Pain Management: Basic Principles

Chapter: Pain Management: Basic Principles
McMaster Section Editor(s): Jenny Legassie
McMaster Author(s): Jenny Legassie, Denise Marshall
Additional Information


Pain is an unpleasant sensory and emotional experience that results from actual (eg, trauma) or potential tissue damage (eg, tissue ischemia). Pain can be purely nociceptive, purely neuropathic, or mixed.

Nociceptive pain is caused by active tissue damage. It can be visceral (cardiac ischemia, renal colic) or somatic (skin laceration, fractured bone).

Neuropathic pain is associated with nervous system disease (diabetic neuropathy) or damage (severed nerves after surgery, compression by tumor).

Myofascial pain is either localized in or referred to a muscle. Myofascial pain is characterized by the presence of trigger points (an area of the muscle that fails to relax, forming a hard spindle-shaped nodule or band that is tender on palpation). Myofascial pain is both nociceptive and neuropathic in nature.

Breakthrough pain (incident pain) refers to a sudden and transient exacerbation of pain that occurs in spite of adequate management of background pain. Breakthrough pain can be nociceptive or neuropathic in origin.


In patients with cancer causes of pain include:

1) Infiltration or compression of various tissues or organs by tumor.

2) Complications of cancer (eg, pathologic vertebral fractures due to skeletal metastases).

3) Cancer treatment (eg, radiation-induced plexopathy, postmastectomy pain syndrome, chemotherapy-induced neuropathy).

4) Non–cancer-related pain (eg, primary headache, angina).

Noncancer pain is caused by injury or compression of various tissues or organs. Mechanisms of this include external trauma, ischemia, or toxins (both external, such as chemical burns, and internal, such as neuropathy caused by uremia).


Principles of Pharmacotherapy

1. Use oral analgesics whenever possible, as this route of administration is the least invasive. If oral treatment is not possible (due to nausea, vomiting, dysphagia), subcutaneous or transdermal administration should be used. Transdermal absorption can be unpredictable in patients with edema or reduced peripheral blood flow (including those actively dying). Initiation of transdermal medications should be avoided in such situations. However, if patients are already receiving these medications at the end of life and find them effective, there is no need to stop this therapy. Subcutaneous injections, when appropriate for selected medication, are preferred over IV injections for patients at home and for those using long-term parenteral analgesics. Repeated IM injections are painful and offer no benefits over the subcutaneous or IV route.

2. Use analgesics in accordance with the World Health Organization (WHO) analgesic ladder (Figure 1.20-1). In patients with mild pain, start treatment with acetaminophen (INN paracetamol), nonsteroidal anti-inflammatory drugs (NSAIDs), and other nonopioid medications, unless contraindicated. If results are unsatisfactory, move up to the next step of the analgesic ladder. Patients with severe pain generally need an opioid regardless of the underlying mechanism of pain; there is no reason to start at the bottom step if pain is severe. On each step of the analgesic ladder coanalgesics and nonopioid medications improve analgesia, reduce opioid requirements, and inhibit the development of opioid tolerance.

3. In patients with ongoing pain analgesics should be administered on a regular basis (around the clock) at intervals adjusted to the pharmacokinetics of a specific agent. Regular dosing provides more consistent pain control than intermittent (as-needed) dosing.

4. Patients with ongoing pain should receive immediate-release breakthrough analgesics for incident pain. Incident or breakthrough pain is pain that occurs despite the regular administration of analgesics. Patients receiving analgesics on the around-the-clock basis should receive immediate-release doses of analgesics to relieve this pain. Patients with only incident pain may achieve good pain control with a breakthrough analgesic alone.

5. Controlled-release (long-acting) opioid formulations should be used only after stable dosing is achieved with immediate-release formulations. Controlled-release opioids provide analgesia with longer intervals between doses, allowing for patient convenience. They have a slower onset of action and cannot be titrated as fast as immediate-release formulations. Pain control may be poor for the first several hours or days of use of a long-acting opioid and the patient will require an immediate-release breakthrough medication. The full effect of a controlled-release medication can take several hours or days to be reached and toxicity can develop if the agent is titrated quickly. Controlled-release formulations should not be used in opioid-naive patients.

