Pain management in patients with cancer

CHAPTER 29


Pain management in patients with cancer


Our topic for this chapter—management of cancer pain—is of note both for its good news and its bad news. The good news is that cancer pain can be relieved with simple interventions in 90% of patients. The bad news is that, despite the availability of effective treatments, pain goes unrelieved far too often. Multiple factors contribute to undertreatment (Table 29–1). Important among these are inadequate prescriber training in pain management; unfounded fears of addiction (shared by prescribers, patients, and families); and a healthcare system that focuses more on treating disease than relieving suffering.



Pain has a profound impact on both the patient and family. Pain undermines quality of life for the patient and puts a heavy burden on the family. Unrelieved pain compromises the patient’s ability to work, enjoy leisure activities, and fulfill his or her role in the family and in society at large. Furthermore, pain can impede recovery, hasten death from cancer, and possibly even create a risk of suicide.


Every patient has the right to expect that pain management will be an integral part of treatment throughout the course of his or her disease. The goal is to minimize pain and thereby maintain a reasonable quality of life, including the ability to function at work and at play, and within the family and society. In addition, if the cancer is incurable, treatment should permit the patient a relatively painless death when that time comes.




Pathophysiology of pain





Neurophysiologic basis of painful sensations

The following discussion is a simplified version of how we perceive pain. Nonetheless, it should be adequate as a basis for understanding the interventions used for pain relief.


Sensation of pain is the net result of activity in two opposing neuronal pathways. The first pathway carries pain impulses from their site of origin to the brain, and thereby generates pain sensation. The second pathway, which originates in the brain, suppresses impulse conduction along the first pathway, and thereby diminishes pain sensation.


Pain impulses are initiated by activation of pain receptors, which are simply free nerve endings. These receptors can be activated by three types of stimuli: mechanical (eg, pressure), thermal, and chemical (eg, bradykinin, serotonin, histamine). In addition, prostaglandins and substance P can enhance the sensitivity of pain receptors to activation, although these compounds do not activate pain receptors directly.


Conduction of pain impulses from the periphery to the brain occurs by way of a multineuron pathway. The first neuron carries impulses from the periphery to a synapse in the spinal cord, where it releases either glutamate or substance P as a transmitter. The next neuron carries the impulse up the cord to a synapse in the thalamus. And the next neuron carries impulses from the thalamus to the cerebral cortex.


The brain is able to suppress pain conduction using endogenous opioid compounds, especially enkephalins and beta-endorphin. These compounds are released at synapses in the brain and spinal cord. Release within the spinal cord is controlled by a descending neuronal pathway that originates in the brain. The opioids that we give as drugs (eg, morphine) produce analgesia by activating the same receptors that are activated by this endogenous pain-suppressing system.



Nociceptive pain versus neuropathic pain

In patients with cancer, pain has two major forms, referred to as nociceptive and neuropathic. Nociceptive pain results from injury to tissues, whereas neuropathic pain results from injury to peripheral nerves. These two forms of pain respond differently to analgesic drugs. Accordingly, it is important to differentiate between them. Among cancer patients, nociceptive pain is more common than neuropathic pain.


Nociceptive pain has two forms, known as somatic and visceral. Somatic pain results from injury to somatic tissues (eg, bones, joints, muscles), whereas visceral pain results from injury to visceral organs (eg, small intestine). Patients generally describe somatic pain as localized and sharp. In contrast, they describe visceral pain as vaguely localized with a diffuse, aching quality. Both forms of nociceptive pain respond well to opioid analgesics (eg, morphine). In addition, they may respond to nonopioids (eg, ibuprofen).


Neuropathic pain produces different sensations than does nociceptive pain and responds to a different group of drugs. Patients describe neuropathic pain with such words as “burning,” “shooting,” “jabbing,” “tearing,” “numb,” “dead,” and “cold.” Unlike nociceptive pain, neuropathic pain responds poorly to opioid analgesics. However, it does respond to drugs known collectively as adjuvant analgesics. Among these are certain antidepressants (eg, imipramine), anticonvulsants (eg, carbamazepine, gabapentin), and local anesthetics/antidysrhythmics (eg, lidocaine).



Pain in cancer patients

Among patients with cancer, pain can be caused by the cancer itself and by therapeutic interventions. Cancer can cause pain through direct invasion of surrounding tissues (eg, nerves, muscles, visceral organs) and through metastatic invasion at distant sites. Metastases to bone are very common, causing pain in up to 50% of patients. Cancer can cause neuropathic pain through infiltration of nerves, and visceral pain through infiltration, obstruction, and compression of visceral structures.


