Brunner & Suddarth's Textbook of Medical-Surgical Nursing 15th Ed PDF

acute pain: pain that results from tissue damage that generally abates as healing occurs; serves as a warning signal that something is wrong or needs attention adjuvant analgesic agent: a substance or medication added to an analgesic medication regimen to improve analgesia (synonym: co-...

acute pain: pain that results from tissue damage that generally abates as healing occurs; serves as a warning signal that something is wrong or needs attention adjuvant analgesic agent: a substance or medication added to an analgesic medication regimen to improve analgesia (synonym: co- analgesic agent) agonist: a medication that binds to an opioid receptor mimicking the way endogenous substances provide analgesia agonist–antagonist: a type of opioid (e.g., nalbuphine and butorphanol) that binds to the kappa opioid receptor site acting as an agonist (capable of producing analgesia) and simultaneously to the mu opioid receptor site acting as an antagonist (reversing mu agonist effects) allodynia: pain due to a stimulus that does not normally provoke pain, such as touch; typically experienced in the skin around areas affected by nerve injury and commonly seen with many neuropathic pain syndromes antagonist: a medication that competes with agonists for opioid receptor binding sites; can displace agonists, thereby inhibiting their action breakthrough pain: a transitory increase in pain that occurs in the context of otherwise controlled persistent pain ceiling effect: an analgesic dose above which further dose increments produce no change in effect central sensitization: a key central mechanism of neuropathic pain; the abnormal hyperexcitability of central neurons in the spinal cord, which results from complex changes induced by the incoming afferent barrages of nociceptors and results in an increased nociceptive neuron response chronic or persistent pain: pain that may or may not be time limited but that persists beyond the usual course/time of tissue healing co-analgesic agent: one of many medications that can either improve the effectiveness of another analgesic agent or independently have analgesic action (synonym: adjuvant analgesic agent) comfort–function goal: the pain rating identified by the individual patient above which the patient experiences interference with function and quality of life (e.g., activities the patient needs or wishes to perform) efficacy: the extent to which a medication or another treatment “works” and can produce the intended effect—analgesia in this context half-life: the time it takes for the plasma concentration (amount of medication in the body) to be reduced by 50% (after starting a medication, or increasing its dose; four to five half-lives are required to 671  approach a steady-state level in the blood, irrespective of the dose, dosing interval, or route of administration; after four to five half-lives, a medication that has been discontinued generally is considered to be mostly eliminated from the body) hydrophilic: a substance or medication that is readily absorbed in aqueous solution hyperalgesia: an increasingly intense experience of pain resulting from a noxious stimulus intraspinal: “within the spine”; refers to the spaces or potential spaces surrounding the spinal cord into which medications can be given lipophilic: a substance or medication that is readily absorbed in fatty tissues metabolite: the product of biochemical reactions during medication metabolism mu agonist: any opioid that binds to the mu opioid receptor subtype and produces analgesic effects (e.g., morphine); used interchangeably with the terms full agonist, pure agonist, and morphinelike medication multimodal analgesia or multimodal pain management: the intentional, concurrent use of more than one pharmacologic or nonpharmacologic intervention with different methods of action with the goal to achieve better analgesia while using lower doses of medications with fewer adverse effects neuraxial: of the central nervous system neuropathic (pathophysiologic) pain: pain caused by injury or dysfunction (lesion or disease) of one or more nerves of the peripheral or central nervous systems with resultant impaired processing of sensory input neuroplasticity: the ability of the peripheral and central nervous systems to change both structure and function as a result of noxious stimuli nociceptive (physiologic) pain: pain that is sustained by ongoing activation of the sensory system that conducts the perception of noxious stimuli; implies the existence of damage to somatic or visceral tissues sufficient to activate the nociceptive system nociceptor: a type of primary afferent neuron that has the ability to respond to a noxious stimulus or to a stimulus that would be noxious if prolonged nonopioid: refers to analgesic medications that include acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs) NSAID: an acronym for nonsteroidal anti-inflammatory drug (pronounced “en said”) 672 opioid: refers to morphine and other natural, semisynthetic, and synthetic medications that relieve pain by binding to multiple types of opioid receptors; term is preferred to “narcotic” opioid dose–sparing effect: occurs when a nonopioid or co-analgesic medication is prescribed in addition to an opioid, enabling the opioid dose to be lower without diminishing analgesic effects opioid-induced hyperalgesia: a phenomenon in which exposure to an opioid induces increased sensitivity, or a lowered threshold, to the neural activity conducting pain perception; it is the “flip side” of tolerance opioid naïve: denotes a person who has not recently taken enough opioid on a regular enough basis to become tolerant to the opioid’s effects opioid tolerant: denotes a person who has taken opioids long enough at doses high enough to develop tolerance to many of the opioid’s effects, including analgesia and sedation pain: an unpleasant experience that is either emotional or sensory resulting from actual or possible damage to tissues and is uniquely experienced and described by each person peripheral sensitization: a key peripheral mechanism of neuropathic pain that occurs when there are changes in the number and location of ion channels; in particular, sodium channels abnormally accumulate in injured nociceptors, producing a lower nerve depolarization threshold, ectopic discharges, and an increase in the response to stimuli physical dependence: the body’s normal response to administration of an opioid for 2 or more weeks; withdrawal symptoms may occur if an opioid is abruptly stopped or an antagonist is given placebo: any medication or procedure, including surgery, that produces an effect in a patient because of its implicit or explicit intent and not because of its specific physical or chemical properties preemptive analgesic agents: pre-injury pain treatments (e.g., preoperative epidural analgesia and preincision local anesthetic infiltration) to prevent the development of peripheral and central sensitization of pain refractory: nonresponsive or resistant to therapeutic interventions such as analgesic agents substance use disorder (SUD): problematic use of substances such as opioids, benzodiazepines, or alcohol based on identification of at least two of the diagnostic criteria listed by the American Psychiatric Association. It is characterized by craving the substance; continuing use despite harm; inability to stop using; and experiencing withdrawal 673  symptoms when abruptly not using the substance; formerly known as addiction titration: upward or downward adjustment of the amount (dose) of an analgesic agent tolerance: a normal physiologic process characterized by decreasing effects of a medication at its previous dose, or the need for a higher dose of medication to maintain an effect withdrawal: result of abrupt cessation or rapid decrease in dose of a substance upon which one is physically dependent. It is not necessarily indicative of substance use disorder Pain serves as a survival tactic that guides individuals not only to avoid damage in the moment, but also to learn to avoid danger in the future (Martin, Power, Boyle, et al., 2017). Nurses in all settings play a key role in the management of pain as experts in assessment, medication administration, and patient education. They are uniquely positioned to assume this role as members of the health care team most consistently at the patient’s bedside. These characteristics have led to nurses’ distinction as the primary managers of patients who are experiencing pain (Curtis & Wrona, 2018). Fundamental Concepts Understanding the definition, effects, and types of pain lays the foundation for proper pain assessment and management. Definition of Pain The American Pain Society (APS, 2016) defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage” (p. 2). This definition describes pain as a complex phenomenon that can impact a person’s psychosocial, emotional, and physical functioning. The clinical definition of pain reinforces that pain is a highly personal and subjective experience: “Pain is whatever the experiencing person says it is, existing whenever he says it does” (McCaffery, 1968, p. 8). The self-report by the patient is the standard; it is considered to be the most reliable indicator of pain and the most essential component of pain assessment (DiMaggio, Clark, Czarenecki, et al., 2018). Effects of Pain Pain affects individuals of every age, gender, race, and socioeconomic class (APS, 2016). It is the primary reason people seek health care and one of the 674 most common conditions that nurses treat (U.S. Department of Health & Human Services [HHS], 2019). Unrelieved pain has the potential to affect every system in the body and cause numerous harmful effects, some of which may last a lifetime (Table 9-1). Despite many advances in the understanding of the underlying mechanisms of pain and the availability of improved analgesic agents and technology, as well as nonpharmacologic pain management methods, all types of pain continue to be undertreated (Jungquist, Vallerand, Sicoutris, et al., 2017). Types and Categories of Pain Pain can be categorized in many ways, and clear distinctions are not always possible. Pain often is described from the perspective of duration, as being acute or chronic (persistent) (APS, 2016). Acute pain involves tissue damage as a result of surgery, trauma, burn, or venipuncture, and is expected to have a relatively short duration and resolve with normal healing. Chronic or persistent pain is subcategorized as being of cancer or noncancer origin and can persist throughout the course of a person’s life. Examples of noncancer chronic pain include peripheral neuropathy from diabetes, back or neck pain after injury, and osteoarthritis pain from joint degeneration. Chronic pain may be intermittent, occurring with flares, or it may be continuous. Some conditions can produce both acute and chronic pain. For example, some patients with cancer have continuous chronic pain and also experience more intense acute exacerbations of pain periodically, which is called breakthrough pain (BTP). Patients may also endure acute pain from repetitive painful procedures during cancer treatment (APS, 2016). Pain is also classified by its inferred pathology as being either nociceptive pain or neuropathic pain (Table 9-2). Nociceptive (physiologic) pain refers to the normal functioning of physiologic systems that leads to the perception of noxious stimuli (tissue injury) as being painful (International Association for the Study of Pain [IASP], 2017). This is the reason why nociception is described as “normal” pain transmission. Neuropathic (pathophysiologic) pain is pathologic and results from abnormal processing of sensory input by the nervous system as a result of damage to the peripheral or central nervous system (CNS) or both (IASP, 2017). 