Debra E. Heidrich and Peg Esper
DEFINITION AND INCIDENCE
The International Association for the Study of Pain (IASP) defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage (IASP, 1979). Pain, however, is a highly personal and subjective experience. McCaffery (1968) proposed the definition most applicable to clinical practice: “Pain is whatever the experiencing person says it is, existing whenever he/she says it does.” The patient’s self-report of pain is its single most reliable indicator. In other words, the patient’s report must be accepted at face value (American Pain Society, 2003).
Pain may be classified based on duration or by inferred pathophysiology. The interventions selected to treat pain will be influenced by both of these types of classification (McCaffery & Pasero, 1999). These classifications are as follows:
Types of Pain Based on Duration
▪ Acute pain is relatively brief in duration. There is a recognized cause of the pain, and the pain diminishes as healing takes place. With acute pain, there may or may not be observable autonomic signs of discomfort (e.g., increased pulse rate and blood pressure) and nonverbal signs (e.g., tense muscles, facial grimace).
▪ Chronic pain is described as pain that persists after the resolution of the initial injury. It is perceived as irreversible and meaningless. Due to physiologic and behavioral adaptation, there are few or no autonomic or nonverbal signs of discomfort.
▪ Breakthrough pain (also called episodic pain) is defined by Portenoy and Hagen (1990) as a “transitory exacerbation of pain that occurs on a background of otherwise stable pain in a patient receiving chronic opioid therapy” (p. 273). Breakthrough pain tends to occur in persons with higher pain severity and is associated with distress and disability (Caraceni, Martini, Zecca et al., 2004; Zeppetella, O’Doherty, & Collins, 2000). The three subtypes of breakthrough pain are listed next (Mercadante & Portenoy, 2001; Portenoy & Hagen, 1990). Assessment of the onset, duration, frequency, and precipitating factors assists in determining the type and guides the treatment.
End-of-dose failure occurs when the blood levels of analgesics are declining. This indicates a need to increase the dose or the frequency of administration of the analgesic.
Nonincident breakthrough pain has no identified precipitant.
Types of Pain Based on Inferred Pathophysiology
▪ Nociceptive pain arises from direct stimulation of the afferent nerves in the skin, soft tissue, or viscera. This type of pain may be further classified as somatic pain, caused by stimulation of nociceptors in the skin, joints, muscle, bone, or connective tissue; or visceral pain, caused by stimulation of nociceptors in the visceral organs (Figure 32-1).
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| Figure 32-1 |
▪ Neuropathic pain results from abnormal processing of sensory input due to nerve damage. This type of pain may be further classified as centrally generated pain or peripherally generated pain.
Patients may experience several different types of pain at the same time; some of these pains may be somatic, some visceral, some neuropathic, and some mixed. Because interventions are based on the type and severity of pain, thorough assessment of each site of pain is critical to appropriate pain management.
Pain is a common symptom with advanced diseases, affecting at least up to 90% of people with metastatic cancer, 90% of those with acquired immunodeficiency syndrome (AIDS), 65% of people with multiple sclerosis, 78% of people with cardiac disease, 8% of people with cerebrovascular disease, and 20% of people with diabetes (Anderson, Vestergaard, Ingeman-Nielsen et al., 1995; Biovie, 1999; Breitbart, Passik, & Rosenfeld, 1999; Corbett, 2005; Levenson, McCarthy, Lynn et al., 2000; McCarthy, Lay, & Addington-Hall, 1996; Ogle & Hopper, 2005). Breakthrough pain occurs in up to 89% of persons with advanced cancer (Zeppetella et al., 2000). The incidence of breakthrough pain in nonmalignant diseases is not investigated as extensively but is reported with many different disease processes (Svendsen, Andersen, Arnason et al., 2005). Zeppetella, O’Doherty, & Collins (2001) reported breakthrough pain in 63% of persons admitted to a hospice with noncancer diagnoses. Important to note and just as significant is the fact that many persons also experience pains unrelated to their primary diagnosis, such as arthritis and chronic low back pain.
