Chronic Pain Management

The editors and publisher would like to thank Dr. Pankaj Mehta for contributing to this chapter in the previous edition of this work. It has served as the foundation for the current chapter.

Anesthesia providers first ventured into the treatment of patients with chronic pain as an extension of their use of regional anesthesia in the operating room setting. Pain medicine is now a well-established subspecialty of anesthesiology, with many practitioners dedicating their entire clinical practice to caring for patients with chronic pain and employing a wide range of diagnostic and therapeutic modalities that now extend far beyond the scope of regional anesthesia. 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” and chronic pain as “pain without apparent biological value that has persisted beyond the normal tissue healing time usually taken to be 3 months.” Chronic pain leads to enormous personal and societal costs in lost productivity and prolonged, often seemingly futile, medical treatment.

Classification of Chronic Pain

Chronic pain can be classified as cancer-related pain or noncancer pain, to distinguish the former, which is often associated with the issues that arise near the end of life. However, as more effective treatments for some cancers have emerged, more patients are surviving for prolonged periods of time on treatment or emerging as long-term survivors, and some of these patients suffer from persistent pain. Chronic pain is often divided into nociceptive pain in which activity in peripheral pain neurons is due to ongoing tissue injury, such as the pain of osteoarthritis, and neuropathic pain in which abnormal function of the nervous system causes ongoing pain, such as the pain associated with postherpetic neuralgia (PHN) or painful diabetic peripheral neuropathy (DPN).

Multidisciplinary Pain Management

Chronic pain is a complex disorder and patients suffering with chronic pain often have biologic disease that is inextricably intertwined with cognitive, affective, behavioral, and social factors. Thus, managing patients with chronic pain necessitates employing the expertise of practitioners from a range of medical disciplines to properly address all the physical and psychological aspects of their illness to allow them to regain control over their lives and optimize their overall level of function. Such a multidisciplinary team approach is the most effective and cost-efficient means for the treatment of chronic pain. The core of the multidisciplinary pain team consists of a physician, a psychologist, and a physical therapist often working in conjunction with an occupational therapist and nurse specialists. The physician coordinates diagnosis and medical treatment, including drug therapy and appropriate pain-relieving interventions; the psychologist typically incorporates patient education, cognitive behavioral therapy (CBT), and relaxation training; and the physical therapist plans various exercise regimens, including muscle conditioning and aerobics, aimed at optimizing the patient’s overall function.

Common Pain Syndromes

Low Back Pain


Low back pain, a nonspecific term, refers to pain centered over the lumbosacral junction. The diagnosis and treatment must be as precise as possible. Low back pain can be differentiated as pain that is centered primarily over the axis of the spinal column from pain that refers primarily to the leg ( Fig. 44.1 ). Lumbar spinal pain is pain inferior to the tip of the twelfth thoracic spinous process and superior to the tip of the first sacral spinous process. Sacral spinal pain is inferior to the first sacral spinous process and superior to the sacrococcygeal joint. Lumbosacral spinal pain is in either or both regions and constitutes “low back pain.” Other patients present with “sciatica,” or pain predominantly localized in the leg. The proper term is radicular pain because stimulation of the spinal nerve or the dorsal root ganglion of a spinal nerve evokes the pain.

Fig. 44.1

The definition of low back pain. (A) “Low back pain” is more precisely termed lumbosacral spinal pain, which encompasses both lumbar spinal pain (L) and sacral spinal pain (S). (B) Radicular pain describes pain that is referred to the lower extremity and is caused by stimulation of a spinal nerve.

Pain is a normal physiologic process and serves as a signal of actual or impending tissue injury. Pain from tissue injury is usually well localized and associated with sensitivity in the region. Pain signals are carried toward the central nervous system (CNS) via the peripheral sensory nerves. This type of pain is termed nociceptive pain, or physiologic pain. In contrast, persistent pain following injury to the nervous system is termed neuropathic pain.


