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Evaluating Pain Intervention Effectiveness and Compliance

Innovative ways to identify patients with severe, chronic pain and assess effective pain control by various standardized, objective measures to monitor clinical progress.
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Editor’s Note: This article was originally prepared for the 4th Annual VA Pain Management Update in Jackson, Mississippi, June 20, 2008.

Robert Foery, PhD, DABCC/TC

Pain treatment is a relatively new discipline that has not yet significantly addressed the issue of treatment effectiveness or outcomes. Even the diagnosis of pain has been controversial since much debate continues to center around the issue as to whether pain is psychologic or anatomic. The severity of pain is believed by some to be purely whatever the patient says it is on a scale of 1 to 10. Treatment of pain is argued as to whether it should be medical, psychological, or interventional. There is acute, chronic, intractable, malignant, non-malignant, baseline, persistent, breakthrough, rescue, incident, and flare pain, just to name some of the terms promulgated in recent years. Interestingly, the usual terms of mild, moderate, and severe that are applied to all other medical conditions, is conspicuously absent in contemporary pain language. Recently, some opioid drugs have been approved by the US Food and Drug Administration for moderate to severe pain, but there are no guidelines or definitions as to how a clinician is to determine whether pain is moderate or severe. While progress in pain treatment has certainly occurred, the journey has been an arduous process. Presented here is a paradigm in which a sub-class of pain patients is objectively diagnosed as having severe, chronic pain and treated with objective outcome measures of effectiveness. The objective diagnosis and evaluation techniques described here are recommended as a means to eliminate some of the subjectivity that has characterized ambulatory pain treatment.

Biologic Basis of Severe Chronic Pain

The paradigm of diagnosis, treatment, and evaluation of both are based on the following fundamental tenets that have evolved from a plethora of scientific studies.

  1. Severe, chronic pain produces many measurable objective physical signs that can confirm the patient’s perception of severe pain.1-7
  2. Severe, chronic pain produces hyper-function of the hypothalamic-pituitary-adrenal axis and profound hyperelectro-transmission in the peripheral and central nervous systems.4-9
  3. Severe, chronic pain—via its hormonal alterations, cardiovascular affects, and hyperelectro-transmission—causes many pathologic, and even fatal, consequences and complications7-13 (see Table 1). It should, therefore, be considered a disease, per se, and the prevention of its complications and consequences is the basic element of treatment.
  4. Severe, chronic pain may impair eating, ambulation, sleep, activities of daily living, health habits, marital or social relations, and vocational pursuits.4,7
Table 1. Some Complications of Severe, Chronic Pain
  • Hypertension
  • Tachycardia
  • Hypercortisolemia
  • Hyperlipidemia
  • Diabetes
  • Osteoporosis
  • Arteriosclerosis
  • Coronary or Cerebral Vascular Accident
  • Adrenal Exhaustion
  • Fatigue
  • Impotence/Loss of Libido
  • Depression/Suicide
  • Anorexia
  • Insomnia
  • Immobility
  • Loss of Mental Capacity
  • Contractures
  • Body Asymmetry
  • Impaired Activities of Daily Living
  • Loss of Social, Vocational Abilities

The Clinical Diagnosis of Severe, Chronic Pain

Acute, chronic, malignant, non-malignant, and intractable are all terms that describe pain but it is more critical to ascertain if the pain is severe, as opposed to mild or moderate. Again, a knowledge of the underlying cause—be it cancer, non-cancer, rheumatologic, traumatic, or post-surgical—is essential but it is more critical to know if the pain is severe. The premise is that potent (Schedule II) opioid drugs should only be prescribed to severe pain patients rather than those whose pain is classified as mild or moderate.

Severe, chronic pain is diagnosed in this paradigm by not only the patient’s history and perception of severity, but by objective physical signs and laboratory tests. Once a diagnosis of severe, chronic pain has been made, treatment with potent opioids and ancillary measures can be initiated.

The components used to make a diagnosis of severe, chronic pain are listed here. Although no patient will have every component, a diagnosis of severe, chronic pain should demonstrate a majority of these components:

  1. A history of failure of past non-opioid treatments
  2. Impairment of activities of daily living and normal biologic functions
  3. Objective, physical signs of sympathetic discharge and other physical signs
  4. Laboratory evidence of adrenal gland abnormalities

A summary table of diagnosis of severe pain (see Table 2) provides additional detail. Given here are more details of objective physical signs, because a knowledge of these is not well appreciated or utilized. It is the contention of this paradigm that potent opioids should not be used unless objective physical signs of severe, chronic pain are present. Furthermore, treatment effectiveness needs to be objective, and this may be done, in great part, by monitoring objective physical signs.

Table 2. Summary Diagnosis of Severe Pain
  • Patient describes pain as constant and debilitating
  • Objective physical signs of:
    Sympathetic (adrenergic) discharge
    Sensory avoidance
    Positional relief
    Pain distraction
  • Impairment of:
    Activities of daily living
    Diet, sleep, ambulation
    Social, marital, vocational relationships
  • Laboratory evidence of adrenal hormone abnormalities (pregnenolone, and cortisol)

Sympathetic Discharge Signs

Sympathetic or adrenergic discharge is caused by two concomitant mechanisms. Adrenergic receptors in the central nervous system are activated by uncontrolled pain, and these central receptors, in turn, activate the autonomic nervous system by sending electrical impulses downward into the periphery via the vagus nerve and the autonomic nerve network.7-9 The second mechanism is activation of the hypothalamic-pituitary-adrenal axis and the out-pouring of catecholamines (adrenalin, dopamine, and noradrenalin) and glucocorticoids (pregnenolone, cortisol) into the blood stream.5-7

Last updated on: January 30, 2012
First published on: July 1, 2008