Chronic pain is a painful condition that lasts >3 months, pain that persists beyond the reasonable time for an injury to heal, or pain that persists 1 month beyond the usual course of an acute disease. Chronic pain lacks the essential function of acute pain. Whereas acute pain is a vital biologic signal to stop the individual from a potentially injurious activity or to pursue medical care, chronic pain serves no obvious biologic function. Complete pain relief is unrealistic in cases of chronic pain. Rather, the goal of therapy is pain reduction and return to functional status. Chronic pain syndromes discussed in this chapter are divided into neuropathic and nonneuropathic conditions. Aberrant drug-related behavior, also called drug-seeking behavior, is discussed.
Chronic pain is a common problem affecting 30.7% of the U.S. population and is more prevalent in women (34.3%) than in men (26.7%).1 Back pain is the most common site for chronic pain, followed by the knee and neck.1 The prevalence of neuropathic pain is 6.9% to 10% of the population.2 Risk factors for chronic pain include increasing age, female gender, higher body mass, and chronic illness.3 An exacerbation of chronic pain is part of the presentation of 11% to 15% of ED visits.4 Compared to patients with acute pain, chronic pain patients are more likely to report their pain as severe and more likely to be frequent visitors to the ED.5
The pathophysiology of chronic pain is incompletely understood. Many chronic pain syndromes follow nerve or tissue injury, producing nerve dysfunction secondary to the mechanical injury or in response to chemical mediators released from adjacent cell injury. Peripheral nerves, the CNS, or both become abnormally sensitive and develop pathologic spontaneous activity through upregulation of sodium channels and receptors.6 Neuroplastic changes in the central descending pain modulatory systems, inhibitory or facilitatory, may lead to further hyperexcitability. These changes lead to hyperalgesia (exaggerated response to a normally painful stimulus) and allodynia (pain from a normally nonpainful stimulus). In several disorders, a history of injury may be lacking, such as for fibromyalgia, where central sensitization is thought to play a key role.7 Psychological factors frequently precede or follow the onset of chronic pain and frequently predispose individuals to physiologic changes, through the fear-avoidance model. The fear of pain may lead to disuse disability, which leads to nerve hyperexcitability and dysfunction, and ultimately, may result in a chronic pain syndrome.8
The nonneuropathic syndromes share certain characteristics, the most common feature being muscle-related pain (Table 38-1). A feature common to most neuropathic syndromes is allodynia (Table 38-2).
TABLE 38-1Symptoms and Signs of Nonneuropathic Pain Syndromes ||Download (.pdf) TABLE 38-1 Symptoms and Signs of Nonneuropathic Pain Syndromes
|Disorder ||Pain Symptoms ||Signs |
|Myofascial headache ||Constant dull pain, occasionally shooting pain ||Trigger points on scalp, muscle tenderness and tension |
|Chronic tension headache ||Constant dull pain ||Diffuse tenderness of the scalp and associated tension |
|Transformed migraine ||Initially migraine-like, becomes constant, dull; nausea, vomiting ||Muscle tenderness and tension, normal neurologic exam |
|Myofascial neck pain ||Constant dull pain, occasionally shooting pain; pain does not typically follow nerve distribution ||Trigger points in area of pain, usually no muscle atrophy, poor ROM in involved muscle |
|Chronic neck pain ||Constant dull pain, occasionally shooting pain; pain does not follow nerve distribution ||No trigger points, poor ROM in involved muscle due to pain |
|Chronic back pain ||Constant dull pain, occasionally shooting pain; pain does not follow nerve distribution ||No trigger points, poor ROM in involved muscle due to pain |
|Myofascial back pain syndrome ||Constant dull pain, occasionally shooting pain; pain does not typically follow nerve distribution ||Trigger points in area of pain, usually no muscle atrophy, poor ROM in involved muscle |
TABLE 38-2Symptoms and Signs of Neuropathic Pain Syndromes ||Download (.pdf) TABLE 38-2 Symptoms and Signs of Neuropathic Pain Syndromes
|Disorder ||Pain Symptoms ||Signs |
|Painful diabetic neuropathy ||Symmetric numbness and burning or stabbing pain in lower extremities; allodynia may occur ||Sensory loss in lower extremities |
|Phantom limb pain ||Variable: aching, cramping, burning, squeezing, or tearing sensation ||May have peri-incisional sensory loss |
|Trigeminal neuralgia ||Paroxysmal, short bursts of sharp, electric-like pain in nerve distribution ||Tearing or red eye may be present |
|HIV-associated sensory neuropathy ||Symmetric pain and paresthesias, most prominent in toes and feet ||Sensory loss in areas of greatest pain symptoms |
|Postherpetic neuralgia ||Allodynia; shooting, lancinating pain ||Sensory changes in the involved dermatome |
