COGNITIVE FACTORS

A person with any pain, but particularly unresolved or chronic pain, develops a set of beliefs to explain the pain experience, beliefs about the cause and onset of pain, the meaning of symptoms, ability to control pain and the impact of pain, now and in the future.⁵ Pain can be seen as a stressor that is appraised like any other stressor.

Appraisal involves a consideration of the threat the pain poses and the coping strategies available to cope with it. How the pain is appraised is influenced by the person’s beliefs and previous experiences and will impact on how the person deals with the pain, from ignoring it and maintaining usual activities to taking on the sick role. Beliefs have been found to be central to the functioning of the patient with pain (especially chronic pain), impacting on psychological and physical functioning, coping efforts, behavioural responses and responses to treatment.⁵ Self-efficacy is defined as the belief that one is capable of doing what is required in a particular situation. Self-efficacy appears to be important in the perception of pain, adjustment to it and level of disability.⁵ If you believe that your thoughts and behaviours can have a positive impact on your pain, then you are more likely to try a range of strategies to moderate the pain and to persevere in your efforts and have a sense of control. For example, those taking some control of analgesia and who are active rather than passive show less distress and disability.^5,19 If patients are less distressed they are likely to experience less physiological arousal and bodily tension, which act to exacerbate pain sensation.

AFFECTIVE FACTORS

Fear and anxiety are an inevitable and primary aspect of pain because pain signals danger requiring an immediate response. In chronic pain, in particular, fear and anxiety will be ongoing because the patient’s efforts at responding often have little effect.

Previous pain experiences impact on current pain episodes, influencing the intensity of pain and pain behaviours. Patients may:

Depression is commonly present in adult patients with chronic pain who present at pain clinics and can be caused by the disabling consequences of pain and its impact on quality of life.²² Anger may be associated with depression. Anger may be an outcome of severe frustration at the impact on quality of life or may be more specifically directed at failed treatments and healthcare professionals. Ongoing fear, depression and/or anger will interfere with the patient’s ability to engage with a range of pain therapies and these feelings should be addressed as part of the overall pain management regimen.^22,23

Attention and vigilance to pain are likely to occur when the threat of pain is ongoing. Heightened attention and hyper-vigilance to ongoing pain is, however, counterproductive as a long-term coping strategy. In addition, it is associated with high levels of disability and distress and lower pain thresholds, anxiety and poor concentration.^22,23 Catastrophic thinking about pain appears to be best understood as an extreme type of worrying about pain and is also seen as a manifestation of depression.²¹

BEHAVIOURAL FACTORS

What people believe and feel about their pain will impact on their behaviour. Intervening to change thoughts and feelings can help change behaviour in positive ways, improving the sense of wellbeing and decreasing pain and disability. Similarly, changing behaviour, for example by increasing activity, can have a positive impact on thoughts and feelings.^5,16

In addition to cognitive and affective influences on behaviour, learning mechanisms, such as operant conditioning, have been shown to have an impact on pain behaviour. Operant conditioning defines pain behaviour as behaviour like any other in that its manifestation, strength and frequency may come under the control of external stimuli, which may be rewarding or reinforcing—for example, attention from a partner or nurse. Escape from punishing or negative reinforcement, such as avoidance of some painful movements, will also maintain pain behaviour.

SOCIOCULTURAL FACTORS

In relation to gender, women are generally said to report more frequent and severe pain of longer duration than men.⁵ In New Zealand, the 2006/2007 National Health Survey found that men and women reported the same incidence of chronic pain, but when the data were adjusted for age, Māori men were found to have a significantly increased incidence of chronic pain compared to men in the total population. Pacific Islander women, Asian men and Asian women were significantly less likely to report chronic pain.³

Families and carers influence the patient’s response to pain through their beliefs and behaviours.²⁴ People learn behaviours appropriate to their culture by a process of socialisation. These behaviours include pain behaviours and some differences have been reported in the cultural expression, but not experience, of pain.²⁵ For example, in Australia, in one study Aboriginal patients were reported as having a higher pain threshold than non-Aboriginal patients²⁶ and to be less likely to complain of pain. The same study reported that men in particular did not complain as they did not want to appear weak. Many traditional Aboriginal people may be quiet and reserved when experiencing pain, and may be labelled by health professionals as not needing pain relief.²⁷ A study of Aboriginal women after surgery found that they had culturally appropriate ways of expressing and managing pain that were not well-understood by non-Aboriginal nurses.²⁸ It was reported that the Aboriginal women were generally silent about their pain, even when asked, and that, in part at least, this arose from fear of pain (including its origin and significance in relation to themselves and the external world).¹⁹ Many traditional Aboriginal people believe that nurses will know about the pain they are experiencing, so that there is no need to tell them.²⁸ Nurses need to realise that they may underestimate the pain of those who are from a culture different from their own and whose language is different.

Pain

HEALTH DISPARITIES

Some people cope with pain by distracting themselves, whereas others convince themselves that the pain is permanent, untreatable and overwhelming. Research has shown that people who believe that their pain in uncontrollable and overwhelming are more likely to have poorer clinical outcomes.^21,22

TRANSDUCTION

Transduction involves the conversion of a noxious mechanical, thermal or chemical stimulus into an electrical signal called an action potential. Noxious (tissue-damaging) stimuli, including thermal (e.g. sunburn), mechanical (e.g. surgical incision) and chemical stimuli (e.g. toxic substances), cause the release of numerous chemicals such as hydrogen ions, substance P and adenosine triphosphate (ATP) into the damaged tissues. Other chemicals are released from mast cells (e.g. serotonin, histamine, bradykinin and prostaglandins) and macrophages (e.g. bradykinin, interleukins and tumour necrosis factor [TNF]). These chemicals activate nociceptors, which are specialised receptors or free nerve endings that respond to painful stimuli. Activation of nociceptors results in an action potential that is carried from the nociceptors to the spinal cord, primarily via small, rapidly conducting, myelinated A-delta fibres and slowly conducting unmyelinated C fibres.

In addition to stimulating nociceptors to fire, inflammation and the subsequent release of chemical mediators promote lowered nociceptor thresholds. As a result, nociceptors may fire in response to stimuli that previously were insufficient to elicit a response; they may also fire in response to non-noxious stimuli, such as light touch. This increased susceptibility to nociceptor activation is called peripheral sensitisation. Cyclooxygenase (COX), an enzyme produced in the inflammatory response, plays an important role in peripheral sensitisation,²⁹ and leukotrienes, prostaglandins, cytokines and substance P are also involved in peripheral sensitisation. A clinical example of this process is sunburn. This thermal injury causes inflammation that results in a sensation of pain when the affected skin is touched lightly. Peripheral sensitisation also amplifies signal transmission, which in turn contributes to central sensitisation (discussed under dorsal horn processing later in the chapter).

The pain produced from activation of peripheral nociceptors is called nociceptive pain. There is a second source of pain-related action potentials arising from abnormal processing of stimuli by the nervous system. This kind of pain is called neuropathic pain. Both types of pain are described later in the chapter.

Therapies that alter either the local environment or the sensitivity of the peripheral nociceptors can prevent transduction and initiation of an action potential. Decreasing the effects of chemicals released at the periphery is the basis of several drug approaches to pain relief. For example, non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen and naproxen, and corticosteroids, such as dexamethasone, exert their analgesic effects by blocking pain-sensitising chemicals. NSAIDs block the action of COX, thereby interfering with the production of prostaglandins. Corticosteroids block the action of phospholipase, thereby reducing the production of both prostaglandins and leukotrienes (see Ch 12). Drugs that stabilise the neuronal membrane and inactivate peripheral sodium channels inhibit the production of the nerve impulse. These medications include local anaesthetics (e.g. injectable or topical lignocaine, bupivacaine and ropivacaine) and antiseizure drugs (e.g. carbamazepine and lamotrigine).

TRANSMISSION

Transmission is the process by which pain signals are relayed from the periphery to the spinal cord and then to the brain. The nerves that carry pain impulses from the periphery to the spinal cord are called primary afferent fibres and include A-delta fibres and C-fibres, each of which is responsible for a different pain sensation (see Fig 8-3). A-delta fibres are small, myelinated fibres that conduct pain rapidly and are responsible for the initial sharp pain that accompanies tissue injury. C-fibres are small, unmyelinated fibres that transmit painful stimuli more slowly and produce pain that is typically aching or throbbing in quality. Primary afferent fibres terminate in the dorsal horn of the spinal cord, which contains the cell bodies for afferent nerve fibres. Activity in the dorsal horn integrates and modulates pain inputs from the periphery. The propagation of pain impulses from the site of transduction to the brain is shown in Figure 8-2. Three segments are involved in nociceptive signal transmission: (1) transmission along the peripheral nerve fibres to the spinal cord; (2) dorsal horn processing; and (3) transmission to the thalamus and cerebral cortex.

