The management of pain is a very important aspect of nursing care in a variety of settings and across the lifespan. Pain is the most common reason that patients seek health care, resulting in some 70 million office visits annually in the United States. Surgical and diagnostic procedures often require pain management, as do several diseases including arthritis, diabetes, multiple sclerosis, cancer, and acquired immunodeficiency syndrome (AIDS). Pain leads to much suffering and is a tremendous economic burden in terms of lost workplace productivity, workers’ compensation payments, and other related health care costs.

To provide quality patient care, you must be well informed about both pharmacologic and nonpharmacologic methods of pain management. This chapter focuses on pharmacologic methods of pain management. Nonpharmacologic methods of pain management are listed in Box 10-1.

BOX 10-1

NONPHARMACOLOGIC TREATMENT OPTIONS FOR PAIN

• Acupressure

• Therapeutic communication

• Therapeutic touch

• Transcutaneous electric nerve stimulation

• Yoga

Medications that relieve pain without causing loss of consciousness are classified as analgesics. They are also commonly referred to as painkillers. There are various classes of analgesics, determined by their chemical structures and mechanisms of action. This chapter focuses primarily on the opioid analgesics, which are used to manage moderate to severe pain. Often drugs from other chemical categories are added to the opioid regimen as adjuvant analgesic drugs (or adjuvants) and are described later.

Pain is most commonly defined as an unpleasant sensory and emotional experience associated with either actual or potential tissue damage. It is a very personal and individual experience. Pain can be defined as whatever the patient says it is, and it exists whenever the patient says it does. Although the mechanisms of pain are becoming better understood, a patient’s perception of pain is a complex process. Pain involves physical, psychological, and even cultural factors (see Patient-Centered Care: Cultural Implications box). Because pain intensity cannot be precisely quantified, health care providers must cultivate relationships of mutual trust with their patients to provide optimal care.

PATIENT-CENTERED CARE: CULTURAL IMPLICATIONS

The Patient Experiencing Pain

• Each culture has its own beliefs, thoughts, and ways of approaching, defining, and managing pain. Attitudes, meanings, and perceptions of pain vary with culture, race, and ethnicity.

• African Americans believe in the power of healers who rely strongly on the religious faith of people and often use prayer and the laying on of hands for relief of pain.

• Hispanic Americans believe in prayer, the wearing of amulets, and the use of herbs and spices to maintain health and wellness. Specific herbs are used in teas and therapies, often including religious practices, massage, and cleansings.

• Some traditional methods of healing for the Chinese include acupuncture, herbal remedies, yin and yang balancing, and cold treatment. Moxibustion, in which cones or cylinders of pulverized wormwood are burned on or near the skin over specific meridian points, is another form of healing.

• Asian and Pacific Islander patients are often reluctant to express their pain because they believe that the pain is God’s will or is punishment for past sins.

• For many Native Americans, treatments for pain include massage, the application of heat, sweat baths, herbal remedies, and being in harmony with nature.

• In Arab culture, patients are expected to express their pain openly and anticipate immediate relief, preferably through injections or intravenous drugs.

• Remain aware of all cultural influences on health-related behaviors and on patients’ attitudes toward medication therapy and thus, ultimately, on its effectiveness. A thorough assessment that includes questions about the patient’s cultural background and practices is important to the effective and individualized delivery of nursing care.

There is no single approach to effective pain management. Instead, pain management is tailored to each patient’s needs. The cause of the pain, the existence of concurrent medical conditions; the characteristics of the pain; and the psychological and cultural characteristics of the patient need to be considered. It also requires ongoing reassessment of the pain and the effectiveness of treatment. The patient’s emotional response to pain depends on his or her psychological experiences of pain. Pain results from the stimulation of sensory nerve fibers known as nociceptors. These receptors transmit pain signals from various body regions to the spinal cord and brain, which leads to the sensation of pain, or nociception (Figure 10-1).

FIGURE 10-1 Illustration of the four processes of nociception. (From Jarvis C: *Physical examination and health assessment,* ed 6, St Louis, 2012, Saunders.)

The physical impulses that signal pain activate various nerve pathways from the periphery to the spinal cord and to the brain. The level of stimulus needed to produce a painful sensation is referred to as the pain threshold. Because this is a measure of the physiologic response of the nervous system, it is similar for most persons. However, variations in pain sensitivity may result from genetic factors.

