Principles of Pharmacology in Pain Management
Maria C. Foy
One of the most widely encountered clinical situations is a patient in pain. Treatment of pain is one of the most difficult aspects of patient care. Pain is defined by the International Association for the Study of Pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (Merskey & Bogduk, 1994). Pain is subjective, and its intensity varies from patient to patient, day to day. The clinician has a large array of medications available to assist patients in relieving their pain. Principles of managing various types of pain will be described in this chapter and will introduce the practicing nurse to the many types and classes of drugs available for the therapeutic management of pain.
Analgesics represent one of the most frequently prescribed and administered classes of medications used in the treatment of pain. Managing pain in the acutely or chronically ill patient requires both a sound comprehension of the clinical pharmacology of analgesics and a clear understanding of how pain is perceived. Clinicians caring for chronically ill patients not only find themselves assisting the patient in dealing with the physical component of pain but often are confronted by the patient’s psychological, spiritual, and social perceptions of pain and pain medications.
Age is a major consideration in assessing pain. For example, elderly patients are less likely to complain about pain and request fewer analgesics to alleviate pain, secondary to incorrect beliefs and biases. A corollary exists in pediatric patients, whose inability to adequately express suffering leads some clinicians to believe that children cannot feel pain. Clinicians, however, now realize that pediatric patients experience as much pain as adults. Because of the identified communication barrier, clinicians need to evaluate a child in pain by utilizing special pain assessment tools developed for children. Similar assessment tools are utilized for adults who may not be able to verbally communicate their pain.
TYPES OF PAIN
Pain can be categorized as nociceptive, neuropathic, or inflammatory based on the presumed underlying cause. Nociceptive pain occurs as a result of nerve receptor stimulation following a mechanical, thermal, or chemical insult. Nociceptive pain is purposeful, where the pain tells you to stop doing whatever is causing the pain. Nociceptive pain can be further classified as somatic or visceral. Somatic pain associated with muscle, skin, or bone injury is often well localized. When pain affects the visceral organs, such as pain seen in pancreatitis, it is referred to as visceral pain. Inflammatory pain is a subtype of nociceptive pain, which results from the release of proinflammatory cytokines at the site of tissue injury. Inflammatory pain may be present in acute pain from bruises or infection and chronically in pain from rheumatoid arthritis or osteoarthritis.
Neuropathic pain is caused by abnormal signal processes in the central nervous system (CNS). Neuropathic pain can be peripheral or central in origin and is no longer protective in nature. Peripheral neuropathies include pain from diabetes and postherpetic neuralgia. Examples of central neuropathic pain syndromes include pain from multiple sclerosis, spinal cord injuries, migraine, and poststroke syndrome. Descriptors of neuropathic pain, such as electric-like, burning, tingling, stabbing, or shooting, can differentiate nerve pain from nociceptive pain and help determine appropriate treatment.
More than one type of pain may occur simultaneously. Failed back surgery syndrome, cancer pain, and chronic regional pain syndrome (CRPS) may have characteristics of a mixed nociceptive/neuropathic pain picture.
New evidence is now leading toward considering pain as a disease of the brain, especially when pain persists long after anticipated healing of the initial injury (Henry et al., 2011).
Noxious stimulants are no longer present and no pathology exists that would explain the pain. This type of pain is often referred to as maldynia, Greek for “bad pain,” which results from changes in the pain pathway. Pain resulting from nervous system changes and cortical reorganization is referred to as neuroplasticity. Structural changes consist of increase nerve endings and receptive fields, and a decreased threshold for nerve activation.
Noxious stimulants are no longer present and no pathology exists that would explain the pain. This type of pain is often referred to as maldynia, Greek for “bad pain,” which results from changes in the pain pathway. Pain resulting from nervous system changes and cortical reorganization is referred to as neuroplasticity. Structural changes consist of increase nerve endings and receptive fields, and a decreased threshold for nerve activation.