675 TABLE 9-1 Harmful Effects of Unrelieved Pain Domains Specific Responses to Pain Affected Endocrine ↑ Adrenocorticotrophic hormone (ACTH), ↑ cortisol, ↑ antidiuretic hormone (ADH), ↑ epinephrine, ↑ norepinephrine, ↑ growth hormone (GH), ↑ catecholamines, ↑ renin, ↑ angiotensin II, ↑ aldosterone, ↑ glucagon, ↑ interleukin-1; ↓ insulin, ↓ testosterone Metabolic Gluconeogenesis, hepatic glycogenolysis, hyperglycemia, glucose intolerance, insulin resistance, muscle protein catabolism, ↑ lipolysis Cardiovascular ↑ Heart rate, ↑ cardiac workload, ↑ peripheral vascular resistance, ↑ systemic vascular resistance, hypertension, ↑ coronary vascular resistance, ↑ myocardial oxygen consumption, hypercoagulation, deep vein thrombosis Respiratory ↓ Flows and volumes, atelectasis, shunting, hypoxemia, ↓ cough, sputum retention, infection Genitourinary ↓ Urinary output, urinary retention, fluid overload, hypokalemia Gastrointestinal ↓ Gastric and bowel motility Musculoskeletal Muscle spasm, impaired muscle function, fatigue, immobility Cognitive Reduction in cognitive function, mental confusion Immune Depression of immune response Developmental ↑ Behavioral and physiologic responses to pain, altered temperaments, higher somatization; possible altered development of the pain system, ↑ vulnerability to stress disorders, addictive behavior, and anxiety states Future pain Debilitating chronic pain syndromes: postmastectomy pain, post thoracotomy pain, phantom pain, postherpetic neuralgia Quality of life Sleeplessness, anxiety, fear, hopelessness, ↑ thoughts of suicide Copyright 1999, Pasero, C., & McCaffery, M. Used with permission from Pasero, C., & McCaffery, M. (2011). Pain assessment and pharmacologic management. St. Louis, MO: Mosby-Elsevier. Patients may have a combination of nociceptive and neuropathic pain. For example, a patient may have nociceptive pain as a result of tumor growth, and also report radiating sharp and shooting neuropathic pain if the tumor is pressing against a nerve plexus. Sickle cell disease pain is usually a combination of nociceptive pain from the various hematologic changes of sickled cells as well as neuropathic pain from nerve ischemia (Belvis, Henderson, & Benzon, 2018). Nociceptive Pain Nociception includes four specific processes: transduction, transmission, perception, and modulation (Ellison, 2017). Figure 9-1 illustrates these processes and following is an overview of each. 676 TABLE 9-2 Classification of Pain by Inferred Pathology 677  Nociceptive Pain Neuropathic Pain Mixed Pain Physiologic Normal processing of Abnormal processing Components of Processes stimuli that damages of sensory input by both tissues or has the the peripheral or nociceptive and potential to do so if central nervous neuropathic prolonged; can be system or both pain; poorly somatic or visceral defined Categories and Somatic Pain: Arises from Centrally Generated No identified Examples bone joint, muscle, skin, Pain categories or connective tissue. It is Deafferentation pain: Examples: usually described as Injury to either the Fibromyalgia; aching or throbbing in peripheral or some types of quality and is well central nervous neck, shoulder, localized system; burning and back pain; Examples: Surgical, pain below the some trauma; wound and burn level of a spinal headaches; pain pain; cancer pain (tumor cord lesion reflects associated with growth) and pain injury to the HIV; some associated with bony central nervous myofascial metastases; labor pain system pain; pain (cervical changes and Examples: Phantom associated with uterine contractions); pain as a result of Lyme disease osteoarthritis and peripheral nerve rheumatoid arthritis damage; poststroke pain; osteoporosis pain; pain; pain pain of Ehlers–Danlos following spinal syndrome; ankylosing cord injury spondylitis Sympathetically Visceral Pain: Arises from maintained pain: visceral organs, such as Associated with the GI tract and dysregulation of pancreas. This may be the autonomic subdivided: nervous system Tumor involvement Example: Complex of the organ capsule regional pain that causes aching syndrome and fairly well- Peripherally localized pain Generated Pain Obstruction of Painful hollow viscus, which polyneuropathies: causes intermittent Pain is felt along cramping and poorly the distribution of localized pain many peripheral nerves. Examples: Organ-involved Examples: Diabetic cancer pain; ulcerative neuropathy; colitis; irritable bowel postherpetic syndrome; Crohn’s neuralgia; alcohol– disease; pancreatitis nutritional 678  neuropathy; some types of neck, shoulder, and back pain; pain of Guillain–Barré syndrome Painful mononeuropathies: Usually associated with a known peripheral nerve injury; pain is felt at least partly along the distribution of the damaged nerve Examples: Nerve root compression, nerve entrapment; trigeminal neuralgia; some types of neck, shoulder, and back pain Pharmacologic Most responsive to Co-analgesic agents, Co-analgesic Treatment nonopioids, opioids, and such as agents, such as local anesthetics antidepressants, antidepressants, anticonvulsants, anticonvulsants, and local and local anesthetics, but anesthetics, but there is wide there is wide variability in terms variability in of efficacy and terms of adverse-effect efficacy and profiles adverse-effect profiles GI, gastrointestinal; HIV, human immune deficiency virus. Copyright 1999, Pasero, C., & McCaffery, M. Used with permission from Pasero, C., & McCaffery, M. (2011). Pain assessment and pharmacologic management. St. Louis, MO: Mosby-Elsevier. Transduction Transduction refers to the processes by which noxious stimuli, such as a surgical incision or burn, activate primary afferent neurons called nociceptors, located throughout the body in the skin, subcutaneous tissue, and visceral (organ), and somatic (musculoskeletal) structures (Montgomery, Mallick- Searle, Peltier, et al., 2018). These neurons have the ability to respond selectively to noxious stimuli generated as a result of tissue damage from 679 mechanical (e.g., incision, tumor growth), thermal (e.g., burn, frostbite), chemical (e.g., toxins, chemotherapy), and infectious sources. Noxious stimuli cause the release of a number of excitatory compounds (e.g., serotonin, bradykinin, histamine, substance P, and prostaglandins), which move pain along the pain pathway (Ringkamp, Dougherty, & Raja, 2018) (see Fig. 9-1A). In addition, sodium, calcium, and potassium ion channels are stimulated to open, resulting in electrical impulses that are transmitted through the large, rapid conducting A-delta and smaller, peripheral C-fiber nociceptors (Ellison, 2017). Prostaglandins are lipid compounds that initiate inflammatory responses that increase tissue swelling and pain at the site of injury (Baral, Udit, & Chiu, 2019). They form when the enzyme phospholipase breaks down phospholipids into arachidonic acid. In turn, the enzyme cyclo-oxygenase (COX) acts on arachidonic acid to produce prostaglandins (Fig. 9-2). COX-1 and COX-2 are isoenzymes of COX and play an important role in producing the effects of the nonopioid analgesic agents, which include the nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen. NSAIDs produce pain relief by mediating inflammation at the site of trauma, primarily by blocking the formation of prostaglandins (Leppert, Malec-Milewska, Zajaczkowska, et al., 2018). The nonselective NSAIDs, such as ibuprofen, naproxen, diclofenac, and ketorolac, inhibit both COX-1 and COX-2, and the COX-2 selective NSAIDs, such as celecoxib, inhibit only COX-2. As Figure 9-2 illustrates, both types of NSAIDs produce anti-inflammation and pain relief through the inhibition of COX-2. Acetaminophen is known to be a COX inhibitor that has minimal peripheral effect, is not anti-inflammatory, and can both relieve pain and reduce fever by preventing the formation of prostaglandins in the CNS (Slattery & Klegeris, 2018). 680 Figure 9-1 Nociception. A. Transduction. B. Transmission. C. Perception. D. Modulation. Redrawn from Pasero, C., & McCaffery, M. (2011). Pain assessment and pharmacologic management (p. 5). St. Louis, MO: Mosby-Elsevier. Copyright 2011, Pasero, C., & McCaffery, M. Used with permission. 681 Figure 9-2 Enzyme pathway: COX-1 and COX-2. Redrawn from Pasero, C., & McCaffery, M. (2011). Pain assessment and pharmacologic management (p. 6). St. Louis, MO: Mosby-Elsevier. Copyright 2004, Pasero, C., & McCaffery, M. Used with permission. 682  Other analgesic agents work at the site of transduction by affecting the flux of ions. For example, sodium channels are closed and inactive at rest but undergo changes in response to nerve membrane depolarization. Transient channel opening leads to an influx of sodium that results in nerve conduction (Nouri, Osuagwu, Boyette-Davis, et al., 2018). Local anesthetics reduce nerve conduction by blocking sodium channels. The calcium channel blocking anticonvulsants that are used to treat neuropathic pain facilitate analgesia by reducing the flux of calcium ions and limiting glutamate, norepinephrine, and substance P release (Peterson, Benson, & Hurley, 2018). Transmission Transmission is another process involved in nociception. Effective transduction generates an action potential that is transmitted along the lightly myelinated rapid conducting A-delta fibers and the unmyelinated slower impulse conducting C fibers (Ellison, 2017) (see Fig. 9-1B). The endings of A- delta fibers detect thermal and mechanical injury, allow relatively quick localization of pain, and are responsible for a rapid reflex withdrawal from the painful stimulus. Unmyelinated C fibers respond to mechanical, thermal, and chemical stimuli. They produce poorly localized and often aching or burning pain. A-beta (β) fibers are the largest of the fibers and respond to touch, movement, and vibration but do not normally transmit pain (Ellison, 2017; Vardeh & Naranjo, 2017). The action potential impulse with the noxious information passes through the dorsal root ganglia, then synapses in the dorsal horn of the spinal cord, and then ascends up to the spinal cord and transmits the information to the brain, where pain is perceived (Ellison, 2017; Ringkamp et al., 2018) (see Fig. 9-1B). Extensive modulation occurs in the dorsal horn via complex neurochemical mechanisms (see Fig. 9-1B inset). The primary A-delta fibers release glutamate and C fibers release substance P and other neuropeptides (Schliessbach & Maurer, 2017). Glutamate is a key neurotransmitter because it binds to the N-methyl-D-aspartate (NMDA) receptor and promotes pain transmission (Zhou, 2017). Perception An additional process involved in nociception is perception, which is the result of the neural activity associated with transmission of noxious stimuli (Ringkamp et al., 2018). It requires activation of higher brain structures for the occurrence of awareness, emotions, and impulses associated with pain (see Fig. 9-1C). Although the physiology of pain perception continues to be studied, it can be targeted by nonpharmacologic therapies, such as distraction, which are based on the belief that innate brain processes can strongly influence pain perception (Chayadi & McConnell, 2019). 