Pain control at the end-of-life remains an important, yet often neglected, issue. Data from the SUPPORT study showed a high incidence of uncontrolled pain (from 74% to 95%) in very ill and dying hospitalized adults despite planned interventions from nurses encouraging physicians to attend to pain control (SUPPORT Study Principal Investigators, 1995). A recent study shows that patient satisfaction with pain control has improved only slightly since the implementation of pain standards by the Joint Commission on the Accreditation of Healthcare Organizations in 2001 (Leddy & Wolosin, 2005).
Uncontrolled pain causes physical, psychosocial, emotional, spiritual, and financial burdens and decreases quality of life. Pain interferes with activities of daily living, decreases strength and endurance, stimulates nausea, impairs appetite, interferes with sleep, and impairs immune response (Page, 2005); it interferes with social and intimate relations, contributing to isolation. Pain is also associated with high emotional distress (Vachon, 2004). A study by Sela, Bruera, Conner-Spady et al. (2002) showed gender differences in the affective responses to cancer pain: men most often reported frustration, anger, and exhaustion due to pain, and women described exhaustion, helplessness, frustration, hopelessness, and anger as their top concerns. Spiritual distress may be a cause or an effect of pain (Georgesen & Dungan, 1996). In addition, pain increases caregiver burden and diminishes important social supports for both the patient and the family. Finally, some pain medications and other treatment regimens are expensive, causing economic stress at a particularly vulnerable time.
ETIOLOGY AND PATHOPHYSIOLOGY
Nociceptive pain occurs when a pain stimulus is generated from either somatic or visceral structures. Pain from somatic structures, including bone, joints, muscle, skin, and connective tissue, is usually described as “aching” or “throbbing,” and the patient can often point to the exact area where the painful stimulus is occurring (i.e., it is well localized). Stimuli from visceral tissues (mainly thoracic, abdominal, and pelvic organs) cause pain that is described as gnawing and aching. Visceral pain may or may not be well localized. In fact, visceral pain may be felt in areas other than the original site, a phenomenon known as referred pain (Hudspith, Siddall, & Munglani, 2006). Figure 32-2 illustrates some commonly reported sites where pain may be referred from visceral organs.
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| Figure 32-2
(From Brockrath, M. [1985]. Fundamentals. Nursing Now [p. 18]. Springhouse, Pa.: Springhouse.)
Springhouse
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Neuropathic pain is not as clearly understood as nociceptive pain. Peripherally generated neuropathic pains involve abnormal processing of sensory input from the peripheral nerves and may be described as “aching,” “burning,” “tingling,” or “shocklike.” Centrally generated neuropathic pains involve abnormal processing of sensory input at the spinal cord level, leading to hyperexcitability. This causes an abnormal continuation of pain impulses, even in the absence of further pain stimuli, or an abnormal processing of stimuli such that normally nonpainful stimuli are perceived as painful (allodynia). Neuropathic pain syndromes can be difficult to treat. The words used to describe an individual’s pain assist in determining the type of pain and inferring a cause (Table 32-1).
| Pain Type | Subtype | Descriptors | Examples |
|---|---|---|---|
| Nociceptive | Somatic |
Aching
Throbbing
Well-localized
|
Acute somatic pain:
Surgical incisions
Muscle or joint sprain
Chronic somatic pain:
Arthritis
Metastatic cancer to the bone
|
| Nociceptive | Visceral |
Aching
Gnawing
Deep and squeezing
Intermittent cramping
Poorly localized; referred
|
Acute visceral pain:
Angina
Bladder irritation (e.g., infection)
Acute bowel obstruction
Chronic visceral pain:
Pancreatic cancer
Metastatic cancer to the liver
|
| Neuropathic: centrally generated | Deafferentation |
Burning
Aching
Lancinating
Pricking
Lacerating
Pressing
|
Phantom limb pain (may have both central and peripheral mechanisms)
Spinal cord injury
Stroke
PHN
|
| Sympathetically maintained |
Burning
Hyperalgesia
Allodynia
Accompanied by excessive sweating and vasomotor changes
|
Complex regional pain syndrome types I and II | |
| Neuropathic: peripherally generated | Polyneuropathies |
Deep aching
Superficial burning, stinging, or prickling
Shocklike; lancinating
Pain felt along distribution of many peripheral nerves
|
Diabetic neuropathy
Drug-induced neuropathy (e.g., due to vinca alkaloid chemotherapy)
|
| Mononeuropathies |
Burning
Severe aching
Intermittent stinging or electric shocklike
Pain along distribution of single nerve or dermatome
|
Mononeuropathies:
Nerve root compression
Trigeminal neuralgia
Multiple mononeuropathies: Postherpetic neuralgia
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Nociceptive Pain Processes
There are four processes involved in nociceptive pain: transduction, transmission, perception, and modulation. Transduction begins when mechanical, thermal, or chemical stimuli cause tissue damage. The damage itself and the inflammatory response to the damage release substances that stimulate or sensitize the pain fibers (Figure 32-3). In the presence of sufficient stimulation, the nerve membrane becomes permeable to sodium, leading to depolarization. An efflux of potassium causes repolarization. Repeated depolarization and repolarization generate an impulse and transduction is complete (Hudspith et al., 2006; McCaffery & Pasero, 1999; Wilke, 1995). In addition to transduction, peripheral pain fibers have the ability to release substances in response to injury (including substance P) that contribute to the inflammatory process and further increase the sensitization of the pain fibers (Hudspith et al., 2006). This explains why light touch of an inflamed area is perceived as painful.