6. Always use lower starting doses in the elderly and those with renal or hepatic impairment. Opioid metabolism is slower in the elderly, increasing the risk of adverse events and toxicity. Most opioids and their metabolites are excreted by the kidneys (hydromorphone and fentanyl are notable exceptions), requiring lower doses in patients with renal failure. Patients with significant hepatic impairment are particularly sensitive to neurologic adverse effects of opioids.

Nonopioid Analgesics

1. Acetaminophen has a rapid onset (15-30 minutes) and short duration of action (up to 4-6 hours). The maximum daily dose in adults (>12 years) who are not at increased risk of hepatotoxicity is 3 to 4 g/24 h. Doses ≤2.6 g/d are recommended in the elderly and even lower doses are recommended in those with liver disease or alcohol abuse.

2. NSAIDs, with analgesic and anti-inflammatory properties, have the most potent analgesic effect in bone pain, myofascial pain, and pain caused by inflammation. The onset and duration of action varies by formulation and includes ibuprofen with a rapid onset (15-30 minutes) and short duration (4-6 hours) and celecoxib with a slower onset (3 hours) and long duration (14 hours). Before using NSAIDs, the risk of cardiovascular, gastrointestinal, and renal adverse effects must be evaluated. Use of selective cyclooxygenase-2 (COX-2) inhibitors, proton pump inhibitors (PPIs), or both will reduce (but not eliminate) the risks of gastrointestinal bleeding. There is no evidence that COX-2 inhibitors have a reduced renal or cardiac risk compared with nonselective COX inhibitors.

Weak Opioid Analgesics

The provided trade (brand) names are valid for Canada.

Weak opioids are so named not because they are inherently less effective than other opioids. At equianalgesic doses, they are just as effective as stronger opioids, such as fentanyl or morphine. Rather, they are called weak opioids because they are commonly combined with other medications that limit the maximum daily dose. When used alone (without the dose-limiting presence of another drug), weak opioids could be considered strong opioids. The distinction between weak and strong opioids is thus, to a certain degree, arbitrary.

1. Codeine: Start immediate-release oral codeine 15 mg to 30 mg every 4 to 6 hours. If necessary, titrate the dose up to a maximum of 240 mg/d. Immediate-release and controlled-release formulations are available. Immediate-release formulations contain codeine alone or combined with acetaminophen (marketed as Tylenol with codeine) or acetylsalicylic acid (previously available as 222’s), limiting the maximum daily dose. Oral formulations are the only formulations available in Canada. Codeine should not be used in moderate or severe renal failure, as metabolites accumulate, causing sedation and altered level of consciousness.

2. Dihydrocodeine (not available in Canada): Start from 60 mg orally every 12 hours. If necessary, titrate the dose up to 120 mg every 12 hours. Dihydrocodeine is a synthetic opioid. Immediate-release formulations are available as dihydrocodeine alone or combined with acetaminophen, aspirin, ibuprofen, antihistamines, or decongestants, limiting the maximum daily dose.

3. Oxycodone: Start from 5 mg every 4 hours. Titrate the dose to achieve an adequate analgesic effect. Immediate-release and controlled-release formulations are available. Immediate-release formulations contain oxycodone alone (in which case it should be considered a strong opioid) or combined with acetaminophen (marketed as Percocet), limiting the maximum daily dose. Oral formulations only in Canada. Oxycodone is available in combination with naloxone (in Canada marketed as Targin), which helps to minimize the adverse effect of constipation.

4. Tramadol: The usual starting dose is 25 to 50 mg every 4 hours in an immediate-release oral formulation. Titrate the dose as needed at a rate no faster than 25 mg every 3 days up to a maximum of 400 mg/d. Tramadol works through opioid receptors and serotonin receptors. Nausea and vomiting are common at the beginning of treatment. Immediate-release and controlled-release formulations are available. Immediate-release formulations contain tramadol alone or combined with acetaminophen (marketed as Tramacet), limiting the maximum daily dose. Oral formulations are the only formulations available in Canada. Caution and lower initial doses are needed in the elderly and in those with renal or hepatic failure. Do not use in patients with poorly controlled seizure disorders. Tramadol is associated with serotonin syndrome.

