Pain Management: Approach to the Patient with Chronic Nonmalignant Pain



Pain Management: Approach to the Patient with Chronic Nonmalignant Pain


Mihir M. Kamdar

Shane J. Volney

Eric L. Krakauer



Chronic pain is an important problem not only for primary care but also for public health, affecting more than 116 million people in the United States and costing an estimated $560 to $645 billion each year, exceeding the annual US expenditures on cancer, diabetes, and heart disease combined. Many clinicians find patients with chronic pain challenging to treat, in part due to the inherent complexities of the chronic pain state and the lack of an adequate number of clinicians well trained in pain medicine.


PATHOPHYSIOLOGY AND CLINICAL PRESENTATIONS (1, 2, 3, 4, 5, 6, 7 and 8)


Definition and the Biopsychosocial Model of Pain

Pain is defined by the International Association for the Study of Pain as “an unpleasant sensory and emotional experience arising from actual or potential tissue damage.” Pain is an inherently subjective phenomenon, originating from a biologic source, but influenced by psychological factors. Unlike acute pain, chronic pain tends to be more multifactorial, less amenable to “cure,” and more influenced by both psychological and social factors. It typically requires continuous long-term and multidisciplinary management. These characteristics necessitate an appropriate adjustment of expectations and approach by both clinicians and patients to achieve a satisfactory outcome. The principal goal is improvement in quality of life and function, rather than complete elimination of the pain.


Biologic Components

Pain derives from afferent signals from nociceptive fibers in the periphery, triggered by tissue damage (nociceptive pain) or by direct neuronal injury (neuropathic pain). These primary afferent nociceptive fibers transduce pain signals to the central nervous system (CNS) via synapses in the dorsal horn of the spinal cord. From the dorsal horn, second-order nociceptors then carry the pain signals mainly via the spinothalamic tracts to the thalamus. Thalamic projections then transmit pain signals to both the somatosensory and frontal cortex. Modulation networks from the frontal cortex and limbic system create a final conscious perception. These networks are the medium by which psychological factors and the psychosocial context alter the sensation of pain.

The biologic component of chronic pain is less well understood than that of acute pain. On occasion, chronic pain can be triggered with a seemingly minor biologic stimulus or persist long after an injury has healed. Generation and maintenance of chronic pain is thought to occur via neuromodulation, primarily through the phenomena of peripheral and central sensitization. Furthermore, psychological and social factors may play a role in modulating the perception and perpetuation of pain.

In peripheral sensitization, primary nociceptors in the peripheral nervous system can be influenced by repetitive stimuli resulting in a decreased threshold for activating nociceptors and/or increased pain responses to suprathreshold stimuli. These changes can generate pain even when the stimulus is minimal. Clinically, these changes may manifest as allodynia (pain elicited from a nonpainful stimulus) or hyperalgesia (an increased responsiveness to noxious stimuli producing a heightened response to pain).

Central sensitization involves the dorsal horn, the site of neural transmission between primary and second-order nociceptors; it is the target of numerous analgesic agents. With chronic pain states, neuroplastic changes occur in the dorsal horn that lead to a decreased threshold for signal transmission between the peripheral and the CNSs. For example, up-regulation in N-methyl-D-aspartate (NMDA) receptor activity in the dorsal horn is thought to play a significant role in the development of chronic pain and neuropathic pain.

In addition to a lowered threshold for pain signaling, there are other changes in the CNS that may occur with chronic pain. In a normal state, there are descending pathways within the central nervous system that dampen pain transmission; with chronic pain, there is down-regulation of these inhibitory mechanisms leading to a heightened state of activity. It also is possible that immunomodulatory changes through microglial activation may play a role in maintaining chronic pain. The combination of these neural changes that occur with central sensitization is thought to potentiate chronic pain, even when the initial peripheral signal may have diminished.


Psychological Components

The interaction of physiologic and psychological factors in chronic pain is complex. Psychological components are often a consequence of chronic pain as well as a modulator and sometimes a cause. Psychological conditions associated with chronic pain include major depressive disorder (see Chapter 227), anxiety disorders (see Chapter 226), somatoform or personality disorders (see Chapters 230 and 231), substance abuse (see Chapter 235), and malingering (see Chapter 230 and Table 236-1).