683 Modulation Modulation is another process involved in nociception. Modulation of the information generated in response to noxious stimuli occurs at every level from the periphery to the cortex and involves many different neurochemicals (Damien, Colloca, Bellei-Rodriguez, et al., 2018) (see Fig. 9-1D). For example, serotonin and norepinephrine are inhibitory neurotransmitters that are released in the spinal cord and the brain stem by the descending (efferent) fibers of the modulatory system (Nouri et al., 2018). Some antidepressants provide pain relief by blocking the body’s reuptake (resorption) of serotonin and norepinephrine, extending their availability to fight pain (Martin et al., 2017). Endogenous opioids are located throughout the peripheral and central nervous systems, and like exogenous opioids, they bind to opioid receptors in the descending system and inhibit pain transmission (Nouri et al., 2018). Neuropathic Pain Neuropathic pain is caused by either a lesion or a disease involving the somatosensory nervous system (Bouhassira, 2019). Injuries to peripheral nerves can either be traumatic or nontraumatic, such as diabetic or compression neuropathies (Osborne, Anastakis, & Davis, 2018). Although specific causes may vary based on the underlying pathology, it is theorized that there are changes in the ion channels; imbalance of the stimuli processing between excitatory and inhibitory somatosensory signals; activity of glial cells; or potential differences in modulation of pain that occur with neuropathic pain (Colloca, Ludman, Bouhassira, et al., 2017; Liu, Zhu, Ju, et al., 2019) (Fig. 9- 3). Recent research findings suggest that dysfunction in autophagy (i.e., cellular degradation of unnecessary materials) is involved with neuropathic pain (Liu et al., 2019). Research is ongoing to better define the peripheral and central mechanisms that initiate and maintain neuropathic pain (García, Gutiérrez-Lara, Centurión, et al., 2019; Kwiatkowski & Mika, 2018; Liu et al., 2019; Nishimura, Kawasaki, Suzuki, et al., 2019). 684  Figure 9-3 Neuropathic pain. Nociceptive injury or inflammation may result in an altered physiologic response within the nociceptive system. These changes cause release of inflammatory cytokines that may alter gene expression and sensitivity in nociceptive fibers. In turn, these alter nociceptive activity, causing neuropathic pain. Used with permission from Golan, D. E., Tashjian, A. H., & Armstrong, E. J. (2017). Principles of pharmacology: The pathophysiologic basis of drug therapy (4th ed.). Baltimore, MD: Wolters Kluwer Health | Lippincott Williams & Wilkins. Peripheral Mechanisms At any point from the periphery to the CNS, the potential exists for the development of neuropathic pain. Nerve endings in the periphery can become damaged, leading to abnormal reorganization in the nervous system called maladaptive neuroplasticity, an underlying mechanism of some neuropathic pain states (Osborne et al., 2018). Changes in ion channels can occur, such as increased sodium channel activity in sensory nerves resulting in heightened excitability, increased transduction, and release of neurotransmitters (Colloca et al., 2017). These and many other processes lead to a phenomenon called peripheral sensitization, which is thought to contribute to the maintenance of neuropathic pain and is thought to be reflected in allodynia and hyperalgesia (Osborne et al., 2018). Allodynia, or pain from a normally non-noxious stimulus (e.g., touch), is one such type of abnormal sensation and a common feature of neuropathic pain (Chekka & Benzon, 2018; Osborne et al., 2018). In patients with allodynia, the mere weight of clothing or bedsheets on the skin can be excruciatingly painful. Hyperalgesia is an increased response of pain sensation from a stimulus which at a usual pain threshold produces a less intense pain response. Central Mechanisms Central mechanisms also play a role in the establishment of neuropathic pain. Central sensitization is defined as abnormal hyperexcitability of central 685 neurons in the spinal cord, which results from complex changes induced by incoming afferent barrages of nociceptors, which also can result in allodynia and hyperalgesia (Osborne et al., 2018). Extensive release and binding of excitatory neurotransmitters, such as glutamate, activate the NMDA receptor and cause an increase in intracellular calcium levels into the neuron, resulting in pain (Yan, Li, Zhou, et al., 2017). Similar to what happens in the peripheral nervous system, an increase in the influx of sodium is thought to lower the threshold for nerve activation, increase response to stimuli, and enlarge the receptive field served by the affected neuron (Osborne et al., 2018; Yan et al., 2017). As in the peripheral nervous system, anatomic changes can occur in the CNS. For example, when the NMDA receptor cells are continuously activated, reorganization in the dorsal horn of the spinal cord can occur (Nouri et al., 2018). Nerve fibers can invade other locations and create abnormal sensations, such as allodynia, in the area of the body served by the injured nerve. Pain Assessment The highly subjective nature of pain causes challenges in assessment and management; however, the patient’s self-report is the undisputed standard for assessing the existence and intensity of pain (APS, 2016; Herr, Coyne, McCaffery, et al., 2011; McCaffery, Herr, & Pasero, 2011). Self-report is considered the most reliable measure of the existence and intensity of the patient’s pain and is recommended by The Joint Commission (Baker, 2017). Accepting and acting on the patient’s report of pain are sometimes difficult. Because pain cannot be proven, clinicians may feel vulnerable to inaccurate or untruthful reports of pain. Although clinicians are entitled to their personal opinions, those thoughts cannot interfere with appropriate patient care. Chart 9-1 provides strategies to use when the patient’s report of pain is not accepted. Chart 9-1 686  Strategies to Use When the Patient’s Report of Pain Is Not Accepted Acknowledge that everyone is entitled to a personal opinion, but personal opinion does not form the basis for professional practice. Clarify that the sensation of pain is subjective and cannot be proved or disproved. Quote recommendations from clinical practice guidelines, especially those published by the American Pain Society. Ask, “Why is it so difficult to believe that this person hurts?” Copyright 2011, Pasero, C., & McCaffery, M. Used with permission from Pasero, C., & McCaffery, M. (2011). Pain assessment and pharmacologic management. St. Louis, MO: Mosby-Elsevier. Quality and Safety Nursing Alert Although accepting and responding to the report of pain may result in administering analgesic agents to an occasional patient who does not have pain, doing so helps to ensure that everyone who does have pain receives appropriate care. Health care professionals do not have the right to deprive any patient of appropriate assessment and treatment simply because they believe a patient is not being truthful. Pain is an extremely personal experience manifested uniquely by each person. It is important to carefully assess and reassess pain when administering analgesic medications. Performing the Comprehensive Pain Assessment: Patient Interview A comprehensive pain assessment should be conducted during the admission assessment or initial interview with the patient, with each new report of pain, and whenever indicated by changes in the patient’s condition or treatment plan. It serves as the foundation for developing and evaluating the effectiveness of the pain treatment plan. The following are components of a comprehensive pain assessment and tips on how to elicit the information from the patient: Location(s) of pain: Ask the patient to state or point to the area(s) of pain on the body. Sometimes allowing patients to make marks on a body diagram is helpful in gaining this information. Intensity: Ask the patient to rate the severity of the pain using a reliable and valid pain assessment tool. Chart 9-2 provides guidance for educating patients and their families on how to use a pain rating scale. Various scales translated in several languages have been 687  evaluated and made available for use in clinical practice and for educational practice. The most common include the following: Chart 9-2 PATIENT EDUCATION 688 Educating Patients and Their Families How to Use a Pain Rating Scalea Step 1. Show the pain rating scale to the patient and the family and explain its primary purpose. Example: “This is a pain rating scale that many of our patients use to help us understand their pain and to set goals for pain relief. We will ask you regularly about pain, but any time you have pain you must let us know. We do not always know when you hurt.” Step 2. Explain the parts of the pain rating scale. If the patient does not like it or understand it, switch to another scale (e.g., vertical presentation, VDS, or faces). Example: “On this pain rating scale, 0 means no pain and 10 means the worst possible pain. The middle of the scale, around 5, means moderate pain. A 2 or 3 would be mild pain, but 7 or higher means severe pain.” Step 3. Discuss pain as a broad concept that is not restricted to a severe and intolerable sensation. Example: “Pain refers to any kind of discomfort anywhere in your body. Pain also means aching and hurting. Pain can include pulling, tightness, burning, knifelike feelings, and other unpleasant sensations.” Step 4. Verify that the patient understands the broad concept of pain. Ask the patient to mention two examples of pain they have experienced. If the patient is already in pain that requires treatment, use the present situation as the example. Example: “I want to be sure that I have explained this clearly, so would you give me two examples of pain you have had recently?” If the patient’s examples include various parts of the body and various pain characteristics, that indicates that they understand pain as a fairly broad concept. An example of what a patient might say is “I have a mild, sort of throbbing headache now, and yesterday my back was aching.” Step 5. Ask the patient to practice using the pain rating scale with the present pain or select one of the examples mentioned. Example: “Using the scale, what is your pain right now? What is it at its worst?” OR “Using the pain rating scale and one of your examples of pain, what is that pain usually? What is it at its worst?” Step 6. Set goals for comfort and function/recovery/quality of life. Ask patients what pain rating would be acceptable or satisfactory, considering the activities required for recovery or for maintaining a satisfactory quality of