Low back pain is among the most common problems leading patients to seek medical attention. In a nationwide health survey, 28% of U.S. adults reported low back pain in the 3 months preceding the survey. The majority of episodes of acute low back pain, with or without radicular pain, resolve without treatment. Overall, 60% to 70% of those affected recover by 6 weeks, and 80% to 90% recover by 12 weeks ( Fig. 44.2 ). However, recovery after 12 weeks is slow and uncertain. Fewer than half of patients disabled for longer than 6 months will return to work. The return-to-work rate for those out of work for 2 years is near zero. Low back pain is frequently recurrent; the vast majority of patients with a single episode experience another episode at some later time. Risk factors for developing chronic low back pain include age, gender, socioeconomic status, education level, body mass index, tobacco use, perceived general health status, physical activity (e.g., bending, lifting, twisting), repetitive tasks, job dissatisfaction, depression, spinal anatomic variations, and imaging abnormalities.

Fig. 44.2

The time course of acute low back pain.

Redrawn from Andersson GB. Epidemiological features of chronic low-back pain. Lancet. 1999;354(9178):581-585, used with permission.


The basic functional unit of the spine is composed of two adjacent vertebral bodies with two posterior facet joints, an intervertebral disk, and the surrounding ligamentous structures. The intervertebral disk absorbs energy and distributes weight evenly from one spinal segment to the next while allowing movement of the protective bony elements. Lifting, bending, twisting, or whole body vibration can damage elements of the spine. With injury and aging, progressive degenerative changes appear in each element of the functional spinal unit, along with the onset of characteristic symptoms ( Fig. 44.3 ). The earliest change in the lumbar facet joints is synovitis, which progresses to degradation of the articular surfaces, capsular laxity and subluxation, and finally enlargement of the articular processes (facet hypertrophy). Progressive degeneration also occurs within the intervertebral disks, starting with loss of hydration of the nucleus pulposus followed by the appearance of circumferential or radial tears within the annulus fibrosis (internal disk disruption). Lumbosacral pain can arise from the facet joints or the annulus fibrosis. With internal disruption of the annulus, some of the gelatinous central nucleus pulposus can extend beyond the disk margin as a disk herniation (herniated nucleus pulposus, or HNP). When an HNP extends to the region adjacent to the spinal nerve, it incites an intense inflammatory reaction. Patients with HNP typically present with acute radicular pain. Hypertrophy of the facet joints and calcification of the ligamentous structures can reduce the size of the intervertebral foramina and central spinal canal (spinal stenosis), with onset of radicular pain and neurogenic claudication.

Fig. 44.3

The functional spinal unit and the degenerative changes that lead to lumbosacral and radicular pain. (A) The normal functional spinal unit. (B) The degenerative changes leading to lumbosacral pain (disk disruption, facet joint arthropathy) and radicular pain (herniated nucleus pulposus). (C) The degenerative changes of lumbar spondylosis leading to lumbosacral (facet joint) pain, radicular (foraminal stenosis) pain, and neurogenic claudication (central canal stenosis).

Patients with prior lumbar surgery and either recurrent or persistent low back pain, often termed failed back surgery syndrome , may require a more complex evaluation. Knowing the type of surgery performed, the indications for and results of the surgery, and the time course and characteristics of any changes in the pattern and severity of postoperative pain is essential. Recurrent pain or progressive symptoms signal the need for further diagnostic evaluation.

Initial Evaluation and Treatment

When first evaluating a patient with low back pain, several features termed red flag conditions require prompt investigation, including new-onset or worsening back pain after trauma, infection, or previous cancer. Patients with progressive neurologic deficits (i.e., typically worsening numbness or weakness) or bowel or bladder dysfunction also warrant immediate radiologic imaging to rule out a compressive lesion. Diagnosis and treatment usually rely on location and duration of symptoms, and determining if the pain is acute or chronic and primarily radicular or lumbosacral in nature. Acute low back pain is pain that is present for less than 3 months, and chronic low back pain is defined as being present for a longer period of time.