Figure 8-3 Possible ascending and descending pathways of A-delta fibres and C-fibres from the dorsal horn in the spinal cord to the thalamus and other centres. These pathways are not definitive and may cross over.

Dorsal horn processing

Once a nociceptive signal arrives in the CNS, it is processed within the dorsal horn of the spinal cord. Neurotransmitters released from the afferent fibre bind to receptors on nearby cell bodies and dendrites of cells. Some of these neurotransmitters produce activation (e.g. glutamate, aspartate, substance P), whereas others inhibit activation of nearby cells (e.g. gamma-aminobutyric acid [GABA], serotonin, noradrenalin). In this area, exogenous and endogenous opioids also play an important role by binding to opioid receptors and blocking the release of neurotransmitters, particularly substance P. Endogenous opioids, which include encephalin and β-endorphin, are chemicals that are synthesised and secreted by the body. They are capable of producing analgesic effects similar to those of exogenous opioids such as morphine.

When enhanced excitability occurs in spinal neurons, it is termed central sensitisation. Peripheral tissue damage or nerve injury can cause central sensitisation, and continued nociceptive input from the periphery is necessary to maintain it. Central sensitisation plays a crucial role in the pathogenesis of chronic pain.¹³ It is defined by an increase in the excitability of neurons within the CNS, so that normal sensory inputs cause abnormal sensing and responses to painful and other stimuli. This explains why some people experience significant pain from touch or tactile stimulation in and around the areas of tissue or nerve injury. With central sensitisation, the central processing circuits are disrupted. Some aspects of central sensitisation can persist after peripheral inputs cease; however, peripheral and central neural mechanisms involved in causing central sensitisation can be long-lasting.³⁰

With ongoing stimulation of slowly conducting unmyelinated C-fibre nociceptors, firing of specialised dorsal horn neurons gradually increases. These inputs create many problems, including the sprouting of wide dynamic range (WDR) neurons and the induction of glutamate-dependent N-methyl-d-aspartate (NMDA) receptors. WDR neurons respond to both nociceptive and non-nociceptive inputs that are of varying levels of stimulus intensity. When sprouting of these neurons occurs, they grow into areas where pain-receiving nerve cell bodies are located. This results in the capacity to transmit a broader range of stimuli-producing signals, which are then passed up the spinal cord and brain. This process is known as ‘windup’ and is dependent on the activation of NMDA receptors. NMDA receptor antagonists, such as ketamine, are agents that can potentially interrupt or block mechanisms that lead to or sustain central sensitisation. Windup, like central sensitisation and hyperalgesia (increased pain responses to noxious stimuli), is induced by C-fibre inputs. Windup, however, is different as it can be short-lasting, whereas central sensitisation and hyperalgesia persist over time.³¹

It is important for nurses to appreciate that acute unrelieved pain can lead to chronic pain through the process of central sensitisation.^5,19 Acute tissue injury produces a cascade of events that involve the release of certain excitatory neurotransmitters (e.g. glutamate) and neuropsychological responses. Even brief intervals of acute pain are capable of inducing long-term neuronal remodelling and sensitisation (plasticity), chronic pain and lasting psychological distress. Neuroplasticity refers to an intricate group of processes that allow neurons in the brain to compensate for injury and adjust their responses to new situations or changes in their environment.³² Neuroplasticity contributes to adaptive mechanisms for reducing pain but also can result in maladaptive mechanisms that enhance pain. Genetic make-up and variability among individuals may play important roles in affecting the plasticity of the CNS.³³ Understanding this phenomenon helps to explain individual differences in responses to pain, and why some patients develop chronic pain conditions while others do not.

Clinically, central sensitisation of the dorsal horn results in: (1) hyperalgesia; (2) painful responses to normally innocuous stimuli (termed allodynia); (3) prolonged pain after the original noxious stimulus ends (called persistent pain); and (4) the extension of tenderness or increased pain sensitivity outside of an area of injury to include uninjured tissue (i.e. referred pain or secondary hyperalgesia).³⁴

Referred pain must be considered when interpreting the location of pain reported by the patient with injury to or disease involving visceral organs. The location of a tumour may be distant from the pain location reported by the patient (see Fig 8-4). For example, pain from liver disease is frequently located in the right upper abdominal quadrant, but can also be referred to the anterior and posterior neck region and to a posterior flank area. If referred pain is not considered when evaluating a pain location report, diagnostic tests and therapy could be misdirected.

Figure 8-4 Typical areas of referred pain.

PERCEPTION

Perception occurs when pain is recognised, defined and responded to by the individual experiencing the pain. In the brain, nociceptive input is perceived as pain. There is no single, precise location where pain perception occurs. Instead, pain perception involves several brain structures. For example, it is believed that the reticular activating system (RAS) is responsible for warning the individual to attend to the pain stimulus; the somatosensory system is responsible for the localisation and characterisation of pain; and the limbic system is responsible for the emotional and behavioural responses to pain. Cortical structures are also crucial to constructing the meaning of the pain. Therefore, behavioural strategies such as distraction and relaxation are effective pain-reducing therapies for many people. By directing attention away from the pain sensation, patients can reduce the sensory and affective components of pain. Opioids are one class of analgesic drugs that modify pain perception, and one mechanism of action is through their ability to activate descending pathway inhibition of pain. Other classes of analgesics such as some antiseizure drugs and antidepressants act in a similar manner.

MODULATION

Modulation involves the activation of descending pathways that exert inhibitory or facilitatory effects on the transmission of pain (see Fig 8-2). Depending on the type and degree of modulation, nociceptive stimuli may or may not be perceived as pain. Modulation of pain signals can occur at the level of the periphery, spinal cord, brainstem and cerebral cortex. Descending modulatory fibres release chemicals such as serotonin, noradrenalin, GABA and endogenous opioids that can inhibit pain transmission.

Several antidepressants exert their effects through the modulatory systems. For example, tricyclic antidepressants (e.g. amitriptyline) and serotonin noradrenalin reuptake inhibitors (SNRIs) (e.g. venlafaxine and duloxetine) are used in the management of chronic non-malignant and cancer pain. These agents interfere with the reuptake of serotonin and noradrenalin, thereby increasing their availability to inhibit noxious stimuli. Noradrenalin appears to play a greater role in centrally inhibiting pain than does serotonin, which explains why SNRIs have greater analgesic effects than selective serotonin reuptake inhibitors (SSRIs) (e.g. fluoxetine, paroxetine and sertraline).³⁵

NOCICEPTIVE PAIN

Nociceptive pain is caused by damage to somatic or visceral tissue. Somatic pain is often further categorised as superficial or deep. Superficial pain arises from skin, mucous membranes and subcutaneous tissues, and is often described as sharp, burning or prickly. Deep pain is often characterised as deep, aching or throbbing and originates in bone, joint, muscle, skin or connective tissue. Visceral pain comes from the activation of nociceptors in the internal organs and lining of the body cavities such as the thoracic and abdominal cavities. Visceral nociceptors respond to inflammation, stretching and ischaemia. Stretching of hollow viscera in the intestines and bladder that occurs from tumour involvement or obstruction can produce intense cramping pain. Examples of nociceptive pain include pain from a surgical incision, a broken bone, arthritis, pancreatitis and inflammatory bowel disease. Nociceptive pain is generally responsive to non-opioid medications, such as NSAIDs, as well as opioids.

NEUROPATHIC PAIN

Neuropathic pain is caused by damage to peripheral nerves or structures in the CNS. Typically described as numbing, hot-burning, shooting, stabbing, sharp or electric shock–like in nature, neuropathic pain can be sudden, intense, short-lived or lingering. Paroxysmal firing of injured nerves is responsible for shooting and electric shock–like sensations. Common causes of neuropathic pain include trauma, inflammation (e.g. secondary to a herniated disc inflaming the adjacent nerve and dorsal root ganglion), metabolic diseases (e.g. diabetes mellitus), alcoholism, infections of the nervous system (e.g. herpes zoster, human immunodeficiency virus), tumours, toxins and neurological diseases (e.g. multiple sclerosis).

Deafferentation pain results from loss of afferent input secondary to either the peripheral nerve injury or CNS disease. Sympathetically maintained pain is associated with dysregulation of the autonomic nervous system and central pain is caused by CNS lesions or dysfunction. Painful peripheral polyneuropathies (pain felt along the distribution of multiple peripheral nerves) and painful mononeuropathies (pain felt along the distribution of a damaged nerve) arise from damage to peripheral nerves and generate pain that may be described as burning, paroxysmal or shock-like. Examples of neuropathic pain include postherpetic neuralgia, phantom limb pain, diabetic neuropathies and trigeminal neuralgia.