life. Example for a surgical patient: “I have explained the importance of coughing and deep breathing to prevent pneumonia and other complications. Now we need to determine the pain rating that will not interfere with this so that you may recover quickly.” Example for patient with chronic pain or terminal illness: “What do you want to do that pain keeps you from doing? What pain rating would allow you to do this?” 689 aWhen a patient is obviously in pain or not focused enough to learn to use a pain rating scale, pain treatment should proceed without pain ratings. Education can be undertaken when pain is reduced to a level that facilitates understanding how to use a pain scale. VDS, verbal descriptor scale. Copyright 2011, Pasero, C., & McCaffery, M. Used with permission from Pasero, C., & McCaffery, M. (2011). Pain assessment and pharmacologic management. St. Louis, MO: Mosby-Elsevier. Numeric Rating Scale (NRS): The NRS is most often presented as a horizontal 0- to 10-point scale, with word anchors of “no pain” at one end of the scale, “moderate pain” in the middle of the scale, and “worst possible pain” at the end of the scale. It may also be put on a vertical axis, which may be helpful for patients who read from right to left. Wong–Baker FACES Pain Rating Scale: The FACES scale consists of six cartoon faces with word descriptors, ranging from a smiling face on the left for “no pain (or hurt)” to a frowning, tearful face on the right for “worst pain (or hurt).” Patients are asked to choose the face that best reflects their pain. The faces are most commonly numbered using a 0, 2, 4, 6, 8, 10 metric, although 0 to 5 can also be used. Patients are asked to choose the face that best describes their pain. The FACES scale is used in adults and children as young as 3 years (McCaffery et al., 2011). It is important to appreciate that FACES scales are self-report tools; clinicians should not attempt to match a face shown on a scale to the patient’s facial expression to determine pain intensity. Patients may be able to understand the tool better if it is displayed vertically with no pain as the anchor at the bottom. Faces Pain Scale—Revised (FPS-R): The FPS-R has six faces to make it consistent with other scales using the 0 to 10 metric. The faces range from a neutral facial expression to one of intense pain and are numbered 0, 2, 4, 6, 8, and 10. As with the Wong–Baker FACES scale, patients are asked to choose the face that best reflects their pain. Faces scales have been shown to be reliable and valid measures in children as young as 3 years of age; however, the ability to optimally quantify pain (identify a number) is not acquired until approximately 8 years of age (Spagrud, Piira, & Von Baeyer, 2003). Ongoing research suggests that the FPS-R is preferred by both patients who are cognitively intact and older adults who are cognitively impaired, and by minority populations (Kang & Demiris, 2018). 690  Verbal descriptor scale (VDS): A VDS uses different words or phrases to describe the intensity of pain, such as “no pain, mild pain, moderate pain, severe pain, very severe pain, and worst possible pain.” The patient is asked to select the phrase that best describes pain intensity. Visual Analogue Scale (VAS): The VAS is a horizontal (sometimes vertical) 10-cm line with word anchors at the extremes, such as “no pain” on one end and “pain as bad as it could be” or “worst possible pain” on the other end. Patients are asked to make a mark on the line to indicate intensity of pain, and the length of the mark from “no pain” is measured and recorded in centimeters or millimeters. Although often used in research, the VAS is impractical for use in daily clinical practice and rarely used in that setting. Quality: Ask the patient to describe how the pain feels. Descriptors such as “sharp,” “shooting,” or “burning” may help identify the presence of neuropathic pain. Onset and duration: Ask the patient when the pain started and whether it is constant or intermittent. Aggravating and relieving factors: Ask the patient what makes the pain worse and what makes it better. Effect of pain on function and quality of life: The effect of pain on the ability to perform recovery activities should be regularly evaluated in the patient with acute pain. It is particularly important to ask patients with persistent pain about how pain has affected their lives, what they could do before the pain began that they can no longer do, or what they would like to do but cannot do because of the pain. Comfort–function goal (pain intensity): For patients with acute pain, identify short-term functional goals and reinforce to the patient that good pain control will more likely lead to successful achievement of the goals. For example, surgical patients are told that they will be expected to ambulate or participate in physical therapy postoperatively. Patients with chronic pain can be asked to identify their unique functional or quality-of-life goals, such as being able to work or walk the dog. Success is measured by progress toward meeting those functional goals (Topham & Drew, 2017). Other information: The patient’s culture, past pain experiences, and pertinent medical history such as comorbidities, laboratory tests, and diagnostic studies are considered when establishing a treatment plan. 691  Patients who are unable to report their pain are at higher risk for undertreated pain than those who can report (Horgas, 2017; McCaffery et al., 2011). In the adult population, this includes patients who are cognitively impaired, critically ill (intubated, unresponsive), comatose, or imminently dying. Patients who are receiving neuromuscular blocking agents or are sedated from anesthesia and other medications given during surgery are also among this at-risk population. The Hierarchy of Pain Measures is recommended as a framework for assessing pain in patients who are nonverbal (Herr et al., 2011; McCaffery et al., 2011). The key components of the hierarchy require the nurse to (1) attempt to obtain self-report, (2) consider underlying pathology or conditions and procedures that might be painful (e.g., surgery), (3) observe behaviors, (4) evaluate physiologic indicators, and (5) conduct an analgesic trial. Chart 9-3 provides detailed information on each component of the Hierarchy of Pain Measures. When patients cannot self-report their pain, some observational tools may be used to help with clinical decision making. Some of these assign a score by observing behaviors that tend to be associated with pain. These observational scores are not considered equivalent to a patient’s self-reported pain intensity score, however. It is imperative to remember that behaviors can indicate the presence of pain, but the absence of behavior does not indicate the absence of pain. Patients who are not moving or making any sounds may still be experiencing intense pain. For instance, older adults with moderate and severe dementia frequently have comorbid disorders that may cause pain (Mueller, Schumacher, Holzer, et al., 2017). Accurately assessing and treating their pain can be difficult to achieve (see Chart 9-4 Nursing Research Profile: Evaluation of a Tool to Assess Pain in Older Adults with Dementia). The following tools are examples of validated measures that are appropriate for different populations of patients unable to self-report their pain (Fry & Elliott, 2018; Kochman, Howell, Sheridan, et al., 2017; Rijkenberg, Stilma, Bosman, et al., 2017; Schofield & Abdulla, 2018). Chart 9-3 692 Hierarchy of Pain Measures 1. Attempt to obtain the patient’s self-report, the single most reliable indicator of pain. Do not assume that a patient cannot provide a report of pain; many patients who are cognitively impaired are able to use a self-report tool if simple actions are taken. Try using standard pain assessment tools (see text). Increase the size of the font and other features of the scale. Present the tool in vertical format (rather than the frequently used horizontal). Try using alternative words, such as “ache,” “hurt,” and “sore,” when discussing pain. Ensure eyeglasses and hearing aids are functioning. Ask about pain in the present. Repeat instructions and questions more than once. Allow ample time to respond. Remember that head nodding and eye blinking or squeezing the eyes tightly can also be used to signal presence of pain and sometimes used to rate intensity. Ask patients who are intubated and who are awake and oriented to point to a number on the numerical scale if they are able. Repeat instructions and show the scale each time pain is assessed. 2. Consider the patient’s condition or exposure to a procedure that is thought to be painful. If appropriate, assume pain is present and document as such when approved by institution policy and procedure. As an example, pain should be assumed to be present in a patient who is unresponsive, mechanically ventilated, and critically ill due to trauma. 3. Observe behavioral signs, for example, facial expressions, crying, restlessness, and changes in activity. A pain behavior in one patient may not be in another. Try to identify pain behaviors that are unique to the patient (“pain signature”). Many behavioral pain assessment tools are available that will yield a pain behavior score and may help determine whether pain is present. However, it is important to remember that a behavioral score is not the same as a pain intensity score. Behavioral tools are used to help identify the presence of pain, but the pain intensity is unknown if the patient is unable to provide it. A surrogate who knows the patient well (e.g., parent, spouse, or caregiver) may be able to provide information about underlying painful pathology or behaviors that may indicate pain. 4. Evaluate physiologic indicators with the understanding that they are the least sensitive indicators of pain and may signal the existence of conditions other than pain or a lack of it (e.g., hypovolemia, blood loss). Patients quickly adapt physiologically despite pain and may have normal or below normal vital signs in the presence of severe pain. The overriding principle 693  is that the absence of an elevated blood pressure or heart rate does not mean the absence of pain. 5. Conduct an analgesic trial to confirm the presence of pain and to establish a basis for developing a treatment plan if pain is thought to be present. An analgesic trial involves the administration of a low dose of nonopioid or opioid and observing patient response. The initial low dose may not be enough to elicit a change in behavior and should be increased if the previous dose was tolerated, or another analgesic agent may be added. If behaviors continue despite optimal analgesic doses, other possible causes should be investigated. In patients who are completely unresponsive, no change in behavior will be evident and the optimized dose of the analgesic agent should be continued. Copyright 2011, Pasero, C., & McCaffery, M. Used with permission. Adapted from Pasero, C. (2009). Challenges in pain assessment. Journal of PeriAnesthesia Nursing, 24(1), 50–54; Pasero, C., & McCaffery, M. (2011). Pain assessment and pharmacologic management. St. Louis, MO: Mosby- Elsevier. Chart 9-4 NURSING RESEARCH PROFILE 694 Evaluation of