Acute Radicular Pain

HNP typically causes acute radicular pain, with or without radiculopathy (signs of dysfunction including numbness, weakness, or loss of deep tendon reflexes referable to a specific spinal nerve). In elderly patients and those with extensive lumbar spondylosis, acute radicular symptoms caused by narrowing of one or more intervertebral foramina can occur. Initial treatment is symptomatic, and following HNP, symptoms resolve without specific treatment in about 90% of patients. Epidural steroid injections have shown efficacy for symptom control in acute radicular pain from HNP. For those with more than 6 weeks of persistent pain after HNP, lumbar diskectomy may be indicated. A controlled trial of surgical versus nonoperative treatment in selected patients showed significant improvement in pain alleviation, quality of life, and physical functioning among both groups over short- and long-term follow-up but remained inconclusive about the superiority of either approach.

Chronic Radicular Pain

Persistent leg pain in the distribution of a spinal nerve may occur in patients with a disk herniation with or without subsequent surgery. In those with persistent pain, a search for a reversible cause of nerve root compression is warranted. In many individuals, scarring around the spinal nerve at the operative site on magnetic resonance imaging and abnormalities on electrodiagnostic studies can suggest chronic radiculopathy. There is a lack of consensus in the field of pain management on how to approach the workup and treatment of chronic radicular pain. As this patient group has characteristics similar to those suffering from other nerve injuries who respond to specific drugs, it is reasonable that initial management consist of pharmacologic treatment for neuropathic pain using gabapentin, pregabalin, tricyclic antidepressants (TCAs), or serotonin-norepinephrine reuptake inhibitors (SNRIs).

Acute Lumbosacral Pain

Most patients presenting with acute onset of lumbosacral pain without radicular symptoms have no obvious abnormal physical findings, and radiologic imaging is unlikely to be helpful. Traumatic sprain of the muscles and ligaments of the lumbar spine or the zygapophyseal joints, and early internal disk disruption, are significant causes of acute lumbosacral pain. As with patients with acute radicular pain, this group is best managed symptomatically.

Chronic Lumbosacral Pain

There are many causes of chronic lumbosacral pain, and identification of the anatomic cause cannot be done with certainty in many cases. The structures most commonly implicated include the sacroiliac joint, lumbar facets, and lumbar intervertebral disks. In chronic low back pain, the incidence of internal disk disruption has been estimated to be 39% (range 29% to 49%), facet joint pain 15% (10% to 20%), and sacroiliac joint pain 15% (7% to 23%). The gold standard for diagnosing sacroiliac and facet joint pain is injection of local anesthetic at the site. However, the use of uncontrolled local anesthetic blocks for diagnostic purposes is plagued by placebo response. For patients achieving significant short-term pain relief with diagnostic blocks, radiofrequency treatment offers a simple, minimally invasive intervention that can provide pain reduction for 3 to 6 months in those with facet-related pain. Pain from degenerating intervertebral disks is also a source of chronic axial back pain. Spinal cord stimulators with implanted epidural electrodes have shown efficacy in selected patients who fail medical and surgical therapy for chronic axial low back pain.

Neuropathic Pain

Persistent pain following injury to the nervous system is termed neuropathic pain and has unique characteristics:

  • Spontaneous pain—pain that occurs with no stimulus (e.g., sudden lancinating pain described with PHN)

  • Hyperalgesia—an exaggerated painful response to a normally mildly noxious stimulus (e.g., light pinprick leading to extreme, prolonged pain)

  • Allodynia—a painful response to a normally non-noxious stimulus (e.g., light touch causing pain)

Neuropathic pain is believed to arise when the normal protective physiologic systems of the nervous system that produce sensitization of the peripheral and central nervous systems (sensitization that affords protection during the healing process) persist after the injured tissue has healed. Three of the most common forms of neuropathic pain include PHN, painful DPN, and complex regional pain syndrome (CRPS).

Painful Diabetic Peripheral Neuropathy

Diabetes mellitus is the most common cause of neuropathic pain, and DPN is caused by damage to small unmyelinated nerve fibers. DPN can result in painless sensory loss or painful neuropathy. DPN typically begins with symmetric numbness in the toes associated with paresthesias, dysesthesias, and pain. The pain is often described as burning but equally common is a simple deep aching pain in the area affected. The neuropathy progresses slowly over many years. As the sensory changes reach the proximal portion of the feet, the same symptoms often appear in the hands. The incidence of painful DPN is directly related to glycemic control, with marked reduction in the incidence, severity, and rate of progression of the neuropathy in those with the tightest control of blood glucose levels. The strongest evidence for efficacy in pharmacologic management of pain-related symptoms exists for TCAs (amitriptyline, desipramine, and imipramine), SNRIs (duloxetine, venlafexine), and anticonvulsants (gabapentin, pregabalin, carbamazapine, oxcarbezapine). Use of opioids is controversial because of potential for long-term dependence, abuse, and their significant adverse effects profile. In clinical trials, tepentadol extended release and oxycodone are more effective than other opioids in treatment of DPN.