CLASSIFICATION OF PAIN
Pain can be classified into two categories, acute and chronic, which help identify the derivation of the pain and provide a framework for treatment. Pain can subsequently be categorized and treated based on expected chronicity of the pain and whether the pain is nociceptive, neuropathic, or mixed in origin.
Acute Pain
Acute pain has a sudden onset, usually subsides quickly, and is characterized by sharp, localized sensations with an identifiable cause. Acute pain is a natural physiologic response to injury, useful in warning individuals of disease or harmful situations. This process is often seen as a signal that the body is invoking critical immunologic and physiologic responses to cellular or tissue damage. Concomitant physiologic responses include excessive sympathetic nervous system activity, such as tachycardia, diaphoresis, and increased blood pressure and respiratory rate. Acute pain is somewhat instructive and purposeful by signaling danger. Pain is usually brief and resolves within a few months of onset. Surgical intervention and trauma are common sources of acute pain.
When acute pain responses become unremitting, constant, or undertreated, the biologic responses outlive their usefulness and can lead to chronic pain. Patients with chronic pain become tolerant to the physiologic response seen in acute pain. In addition, these patients often do not appear to be suffering from pain. The body becomes tolerant to the autonomic indicators where heart rate, blood pressure, and respiratory rate normalize as pain persists. Undesired consequences, such as anxiety and depression, are often associated with constant, long-term pain. The goal of acute pain management is to avoid progression to a chronic pain state. Early pain control will often prevent the development of chronic pain.
Chronic Pain
Chronic pain is defined by the Institute of Clinical Systems Improvement as “pain without biological value that has persisted beyond the normal time and despite the usual customary efforts to diagnose and treat the original condition and injury” (Hooten et al., 2013). Chronic pain may have a verifiable source, as in patients with arthritis, diabetic peripheral neuropathy, and postherpetic neuralgia. In some patients, however, no evidence of structural or nerve damage exists to explain the reason for pain. In these patients, the pain is most likely from peripheral and central sensitization of the pain pathways, explained later in this chapter.
Evidence is now showing that chronic pain is primarily a biopsychosocial disease, with cognitive factors such as pain catastrophizing and anxiety having a strong correlation to pain and disability. The current biomedical approach focusing only on tissue and tissue injury as the cause for the pain has often been ineffective. Patients are often complicated and need an individualized approach to therapy.
Identifying and differentiating pain through careful history of the location, quality, chronicity, and presence of psychological comorbidities is important because treatment choices are dictated by the cause and type of pain. The primary goal of therapy in chronic pain is to decrease the pain to a tolerable level using a combination of various types of therapies to help improve function and quality of life. Examples of types of chronic pain are shown in Box 7.1.
BOX 7.1
Classification of Chronic Pain
Classification of Chronic Pain
NOCICEPTIVE PAIN
Postoperative pain
Mechanical low back pain
Arthropathies (e.g., rheumatoid arthritis, osteoarthritis, gout)
Ischemic disorders
Myalgia (e.g., myofascial pain syndromes)
Nonarticular inflammatory disorders (e.g., polymyalgia rheumatica)
Skin and mucosal ulcerations
Superficial pain (sunburn, thermal burns, skin cuts)
Visceral pain (appendicitis, pancreatitis)
NEUROPATHIC PAIN
Alcoholic neuropathy
Cancer-related pain and some cancer treatments
Vitamin B12 deficiency
Chronic regional pain syndrome
Human immunodeficiency virus (HIV)-related pain and some HIV treatments
Multiple sclerosis-related pain
Diabetic peripheral neuropathy
Phantom limb pain
Postherpetic neuralgia
Poststroke pain
Trigeminal neuralgia
MIXED OR UNDETERMINED PATHOPHYSIOLOGY
Low back pain with radiculopathy
Carpal tunnel syndrome
Chronic recurrent headaches
Painful vasculitis
Cancer-Related Pain
Cancer-related pain is pain associated with malignancy and can result from the disease itself or damage to secondary tissue. Disease-induced pain includes pain secondary to direct tumor involvement of bone, nerves, viscera, or soft tissue. In addition, muscle spasm, muscle imbalance, or other body structure/function changes secondary to the tumor are considered disease induced. Pain may be associated with treatment of the disease and may be seen with biopsies, surgeries, and/or chemotherapy and radiation treatments. Pain may be present in sites where cancer has metastasized (i.e., bone pain). Cancer and treatment interventions may activate peripheral nociceptors, causing somatic and visceral nociceptive pain. Neuropathic pain involving the sympathetic nervous system may also be seen.