There are three main receptors believed to be involved in pain. The mu receptors in the dorsal horn of the spinal cord appear to play the most crucial role. Less important but still involved in pain sensations are the kappa and delta receptors. Pain receptors are located in both the central nervous system (CNS) and various body tissues. Pain perception—and, conversely, emotional well-being—is closely linked to the number of mu receptors. This number is controlled by a single gene, the mu opioid receptor gene. When the number of receptors is high, pain sensitivity is diminished. Conversely, when the receptors are reduced or missing altogether, relatively minor noxious stimuli may be perceived as painful.

The patient’s emotional response to the pain is also molded by the patient’s age, sex, culture, previous pain experience, and anxiety level. Whereas pain threshold is the physiologic element of pain, the psychological element of pain is called pain tolerance. This is the amount of pain a patient can endure without its interfering with normal function. Because it is a subjective response, pain tolerance can vary from patient to patient. Pain tolerance can be modulated by the patient’s personality, attitude, environment, culture, and ethnic background. Pain tolerance can even vary within the same person depending on the circumstances involved. Table 10-1 lists the various conditions that can alter one’s pain tolerance.

TABLE 10-1

CONDITIONS THAT ALTER PAIN TOLERANCE

PAIN THRESHOLD	CONDITIONS
Lowered	Anger, anxiety, depression, discomfort, fear, isolation, chronic pain, sleeplessness, tiredness
Raised	Diversion, empathy, rest, sympathy, medications (analgesics, antianxiety drugs, antidepressants)

Pain can also be further classified in terms of its onset and duration as either acute or chronic. Acute pain is sudden and usually subsides when treated. One example of acute pain is postoperative pain. Chronic pain is persistent or recurring, lasting 3 to 6 months. It is often more difficult to treat, because changes occur in the nervous system that often require increasing drug dosages. This situation is known by the general term tolerance or physical dependence (see Chapter 17). Acute and chronic pain differ in their onset and duration, their associated diseases or conditions, and the way they are treated. Table 10-2 lists the different characteristics of acute and chronic pain and various diseases and conditions associated with each.

TABLE 10-2

ACUTE VERSUS CHRONIC PAIN

TYPE OF PAIN	ONSET	DURATION	EXAMPLES
Acute	Sudden (minutes to hours); usually sharp, localized; physiologic response (SNS: tachycardia, sweating, pallor, increased blood pressure)	Limited (has an end)	Myocardial infarction, appendicitis, dental procedures, kidney stones, surgical procedures
Chronic	Slow (days to months); long duration; dull, persistent aching	Persistent or recurring (endless)	Arthritis, cancer, lower back pain, peripheral neuropathy

SNS, Sympathetic nervous system.

Pain can be further classified according to its source. The two most common sources of pain are somatic and visceral. Somatic pain originates from skeletal muscles, ligaments, and joints. Visceral pain originates from organs and smooth muscles. Sometimes pain is described as superficial. Superficial pain originates from the skin and mucous membranes. Deep pain occurs in tissues below skin level. Pain may be appropriately treated when the source of the pain is known. For example, visceral and superficial pain usually require opioids for relief, whereas somatic pain (including bone pain) usually responds better to nonopioid analgesics such as nonsteroidal antiinflammatory drugs (NSAIDs) (see Chapter 44).

Pain may be further subclassified according to the diseases or other conditions that cause it. Vascular pain is believed to originate from the vascular or perivascular tissues and is thought to account for a large percentage of migraine headaches. Referred pain occurs when visceral nerve fibers synapse at a level in the spinal cord close to fibers that supply specific subcutaneous tissues in the body. An example is the pain associated with cholecystitis, which is often referred to the back and scapular areas. Neuropathic pain usually results from damage to peripheral or CNS nerve fibers by disease or injury but may also be idiopathic (unexplained). Phantom pain occurs in the area of a body part that has been removed—surgically or traumatically—and is often described as burning, itching, tingling, or stabbing. It can also occur in paralyzed limbs following spinal cord injury. Cancer pain can be acute or chronic or both. It most often results from pressure of the tumor mass against nerves, organs, or tissues. Other causes of cancer pain include hypoxia from blockage of blood supply to an organ, metastases, pathologic fractures, muscle spasms, and adverse effects of radiation, surgery, and chemotherapy. Central pain occurs with tumors, trauma, inflammation, or disease (e.g., cancer, diabetes, stroke, multiple sclerosis) affecting CNS tissues.