Sympathetically Maintained Pain

Sympathetically mediated pain is a subset of neuropathic pain in which sympathetic efferent activity augments chronic pain and loss of function. As a result, early blockade of sympathetic neurotransmission during certain acute pain conditions may reduce the development of chronic pain. Typical examples of sympathetically mediated pain are PHN, CRPS, and stump neuroma in amputees.

Postherpetic Neuralgia

The varicella-zoster virus produces a highly contagious primary viral infection called chickenpox that is common in childhood, characterized by the appearance of a diffuse vesicular rash that typically heals without scarring. The varicella-zoster virus lies dormant in the dorsal root ganglia following resolution of the primary infection. In individuals with immunosuppression or with aging of the immune system, the virus can produce a secondary infection called shingles in which the virus replicates and travels from the ganglia along one or more spinal nerves erupting in an acute vesicular rash that is typically limited to one or two dermatomes on one side of the body. This secondary infection leads to damage to small unmyelinated nerve fibers and can lead to severe and persistent pain, PHN. PHN is characterized by episodic lancinating pain and severe allodynia in the affected dermatome. The incidence of PHN has been reduced in recent years with the emergence of an effective vaccine. Antiviral therapy with acyclovir, famcyclovir, or valacyclovir started within the first few days after eruption of vesicles also appears to reduce the incidence of PHN. The incidence rate of herpes zoster ranges from 1.2 to 3.4 per 1000 person-years among healthy individuals, increasing to 3.9 to 11.8 per 1000 person-years among those older than 65 years. Sympathetic blockade during acute herpes zoster can produce excellent analgesia, but is ineffective in treating established PHN. Treatment of established PHN is difficult. Topical lidocaine can reduce pain in those with marked allodynia. TCAs and anticonvulsants remain the primary treatment for PHN.

Complex Regional Pain Syndrome

CRPS develops as a localized pain disorder within 4 to 6 weeks following a trauma to an extremity ( Box 44.1 ). The incidence of CRPS is between 5.5 to 26.2 per 100,000 per year. Women are twice as frequently affected. Typically, symptoms are preceded by trauma. As the traumatized area heals, patients who develop CRPS are left with persistent pain that has the characteristics of neuropathic pain associated with signs and symptoms of dysfunction of the sympathetic nervous system (swelling, edema, erythema or bluish discoloration, temperature asymmetry when compared with the contralateral limb). CRPS can be divided into two subgroups based on absence (CRPS type 1) or presence (CRPS type 2) of distinct nerve lesions.

Box 44.1

Budapest Clinical Diagnostic Criteria for Complex Regional Pain Syndrome

  • 1.

    Continuing pain, which is disproportionate to any inciting event

  • 2.

    Must report at least one symptom in three of the four following categories:

    • Sensory: reports of hyperesthesia or allodynia

    • Vasomotor: reports of temperature asymmetry or skin color changes or skin color asymmetry

    • Sudomotor/edema: reports of edema or sweating changes or sweating asymmetry

    • Motor/trophic: reports of decreased range of motion or motor dysfunction (weakness, tremor, dystonia) or trophic changes (hair, nail, skin)

  • 3.

    Must display at least one sign at time of evaluation in two or more of the following categories:

    • Sensory: evidence of hyperalgesia (to pinprick) or allodynia (to light touch or deep somatic pressure or joint movement)

    • Vasomotor: evidence of temperature asymmetry or skin color changes or asymmetry

    • Sudomotor/edema: evidence of edema or sweating changes or sweating asymmetry

    • Motor/trophic: evidence of decreased range of motion or motor dysfunction (weakness, tremor, dystonia) or trophic changes (hair, nail, skin)

  • 4.