Chronic Noncancer Pain
Chronic noncancer pain (CNCP) is persistent pain seen in patients not affected by cancer. Some examples of CNCP are rheumatoid arthritis, osteoarthritis, fibromyalgia, and peripheral neuropathies. Alternately, chronic pain may be thought of as the disease itself when no cause of pain is identified. CNCP may be nociceptive, neuropathic, or mixed in origin (see Box 7.1). Nociceptive mechanisms usually respond well to traditional approaches to pain management, including common analgesic medications and nonpharmacologic strategies. Neuropathic pain will respond to most traditional approaches including opioid therapy. However, higher doses of opioids are required to control this type of pain. Therefore, adjunctive treatment choices including anticonvulsants, antidepressants, or dual-mechanism medications may be considered to replace or add to traditional treatment modalities.
Breakthrough Pain
Breakthrough pain (BTP) is defined as a transitory pain often seen in conjunction with chronic pain, where moderate to severe pain occurs in patients with otherwise well-controlled pain. True BTP is characterized as brief, lasting minutes to hours, and can interfere with functioning and quality of life. True BTP has historically been associated with cancer pain. BTP can also be seen in many other chronic pain conditions, such as neuropathic pain and chronic lower back pain.
Other types of BTP include pain caused by certain activities (incident pain) or when the duration of analgesia is less than the dosing interval (end-of-dose failure). Giving an analgesic prior to the incident known to cause pain will often allow the activity to be performed with minimal discomfort. Shortening the dosing interval is recommended in patients with end-of-dose failure.
PAIN PATHOPHYSIOLOGY
Several theories exist as to how information resultant from tissue damage is perceived by the brain as pain. Noxious stimuli from the point of the initial injury move through specialized nerve fibers within the spinal cord where the signal reaches the brain and is interpreted by the brain as pain. This transmission of the pain signal through the CNS is termed nociception. Free nerve endings of small myelinated A-delta fibers and larger unmyelinated C fibers are called nociceptors and are responsible for delivering pain signals to the brain. In the past, the “Gate Control Theory” proposed that “closing of the gate” to pain signals was accomplished primarily through stopping the transmission of the pain signal to the brain. However, recent studies theorize that changes in the brain and CNS have a much larger role in the perception of pain (Woo et al., 2015). Anxiety, fear, depression, and previous pain experiences may influence an individuals’ perception of pain, especially when pain becomes chronic.
Description of nociception can be divided into four main categories: transduction, transmission, perception, and modulation (Figure 7.1).
Transduction
Transduction refers to a process of nociceptor activation due to mechanical, thermal, or chemical injury. Nerve endings are activated through the release of various excitatory chemical neurotransmitters, such as prostaglandins (PGs), substance P, histamine, bradykinin, and serotonin.
Transmission
Transduction results in an action potential transmitted via the myelinated A-delta and unmyelinated C fibers, by way of the dorsal root ganglia, synapsing in the dorsal horn of the spinal cord. Second-order neurons are then activated and convey pain signals to the higher centers of the CNS. Neurotransmitters in the dorsal horn directly or indirectly depolarize the second-order neurons, facilitating transmission of information to the brain leading to the perception of pain. Inhibitory substances are also released in the dorsal horn (see section on modulation) and may decrease the number of signals reaching the brain, thereby lessening transmission.
