cheerful morning. In chronic pain, it is sometimes very hard to disentangle depression from pain. Pain makes depression worse and depression makes pain worse. This pattern is all too familiar to those who manage pain. The thinking clinician needs to deal with both the pain and the depression. In chronic pain, distress and disability may also amplify the pain, and good pain relief will not improve disability. Expectations need to be realistic.

Pain is necessarily subjective. It is what one human being reports to another. There may be few objective signs to judge the severity of reported pain, and many patients have no visibly obvious handicap. The most important principle is that the patient and the doctor are best served if the doctor believes the patient’s report. Their problems may be ill understood, even disbelieved, at work and at home. Chronic pain changes people, affecting their personal and working lives, and ultimately their personalities. Often, such changes are reversible with successful treatment. Much time and energy is wasted on procedures designed to ‘catch the patient out’. Labelling patients as malingerers or the pain as psychogenic may be easier than admitting that there is no successful treatment.

Pain mechanisms and pain syndromes

Sacrificing precision for the sake of clarity, we can distinguish by mechanism two broad types of pain (Table 30.1.1). The distinction here is between normal or nociceptive pain and nerve damage or neuropathic pain. The importance of the distinction is that successful drug treatment of these two types requires different classes of drugs.

Table 30.1.1 Pain syndromes and mechanisms

1. Nociceptive

2. Neuropathic

3. Visceral

Combined

a. Peripheral

b. Central

Acute

  • Postoperative

  • Burns

  • ‘Sprains and strains’

  • ‘Stone’ pain

  • ulcer

  • Intermittent/

  • Incidental

  • Headache

  • Migraine

  • Osteoarthritis

Trigeminal

  • Dysmenorrhea

  • Endometriosis

  • Pelvic

  • IBS

  • Dyspepsia

Cancer (1, 2, 3)

Chronic

Rheumatoid arthritis

PHN

Spinal cord injury

Pelvic

Cancer (1, 2, 3)

Osteoarthritis

Diabetic mono/poly neuropathy

Central post stroke

LBP with radiculopathy (1, 2a)

  • FM

  • Myofascial (e.g. neck–shoulder)

  • Low back pain

Nerve trauma

  • Multiple sclerosis

  • Parkinson’s disease

Whiplash (1, 2a)

FM, Fibromyalgia; IBS, irritable bowel syndrome; LBP, low back pain; PHN, postherpetic neuralgia.

Conventional analgesics, from aspirin through to morphine, work well in nociceptive pain but not so well in neuropathic pain. Unconventional analgesics, antidepressants, or antiepileptics work well in neuropathic pain and not so well in nociceptive pain.

The incidences of each of the classic neuropathic pain conditions, postherpetic neuralgia, painful diabetic neuropathy, and trigeminal neuralgia (Table 30.1.1) is about 30 per 100 000 person-years observation. Neuropathic pain resulting from surgery and neuropathic pain as a consequence of back problems are very much commoner.

Further mechanistic subdivisions are possible, e.g. ‘inflammatory pain’ or ‘visceral pain’ are categories often used by scientists working on pain mechanisms, but pragmatically the same remedies work in these groupings as work in nociceptive pain generally, and the neuropathic remedies do not. Most difficult are the pain syndromes which are not clearly either nociceptive or neuropathic, but which undoubtedly impair function. Examples in this dysfunctional grouping include migraine, fibromyalgia, and irritable bowel syndrome. Migraine can be helped by the conventional analgesics used in nociceptive pain and it may respond to the triptans, which do not work in nociceptive pain, and can be prevented by antiepileptic drug prophylaxis. This crossover is apparent too in the effective treatment of fibromyalgia and irritable bowel syndrome with the unconventional analgesic classes of drugs.

Implicit in this scheme is the important distinction between acute, chronic, and ‘acute on chronic’ timing. Most pains wax and wane, and treatment needs to be sufficiently flexible to deal with both moderate and severe fluctuations. Most patients need a regime to deal with their baseline pain and a regime to deal with a flare of pain.

Pain histories

Asking whether sensation is normal in the painful area and whether the pain is shooting or stabbing in character may help to identify the pains variously known as dysaesthetic, deafferentational, or neuropathic. The distinction is important, because response to conventional analgesics is unlikely. These pains often have little pattern, but are less troublesome when the patient is distracted. Pain may be spontaneous or evoked in response to a normally nonpainful stimulus (allodynia) or it may be exaggerated in response to a marginally painful stimulus.