|Fibromyalgia ||Widespread muscular pain and stiffness, fatigue, sleep disturbance, and cognitive dysfunction (forgetfulness, inability to concentrate or recall simple words or numbers, confusion) ||Muscle tenderness in >6 body areas out of 19 total regions |
|Poststroke pain ||Same side as weakness; throbbing, shooting pain; allodynia ||Loss of hot and cold differentiation |
|Sciatica (neurogenic back pain) ||Constant or intermittent, burning or aching, shooting or electric shock–like pain; may follow dermatome; leg pain > back pain ||Possible muscle atrophy in area of pain, possible reflex changes |
|Complex regional pain type I ||Burning persistent pain, allodynia, associated with immobilization or disuse, not associated with nerve injury || |
Early: edema, warmth, local sweating
Late: above alternates with cold, pale, cyanosis, eventually atrophic changes
|Complex regional pain type II ||Burning persistent pain, allodynia, associated with peripheral nerve injury, associated with nerve injury, usually more painful and difficult to control than Type I || |
Early: edema, warmth, local sweating
Late: above alternates with cold, pale, cyanosis, eventually atrophic changes
Clinical assessment should be appropriate to the circumstances, and can be focused or comprehensive. A comprehensive evaluation starts with assessing the quality and character of the patient's current pain, including initiating, exacerbating, or relieving factors. Compare and quantify prior episodes to the current episode. Determine sources, modes, and success or failure of prior treatment, including medications and dosages for physician-prescribed, over-the-counter, or alternative medications. Determine the patient's functional status across the course of the illness and treatment. Treatments that have provided pain relief yet have led to disability cannot be considered a success. Assess any history of alcohol or drug addiction, need for prior detoxification, or psychiatric illness that may impact decisions about choice of medication. A review of systems should assess for potential life- or limb-threatening conditions.
Objective findings of acute pain include tachycardia, hypertension, diaphoresis, and muscle spasms on stimulation. Objective evidence of chronic pain includes muscle atrophy in the distribution of pain due to disuse and skin temperature changes due to the effects of the sympathetic nervous system after disuse or secondary to nerve injury. Trigger points, another objective sign, are focal points of muscle tenderness and tension that, when stimulated with pressure, provoke referred pain, typically in the distribution of the involved muscle. Trigger points are differentiated from simple focal tender portions of the muscle, as trigger points provoke referred pain throughout the affected muscle. Trigger points lack a biologic basis and interexaminer agreement, yet they remain an essential feature of the diagnosis of myofascial pain syndromes.9 Objective evidence of pain is not observed for the pain to be factual. For ED patients, there is no observed correlation between numeric pain scores and vital signs.10
CLINICAL FEATURES OF SELECTED CHRONIC PAIN SYNDROMES
Further discussion including treatment of chronic back pain, neck pain, and sciatica is found in chapter 279, Neck and Back Pain. Migraine headaches and tension headaches are discussed in chapter 165, Headache.
Transformed migraine is a syndrome in which classic or common migraine headaches change over time and develop into a chronic pain syndrome, most commonly from medication overuse.11 Chronic migraine (15 or more migraine days a month) is a precursor to transformed migraine. Medications implicated in this transition are barbiturates taken 5 or more days per month, opioids taken 8 or more days per month, and triptans or nonsteroidal anti-inflammatory drugs (NSAIDs) taken 10 or more days per month.11 Patients with chronic migraine may have more symptoms similar to tension headache with tenderness and tension of scalp musculature. Nausea and vomiting or failure of an oral antimigraine medication often prompts an ED visit. In addition to increased headache frequency, headache duration is longer in chronic migraine.
Fibromyalgia is widespread muscular pain involving greater than six body areas out of 19 total regions and a symptom severity score of 5 or more, rating four areas: fatigue, sleep disturbance, and cognitive dysfunction (e.g., forgetfulness, inability to concentrate or recall simple words or numbers, confusion and associated non-muscle pain symptoms).12,13 Prevalence is thought to be 5.4% of the population.14
The symptoms of painful diabetic neuropathy are symmetric numbness associated with burning, electrical, or stabbing pain in lower extremities. Patients may have hyperesthesia, dysesthesias, and/or deep aching pain. Pain may be provoked with a gentle touch to the skin in the areas of abnormal sensation.