Perception
Nociceptive information travels through different areas of the CNS to the brain where the pain is perceived. Perception is the end result of the pain transmission to the brain; at this point, we become consciously aware of the pain. Pain perception is not just a manifestation of physical injury but is affected by psychosocial factors and previous experiences of pain. In a chronic pain state, the perception of pain is no longer influenced by the initial noxious stimuli. The presence of psychological comorbidities in many patients with chronic pain may result in fear of the pain and pain catastrophizing, thereby increasing pain perception.
Modulation
Pain modulation occurs at various levels of the CNS. Endogenous opioids work through binding of opioid receptors in both the periphery and CNS. The main central inhibitory neurotransmitters involved in modulation of pain include serotonin and
norepinephrine. These neurotransmitters fight pain by increasing their concentration in the spinal cord and brainstem.
norepinephrine. These neurotransmitters fight pain by increasing their concentration in the spinal cord and brainstem.
Peripheral and Central Sensitization
Often, pain persists despite healing, and no reason for the pain can be found. Pain pathways become “broken,” and pain is seen without an obvious cause. Modifications occurring in the pain conduction pathways of the peripheral nervous system and CNS where hypersensitivity to pain stimulus and neuronal structural changes result in chronic pain syndromes are referred to as peripheral and central sensitization.
Peripheral Sensitization
When pain receptors in the periphery are continually stimulated (i.e., untreated acute pain), the threshold for stimulation becomes lowered and increased nerve firing occurs. Increased frequency of nerve impulses results in more pain signals reaching the dorsal horn of the spinal cord. These processes contribute to the development of central sensitization.
Central Sensitization
Central sensitization is defined as “an amplification of neural signaling within the CNS that elicits pain hypersensitivity” (Woolf, 2011). When nociceptive information repeatedly stimulates nerve fibers, increased dorsal horn neuronal activity is seen. With actual or potential nerve damage as in many cases of uncontrolled pain, the increase in firing causes increased excitability and responsiveness, termed central sensitization. The end result is a decrease of central pain inhibition, increased spontaneous neuronal activity in the dorsal horn,
formation of neuromas causing an increase in receptive fields, and a decreased threshold for neuronal firing. Sensitization of the NMDA (N-methyl-D-aspartic acid) receptor in the area of the dorsal horn also contributes to central sensitization. Allodynia (pain response to something painless), hyperalgesia (increased response to pain), persistent pain, or referred pain may result.
formation of neuromas causing an increase in receptive fields, and a decreased threshold for neuronal firing. Sensitization of the NMDA (N-methyl-D-aspartic acid) receptor in the area of the dorsal horn also contributes to central sensitization. Allodynia (pain response to something painless), hyperalgesia (increased response to pain), persistent pain, or referred pain may result.
Central sensitization can occur in many chronic pain states, especially when associated with nerve injury or dysfunction. Alternately, inadequate treatment of acute pain, concomitant psychological comorbidities, and poor coping skills may lead to the development of chronic pain through the sensitization of the CNS. Pain associated with central sensitization often responds poorly to traditional pain therapies. The addition of coanalgesics, reviewed later in this chapter, should be used for the treatment of chronic pain associated with central sensitization.
Chemical Mediators
Coupled with the neuronal component of pain is the release of chemical mediators initiating or continuing the stimulation of pain-conducting fibers. Peripheral chemical mediators include the neurotransmitters norepinephrine, serotonin, and histamine and polypeptides such as bradykinin, PGs, and substance P. Their role in the pain pathway is activating and sensitizing nociceptors and increasing neuronal excitability. Blocking the production of these mediators, particularly inhibiting the production of PGs with anti-inflammatory medications or similar compounds, minimizes nociceptor activation and neuronal firing, thereby lessening the transmission of pain through the CNS. Because of their role in initiating the pain pathway, these chemicals are targets for many of the medications currently available to treat pain.
Both excitatory and inhibitory neurotransmitters can be found in the dorsal horn of the spinal cord. Excitatory amino acids, glutamate and aspartate, along with substance P facilitate activation of second-order neurons in the dorsal horn primarily through activation of the NMDA receptors.