It is important to enquire specifically about the efficacy of each particular class of drug. This information prevents the inept prescription of drugs which have failed previously, and may give important clues to the kind of pain and its sensitivity to different classes of drugs.

It is also important to know the dose size, frequency, duration of prescription, and the side-effect problems for each drug that has been prescribed. Dose–response relationships apply with analgesics, and therapeutic failure should not be presumed if the dosage was inadequate. A good example is the use of carbamazepine in trigeminal neuralgia. The question we ask ourselves is, ‘Has this patient had an adequate trial of this drug?’, meaning has the dose been increased to the point of unmanageable or intolerable adverse effects without or precluding benefit. Is the patient taking drugs other than analgesics? Anticoagulation, for instance, is not only a virtually absolute contraindication to pain management by injection procedures, but also contraindicates most anti-inflammatory drugs.

It is important to be sure whether nerve blocks used previously were technically effective (e.g. did the patient have any numbness after an epidural which included local anaesthetic?), before dismissing them as being useless for this patient. Other measures, such as transcutaneous nerve stimulation (TENS), may not have been used correctly, and may succeed if the patient receives proper instruction in their use.

Recording pain

In cases of chronic pain, when patients record pain over long periods, we tend to use diaries with word categories, and ask about both pain intensity (none, mild, moderate, or severe) and pain relief (none, slight, moderate, good, or complete). Another useful scale is the patient’s ‘global report’. Using the same categories as the pain relief scale, this is a composite view encompassing both pain itself and any adverse effects of treatment. The clinician’s ‘global view’ is notoriously unreliable and should not be used.

Most important and simplest is the idea of including a binary scale because of its clinical relevance. The question is phrased in various forms, around the idea: ‘Is your pain at least 50% relieved?’, to which the patient answers yes or no.

The argument for using pain charts as part of normal practice is to improve the quality of care. It is the fact of a chart rather than its form that is the more important. These should be completed, together with vital signs, and can then be used for both clinical care and for audit.

Some index of function is necessary as a baseline so that improvement or deterioration may be monitored. Useful clinical outcome measures are notoriously difficult, but simple pain charts and indices of activity can work well, using the patient’s definition of impaired activity such as walking or gardening.

Treating pain

Drugs are the mainstay of treating both normal (nociceptive) and neuropathic pain. The menu of remedies also includes stimulation devices, from trans-cutaneous through to implanted stimulators, cognitive–behavioural therapy (pain programmes), complementary techniques, and invasive methods from injection through to surgery designed to block transmission of the pain message (Fig. 30.1.1).

Fig. 30.1.1 Treatment options for acute and chronic pain.

Fig. 30.1.1
Treatment options for acute and chronic pain.

Treating normal (nociceptive) pain

The basic algorithm for treating nociceptive pain, acute, chronic, or acute on chronic, is shown in Fig. 30.1.2, derived from the pain ‘ladder’ which is widely used in palliative care (see Section 31). This ladder was formulated originally in the 1980s under the aegis of the World Health Organization (WHO). In its raw form, it captured the treatment care pathway for pain by representing increasing strengths of analgesia as further steps or rungs up the ladder. At the bottom rung, or step 1, is a nonopioid analgesic, usually paracetamol (acetaminophen); at step 2, a nonsteroidal anti-inflammatory drug (NSAID) or a combination of minor opioid with paracetamol; and, at step 3, addition of a strong opioid, morphine by mouth or injection. This simple pathway has had enormous global impact in palliative care, even though the drugs that are available vary in different countries.

Fig. 30.1.2 Algorithm for analgesics in nociceptive pain.

Fig. 30.1.2
Algorithm for analgesics in nociceptive pain.

This algorithm is equally applicable and useful outside palliative care, e.g. in primary care and in postoperative pain. In acute pain, perioperative or traumatic, one is working right to left (in terms of Fig. 30.1.2) as pain decreases. In chronic pain, the patient needs to use the three strengths of analgesic as the pain increases or decreases, the ‘three pot’ system. The basic algorithm is thus the same across the different pain intensities, making teaching and implementation more effective, but the choice of particular drugs will vary locally with availability.

The visual presentation of the ladder differs from the original WHO palliative care ladder in two main ways. The first is that the analogy is with building blocks rather than with rungs on a ladder. What we wanted to convey visually was the principle of ‘add rather than replace’, by which we meant that if the pain becomes more severe you add a stronger analgesic to your other analgesics, adding rather than replacing. We believe that ‘add rather than replace’ is easier to understand using the building block analogy compared to rungs on a ladder, because one rarely stands simultaneously on multiple rungs on a ladder.

