CHRONIC PAIN MEDICAL TREATMENT GUIDELINES
Forum Posting December 2014
Part 1: Introduction……………………….……………………………………..……………2
References (for Introduction)…………………………………………..……….…………......12
Part 2: Procedure Summary ─ Pain…………………………………………………….......14
References (for Procedure Summary)………………………………………..…...…………..188
(Including findings, evaluations, and ratings; click on PMID# for complete abstracts)
Explanation of ODG Medical Literature Ratings (see Contents for more detail)
Ranking by Type of Evidence:
1. Systematic Review/Meta-Analysis
2. Controlled Trial – Randomized (RCT) or Controlled
3. Cohort Study - Prospective or Retrospective
4. Case Control Series
5. Unstructured Review
6. Nationally Recognized Treatment Guideline (from guidelines.gov)
7. State Treatment Guideline
8. Other Treatment Guideline
10. Conference Proceedings/Presentation Slides
Ranking by Quality within Type of Evidence:
a. High Quality
b. Medium Quality
c. Low Quality
DWC Evidence Ratings for Selected References:
See MTUS Hierarchy of Evidence (Currently in Public Comment)
With the permission of the publisher (Work Loss Institute) the Department of Workers’ Compensation has modified the Official Disability Guidelines chapter titled “Pain (Chronic),” published in April 2014 and most recently modified on November 21, 2014, for adoption as part of the Medical Treatment Utilization Schedule regulations.
PART 1: Introduction
These Chronic Pain Medical Treatment Guidelines apply when the patient has chronic pain as determined by following the clinical topics section of the Medical Treatment Utilization Schedule (MTUS). In following the clinical topics section, the physician begins by assessing the presenting complaint and determining whether there is a “red flag for a potentially serious condition” that would trigger an immediate intervention. Upon ruling out a potentially serious condition, the physician should provide conservative management. If the complaint persists, the physician needs to reconsider the diagnosis and decide whether a specialist evaluation is necessary.
If the patient continues to have pain that persists beyond the anticipated time of healing without plans for curative treatment that meet MTUS Guidelines, such as surgical options, the chronic pain medical treatment guidelines apply. They provide a framework to manage all chronic pain conditions, even when the injury is not addressed in the clinical topics section of the MTUS.
The chronic pain medical treatment guidelines consist of an introduction (Part 1) and specific information on interventions and treatments for chronic pain (Part 2), an edited version of evidence-based treatment guidelines from the April 10, 2014, version of the Work Loss Data Institute’s Official Disability Guidelines (ODG) Treatment in Workers’ Compensation – Chapter on Pain (Chronic), adapted with permission from the publisher. For specific guidance on opioid use, refer to the Division of Workers’ Compensation (DWC) “Guideline for the Use of Opioids to Treat Work-Related Injuries.”
Pain: The International Association for the Study of Pain (IASP) defines pain as “an unpleasant sensory or emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” This definition describes pain as a subjective experience; therefore, unlike hypertension or diabetes, there is no objective measurement for pain intensity. Analysis of the objective data (history, psychosocial assessment, physical findings, imaging results, lab tests, etc.) is needed to evaluate the patient’s subjective report of pain.
Types of Pain (Acute vs Chronic): Pain comes in many forms. Understanding which kind or kinds of pain a person is experiencing is a first step toward treatment. Although acute and chronic pain are considered separately below, an individual can experience them simultaneously. Furthermore, current research shows that pain exists more on a continuum than in discrete categories of “acute” or “chronic” pain. This means that, for some patients, the mechanisms responsible for pain persistence are engaged early in the injury process. Therefore, it is important to identify persons at risk for the development of chronic pain and to establish preventative measures to reduce the likelihood of pain persistence.
Acute pain, by definition, is of sudden onset and expected to be of short duration. It can usually be linked to a specific event, injury, or illness—a muscle strain, a bone fracture, severe sunburn, or a kidney stone, for example. People can self-manage many types of acute pain with over-the-counter medications or a short course of stronger analgesics and rest. Acute pain usually subsides when the underlying cause resolves, such as when a fracture heals, or kidney stone or diseased tooth is removed. In the DWC “Guideline for the Use of Opioids to Treat Work-Related Injuries,” acute pain is defined as pain lasting up to one month and subacute pain as pain last between one and three months.