Pain-Modulating Receptors
Historically, pain modulation was thought to be primarily due to descending inhibitory information from the brain. Pain experts now theorize that both descending inhibitory pain pathways and inhibitory neurotransmitters decrease the perception of pain. Inhibitory substances, such as endogenous opioids, norepinephrine, and serotonin are released in various areas of the CNS and attenuate the transmission of pain by modulating the pain signals in the dorsal horn (Pasero & McCaffrey, 2011). Endogenous opioid substances, primarily β-endorphins, stimulate inhibitory neuronal receptors known as the opioid receptors. Stimulation of these receptors, particularly the mu opioid receptor, inhibits the transmission of pain signals to and from the higher brain centers. These receptors are stimulated by morphine-like drugs (opioids) and account for a great deal of the pain relief associated with this class of analgesics.
In contrast, neuropathic pain syndromes do not respond as well to conventional analgesic therapy. Neuropathic pain is often the result of peripheral and central sensitization. Sensitization of the NMDA receptors by various mechanisms is primarily responsible for this type of pain. Use of coanalgesic agents, such as antidepressants, anticonvulsants, and antiarrhythmic agents are recommended for neuropathic pain treatment. Details on the use of coanalgesics are found later in this chapter.
GENERAL PRINCIPLES OF PAIN MANAGEMENT
Treatment of pain in today’s society rests on two major principles: appropriate assessment of the severity and intensity of the pain and selection of the most appropriate agent to relieve pain with minimal side effects. Pain relief often requires a multimodal approach, using multiple agents that target different receptors and neurotransmitters in the CNS. Additional mind body approaches such as cognitive-behavioral therapy, massage, acupuncture, and mindful meditation are often recommended to be used in addition to pharmacologic therapy in patients suffering from chronic nonmalignant pain.
Pain Assessment
The individual assessment of pain is extremely important for determining proper treatments as well as monitoring effectiveness over time. According to the National Institutes of Health (NIH), self-reporting by patients is “the most reliable indicator of the existence and intensity of pain” (Herr & Garand, 2001). Along with self-reporting, involving the caregiver’s assessment of pain, especially in the very young or noncommunicating older patient, may be helpful. The self-report should include a description of the pain, location, intensity/severity, aggravating and relieving factors, and effect of pain on quality of life. Assessment tools are recommended to be brief and easy to use in order to reliably document pain intensity and pain relief. These tools will also evaluate other factors effecting pain, such as the presence of psychological comorbidities. One routine clinical approach to pain assessment and management is summarized by the mnemonic PQRSTU (Box 7.2). Assessment tools should be used initially to obtain a baseline level of pain and impaired function. Follow-up assessments should be performed to measure the progress toward acceptable pain relief based on the individual functional goals of the patient.
Because pain is subjective and is not easily quantifiable, several tools are available to determine the quantity and quality of a patients’ pain. The various pain scales can be classified as single or multidimensional and self-report or observational. Common single-dimension tools include the visual analog
scale (VAS), numerical rating scale (NRS), and verbal description scale (Figure 7.2). The single-dimension scales evaluate the intensity of pain. However, single-dimensional scales alone do not take into account function, which may be a more reliable indicator of pain control, especially chronic pain. Multidimensional scales consider location, pattern, and affective responses in addition to a severity score alone. Examples of multidimensional scales include the Brief Pain Inventory and the Initial Pain Assessment Tool (Pasero & McCaffrey, 2011).
scale (VAS), numerical rating scale (NRS), and verbal description scale (Figure 7.2). The single-dimension scales evaluate the intensity of pain. However, single-dimensional scales alone do not take into account function, which may be a more reliable indicator of pain control, especially chronic pain. Multidimensional scales consider location, pattern, and affective responses in addition to a severity score alone. Examples of multidimensional scales include the Brief Pain Inventory and the Initial Pain Assessment Tool (Pasero & McCaffrey, 2011).