Several theories attempt to explain pain transmission and pain relief. The most common and well described is the gate theory. This theory, proposed by Melzack and Wall in 1965, uses the analogy of a gate to describe how impulses from damaged tissues are sensed in the brain. First, the tissue injury causes the release of several substances from injured cells, such as bradykinin, histamine, potassium, prostaglandins, and serotonin. Some current pain medications work by altering the actions and levels of these substances (e.g., NSAIDs → prostaglandins; antidepressants → serotonin). The release of these pain-mediating chemicals initiates action potentials (electrical nerve impulses) at the distal end of sensory nerve fibers through pain receptors known as nociceptors. These nerve impulses are conducted along sensory nerve fibers and activate pain receptors in the dorsal horn of the spinal cord. It is here that the so-called gates are located. These gates regulate the flow of sensory nerve impulses. If impulses are stopped by a gate at this junction, no impulses are transmitted to the higher centers of the brain. Conversely, if the gates permit a sufficient number and intensity of action potentials to be conducted from the spinal cord to the cerebral cortex, the sensation of pain is then felt. This is known as nociception. Figure 10-2 depicts the gate theory of pain transmission.

FIGURE 10-2 Gate theory of pain transmission. *CNS,* Central nervous system.

Both the opening and the closing of this gate are influenced by the relative activation of large-diameter A fibers and small-diameter C fibers (Table 10-3). Closing of the gate seems to be affected by the activation of A fibers. This causes the inhibition of impulse transmission to the brain and avoidance of pain sensation. Opening of the gate is affected by the stimulation of C fibers. This allows impulses to be transmitted to the brain and pain to be sensed. The gate is innervated by nerve fibers that originate in the brain and modulate the pain sensation by sending impulses to the gate in the spinal cord. These nerve fibers enable the brain to evaluate, identify, and localize the pain. Thus, the brain can control the gate, either keeping the gate closed or allowing it to open so that the brain is stimulated and pain is sensed. The cells that control the gate have a threshold. Impulses that reach these cells must rise above this threshold before an impulse is permitted to travel up to the brain.

TABLE 10-3

A AND C NERVE FIBERS

TYPE OF FIBER	MYELIN SHEATH	FIBER SIZE	CONDUCTION SPEED	TYPE OF PAIN
A	Yes	Large	Fast	Sharp and well localized
C	No	Small	Slow	Dull and nonlocalized

The body is also equipped with certain endogenous neurotransmitters known as enkephalins and endorphins. These substances are produced within the body to fight pain and are considered the body’s painkillers. Both are capable of bonding with opioid receptors and inhibiting the transmission of pain impulses by closing the spinal cord gates, in a manner similar to that of opioid analgesic drugs. The term endorphin is a condensed version of the term “endogenous morphine.” These endogenous analgesic substances are released whenever the body experiences pain or prolonged exertion. For example, they are responsible for the phenomenon of “runner’s high.” Figure 10-1 depicts this entire process.

Another phenomenon of pain relief that may be explained by the gate theory is the fact that massaging a painful area often reduces the pain. When an area is rubbed or liniment is applied, large sensory A nerve fibers from peripheral receptors carry pain-modulating impulses to the spinal cord. Remember, the A fibers tend to close the gate, which reduces pain sensation in the brain.

Treatment of Pain in Special Situations

It is estimated that one of every three Americans experiences ongoing pain. Pain is poorly understood and often undertreated. In addition to enduring their baseline chronic pain, patients with illnesses such as cancer, AIDS, and sickle cell anemia may also experience crisis periods of acute pain. Effective management of acute pain is often different from management of chronic pain in terms of medications and dosages used. Routes of drug administration may include oral, intravenous (IV), intramuscular (IM), subcutaneous (subcut), transdermal, and rectal. One intravenous route commonly used in the hospital setting is patient-controlled analgesia (PCA). In this situation, patients are able to self-medicate by pressing a button on a PCA infusion pump. This has been shown to be very effective and reduces the total opioid dose used. Morphine and hydromorphone are commonly given by PCA. Potential hazards of PCA include well-meaning family members’ pressing the dosing button rather than letting able patients do so on their own. For patients truly not able to self-medicate using the PCA pump, a different method of pain control needs to be used. Numerous deaths have occurred when well-meaning family members have administered too much of the opioid drug. This is called PCA by proxy. The Institute for Safe Medication Practices (www.ismp.org) advises against PCA by proxy.