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| Figure 32-3
(Data from Wilke, D.J. [1995]. Neural mechanisms of pain: A foundation for cancer pain assessment and management. In D.B. McGuire, C.H. Yarbro, & B.R. Ferrell [Eds.]. Cancer pain management [2nd ed., pp. 61-87]. Boston: Jones & Bartlett; and Hudspith, M.J., Siddall, P.J., & Munglani, R. [2006]. Physiology of pain. In H.B. Hemmings & P.M. Hopkins [Eds.]. Foundations of anesthesia: Basic sciences for clinical practice [2nd ed., pp. 267-285]. St. Louis: Mosby.)
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The second phase of nociception is transmission of the impulse from the site of injury to the dorsal horn of the spinal cord, up to the brainstem, and out to the thalamus and cortex. Nociceptive fibers carry the impulse to the dorsal horn of the spinal cord, where these fibers end. In order to transmit the impulse to dorsal horn neurons, neurotransmitters are required. These neurotransmitters include glutamate, substance P, neurokinin A, and calcitonin gene–related peptide (CGRP). Glutamate plays a major role in nociceptive transmission by binding with α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors. AMPA receptors are responsible for fast transmission of nociceptive impulses. Sustained activation of AMPA and/or sustained activation of neurokinin receptors primes the NMDA receptor so that it reaches a state ready for activation. Activation of NMDA receptors causes large and prolonged depolarization; prolonged activation initiates processes that contribute to changes observed in chronic pain states, including central sensitization (Hudspith et al., 2006). Thus, prolonged exposure to nociceptive pain may lead to neuropathic pain.
Once transmitted across the synaptic space in the dorsal horn, the impulse is transmitted through several different ascending pathways to the brainstem, thalamus, and higher brain centers. This ends the transmission phase of nociception and begins the phase of perception. Precisely where pain is perceived in the brain is not clear, but this is thought to occur at several cerebral levels. Processing by the somatosensory cortex allows an individual to localize and characterize the pain. The emotional and behavioral responses to pain occur when the pain stimulus is processed in the limbic system. The reticular activating system is responsible for the autonomic responses to pain (Hudspith et al., 2006; McCaffery & Pasero, 1999; Wilke, 1995).
The fourth process in nociception is modulation. This involves the descending pathways from the brain to the dorsal horn of the spinal cord. Substances that inhibit the transmission of pain may be released by these descending fibers. Among these substances are endogenous opioids (enkephalin), serotonin, norepinephrine, γ-aminobutyric acid (GABA), α 2-adrenergic substances, acetylcholine, thyrotropin-releasing hormone, and somatostatin (Hudspith et al., 2006).
Neuropathic Pain Processes
As mentioned, neuropathic pain processes are not as clearly understood but involve abnormal processing of sensory input. Peripheral neuropathic pains may be caused by injury to the nerve that causes a spontaneous generation of an action potential (Coderre & Melzack, 1992; Paice, 2003). The pain pathway is typically along a single dermatome, affected nerve, or plexus. Combined motor and sensory involvement is suspected if the individual is found to have altered reflexes, muscle atrophy, or weakness (Paice, 2003). There are three categories of damage that cause neuropathic pain: physical (e.g., surgery, trauma), chemical (e.g., neurotoxic medications, hyperglycemia), and viral (e.g. HIV, herpes zoster).