Social Contributors

Social contributors to chronic pain include demographic variables that may influence the clinical course (Table 236-1).
They may also emanate from home life or work (e.g., ongoing litigation or a work’s compensation claim), complicating a chronic pain state or persist due to a potential secondary gain. Injured workers respond less well to treatment than do individuals with similar medical conditions who do not have workers’ compensation claims. Chronic pain presentations may also result from partner (domestic) violence, the presence of which greatly increases the risk of a chronic pain syndrome. Estimates of lifetime risk among women for partner violence range from 10% to 30%.








TABLE 236-1 Myths Surrounding Chronic Pain

















Patients’ complaints stem from secondary gains; they do not really suffer “pain.”


Patients with chronic pain are inherently noncompliant and manipulative.


Patients given opiates will refer manipulative friends.


Opiates in therapeutic doses will cause respiratory depression.


Patients given opiates will become “addicted.”


Giving patients opiates for chronic nonmalignant pain will result in investigations by state and federal review boards.


Chronic pain can be fixed.



Partner (Domestic) Violence.

The vast majority of partner violence victims are women, outnumbering men by a ratio of 9:1. The condition occurs among people of all sociodemographic and age groups, including the elderly (sometimes referred to as elder abuse). Such violence greatly increases the risk of developing adverse physical and psychological consequences. Physical manifestations range from telltale “falls,” ecchymoses, and forearm injuries (from trying to protect oneself) to more subtle, otherwise unexplained chronic pain presentations such as headache, pelvic pain, back pain, abdominal pain, or dyspareunia. Severe premenstrual cramping and irritable bowel symptoms may ensue. Persons suffering from a preexisting chronic condition may experience a worsening of symptoms. Psychological presentations include anxiety, depression, and alcohol and substance abuse. Patients are at increased risk for somatization disorders, complications of pregnancy, sexually transmitted diseases, eating disorders, and noncompliance with medical regimens.


Categorizations of Pain

Pain can be categorized by either clinical presentation (acute vs. chronic) or underlying mechanism (neuropathic vs. nociceptive).


Acute versus Chronic

In general, acute pain emanates from an identifiable biologic stimulus, is more amenable to pure pharmacologic intervention, and is generally self-limited due to the natural resolution of tissue injury. Chronic nonmalignant pain, defined as pain lasting beyond 3 months by the International Association for the Study of Pain, may or may not have an identifiable or overt biologic stimulus, may be more challenging to treat pharmacologically, and may have greater psychosocial underpinnings.


Nociceptive versus Neuropathic Pain


Nociceptive Pain.

This type of pain develops from actual or potential tissue or organ damage. Somatic nociceptive pain is typically attributable to a specific anatomic location of tissue injury. Patients present with pain that is well localized and stabbing, throbbing, or achy. Examples of somatic nociceptive pain include incisional pain at the site of a recent surgery or focal extremity pain at the site of a bony fracture. Visceral nociceptive pain is secondary to actual or potential injury to an internal organ. Visceral nociceptive pain is often more difficult to localize and may have a referred component due to persistence of embryologic nociceptive innervation of the visceral structures. Examples of visceral nociceptive pain include the spasmodic pain of biliary colic that may radiate to the shoulder blades or the dull, aching pain of pancreatic cancer.


Neuropathic Pain.

This form derives from direct neural trauma or injury. It may occur with or without a nociceptive component. The pain is typically characterized as burning, tingling, and lancinating, often occurring in a dermatomal distribution. Peripheral and central sensitization can lead to the nerves firing in the absence of any peripheral stimulus. Patients may experience allodynia (pain induced by a nonpainful stimulus) or hyperalgesia (a state of increased sensitivity to a pain stimulus). Examples of neuropathic pain include postherpetic neuralgia, diabetic neuropathy, sciatica, trigeminal neuralgia, complex regional pain syndrome, and phantom limb pain.


DIFFERENTIAL DIAGNOSIS (2,3,5,9)

Differential diagnosis includes reversible organic causes of pain, pathologies such as malignancy or evolving neuropathy, and psychosocial factors that could trigger, sustain, or aggravate pain. While chronic pain sometimes remain idiopathic, determination of the most likely diagnosis enables implementation of the most targeted and effective therapies. Potential organic causes of pain should be grouped by pain location (Table 236-2).