The incidence and intensity of cancer-induced pain is a function of cancer type and the stage of disease progression. Among patients with advanced disease, about 75% experience significant pain. Of these, 40% to 50% report moderate to severe pain, and 25% to 30% report very severe pain.


Therapeutic interventions—especially chemotherapy, radiation, and surgery—cause significant pain in at least 25% of patients, and probably more. Chemotherapy can cause painful mucositis, diffuse neuropathies, and aseptic necrosis of joints. Radiation can cause osteonecrosis, chronic visceral pain, and peripheral neuropathy (secondary to causing fibrosis of nerves). Surgery can cause a variety of pain syndromes, including phantom limb syndrome and postmastectomy syndrome.



Management strategy


Management of cancer pain is an ongoing process that involves repeating cycles of assessment, intervention, and reassessment. The goal is to create and implement a flexible treatment plan that can meet the changing needs of the individual patient. The flow chart in Figure 29–1 summarizes the steps involved. Management begins with a comprehensive assessment. Once the nature of the pain has been determined, a treatment modality is selected. Analgesic drugs are preferred, and hence are usually tried first. If drugs are ineffective, other modalities can be implemented. Among these are radiation, surgery, and nerve blocks. After each intervention, pain is reassessed. Once relief has been achieved, the effective intervention is continued, accompanied by frequent reassessments. If severe pain returns or new pain develops, a new comprehensive assessment should be performed—followed by appropriate interventions and reassessment. Throughout this process, the healthcare team should make every effort to ensure active involvement of the patient and his or her family. Without their involvement, maximal benefits cannot be achieved. The importance of patient and family involvement is reflected in the clinical approach to pain management recommended by the Agency for Healthcare Research and Quality (AHRQ):


image
Figure 29–1  Flow chart for pain management in patients with cancer.
NSAID = nonsteroidal anti-inflammatory drug. (Adapted from Jacox A, Carr DB, Payne R, et al: Management of Cancer Pain [Clinical Practice Guideline No. 9; AHCPR Publication No. 94-0592]. Rockville, MD: Agency for Health Care Policy and Research, 1994.)



Assessment and ongoing evaluation


Assessment is the foundation of treatment. In the absence of thorough assessment, effective pain management is impossible. Assessment begins with a comprehensive evaluation and then continues with regular follow-up evaluations. The initial assessment provides the basis for designing the treatment program. Follow-ups let us know how well treatment is working.



Comprehensive initial assessment


The initial assessment employs an extensive array of tests. The primary objective is to characterize the pain and identify its cause. This information provides the basis for designing a pain management plan. In addition, by documenting the patient’s baseline pain status, the initial assessment provides a basis for evaluating the efficacy of treatment.



Assessment of pain intensity and character: the patient self-report

The patient’s description of his or her pain is the cornerstone of pain assessment. No other component of assessment is more important! Remember, pain is a personal experience. Accordingly, if we want to assess pain, we must rely on the patient to tell us about it. Furthermore, we must act on what the patient says—even if we personally believe the patient may not be telling the truth.


The best way to ensure an accurate report is to ask the right questions and listen carefully to the answers. We cannot elicit comprehensive information by asking, “How do you feel?” Rather, we must ask a series of specific questions. The answers should be recorded on a pain inventory form. The following information should be obtained:



Onset and temporal pattern—When did your pain begin? How often does it occur? Has the intensity increased, decreased, or remained constant? Does the intensity vary throughout the day?


Location—Where is your pain? Do you feel pain in more than one place? Ask patients to point to the exact location of the pain, either on themselves, on you, or on a full-body drawing.


Quality—What does your pain feel like? Is it sharp or dull? Does it ache? Is it shooting or stabbing? Burning or tingling? These questions can help distinguish neuropathic pain from nociceptive pain.


Intensity—On a scale of 0 to 10, with 0 being no pain and 10 the most intense pain you can imagine, how would you rank your pain now? How would you rank your pain at its worst? And at its best? A pain intensity scale (see below) can be very helpful for this assessment.


Modulating factors—What makes your pain worse? What makes it better?


Previous treatment—What treatments have you tried to relieve your pain (eg, analgesics, acupuncture, relaxation techniques)? Are they effective now? If not, were they ever effective in the past?


Impact—How does the pain affect your ability to function, both physically and socially? For example, does the pain interfere with your general mobility, work, eating, sleeping, socializing, or sex life?