Postherpetic neuralgia may follow the course of an acute episode of herpes zoster in 5% to 30% of cases; pain lasts more than 1 year for 30% of patients.15 Pain is characterized by allodynia and shooting, lancinating (tearing or sharply cutting) pain. Often, patients have hyperesthesia in the involved dermatome. Occasionally there are pigmentation changes in the distribution of the involved dermatome, but this is not unique to postherpetic neuralgia.
Typical symptoms of trigeminal neuralgia include paroxysmal, short bursts of sharp, electric shock–like pain in the nerve distribution of the trigeminal nerve. Pain is often triggered by chewing, speaking, washing, brushing teeth, or something touching the face. Tearing of the eyes or red eye may be present.
Phantom limb pain is quite variable in presentation but is more frequent in patients who had pain in the extremity before amputation. Pain may be aching, cramping, burning, tearing, or squeezing. Phantom limb pain occurs in 30% to 81% of amputations and changes over years, becoming less "knife-like" and more "burning" in character.16
There are two types of complex regional pain syndrome: type I, from prolonged immobilization or disuse, as after stroke; and type II, from a peripheral nerve injury (e.g., due to fracture or gunshot). Symptoms include allodynia and a persistent burning or shooting pain on the affected side or limb. Associated signs early in the course of the disease include edema, warmth, and localized abnormal sweating. It may be difficult to distinguish this stage from an underlying wound infection or osteomyelitis. Later signs include periods of edema and warmth that alternate with cold, pale, cyanotic skin, and, eventually, atrophic changes.
Patients with acquired immunodeficiency syndrome can develop distal sensory polyneuropathy characterized by shooting pain, numbness, and burning sensations primarily on the soles, dorsum of the feet, and toes. This human immunodeficiency virus–associated sensory neuropathy is associated with antiretroviral therapy, but not with low CD4 counts.17 Sensory loss is common in the areas of greatest pain symptoms. As the neuropathy progresses, walking becomes difficult, and quality of life is diminished.
The most important task is to distinguish an exacerbation of chronic pain from a life- or limb-threatening condition. The history and physical examination should either confirm the chronic condition or point to the need for further evaluation when unexpected signs or symptoms are elicited. Because patients with chronic pain may be frequent visitors to the ED, the entire staff may prejudge complaints as simply chronic or even factitious. Follow routine procedures, including a standard triage assessment and a complete set of vital signs.
After eliminating potential conditions that require emergent treatment, clinical judgment determines if focused management of pain is an appropriate course of action in the ED. The principles of focused management are to identify that symptoms are an exacerbation or continuation of a chronic pain pattern, provide appropriate rescue therapy for pain relief, and reinforce the need for a single provider (physician or clinic) for ongoing pain management.
Rarely is a provisional diagnosis of a chronic pain condition made for the first time in the ED. Definitive assessment for chronic pain conditions is difficult and requires expert opinion and often advanced procedures such as MRI, CT, and thermography. Furthermore, abnormal results do not confirm with certainty the cause of pain. For example, abnormalities on MRI of the spine and extremities are common in both asymptomatic and symptomatic patients. Therefore, referral back to the primary source of care is warranted to confirm the diagnosis.
In 1986, Portenoy and Foley18 reported a case series of 38 patients treated with long-acting opioids for chronic, noncancer pain claiming that this therapy was safe and effective and that the risk of addiction was less than 1%, citing unrelated data. Without randomized controlled trials to support their assertions, the use of opioids to treat chronic, noncancer pain rapidly gained popularity with physicians who were twice as likely to prescribe an opioid for chronic pain in 2000, compared to 1980, and with prescriptions for strong opioids (oxycodone compared to codeine) quadrupled.19 From 2001 to 2010, the percentage of patients receiving an opioid prescription at ED discharge increased from 20.8% to 31.0%, while the percentage of visits for painful conditions increased only 4.0%.20 ED visits for nonmedical use of opioids (adverse events including nonfatal overdose) increased 111% from 2004 to 2008.21 The age-adjusted rate for opioid-analgesic poisoning deaths nearly quadrupled from 1.4 per 100,000 in 1999 to 5.4 per 100,000 in 2011;22 poisoning is now the most common cause of injury-related death in the United States, surpassing motor vehicle–related death.