One particularly debilitating type of neuropathic pain is complex regional pain syndrome (CRPS). Typical features include dramatic changes in the colour and temperature of the skin over the affected limb or body part, accompanied by intense burning pain, skin sensitivity, sweating and swelling. CRPS type I is frequently triggered by tissue injury; the term describes all patients with the above symptoms but with no underlying nerve injury. CRPS type II is associated with diverse sympathetic dysfunction.³⁵

Often, neuropathic pain is not well controlled by opioid analgesics alone. Treatment is typically augmented with adjuvant therapies including tricyclic antidepressants (e.g. amitriptyline, nortriptyline, desipramine), SNRIs (e.g. venlafaxine, duloxetine, bupropion), antiseizure drugs (e.g. gabapentin, pregabalin), and α₂-adrenergic agonists (e.g. clonidine). More recently, NMDA receptor antagonists such as ketamine have shown promise in alleviating neuropathic pain refractory to other drugs.³⁶

ACUTE AND CHRONIC PAIN

Acute pain and chronic pain are different as reflected in their cause, course, manifestations and treatment (see Table 8-3). Examples of acute pain include postoperative pain, labour pain, pain from trauma (e.g. lacerations, fractures, sprains), infection (e.g. dysuria from cystitis) and angina. For acute pain, treatment includes analgesics for symptom control and treatment of the underlying cause (e.g. splinting for a fracture, antibiotic therapy for an infection). Normally, acute pain diminishes over time as healing occurs. However, acute pain that persists can ultimately lead to disabling chronic pain states. For example, pain associated with herpes zoster (shingles) subsides as the acute infection resolves, usually within a month. However, sometimes the pain persists and develops into a chronic pain state called postherpetic neuralgia (PHN).

Chronic pain, or persistent pain, lasts for longer periods—often defined as longer than 3 months or past the time when an expected acute pain or acute injury should subside.⁵ The severity and functional impact of chronic pain is frequently disproportionate to objective findings. Whereas acute pain functions as a signal, warning the person of potential or actual tissue damage, chronic pain does not appear to have an adaptive role. Chronic pain can be disabling and is often accompanied by anxiety and depression. As previously discussed, untreated acute pain leads to chronic pain through central sensitisation and neuroplasticity. Consequently, it is imperative to treat acute pain aggressively and effectively to prevent chronic pain.

Chronic pain is strongly associated with markers of social disadvantage, such as lower levels of completed education, not having private health insurance, receiving a disability benefit or unemployment benefit and being unemployed for health reasons.⁵

ELEMENTS OF A PAIN ASSESSMENT

Most components of a pain assessment involve direct interview or observation of the patient. Diagnostic studies and physical examination findings complete the initial assessment. Although the assessment will differ according to the clinical setting, patient population and point of care (i.e. whether it is part of an initial assessment or a reassessment of pain following therapy), the evaluation of pain should always be multidimensional. The first assessment is the presence or absence of pain (see Fig 8-5, which shows an initial pain assessment tool).

Figure 8-5 Initial pain assessment tool. (May be duplicated for use in clinical practice.)

Source: McCaffery M, Pasero C. Pain: clinical manual. 2nd edn. St Louis: Mosby; 1999:60. Copyright © 1999, Mosby.

Before beginning any assessment, the nurse needs to recognise that patients may use words other than ‘pain’. For example, older adults may deny that they have pain but respond positively when asked if they have soreness or aching. The nurse should document the specific words that the patient uses to describe pain, then consistently ask the patient about pain using those words.

Pain intensity

Assessing the severity, or intensity, of pain provides a reliable measure to determine the type of treatment and its effectiveness. Pain scales help patients to communicate pain intensity. Scales must be adjusted to age and cognitive development. Most adults can rate the intensity of their pain using numeric scales (e.g. 0 = no pain, 10 = the worst pain) or verbal descriptor scales (e.g. none, a little, moderate, severe). These tools are sometimes easier for patients to use if they are oriented vertically or include a visual component. The pain thermometer scale is an example of this type of scale (see Fig 8-6).

Figure 8-6 Pain thermometer scale. The patient is asked to circle words next to the thermometer or to mark the area on the thermometer to indicate the intensity of pain.

Used with permission of Keela Herr, PhD, RN, AGSF, FAAN, The University of Iowa.

Although intensity is an important factor in determining analgesic approaches, it is essential not to dose patients with opioids solely based on reported pain scores. Opioid ‘dosing by numbers’ without taking into account a patient’s sedation level and respiratory status can lead to unsafe practices and serious adverse events. Safer analgesic administration can be achieved by balancing the patient’s pain with analgesic side effects. Adjustments in therapy can be made to promote better pain control and minimise adverse outcomes.

DOCUMENTATION

Documentation of the pain assessment is critical to ensure effective communication between team members and appropriate care planning and implementation. Many healthcare facilities and agencies have adopted specific tools to record the initial pain assessment, treatment and reassessment. There also are many multidimensional pain assessment tools. Fig 8-7 illustrates an assessment chart for patients postoperatively. Fig 8-8 illustrates the Abbey pain scale, which was developed for people with dementia who are unable to report their pain.³⁷

Figure 8-7 Pain indicator and assessment (PINDA) chart. C & B, coughing and breathing; IMI, intramuscular injection; IV, intravenous; NSAID, non-steroidal anti-inflammatory drug; OP site, operation site; PCA, patient-controlled analgesia; SaO₂%, saturation percentage; SC, subcutaneous; SOOB, sit out of bed; VAS, visual analogue scale.

Figure 8-8 The Abbey pain scale.

REASSESSMENT

It is critical that the nurse reassess the patient’s pain at appropriate intervals. For example, reassessment for a postoperative patient is done within 30 minutes of an intravenous (IV) dose of an analgesic. In a long-term care facility, residents with chronic pain are reassessed at least quarterly or with a change in condition or functional status. The frequency and scope of reassessment are guided by factors such as pain severity, physical and psychosocial condition, and institutional policy.

BASIC PRINCIPLES

All pain treatment plans are based on the following principles and practice standards:

DRUG THERAPY FOR PAIN

Pain medications are generally divided into three categories: non-opioids, opioids and adjuvant drugs. Treatment regimens may include medications from one or more of these groups. Mild pain may be relieved using non-opioids alone. Moderate to severe pain usually requires an opioid. Certain types of pain, such as neuropathic pain, often require adjuvant drug therapy alone or in combination with an opioid or another class of analgesics. Pain caused by specific medical conditions, such as cancer and rheumatoid arthritis, may be treated with curative or disease-modifying therapies (e.g. chemotherapy for cancer; TNF antagonists such as etanercept for rheumatoid arthritis), as well as pain medications.

Non-opioids

Non-opioid analgesics include paracetamol, aspirin and other salicylates, and NSAIDs (see Table 8-6). These agents are characterised by the following: (1) there is an analgesic ceiling to their analgesic properties—that is, increasing the dose beyond an upper limit provides no greater analgesia; (2) they do not produce tolerance or physical dependence; and (3) many are available without a prescription. It is important to monitor over-the-counter analgesic use to avoid serious problems related to drug interactions, side effects and overdose. Non-opioids are effective for mild to moderate pain. They are often used in conjunction with opioids because they allow for effective pain relief using lower opioid doses (thereby causing fewer opioid side effects); this phenomenon is called the opioid-sparing effect.

TABLE 8-6 Selected non-opioid analgesics and NSAIDS

DRUG THERAPY

GI, gastrointestinal; NSAIDS, non-steroidal anti-inflammatory drugs.

Aspirin is effective for mild pain but its use is limited by its common side effects, including increased risk for platelet dysfunction and bleeding, especially GI bleeding. Other salicylates such as choline magnesium trisalicylate cause fewer GI disturbances and bleeding abnormalities. Like aspirin, paracetamol has analgesic and antipyretic effects, but, unlike aspirin, it has no antiplatelet or anti-inflammatory effects. Although paracetamol is well tolerated, it is metabolised by the liver; chronic dosing greater than 4 g/day, acute overdose or use by patients with severe pre-existing liver disease may result in hepatotoxicity.

NSAIDs represent a broad class of drugs with varying efficacy and side effects. All NSAIDs inhibit COX, the enzyme that converts arachidonic acid into prostaglandins and related compounds. There are two forms of this enzyme: COX-1 and COX-2. COX-1 is found in almost all tissues and is responsible for several protective physiological functions. In contrast, COX-2 is produced mainly at the sites of tissue injury, where it mediates inflammation (see Fig 8-9). Inhibition of COX-1 causes many of the untoward effects of NSAIDs, such as impairment of renal function, bleeding tendencies, GI irritation and ulceration. Inhibition of COX-2 is associated with the therapeutic, anti-inflammatory effects of NSAIDs. Older NSAIDs, such as ibuprofen, inhibit both forms of COX and are referred to as non-selective NSAIDs. In the late 1990s, NSAIDs that selectively inhibit COX-2 were introduced. These medications, which include celecoxib, are called COX-2 inhibitors.