a Tool to Assess Pain in Older Adults with Dementia Mueller, G., Schumacher, P., Holzer, E., et al. (2017). The inter-rater reliability of the observation instrument for assessing pain in elderly with dementia: An investigation in the long-term care setting. Journal of Nursing Measurement, 25(3), E173–E184. Purpose The aim of this study was to examine the interrater reliability of the German version of the observation instrument for assessing pain in older adults with dementia called the BISAD for the German (Beobachtungsinstrument für das Schmerzassessment bei alten Menschen mit Demenz). This is a tool that is commonly used to assess pain among older adults with moderate and severe dementia who reside in long-term care facilities in both Germany and Austria; however, interrater reliability was not previously done to ensure its validity. Design This study used a quantitative multicenter-descriptive cross-sectional design with a convenience sample of 71 participants who resided in one of three nursing homes in Austria. The nursing participants consisted of 46 registered nurses who had been working at one of the same three nursing homes for at least 2 y. Nurse participants were paired to independently evaluate a resident participant within the same hour using the eight-item BISAD observational pain assessment tool. Findings Although modest agreement between raters was noted, the absolute concordance of the total was only 25.32%. The analysis of interrater reliability was low and did not support reliability of the items in the BISAD. There was agreement that pain was greater with movement than when the participant residents were at rest. Nursing Implications Findings of this study are important since they indicate the items used in the BISAD tool are not reliable for assessing pain in older adult residents with moderate and severe dementia in nursing homes in Austria, although it is commonly used. This is an important finding since use of this tool with that population could yield inaccurate data upon which nurses could base pain management care. One interesting aspect of this study was that behaviors did demonstrate greater pain with activity than when at rest. Finally, the authors note that there may be cultural and language issues that affected the results and encourage a translated version of the tool be assessed in long- term care facilities where English is the primary language. 695  FLACC: indicated for use in young children. Scores are assigned after assessing Facial expression, Leg movement, Activity, Crying, and Consolability, with each of these five categories assigned scores from 0 to 2, yielding a total composite score of 0 to 10. Scores of “0” are interpreted as reflecting that the patient is relaxed and comfortable, scores of “1” to “3” are interpreted as consistent with mild discomfort, scores from “4” to “6” are considered consistent with moderate pain, and scores from “7” to “10” are considered consistent with severe discomfort or pain. PAINAD (Pain Assessment IN Advanced Dementia): indicated for use in adults with advanced dementia who are not able to verbalize their needs. Patterned after the FLACC, this tool was developed by the U.S. Department of Veterans Affairs for patients who have dementia. CPOT (Critical Care Pain Observation Tool): indicated for use in patients in critical-care units who cannot self-report pain, whether or not they may be intubated. It is also patterned after the FLACC. Reassessing Pain Following initiation of the pain management plan, pain is reassessed and documented on a regular basis to evaluate the effectiveness of treatment. At a minimum, pain should be reassessed with each new report of pain and before and after the administration of analgesic agents (McCaffery et al., 2011). The frequency of reassessment depends on the stability of the patient and the timing of peak effect of the medication administered, which is generally between 15 and 30 minutes following parenteral administration and between 1 and 2 hours following oral administration (Chou, Gordon, de Leon-Casasola, et al., 2016). For example, in the postanesthesia care unit (PACU), reassessment may be necessary as often as every 10 minutes when pain is unstable during intravenous (IV) opioid titration but may be done an hour following administration of oral medication in patients with satisfactory and stable pain control the day following surgery. Veterans Considerations Nurses should be aware that research has demonstrated a high prevalence of pain associated disorders, including arthritis, fibromyalgia, headaches and generalized abdominal, back, and joint pain in veteran populations (Nahin, 2017). In addition, reports of severe pain are more common in military veterans compared to nonveterans, especially in those who served, more recently, in conflicts in Iraq and Afghanistan (Nahin, 2017). In particular, younger veterans (18 to 39 years of age) and male veterans report significantly 696 higher levels of pain compared to matched age groups and men in the general public (Nahin, 2017). As a result, it is important for the nurse to determine during assessment if a patient has served in the U.S. military, to recognize that this group may have unique needs related to their service, and to advocate for multimodal and multidisciplinary approaches to help veterans better cope with pain. For example, Groessi, Liu, Change, and colleagues (2017) found that yoga was a safe and beneficial intervention in helping veterans to reduce pain and disability, while taking fewer opioid medications. Pain Management Achieving optimal pain relief is best viewed on a continuum, with the primary objective being to provide both effective and safe analgesia (Pozek, De Ruyter, & Khan, 2018). The quality of pain control should be addressed whenever patient care is passed on from one clinician to another, such as at change of shift and transfer from one clinical area to another. Optimal pain relief is the responsibility of every member of the health care team and begins with titration of the analgesic agent, followed by continued prompt assessment, analgesic agent administration, and nonpharmacologic interventions during the course of care to safely achieve pain intensities that allow patients to meet their functional goals with relative ease. Although it may not always be possible to achieve a patient’s pain intensity goal within the short time the patient is in an area like the PACU or emergency department, this goal provides direction for ongoing analgesic care. Important information to provide during transfer report is the patient’s comfort–function goal, how close the patient is to achieving it, what has been done thus far to achieve it (analgesic agents and doses and/or nonpharmacologic interventions), and how well the patient has tolerated administration of the analgesic agent (adverse effects). There is growing interest among both clinicians and researchers in linking pain management to functional goals. One effort in this work is the Clinically Aligned Pain Assessment (CAPA) Tool, which is used to assess various degrees of comfort, pain control, function, and sleep (Topham & Drew, 2017). Pain management interventions should improve and not inhibit progress toward healing and rehabilitation. Pharmacologic Management of Pain: Multimodal Analgesia Pain is a complex phenomenon involving multiple underlying mechanisms that requires more than one analgesic agent to manage it safely and effectively. The recommended approach for the treatment of all types of pain in all age groups is called multimodal analgesia or multimodal pain management. A 697 multimodal regimen intentionally and simultaneously combines medications with different underlying mechanisms, along with nonpharmacologic interventions, which allows for lower doses of each of the medications in the treatment plan, reducing the potential for adverse effects. Furthermore, multimodal analgesia can result in comparable or greater pain relief with fewer adverse effects than can be achieved with any single analgesic agent (Beverly, Kaye, Ljungqvist, et al., 2017; Blackburn, 2018). Routes of Administration Oral is the preferred route of analgesic administration and should be used whenever feasible (Chou et al., 2016). Medications administered via the oral route are generally best tolerated, easiest to administer, and most cost- effective. When the oral route is not possible, such as when patients cannot swallow, are NPO (nothing by mouth), or nauseated, other routes of administration are used. For example, patients with cancer pain who are unable to swallow may take analgesic agents by the transdermal, rectal, or subcutaneous route of administration (Burchum & Rosenthal, 2019). In the immediate postoperative period, the IV route is most often the first- line route of administration for analgesic delivery, and patients are transitioned to the oral route as tolerated (see Chapter 16 for the management of postoperative pain). The rectal route of analgesic administration is an alternative route when oral or IV analgesic agents are not an option (e.g., for palliative purposes during end-of-life care). The rectum allows passive diffusion of medications and absorption into the systemic circulation. This route can be less expensive and does not involve the skill and expertise required of the parenteral route of administration. Limitations are that medication absorption can be unreliable and depends on many factors including rectal tissue health and administrator technique. Some patients may be resistant to or fearful of rectal administration. The rectal route is contraindicated in patients who are neutropenic or thrombocytopenic because of potential rectal bleeding. Diarrhea, perianal abscess or fistula, and abdominoperineal resection are also relative contraindications (Burchum & Rosenthal, 2019). The topical route of administration is used for both acute and chronic pain. For example, the nonopioid diclofenac is available in patch and gel formulations for application directly over painful areas. Local anesthetic creams, such as eutectic mixture or emulsion of local anesthetics and lidocaine cream 4%, can be applied directly over the injection site prior to painful needle stick procedures; the lidocaine patch 5% is often used for well-localized types of neuropathic pain, such as postherpetic neuralgia. It is important to distinguish between topical and transdermal medication delivery. Although both routes require the medication to cross the stratum corneum to produce analgesia, transdermal delivery requires absorption into the systemic 698 circulation to achieve effects, whereas topical agents produce effects in the tissues immediately under the site of application (referred to as targeted peripheral analgesia). Compounding pharmacies may be consulted to custom blend antispasmodic agents, such as topical morphine or gabapentin, for topical application at the painful site. A more invasive method used to manage pain is accomplished using neuraxial analgesia, which involves administering medication in the epidural or subarachnoid space (American Society of Regional Anesthesia and Pain Medicine, 2016). Delivery of analgesic agents by the neuraxial route is accomplished by