Patients with complex pain syndromes often benefit from a holistic or multimodal clinical approach that involves pharmacologic and/or nonpharmacologic treatment. Effective drug therapy may include use of opioid and/or nonopioid drugs. The goals of pain management include reducing and controlling pain, and improving body function and quality of life.

In situations such as pain associated with cancer, the main consideration in pain management is patient comfort and not trying to prevent drug addiction (or psychologic dependence; see Chapter 17). Opioid tolerance is a state of adaptation in which exposure to a drug causes changes in drug receptors that result in reduced drug effects over time. This can occur in as little as 1 week. Because of increasing pathology (e.g., tumor burden), cancer patients usually require increasingly higher opioid doses and thus do become physically dependent on the drugs. Cancer patients are likely to experience withdrawal symptoms (see Chapter 17) if opioid doses are abruptly reduced or discontinued; however, actual psychological dependence or addiction in such patients is unusual. For long-term pain control, oral, intravenous, subcutaneous, transdermal, and sometimes even rectal dosing routes are favored over multiple intramuscular injections due to associated puncture trauma (bruising) and erratic drug absorption.

One controversial issue in pain management is the use of placebos, inert dosage forms that actually lack medication. Some prescribers feel that this practice may be helpful by taking advantage of the well-documented placebo effect. The placebo effect is a psychological therapeutic effect that occurs even in the absence of actual medication. It is believed to arise from activation of the patient’s own endorphins. It is also attributed to the patient’s belief that any “treatment” is effective, as well as the patient’s high level of trust in the health care provider. Critics argue that the use of placebos is unethical, because it requires that the patient be deceived in the process. The use of placebos for pain management has fallen out of favor, and they are rarely used today (see Chapter 4 for further discussion).

The treatment of acute pain in patients who are addicted to opioids is of great concern to clinicians, who may be reluctant to prescribe opioid therapy. However, habitual street opioid users are opioid tolerant and generally require high dosages. Longer-acting opioids such as methadone or extended-release oxycodone are usually better choices than shorter-acting immediate-release drug products for these patients. This is because the shorter-acting drugs are more likely to produce a psychological “high” or euphoria, which only reinforces addictive tendencies. Genetic differences in cytochrome P-450 enzymes (see Chapters 2 and 8) can cause different patients, whether addicted or not, to respond more or less effectively to a given drug. For this reason, patients must not automatically be viewed with suspicion if they complain that a given drug does not work for them.

The label of “addict” can be used unfairly to justify refusal to prescribe pain medications, resulting in undertreatment of pain, even in patients who do not use street drugs. This is now regarded as an inappropriate and inhumane clinical practice. In these situations, control of the patient’s pain takes ethical and clinical priority over concerns regarding drug addiction. Nonetheless, prescribers must contend with the reality of abuse of street and/or prescription drugs by patients without genuine pain conditions (see Chapter 17). Such patients often request excessive numbers of prescriptions and may use multiple prescribers and/or pharmacies. At times, they may also forge prescriptions and/or use a telephone to call in prescriptions for non–Schedule II opioids such as hydrocodone/acetaminophen (Vicodin). Community pharmacists work collaboratively to detect such abuses and notify law enforcement authorities. Creating a phony prescription for a controlled substance is a felony under federal and state laws.

EVIDENCE-BASED PRACTICE

Student Nurses’ Misconceptions of Adults with Chronic Nonmalignant Pain

Review

The purpose of this study was to identify some of the misconceptions that student nurses have, across 3 years of undergraduate education, about adults who are experiencing chronic nonmalignant pain. Previously identified misconceptions about patients with chronic nonmalignant pain reported in an extensive literature search served as the basis of the study. The rationale for this study was to identify potential gaps in attitudes and knowledge of student nurses. The results were then used to discuss educational approaches focused on improving care of the patient experiencing chronic nonmalignant pain. The two major questions that this study sought to explore included the following: (1) Do student nurses hold misconceptions about adults with chronic nonmalignant pain, and (2) If so, to what extent do they develop during their undergraduate education?