Figure 8-9 Arachidonic acid is oxidised by two different pathways: lipoxygenase and cyclooxygenase. The cyclooxygenase pathway leads to two forms of the enzyme cyclooxygenase: COX-1 and COX-2. COX-1 is known as ‘constitutive’ (always present) and COX-2 is known as ‘inducible’ (meaning its expression varies markedly depending on the stimulus). NSAIDs differ in their actions, with some having more effects on COX-1 and others more on COX-2. Indomethacin acts primarily on COX-1, whereas ibuprofen is equipotent on COX-1 and COX-2. Celecoxib primarily inhibits COX-2.

Some NSAIDs possess analgesic efficacy equal to that of aspirin, whereas others have better efficacy profiles. Patients vary greatly in their responses to a specific NSAID, so when one NSAID does not provide relief, another should be tried. NSAIDs are associated with many side effects, including GI problems ranging from dyspepsia to life-threatening ulceration and haemorrhage. Renal insufficiency and hypertension also occur. Serious side effects of NSAIDs result in thousands of hospitalisations every year.⁴⁰ Thus the use of NSAIDs should be limited in those at highest risk for adverse effects, including the elderly and patients with a history of peptic ulcer disease. If NSAIDs are used in patients at risk for GI bleeding, they should have concomitant therapy with a misoprostol or a proton pump inhibitor (PPI) such as omeprazole. NSAIDs should not be administered concurrently with aspirin, as the risk for bleeding and GI adverse events in increased.

When the COX-2 inhibitors were first introduced, they were thought to be much safer than non-selective NSAIDs, but ultimately two have been withdrawn from the market. There is an increased risk of cardiovascular events associated with both selective COX-2 inhibitors and non-selective NSAIDs⁴¹ and the prescribing practitioner needs to discuss the risks of taking these medications with the patient.

Opioids

Opioids produce their effects by binding to receptors in the CNS. This results in: (1) inhibition of the transmission of nociceptive input from the periphery to the spinal cord; (2) altered limbic system activity; and (3) activation of the descending inhibitory pathways that modulate transmission in the spinal cord. Thus opioids act on several nociceptive processes.

Types of opioids

Opioid analgesics (also known as narcotic analgesics) are a group of both synthetic and natural agonist drugs that have morphine-like properties and interact in the brain with specific opioid receptors (mu, kappa, delta) to lessen the sensation of pain.⁴¹ (Agonist drugs are site-specific drugs that trigger cellular activity; antagonist drugs act to block cellular activity.) Although nociceptive pain appears to be more responsive to opioids than neuropathic pain, opioids are used to treat both types of pain. Pure opioid agonists include morphine, oxycodone, hydrocodone, codeine, methadone and hydromorphone (see Table 8-7). These drugs are effective for moderate to severe pain because they are potent, have no analgesic ceiling and can be administered through several routes.

TABLE 8-7 Opioid analgesics

DRUG THERAPY

IV, intravenous.

* Neuraxial anaesthesia pertains to local anaesthetics placed around the nerves of the central nervous system such as spinal and epidural anaesthesia.

When opioids are prescribed for moderate pain, they are usually combined with a non-opioid analgesic such as paracetamol. Table 8-8 describes selected weak opioids and combination analgesics.

TABLE 8-8 Selected weak opioid and combination analgesics

DRUG THERAPY

Pethidine is a synthetic opioid that acts on mu receptors. It is commonly prescribed in Australia and New Zealand because the analgesic effects are good when used for postoperative pain and the adverse effects (e.g. constipation and urinary retention) are less than they are with other opioids.⁴¹ However, it is not recommended for use in the US as it has been associated with neurotoxicity (e.g. seizures) caused by accumulation of its metabolite, normeperidine.⁴²

Side effects of opioids

Common side effects of opioids include constipation, nausea and vomiting, sedation, respiratory depression and pruritus. With continued use, many side effects diminish, with the exception of constipation. Less common side effects include urinary retention, myoclonus, dizziness, confusion, delirium and hallucinations.

Constipation is the most common side effect. Because tolerance to opioid-induced constipation does not occur, a bowel regimen should be instituted at the beginning of opioid therapy and continued for as long as the patient takes opioids. Although dietary roughage, fluids and exercise should be encouraged to the extent possible, these measures alone may not be sufficient. Most patients should use a gentle stimulant laxative (e.g. senna) plus a stool softener (e.g. docusate sodium). Other agents (e.g. milk of magnesia, bisacodyl or lactulose) can be added if necessary.

Nausea is often a problem in opioid-naive patients (i.e. those who have never or rarely used opioids). The use of antiemetics such as metoclopramide, transdermal scopolamine or a phenothiazine (e.g. prochlorperazine) can prevent or minimise opioid-related nausea and vomiting until tolerance develops, which usually occurs within a week. Metoclopramide is particularly effective when the patient reports a feeling of gastric fullness. Opioids delay gastric emptying, and this effect can be reduced by metoclopramide. If nausea and vomiting are severe and persistent, changing to a different opioid may be necessary. In this case, a serotonergic (5HT₃) antagonist (e.g. ondansetron) may be used.

Concerns about sedation and respiratory depression are two of the most common fears associated with opioids. Sedation is usually seen in opioid-naive patients in the treatment of acute pain. Hospitalised patients receiving opioid analgesics for acute pain should be monitored regularly, especially in the first few days after surgery. Nurses need to be aware that for postoperative patients the risk for sedation is greatest within 4 hours after leaving the recovery unit. Opioid-induced sedation resolves with the development of tolerance. Persistent sedation with chronic opioid use can be effectively treated with psychostimulants such as caffeine, dextroamphetamine, methylphenidate or the anticataleptic drug modafinil.

The risk of respiratory depression is also higher in opioid-naive hospitalised patients who are treated for acute pain. Clinically significant respiratory depression is rare in opioid-tolerant patients and when opioids are titrated to analgesic effect.⁴³ Patients most at risk for respiratory depression include those who are elderly, have underlying lung disease or a history of sleep apnoea, or are receiving other CNS depressants (e.g. sedatives, benzodiazepines, antihistamines). For postoperative patients, the greatest risk for opioid-related respiratory adverse events is within the first 24 hours after surgery.⁴³ Clinically significant respiratory depression cannot occur in patients who are awake. Thus, the sedation level must be monitored in addition to the respiratory rate. A sedation scale can be used for monitoring (see Box 8-2). The patient should be roused and asked to take deep breaths.

BOX 8-2 Sedation assessment scale

N = Normal sleep

1 = Anxious, agitated or restless

2 = Calm, cooperative to tranquil (normal baseline without sedation)

3 = Quiet, drowsy, responds to verbal commands

4 = Asleep, brisk response to forehead tap or loud verbal stimuli

5 = Asleep, sluggish response to increasingly vigorous stimuli

6 = Unresponsive to painful stimuli

Moderate sedation = sedation score of 4

Source: Pain care facts. Available at http://prc.coh.org/pdf/Resp%20Dep-FF%2012-08.pdf, accessed 9 April 2011.

SAFETY ALERT

• If the respirations fall below 8 breaths per minute and the sedation level is 5 or greater, the patient should be stimulated vigorously and if possible kept awake.

• If the patient becomes over-sedated, oxygen should be administered.

• The dose of opioid should be reviewed and decreased.

For patients who are excessively sedated or unresponsive, naloxone (an opioid antagonist that rapidly reverses the effects of opioids) can be administered. Naloxone can be given intravenously or subcutaneously every 2 minutes. If the patient has been taking opioids regularly for more than a few days, naloxone should be used judiciously and titrated carefully because it can precipitate severe, agonising pain, profound withdrawal symptoms and seizures. Naloxone’s half-life is shorter than that of most opiates, so the patient’s respiratory rate should be monitored, because it can drop again 1–2 hours after naloxone administration.

Pruritus (itching) occurs most frequently when opioids are administered via neuraxial (i.e. epidural, intrathecal) routes. Management of opioid-induced pruritus typically involves low-dose infusions of naloxone, mixed agonist-antagonists (e.g. nalbuphine) or a 5HT₃ antagonist such as ondansetron.⁴⁴

A rare but concerning problem with long-term and even short-term use of opioids is the development of opioid-induced hyperalgesia (OIH). OIH is a state of nociceptive sensitisation caused by exposure to opioids. It is characterised by a paradoxical response in which patients actually become more sensitive to certain painful stimuli and report increased pain with opioid use. The exact mechanism for this phenomenon is not clearly understood, but it is believed to be related to neuroplastic changes that lead to sensitisation of pronociceptive pathways.⁴⁵ This may explain why opioids tend to lose their effectiveness in certain patients over time.