Physical and neurologic examinations

The physical and neurologic examinations help to further characterize the pain, identify its source, and identify any complications related to the underlying pathology. The clinician should examine the site of pain and determine if palpation or manipulation makes it worse. Nonverbal cues (eg, protecting the painful area, limited movement in an arm or leg) that may indicate pain should be noted. Common patterns of referred pain should be assessed. For example, if the patient has hip pain, the assessment should determine if the pain actually originates in the hip or if it is referred pain caused by pathology in the lumbar spine. Potential neurologic complications should be considered. For example, patients with back pain should be evaluated for impaired motor and sensory function in the limbs, and for impaired rectal and urinary sphincter function.





Pain intensity scales

Pain intensity scales are useful tools for assessing pain intensity. Representative scales are shown in Figures 29–2 and 29–3. The descriptive scale and numeric scale (Fig. 29–2) are used for adults and older children. The pain affect FACES scale (Fig. 29–3) is used for young children and for patients with cognitive impairment, who may have difficulty understanding the descriptive and numeric scales.


image
Figure 29–2  Linear pain intensity scales.
*If used as a graphic rating scale, a 10-cm baseline is recommended. (From Acute Pain Management Guideline Panel: Acute Pain Management: Operative or Medical Procedures and Trauma [Clinical Practice Guideline No. 1; AHCPR Publication No. 92-0032]. Rockville, MD: Agency for Health Care Policy and Research, 1992.)

image
Figure 29–3  Wong-Baker FACES pain rating scale.
Explain to the patient that the first face represents a person who feels happy because he or she has no pain, and that the other faces represent people who feel sad because they have pain, ranging from a little to a lot. Explain that face 10 represents a person who hurts as much as you can imagine, but that you don’t have to be crying to feel this bad. Ask the patient to choose the face that best reflects how he or she is feeling. The numbers below the faces correspond to the values in the numeric pain scale shown in Figure 29–2. (From Hockenberry MJ, Wilson D: Wong’s Essentials of Pediatric Nursing, 8th ed. St. Louis: Elsevier, 2009.)

Pain intensity scales are valuable not only for assessing pain intensity, but also for setting pain relief goals and evaluating treatment. When setting goals, the patient and prescriber should agree on a target pain intensity rating that will permit the patient to participate in recovery activities, perform activities of daily living, and enjoy activities that contribute to quality of life. The objective of treatment is to reduce pain to the agreed-upon level—and lower, if possible.



Ongoing evaluation


Once a treatment plan has been implemented, pain should be reassessed frequently. The objective is to determine the efficacy of treatment and to allow early diagnosis and treatment of new pain. Each time an analgesic drug is administered, pain should be evaluated after sufficient time has elapsed for the drug to take effect. Because most patients are treated at home, patients and caregivers should be taught to conduct and document pain evaluations. The prescriber will use the documented record to make adjustments to the pain management plan.


Prescribers, patients, and caregivers should be alert for new pain. In the majority of cases, new pain results from a new cause (eg, metastasis, infection, fracture). Accordingly, whenever new pain occurs, a rigorous diagnostic work-up is indicated.



Barriers to assessment


As stressed above, pain assessment relies heavily on a report from the patient. Unfortunately, the report is not always accurate: Some patients report more pain than they have, some report less, and some are unable to report at all. With other patients, cultural and language differences impede assessment. In all cases, reliance on behavioral cues and facial expression is a poor substitute for an accurate report by the patient.


Many patients under-report pain, frequently because of misconceptions. Some fear addiction to opioids, and hence want to minimize opioid use. Some believe they are expected to be stoic and “tough it out.” Some deny their pain because they fear pain signifies disease progression. When under-reporting of pain is suspected, the patient should be interviewed in an effort to discover the reason. If a misconception is responsible for under-reporting, educating the patient can help fix the problem.


Some patients fear they may be denied sufficient pain medication, and hence, to ensure adequate dosing, report more pain than they actually have. When exaggeration is suspected, the patient should be reassured that adequate pain relief will be provided, and should be taught that inaccurate reporting serves only to make appropriate treatment more difficult.


Language barriers and cultural barriers can impede pain assessment. For patients who do not speak English, a translator should be provided. Obtaining a pain rating scale in the patient’s own language would obviously help. A pain affect FACES scale can be useful, since facial expressions reflecting discomfort are the same in all cultures. Cultural beliefs may cause some patients to hide overt expression of pain and report less pain than is present. The interviewer should be alert to this possibility.