inserting a needle into the subarachnoid space (for intrathecal [spinal] analgesia) or the epidural space, and either injecting the analgesic medication directly, or threading a catheter through the needle to enable bolus dosing or continuous administration (Conlin, Grant, & Wu, 2018; Hernandez, Grant, & Wu, 2018). Intrathecal catheters for acute pain management are used most often for providing anesthesia or a single bolus dose of an analgesic agent. Implanted intrathecal pumps deliver very small amounts of medication in a constant infusion for treatment of end-of-life pain or persistent pain (Jamison, Cohen, & Rosenow, 2018). Temporary epidural catheters for acute pain management are removed after 2 to 4 days. Epidural analgesia is administered by clinician-given bolus, continuous infusion (basal rate), and patient-controlled epidural analgesia (PCEA). The most common opioids given intraspinally are morphine, fentanyl, and hydromorphone. These are often combined with a local anesthetic, most often ropivacaine or bupivacaine (Jamison et al., 2018). The multimodal use of local anesthetics with opioids improves analgesia and produces an opioid dose–sparing effect. A pain management technique that involves the use of an indwelling catheter is the continuous peripheral nerve block (also called perineural anesthesia), whereby an initial local anesthetic block is established and followed by the placement of a catheter or catheters through which an infusion of local anesthetic, usually ropivacaine or bupivacaine, is infused continuously to the targeted site of innervation. The effect of local anesthetic is dose dependent: at lower doses, the smaller sensory nerve fibers are affected before the larger motor fibers. Patients thus medicated are able to walk but have well controlled pain (Burchum & Rosenthal, 2019; Ilfeld & Mariano, 2018). Dosing Regimen Achieving, then maintaining, optimal pain management that is safe, effective, and progresses toward realistic functional goals requires patient education with continuing reassessment of analgesic effect and development of any untoward effects (Chou et al., 2016). Accomplishing these goals may require the mainstay analgesic agent to be given on a scheduled around-the-clock (ATC) basis, rather than PRN (as needed) to maintain stable analgesic blood levels when pain is continuous (Eksterowicz & DiMaggio, 2018). ATC dosing 699 regimens are designed to control pain for patients who report pain being present 12 hours or more during a 24-hour period. PRN dosing of analgesic agents is appropriate for intermittent pain, such as prior to painful procedures and for BTP (pain that “breaks through” the pain being managed by the mainstay analgesic agent), for which supplemental doses of analgesia are provided (Palat, 2018). Patient-Controlled Analgesia Patient-controlled analgesia (PCA) is an interactive method of pain management that allows patients to treat their pain by self-administering doses of analgesic agents (Burchum & Rosenthal, 2019). It is used to manage all types of pain by multiple routes of administration, including oral, IV, subcutaneous, epidural, and perineural (Fernandes, Hernandes, de Almeida, et al., 2017). Current guidelines from the APS, the American Society of Regional Anesthesia and Pain Medicine, and the American Society of Anesthesiologists strongly recommended IV PCA for postoperative pain management when it is necessary to use the parenteral route to deliver analgesic medications (Chou et al., 2016). A PCA infusion device is programmed so that the patient can press a button (pendant) to self-administer a dose of an analgesic agent (PCA dose) at a set time interval (demand or lockout) as needed. Patients who use PCAs must be able to understand the relationships among pain, pushing the PCA button or taking the analgesic agent, and pain relief, and must be cognitively and physically able to use any equipment that is necessary to administer the therapy (ECRI Institute Patient Safety Organization, 2017). A basal rate (continuous infusion) may be used for patients who are opioid tolerant, and when PCEA is used. It is discouraged for patients who are opioid naïve and receiving IV PCA due to the risk of oversedation with subsequent respiratory depression (Chou et al., 2016; ECRI Institute Patient Safety Organization, 2017). Essential to the safe use of a basal rate with PCA is close monitoring by nurses of sedation and respiratory status and prompt decreases in opioid dose (e.g., discontinue basal rate) if increased sedation is detected (Pasero, Quinn, Portenoy, et al., 2011). The primary benefit of PCA is that it recognizes that only the patient can feel the pain and only the patient knows how much analgesic will relieve it. This reinforces that PCA is for patient use only and that unauthorized activation of the PCA device by anyone other than the patient (PCA by proxy) should be discouraged (Burchum & Rosenthal, 2019). Quality and Safety Nursing Alert 700  Staff, family, and other visitors should be instructed to contact the nurse if they have concerns about pain control rather than activating the PCA device for the patient. However, for some patients who are candidates for PCA but unable to use the PCA equipment, the nurse or a capable family member may be authorized to manage the patient’s pain using PCA equipment. This is referred to as Authorized Agent Controlled Analgesia; guidelines are available for the safe administration of this therapy (Cooney, Czarnecki, Dunwoody, et al., 2013). Analgesic Medications Analgesic medications are categorized into three main groups: (1) nonopioid antispasmodic agents, which include acetaminophen and NSAIDs; (2) opioid antispasmodic agents, which include, among others, morphine, hydromorphone, fentanyl, and oxycodone; and (3) co-analgesic agents (also referred to as adjuvant analgesic agents). The co-analgesic agents comprise the largest group and include various agents with unique and widely differing mechanisms of action. Examples are local anesthetics, some anticonvulsants, and some antidepressants (APS, 2016). Nonopioid Analgesic Agents Acetaminophen and NSAIDs comprise the group of nonopioid analgesic agents (refer to earlier discussion of the two categories of NSAIDs; see Fig. 9- 2). Indications and Administration Nonopioid medications are analgesic agents used for a wide variety of painful conditions. They are appropriate alone for mild to some moderate nociceptive pain (e.g., from surgery, trauma, or osteoarthritis) and are added to opioids, local anesthetics, and/or anticonvulsants as part of a multimodal analgesic regimen for more severe nociceptive pain (APS, 2016; Chou et al., 2016; Comerford & Durkin, 2020). Since acetaminophen and NSAIDs have different mechanisms of action, they may be administered concomitantly (Chou et al., 2016). Although there is no research supporting staggering the two medications, it may be helpful for some patients. Unless contraindicated, surgical patients should routinely be given acetaminophen and an NSAID in scheduled doses throughout the postoperative course, which can be initiated preoperatively (Chou et al., 2016). Nonopioids are often combined in a single tablet with opioids, such as oxycodone or hydrocodone, and are very popular for the treatment of mild to moderate acute pain. They are traditionally a common choice after invasive pain management therapies are discontinued and for pain treatment after 701 hospital discharge and dental surgery when an opioid is prescribed. Many people with persistent pain also take a combination nonopioid–opioid analgesic agent; however, it is important to remember that these combination medications are not appropriate for severe pain of any type because the maximum daily dose of the nonopioid limits the escalation of the opioid dose (Burchum & Rosenthal, 2019; Comerford & Durkin, 2020). Acetaminophen is versatile in that it can be given by multiple routes of administration, including oral, rectal, and IV. Oral acetaminophen has a long history of safety in recommended doses in all age groups. It is a useful addition to multimodal treatment plans for postoperative pain (Wick, Grant, & Wu, 2017). Findings from one research study suggest that patients who receive scheduled acetaminophen with PRN opioids will use less opioids than if they receive PRN acetaminophen plus opioids (Valentine, Carvalho, Lazo, et al., 2015). These results were supported in a more recent study evaluating opioid use among women who underwent Cesarean deliveries (Holland, Bateman, Cole, et al., 2019). IV acetaminophen is approved for the treatment of pain and fever and is given by a 15-minute infusion in single or repeated doses. It may be given alone for mild to moderate pain or in combination with opioid analgesic agents for more severe pain. The results of several research studies have been inconsistent regarding the opioid sparing effects of IV acetaminophen (Nelson & Wu, 2018). Recommended dosing is 1000 mg every 6 hours for a maximum of 4000 mg in adult patients (Comerford & Durkin, 2020). A benefit of the NSAID group is the availability of a wide variety of agents for administration via noninvasive routes. Ibuprofen, naproxen, and celecoxib are the most widely used oral NSAIDs in the United States. When rectal formulations are unavailable, an intact oral tablet or a crushed tablet in a gelatin capsule may be inserted into the rectum. The rectal route may require higher doses than the oral route to achieve similar analgesic effects (Pasero et al., 2011). Diclofenac can be prescribed in patch and gel form for topical administration, and an intranasal patient-controlled formulation of ketorolac has been approved for the treatment of postoperative pain. IV formulations of ketorolac and ibuprofen are available for acute pain treatment. Both have been shown to produce excellent analgesia alone for moderate nociceptive pain, and significant opioid dose–sparing effects when given as part of a multimodal analgesia plan for more severe nociceptive pain (Comerford & Durkin, 2020; Williams, 2018). Adverse Effects of Nonopioid Analgesic Agents Acetaminophen is widely considered one of the safest, best tolerated, and most cost effective of the analgesic agents (APS, 2016; Williams, 2018). Its most serious complication is hepatotoxicity (liver damage) as a result of overdose. In the healthy adult, a maximum daily dose below 4000 mg is rarely associated 702 with liver toxicity. Nevertheless, one manufacturer of oral acetaminophen voluntarily changed its dosing recommendations in 2011, calling for a maximum daily dose of 3000 mg (Shiffman, Battista, Kelly, et al., 2018). In 2014, the U.S. Food and Drug Administration (FDA) recommended that health care professionals stop prescribing and pharmacists stop dispensing prescription combination medication products that contain more than 325 mg of acetaminophen per tablet, capsule, or other dosage unit in order to reduce the risk of hepatotoxicity (FDA, 2014). Acetaminophen does not increase bleeding time and has a low incidence of gastrointestinal (GI) adverse effects, making it the analgesic agent of choice in many individuals with comorbidities. There are two potential interactions with acetaminophen that warrant caution. Acetaminophen