    No other diagnosis better explains the signs and symptoms

CRPS can lead to long-term, severe, persistent pain, and loss of function related to loss of use of the painful extremity. There is consensus that early therapeutic intervention is desirable and may prevent the transition to chronic CRPS. The central tenet of managing patients with CRPS is to focus on maintenance and restoration of function through aggressive physical and occupational rehabilitative therapy. Patients often fear the transient increase in pain and exacerbation of visible symptoms with use of the affected extremity. Reassurance and pain reduction can facilitate functional restoration. Pain is decreased with bisphosphonates administered both in early (first 6 to 9 months) and established CRPS. Although medications are widely prescribed in CRPS, clinical trial evidence for improvement in long-term pain is either negative (gabapetin) or is lacking (TCAs, carbamazepine). These medications may address the neuropathic components of CRPS. Sympathetic nerve blocks have been used for many years in managing patients with CRPS; they can produce dramatic pain reduction that facilitates physical therapy, but they are rarely useful in the long-term management of these patients. Spinal cord stimulation (SCS) has emerged in recent years as a more effective long-term means to produce pain reduction and facilitate functional restoration in patients with CRPS. Multidisciplinary treatment teams that include a provider that oversees medical management working in close coordination with a physical therapist and a psychologist appear to be the most effective means to help this group of patients.

Musculoskeletal Pain

Two of the most common syndromes involving myofascial or widespread musculoskeletal pain are myofascial pain syndrome (MPS) and fibromyalgia. MPS is typically characterized by regional pain, fibromyalgia by generalized pain. In spite of distinct diagnostic criteria and clinical features in typical cases, they frequently coexist in the same patient and may be pathophysiologically interconnected.

Myofascial Pain Syndrome

Although MPS lacks a consensus on definition and diagnostic criteria, it is characterized by the regional presence of spots of exquisite tenderness and hyperirritability in muscles or fascia, termed myofascial trigger points. Over 30% to 50% of middle-aged men and women, respectively, may complain of acute, recurrent, or chronic forms of regional musculoskeletal pain that may be MPS. Trigger point injections are frequently employed in the treatment of MPS in addition to physical therapy. Although effective in relieving symptoms in a significant proportion of these patients, the pain relief mechanism of trigger point injections is poorly understood.


Fibromyalgia is a condition defined by widespread, chronic musculoskeletal pain, present for more than 3 months, and accompanied by other somatic symptoms such as fatigue, waking unrefreshed, and cognitive dysfunction. Two thirds of the symptom burden is due to pain. It affects over 2% of the U.S. population, predominantly women (3.4% of women vs. 0.5% of men). In 25% to 65% of cases, fibromyalgia co-occurs with other rheumatic conditions such as rheumatoid arthritis, systemic lupus erythmatosus, and ankylosing spondylitis. Prevalence of fibromyalgia increases with aging. Although precise causation of fibromyalgia remains mostly speculative, dysregulation of pain-processing mechanisms and central pain sensitization have been postulated as major mechanisms underlying its clinical manifestations. Nonpharmacologic treatments (primarily promoting increased physical activity) are the cornerstone of therapy. TCAs, typically in doses smaller than those used to treat depression, are the traditional drug treatment. SNRIs, such as duloxetine and milnacipran, consistently augment pain alleviation and function in fibromyalgia. Although widely prescribed, opioids, with the exception of tramadol, have not been formally studied in fibromyalgia. Tramadol has effects on serotonin and norepinephrine uptake, which may explain its positive effects on pain and quality of life in fibromyalgia.