Centrally generated neuropathic pain may occur as a result of repetitive transmission of nociceptive signals to the dorsal horn, causing changes in the processing of these impulses. Hypersensitivity and hyperexcitability result. As mentioned, prolonged activation of NMDA receptors is likely involved in this process. Prevention and prompt treatment of pain may prevent these dorsal horn changes.
Physiologic Rationale for Pain Medications
Medications used to treat pain are discussed in detail in the “Intervention and Treatment” section of this chapter. It is important to understand the rationale for the use of these medications, which is based on the physiologic characteristics of pain. Most medications used to manage pain function by interrupting transduction or transmission or by enhancing modulation, as summarized in Table 32-2. Nociceptive pains tend to respond to traditional analgesics, nonopioids, and opioids. The interplay of the inflammatory process in, particularly, the somatic pains indicates that antiinflammatory medications may be helpful. Neuropathic pains are less responsive to traditional analgesics; often an adjuvant medication, such as an antidepressant or an anticonvulsant, is needed alone or in combination with an opioid.
| Medication Class | Mechanism of Action |
|---|---|
| Nonsteroidal antiinflammatory drugs | Block production of prostaglandins |
| Anticonvulsants | Block influx of sodium ions, preventing depolarization and generation of an action potential |
| Local anesthetics | Block influx of sodium ions, preventing depolarization and generation of an action potential |
| Corticosteroids | Block production of prostaglandins |
| Opioids | Bind with opioid receptors and block release of substance P |
| N-Methyl-D-aspartate receptor antagonists | Inhibit binding of excitatory amino acids, such as glutamate, preventing transmission |
| Tricyclic antidepressants | Prevent reuptake of serotonin and norepinephrine |
| GABA agonists | Enhance release of GABA |
| α-Adrenergic agonists | Inhibit release of substance P |
MYTHS AND MISCONCEPTIONS ABOUT PAIN
The treatment of pain is wrought with myths, misconceptions, and erroneous beliefs. Understanding these myths and correcting them are essential to the assessment and treatment of pain. Unfortunately, these issues are quite common among patients, families, health care professionals, and the general public.
Many patients and families hesitate to report pain or use analgesics because of misperceptions, misinformation, and fear. Ward, Goldberg, Miller-McCauley et al. (1993) identified eight barriers:
1. Fear of opioid side effects
2. Fear of addiction
3. Belief that increasing pain signifies disease progression
4. Fear of injections
5. Concern about drug tolerance
6. Belief that “good” patients do not complain about pain
7. Belief that reporting pain may distract the physician from treating or curing the cancer
8. Fatalism, the belief that pain is inevitable with cancer and that it cannot be relieved
Likewise, health care professionals retain erroneous attitudes and beliefs about pain and the use of medications that negatively affect pain assessment and management:
1. The patient’s self-report of pain is not to be believed; health care professionals are the best judge of pain. The patient’s report of pain must be accepted because there are no diagnostic or “objective” tests for pain. Pain is whatever the experiencing person says it is, existing whenever he or she says it does (McCaffrey, 1968).
2. Addiction to pain medication is common. When pain medications are used to treat pain and there is no history of substance abuse, addiction is rare (Weissman, Burchman, Dahl et al., 1994). To clear up confusion over the meanings and application of these terms, addiction, tolerance, and physical dependence are defined as follows:
▪ “ Addiction is a primary, chronic, neurobiologic disease, with genetic, psychosocial, and environmental factors influencing its development and manifestations. It is characterized by behaviors that include one or more of the following: impaired control over drug use, compulsive use, continued use despite harm, and craving” (American Academy of Pain Medicine, American Pain Society, & American Society of Addiction Medicine, 2001, p. 6).
▪ “ Tolerance is a state of adaptation in which exposure to a drug induces changes that result in a diminution of one or more of the drug’s effects over time” (American Academy of Pain Medicine et al., 2001, p. 7).