Chronic pain is any pain that lasts more than three months following an injury and can be frustratingly difficult to treat. In the DWC “Guideline for the Use of Opioids to Treat Work-Related Injuries,” chronic pain is defined as pain lasting more than three months.
Types of Pain (Mechanisms): Pain mechanisms can be broadly categorized as nociceptive, inflammatory, neuropathic, or unknown.
Nociceptive pain: pain caused by activation of nociceptors, which are sensory neurons found throughout the body. A nociceptor is “a receptor preferentially sensitive to a noxious stimulus or to a stimulus which would become noxious if prolonged.” (Hughes, 2008) Nociceptive pain is the type experienced with tissue damage such as contusion, burn, or injury to a body part.
Inflammatory pain: pain which occurs in response to tissue injury, when inflammation develops and local nociceptors become highly sensitive even to normal stimuli, such as touch. This is another type of “warning” pain, indicating the need for a period of healing, and this pain generally disappears after the injury resolves. In conditions such as rheumatoid arthritis or gout, inflammatory pain persists as long as the inflammation does. (IOM, 2011)
Neuropathic Pain: “pain initiated or caused by a primary lesion or dysfunction of the nervous system.” Neuropathic pain is caused by a malfunction of the peripheral or central nervous system due to an injury or an illness. (Normal nociception would not be considered dysfunction of the nervous system). The cause may be an underlying disease process (as in diabetes) or injury (e.g., stroke, spinal cord damage), but neuropathic pain may not have an observable cause and can be considered maladaptive “in the sense that the pain neither protects nor supports healing and repair.” (Costigan, 2009)
Unknown causes: pain that arises without a defined cause or injury. Examples of such chronic pain conditions are fibromyalgia, irritable bowel syndrome, vulvodynia, chronic headaches, and temporomandibular disorders. Research points to impaired central pain sensitivity and responses in these conditions, but their complex mechanisms have not yet been unraveled. (Kindler, 2011)
Acute and chronic pain affects large numbers of Americans, with at least 100 million adults in the United States burdened by chronic pain alone. The annual national economic cost associated with chronic pain is estimated to be $560–635 billion. Pain is a uniquely individual and subjective experience that depends on a variety of biological, psychological, and social factors, and different population groups experience pain differentially. (IOM, 2011)
Chronic pain has a significant impact on the individual and on society as a whole, and it is the primary reason for delayed recovery and costs (medical and indemnity) in the workers’ compensation system. Most chronic pain problems start with an acute nociceptive pain episode. As a result, effective early care is paramount in preventing chronic pain. Not surprisingly, pain has become the subject of intensive scientific research, and researchers are generating a growing evidence base regarding the diagnosis, treatment, and management of painful conditions.
The experience of pain is a complex phenomenon. Multiple models have evolved over time to explain it. Traditionally, the biomedical model explains pain through etiologic factors (e.g., injury) or disease whose pathophysiology results in pain. It is now understood that this classic biomedical approach (pursuit of a pathoanatomical diagnosis with the view of targeting and treating a specific “pain generator”) is incomplete. Its exclusive application can result in unrealistic expectations on the part of the physician and patient, inadequate pain relief, and excessive disability in those with pain that persists well after the original injury has healed. A strictly biomedical approach to pain is simply too reductionist; rather, what is called for is an approach that recognizes the complexity of the pain experience. Similar to what has been learned about other chronic diseases, chronic pain ultimately affects (and is affected by) many intrinsic and extrinsic aspects of a person’s life.
In general, the early theories of how pain works failed to address some key issues, many of which were described a number of years ago by Melzack and Wall (1996):
The relationship between injury and pain varies (that is, a minor injury may produce great pain, and a significant injury may produce minor pain), as does the relationship between the extent of injury and the resulting disability.
Non-noxious stimuli can sometimes produce pain (allodynia), and minor amounts of noxious stimuli can produce large amounts of pain (hyperalgesia).
The locations of pain and tissue damage are sometimes different (referred pain).
Pain can persist long after tissue heals.
The nature of pain and sometimes its location can change over time.
Pain is a multidimensional experience, with strong psychosocial influences and impacts.