When assessing pain, we must keep in mind that behavior and facial expression may be poor indicators of pain status. For example, in patients approaching the end of life, behavioral cues of pain (eg, vocalizing, grimacing) are often absent. Other patients may simply have good coping skills, and hence may smile and move around in apparent comfort, even though they are in considerable pain. Because appearances can be deceiving, we must not rely on them to assess pain.


Assessment in young children and other nonverbal patients is a special challenge. By definition, nonverbal patients are unable to self-report pain. Accordingly, we must use less reliable methods of assessment, including observing the patient for cues. Assessment in children is discussed further under Pain Management in Special Populations.



Drug therapy


Analgesic drugs are the most powerful weapons we have for overcoming cancer pain. With proper use, these agents can relieve pain in 90% of patients. Because analgesics are so effective, drug therapy is the principal modality for pain treatment. Three types of analgesics are employed:



These classes differ in their abilities to relieve pain. With the nonopioid and adjuvant analgesics, there is a ceiling to how much relief we can achieve. In contrast, there is no ceiling to relief with the opioids.


Selection among the analgesics is based on pain intensity and pain type. To help guide drug selection, the World Health Organization (WHO) devised a drug selection ladder (Fig. 29–4). The first step of the ladder—for mild to moderate pain—consists of nonopioid analgesics: NSAIDs and acetaminophen. The second step—for more severe pain—adds opioid analgesics of moderate strength (eg, oxycodone, hydrocodone). The top step—for severe pain—substitutes powerful opioids (eg, morphine, fentanyl) for the weaker ones. Adjuvant analgesics, which are especially effective against neuropathic pain, can be used on any step of the ladder. Specific drugs to avoid are listed in Table 29–2.



image
Figure 29–4  The WHO analgesic ladder for cancer pain management.
Note that steps represent pain intensity. Accordingly, if a patient has intense pain at the outset, then treatment can be initiated with an opioid (step 2), rather than trying a nonopioid first (step 1). (Adapted from Cancer Pain Relief, 2nd ed. Geneva: World Health Organization, 1996.)

Traditionally, patients have been given opioid analgesics only after a trial with nonopioids has failed. Guidelines from the National Comprehensive Cancer Network (NCCN) recommend a different approach, in which initial drug selection is based on pain intensity. Specifically, if the patient reports pain in the 4 to 10 range (as measured on a numeric rating scale), then treatment should start directly with an opioid; an initial trial with a nonopioid is considered unnecessary. If the patient reports pain in the 1 to 3 range, then treatment usually begins with a nonopioid, although starting with an opioid remains an alternative.


It is common practice to combine an opioid with a nonopioid. Why? Because the combination can be more effective than either drug alone. When pain is only moderate, opioids and nonopioids can be given in a fixed-dose combination formulation, thereby simplifying dosing. However, when pain is severe, these drugs must be given separately. Why? Because, with a fixed-dose combination, side effects of the nonopioid would become intolerable as the dosage grew large, and hence would limit how much opioid could be given.


Drug therapy of cancer pain should adhere to the following principles:




Nonopioid analgesics


The nonopioid analgesics—NSAIDs and acetaminophen—constitute the first rung of the WHO analgesic ladder. These agents are the initial drugs of choice for patients with mild pain. There is a ceiling to how much pain relief nonopioid drugs can provide. Hence, there is no benefit to exceeding recommended dosages (Table 29–3). Acetaminophen is about equal to the NSAIDs in analgesic efficacy but lacks anti-inflammatory actions. Because of this difference and others, acetaminophen is considered separately below. The NSAIDs and acetaminophen are discussed at length in Chapter 71. Accordingly, discussion here is brief.




Nonsteroidal anti-inflammatory drugs

NSAIDs (eg, aspirin, ibuprofen) can produce a variety of effects. Primary beneficial effects are pain relief, suppression of inflammation, and reduction of fever. Primary adverse effects are gastric ulceration, acute renal failure, and bleeding. In addition, all NSAIDs except aspirin increase the risk of thrombotic events (eg, myocardial infarction, stroke). In contrast to opioids, NSAIDs do not cause tolerance, physical dependence, or psychologic dependence.


NSAIDs are effective analgesics that can relieve mild to moderate pain. All of the NSAIDs have essentially equal analgesic efficacy, although individual patients may respond better to one NSAID than to another. NSAIDs relieve pain by a mechanism different from that of the opioids. As a result, combined use of an NSAID with an opioid can produce greater pain relief than either agent alone.