BOX 7.2
P-Q-R-S-T-U Mnemonic for Assessing Pain
P-Q-R-S-T-U Mnemonic for Assessing Pain
P—Presenting, precipitating, palliating. When and how did the pain start? What makes the pain better? What have you used for pain in the past that wasn’t effective?
Q—Quality of the pain. What does the pain feel like? (descriptors such as sharp, stabbing, burning)
R—Region, radiation. Where is the pain? Does the pain stay in one location or does the pain radiate?
S—Severity. On a scale of 0 to 10, 0 being no pain, 10 being the worst pain imaginable, what is your pain now? In the last 24 hours? After a pain medication?
T—Temporal pattern. Is the pain constant, intermittent, associated with movement?
U—How does the pain affect you? Quality-of-life indicator.
The information assessed, particularly from the NRS and VAS, is helpful in determining appropriate treatment and drug selection. The Institute for Clinical Systems Improvement (ICSI) and the NIH have published guidelines on the appropriate evaluation and treatment of acute and chronic pain. Pain is recommended to be assessed with a 0-to-10 scale to assess a patient’s current level of pain. Zero defines a pain-free state, and a 10 describes the most severe pain imaginable by the patient. Pain rated at 1 to 3 is classified as mild; 4 to 7, moderate; and 8 to 10, severe. Other validated scales are available for use in special populations, such as in children and adults unable to self-report.
Subsequent assessments should evaluate the effectiveness of the treatment plan. First, determine if the cause of increased pain is related to the progression of disease, disease treatments, or a new cause of pain, as in cancer that has metastasized. Unrelieved pain may also be due to the development of opioid tolerance where the same amount of pain requires increasing doses of opioids in order to provide relief. The assessment of the patient’s pain and the efficacy of the treatment plan should be ongoing, and the pain reports should be documented. Continued use of the same pain scale is crucial to the continued assessment of treatment progress and communication between health care providers.
Pain Management
Treatment options for pain control include nonpharmacologic and pharmacologic therapies. Box 7.3 lists treatments that complement medication management of pain. Often, a multimodal, multidisciplinary approach using a combination of both pharmacologic and nonpharmacologic treatments is necessary to reduce pain to an acceptable level and provide an improvement in function, especially when opioid therapies are used. Maximizing the patient’s quality of life and function, while minimizing adverse effects of treatments, is the goal of the pain management treatment plan. Individualization of drug regimens according to the type and severity of pain is essential principles when using medications to manage both acute and chronic pain states.
For mild to moderate pain, acetaminophen, aspirin, or a nonsteroidal anti-inflammatory drug (NSAID) is usually considered initial therapy. Acetaminophen is used for mild pain across all age groups, mainly due to its favorable side effect profile. NSAIDs are very effective in pain associated with inflammation. However, patients may be at risk for gastrointestinal (GI), cardiac, or renal toxicities. Discussion of risk versus benefits of NSAID therapies will be discussed later in this chapter.
BOX 7.3
Adjunctive Pain Control Options
Adjunctive Pain Control Options
Physical methods (stretching, exercise, gait training, immobilization, hot or cold applications)
Patient education (Therapeutic Neuroscience Education)
Coping skills training
Cognitive-behavioral therapy
Massage
Transcutaneous electrical nerve stimulation
Acupuncture
Mindful meditation
For pain assessed as moderate to severe, combination opioids, such as oxycodone, hydrocodone, or codeine in combination with acetaminophen or ibuprofen, can be used. More potent opioids, such as morphine, hydromorphone, or fentanyl, are used for the treatment of severe pain. Moderate to severe pain can also be treated with low-dose opioids when a patient has contraindications to NSAIDs or acetaminophen. Opioids may be combined with other coanalgesic medications based on severity, description, and type of pain. The combination of an opioid with a coanalgesic medication may provide more pain control than either of the drug classes alone.