Adjuvant analgesic therapy

These medications comprise classes of drugs that can be used alone or in conjunction with opioid and non-opioid analgesics. Generally, these agents were developed for other purposes (e.g. antiseizure drugs, antidepressants) and found later to be effective for pain. Commonly used analgesic adjuvants are listed in Table 8-9.

TABLE 8-9 Adjuvant drugs used for pain management

DRUG THERAPY

Corticosteroids

These drugs, which include dexamethasone, prednisone and methylprednisolone, are used for management of acute and chronic cancer pain, pain secondary to spinal cord compression and inflammatory joint pain syndromes. Mechanisms of action are unknown but may be due to the ability of corticosteroids to decrease oedema and inflammation. They also may decrease activation of an inflamed neuron. Because of this effect, corticosteroids are useful when injected epidurally for acute or subacute disc herniations. Corticosteroids have many side effects, especially when given chronically in high doses. Adverse effects include hyperglycaemia, fluid retention, dyspepsia and GI bleeding, impaired healing, muscle wasting, osteoporosis, adrenal suppression and susceptibility to infection. Because they act through the same final pathway as NSAIDs, corticosteroids should not be given at the same time as NSAIDs.

Antidepressants

Tricyclic antidepressants (TCAs) enhance the descending inhibitory system by preventing the cellular reuptake of serotonin and noradrenalin. Higher levels of serotonin and noradrenalin in the synaptic cleft inhibit the transmission of nociceptive signals in the CNS. Other potential beneficial actions of TCAs include sodium channel modulation, α₁-adrenergic antagonist effects and a weak NMDA receptor modulation. They appear to be effective for a variety of pain syndromes, especially neuropathic pain syndromes. However, side effects such as sedation, dry mouth, blurred vision and weight gain limit their usefulness. Antidepressants that selectively inhibit reuptake of serotonin and noradrenalin (SSRIs and SNRIs) are effective for many neuropathic pain syndromes and have a better side effect profile than the TCAs. These agents include venlafaxine, duloxetine and bupropion.⁴⁶

Antiseizure drugs

Antiseizure drugs affect both peripheral nerves and the CNS in several ways, including sodium channel modulation, central calcium channel modulation and changes in excitatory amino acids and other receptors. Agents such as gabapentin, lamotrigine and pregabalin are valuable adjuvant agents in chronic pain therapy and are being increasingly used in the treatment of acute pain.

GABA receptor agonists

Baclofen, an analogue of the inhibitory neurotransmitter GABA, can interfere with the transmission of nociceptive impulses and is mainly used for muscle spasms. It crosses the blood–brain barrier poorly and is much more effective for spasticity when delivered intrathecally.

α₂-adrenergic agonists

Currently, clonidine is the most widely used α₂-adrenergic agonist. α₂-adrenergic agonists are thought to work on the central inhibitory α-adrenergic receptors and may also decrease noradrenalin release peripherally. They are used for chronic headache and neuropathic pain.

Local anaesthetics

For acute pain from surgery or trauma, local anaesthetics such as bupivacaine and ropivacaine can be administered epidurally by continuous infusion, and also by intermittent or continuous infusion with regional nerve blocks. Topical applications of local anaesthetics are used to interrupt transmission of pain signals to the brain.

Mixed mu agonist opioid and NE/5HT reuptake inhibitors

Some analgesics have two distinct actions, or dual mechanisms. Tramadol is a weak mu agonist and also inhibits the reuptake of noradrenalin and serotonin. It is effective in low back pain, osteoarthritis, diabetic peripheral neuropathic pain, polyneuropathy and post-herpetic neuralgia. The most common side effects are similar to those of other opioids, including nausea, constipation, dizziness and sedation. As with other medications that increase serotonin and noradrenalin, this agent should be avoided in patients with a history of seizures because it lowers seizure threshold.

Tapentadol is the newest dual-mechanism agent. It is available by restricted prescription in Australia and New Zealand for treatment of chronic disabling pain that does not respond to other analgesics. It acts via mu opioid receptors and also by inhibition of serotonin and noradrenalin reuptake. In clinical trials, tapentadol showed comparable pain relief to oxycodone for surgical pain and has been shown to be effective for non-surgical joint and back pain.⁴⁷ The side effects are similar to conventional opioids, except that it is associated with less nausea and constipation.

Cannabinoids

Cannabinoid-derived medications have been approved for use in Canada, the UK, the US and New Zealand, but are not currently approved by the Therapeutic Goods Administration (TGA) for therapeutic use in Australia. Cannabinoid-derived medications show promise in the treatment of certain pain syndromes and symptoms, but these preparations have sparked considerable controversy, prejudice and confusion, mostly because cannabinoids have some relationship to the cannabis plant—also known as marijuana. Smoking marijuana or cannabis rapidly increases plasma levels of tetrahydrocannabinol (THC), but the amount is highly dependent on the composition of the marijuana cigarette and inhalation technique, so this form of use is associated with highly variable results in relief of pain and symptoms.⁴⁸ With commercially available oral preparations, the absorption and bioavailability are much more reliable and predictable.

Cannabinoids exert their analgesic effects primarily mediated through the cannabinoid-l (CB1) receptor in nociceptive areas in the periphery and CNS. CB1 stimulation modulates neurotransmission in the serotoninergic, dopaminergic and glutamatergic systems, as well as other systems. It is also believed that cannabinoids enhance the endogenous opioid system. Other beneficial effects include alleviation of nausea and increased appetite. Cannabinoids may also have opioid-sparing effects, possibly reduce opioid tolerance and even ameliorate symptoms of opioid withdrawal.⁴⁹

Administration

Scheduling

Appropriate analgesic scheduling focuses on prevention or control of pain, rather than the provision of analgesics after the patient’s pain has become severe. A patient should be premedicated before painful procedures and activities that are expected to produce pain. Similarly, a patient with constant pain should receive analgesics around the clock rather than on an ‘as needed’ (prn) basis. These strategies control pain before it starts and usually result in lower analgesic requirements. Fast-acting drugs should be used for incident or breakthrough pain, whereas long-acting analgesics are more effective for constant pain. Examples of fast-acting and sustained-release analgesics are described later in this section.

Titration

Analgesic titration is dose adjustment based on assessment of the adequacy of analgesic effect versus the side effects produced. There is wide variability in the amount of analgesic needed to manage pain, and titration is an important strategy in addressing this variability. An analgesic can be titrated upwards or downwards, depending on the situation. For example, in a postoperative patient the dose of analgesic generally decreases over time as the acute pain resolves. On the other hand, opioids for chronic, severe cancer pain may be titrated upwards many times over the course of therapy to maintain adequate pain control. The goal of titration is to use the smallest dose of analgesic that provides effective pain control with the fewest side effects.

Equianalgesic dosing

The term equianalgesic dose refers to a dose of one analgesic that is equivalent in pain-relieving effects to another analgesic. This equivalence permits substitution of analgesics in the event that a particular drug is ineffective or causes intolerable side effects. Generally, equianalgesic doses are provided for opioids and are important because there is no upper dosage limit for many of these drugs. Equianalgesic charts and conversion programs are widely available in pharmacology textbooks, clinical guidelines, healthcare facility pain protocols and on the internet. They are useful tools, but healthcare providers need to understand their limitations. Equianalgesic dosages are estimates, and some are based on small, single-dose studies on healthy volunteers.⁵⁰ Differences exist among various published charts. For these reasons, all changes in opioid therapy must be monitored carefully and adjusted for the individual patient. When possible, healthcare providers should use equianalgesic conversions that have been approved for their facility or clinic and, if concerned, should consult an expert in pain control or a pharmacist before making changes.

Administration routes

Opioids and other analgesic agents can be delivered via many routes. This flexibility allows the healthcare provider to: (1) target a particular anatomical source of the pain; (2) achieve therapeutic blood levels rapidly when necessary; (3) avoid certain side effects through localised administration; and (4) provide analgesia when patients are unable to swallow. The following discussion highlights the uses and nursing considerations for analgesic agents delivered through a variety of routes.

Oral route

Generally, oral administration is the route of choice for the patient with a functioning GI system. Most pain medications are available in oral preparations, such as liquid and tablet formulations. For opioids, larger oral doses are needed to achieve the equivalent analgesia as doses administered intramuscularly (IM) or intravenously. For example, 10 mg of parenteral morphine is equivalent to approximately 30 mg of oral morphine.⁵⁰ The reason larger doses are required is related to the first-pass effect of hepatic metabolism. This means that oral opioids are absorbed from the GI tract into the portal circulation and shunted to the liver. Partial metabolism in the liver occurs before the drug enters the systemic circulation and becomes available to peripheral receptors or can cross the blood–brain barrier and access CNS opioid receptors, which is necessary to produce analgesia. Oral opioids are as effective as parenteral opioids if the dose administered is large enough to compensate for the first-pass metabolism.