The second main difference is the inversion of the diagram. The basic building block (step 1) is at the top of the picture. This is different from the original WHO palliative care ladder, where the step 1 drug was at the bottom, to emphasize the ‘add not replace’ concept, because putting the step 1 drugs at the bottom of the algorithm makes it more likely that they will be overlooked and omitted in the management of moderate or severe pain.

Fleshing out the detail of the drugs and the route of administration for each of the drug choices for each section of the algorithm in each of the pain intensities, keeping as much in common as possible, will vary with available drug choice and clinical situation. Both choice of particular drug and dose might differ; e.g. lower starting doses might be used in older people. Some of the detail will rightly be determined by local custom and practice, and where the detail on the pathway is at variance with local belief, even if in just one tiny detail, then the whole pathway loses credibility. A simple example for trauma pain is the issue of NSAIDs and bone healing. When staff have been taught or instructed not to use NSAIDs because they are said to impair bone healing, including NSAIDs on the pathway will not work. Although many may doubt that NSAIDs have significant clinical impact on bone healing, the detailed algorithm will need to be subject to this local variation to give it the local ownership that it needs if it is to be part of everyday clinical practice.

The step 2 drugs in the algorithm are the NSAIDs and the minor opioids, such as codeine. NSAIDs are powerful analgesics. Standard oral NSAID doses provide analgesia equivalent to that from intramuscular morphine 10 mg. However, the adverse effects of NSAIDs at therapeutic doses limit their utility, particularly for extended use in chronic pain. In those for whom NSAIDs are contraindicated and paracetamol (acetaminophen) is not sufficient, a minor opioid should be added to the paracetamol to improve analgesia.

The choice of strong opioid will vary according to local availability, custom, and practice. Morphine is the gold standard, orally in chronic pain or by injection in acute pain, but other formulations or alternative opioids are used. When swallowing or gastrointestinal function is impaired, for instance, routes other than oral, such as injected, sublingual, topical, nasal or inhaled may be necessary. In perioperative care, patients self-administer strong opioid via patient-controlled analgesia systems. Pressing the button delivers an injected dose.

In chronic pain, modified-release oral formulations are convenient for patients, allowing the greater part of the daily opioid requirement to be taken just twice a day, using a normal-release formulation to deal with flares of pain. Faster-acting nasal and inhaled formulations to give improved control of these flares, ‘breakthrough’ pain, are emerging.

These drug regimes may fail to control pain. It is estimated that in cancer pain 5 to 10% of patients need a different approach. Perhaps the most important change in the last 30 years is the realization that destructive invasive techniques rarely produce long-term benefit because the system eventually rewires, and the pain may be more difficult to manage than before. Reversible invasive techniques such as long-term epidural infusions using local anaesthetic, opioids, and other drugs such as clonidine can provide the necessary control, and can be withdrawn if the pain improves, without making the situation worse.

Treating nerve damage (neuropathic) pain

Peripheral neuropathic pain can rarely be managed adequately over the long term with the conventional analgesics described earlier. The dose–response for opioids is shifted to the right in neuropathic pain compared to nociceptive pain, and response is often minimal. Precisely why is still a mystery. In central neuropathic pain, e.g. with multiple sclerosis, opioids may be more effective.

The unconventional analgesics listed in the lower panel of Fig. 30.1.1 are antidepressants and antiepileptics. Both classes of drugs have proved effective in a wide variety of neuropathic pain syndromes, and also in fibromyalgia and irritable bowel, which fall outside the usual lists of causes of neuropathic pain. An algorithm for drug management of neuropathic pain, using an analogous format to that for nociceptive pain, is shown in Fig. 30.1.3.

Fig. 30.1.3 Algorithm for analgesics in neuropathic pain.

Fig. 30.1.3
Algorithm for analgesics in neuropathic pain.

The evidence suggests that antidepressants have better (lower) numbers needed to treat (NNT) than antiepileptic drugs in the classic test beds of postherpetic neuralgia and painful diabetic neuropathy. This conclusion may be biased by the older, successful and small crossover trials of tricyclic antidepressants, producing NNTs of 3 or less for at least 50% pain relief over 6 to 8 weeks. The more recent and larger parallel group trials of antiepileptic and newer antidepressant drugs yielded NNTs of between 4 and 5.