When developing a treatment plan, members of the health care team should take into account the preferences and needs of patients whose education or cultural traditions may impede effective treatment. Certain cultures have strong beliefs about pain and its management. Members of these cultures may hesitate to report unrelieved pain or may have alternative methods of treating pain. Clinicians should be aware of the unique needs and circumstances of patients from different age groups or various ethnic and cultural backgrounds. In addition, many biases to opioids continue to exist in some patients and prescribers. Patient and provider education may be effective in addressing cultural concerns and alleviating biases associated with pain treatments.
Pharmacologic treatment is the most common modality in pain control. However, nonpharmacologic options and therapies have been shown to be effective, especially in patients with chronic pain. Nonpharmacologic approaches include the use of therapies such as heat, cold, exercise, and physical therapy. Complementary therapies such as acupuncture, meditation, and massage may also be effective.
More data is emerging on how CNCP needs to be seen as a biopsychosocial and not a purely biological condition especially when pain has no obvious cause. Behavioral therapies, including systematic coping approaches and relaxation strategies, have been shown to be essential in these patients in order to improve function and quality of life. Transcutaneous electrical nerve stimulation therapy can be used to help control certain types of nerve-related pain. Treatment of difficult pain conditions that cannot be managed by noninvasive and/or pharmacologic treatments may require a consultation with a pain specialist or a pain psychologist to evaluate other options or interventions.
Drug Therapy by Type of Pain
Assessment of pain intensity is important when determining initial analgesic therapies. Mild to moderate pain can be treated with lower-potency medications such as acetaminophen and NSAIDs. These agents can also be part of a multimodal therapy plan in combination with opioids for severe pain. Historically, aspirin had been used as a pain modality for short-term pain treatment. However, increased adverse effects limit its chronic use. Aspirin is mostly used today to prevent cardiac events and is not routinely used as first-line pain management therapy.
Combination opioids, ketorolac, and tramadol are commonly used to treat moderate pain. The combination opioids contain the addition of a “nonopioid,” such as acetaminophen or ibuprofen, creating a treatment ceiling dose (maximum dose). Low doses of strong opioids may also be utilized for moderate pain in patients who have contraindications for NSAIDs or tramadol.
Opioids are the most common therapy recommended for severe pain. Morphine is the gold standard and the most studied opioid. When used in equivalent doses, most pure opioids (mu receptor agonists) are equally effective in controlling pain, but individual variation may exist among patients. Morphine, oxycodone, hydromorphone, oxymorphone, and fentanyl are pure mu opioid agonists indicated for the treatment of severe pain. Morphine is considered the opioid of first choice unless a contraindication exists or the patient has failed prior morphine therapy. Meperidine is another opioid that has historically been utilized for the treatment of severe pain. Use of this agent is no longer recommended due to neurotoxicity associated with accumulation of the active metabolite in patients with renal insufficiency or with chronic use.
In most persistent pain cases, pain medications should be administered around the clock (ATC), with as-needed medications used to treat BTP. This recommendation is based on the finding that regularly scheduled medications maintain a constant level of drug in the body and help prevent a recurrence of pain. BTP medications are indicated when intermittent pain occurs despite ATC therapy.
An essential principle in using medications to manage chronic pain is to individualize medication regimens according to the type and severity of pain. For mild to moderate pain, acetaminophen or an NSAID is usually considered initial therapy. Management of moderate to severe pain may utilize a combination opioid, tramadol, or low doses of opioids. Severe pain is treated with higher-potency opioids, such as morphine, hydromorphone, or oxycodone. Various classes of coanalgesics, such as anticonvulsants and antidepressants, can also be utilized in combination with the opioids (Table 7.1).
Acute Pain
Acute pain is often a response to tissue injury or trauma and is usually nociceptive in nature. Treatment includes nonopioids such as NSAIDs and acetaminophen for mild to moderate pain and opioid medications for moderate to severe pain. As acute pain increases and persists, it becomes more difficult to manage. Therefore, it is important to treat acute pain promptly and effectively. Also, untreated acute pain is often the catalyst in the development of chronic pain conditions in which pain persists despite healing of the original injury.