Many opioids are available in short-acting (immediate-release) and long-acting (sustained-release) oral preparations. Immediate-release products are effective in providing rapid, short-term pain relief. Sustained-release preparations generally are administered every 8–12 hours. As with other sustained-release preparations, these products should not be crushed, broken or chewed.

Sublingual and buccal routes

Opioids can be administered under the tongue or held in the mouth and absorbed into the systemic circulation, which exempts them from the first-pass effect. Although morphine is commonly administered to patients with cancer pain via the sublingual route, little of the drug is actually absorbed from the sublingual tissue. Instead, most of the drug is dissolved in saliva and swallowed, making its metabolism the same as that of oral morphine.

Fentanyl citrate is administered transmucosally. The fentanyl dose is embedded in a flavoured lozenge on a stick. The drug is absorbed by the permeable buccal mucosa after being rubbed actively over it (not sucked as a lollipop), allowing the drug to enter the bloodstream and travel directly to the CNS. Pain relief typically occurs within 5–7 minutes after administration. This agent should be used only for patients who are already receiving and who are tolerant to opioid therapy.

An oromucosal spray delivery of cannabinoid extract (Sativex) shows promise in treating chronic, neuropathic pain conditions. It has been approved in Canada for the treatment of pain in multiple sclerosis.

Intranasal route

Intranasal administration allows delivery of medication to highly vascular mucosa and avoids the first-pass effect. Butorphanol is one of the few intranasal analgesics currently available. This drug is indicated for acute headache and other intense, recurrent types of pain. Intranasal delivery of other opioids is being investigated.

Rectal route

The rectal route is often overlooked but is particularly useful when the patient cannot take an analgesic by mouth, such as those patients with severe nausea and vomiting. Analgesics that are available as rectal suppositories include hydromorphone, oxymorphone, morphine and paracetamol. If rectal preparations are not available, many oral formulations can be given rectally if the patient is unable to take medications by mouth.

Transdermal route

Fentanyl is available as a transdermal patch system for application to non-hairy skin. This delivery system is useful for the patient who cannot tolerate oral analgesic drugs. Absorption from the patch is slow and it takes 12–17 hours to reach full effect with the first application. Therefore, transdermal fentanyl is not suitable for rapid dose titration, but it can be effective if the patient’s pain is stable and the dose required to control it is known. Patches may need to be changed every 48 hours rather than the recommended 72 hours based on individual patient responses. Rashes caused by the patch adhesive may be reduced by preparing the skin 1 hour before placement with a weak corticosteroid cream. Bio-occlusive dressings are available if the patch keeps falling off because of excessive sweating.

DRUG ALERT—fentanyl patches

• Fentanyl patches may cause death from overdose.

• Signs of overdose include trouble breathing or shallow respirations; tiredness, extreme sleepiness or sedation; inability to think, talk or walk normally; and feeling faint, dizzy or confused.

Transdermal medications are also available over-the-counter. Creams and lotions containing capsaicin available in Australia and New Zealand include Zostrix, which is available in two strengths: capsaicin 0.025%w/w topical cream and capsaicin 0.075%w/w topical cream. Derived from red chilli pepper, capsaicin acts on the vanilloid heat receptors of the C-fibres. If used regularly three or four times a day for 4–6 weeks, it will cause the C-fibres to become inactive because of excessive calcium entering the nerve cell. The result is neuronal resistance to painful stimuli. Capsaicin can control pain associated with post-herpetic neuralgia, diabetic neuropathy and arthritis.

Parenteral routes

The parenteral route includes subcutaneous, intramuscular and intravenous administration. Single, repeated or continuous dosing (subcutaneous or IV) is possible via parenteral routes. Although it is frequently used, the IM route is not recommended because injections cause significant pain, result in unreliable absorption and, with chronic use, can result in abscesses and fibrosis. Onset of analgesia following subcutaneous administration is slow and thus the subcutaneous route is rarely used for acute pain management. However, continuous subcutaneous infusions are effective for pain management at the end of life. This route is especially helpful for people with abnormal GI function and limited venous access. IV administration is the best route when immediate analgesia and rapid titration are necessary. Continuous IV infusions provide excellent steady state analgesia through stable blood levels.

Intraspinal delivery

Intraspinal (epidural or intrathecal) opioid therapy involves inserting a catheter into the subarachnoid space (intrathecal delivery) or the epidural space (epidural delivery) (see Fig 8-10). Analgesics are injected by either intermittent bolus doses or continuous infusion.

Figure 8-10 Spinal anatomy. The spinal cord extends from the foramen magnum to the first or second lumbar vertebral space. The subarachnoid space (intrathecal space) is filled with cerebrospinal fluid that continually circulates and bathes the spinal cord. The epidural space is a potential space filled with blood vessels, fat and a network of nerve extensions.

Percutaneously placed temporary catheters are used for short-term therapy (2–4 days) and surgically implanted catheters are used for long-term therapy. Although the lumbar region is the most common site of placement, epidural catheters may be placed at any point along the spinal column (cervical, thoracic, lumbar or caudal). The tip of the epidural catheter is placed as close to the nerve supplying the painful dermatome as possible. For example, a thoracic catheter is placed for upper abdominal surgery and a high lumbar catheter is used for lower abdominal surgery. Fluoroscopy is used to ensure correct placement of the catheter.

Intraspinally administered analgesics are highly potent because they are delivered close to the receptors in the spinal cord dorsal horn. Thus much smaller doses of analgesics are needed when compared with other routes, including IV. For example, 1 mg of intrathecal morphine is approximately equivalent to 10 mg of epidural morphine, 100 mg of IV morphine and 300 mg of oral morphine. Drugs that are delivered intraspinally include morphine, fentanyl, hydromorphone, ziconotide (a calcium channel receptor modulator for use in neuropathic pain syndromes) and clonidine. Nausea, itching and urinary retention are common side effects of intraspinal opioids.

Complications of intraspinal analgesia include catheter displacement and migration, accidental infusions of neurotoxic agents, and infection. Clinical manifestations of catheter displacement or migration depend on catheter location and the drug being infused. A catheter that migrates out of the intrathecal or epidural space will cause a decrease in pain relief with no improvement, even with additional boluses or increases in the infusion rate. If an epidural catheter migrates into the subarachnoid space, an increase in side effects will become quickly apparent. Somnolence, confusion and an increased anaesthesia (if the infusate contains an anaesthetic) occur. Correct placement of an intrathecal catheter can be checked by aspirating cerebrospinal fluid (CSF). Migration of a catheter into a blood vessel may cause an increase in side effects because of systemic drug distribution.

Many drugs and chemicals are highly neurotoxic when administered intraspinally. These include many preservatives such as alcohol and phenol, antibiotics, chemotherapy agents, potassium and parenteral nutrition. To avoid inadvertent injection of IV drugs into an intraspinal catheter, the catheter should be clearly marked as an intraspinal access device, and only preservative-free drugs should be injected.

Infection is a rare but serious complication of intraspinal analgesia. The skin around the exit site should be assessed carefully for inflammation, drainage or pain. Signs and symptoms of an intraspinal infection include diffuse back pain, pain or paraesthesia during bolus injection, and unexplained sensory or motor deficits in the lower limbs. Fever may or may not be present. Acute bacterial infection (meningitis) is manifested by photophobia, neck stiffness, fever, headache and altered mental status (see Ch 56). Infection is avoided by providing regular, meticulous wound care and using sterile technique when caring for the catheter and injecting drugs.

Long-term epidural catheters may be placed for terminal cancer patients or patients with certain pain syndromes that are unresponsive to other treatments. If a long-term indwelling epidural catheter is used, double bacterial filters are recommended. Because the highest infective risk occurs when the medication bags are changed, the concentration and volume in the infusing bag should be optimised to reduce the number of bag changes.

Implantable pumps

Intraspinal catheters can be surgically implanted for long-term pain relief. The surgical placement of an intrathecal catheter to a subcutaneously placed pump and reservoir allows for the delivery of drugs directly into the intrathecal space. The pump, which is normally placed in a pocket made in the subcutaneous tissue of the abdomen, may be programmable or fixed. Changes are made by either reprogramming the pump or changing the mixture or concentration of drug in the reservoir. The pump is refilled every 30–90 days depending on flow rate, mixture and reservoir size.

Patient-controlled analgesia

A specific type of IV delivery system is patient-controlled analgesia (PCA), or demand analgesia. It can also be connected to an epidural catheter (patient-controlled epidural analgesia [PCEA]). With PCA, a dose of opioid is delivered when the patient decides a dose is needed. PCA uses an infusion system in which the patient pushes a button to receive a bolus infusion of an analgesic. PCA is used widely for the management of acute pain, including postoperative pain and cancer pain.