should be avoided when consuming alcohol because the combination can result in serious liver damage; acetaminophen also should be avoided when warfarin is prescribed because it can inhibit metabolism of warfarin resulting in toxicity with bleeding risk (Burchum & Rosenthal, 2019). NSAIDs have considerably more adverse effects than acetaminophen, with gastric toxicity and ulceration being the most common (Comerford & Durkin, 2020). The primary underlying mechanism of NSAID-induced gastric ulceration is the inhibition of COX-1, which leads to a reduction in GI- protective prostaglandins (see Fig. 9-2). This is a systemic (rather than local) effect and can occur regardless of the route of administration of the NSAID. Risk factors include advanced age (older than 60 years), presence of prior ulcer disease, and cardiovascular (CV) disease and other comorbidities (Williams, 2018). In patients with elevated risks, the use of a COX-2 selective NSAID (e.g., celecoxib) or the least ulcerogenic nonselective NSAID (e.g., ibuprofen) plus a proton pump inhibitor is recommended; however, there are risks with proton pump inhibitors as well (Gwee, Goh, Lima, et al., 2018). Proton pump inhibitors may decrease the absorption of some other medications such as itraconazole and rilpivirine (Burchum & Rosenthal, 2019). As with all medications, it is important to frequently reassess the need for continued use and to discontinue when appropriate. GI adverse effects are also related to the dose and duration of NSAID therapy; the higher the NSAID dose and the longer the duration of NSAID use, the higher the risk of GI toxicity (Williams, 2018). A principle of nonopioid analgesic use is to administer the lowest dose for the shortest time necessary (Pasero, Portenoy, & McCaffery, 2011). All NSAIDs carry a risk of CV adverse effects through prostaglandin inhibition, and the risk is increased with COX-2 inhibition, whether it is produced by a COX-2 selective NSAID (e.g., celecoxib) or by NSAIDs that are nonselective inhibitors of both COX-1 and COX-2 (e.g., ibuprofen, naproxen, and ketorolac). Findings from a recent meta-analysis suggest that the risk of acute myocardial infarction is greatest during the first month of treatment with NSAIDs, with this risk developing during the first week of 703 treatment (Bally, Dendukuri, Rich, et al., 2017). All patients prescribed NSAIDs should receive the lowest effective dose for the shortest time period to decrease risks. NSAIDs can negatively impact renal function, and are associated with diminished renal prostaglandin formation, interstitial nephritis, reduced secretion of renin, and greater reabsorption of water and sodium (APS, 2016). NSAID-induced renal toxicity can occur, but is relatively rare in otherwise healthy adults who are given NSAIDs for short-term pain management (e.g., in the perioperative period); however, individuals with acute or chronic volume depletion or hypotension rely on prostaglandin synthesis to maintain adequate renal blood flow, and NSAID inhibition of prostaglandin synthesis in such patients can cause acute kidney injury (Burchum & Rosenthal, 2019). Attention to adequate hydration is essential when administering NSAIDs to prevent this complication (Pasero et al., 2011). Most nonselective NSAIDs increase bleeding time through inhibition of COX-1. This is both medication and dose related, so the lowest dose of nonopioids with minimal or no effect on bleeding time should be used in patients having procedures with high risk for bleeding. Options include acetaminophen, celecoxib, choline magnesium trisalicylate, salsalate, and nabumetone (APS, 2016; Burchum & Rosenthal, 2019). Opioid Analgesic Agents Although it is often used, the term narcotic is inaccurate and considered obsolete when discussing the use of opioids for pain management, in part because it is a term used loosely by law enforcement and the media to refer to various substances of potential abuse, which include opioids as well as cocaine and other illicit substances. Legally, controlled substances classified as narcotics include opioids, cocaine, and others. The accurate term, when discussing these agents in the context of pain management, is opioid analgesics (Burchum & Rosenthal, 2019). Opioid analgesic agents are divided into two major groups: (1) mu agonist opioids (also called morphinelike medications) and (2) agonist–antagonist opioids. The mu agonist opioids comprise the larger of the two groups and include morphine, hydromorphone, hydrocodone, fentanyl, oxycodone, and methadone, among others. The agonist–antagonist opioids include buprenorphine, nalbuphine, and butorphanol (APS, 2016). Opioid analgesic agents exert their effects by interacting with opioid receptor sites located throughout the body, including in the peripheral tissues, GI system, and CNS; they are abundant in the dorsal horn of the spinal cord. There are three major classes of opioid receptor sites involved in analgesia: the mu, delta, and kappa. The pharmacologic differences in the various opioids are the result of their interaction with these opioid receptor types (Burchum & Rosenthal, 2019; Sheth, Holtsman, & Mahajan, 2018). When an opioid binds 704 to the opioid receptor sites, it produces analgesia as well as unwanted effects, such as constipation, nausea, sedation, and respiratory depression (Arthur & Hui, 2018). The opioid analgesic agents that are designated as first line (e.g., morphine, hydromorphone, fentanyl, and oxycodone) belong to the mu opioid agonist class because they bind primarily to the mu-type opioid receptors. The agonist–antagonist opioids are designated as “mixed” because they bind to more than one opioid receptor site. They bind as agonists, producing analgesia, at the kappa opioid receptor sites, and as weak antagonists at the mu opioid receptor sites. Their propensity to antagonize the effects of mu opioid analgesic agents limits their usefulness in pain management (Burchum & Rosenthal, 2019). They should be avoided in patients receiving long-term mu opioid therapy because their use may trigger severe pain and opioid withdrawal syndrome characterized by rhinitis, abdominal cramping, nausea, agitation, and restlessness. Antagonists (e.g., naloxone, naltrexone, naloxegol) are medications that also bind to opioid receptors but produce no analgesia. If an antagonist is present, it competes with opioid molecules for binding sites on the opioid receptors and has the potential to block analgesia and other effects. Antagonists are used most often to reverse adverse effects, such as respiratory depression (Burchum & Rosenthal, 2019). Antagonists have been incorporated in the manufacture of some opioids in an effort to deter abuse of the opioid (Li, 2019) Administration Safe and effective use of opioid analgesic agents requires the development of an individualized treatment plan based on a comprehensive pain assessment, which includes clarifying the goals of treatment and discussing options with the patient and the family when appropriate (Chou et al., 2016; Sheth et al., 2018). Goals are periodically reevaluated, and changes made depending on patient response and in some cases disease progression. Many factors are considered when determining the appropriate opioid analgesic agent for the patient with pain. These include the unique characteristics of the various opioids and patient factors, such as pain intensity, age, coexisting disease, current medication regimen and potential medication interactions, prior treatment outcomes, and patient preference (APS, 2016; Sheth et al., 2018). In all cases, a multimodal approach that may rely on the selection of appropriate analgesic agents from the nonopioid, opioid, and co- analgesic agent groups is recommended to manage all types of pain (APS, 2016; Li, 2019). Chart 9-5 lists the key considerations when developing an opioid pain treatment plan. Titration of the opioid dose is usually required at the start and throughout the course of treatment when opioids are given. Whereas patients with cancer 705 pain most often are titrated upward over time for progressive pain, patients with acute pain, particularly postoperative pain, are eventually titrated downward and discontinued as pain resolves (Chou et al., 2016; FDA, 2017; Sheth et al., 2018). The dose and analgesic effect of mu agonist opioids have no ceiling effect, although the dose may be limited by adverse effects. The absolute dose given is based on a balance between pain relief and tolerability of adverse effects. The goal of titration is to use the smallest dose that provides satisfactory pain relief with the fewest adverse effects (Sheth et al., 2018). The time at which the dose can be increased is determined by the onset and peak effects of the opioid and its formulation. Chart 9-5 706 Use of Opioids Perform a comprehensive assessment that addresses pain, comorbidities, and functional status. Develop an individualized treatment plan that includes specific goals related to pain intensity, activities (function/quality of life), and adverse effects (e.g., pain intensity rating of 3 on a 0–10 numerical rating scale to ambulate accompanied by minimal or no sedation). Use multimodal analgesia (e.g., add acetaminophen and NSAID; anticonvulsant in patients at risk for persistent postsurgical pain). Assess for presence preoperatively of underlying persistent pain in surgical patients and optimize its treatment. Consider preemptive analgesic agents before surgery, particularly for those at risk for severe postoperative pain or a persistent postsurgical pain syndrome. Provide analgesic agents prior to all painful procedures. Medication selection Consider diagnosis, condition, or surgical procedure, current or expected pain intensity, age, presence of major organ dysfunction or failure, and presence of coexisting disease. Consider pharmacologic issues (e.g., accumulation of metabolites and effects of concurrent medications). Consider prior treatment outcomes and patient preference. Be aware of available routes of administration (oral, transdermal, rectal, intranasal, IV subcutaneous, perineural, intraspinal) and formulations (e.g., short acting, modified release). Be aware of cost differences. Route of administration selection Use least invasive route possible. Consider convenience and patient’s ability to adhere to the regimen. Consider staff’s (or patient’s or caregiver’s) ability to monitor and provide care required. Dosing and titration Consider previous dosing requirement and relative analgesic potencies when initiating therapy. Use equianalgesic dose chart (Table 9-3) to determine starting dose with consideration of patient’s current status (e.g., sedation and respiratory status) and comorbidities (e.g., medical frailty), and then titrate until adequate analgesia is achieved or dose-limiting adverse effects are encountered. Use appropriate dosing schedule (e.g., around-the-clock for continuous pain; PRN for intermittent pain). When dose is safe but additional analgesia is desired, titrate upward as prescribed by 25% for slight increase, 50% for moderate 707  increase, and 100% for considerable increase in analgesia. Provide supplemental doses for breakthrough pain; consider PCA if appropriate. Treatment of