Strong Opioid Analgesics

At equianalgesic doses, weak and strong opioids have the same level of effect. Some weak opioids are actually more potent than certain strong opioids. Examples of drug conversions: Table 1.20-1, Table 1.20-2.

1. Morphine: Start from 5 to 10 mg orally every 4 hours. Titrate the dose to achieve adequate analgesia or based on adverse effects. Immediate-release and controlled-release formulations are available. Oral, rectal, subcutaneous, and IV formulations in Canada (conversion between routes of administration: Table 1.20-1, Table 1.20-2). Morphine and its active metabolites are excreted by the kidneys. Not advised in patients with renal failure.

2. Hydromorphone: Start from 0.5 mg to 1 mg orally every 4 hours. Titrate the dose to achieve adequate analgesia or based on adverse effect. Immediate-release and controlled-release formulations are available. Oral, subcutaneous, and IV formulations in Canada (conversion between routes of administration: Table 1.20-1, Table 1.20-2). Hydromorphone is a semisynthetic (morphine-based) opioid. Patients with a true allergy to morphine should try a different fully synthetic opiate where there is no known cross-reactivity. Hydromorphone has relatively inert metabolites that are excreted by the kidneys. It can be safely used in patients with renal failure.

3. Buprenorphine: An intermediate-acting opioid available in Canada in transdermal form only. Buccal and sublingual formulations are available outside of Canada. Dosing is based on prior exposure to opioids. Buprenorphine can be used in opioid-naive patients at low doses with caution. Conversion from other opioids: Table 1.20-1. All routine dosing of alternative opioids should be stopped when buprenorphine is started. Intermittent breakthrough opioids can be used to prevent increases in pain or symptoms of withdrawal. Buprenorphine is safe for use in patients with renal failure.

1) Transdermal patches (up to 20 microg/h) are changed every 7 days. Dose adjustments should occur only after 3 to 7 days. Higher-dose preparations of transdermal patches (from 35 microg/h) changed every 3 to 4 days are used in some European countries.

2) Buccal film and sublingual tablets are taken every 12 hours. Dose adjustments should occur no quicker than every 4 days. Lower doses and slower titration are advised in patients with oral lesions.

3) Sublingual tablets that contain both buprenorphine and naloxone are available in 2 dosage forms but currently in Canada these are approved only for use in opioid addiction.

4. Fentanyl: A strong opioid reserved for opioid-tolerant patients. Immediate-release (buccal and IV) and controlled-release formulations (transdermal patches) are available. Starting doses depend on prior opioid use. Not recommended for patients using <45 mg to 60 mg of morphine (or equivalent) per day. IV dosing should be reserved for monitored settings, such as operating rooms and intensive care units. Patients using controlled-release formulations will need breakthrough analgesics for incident pain. Controlled-release formulations should be titrated no quicker than once a week because of their long half-life. When a patch is removed, drug levels may be found in blood for up to 1 day. Conversion from alternative opioids to fentanyl is not as exact as in other opioid conversions. Deaths have occurred in Canada when opioid-naive patients started using fentanyl patches, even the smallest doses possible. Prescription of fentanyl patches should be reserved for practitioners experienced in opiate dosing. It is suggested that for critically ill patients, transdermal fentanyl dosing can be converted directly to IV (and back again when the patient’s condition improves and they are able to take oral formulations) at a 1:1 ratio.Evidence 1Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients) Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to purely observational data of a very small number of patients (very low confidence). Samala RV, Bloise R, Davis MP. Efficacy and safety of a six-hour continuous overlap method for converting intravenous to transdermal fentanyl in cancer pain. J Pain Symptom Manage. 2014 Jul;48(1):132-6. doi: 10.1016/j.jpainsymman.2013.09.001. Epub 2013 Dec 2. PubMed PMID: 24291296. Kornick CA, Santiago-Palma J, Schulman G, et al. A safe and effective method for converting patients from transdermal to intravenous fentanyl for the treatment of acute cancer-related pain. Cancer. 2003 Jun 15;97(12):3121-4. PubMed PMID: 12784350. This should be done in a monitored setting. Fentanyl is safe for use in patients with renal failure.

5. Methadone: An intermediate-acting opioid used in opioid-tolerant patients. Only oral formulation is available. Dosing is based on use of other opioids and goals of therapy (pain management or addiction therapy). Methadone may be used in patients with end-stage renal disease. It is safe for use in patients with renal disease. Methadone prolongs the cardiac QT interval. It must be used with caution in patients taking other medications.

6. Oxycodone: Described in the weak opioids section (see above), it can be considered a strong opioid when administered without dose-limiting medications. The starting doses and rate of titration are the same with and without additional medications.

Management of Adverse Effects of Opioids

1. Sedation (manifesting as daytime somnolence) usually occurs at the beginning of opioid treatment or after a considerable dose increase and resolves within several days. If somnolence persists or worsens, the dose of opioid can be decreased to the lowest dose that ensures pain control. Other causes of sedation (eg, other medications, dehydration, renal failure, disease progression, hypercalcemia) should be excluded and treated where possible. Persistent somnolence may be an indication for switching to another opioid. Patients should be advised not to drive or operate heavy equipment until they are aware how their opioids will affect them (in some countries driving when using opioids is not allowed).

2. Nausea and vomiting may develop in the first days of starting an opioid or following a dose increase and usually resolve spontaneously. Opioids can elicit nausea and vomiting through direct effects on the vomiting center in the brain or by way of reduced gut motility (with or without constipation). Always inform the patient about the risk of nausea or vomiting (or both) and explain these are likely to be transient (to prevent patients from discontinuing the drug on their own). Consider providing the patient with an antiemetic agent to be used at home in case of nausea or vomiting associated with opioid treatment. Other causes of nausea and vomiting (eg, other medications, renal failure, disease progression, constipation) should be excluded and treated where possible. Opioid-induced nausea and vomiting respond best to prokinetic antiemetics (metoclopramide) or dopamine antagonists (haloperidol). If nausea and vomiting cannot be managed medically, consider rotation to a different opioid or to another form of the medication (eg, long-acting, transdermal).

3. Constipation is the most frequent adverse effect of opioids. Patients using opioids on a regular basis should be provided with prophylactic laxative therapy. Opioid-induced constipation often requires a combination of medications. Stimulant (senna) and osmotic (lactulose) laxatives are most effective.

4. Delirium may occur with initiation of opioids, dose changes, or accumulation of metabolites (ie, acute renal failure). Subtle cognitive changes may occur in the absence of clinically evident delirium. Cognitive changes are often caused by opioid metabolites rather than the given opioid itself. Cognitive changes can be reduced by decreasing opioid dose to the lowest dose that provides adequate pain control. Opioid rotation, particularly to one with minimally active metabolites (hydromorphone, fentanyl), may reduce cognitive effects. Delirium that does not resolve or is distressing can be treated with low doses of a dopamine antagonist (haloperidol 0.125-1 mg orally or subcutaneously). Other causes of cognitive impairment (eg, other medications, renal failure, disease progression, or hypercalcemia) should be excluded and treated where possible.

5. Hyperalgesia: Opioid-induced hyperalgesia is a poorly understood phenomenon where use of opioids leads to overstimulation of nociceptors and sensation of pain. Typically hyperalgesia develops simultaneously with neurotoxicity. Patients with hyperalgesia experience no pain relief with increasing opioid doses. Opioid-induced hyperalgesia is a diagnosis of exclusion, and alternative causes of pain such as disease progression must be ruled out. Hyperalgesia should be managed urgently by decreasing opioid dose (typically by a third or half) to reduce stimulation of the opioid receptor. Opioid rotation (including a dose decrease) and careful use of opioid-sparing analgesics can be helpful as well.

6. Neurotoxicity: Opioid-induced neurotoxicity is a clinical syndrome in which the given opioid or its metabolites cause neurologic adverse effects. Symptoms can include hallucinations, delirium, somnolence, myoclonus, dysesthesia, and hyperalgesia. Opioid neurotoxicity does not appear to be mediated through opioid receptors and thus does not respond to opioid antagonists such as naloxone. Management of opioid-induced neurotoxicity requires reduction of opioid dosing and hydration to assist in the clearance of metabolites. Severe cases may require switching to an alternative opioid. Specific symptoms can be managed with directed therapies, such as benzodiazepines (myoclonus); these therapies must be used with care as they will contribute to the altered cognitive status of the patient.

7. Overdose: Features of opioid overdose include depressed respiratory rate, depressed mental status, decreased bowel sounds, and constricted pupils. Overdose can occur with one large dose or as metabolites accumulate in patients with dehydration or renal failure. Management of a mild overdose includes reduction of opioid dosing and IV fluids to assist in the clearance of metabolites. Low doses of naloxone (0.05-0.1 mg IV, intranasally, or subcutaneously) can be used if necessary but often this is not needed.

Management of a severe opioid overdose (respiratory depression, airway compromise, unresponsiveness) requires reduction of opioid dosing, IV fluids, and an opioid antagonist (naloxone). Initial doses of 0.4 to 1 mg of naloxone IV, intranasally, or subcutaneously are advised. As the half-life of naloxone is shorter than that of therapeutic opioids, many patients require a continuous infusion of naloxone to provide support until clearance of all metabolites is achieved.

Of note, patients at the end of life have symptoms similar to those of opioid toxicity (see Last Days and Hours). As long as death is not related to opioid toxicity, it is important not to give naloxone to actively dying patients, as this will cause pain and distress and not reverse the symptoms.

8. Other adverse effects: Dry mouth, pruritus, urinary retention, and sweating commonly occur and can be treated symptomatically. With long-term use, suppression of luteinizing hormone, follicle-stimulating hormone, adrenocorticotropic hormone, and growth hormone secretion can occur and can be associated with osteoporosis.

Opioid Rotation

Opioid rotation (switching from one opioid to another) is used in patients who develop unacceptable refractory adverse effects to or tolerance of a certain opioid. Opioid rotation is also used when patients are no longer able to swallow opioids that come only in oral formulations. The method of rotation needs to account for the type of opioid the patient is taking (controlled-release or immediate-release formulation) and the dose of the opioid. Opioid receptors have incomplete cross-tolerance for opioids and tend to take up a novel opioid with greater affinity than the one the patient has been using for some time. As a result, guidelines suggest calculating equianalgesic doses of the new medication and then decreasing this dose by as much as a third to a half. A breakthrough immediate-release opioid can be used to improve analgesia during the transition period. Consultation with a palliative care or pain medicine specialist is recommended for opioid rotation.


Coanalgesics are agents that are not classified as analgesics but in certain types of pain have inherent analgesic effects or enhance the effects of analgesics. When appropriate, coanalgesics should be used at all steps of the WHO analgesic ladder.

1. Antiepileptic drugs:

1) Gabapentin: Originally designed as an anticonvulsant, gabapentin is now approved in Canada for treatment of neuropathic pain. The usual starting dose is 200 to 300 mg (100 mg in elderly patients and those with renal impairment) in the evening, with the dose titrated up every 2 to 3 days by 200 to 300 mg/d (100 mg/d in the elderly) until an adequate analgesic effect is achieved or adverse effects develop. Similarly to opioids, there is no maximum dose, although benefits from increases beyond 1200 mg tid are minimal. The goal should be the lowest dose (in a bid or tid dosing) that achieves pain control and minimizes adverse effects. Somnolence is the most common adverse effect that limits the rate at which the dose may be increased. Unsteady gait and falls are common.

2) Pregabalin: Pregabalin is an analgesic designed to mimic the neuropathic analgesic properties of gabapentin. Start from 75 mg bid (25 mg bid in the elderly and those with renal impairment). If necessary, titrate the dose up by 25 to 50 mg every 3 to 7 days. The maximum recommended effective dose is 300 mg bid (total daily doses of 50 mg may be effective in patients with renal impairment and in the elderly). Common adverse effects include confusion and volume overload (from sodium and water retention). These effects can be severe and require discontinuation of the medication. The mechanism of action mimics that of gabapentin, thus there is no reason to use these two medications at the same time.

3) Carbamazepine: An anticonvulsant with analgesic effects as a neuropathic agent. Start from 50 to 100 mg bid. The dose can be titrated up to a maximum of 800 to 1200 mg/d. Lower doses are needed in those with renal impairment and in the elderly. The main adverse effect is sedation, which can be managed with dose reduction. Carbamazepine is the first-line therapy recommended for trigeminal neuralgia. The effectiveness of analgesia is not related to drug levels, unlike when it is used as an anticonvulsant. There is no need to regularly measure drug levels unless toxicity is suspected (based on the clinical situation or high drug doses).

2. Tricyclic antidepressants (TCAs): This class of medications has been shown to be effective in the management of migraine, arthritis, chronic low back pain, postherpetic neuralgia, fibromyalgia, and diabetic neuropathy. The adverse effect profile of TCAs is that of anticholinergic medications (eg, sedation, dry mouth, constipation, urinary retention, or confusion) and will often limit dosing.

1) Amitriptyline: Starting dose 10 mg at bedtime, increased to 25 mg after 3 to 7 days, and then increased by 25 mg/d every 1 to 2 weeks. Effective analgesia (or adverse effects) can often develop with doses <50 mg/d.

2) Nortriptyline: Starting dose 10 mg at bedtime, increased to 25 mg after 3 to 7 days, and then increased by 25 mg/d every 1 to 2 weeks. Effective analgesia (or adverse effects) can often develop with doses <75 mg/d.

3. Other antidepressants: Other antidepressants have been shown to have coanalgesic effects. They modulate this effect through management of comorbid mood disorders as well as through mechanisms not yet understood. Evidence suggests that selective serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine reuptake inhibitors (SNRIs) have inferior efficacy in neuropathic pain management when compared with TCAs. However, the adverse effect profile of SSRIs and SNRIs is better tolerated by most patients, making these agents a suitable option to consider for the management of neuropathic pain.

Duloxetine: The only SNRI officially approved in Canada for management of diabetic neuropathy, fibromyalgia, and chronic musculoskeletal pain. The starting dose of 30 mg is effective in some patients. Others need to have their dose increased to a maximum of 60 mg daily after 1 week of treatment with the starting dose. Duloxetine should not be used in patients with end-stage renal disease or cirrhosis.

4. Other coanalgesics: There are many other agents used as coanalgesics in specific situations.

1) Glucocorticoids (dexamethasone) provide pain relief in the setting of inflammatory conditions and when pain is caused by compression, stretch, or infiltration by tumor. They are useful for pain management in patients with rheumatologic disease, solid tumor, or lymphoma.

2) Bisphosphonates help to reduce bone pain associated with malignant infiltration through inhibition of osteoclast activity. Not sufficient as a single analgesic agent.

3) Topical lidocaine and capsaicin are effective in treating localized pain due to neuropathy, vasculitis, or trauma.

Nonpharmacologic Management

An in-depth analysis of nonpharmacologic interventions of pain management is beyond the scope of this chapter. However, in many situations they can be an adjuvant to pharmacologic therapy.

1. Nerve blocks and neurodestructive procedures: Use anesthetic agents to temporarily anesthetize or alcohol to permanently destroy the nerve plexus at the source of pain. Performing such procedures with imaging guidance improves success rates. The availability of interventional procedures is site-dependent and not all clinics and hospitals are able to provide such services.

1) Celiac plexus neurolysis may be used in the treatment of pain caused by pancreatic, gastric, liver, gallbladder, intestinal, or renal cancers; retroperitoneal metastases; or splenomegaly.

2) Hypogastric plexus neurolysis or blocks may be used in patients with pelvic pain secondary to malignant and nonmalignant causes, tenesmus secondary to radiation therapy to the rectum, or malignancy-related rectal pain.

3) Blocks of the stellate ganglion, lumbar sympathetic trunk, and ganglion impar (ganglion of Walther) can be used to ease pain in the limbs, face, and pelvic region.

4) Continuous central neuraxial blocks (subarachnoid and epidural) are most commonly performed when systemic administration of opioids is ineffective or results in unacceptable adverse effects. These blocks can be used to treat intractable neuropathic and nociceptive pain. The most significant benefit of continuous spinal opioid delivery is typically in the reduction of adverse effects rather than in improved pain control.

5) Peripheral nerve blocks are often used for procedures and interventions. A long-term anesthetic effect could be achieved through alcohol lysis of the same nerves.

6) Trigger point injections are injections of an anesthetic agent with or without glucocorticoid into a muscle knot (trigger point). The exact mechanism of pain control is not clear but improvement in local pain has been shown in patients with myofascial pain and fibromyalgia.

2. Radiotherapy is first-line treatment for localized pain associated with metastatic bone disease and direct nerve injury from solid tumor growth. The number of treatments and total size of radiation dose varies based on the nature of pain and the type of cancer.

3. Surgery can be a useful method of pain relief. Prophylactic and postfracture bone fixation provides rapid and profound pain control. Spinal decompression, vertebroplasty, and kyphoplasty have shown mixed results in the management of pain from degenerative disc disease and vertebral compression fractures.

4. Transcutaneous electrical nerve stimulation (TENS) uses electrical stimulation applied to the skin to stimulate nerve endings, in this way altering or eradicating pain. This form of analgesia is easily performed in the outpatient setting. Results are most beneficial when TENS is used for acute and subacute pain from injury or surgery.

5. Physiotherapy, including massage, and exercise are most effective in the management of bone, soft tissue, and neuropathic pain. Physiotherapy is important in maintaining mobility despite ongoing pain and disease.

6. Occupational therapy does not directly provide analgesia. Thanks to modifications in behavior, gait aids, and tools, occupational therapy can indirectly reduce pain through altered body mechanics and minimization of ongoing injury.

7. Cognitive behavioral therapy and behavior therapy have been shown to have very small benefits in overcoming disability, managing mood, and reducing catastrophic thinking associated with chronic pain. It is not clear at this time how long the therapy should be continued or which patients benefit most from such interventions.

Tables and FiguresTop


Table 1.20-1. Analgesic equivalencies


PO dose

To convert to PO morphine equivalent multiply by:

To convert from PO morphine equivalent multiply by:

To convert PO to SC or IVa (same drug) multiply by:


100 mg



0.5 (SC only; IV not available in Canada)


10 mg



7.5 mg



Not available in Canada


2 mg




Methadone and tramadol

Morphine dose equivalence not reliably established


5 microg/h patch = 30 mg morphine PO (daily dose)

10 microg/h patch = 30-80 mg morphine PO (daily dose)

Higher doses (35, 52.5, 70 microg/h) available is some countries


Should be reserved for monitored settings (IV formulations) and opioid-experienced patients (PO, buccal, transdermal formulations)

a SC dosing limited to 2 mL per injection site. If concentration of the drug does not allow for this, >1 injection site or conversion to IV dose is required.

Adapted from Canadian Guideline for Safe and Effective Use of Opioids for Chronic Non-Cancer Pain. Canada: National Opioid Use Guideline Group (NOUGG); 2010. Available from: and Health Canada. Important Changes to the Dose Conversion Guidelines for Fentanyl Transdermal Systems – For Health Professionals. Published January 7, 2009.

IV, intravenous; PO, oral; SC, subcutaneous.

Table 1.20-2. Dosage conversion guidelines for transdermal fentanyla by Health Canada

Current analgesic

Daily dose (mg/d)

Morphine PO








Morphine IM/IVb








Oxycodone PO








Codeine PO








Hydromorphone PO








Hydromorphone IV








Recommended FTS dose

25 microg/h

37 microg/h

50 microg/h

62 microg/h

75 microg/h

87 microg/h

100 microg/h

Conversion method for adult patients taking opioids or doses not listed here: Table 1.20-1.

This table should not be used for conversion in the other direction (from FTS to other opioids), because this conversion to FTS is conservative. Its use for conversion to other analgesics can overestimate the dose of the new agent and result in overdosage.

a The usual starting dose is 25 microg/h. Lower doses could be occasionally used if considered required. FTS at any dose is contraindicated in opioid-naive patients.

b Calculation in this table is based on a 1:2 ratio of parenteral to PO morphine doses. For some patients, a 1:3 parenteral to PO dose ratio may be more appropriate (10 mg parenteral morphine = 30 mg PO morphine).

FTS, fentanyl transdermal system; IM, intramuscular; IV, intravenous; PO, oral.

Source: Health Canada. Important Changes to the Dose Conversion Guidelines for Fentanyl Transdermal Systems – For Health Professionals. Published January 7, 2009.

Figure 1.20-1. The World Health Organization analgesic ladder.

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