WORKUP (2,3,5,9)

As with any initial presentation of a chronic condition, a thorough history and physical examination is imperative for optimal assessment and treatment. The heterogeneity of chronic pain complaints and the variety of mechanisms and presentations necessitate an exploration of both physical and psychosocial dimensions of the problem.


Pain History

A pain history should review prior pain diagnostics and therapies, explore the possibility of serious underlying pathology, serve to classify the pain process, and elicit any potentially contributory psychosocial factors.


Characterizing the Pain for Classification

The cardinal features of pain should always be documented: onset/duration, circumstances surrounding the onset, quality/severity, location/spread, alleviating/aggravating factors, and associated symptoms. Circumstances surrounding onset are especially important in elucidating the underlying cause or causes. The pain history enables accurate classification—acute or chronic, localized or diffuse, somatic or visceral, and nociceptive or neuropathic—which guides further workup and targeted treatment.

Pain severity can be assessed by standard severity scales, most of which are cross-culturally reproducible. Examples include the visual analogue pain scale or 0-to-10 numerical rating scale. These scales also are useful when assessing response to stepwise
pharmacologic therapy; pain severity should be documented frequently when pain treatment is initiated and when it is changed in response to a changing clinical situation.








TABLE 236-2 Differential Diagnoses of Chronic Pain Based on Location




























































































































Location


Differential of Reversible Etiologies


Headache/Facial Pain (See Chapters 165 and 214)


Tension


Sinusitis


Glaucoma


Migraine


Chronic otitis


Medication


Cluster


Chronic meningitis


Trigeminal neuralgia


Temporal arteritis


Abscess


Postconcussive


Large AVM


Subdural


Glaucoma


Hypertension


Tumor


Bruxism


Dentalgia


TMJ


Sialadenitis


Musculoskeletal Pain (See Chapters 147, 148, 149, 150, 151, 152, 153, 154)


Fibromyalgia


Rheumatoid arthritis


Paget disease


PMR


Osteoarthritis


Tumor


Polymyositis


Gout/pseudogout


Cramps


Dermatomyositis


SLE


Bursitis/tendinitis


Drug myositis


Osteomyelitis


Reflex sympathetic dystrophy


Hypothyroidism


Trichinosis


Sickle cell disease


Trauma


Lyme disease


Secondary syphilis


Low Back Pain (See Chapter 147)


Chronic disk disease


Osteoporotic fracture


Tumor (bone/retroperitoneum)


Sciatica


Spinal stenosis


Seronegative spondylosis


Vertebral osteoarthropathy


Epidural abscess


Abdominal/Pelvic Pain (See Chapters 58 and 116)


Irritable bowel


IBD


Kidney stones


Biliary colic


Diverticulitis


Chronic pyelonephritis


Esophagitis


Gastritis/PUD


Polycystic kidney


Pancreatitis


Hepatitis


Endometriosis


Parasitosis


Tumor (GI/GU/GYN)


Ovarian cysts


Aortic aneurysm


Abdominal angina


PID/TOA


Sickle cell disease


Poisoning (e.g., lead)


FMF


Medicines


Internal hernias PMS


Porphyria


Peripheral Nerve Pain (See Chapter 167)


DM neuropathy


B12 deficiency


Charcot-Marie-Tooth disease


HIV neuropathy


CTDz


Hypothyroidism


Paraneoplastic


Renal failure


Poisoning (EtOH, Pt, INH)


AVM, arteriovenous malformation; CTDz, connective tissue disease; DM, diabetes mellitus; EtOH, ethanol; FMF, familial Mediterranean fever; GI, gastrointestinal; GU, genitourinary; GYN, gynecologic; IBD, inflammatory bowel disease; INH, isoniazid; PID, pelvic inflammatory disease; PMR, polymyalgia rheumatica; PMS, premenstrual syndrome; PUD, peptic ulcer disease; Pt, platinum; SLE, systemic lupus erythematosus; TMJ, temporomandibular joint; TOA, tuboovarian abscess.