▪ “ Physical dependence is a state of adaptation that is manifested by a drug class specific withdrawal syndrome that can be produced by abrupt cessation, rapid dose reduction, decreasing blood level of the drug, and/or administration of an antagonist” (American Academy of Pain Medicine et al., 2001, p. 8).
Tolerance and physical dependence are physiologic responses to prolonged use of many substances and medications, including caffeine (e.g., caffeine withdrawal headache), and are not signs of addiction. Requests for pain medication, “clock watching,” and other “drug-seeking” behaviors due to poorly controlled pain are often mistaken for addiction. This is referred to as opioid pseudo-addiction.
▪ Opioid pseudo-addiction is an iatrogenic (meaning “health care system– acquired”) syndrome in which certain behavioral characteristics of psychologic dependence develop as a consequence of inadequate pain treatment (American Academy of Pain Medicine et al., 2001).
3. Respiratory depression is a frequent, serious complication with opioid use. Respiratory depression is feared and misunderstood by patients, families, and health care professionals. Tolerance develops rapidly to respiratory depression; thus, it is rarely a problem except in the opioid-naïve patient. Keep in mind that respiratory rate alone is not an indicator of respiratory depression; careful assessment of the whole patient, not just respiratory rate, is required. Most important, adequate pain management does not shorten life or hasten death (Fohr, 1998; Sykes & Thorns, 2003).
There are other barriers to adequate pain management including the “antidrug” culture and perceived regulatory barriers that vary from state to state. Such restrictions include triplicate prescription programs or other systems that monitor prescribing patterns or a lack of laws facilitating pain management in end-stage illness, including partial filling of scheduled medications. Be familiar with the state’s nurse practice act, regulations, and controlled substances laws.
ASSESSMENT AND MEASUREMENT
If pain is not assessed, appropriate management is impossible. Pain is a multidimensional human experience and thus requires a comprehensive, holistic evaluation. Each new pain report requires a systematic assessment, appropriate treatment, and follow-up. A complete pain assessment includes the following:
▪ Site: The patient identifies primary sites as well as sites of radiation on his or her body or a diagram. Remember also that the patient may have several sites of pain; it may be helpful to number pains to organize assessment, interventions, and evaluations.
▪ Character: Use the patient’s own words; a careful description will lead to the diagnosis of pain type and assist in determining appropriate analgesics (i.e., sharp, shooting describes neuropathic pain syndromes).
▪ Onset: When did it start? Did (or does) a specific event trigger the pain? Carefully distinguish between new and preexisting pain (i.e., arthritis, chronic low back pain syndromes).
▪ Duration and frequency: How long has the pain persisted? Is it constant or intermittent?
▪ Intensity: Intensity is commonly defined on a scale, most frequently of 0 to 10. The 0-to-10 scale has been validated in international populations (Serlin, Mendoza, Nakamura et al., 1995). However, the pain intensity measure must be adapted to the patient. Have an alternate scale available for patients unable or unwilling to use the 0-to-10 scale. For example, some patients prefer a verbal descriptor scale or a modification of a smile-to-sad scale. Find a scale that is meaningful to the patient. Ask patients to rate their pain intensity “now,” at its “worst,” and at its “least.” Note that ratings of pain intensity are the most important pain assessment data to collect if time is short; pain intensity directly correlates with interference with the patient’s quality of life.
▪ Exacerbating factors: What times, activities, or other circumstances make the pain worse?
▪ Associated symptoms: What other symptoms occur before, with, or after the pain? Nausea is frequently associated with pain and often attributed to pain medications and not the pain itself. If nausea occurs at the peak of the drug, it may be drug related; if it occurs at the end of the dose, it may be pain related.
▪ Alleviating factors: What makes the pain better? What treatments have been successful in the past? What treatments have been unsuccessful? Remember that treatments that did not work in the past may work now if the previous dose was inappropriate or the type of pain problem is different. Include a thorough medication history, especially for the past 24 hours.
▪ Effect on quality of life: How does the pain affect the patient’s ability to perform activities of daily living? How does the pain affect relationships with close others? What does the pain mean to the patient and family? How has this pain affected them? How much do the patient and family know about pain? Do they have the expectation that it can be relieved? Are there emotional or spiritual components to the pain? Does unrelieved pain lead to increased fear or anxiety, or to fears that death is imminent?