Cancer-Related Pain

Pain related to cancer and its treatment is common; indeed, pain is the most common presenting symptom of undiagnosed malignancy. The pain may be due to direct invasion of the malignancy or result from cancer treatment; chronic pain of various types often coexists with cancer-related pain. The primary focus of pain reduction in cancer patients is direct treatment of the malignancy, because successful treatment often leads to complete pain resolution. Nonetheless, ongoing pain during the course of treatment or as the disease progresses is all too common. More than 3 decades ago, the World Health Organization (WHO) revolutionized the treatment of cancer pain by introducing a simple, three-step analgesic ladder ( Box 44.2 ). This approach has been adopted worldwide and promotes the aggressive treatment of cancer-related pain by tailoring the analgesic used to the severity of the pain, starting with oral nonopioids and moving toward more potent oral and parenteral nonopioid and opioid analgesics as necessary to control pain. Anesthesia providers are often called upon to apply their knowledge of regional anesthesia and neuraxial drug delivery in caring for a small group of patients whose pain cannot be controlled with the more conservative approaches specified in the WHO approach. One of the more common nerve blocks used to successfully treat patients with pain associated with abdominal malignancy is the neurolytic celiac plexus block (described later). With the advent of implantable intrathecal drug delivery systems, long-term treatment of patients with intractable cancer-related pain using intrathecal opioids and other drugs (local anesthetics, clonidine, ziconotide) has become routine.

Box 44.2

World Health Organization (WHO) Analgesic Ladder for the Treatment of Cancer Pain

Step 1: Mild Pain

Nonopioid analgesics (acetaminophen, NSAIDs)

± adjuvant analgesics (TCAs, anticonvulsants) for neuropathic pain

Step 2: Moderate Pain

Use of short-acting opioids (e.g., hydrocodone, oxycodone) in starting doses

± nonopioid analgesics (acetaminophen, NSAIDs)

± adjuvant analgesics (TCAs, anticonvulsants) for neuropathic pain

Step 3: Severe Pain

Use of potent opioids (e.g., morphine, hydromorphone) in higher doses

± nonopioid analgesics (acetaminophen, NSAIDs)

± adjuvant analgesics (TCAs, anticonvulsants) for neuropathic pain

NSAIDs, Nonsteroidal antiinflammatory drugs; TCAs, tricyclic antidepressants.

Pharmacologic Management of Chronic Pain

Acetaminophen and Nonsteroidal Antiinflammatory Drugs

Acetaminophen and the nonsteroidal antiinflammatory drugs (NSAIDs) are among the most common medications used to treat mild to moderate pain, ranging from headache to acute muscle sprain and strain. The NSAIDs reduce the long-term pain and stiffness associated with osteoarthritis. Acetaminophen is a novel nonopioid analgesic with a poorly understood mechanism of action; aspirin and the NSAIDs produce potent inhibition of the enzyme cyclooxygenase, resulting in decreased levels of prostaglandins. The long-term use of NSAIDs and acetaminophen in other chronic painful conditions such as low back pain is common but poorly supported by scientific evidence, which shows little utility in the use of these drugs. These two groups of analgesics also represent the first step in the WHO analgesic ladder and are recommended as the initial drugs to treat mild to moderate cancer-related pain.


TCAs (e.g., amitriptyline, nortriptyline, desipramine) and newer selective SNRIs (e.g., venlafaxine, duloxetine) have a long history of use as first-line drugs in the treatment of neuropathic pain, including PHN and painful DPN. In this setting, TCAs are usually prescribed in doses smaller than those indicated for treatment of depression. Side effects can be problematic in maintaining long-term therapy. Common side effects of the TCAs include dry mouth and urinary retention; TCAs can also worsen preexisting heart block. The SNRIs have a more favorable side-effect profile at the cost of lesser efficacy when compared with the TCAs. Milnacipran is a recently introduced SNRI that has shown modest benefit for fibromyalgia pain relief. Although clinical experience with milnacipran for chronic neuropathic pain has been positive, strong research evidence to support its use for this indication is awaited.


Antiepileptic drugs (e.g., gabapentin, pregabalin) are effective as first-line treatment for neuropathic pain. These drugs are generally well tolerated; the most common side effects are dizziness, somnolence, and peripheral edema. Decisions regarding pharmacologic treatment of neuropathic pain ( Box 44.3 ) may be based on an analysis of the number needed to treat (NNT); the NNT (with 95% confidence interval [CI]) are TCA 3.6 (3.0 to 4.4), SNRI 6.4 (5.2 to 8.4), gabapentin 7.2 (5.9 to 9.1), and pregabalin 7.7 (6.5 to 9.4).

Oct 21, 2019 | Posted by in ANESTHESIA | Comments Off on Chronic Pain Management
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