«CHRONIC PAIN MEDICAL TREATMENT GUIDELINES Part 1: Introduction The chronic pain medical treatment guidelines apply when the patient has chronic pain ...»
CHRONIC PAIN MEDICAL TREATMENT GUIDELINES
Part 1: Introduction
The 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 with an assessment of the presenting
complaint and a determination as to whether there is a “red flag for a potentially serious condition” which would trigger an immediate intervention. Upon ruling out a potentially serious condition, conservative management is provided. 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, such as surgical options, the chronic pain medical treatment guidelines apply. This provides 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 two parts. Part 1 is the introduction. Part 2 consists of pain interventions and treatments. With a few exceptions, Part 2 is primarily an adaptation of evidence-based treatment guidelines, from the Work Loss Data Institute’s Official Disability Guidelines (ODG) Treatment in Workers’ Comp – Chapter on Pain (Chronic). The version adapted is dated October 23, 2008, and it is being adapted with permission from the ODG publisher. Any section not adapted directly from ODG is labeled “[DWC]”.
Chronic Pain: Chronic pain is defined as “any pain that persists beyond the anticipated time of healing.” Types of Pain: Pain mechanisms can be broadly categorized as nociceptive or neuropathic.
Nociceptive pain: Nociceptive pain is the 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.” Neuropathic Pain: Neuropathic pain is “pain initiated or caused by a primary lesion or dysfunction of the nervous system.” Normal nociception would not be considered dysfunction of the nervous system.
Overview Chronic pain has a huge impact on the individual and society as a whole. It is the primary reason for delayed recovery and costs in the workers’ compensation system. Most chronic pain problems start with an acute nociceptive pain episode. Therefore, effective early care is paramount in managing chronic pain. Given the importance of pain in healthcare, it is presently the subject of intensive scientific research which in turn has generated a growing evidence base regarding the diagnosis, treatment and management of painful conditions.
The International Association for the Studyof Pain (IASP) states that pain is “an unpleasant sensory or emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” (Merskey and Bogduk 1994) This describes pain as a subjective experience; therefore, unlike hypertension or diabetes, there is no objective measurement for pain intensity. Analysis of the objective
data (psychosocial assessment, physical exam findings, imaging results, lab tests) is needed to evaluate the patient’s subjective report of pain.
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 to understanding and treating pain 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.
The biopsychosocial model of pain instead recognizes that pain is ultimately the result of the pathophysiology plus the psychological state, cultural background/belief system, and relationship/interactions with the environment (workplace, home, disability system, and health care providers). Current research is investigating the neurobiological causes for persistent pain and how structural and functional changes in the central nervous system may serve to amplify and maintain the experience and disability of certain pain condition. (Siddall and Cousins 2007) This is an area of intensive research which will contribute to the scientific evidence base in years to come.
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 greater 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 cortical pathways to the brain. Nociceptive signals within the brain are sent to two major areas: the somatosensory cortex, where the sensory component of pain is represented in the brain, and the limbic forebrain system, which is the neural substrate for the emotional component of pain experience responsible for feelings of suffering.
Since these 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 approach to the management of pain.
Neuropathic pain is “pain initiated or caused by a primary lesion or dysfunction of the nervous system.” (Turk and Okifuji 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 and Maeda 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, and Complex Regional Pain Syndrome (CRPS)/Reflex Sympathetic Dystrophy (RSD). (Mackey and Maeda 2004) 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 there is an increase in neuronal excitability and responsiveness in the dorsal horn. In central sensitization, chemical mediators for inflammation can also upregulate the expression of genes that alter synaptic transmission.
Because of neuronal plasticity, current research is showing that 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 to understand pain and serve to establish parameters for reasonable outcomes and acceptable standards of care. These 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 can be distinguished from acute pain by 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 ultimately leading 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 “chronic pain persists beyond the usual course of healing of an acute disease or beyond a reasonable time for an injury to heal.” (ACOEM Medical Treatment Guidelines Chapter 6 page 108.) The Division of Workers’ Compensation definition of chronic pain, “any pain that persists beyond the anticipated time of healing,” is derived from Bonica’s Management of Pain (Turk and Okifuji, 2001). Therefore, it is a clinical decision to recognize chronicity or persistence of pain when 1) the condition is not improving over time, 2) fails to improve 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 (see Clinical Topics section of the MTUS).
Often it takes a number of months for the clinician to recognize when pain becomes 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 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 may 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 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 1977). Thus 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 there has been an approach 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 and Gerber 1993):
Linton identified strong evidence that psychosocial variables are strongly linked to the transition from acute to chronic pain disability and that psychosocial variables generally have more impact than biomedical or biomechanical factors on back pain disability. (Linton 2000) Thus, when clinical progress is insufficient, the clinician should always be prepared to address confounding psychosocial variables, in a coordinated, multidisciplinary manner.
Medical vs. Self-Management Model