▪ Patient’s goal for relief: Consider using either a pain intensity score or a functional goal, for example, the ability to walk without pain. What would you like to do that your pain is preventing you from doing? What pain score would allow you to perform that activity?
▪ Physical examination: Observe the site of the pain, and validate with the patient the pain’s location. Note skin color, warmth, irritation, integrity, and any other unusual findings (Berry, Eagan, Eighmy et al., 1999).
▪ Other effects of pain: Assess for the presence of depression, anxiety, and other emotional aspects of the pain experience.
There are multiple pain assessment forms and scales available. Figure 32-4, one example, presents a 0-to-10 scale and other alternate scales.
Assessment of the Cognitively Impaired
Assessment of patients who lack verbal skills because of cognitive impairment requires astute observation of behavior. A change in behavior is the gold standard for suspecting pain or discomfort in a cognitively impaired person. Several pain rating scales have been proposed for use with nonverbal patients; most include monitoring for changes in breathing patterns, negative vocalizations, frowning or grimacing, tense body language or agitation, and the ability to console the person (Warden, Hurley, & Volicer, 2003). Kovach, Weissman, Griffie et al. (1999) suggest the following protocol for assessing discomfort in patients with dementia who exhibit a change in behavior:
▪ Perform a physical assessment for a cause of discomfort and pain. If a cause is found, treatment is initiated.
▪ Review the patient’s history for possible causes of pain through medical records and family members.
▪ Trial nonpharmacologic interventions appropriate to the circumstances; levels of environmental stimuli should also be evaluated and adjusted for the patient’s comfort.
▪ If the preceding steps are unsuccessful, trial of a nonopioid analgesic is indicated.
▪ If the nonopioid is unsuccessful, choose a stronger medication, using the World Health Organization (WHO) analgesic ladder as a guide (Figure 32-5); for example, a smaller dose of an opioid in combination with acetaminophen such as hydrocodone (WHO, 1990).
The importance of including a caring approach and the use of nonpharmacologic interventions that enhance the dignity and self-esteem of the individual cannot be overstressed in the care of persons with cognitive impairment.
HISTORY AND PHYSICAL EXAMINATION
Physical examination, appropriate to each identified location of pain, should be performed. Additional history may be suggested by physical findings.
DIAGNOSTICS
Radiologic examinations may be appropriate to direct treatment of the underlying cause of pain within the patient’s goals of care. As discussed in the previous chapters, decisions to pursue further diagnostics are based on the patient’s place on the disease trajectory and the goals of care.
Laboratory evaluation may or may not be appropriate. In any case, the most recent laboratory values should be reviewed. Blood urea nitrogen (BUN) and creatinine levels may be indicated to ascertain renal function before the initiation of opioid therapy if renal insufficiency is suspected. Likewise, liver function tests may be indicated if hepatic insufficiency is suspected.
INTERVENTION AND TREATMENT
Basic Principles of Pain Management
The following principles serve as a guide to the basics of pain management (American Pain Society, 2003; Gordon, Dahl, Miaskowski et al., 2005; National Cancer Institute, 2005; National Comprehensive Cancer Network [NCCN], 2005).
1. Document the pain assessment data so that pain syndrome can be identified and appropriately treated.
2. Match the choice of drug with the intensity and type of pain.
4. Use the oral route whenever possible. If the patient is unable to swallow oral medications, buccal, sublingual, rectal, and transdermal routes are considered before parenteral routes. The intramuscular route is avoided.
5. Continuous pain requires treatment with a scheduled sustained-release (modified-release) or long-acting opioid and a short-acting medication for breakthrough pain. Patients and families, however, need to be educated about taking the medication when the pain is first perceived—not when it has become severe or unbearable.
6. Educate patients and families about side effects of opioids to avoid the perception that these are allergic reactions.
7. Use an adequate rescue dose for breakthrough pain: 10% to 20% of the 24-hour dose every 1 to 2 hours is the customary rescue dose.
8. Increase the baseline dose if the patient needs more than three rescue doses in 24 hours.
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