Opioids such as morphine and hydromorphone are commonly administered for IV PCA therapy for both acute and chronic pain management. Fentanyl is used less often for acute pain. Sometimes IV PCA is administered with a continuous or background infusion called a basal rate depending on the patient’s opioid requirement. For acute pain (e.g. postoperative pain), basal rates are not recommended when initiating therapy in opioid-naive patients. The addition of a basal rate does not improve pain control, reduce the number of demand doses or improve sleep. Furthermore, the addition of a basal rate in opioid-naive patients and those at risk for adverse respiratory outcomes (e.g. patients who are older, who have obstructive sleep apnoea or existing pulmonary disease) may lead to serious respiratory events.¹⁹

Use of PCA begins with patient teaching. The nurse should help the patient to understand the mechanics of getting a drug dose and how to titrate the drug to achieve good pain relief. The patient should be taught to self-administer the analgesic before pain intensity is greater than the patient’s desired pain intensity goal. Patients should be assured that they cannot ‘overdose’ because the pump is programmed to deliver a maximum number of doses per hour. The dose of medication is ordered to achieve what is known as a therapeutic window—that is, the ideal plasma concentration needed to achieve effective pain relief (see Fig 8-11). Pressing the button after the maximum dose is administered will not result in additional analgesic. If the maximum dose is inadequate to relieve pain, the pump can be reprogrammed to increase the amount or frequency of dosing. In addition, bolus doses can be given if they are ordered. To make a smooth transition from infusion PCA to oral drugs, the patient should receive increasing doses of oral drug as the PCA analgesic is tapered.

Figure 8-11 Therapeutic window for morphine. PCA, patient-controlled analgesia.

Interventional therapy

Therapeutic nerve blocks

Nerve blocks generally involve one-time or continuous infusion of local anaesthetics into a particular area to produce pain relief. These techniques are also called regional anaesthesia. Nerve blocks interrupt all afferent and efferent transmission to the area and thus are not specific to nociceptive pathways. They include local infiltration of anaesthetics into a surgical area (e.g. chest incisions, inguinal hernia, joints) and injection of anaesthetic into a specific nerve (e.g. occipital or pudendal nerve) or nerve plexus (e.g. brachial or coeliac plexus). Nerve blocks can be used during and after surgery to manage pain. For longer-term relief of chronic pain syndromes, local anaesthetics can be administered via a continuous infusion.

The adverse effects of nerve blocks are similar to those for local anaesthetics delivered via other systemic routes and include arrhythmias, confusion, nausea and vomiting, blurred vision, tinnitus and metallic taste. Temporary nerve blocks affect both motor function and sensation and typically last 2–24 hours depending on the agent and site of injection. Motor ability generally returns before sensation.⁵¹

Neuroablative techniques

Neuroablative interventions are performed for severe pain that is unresponsive to all other therapies. Neuroablative techniques destroy nerves, thereby interrupting pain transmission. Destruction is accomplished by surgical resection or thermocoagulation, including radiofrequency coagulation. Neuroablative interventions that destroy the sensory division of a peripheral or spinal nerve are classified as neurectomies, rhizotomies and sympathectomies. Neurosurgical procedures that ablate the lateral spinothalamic tract are classified as cordotomies if the tract is interrupted in the spinal cord, or tractotomies if the interruption is in the medulla or the midbrain of the brainstem. Figure 8-12 identifies the sites of neurosurgical procedures for pain relief. Both cordotomy and tractotomy can be performed with the aid of local anaesthesia by a percutaneous technique under fluoroscopy.

Figure 8-12 Sites of neurosurgical procedures for pain relief.

Neuroaugmentation

Neuroaugmentation involves electrical stimulation of the brain and the spinal cord. Spinal cord stimulation is performed much more often than deep brain stimulation. Recent advances have allowed the use of multiple leads and multiple electrode terminals to stimulate large areas. The most common use of spinal cord stimulation is for chronic back pain secondary to nerve damage that is unresponsive to other therapies. Other uses include complex regional pain syndrome, spinal cord injury pain and interstitial cystitis. Potential complications include those related to the surgery (bleeding and infection), migration of the generator (which is usually implanted in the subcutaneous tissues of the upper gluteal or pectoralis area) and nerve damage.⁵²

Non-drug therapies for pain

Non-drug strategies play a critical role in pain management (see Table 8-10). They can reduce the dose of an analgesic required to relieve pain and thereby minimise side effects of drug therapy. Moreover, they can increase the patient’s sense of personal control about managing pain and bolster coping skills. Some strategies are believed to alter ascending nociceptive input or stimulate descending pain modulation mechanisms. Some non-drug therapies are used independently by patients as self-management strategies. They are especially important in the treatment of chronic pain.⁵³

TABLE 8-10 Non-drug therapies for pain

Physical pain relief strategies

Massage

Massage is a common therapy for pain. There is good evidence to support the use of massage for acute and chronic pain.⁵⁴ Many different massage techniques exist, including moving the hands or fingers over the skin slowly or briskly with long strokes or in circles (superficial massage) or applying firm pressure to the skin to maintain contact while massaging the underlying tissues (deep massage). Another example is trigger point massage. A trigger point is a circumscribed hypersensitive area within a tight band of muscle. It is caused by acute or chronic muscle strain and can often be felt as a tight knot under the skin. Trigger point massage is performed by applying strong sustained digital pressure, deep massage or gentle massage with ice followed by muscle heating. (Massage is discussed in Ch 7.)

Exercise

Exercise is a critical part of the treatment plan for patients with chronic pain, particularly those with musculoskeletal pain. Research supports the effectiveness of many types of exercise for a variety of painful conditions.^55,56 Many patients become physically deconditioned as a result of their pain, which in turn leads to more pain. Exercise acts via many mechanisms to relieve pain. It enhances circulation and cardiovascular fitness, reduces oedema, increases muscle strength and flexibility, and enhances physical and psychosocial functioning. An exercise program should be tailored to the physical needs and lifestyle of the patient and should include aerobic exercise, stretching and strengthening exercises. The program should be supervised by trained personnel (e.g. exercise physiologist, physiotherapist). Examples of exercise programs include yoga, Tai Chi and water aerobics.

Transcutaneous electrical nerve stimulation

Transcutaneous electrical nerve stimulation (TENS) involves the delivery of an electric current through electrodes applied to the skin surface over the painful region, at trigger points or over a peripheral nerve. A TENS system consists of two or more electrodes connected by lead wires to a small battery-operated stimulator (see Fig 8-13). Initially, a physiotherapist may be responsible for administering TENS therapy, although nurses can be trained in the technique. TENS may be used for acute pain, including postoperative pain and pain associated with physical trauma.⁵⁷ The effects of TENS on chronic pain are less clear but the procedure may be effective for some chronic pain patients.⁵⁸

Figure 8-13 Initial TENS treatment being given by a physiotherapist to assess value in pain relief.

Acupuncture

Acupuncture is a technique of traditional Chinese medicine in which very thin needles are inserted into the body at designated points. Acupuncture is used for many different kinds of pain. (Acupuncture is discussed in Ch 7.)

Heat therapy

Heat therapy is the application of moist or dry heat to the skin. Heat therapy can be either superficial or deep. Superficial heat can be applied using an electric heating pad (dry or moist), a hot pack, hot moist compresses, warm wax (paraffin) or a hot water bottle. For exposure to large areas of the body, patients can immerse themselves in a hot bath, shower or whirlpool. Physiotherapy departments provide deep-heat therapy through such techniques as short-wave diathermy, microwave diathermy and ultrasound therapy. Patient teaching regarding heat therapy is outlined in Box 8-3.

BOX 8-3 Heat and cold therapy

PATIENT & FAMILY TEACHING GUIDE

Include the following instructions when teaching the patient and/or family about superficial heat techniques.

• Do not use heat on an area that is being treated with radiation therapy, is bleeding, has decreased sensation or has been injured in the past 24 hours.

• Do not use any menthol-containing products (e.g. Dencorub, Vicks, Icy Hot) with heat applications because this may cause burns.

• Cover the heat source with a towel or cloth before applying to the skin to prevent burns.

Include the following instructions when teaching the patient and/or family about superficial cold techniques.

• Cover the cold source with a cloth or towel before applying to the skin to prevent tissue damage.

• Do not apply cold to areas that are being treated with radiation therapy, have open wounds or have poor circulation.

• If it is not possible to apply the cold directly to the painful site, try applying it just above or below the painful site or on the opposite side of the body on the corresponding site (e.g. left elbow if the right elbow hurts).

Cold therapy

Cold therapy involves the application of either moist or dry cold to the skin. Dry cold can be applied by means of an ice pack, moist cold by means of towels soaked in ice water, cold hydrocollator packs or immersion in a bath or under running cold water. Icing with ice cubes or blocks of ice made to resemble ice blocks is another technique used for pain relief. Cold therapy is believed to be more effective than heat for a variety of painful conditions, including acute pain from trauma or surgery, acute flare-ups of arthritis, muscle spasms and headache. Patient teaching regarding cold therapy is described in Box 8-3.