adverse effects Be aware of the prevalence and impact of opioid adverse effects. Remember that most opioid adverse effects are dose dependent; always consider decreasing the opioid dose as a method of treating or eliminating an adverse effect; adding nonopioid analgesic agents for additive analgesia facilitates this approach. Use a preventive approach in the management of constipation, including for patients receiving short-term opioid treatment. Prevent respiratory depression by monitoring sedation levels and respiratory status frequently and decreasing the opioid dose as soon as increased sedation is detected. Monitoring Continually and consistently evaluate the plan on the basis of the specific goals identified at the outset and assess pain intensity, adverse effects, and activity levels. Make necessary modifications to treatment plan to maintain efficacy and safety. Tapering and cessation of treatment If a decrease in dose or cessation of treatment is appropriate, do so in accordance with decreased pain intensity and after evaluation of functional outcomes. Be aware of the potential for withdrawal syndrome (rhinitis, abdominal cramping, diarrhea, restlessness, agitation) and need for tapering schedule in patients who have been receiving opioid therapy for more than a few days. IV, intravenous; NSAID, nonsteroidal anti-inflammatory drug; PCA, patient- controlled analgesia; PRN, as needed. Copyright 2011, Pasero, C., & McCaffery, M. Modified and used with permission from Pasero, C., & McCaffery, M. (2011). Pain assessment and pharmacologic management. St. Louis, MO: Mosby-Elsevier. Equianalgesia. The term equianalgesia means approximately “equal analgesia.” An equianalgesic chart provides a list of doses of analgesic agents, both oral and parenteral (IV, subcutaneous, and intramuscular), that are approximately equal to each other in ability to provide pain relief. Equianalgesic conversion of doses is developed from the ratio representing the difference in the potency of the two medications (Treillet, Laurent, & Hadjiat, 2018). The information is used to help ensure that patients are not overdosed or underdosed when they are switched from one opioid or route of administration to another. It requires a series of calculations based on the daily dose of the current opioid to determine the equianalgesic dose of the opioid to 708 which the patient is to be switched. Several excellent guidelines are available to assist in calculating equianalgesic doses (Burchum & Rosenthal, 2019) (see Table 9-3). Equianalgesic tools available in electronic health records enable all clinicians at any facility to easily convert analgesic dosages (APS, 2016). 709 TABLE 9-3 Equianalgesic Dose Chart for Common mu Opioid Analgesic Agents Equianalgesic means approximately the same pain relief. The equianalgesic chart is a guideline for selecting doses for patients who are opioid- naïve. Doses and intervals between doses are titrated according to individuals’ responses. The equianalgesic chart is helpful when switching from one medication or route of administration to another. Opioid Oral Parenteral Comments Morphine 30 mg 10 mg Standard for comparison; first-line opioid via multiple routes of administration; once- and twice-daily oral formulations; clinically significant metabolites Fentanyl No formulation 100 mcg IV First-line opioid via IV, 100 mcg/h of transdermal, and transdermal fentanyl intraspinal routes; is approximately available in oral equal to 4 mg/h of transmucosal and buccal IV morphine; 1 formulations for mcg/h of breakthrough pain in transdermal fentanyl patients who are opioid- is approximately tolerant; no clinically equal to 2 mg/24 h relevant metabolites of oral morphine Hydrocodone 30 mg (not No formulation Available only in recommended) combination with acetaminophen and as such is appropriate only for mild to some moderate pain Hydromorphone 7.5 mg 1.5 mg First-line opioid via multiple routes of administration; once-daily oral formulation; clinically significant metabolites noted with long-term and high-dose infusion Oxycodone 20 mg No formulation in the Short-acting and twice-daily United States oral formulations Oxymorphone 10 mg 1 mg Parenteral and short-acting and twice-daily oral formulations 710 IV, intravenous. Adapted from Comerford, K. C., & Durkin, M. T. (2020). Nursing 2020 drug handbook. Philadelphia, PA: Wolters Kluwer; Pasero, C., & McCaffery, M. (2011). Pain assessment and pharmacologic management. St. Louis, MO: Mosby-Elsevier. Formulation terminology. The terms short acting, immediate release, and normal release have been used interchangeably to describe oral opioids that have an onset of action of approximately 30 minutes and a relatively short duration of 3 to 4 hours. The term immediate release is misleading because none of the oral analgesic agents have an immediate onset of analgesia; short acting is preferred. The terms modified release, extended release, sustained release, controlled release, and long acting are used to describe opioids that are formulated to release over a prolonged period of time. For the purposes of this chapter, the term modified release will be used when discussing these opioid formulations. Substance Use Disorder, Physical Dependence, and Tolerance In 2013 the American Psychological Association (APA) renamed addiction as substance use disorder (SUD) (Lo Coco, Melchiori, Oiendi, et al., 2019). SUD includes a number of subcategories, including opioid use disorder. The terms physical dependence and tolerance often are confused with substance use disorder, previously understood as addiction; thus, clarification of definitions is important (Burchum & Rosenthal, 2019). Physical dependence is a normal response that occurs with repeated administration of the opioid, with intensity and duration dependent upon the half-life of the medication and how long it has been used. It is manifested by the occurrence of withdrawal symptoms when the opioid is suddenly stopped or rapidly reduced, or an antagonist such as naloxone is given. Withdrawal symptoms may be suppressed by the natural, gradual reduction of the opioid as pain decreases or by gradual, systematic reduction, referred to as tapering (Burchum & Rosenthal, 2019). Withdrawal occurs with prolonged use of opioids, regardless of whether the use of opioids is prescribed for pain management or because of SUD (Sheth et al., 2018). Tolerance is also a normal physiologic response that can occur with regular administration of an opioid and consists of a decrease in one or more effects of the opioid (e.g., decreased analgesia, sedation, or respiratory depression). Although it may occur in conjunction with SUD, it cannot be equated with SUD. It may be treated with increases in dose to attain the previous effect. With the exception of constipation, tolerance to the opioid adverse effects develops with regular daily dosing of opioids over several days (Burchum & Rosenthal, 2019; Sheth et al., 2018). 711  Substance Use Disorder (SUD) was historically known as addiction or addictive disease, and defined as a chronic, relapsing, treatable neurologic disease. The APA has since described SUD as the impaired use of a substance, such as opioids, even while experiencing major problems, characterized by impaired control over use, compulsive use, continued use despite harm, and craving for the substance. With SUD, use of the opioid is for nontherapeutic reasons and is thus independent of pain relief. The development and characteristics of SUD are influenced by genetic, psychosocial, and environmental factors (Auriacombe, Serre, Denis, et al., 2019; Lo Coco et al., 2019; Sheth et al., 2018). Withdrawal occurs when a medication or substance to which the body has become dependent is abruptly reduced or discontinued. This is true of prescribed medications as well as illicitly obtained substances. Withdrawal is exhibited by a cascade of unpleasant symptoms including anxiety, nausea, vomiting, rhinitis, sneezing, chills, hot flashes, abdominal cramping, tremors, diaphoresis, hyperreflexia, diarrhea, piloerection, and/or insomnia (APS, 2016; Burchum & Rosenthal, 2019; Sheth et al., 2018). Pseudoaddiction is a mistaken diagnosis of substance use disorder that occurs when a patient’s pain is not well controlled; the patient may begin to manifest symptoms suggestive of SUD. In an effort to obtain adequate pain relief, the patient may respond with demanding behavior, escalating demands for more or different medications, and repeated requests for opioids on time or before the prescribed interval between doses has elapsed. Pain relief typically eliminates these behaviors and is often accomplished by increasing opioid doses or decreasing intervals between doses (Sheth et al., 2018; Weissman & Haddox, 1989). Pain management specialists have increasingly come to realize that the progression from prescribed opioid use to the disease of opioid SUD is poorly understood and complex. The National Institute on Drug Abuse (2014) estimated that the rates of SUD among patients with chronic pain vary widely, from 3% to 40%. A government effort to address the issue of SUD is the Comprehensive Addiction and Recovery Act of 2016 which provides prevention, treatment, and rehabilitative support (Burchum & Rosenthal, 2019). There is real concern for adequately treating the 2 million Americans who are living with opioid SUD and the 50 million people who are living with chronic pain (National Institutes of Health [NIH], 2019). The patients in both groups need and deserve to receive informed, evidence-based, compassionate nursing care. Opioid naïve versus opioid tolerant. Patients are often characterized as being either opioid naïve or opioid tolerant. Whereas an opioid naïve person 712 has not recently taken enough opioid on a regular basis to become tolerant to the effects of an opioid, an opioid tolerant person has taken an opioid long enough at doses high enough to develop tolerance to many of the effects, including analgesia and sedation. There is no set time for the development of tolerance, and there is great individual variation, with some not developing tolerance at all. By convention, most clinicians consider a patient who has taken opioids regularly for approximately 7 or more days to be opioid tolerant (Pasero et al., 2011). Opioid-Induced Hyperalgesia Opioid-induced hyperalgesia (OIH) is a paradoxical situation in which increasing doses of an opioid result in increasing sensitivity to pain. The incidence of clinically significant OIH has not been determined; however, it is a serious consequence of opioid administration. At this time, it is not possible to predict who will develop OIH as a result of opioid exposure, and the mechanisms underlying OIH are largely unknown. In general, OIH is thought to be the result of changes in the central and peripheral nervous systems that produce increased transmission of nociceptive signals (APS, 2016; Higgins, Smith, & Matthews, 2018; Ringkamp et al., 2018; Spofford & Hurley, 2018). Some experts characterize OIH and analgesic tolerance as “opposite sides of the coin” (Pasero et al., 2011). In tolerance, increasing doses of opioid are needed to provide the same level of pain relief because opioid exposure induces neurophysi