NSAIDs produce their effects—both good and bad—by inhibiting cyclooxygenase (COX), an enzyme that has two forms, known as COX-1 and COX-2. Most NSAIDs inhibit both COX-1 and COX-2, although a few are selective for COX-2. The selective COX-2 inhibitors (eg, celecoxib [Celebrex]) cause less GI damage than the nonselective inhibitors. Unfortunately, the selective inhibitors pose a greater risk of thrombotic events, and hence long-term use of these drugs is not recommended.


For patients undergoing chemotherapy, inhibition of platelet aggregation by NSAIDs is a serious concern. Many anticancer drugs suppress bone marrow function, and thereby decrease platelet production. The resultant thrombocytopenia puts patients at risk of bruising and bleeding. Obviously, this risk will be increased by drugs that inhibit platelet function. Among the conventional NSAIDs, only one subclass—the nonacetylated salicylates (eg, magnesium salicylate)—does not inhibit platelet aggregation, and hence is safe for patients with thrombocytopenia. All other conventional NSAIDs should be avoided. Aspirin is especially dangerous because it causes irreversible inhibition of platelet aggregation. Hence, its effects persist for the life of the platelet (about 8 days). Because COX-2 inhibitors do not affect platelets, these drugs are safe for patients with thrombocytopenia.



Acetaminophen

Acetaminophen [Tylenol, others] is similar to the NSAIDs in some respects and different in others. Like the NSAIDs, acetaminophen is an effective analgesic, and hence can relieve mild to moderate pain. Benefits derive from inhibiting COX in the central nervous system (CNS), but not in the periphery. Combining acetaminophen with an opioid can produce greater analgesia than either drug alone (because acetaminophen and opioids relieve pain by different mechanisms).


Acetaminophen differs from the NSAIDs in several important ways. Because it does not inhibit COX in the periphery, acetaminophen lacks anti-inflammatory actions, does not inhibit platelet aggregation, and does not promote gastric ulceration, renal failure, or thrombotic events. Because acetaminophen does not affect platelets, the drug is safe for patients with thrombocytopenia.


Acetaminophen has important interactions with two other drugs: alcohol and warfarin (an anticoagulant). Combining acetaminophen with alcohol, even in moderate amounts, can result in potentially fatal liver damage. Accordingly, patients taking acetaminophen should minimize alcohol consumption. Acetaminophen also can increase the risk of bleeding in patients taking warfarin. The mechanism appears to be inhibition of warfarin metabolism, which causes warfarin to accumulate to dangerous levels.



Opioid analgesics


Opioids are the most effective analgesics available, and hence are the primary drugs for treating moderate to severe cancer pain. With proper dosing, opioids can safely relieve pain in about 90% of cancer patients. Unfortunately, many patients are denied adequate doses, owing largely to unfounded fears of addiction. In the past, opioids were known as narcotics, a term that is now obsolete.


Opioids produce a variety of pharmacologic effects. In addition to analgesia, they can cause sedation, euphoria, constipation, respiratory depression, urinary retention, and miosis. With continuous use, tolerance develops to most of these effects, with the notable exception of constipation. Continuous use also results in physical dependence, which must not be equated with addiction.


The opioids are discussed at length in Chapter 28. Discussion here focuses on their use in patients with cancer.



Mechanism of action and classification

Opioid analgesics relieve pain by mimicking the actions of endogenous opioid peptides (enkephalins, dynorphins, endorphins), primarily at mu receptors and partly at kappa receptors.


Based on their actions at mu and kappa receptors, the opioids fall into two major groups: (1) pure (full) agonists (eg, morphine) and (2) agonist-antagonists (eg, butorphanol). The pure agonists can be subdivided into (1) agents for mild to moderate pain and (2) agents for moderate to severe pain. The pure agonists act as agonists at mu receptors and at kappa receptors. In contrast, the agonist-antagonists act as agonists only at kappa receptors; at mu receptors, these drugs act as antagonists. Because their agonist actions are limited to kappa receptors, the agonist-antagonists have a ceiling to their analgesic effects. Furthermore, because of their antagonist actions, the agonist-antagonists can block access of the pure agonists to mu receptors, and can thereby prevent the pure agonists from relieving pain. Accordingly, agonist-antagonists are not recommended for managing cancer pain.

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Jul 24, 2016 | Posted by in NURSING | Comments Off on Pain management in patients with cancer

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