Type of Evidence

The researchers developed, tested, and validated a survey tool specifically for this cross-sectional study to evoke responses from students at three points during their undergraduate nursing education in New Zealand. The survey began with a vignette of a 22-year-old client who was experiencing back pain for 6 months. The injury that caused the pain resulted when the woman suffered a fall while lifting a patient. It was thought that the vignette represented demographics that would be most familiar to the participants. Part of the vignette also purposely alluded to some of the basic details of misconceptions of pain (McCaffery and Pasero, 1999) but without giving many specific details. The patient in the vignette was also someone who was a healthy, fit young adult prior to the injury. There were two slight variations in the vignettes with the hopes of eliciting possible differences in responses toward patients, depending on whether a specific pathology had been identified. A series of eight items, the misconception items, were directly linked to each of the misconceptions identified by McCaffery and Pasero (1990), and the responses were gathered using a seven-point Likert scale seeking differing levels of agreement in relation to the items. A tool was designed and used with another group of students from a different discipline but within the same facility. This was done to get feedback from a group of students similar to the participants but prior to the final study. Some minor changes were made in the tool before moving forward with the study.

Results of Study

Some 435 students were approached to participate in the research study, and 430 completed and returned the surveys for a total response rate of 99%. A convenience sampling was used because the students were easily accessible; they represented about 75% of students enrolled in the facility in semesters one, four, and six of the undergraduate nursing degree program in the city of Auckland and around 13% of those enrolled in New Zealand. These participants were distributed over a 3-year period of undergraduate studies during six semesters of full-time studies. The majority were female students, although there was no further specific demographic data collected about the participants. A cross-sectional design meant that data gathered came from each participant only once during the study. A research assistant, and one who had not taught the students, met with the students and invited them to participate in the study. Sessions were held in the middle of the semester to increase the response rate as well as diminish anxiety during final exam time. More than 38% of the participants demonstrated a misconception about people with chronic pain and that they were tolerant to some degree of pain. More than 60% did not hold this misconception about tolerance to pain. More than one-half of the students’ (59%) responses indicated that they held the misconception that psychological impairment is related to chronic pain. Approximately 79% of the students suggested that they believed stress was a contributory cause of chronic pain, whereas less than one-fourth indicated that they accurately understood that this was not the case. The misconception of compensation and exaggeration in chronic pain was held by 47.9% of the participants, and 51.7% did not hold this same misconception. About one-third of the students indicated that they held the misconception that patients with chronic pain were manipulative, and the majority indicated that they did not.

Approximately 64% of the participants held the misconception that depression plays a role in the chronic pain experience. Opioid addiction was a misconception held by about one-half of the participants, such that 54.8% believed that patients taking opioids were likely to be addicted. Some 58% of the students indicated that they did hold the misconception that patients with chronic pain were noncompliant and dependent, whereas 41.4% indicated that they did not hold this misconception. Another question that was posed to the students was the extent to which they had developed their misconceptions of patients with chronic pain during their undergraduate education. There were significantly positive trends across the semesters, suggesting that students held their misconceptions to a lesser degree as they progressed through their course of study. In summary, analysis of the results indicate that a substantial proportion of students who participated in the study hold misconceptions about patients with chronic pain to some extent.

The analysis of the misconception scores across the semesters indicates that the knowledge and attitudes of students toward adults experiencing chronic nonmalignant pain developed to some degree because their misconceptions were held to a lesser degree by the end of the program of study.

Link of Evidence to Nursing Practice

It is a known phenomenon that a gap exists between theory and practice across many areas of professional nursing practice. Therefore, it would be ideal for nursing educators and the nursing educational experience to equip students with the knowledge, skills, and attitudes to participate in the discussion, planning, and implementing of care for patients suffering from chronic nonmalignant pain. Nursing faculty and schools of nursing need to make available experiential learning situations that will enhance the blending of knowledge, skills, and attitudes into professional nursing practice so that these gaps in care are closed. The findings of this study show that students, like many practicing nurses, hold misconceptions about adults with chronic nonmalignant pain, representing a lack of knowledge and inappropriate attitudes. An integrated approach to teaching chronicity and disability needs to be included in the nursing curriculum; however, critical thinking, linking theory to practice, and developing compassion also need to be part of the educational process.

