Letters to the Editor

Sympathetic Dystrophy: New Name, New Concepts, New Treatment? To the Editor: We have read with interest the preliminary results by Vanos et al. (1)about the use of ketorolac in patients with sympathetic maintained pain (formerly sympathetic reflex dystrophy). We agree that it is compulsory to perform prospective, controlled and double-blind studies before accepting this new treatment. An excessive production or response of some prostaglandins in this type of pain is supported by more scientific data. Perhaps prostaglandininduced hyperalgesia is mediated by a presynaptic (postganglionic sympathetic neurons) release of prostaglandins stimulated by norepinephrine (2,3). Taiwo et al. (4) reported the direct effect of cyclic adenosine monophosphate as second messenger in peripheral hyperalgesia in primary afferent nociceptors. Also they suggested that it could be the final common pathway for many agonists in nociception, including the direct acting prostaglandin E,. In another publication, the same authors (5) demonstrated the blocking effect of morphine (by stimulation of preceptor in the primary afferents) on prostaglandin E,’s induced hyperalgesia, but not on the intracellular effects of 8-bromo cyclic adenosine monophosphate (a cell membrane diffusible cyclic adenosine monophosphate analogue). Kimbal (6) has described a new scheme to understand the interaction of physiologic products in neurogenic inflammation that binds prostaglandin E,, interleukin (IL), histamine, bradykinin, and others, all linked to substance P. Regarding sympathetic maintained pain, IL-8 could have a direct pain generating role successfully blocked by antiadrenergic drugs, but not by the cyclooxygenase inhibitor. Cunha et al. (7) proposed that IL-8 could be an intermediator between tissue damage and sensitization of pain receptors, leading to the development of sympathetic hyperalgesia. Recently, Drummond et al. (8) challenged the classical conceptions of sympathetic maintained pain as being an increase of sympathetic outflow in the diseased limb. Instead they observed a decrease of 3,4-dihydroxyphenylethyleneglycol and catecholamines in venous samples of affected limbs in patients diagnosed with sympathetic maintained pain, therefore, probably finding a decrease in sympathetic outflow! If sympathetic control is still the probable main factor in the physiopathology of sympathetic maintained pain, several other mediators (as suggested above) could also be

01992 by the International Anesthesia Research Society

involved. That could explain the usefulness of treatments different than sympathetic blockade. Francisco Asenjo, MD Gilbert Blaise, MD Department of Anesthesia Montreal Uniuersify Notre-Dame Hospital Montreal, P. Q., Canada

References 1. Vanos DN, Ramamurthy S, Hoffman J. Intravenous regional block using ketorolac: preliminary results in the treatement of sympathetic dystrophy. Anesth Analg 1992;7413941. 2. Ferreira SH, Nakamura M. Prostaglandin hyperalgesia: the peripheral analgesic activity of morphine, enkephalins and opioids antagonist. Prostaglandins 1979;18:191-200, 3. Levine JD, Taiwo YO, Collins SD, Tam JK. Noradrenaline hyperalgesia is mediated through interaction with sympathetic postganglionic neurone terminals rather than activation of primary afferent nociceptors. Nature 1986;323:158-60. 4. Taiwo YO, Bjerknes JK, Goetzl EJ, Levine ID.Mediation of primary afferent peripheral hyperalgesia by the CAMPsecond messenger system. Neuroscience 1989;32:577-80. 5. Levine JD, Taiwo YO. Involvement of the mu-opiate receptor in peripheral analgesia. Neuroscience 1989;32:5715. 6. Kimbal ES. Involvement of cytokines in neurogenic inflammation. In: Kimbal ES, ed. Cytokines and inflammation. Boston: CRC Press, 1991; 169439. 7. Cunha FQ, Lorenzetti BB, Poole S, Ferreira SH. Interleukin-8 as a mediator of sympathetic pain. Br J Pharmacol 1991;104:765-7. 8. Drummond I‘D, Finch PM, Smythe GA. Reflex sympathetic dystrophy: the significance of differing plasma catecholamine concentration in affected and unaffected limbs. Brain 1991;114:202536.

Wet Tap Due to Epidural Needle Defect To the Editor:

Most anesthesiologists use the loss of resistance technique to locate the appropriate endpoint when placing an epidural catheter. Soft interspinous ligaments or a leak at the Luer lock between the syringe and needle may cause a decrease in resistance below the expected amount. This case demonstrates another cause of decreased resistance and reminds us to inspect and test the whole syringeneedle unit for integrity before starting the procedure. Recently, on our chronic pain service, we evaluated a 47-yr-old woman with syringomyelia and a spinal cord injury resulting from a complication during biopsy of her thoracic syrinx. She presented with severe right-sided pain refractory to all employed modes of therapy and was to undergo a trial of continuous epidural narcotic therapy. For the epidural placement, the patient was placed in the sitting fetal position with her feet on a chair, and with head down on her bedtable to provide maximum thoracic kyphosis. After betadine preparation and 1%lidocaine infiltration

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Sympathetic dystrophy: new name, new concepts, new treatment?

Letters to the Editor Sympathetic Dystrophy: New Name, New Concepts, New Treatment? To the Editor: We have read with interest the preliminary results...
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