Responses to a given therapy vary among individuals.
Earlier theories have not led to adequate pain treatment.
The biopsychosocial model of pain recognizes that pain is ultimately the result of the patient’s pathophysiology and psychological state, cultural background/belief system, and relationship/interactions with the environment (workplace, home, disability system, and health care providers). Therefore, pain has become understood as a complex condition involving numerous areas of the brain. Multiple two-way communication pathways in the central nervous system (from the site of pain to the brain and back again) and emotional, cognitive, and environmental elements work together to form a complete, interconnected pain apparatus. Because it has numerous interacting and contributing causes and multiple effects, chronic pain resembles many other chronic diseases. (Gatchel, 2007; IOM, 2011)
Within the biomedical model, pain mechanisms are broadly categorized as nociceptive or neuropathic. Inflammatory mechanisms may also play a role. While there are similarities, each mechanism has unique features and characteristics. This mechanistic approach may provide insight into appropriate therapeutic strategies.
Several reviews have detailed the mechanisms and mediators of pain and the components of the ascending and descending pain pathways. In nociceptive pain, signal transduction in nociceptor somatosensory afferent terminals converts mechanical, electrical, thermal, or chemical energy into an action potential which is transmitted to the dorsal horn of the spinal cord by specialized nerve fibers. The signal is then transmitted through ascending spinal-cortical pathways to the brain. These signals evoke a response in multiple brain systems, a “distributed network,” consistent with the variety of physical, cognitive, affective, and reflexive reactions to pain that people experience.
Since multiple areas of the brain interact with other areas of the brain, past memories, external environmental factors, and internal cognitive factors (i.e., psychosocial factors) influence or modulate the pain experience. How the brain integrates all the input is, in part, the basis for the biopsychosocial model for, and approach to, the management of pain.
In contrast to nociceptive pain, neuropathic pain is “pain initiated or caused by a primary lesion or dysfunction of the nervous system.” (Turk, 2001) The altered modulation of the pain response in patients with neuropathic pain causes a state of hyperexcitability and continuous pain signal output in the absence of peripheral tissue damage. “‘Neuropathic pain can result from injury or trauma (e.g., surgery), infection (e.g., post-herpetic neuralgia), endocrine (e.g., diabetes, hypothyroidism), demyelination (e.g., multiple sclerosis), errors in metabolism, neurodegenerative disorders (e.g., Parkinson’s disease), or damage directly to the spinal cord or brain (e.g., thalamic stroke).” (Backonja in Loeser, 2001; Mackey, 2004)
Neuropathic pain is characterized by symptoms such as lancinating, electric shock-like, paroxysmal, tingling, numbing, and burning sensations that are distinct from nociceptive pain.
Many neuropathic pain states have traditionally been thought of as having a primary peripheral etiology. Recent investigation, however, using functional neuroimaging techniques, demonstrates that many neuropathic and other chronic pain conditions may have a large centralized component (central vs. peripheral model). These conditions include, but are not limited to, chronic low back pain (CLBP), fibromyalgia, irritable bowel syndrome, temporomandibular disorders, and Complex Regional Pain Syndrome (CRPS)/Reflex Sympathetic Dystrophy (RSD).
Inflammation can play a significant role in both nociceptive and neuropathic pain. Inflammation occurs when cells and tissue are damaged and release chemical mediators (commonly referred to as “the inflammatory soup”) that not only induce an inflammatory response but also sensitize nociceptors and other somatosensory components of the nervous system. Peripheral sensitization occurs when inflammatory mediators cause a reduction in the threshold required for nociceptor activation. A similar short-term central sensitization can occur in which neuronal excitability and responsiveness in the dorsal horn increase. In central sensitization, chemical mediators for inflammation can also upregulate the expression of genes that alter synaptic transmission.
Current research indicates that because of neuronal plasticity, protracted central sensitization (neuronal hyperexcitability) can result in long-term changes that may be important in the transition from acute to chronic pain and the development of chronic pain syndromes. Patients with these syndromes generally have severe and persistent pain that is disproportionate to the tissue injury.