References: Shaw S, Lee A: Student nurses’ misconceptions of adults with chronic nonmalignant pain, Pain Manag Nurs 11(1):2-14, 2010; McCaffery M, Pasero C: Pain: clinical manual, St Louis, 1990, Mosby; McCaffery M, Pasero C: Pain: clinical manual, ed 2, St Louis, 1999, Mosby.

For patients receiving long-acting opioids, breakthrough pain often occurs between doses of pain medications. This is because the analgesic effects wear off as the drug is metabolized and eliminated from the body. Treatment with prn (as needed) doses of immediate-release dosage forms (e.g., oxycodone IR) given between scheduled doses of extended-release dosage forms (e.g., oxycodone ER) is often helpful in these cases. Chewing or crushing of any extended-release opioid drug can cause oversedation, respiratory depression, and even death due to rapid drug absorption. If the patient is requiring larger doses for breakthrough pain, the dose of the scheduled extended-release opioid may need to be shortened or a more potent drug started.

Drugs from other chemical categories are often added to the opioid regimen as adjuvant drugs. These assist the primary drugs in relieving pain. Such adjuvant drug therapy may include NSAIDs (see Chapter 44), antidepressants (see Chapter 16), antiepileptic drugs (see Chapter 14), and corticosteroids (see Chapter 33), all of which are discussed further in their corresponding chapters. This approach allows the use of smaller dosages of opioids and reduces some of the adverse effects that are seen with higher dosages of opioids, such as respiratory depression, constipation, and urinary retention. It permits drugs with different mechanisms of action to produce synergistic effects. Antiemetics (see Chapter 52) and laxatives (see Chapter 51) may also be needed to prevent or relieve associated constipation, nausea, and vomiting (Box 10-2).

BOX 10-2

POTENTIAL OPIOID ADVERSE EFFECTS AND THEIR MANAGEMENT

Constipation

Opioids decrease gastrointestinal (GI) tract peristalsis because of their central nervous system (CNS) depression, with subsequent constipation as an adverse effect. Stool becomes excessively dehydrated because it remains in the GI tract longer. Preventative measures: Constipation may be managed with increased intake of fluids, stool softeners such as docusate sodium, or the use of stimulants such as bisacodyl or senna. Agents such as lactulose, sorbitol, and polyethylene glycol (Miralax) have been proven effective. Less commonly used are bulk-forming laxatives such as psyllium, for which increased fluid intake is especially important to avoid fecal impactions or bowel obstructions.

Nausea and Vomiting

Opioids decrease GI tract peristalsis, and some also stimulate the vomiting center in the CNS, so nausea and vomiting are often experienced. Preventative measures: Nausea and vomiting may be managed with the use of antiemetics such as phenothiazines.

Sedation and Mental Clouding

Any change in mental status should always be evaluated to ensure that causes other than drug-related CNS depression are ruled out. Preventative measures: Persistent drug-related sedation may be managed with a decrease in the dosage of opioid or change in drug used. The prescriber may also order various CNS stimulants (see Chapter 13).

Respiratory Depression

Long-term opioid use is generally associated with tolerance to respiratory depression. Preventative measures: For severe respiratory depression, opioid antagonists (naloxone) may be used to improve respiratory status and, if they are titrated in small amounts, the respiratory depression may be reversed without analgesia reversal.

Subacute Overdose

Subacute overdose may be more common than acute respiratory depression and may progress slowly (over hours to days), with somnolence and respiratory depression. Before analgesic dosages are changed or reduced, advancing disease must be considered, especially in the dying patient. Preventative measures: Often, holding one or two doses of an opioid analgesic is enough to judge if the mental and respiratory depression is associated with the opioid. If there is improvement with this measure, the opioid dosage is often decreased by 25%.

Other Opioid Adverse Effects

Dry mouth, urinary retention, pruritus, myoclonus, dysphoria, euphoria, sleep disturbances, sexual dysfunction, and inappropriate secretion of antidiuretic hormone may occur but are less common than the aforementioned adverse effects. Preventative measures: Ongoing assessment is needed for each of the adverse effects so that appropriate measures may be implemented (e.g., sucking of sugar-free hard candy or use of artificial saliva drops or gum for dry mouth; use of diphenhydramine for pruritus).