Psychiatric History

Any history of psychological evaluation or treatment is equally important, particularly in light of evidence that early psychological intervention has a considerable effect on a patient’s reported pain level, return of function, and compliance with treatment. A history of any prior psychiatric diagnoses and treatments should be obtained. In addition, signs of abnormal mood or affect on examination should be noted, and validated screening tools for depression, anxiety, and substance abuse should be used. The possibility of past physical, sexual, or emotional abuse should always remain a consideration when evaluating a patient with chronic pain.








TABLE 236-3 Previous Pain History




























1. Prior pain diagnostics:



▪ Imaging (x-ray, CT scan, MRI)


▪ Electromyography (EMG)


▪ Blood tests


2. Interventions:



▪ Prior injection therapies (including both diagnostic and therapeutic injections and blocks)


▪ Prior surgeries targeting chronic pain


3. Current and previous pain medications:



▪ Prescription, nonprescription, herbal remedies


▪ Include dose, frequency, side effects/reason medication was stopped (where applicable), effect on pain


4. Other nonpharmacologic therapies:



▪ Physical or occupational therapy


▪ Functional restoration/work-hardening programs


▪ Complementary therapies (acupuncture, mind-body therapies, acupuncture)


▪ Transcutaneous electrical nerve stimulation (TENS) unit trial


▪ Chiropractor visits


5. Psychological treatment:



▪ Previous treatment for emotional/behavioral disorders, history of suicidal thoughts or attempts, current or past medications




Social History and Perceived Functional Status

The social history for chronic pain should include a review of home, work, and leisure activities; a review of personal relationships; and a thorough functional review (e.g., ability to carry out activities of daily living, ability to work, and any current pain-related physical restrictions). Some potentially important contributing factors may be difficult to elicit and require special attention during the workup. These include partner violence and posttraumatic stress disorder (see Chapter 239).


Case Finding for Partner (Domestic) Violence

When the cause of chronic pain remains unexplained or there is other clinical suspicion of partner violence (e.g., repeated visits to the ER for “falls” or forearm injuries), partner violence deserves consideration. Screening asymptomatic persons in the primary care setting remains somewhat controversial (detection is possible, but evidence of improved outcomes remains sparse); however, case finding in patients with conditions such as unexplained chronic pain syndrome may be more productive. Use of validated screening questions can be helpful in case finding. These include a two-question approach:

“Do you ever feel unsafe at home?”

“Has anyone at home hit you or tried to injure you in any way?”

Sensitivity for this approach is 71% with a specificity of 85%. Some authorities also suggest questions that can elicit evidence of fear of a current or previous partner’s intimidating or controlling behavior:

“Have you ever been afraid of your partner?”

“Has anyone every threatened you or tried to control you?”

If the response to any of these questions is positive, the physician should obtain a full description of any evidence of injury and perform a directed physical exam (see next section). Confidentiality is essential to patient safety, and all records (including telephone numbers and billing diagnoses) should be handled carefully with patient protection as a priority.


Perceived Functional Status

There are a number of validated tools for assessing a person’s perceived disability due to pain, such as the Brief Pain Inventory (BPI) (Fig. 236-1) and the Oswestry Disability Index.



Laboratory Study

If a neurologic deficit is noted, further workup such as CNS imaging, neurophysiologic testing, or neurologic consultation may be warranted. Checking inflammatory biomarkers in a patient with diffuse, multifocal pain can help rule out inflammatory arthritis. Evidence of organ pathology may be an indication for imaging, most useful in the context of cancer-induced pain (see Chapter 90).


Determining the Likelihood of Serious Underlying Organic Pathology

If the pain complaint is relatively new and accompanied by constitutional or other objective findings, then the likelihood of a primary organic process increases markedly, and the workup should focus on the appropriate physical examination and laboratory testing. Specific “red flag” findings include new onset of neurologic deficits (motor weakness, sensory deficits, meningeal signs, new bowel or bladder dysfunction, etc.), new constitutional symptoms, or other rapidly evolving symptoms associated with pain.

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Aug 23, 2016 | Posted by in CRITICAL CARE | Comments Off on Pain Management: Approach to the Patient with Chronic Nonmalignant Pain

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