Models are the conceptual framework for understanding pain. They serve to establish parameters for reasonable outcomes and acceptable standards of care, which are helpful for physicians, patients, families, healthcare providers, carriers, and compensation systems. Several different models of pain have developed over time, each with strengths and weaknesses.
Acute vs. Chronic Pain Model
In many situations, acute pain serves as a highly adaptive and beneficial experience. Fundamentally, it serves as a protective warning of actual or impending tissue damage. Acute musculoskeletal pain is a common example in the injured worker and is often a signal of real or impending tissue damage.
Most acute pain is self-limited and may respond to short-term administration of analgesics and conservative therapies. However, continued activation of nociceptors with less than adequate pain control can lead to peripheral and central sensitization, a risk factor for persistent pain with prolonged disability, delayed return to baseline function, and delayed return to work.
Chronic pain differs from acute pain in more than just the time course. Whereas acute pain serves as a protective warning signal, chronic pain has no known survival benefit. Evidence suggests that generation and subsequent maintenance of chronic pain, as opposed to acute pain, may involve changes in central pain processing mediated through mechanisms of neural plasticity and may ultimately lead to hyper-excitability of central structures in the spinal cord and brain. To complicate matters, unremitting pain may be associated with depression and/or anxiety.
As a practical matter, it is noted that “[t]he distinction between acute and chronic pain is somewhat arbitrary” and “[c]hronicity may be reached from one to six months postinjury.” ACOEM recognizes that the most clinically useful definition might be that “chronic pain persists beyond the usual course of healing of an acute disease or beyond a reasonable time for an injury to heal.” (ACOEM, 2014) The DWC definition of chronic pain, “any pain that persists beyond the anticipated time of healing,” is derived from Bonica’s Management of Pain. (Turk, 2001) Therefore, it is a clinical decision to recognize chronicity or persistence of pain: (1) when the condition is not improving over time; (2) when there is a lack of improvement with treatments directed to the specific injured body part (see Clinical Topics section of the MTUS); or (3) in the absence of a specifically correctable anatomic lesion (refer to the relevant Clinical Topics section of the MTUS). It often takes a number of months for the clinician to recognize when pain has become chronic.
Illness Behavior Model
As previously stated, pain is a subjective experience, influenced and modulated by cognitive, emotional, and environmental elements. Psychosocial factors can affect the perception and expression of pain. These might include, but are not limited to, a tendency toward anxiety, depression, somatization, fear avoidance, emotional lability, catastrophizing, job dissatisfaction, perceived injustice, and embellishment.
Further, while frank malingering is rare, secondary gain factors, such as disability income and avoidance of perceived unpleasant tasks can impact the overall clinical presentation. Taken together, psychosocial factors often play a larger role in eventual patient outcome than obvious somatic factors as determined by the nature and extent of the original injury. Efforts directed solely to the management of possible physical pain generators without addressing psychosocial factors may result in a suboptimal outcome.
Biomedical vs. Biopsychosocial Model
The traditional biomedical model “assumes disease to be fully accounted for by deviations from the norm of measurable biological (somatic) variables.” (Engel, 1997) According to this model, there is always a direct causal relationship between a specific pathophysiologic process and the presence and extent of a particular symptom. While this model has served the medical community well in the treatment and cure of certain diseases (e.g., infectious diseases), it has generally failed in the treatment of chronic illness, including persistent pain. For example, for decades the prevailing approach has been to identify the “pain generator” and remove it by cutting it out or blocking it.
In 1977 Engel proposed an alternative, the biopsychosocial model, which focuses greater attention on the patient, rather than presumed pathophysiology. The biopsychosocial model approaches pain and disability as a complex interplay of biological, psychological, and social factors. These psychosocial factors can be easily assessed.
The following chart contrasts these two pain models (Hanson, 1993):
Most appropriate for treating acute pain conditions
More useful for those with chronic pain conditions
Emphasizes peripheral nociception
Recognizes the role that central mechanisms play in modulating peripheral nociception or generating the experience of pain in the absence of nociception
Focuses on physical disease mechanisms
Recognizes the importance of illness behavior including cognitive and emotional responses to pain
Takes a reductionistic approach to understanding and treating pain
Takes a multidimensional systems approach to understanding and treating pain
Relies on medical management approaches
Uses self-management approaches in addition to medical management