One common use of adjuvant drugs is in the treatment of neuropathic pain. Opioids are not completely effective in such cases. Neuropathic pain usually results from some kind of nerve damage secondary to disease (e.g., diabetic neuropathy, postherpetic neuralgia secondary to shingles, trigeminal neuralgia, AIDS or injury, including nerve damage secondary to surgical procedures [e.g., post-thoracotomy pain syndrome occurring after cardiothoracic surgery]). Common symptoms include hypersensitivity or hyperalgesia to mild stimuli such as light touch or a pinprick, or the bed sheets on a person’s feet. This is also known as allodynia. It can also manifest as hyperalgesia to uncomfortable stimuli, such as pressure from an inflated blood pressure cuff on a patient’s limb. It may be described as heat, cold, numbness and tingling, burning, or electrical sensations. Examples of adjuvants commonly used in these cases are the antidepressant amitriptyline and the anticonvulsants gabapentin and pregabalin.

The three-step analgesic ladder defined by the World Health Organization (WHO) is often applied as the pain management standard for cancer pain. Examples of nonopioid analgesic drugs include NSAIDs (see Chapter 44) as well as acetaminophen and tramadol (see Drug Profiles). Step 1 is the use of nonopioids (with or without adjuvant medications) once the pain has been identified and assessed. If pain persists and/or increases, treatment moves to step 2, which is defined as the use of opioids with or without nonopioids and with or without adjuvants. If pain persists or increases, management then rises to step 3, which is the use of opioids indicated for moderate to severe pain, administered with or without nonopioids or adjuvant medications. Many experts now question the effectiveness of Step 2, and the WHO is considering adjusting the ladder. Not all patients will be treated effectively using the ladder method and may need to seek an experienced pain management physician.

Pharmacology Overview

Opioids are classified as both mild agonists (codeine, hydrocodone) and strong agonists (morphine, hydromorphone, levorphanol, oxycodone, oxymorphone, meperidine, fentanyl, and methadone). Meperidine is not recommended for long-term use because of the accumulation of a neurotoxic metabolite, normeperidine. In fact, many hospitals have tried to prohibit the use of meperidine due to its adverse CNS effects, including seizures. In 2010, the mild agonist, propoxyphene (Darvocet) was withdrawn from the market due to adverse effects. The opiate agonists-antagonists such as pentazocine and nalbuphine are associated with an analgesic ceiling effect. This means that the drug reaches a maximum analgesic effect, so that analgesia does not improve even with higher dosages (see Drug Profiles). Such drugs are useful only in patients who have not been previously exposed to opioids and can be used for nonescalating moderate to severe pain. Finally, because of associated bruising and bleeding risks, as well as injection discomfort, there is now a strong trend away from intramuscular injections in favor of intravenous, oral, and transdermal routes of drug administration.

Opioid Drugs

The pain-relieving drugs currently known as opioid analgesics originated from the opium poppy plant. The word opium is a Greek word that means “juice.” More than 20 different alkaloids are obtained from the unripe seed of the poppy. The properties of opium and its many alkaloids have been known for centuries. Opium-smoking immigrants brought opium to the United States, where unrestricted availability of opium prevailed until the early twentieth century.

Chemical Structure

Opioid analgesics are very strong pain relievers. They can be classified according to their chemical structure or their action at specific receptors. Of the 20 different natural alkaloids available from the opium poppy plant, only three are clinically useful: morphine, codeine, and papaverine. Of these, only morphine and codeine are pain relievers; papaverine is a smooth muscle relaxant. Relatively simple synthetic chemical modifications of these opium alkaloids have produced the three different chemical classes of opioids: morphine-like drugs, meperidine-like drugs, and methadone-like drugs (Table 10-4).