Placing antidepressants at step 1 in the algorithm reflects these lower NNTs. Tricyclics are usually given as a single night-time dose, 1 h before lights out. The differences between tricyclics used to treat pain rather than depression are that onset of effect is in days rather than weeks, the average effective dose is lower, and the analgesic effect is distinguishable from any mood effect. Titration to optimal dose, optimal balance between effect and adverse effect, can be managed by increasing the dose at weekly intervals, e.g. with 25-mg increments of amitriptyline. Continuing controversy exists over whether or not switching between different tricyclics to achieve a better balance is worthwhile, e.g. from amitriptyline to desipramine or nortriptyline; whether selective serotonin reuptake inhibitors are effective in these pain syndromes; and whether serotonin and noradrenaline (norepinephrine) reuptake inhibitors offer a better balance.

Gabapentin and pregabalin have become the first choice antiepileptic drugs, apart from carbamazepine in trigeminal neuralgia. Dosing is the same as in epilepsy. As with antidepressants, there is insufficient evidence about these drugs to allow certainty. Anecdote suggests that nonresponders may respond to antiepileptic drugs with a different mode of action, so that switching may be worthwhile.

There is evidence to support the use of both lidocaine (lignocaine) patches (in postherpetic neuralgia) and capsaicin. They may supplement antidepressant and antiepileptic analgesia. Oral steroids may be very effective, particularly in palliation of neuropathic pain from head and neck cancer. N-methyl-d-aspartate blockade with ketamine can also be useful to control severe neuropathic pain that is responding poorly to the algorithm. Regional blocks such as epidurals and spinals may be necessary to control really severe neuropathic pain. Clonidine given epidurally or intrathecally, usually with local anaesthetic and opioid, may usefully boost the analgesic effect.

Pain that is both nociceptive and neuropathic

The evidence for efficacy of complementary techniques is very poor. Perhaps the most important distinction is between remedies that make patients feel better, even if only for hours or days, and those that are effective in reducing pain. Studies of complementary techniques using pain outcomes show little sustained benefit, but may make people feel better. Similarly, the evidence for long-term efficacy of stimulation techniques is weak.

Cognitive behavioural therapy has proven benefit in helping patients to cope better with their pain.

Pains that resist treatment

Nothing so far in this chapter has acknowledged the awkward fact that there are many patients who complain of pain for which the diagnosis may never be made, or who fail to respond to any of the treatments described, or whose pain is part of a complicated mental health problem. More difficult still may be managing patients whose drug consumption seems extraordinarily high for the complaint, or indeed whose complaint is extraordinarily loud for the presenting problem. Another on the incomplete list is functional deficit that is greater than expected for the presenting problem.

Some humility is necessary, because each of us has been caught by the diagnosis missed, by the failure of our pattern recognition. That said, there are some constructive solutions. For these difficult pain problems, some form of multidisciplinary management can make a real difference.

The aim is for the patient to move from a distressed state, seeking a cure and bouncing round the health care system, to an acceptance that the best that can be done has been done. Unless a dramatic change occurs, a point will have been reached where all the possible tests have been done, and further treatments are likely to be fruitless. For this ‘acceptance’ conclusion to be reached there has to be a modicum of trust and reassurance. That point is much easier to achieve if and when the patient feels that they have been listened to and that all appropriate efforts have been made.

The ideal settings in which to reach this difficult goal are multidisciplinary assessment and multidisciplinary clinics. Assessment by an expert team may involve psychology, experienced nurses, physiotherapy, and occupational therapy, as well as the medical input. Such assessment may involve interacting with the patient over days and not just at a clinic appointment. The multidisciplinary clinic allows the patient to see the pain team with the specialist relevant to the complaint, so that a joint approach to further diagnostic efforts and to therapy, including a halt to both, can be achieved. Not all clinics need to be so grandiose; rather, the argument is for a ‘hub and spoke’ organization so that the patients with problematic pain unresolved at the spoke can be referred for the additional skill and experience at the hub.

In the end, not giving up on people and being accessible are important. Although an economic case can be made for the savings possible when patients do not have to rotate around the system to multiple clinics and multiple tests, the real yardstick is the quality of care.

Further reading

McMahon S, Koltzenburg M (eds.) (2006). Wall and Melzack’s textbook of pain, 5th edition. Elsevier, Philadelphia, PA.Find this resource:

    Moore A, et al. (2003). Bandolier’s little book of pain. Oxford University Press, Oxford.Find this resource:

      Twycross R, Wilcock A. (2007). Palliative care formulary, 3rd edition. http://palliativebooks.com.

      Urch CE, Dickenson AH (2008). Neuropathic pain in cancer. Eur J Cancer, 44, 1091–6.Find this resource:

      Wall P (1999). Pain: the science of suffering. Weidenfeld & Nicolson, London.Find this resource: