Pain Management

CHAPTER 18 Pain Management



I. DefinitionPain is a common condition that manifests as many different forms and severities. Pain is defined as an unpleasant sensory and emotional experience associated with damage to body tissues, including organs, bones, and muscles. Acute pain occurs after tissue injury and often resolves soon after the body has healed. Chronic pain occurs either from continual damage or constant stimulation of nerve fibers lasting at least 6 months. The cause of some chronic pain may not be known. The treatment of pain depends upon the causes of the pain and the individual’s tolerance of pain.

II. Types of Pain The different types of pain include acute pain, chronic pain, nerve pain, nociceptive pain, and psychogenic pain.
A. Acute pain: results from injury to tissues and/or inflammation. Acute pain generally has a sudden onset. For example, after trauma or surgery, acute pain may be accompanied by anxiety or emotional distress.

B. Chronic pain: Pain signals keep firing in the nervous system for weeks, months, even years. Initial injuries, such as an infection, sprained back, or sprained muscle, may cause acute pain that may lead to chronic pain. There may be an ongoing cause of pain, such as in back pain, arthritis, diabetes (diabetic neuropathy), or cancer.

C. Nerve pain (neuropathic pain): pressure or damage to nerves or the spinal cord. Nerve pain can be caused by tumors; injury, such as during surgery or falls; chemical damage, such as with mercury, lead, chemotherapy, and radiation; or viruses, such as herpes zoster (shingles or chicken pox).

D. Nociceptive pain: aching, sharp, or throbbing pain that includes somatic pain (body surface, deep tissues) and visceral pain (not well localized, pressure-like, deep squeezing)

E. Psychogenic pain: mostly related to psychological disorders. Goals of treatment are to improve comfort and physical and psychological function. Treatment includes antidepressants, psychological counseling.

III. Acute Pain Control
A. Pain management required for a short duration (e.g., following surgery, accident)

B. Known end period for required pain management

C. Monitor for addiction

IV. Chronic Pain Control
A. Disease state management (e.g., cancer, rheumatoid arthritis, osteoarthritis)

B. Pain management required for a long period, possibly until end of life

C. Acute control (e.g., breakthrough pain) may be required for short duration events during chronic control

D. Monitor for addiction

V. Pyramid Control
A. Start with mild agents, increase to narcotics

B. Ceiling effect (i.e., a limited dose requirement) with most analgesics
1. Narcotics (opioids) like morphine do not have a ceiling effect.

C. Controlled substances potentially addictive

D. Start with lowest doses possible

VI. Patient Assessment
A. Use the mnemonic: PQRST
1. P = Palliative factors: What makes the pain better?
a) Provocative factors: What makes the pain worse?

2. Q = Quality: Describe the pain.

3. R = Radiation: Where is the pain?

4. S = Severity: How does this pain compare with other pain you have experienced?

5. T = Temporal factors: Does the intensity of the pain change with time?

VII. Patient Management
A. Identify the source of pain.

B. Eliminate the underlying cause.

C. Select the most effective analgesic with the fewest side effects.

D. Properly titrate the dose for each patient and administer for an appropriate duration.

E. Always consider around-the-clock regimens for acute and chronic pain.

F. Use as-needed regimens for breakthrough pain.

G. Assess for side effects of analgesics (i.e., constipation with opioids).

H. Avoid excessive sedation by titrating the opioids tentatively.

I. Adjust the route of administration to the needs of each patient, using oral administration whenever possible.

J. Use equianalgesic doses when converting from one agent to another and titrate accordingly.

K. Consider antidepressants, anticonvulsants, or opioids for neuropathic pain.

L. Consider a multidisciplinary approach: pharmacologic + nonpharmacologic therapies.

VIII. Pharmacologic Therapies
A. Acetaminophen (paracetamol; tylenol)
1. Mechanism of action: not fully understood at this time; possibly centrally acting; derivative of p-aminophenol; analgesic

2. Maximum dose 4 g/day for adults (lower maximum dosages currently under consideration by Food and Drug Administration [FDA]); less with hepatic dysfunction and/or alcohol use

3. Caution: anemia or cardiac, pulmonary, renal or hepatic disease, alcoholism

4. Interactions: alcohol, liver enzyme inducers

5. Toxicity and side effects: Narrow therapeutic index; do not exceed maximum dose limits. Liver toxicity (acetaminophen is the primary agent associated with liver failure and need for transplantation in the United States), nephrotoxicity
a) Overdose: nausea, vomiting, diarrhea, methemoglobinemia
(1) Treatment with supportive measures and acetylcysteine

B. Nonsteroidal anti-inflammatory drugs (NSAIDs) (Table 18-1)
1. Mechanism of action: nonspecific inhibition of cyclooxygenase (COX)-2 and COX-1 receptors, decreasing prostaglandins produced by the arachidonic acid cascade in response to noxious stimuli, thereby decreasing the number of pain impulses received by the central nervous system (CNS)

2. Use lowest effective dose for shortest possible duration; OTC NSAID not to exceed 10 days unless a physician directs otherwise

3. Caution: Avoid in patients with recent coronary artery bypass graft surgery (CABG). Caution in bleeding disorders, hepatic or renal disease, GI disorders; women who are pregnant or lactating or who are trying to conceive

4. Interactions: Methotrexate, medications which increase the risk of bleeding (anticoagulants, e.g., warfarin), medications causing liver or renal damage, medications causing GI disturbance, diuretics, lithium, aspirin,antihypertensive agents

5. Toxicity and side effects: bleeding, upset stomach, ulcers, nausea, vomiting, diarrhea, constipation, fluid retention, edema, tinnitus, increased risk of bleeding, increased risk of Reye syndrome in children

C. Aspirin
1. Prototype of the salicylates; also a nonsteroidal anti-inflammatory drug (NSAID)

2. Mechanism of action: irreversibly inhibits COX-1 and COX-2, decreasing prostaglandins produced by the arachidonic acid cascade in response to noxious stimuli, thereby decreasing the number of pain impulses received by the CNS

3. Maximum dose 5400 mg per day; less in some situations

4. Caution: bleeding disorders, hepatic and/or renal disease, GI disorders, use in children, pregnancy, fertility, lactation

5. Interactions: other medications that increase the risk of bleeding, medications containing salicylates, medications causing GI disturbance

6. Toxicity and side effects: increased risk of Reye syndrome in children, GI disturbance, GI bleeding and/or mucosal lesions, otic effects (tinnitus and hearing loss at high doses), hepatotoxicity, nephrotoxicity is rare, and increased risk of bleeding

D. COX-2 inhibitors (a subset of NSAID class) (Table 18-2)
1. Mechanism of action: selectively inhibits the activity of the enzyme COX-2, resulting in a decreased prostaglandin production, thereby decreasing the number of pain impulses received by the CNS

2. May have fewer GI effects than COX-1 inhibitors

3. Common side effects: peripheral edema, abdominal pain, diarrhea, dyspepsia, flatulence, nausea, back pain, dizziness, headache, insomnia, pharyngitis, rhinitis, sinusitis

4. Caution: same risks as traditional NSAIDs

5. Avoid in patients with recent coronary artery bypass graft surgery (CABG), creatinine clearance <30 mL/min

6. Interactions: medications that increase the risk of bleeding, hepatotoxic or nephrotoxic medications, medications that cause GI disturbance

7. Toxicity: GI disturbance, hepatotoxicity, nephrotoxicity, increased risk of bleeding GI ulceration, cardiovascular events, including stroke**

E. Narcotic analgesics (Table 18-3)
1. Overview
a. Mechanism of action: binds to opiate receptors in the CNS causing inhibition on ascending pain pathways thereby altering the perception of and response to pain

b. Caution: physically addictive, controlled substances

c. Interactions: additive CNS depression with alcohol

d. Toxicity and side effects: constipation, drowsiness, nausea/vomiting, sedation, itching, difficulty urinating, miosis, toxicity may result in respiratory depression

e. Antidote for opioid overdose: naloxone (Narcan)

2. Morphine
a. The prototype opioid narcotic

b. Schedule II

c. Mechanism of action: Acts on mu, kappa, and sigma receptors
1) Decreases pain by depressing opioid receptors in the limbic system

2) Activates certain midbrain neurons that relay inhibitory impulses from periphery to brain

3) Alter brain’s perception of pain, decrease substance P, decrease nerve conduction of pain

d. Used for relief of severe acute and chronic pain when other drugs have failed

e. No maximum dose: must titrate up slowly to lessen side effects, especially respiratory depression

f. Can suppress cough reflex

g. Adverse effects: euphoria, feelings of relaxation, reduced anxiety, respiratory depression, sedation, constipation, papillary constriction, and cough suppression, itching, sweating, and hypotension (caused by histamine release)

3. Hydromorphone (Dilaudid)
a. Mechanism of action: Similar to morphine
1) Faster onset of action and shorter duration of action

2) 8–10 times stronger than morphine

b. Used for moderate to severe pain

c. Schedule II

4. Codeine (methyl morphine)
a. Mechanism of action: similar to morphine but not as potent and shorter duration of action

b. Combination therapy with other agents in same formulation

c. Also used for suppressive therapy of cough

d. Used for moderate pain

e. Must monitor contents when using multiple agents

f. Schedule II or III

g. Adverse effects: constipation, nausea, and vomiting

5. Synthetic and semisynthetic narcotics
a. Oxycodone (OxyContin)
1) Mechanism of action: similar to morphine; alters perception and response to pain
a) As potent as morphine

b) 10–12 times less potent than codeine

2) Used for moderate to moderately severe pain

3) Schedule II

4) Combination products containing oxycodone
(a) Percocet = acetaminophen + oxycodone

(b) Percodan = aspirin + oxycodone

5) Dose
(a) Percocet: Doses should be given every 4–6 hours as needed and titrated to appropriate analgesic effects. Maximum daily dose based on acetaminophen content: oral 4 g/day for adults

(b) Percodan: 1 tablet every 6 hours as needed for pain; maximum aspirin dose should not exceed 4 g/day for adults

6) Metabolized in liver by cytochrome P-450 (CYP) 2D6

b. Meperidine (Demerol)
1) No maximum dose: must titrate up slowly to lessen side effects, especially respiratory depression

2) Can suppress cough reflex

3) Useful in treatment of rigors

4) Schedule II

5) Contraindicated for use with monoamine oxidase inhibitors (MAOIs)

6) Adverse effects: itching, sweating, and hypotension (caused by histamine release)

7) Toxic metabolite = normeperidine; patient must have good renal function to use medication

c. Propoxyphene (Darvon)
1) Combination therapy with other agents in same formulation

2) Must monitor contents when using multiple agents

3) Less addictive than opioids

4) Used for moderate pain

5) Schedule IV

6) Adverse effects: constipation, GI upset, CNS disturbance

d. Fentanyl (Actiq, Duragesic, Fentora)
1) Mechanism of action: mu agonist

2) Highly lipophilic (rapid onset and short duration of action)

3) No active metabolites

4) Used for breakthrough cancer pain, chronic pain, analgesia and anesthesia

5) No maximum dose: must titrate up slowly to lessen side effects, especially respiratory depression

6) Schedule II

7) Available as oral transmucosal lozenges (“lollipops” [Actiq]), effervescent buccal tablets (Fentora), buccal film (Onsolis) transdermal patches (Duragesic), and injectable formulations

8) Adverse effects: itching, sweating, and hypotension (caused by histamine release)

3. Drugs used in treatment of narcotic dependency
a. Methadone (Dolophine)
1) Mechanism of action: mu-opioid receptor agonist activity; synthetic drug

2) Used for detoxification and maintenance treatment of opioid addiction

3) Also used for pain relief

4) Patients must be in authorized methadone program; prescribers who prescribe for narcotic dependency must have special DEA registration; such registration is not needed for those using methadone for pain

5) High abuse potential

6) Schedule II

b. Buprenorphine (Suboxone and Subutex)
1) Both products are available as 2-mg and 8-mg sublingual (under the tongue) tablets; buprenorphine injection is also available.
a) Subutex contains only buprenorphine.

b) Suboxone is a combination product with buprenorphine and naloxone in a 4:1 ratio, respectively.

2) Mechanism of action: produces effects typical of both pure mu agonists and partial agonists depending on dose and pattern of use

3) Patients must be in authorized opioid maintenance program; prescribers who prescribe for narcotic dependency must have special DEA registration; such registration not needed for those using drug management for pain

4) Schedule III

5) Adverse effects: respiratory depression especially when used with benzodiazepines

F. Narcotic antagonists
1. Naloxone (Narcan)
a. Mechanism of action: opioid antagonists; displaces opiates from receptor site without activating receptor site

b. Used for reversal of opioid depression
1) Diagnosis of suspected opioid tolerance

2) Increase blood pressure (adjunct)

c. May precipitate acute withdrawal symptoms

2. Naltrexone (ReVia)
a. Used as opioid antagonist

b. Also used for alcohol dependence

c. Adverse effect: dose-related hepatocellular injury; will cause narcotic withdrawal symptoms

G. Antidepressants used for pain management
1. Tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs) have been found to provide some relief depending on the type of pain to be treated.

2. Used for chronic pain (e.g., neuropathic pain). Some SSRIs used for fibromyalgia.

3. TCA examples: amitriptyline (Elavil), nortriptyline (Pamelor), desipramine (Norpramin)

4. Narrow therapeutic window for TCA

5. TCAs associated with side effects: sedation, orthostatic hypotension, urinary retention

H. Anticonvulsants used for pain management
1. Used for chronic pain (e.g., neuropathic pain)

2. Liver function tests (LFT) should be obtained at baseline and throughout use with many of these drugs (e.g., phenytoin, valproic acid, carbmazepine).

3. Examples: gabapentin (Neurontin); carbamazepine (Tegretol); phenytoin (Dilantin), valproic acid (Depakote), lamotrigine (Lamictal)
a. Gabapentin is the most promising with the fewest side effects.
1. Initial adult dose: 100 mg twice daily, may titrate up to 1200–2400 mg daily divided in three doses

I. Local anesthetics
1. Topical local anesthetics (e.g., Lidoderm, EMLA) are used for neuropathic pain and postherpetic neuralgia.

2. Use only on intact skin.

J. Capsaicin
1. Over-the-counter (OTC) topical products: Zostrix, Axsain

2. Composed of an extract of chili peppers

3. Also used for rheumatoid arthritis and osteoarthritis

4. Rarely recommended due to overall poor efficacy

5. Adverse effect: burning at site of administration

K. Corticosteroids
1. May be used for neuropathic symptoms when associated with inflammation and edema
a. Also used for bone pain, spinal metastasis, rheumatoid arthritis, other acute inflammatory disorders

2. Example: dexamethasone commonly used

3. Many potential adverse effects: hyperglycemia, insomnia, GI irritation, psychosis, osteoporosis

L. Other neuropathic pain medications
1. Clonidine

2. Baclofen

3. Mexiletine

Table 18-1 Nonsteroidal Anti-inflammatory Drugs (NSAID)


















NSAID Usual Oral Adult Doses Comments
Ibuprofen (Motrin) 200–400 mg PO q4–6h prn Maximum 1200 mg/day (OTC); 3200 mg/day (Rx)
Naproxen (Aleve, Naprosyn, Anaprox) 200–400 mg PO (initial dose), followed by 200 mg PO q8–12h Maximum 600 mg/day (OTC); 1000 mg/day (Rx)
Diclofenac (Cataflam, Voltaren)
May initiate with 100 mg PO followed by 50 mg tid
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Jun 21, 2016 | Posted by in PHARMACY | Comments Off on Pain Management

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