In response to the dramatic increase in opioid-analgesic poisoning, state agencies created statewide prescription drug monitoring programs accessible by the Internet for registered medical providers to view controlled substance prescriptions that a patient has received.23 As of June 2014, 48 states had operational prescription drug monitoring programs.24 Many state medical boards have issued guidelines for the prescription of controlled substances by physicians licensed in that state with specific recommendations for emergency care providers, including Arizona, Arkansas, California, New York, North Carolina, Ohio, Oklahoma, and Washington State;25 additional state guidelines are pending. The American College of Emergency Physicians issued a policy on the prescription of opioids for patients discharged from the ED.26 Table 38-3 summarizes key guideline statements from the American College of Emergency Physicians policy26 and Washington State guidelines.25
TABLE 38-3Guidelines for Prescribing Opioids for Adults in the ED ||Download (.pdf) TABLE 38-3 Guidelines for Prescribing Opioids for Adults in the ED
*For the treatment of back pain, given a lack of demonstrated evidence of superior efficacy of either opioid or nonopioid analgesics, and the individual and community risks associated with opioid use, misuse, and abuse, opioids should be reserved for more severe pain or pain refractory to other analgesics rather than routinely prescribed.
*If opioids are indicated, the prescription should be for the lowest practical dose for a limited duration (e.g., <1 week), and the prescriber should consider the patient's risk for opioid misuse, abuse, or diversion.
*Avoid the routine prescribing of outpatient opioids for a patient with an acute exacerbation of chronic noncancer pain seen in the ED.
*Honor existing patient-physician pain contracts/treatment agreements.
*Consider past prescription patterns from information sources such as prescription drug monitoring programs.
†The administration of intravenous and intramuscular opioids in the ED for the relief of acute exacerbations of chronic pain is discouraged.
†Do not provide replacement prescriptions for controlled substances that were lost, destroyed, or stolen.
†Long-acting or controlled-release opioids (such as OxyContin®, fentanyl patches, and methadone) should not be prescribed from the ED.
†Prescriptions for controlled substances from the ED should state that the patient is required to provide a government-issued picture identification (ID) to the pharmacy filling the prescription.
†Do not provide replacement doses of methadone for patients in a methadone treatment program.
†If opioids are prescribed to a patient with chronic pain, prescribe only enough pills to last until the office of the patient's primary opioid prescriber opens.
TREATMENT OF CHRONIC NONNEUROPATHIC PAIN SYNDROMES
Evidence-based treatment for chronic nonneuropathic pain syndromes is divided into primary and secondary treatment modalities (Table 38-4).27,28,29,30,31,32,33 For management in the ED, an acute exacerbation of a chronic migraine can be treated like an exacerbation of episodic migraine.27 When selecting a standard NSAID, adding a proton pump inhibitor reduces GI complications, and the combination is less expensive than daily use of the cyclooxygenase-2 inhibitors.34
TABLE 38-4Management of Nonneuropathic Chronic Pain Syndromes ||Download (.pdf) TABLE 38-4 Management of Nonneuropathic Chronic Pain Syndromes
|Disorder ||Primary Treatment ||Secondary Treatment ||Possible Referral Outcome |
|Myofascial pain syndromes ||Nonsteroidal anti-inflammatory drugs orally, topical diclofenac patch for single site of pain ||Amitriptyline ||Trigger point injections or dry needling, US treatments, optimization of medical therapy, recommendations for exercise |
|Chronic migraine headache ||See chapter 165 for treatment of acute exacerbations ||Prophylaxis with sodium valproate or topiramate ||Optimization of medical therapy, evaluation for use of prophylactic onabotulinumtoxinA |
|Transformed migraine/medication overuse headache ||Stop prior medications ||Celecoxib or prednisone taper during withdrawal period ||Optimization of medical therapy, withdrawal of prior medications, evaluation for use of prophylactic onabotulinumtoxinA |
Treatment in the ED should never be regarded as definitive, and follow-up care is essential. Many emergency providers will elect to prescribe short-acting nonspecific pain medications (Table 38-3) for patients with chronic pain, deferring initiating of more specific therapy for the primary care physician or pain specialist. Specialty referral may provide optimization of therapy, trigger point injections, and novel treatments, such as onabotulinumtoxinA injections.