Cognitive therapies

Techniques to alter the affective, cognitive and behavioural components of pain include a variety of cognitive strategies and behavioural approaches. Some of these techniques require little training and are often adopted independently by the patient. For others, a trained therapist is necessary.⁵

Distraction

Distraction involves redirecting attention away from the pain and onto something else. It is a simple but powerful strategy to relieve pain. Distraction can be achieved by engaging the patient in any activity that can hold their attention (e.g. watching TV or a movie, conversing, listening to music, playing a game). It is important to match the activity with the patient’s energy level and ability to concentrate.

Hypnosis

Hypnotherapy is a structured technique that enables the patient to achieve a state of heightened awareness and focused concentration that can be used to alter the patient’s pain perception. Hypnosis should be administered and monitored only by specially trained clinicians.⁵⁹

Relaxation strategies

Relaxation strategies are varied, but their goal is to reach a state that is free from anxiety and muscle tension. Relaxation reduces stress, decreases acute anxiety, distracts from pain, alleviates muscle tension, combats fatigue, facilitates sleep and enhances the effectiveness of other pain relief measures.³⁴ Relaxation strategies include relaxation breathing, music, imagery, meditation and progressive muscle relaxation.

NURSING AND COLLABORATIVE MANAGEMENT: PAIN

Nurses are important members of the multidisciplinary pain management team. Nursing roles include planner, educator, patient advocate, interpreter and supporter of the patient and carer. Because patients in any care setting can experience pain, nurses need to be knowledgeable about current therapies and flexible in trying new approaches to pain management. Many nursing roles have been described earlier, including pain assessment, administering therapies, monitoring for side effects, and teaching patients and carers. However, the success of these actions depends on the nurse’s ability to establish a trusting relationship with the patient and carer and to address their concerns about pain and its treatment.

Barriers to effective pain management

Pain is a complex, subjective experience and its management is influenced greatly by psychosocial, sociocultural and legal-ethical factors. These factors include the emotions, behaviours, beliefs and attitudes of patients and carers about pain and the use of pain therapies. Achieving effective pain management requires careful consideration of these factors. Common barriers are tolerance, dependence and addiction. Patients, carers and healthcare providers often share these concerns. It is important for nurses to understand and to be able to explain the differences among these various concepts.

Tolerance

Tolerance occurs with prolonged exposure to a variety of drugs. In the case of opioids, tolerance is characterised by the need for an increased opioid dose to maintain the same degree of analgesia. The incidence of clinically significant opioid tolerance in chronic pain patients is unknown, since dosage needs may also increase as a disease such as cancer progresses. Although tolerance is not as common as once thought, it is essential to assess for increased analgesic needs in patients on long-term therapy. The healthcare team needs to evaluate and rule out other causes of increased analgesic needs, such as disease progression or infection. If significant tolerance to opioids develops and it is believed that an opioid is losing its effectiveness, or if there are intolerable side effects associated with escalation of doses, the practice of opioid rotation may be considered.⁶⁰ This involves switching from one opioid to another, assuming that the new opioid will be more effective at lower equianalgesic doses. As previously discussed, very high opioid doses can result in hyperalgesia rather than pain relief. Thus further increase in the dose can lead to higher pain levels.

Physical dependence

Like tolerance, physical dependence is an expected physiological response to ongoing exposure to drugs (this is not the same as addiction, which is described below). It is manifested by a withdrawal syndrome that occurs when blood levels of the drug are abruptly decreased. Symptoms of opioid withdrawal are listed in Table 8-11. When opioids are no longer needed to provide pain relief, a tapering schedule should be used in conjunction with careful monitoring. A typical tapering schedule begins with calculating the 24-hour dose used by the patient and dividing by 2. Of this decreased amount, 25% is given every 6 hours. After 2 days, the daily dose is reduced by an additional 25% every 2 days until the 24-hour oral dose is 30 mg (morphine equivalent) per day. After 2 days on this minimum dose, the opioid is then discontinued.

TABLE 8-11 Symptoms of withdrawal syndrome from short-acting opioids

Addiction

Addiction is a complex neurobiological condition characterised by aberrant behaviours arising from a drive to obtain and take substances for reasons other than the prescribed therapeutic value (see Ch 10). Tolerance and physical dependence are not indicators of addiction. Rather, they are normal physiological responses to chronic exposure to certain drugs, including opioids.

The risk of developing addiction is associated with certain factors, including younger age, personal or family history of substance abuse, and mood disorders. The risk of addiction, however, should not prevent clinicians from using opioids to treat moderate to severe acute and chronic pain. Several professional organisations and government agencies have issued joint statements about the roles and responsibilities of healthcare professionals in the appropriate use of opioids in the treatment of pain.⁶¹

Assessing and treating pain in people with current or a history of drug and alcohol abuse is challenging, particularly when therapy involves medications that may themselves be abused (e.g. opioids). However, these individuals have the right to receive effective pain management. A comprehensive pain assessment is imperative, including a detailed history, physical examination, psychosocial assessment and diagnostic assessment to determine the cause of the pain. Screening tools are available to assess risk for substance abuse and to evaluate abnormal behaviours in patients with chronic pain.⁶²

Opioids may be used effectively and safely in patients with substance dependence when indicated for pain control. Withholding opioids from chemically dependent patients with pain has not been shown to increase the likelihood of recovery from addiction. Opioid agonists-antagonists (e.g. pentazocine, butorphanol) should not be used in this patient group because they may precipitate withdrawal. The use of ‘potentiators’ and psychoactive drugs that do not have analgesic properties should be avoided. In individuals who are tolerant to CNS depressants, larger doses of opioids or increased frequency of drug administration is necessary to achieve pain relief.

Pain management for people with addiction is challenging and requires a multidisciplinary team approach. When possible, the team should include pain management and addiction specialists. Team members need to be aware of their own attitudes and misconceptions about people with substance abuse problems, which may result in undertreatment of pain.

In addition to the fears about addiction, physical dependence and tolerance, other barriers hinder effective pain management. Table 8-12 lists these and other barriers and includes strategies to address the barriers.

TABLE 8-12 Reducing barriers to pain management

PATIENT & FAMILY TEACHING GUIDE

NSAIDs, non-steroidal anti-inflammatory drugs.

Source: Adapted from Ersek M. Enhancing effective pain management by addressing patient barriers to analgesic use. J Hospice Palliat Nurs 1999; 1:87.

FEAR OF HASTENING DEATH BY ADMINISTERING ANALGESICS

A common concern of healthcare professionals and carers is that providing sufficient drugs to relieve pain will precipitate the death of a terminally ill person. Despite the fear, however, there is no scientific evidence that opioids can hasten death, even among patients at the very end of life. Moreover, nurses have a moral obligation to provide comfort and pain relief at the end of life. Even if there is a concern about the possibility of hastening death, the rule of double effect provides ethical justification. This rule states that if an unwanted consequence (i.e. hastened death) occurs as a result of an action taken to achieve a moral good (i.e. pain relief), the action is justified if the nurse’s intent is to relieve pain and not to hasten death.⁶³

REQUESTS FOR EUTHANASIA

Unrelieved pain is one of the reasons that patients make requests for euthanasia (assisted suicide). In some states in the US and in the Netherlands, Belgium and Switzerland, euthanasia is legal. However, it is currently illegal in New Zealand and Australia. The Death with Dignity Bill 2003 was introduced into the New Zealand Parliament on 6 March 2003. The Bill’s purpose was to provide terminally and/or incurably ill people with the opportunity of requesting assistance from a medically qualified person to end their lives, but the Bill was defeated on 30 July 2003. Voluntary euthanasia was legal in the Northern Territory from 1996 to 1997, and since then several legislative attempts have been made to legalise euthanasia in parts of Australia. However, at present it remains unlawful. Euthanasia has been the subject of much moral, religious, philosophical, legal and human rights debate in both Australia and New Zealand. At the core of this debate is how to reconcile competing values: the desire of individuals to choose to die with dignity when suffering, and the need to uphold the inherent right to life of every person. Currently it is believed that aggressive and adequate pain management will solve the needs of people who are suffering. Euthanasia is a complex issue that extends beyond pain and pain management and the scope of this chapter. Nurses need to be aware of the laws that surround this issue.

USE OF PLACEBOS IN PAIN ASSESSMENT AND TREATMENT

Although their use has declined, placebos are sometimes still used to assess and to treat pain. Using a placebo involves deceiving patients by making them believe that they are receiving an analgesic (usually an opioid) when in fact they are typically receiving an inert substance such as saline. The use of placebos to assess or treat pain is condemned by several professional organisations.⁶⁴