Editor's Memo
by Forest A. Tennant, MD, DrPH
 It’s now been almost 30
years ago that I began my pain management clinic. The early patients were heavily weighted
towards cancer, post-polio, and back-trauma patients. A standard practice in those days
was to do a rheumatic disease blood panel, and I was intrigued at the high percentage of
pain patients with one or more positive immune tests such as C-reactive protein,
anti-nuclear antibody, sedimentation rate, and rheumatoid factor. I developed the theory
that the patients must have some genetic, immune, or collagen disease that made them
susceptible to the development of a painful condition or that prevented proper healing
after trauma or surgery. It turns out my theory didn’t hold much water, but I was so
curious that I began searching the literature for clues as to why pain patients had so
many positive immune tests. I discovered that a reasonable number of good scientific
studies on biochemical changes in pain patients had already been reported particularly by
British physicians. Such changes included abnormal corticoid secretion and serum carbon
dioxide levels.1 This early literature was notable in that observed biochemical
changes were generally believed to be rather innocuous, diagnostic tracers or markers for
the presence of pain and not a serious complication of pain. The idea of a biologic tracer
or marker carried into the 90’s. The military wanted to find a marker to separate
malingerers from legitimate pain patients and believed they found one when a group of pain
patients were discovered to have low serum triiodothyronine levels.2 Others,
including this editor, believed that one or more biologic markers might identify valid
pain patients as opposed to addicts.3
As time and research marched on, it became evident that there are no innocuous tracers
or markers in severe pain patients. The biochemical alterations and markers observed in
severe, chronic pain patients are actually complications of pain itself. Although chronic
pain may exert its dirty work by multiple biologic mechanisms, one stands out. Severe
pain—both acute and chronic—activates the hypothalamus-pituitary-adrenal axis.
Consequently, there is hyper-secretion of catecholamines and glucocorticoids which raise
blood pressure and pulse rate. The abnormal adrenal secretions produced by severe, chronic
pain likely cause some of the immune abnormalities observed in pain patients.
Fundamentally, the most objective, physiologic signs of uncontrolled pain are tachycardia
and hypertension. In addition to adrenal hormone release, elevated pulse rate and blood
pressure are likely to also result from pain over-stimulating central adrenergic centers.
The astute, in-depth practitioner can easily and certainly document adrenal abnormalities
by simple serum screening of cortisol and pregnenolone. No need for a 24-hour urine
collection for catecholamine assay or an ACTH challenge test.
Why is documentation of over-stimulation of the hypothalamus-pituitary-adrenal axis so
critical? Two reasons. One is simply welfare of the patient. Asking the patient to rate
their pain 1 to 10 is fine, but this is hardly an objective way to categorize pain into
the usual clinical categories of mild, moderate, and severe. Simply, all physicians from
the wide-eyed intern to the gray-haired sage need to evaluate every pain patient with a
pulse and blood pressure reading. Obviously, the pain patient with a pulse rate of lets
say, 100 a minute, needs a far more aggressive treatment approach than one with a pulse
rate of 76.
The second reason to put some objectivity to pain categorization is a practical one:
reimbursement. Costs of the most potent pain treatments — be it Schedule II opioids,
intrathecal administration, or a implanted electrical stimulator — can only be
considered catastrophic. We need to give the bill-payors—sometimes known as insurance
companies, HMO’s, health plans, and skin flints—additional, objective
categorization rather than “10 on the pain scale.” Try it. They listen on the
other end of the phone when you mention constant pain, debilitation, pulse rates over 90,
and a high cortisol. This is doctor talk. I personally don’t have much trouble with
reimbursement these days: I just indicate that I’ve documented tachycardia and a low
pregnenolone serum level in the patient.
Bottom line. Pain is now the 5th vital sign, but don’t ignore a couple of the
others.
—Forest A. Tennant, MD, DrPH
Editor in Chief
References
1. Glynn CJ and Lloyd JW. Biochemical changes associated with intractable pain. Br Med J.
1978. 1:280-281.
2. Dons RF and Shaki KMM. Changes in triiodothyronine mark severe pain syndrome: a case
report. Military Med. 1994. 159:465-466.
3. Tennant F and Herman L. Using biologic markers to identify legitimate chronic pain.
Amer Clin Lab. June 2002.
— September 2006
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