TREATMENT OF CHRONIC NEUROPATHIC PAIN SYNDROMES
Evidence-based treatment for chronic neuropathic pain syndromes is divided into primary and secondary treatment modalities (Table 38-5).35,36,37,38,39,40,41,42, 43,44
TABLE 38-5Management of Neuropathic Chronic Pain ||Download (.pdf) TABLE 38-5 Management of Neuropathic Chronic Pain
|Disorder ||Primary Treatment ||Secondary Treatment ||Possible Referral Outcome |
|Fibromyalgia ||Pregabalin ||Duloxetine ||Exercise program, optimization of medical therapy |
|Trigeminal neuralgia ||Carbamazepine ||Oxcarbazepine ||Optimization of medical therapy, consideration for surgery or radiation |
|Human immunodeficiency virus neuropathy pain ||Topical capsaicin ||Gabapentin ||Optimization of medical therapy |
|Spinal cord pain ||Pregabalin ||Tramadol ||Optimization of medical therapy |
|Painful diabetic neuropathy ||Duloxetine ||Gabapentin or Pregabalin ||Optimization of medical therapy |
|Postherpetic neuralgia ||Pregabalin or gabapentin ||Tramadol ||Optimization of medical therapy, regional nerve blockade |
|Phantom limb pain ||Gabapentin ||Tramadol ||Optimization of medical therapy, ketamine infusion |
|Poststroke pain ||Pregabalin ||Gabapentin ||Optimization of medical therapy |
|Complex regional pain syndrome types I and II (reflex sympathetic dystrophy and causalgia) ||Acute phase: prednisone ||Chronic: intermittent infusions of low-dose ketamine by specialist ||Physical therapy, individualized therapy based on neurologic testing |
There is no convincing unbiased evidence to support the use of opioids (specifically oxycodone) in the treatment of neuropathic pain including fibromyalgia.45 Duloxetine is favored over pregabalin and gabapentin in the treatment of painful diabetic neuropathy.40 Human immunodeficiency syndrome–related neuropathy is resistant to many therapies commonly used for neuropathic pain; although topical capsaicin is effective,38 it is best directed by a specialist because pain increases at first application and pretreatment with topical lidocaine may be required.
Tramadol reduces pain in most neuropathic pain syndromes but is considered secondary treatment because it is less effective than the primary treatments (Table 38-5).40,46 Complex regional pain syndrome is the most resistant to pharmacotherapy of all neuropathic pain conditions.44 An IV infusion of ketamine may reduce pain for up to 12 weeks,44 but does not improve function. Corticosteroids (prednisone, 60 milligrams PO once a day) have been recommended at the time of first diagnosis when signs of inflammation are present,44 but steroids do not affect the course of illness. Patients should be informed that NSAIDs and strong opioids are generally ineffective in neuropathic pain. Although considered second line, cyclic antidepressants are effective therapy for most patients with neuropathic pain, except spinal cord injury pain, phantom limb pain, human immunodeficiency syndrome–related neuropathy, and chronic regional pain syndrome. Amitriptyline can be started at 25 milligrams PO nightly, and escalated by the follow-up clinician. Complete relief of pain is an unrealistic goal for patients with chronic pain, both for the ED visit and for follow-up care; patients should be informed of this limitation early in their ED course.
DISPOSITION AND FOLLOW-UP
Referral to an appropriate specialist is one of the most productive means of aiding in the care of chronic pain patients who present to the ED. Chronic pain clinics have been successful in changing the lives of patients by eliminating opioid use, decreasing medication use, reducing pain levels, and increasing work hours. Patients' compliance with pain clinics may improve if these benefits are explained. Admission to the hospital is rarely indicated. However, occasionally patients may be admitted for pain control, possibly using self-controlled analgesic administration.
The prevalence of chronic pain increases with age.1 Opioid analgesic alternatives, such as NSAIDs, have side effects that may limit their use in the elderly who are prone to GI and renal complications; however, when compared to opioids, NSAIDs have fewer side effects overall and are less likely to lead to premature death in the elderly.47 GI bleeding rates are similar for patients treated with opiates or nonselective NSAIDs and lower for those treated with cyclooxygenase-2 inhibitors.47 NSAIDs should not be given to patients with renal dysfunction. Topical analgesics (lidocaine 5%, capsaicin 8%) are effective48 and can be given alone or as adjuncts. Topical NSAIDs provide excellent joint and tissue levels with low plasma levels and are available as diclofenac gel, patch, or topical solution.48
Cognitively and mentally impaired adults with chronic pain are at risk for inadequate pain control due to barriers in communicating the nature and intensity of their pain. Be alert to these potential barriers and look for nonverbal signs of pain: agitation, irregular breathing, facial expressions of pain, stiffened body positioning, and reports of irregular sleep patterns. The ability to monitor undesired side effects, such as sedation, may limit the use of certain pain medications in this population.