TABLE 10-4

CHEMICAL CLASSIFICATION OF OPIOIDS

CHEMICAL CATEGORY	OPIOID DRUGS
Meperidine-like drugs	Meperidine, fentanyl, remifentanil, sufentanil, alfentanil
Methadone-like drugs	Methadone
Morphine-like drugs	Morphine, heroin, hydromorphone, oxymorphone, levorphanol, codeine, hydrocodone, oxycodone
Other	Tramadol, tapentadol

Mechanism of Action and Drug Effects

Opioid analgesics can also be characterized according to their mechanism of action. They are agonists, agonists-antagonists, or antagonists (nonanalgesic). An agonist binds to an opioid pain receptor in the brain and causes an analgesic response—the reduction of pain sensation. An agonist-antagonist, also called a partial agonist or a mixed agonist, binds to a pain receptor and causes a weaker pain response than does a full agonist. Different drugs in this class exert their agonist and/or antagonist effects by binding in different degrees to kappa and mu opioid receptors. Although not normally used as first-line analgesics, they are sometimes useful in pain management in opioid-addicted patients as well as obstetrical patients (because they avoid oversedation of the mother and/or fetus). An antagonist binds to a pain receptor but does not reduce pain signals. It functions as a competitive antagonist because it competes with and reverses the effects of agonist and agonist-antagonist drugs at the receptor sites.

The receptors to which opioids bind to relieve pain are listed in Table 10-5. The mu, kappa, and delta receptors are most responsive to drug activity, with the mu being the most important. Many of the characteristics of a particular opioid, such as its ability to sedate, its potency, and its ability to cause hallucinations, can be attributed to relative affinity for these various receptors.

TABLE 10-5

OPIOID RECEPTORS AND THEIR CHARACTERISTICS

RECEPTOR TYPE	PROTOTYPICAL AGONIST	EFFECTS OF OPIOID STIMULATION
mu	morphine	Supraspinal analgesia, respiratory depression, euphoria, sedation^∗
kappa	ketocyclazocine	Spinal analgesia, sedation,^† miosis
delta	Enkephalins	Analgesia

^∗Moderate level of sedation.

^†Twice as much sedation compared to mu receptors.

Understanding the relative potencies of various drugs becomes important in clinical settings. Equianalgesia refers to the ability to provide equivalent pain relief by calculating dosages of different drugs and/or routes of administration that provide comparable analgesia. Box 10-3 lists equianalgesic doses for several common opioids and shows how to calculate dosage conversions for patients. Because fentanyl is most commonly used transdermally, it is discussed separately in its drug profile.

BOX 10-3

CALCULATING DOSAGE CONVERSIONS BETWEEN COMMONLY USED OPIOIDS

	EQUIANALGESIC DOSES
	ORAL DOSE (mg)	PARENTERAL DOSE (mg)	ORAL-TO-PARENTERAL DOSE RATIO	DOSING INTERVAL (hr)
morphine	30	10	3:1	12 (continuous release) 4 (immediate release)
hydromorphone	7.5	1.5	5:1	4 (immediate release)
oxycodone	15	N/A	N/A	4 (immediate release)
hydrocodone	30	N/A	N/A	N/A
fentanyl	See fentanyl Drug Profile

N/A, Not applicable.

Basic Conversion Equation

24-hour amount of current drugx=EA dose of current drugEA dose of desired drug

Where x = amount of desired opioid in 24 hours and EA = equianalgesic dose obtained from the table above

For example: A patient with colon cancer is currently taking oral oxycodone 80 mg every 12 hours and needs to be converted to intravenous morphine due to a bowel obstruction. What is the equivalent IV morphine dose?

Step 1: Determine the 24-hour amount of oxycodone taken by this patient:

80 mg × 2 doses per 24 hours = 160 mg per 24 hours

Step 2: Using the conversion table above, find the equianalgesic (EA) doses of oxycodone and parenteral morphine:

15 mg oxycodone = 10 mg parenteral morphine

Step 3: Use the above equation and solve for x by cross-multiplying:

24-hour amount of oxycodone (160 mg)x=EA of current oxycodone (15 mg)EA dose of parenteral morphine (10 mg)

Where x = amount of parenteral morphine in 24 hours (solve by cross-multiplying)

160mg×10mg=15mgxx=1600mg15mg

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Tags: Pharmacology and the Nursing Process

May 9, 2017 | Posted by admin in NURSING | Comments Off

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Nurse Key

Fastest Nurse Insight Engine

Analgesic Drugs

Analgesic Drugs

Objectives

Key Terms

Anatomy, Physiology, and Pathophysiology Overview

Treatment of Pain in Special Situations

Pharmacology Overview

Opioid Drugs

Chemical Structure

Mechanism of Action and Drug Effects

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