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• W2065859920 abstract "To the Editor: Although the Bier block has been used as a treatment for sympathetically-maintained pain (SMP) for many years, the selection of agents remains controversial. Different drug classes have been used, including alpha-adrenergic blockers (guanethidine, reserpine, bretylium), alpha-2 agonists (clonidine), nonsteroidal anti-inflammatory agents (ketorolac, tenoxicam), local anesthetics (lidocaine, prilocaine), and NMDA antagonists (ketamine). To our knowledge the use of labetalol for Bier block has not been reported. We here report a case of complex regional pain syndrome (CRPS) that did not respond to a standard Bier block with bretylium and lidocaine, but responded for 7 years to multiple Bier blocks with labetalol and lidocaine. A 42-year-old man sustained a right fifth metatarsal fracture after a heavy block fell upon his right foot in June 1993. His injury was complicated by osteomyelitis. Following healing, he continued to have persistent sharp, burning pain on the lateral side and dorsum of the right foot. The pain was constantly present, varying in intensity between 7 (0–10 scale) at its worst and 3–4 at its best. The clinical findings were consistent with a CRPS. Before presentation to our service, treatments included seven lumbar sympathetic blocks, each with poor or no pain relief; epidural infusions with bupivacaine and fentanyl, with moderate temporary pain relief; and physical therapy. He had a negative phentolamine infusion test. Multiple oral medication trials, which included opioids (levorphanol, morphine, oxycodone), tramadol and sodium channel blockers (IV lidocaine), failed to relieve his pain. At presentation, his medications included amitriptyline 100 mg daily, clonidine 0.2 mg po three times daily, clonazepam 0.5 mg po three times daily, gabapentin 900 mg po three times daily, and dextromethorphan 90 mg po three times daily. He had no pending litigation, drank alcohol socially, and smoked for 20 years. On physical examination his right foot was mottled, mildly swollen, colder than the left, and had excessive sweating and dystrophic changes of the skin. Significant cold allodynia and pinprick-induced hyperalgesia were present on the lateral and dorsal surfaces. Strength was normal, with mild limitation in range of motion secondary to pain. He walked with crutches and was unable to bear weight on the foot, except for the duration of pain relief gained with Bier block. In contrast to a Bier block with bretylium 120 mg and lidocaine, which did not bring him pain relief except for the short duration of local anesthetic, Bier blocks with the combination of labetalol (20–40 mg) and lidocaine (100–200 mg) gave him complete pain relief for 7 to 10 days. During the past seven years, he has received this block 158 times. Initially, the blocks were performed once each month; during the last 5 years, he has undergone this procedure every two to three weeks. Medical and vascular evaluations have identified no contraindications to these serial Bier blocks. Other treatments, including a spinal cord stimulation trial, have been proposed, but the patient refused because he was satisfied with the current treatment. In order to determine whether the effect of Bier block was mediated through A beta fiber conduction block,1Torebjork H.E. Hallin R.G. Perceptual changes accompanying controlled preferential blocking of A and C fiber responses in intact human skin nerves.Exp Brain Res. 1973; 16: 321-332Crossref PubMed Scopus (235) Google Scholar the patient consented to an ischemic tourniquet block of the right foot, with no medication administered; this caused an exacerbation of pain and allodynia. In addition he underwent a Bier block with normal saline and lidocaine (without labetalol) in a blind manner to test the effects of lidocaine alone and a possible placebo effect. This procedure provided him with only minimal pain relief for a few hours, as compared to more than 7 days for the combination of lidocaine and labetalol. Sympathetically-maintained pain (SMP) may or may not be present in patients with CRPS. The treatment of SMP with a Bier block using guanethidine has been used clinically for many years. Guanethidine's site of action is on noradrenergic ganglionic synapses. Guanethidine is transported across the sympathetic nerve membrane by the same mechanism that transports norepinephrine itself. After uptake, guanethidine replaces norepinephrine, causing a gradual depletion of norepinephrine stores in nerve endings. It has been suspected that repeated Bier blocks with guanethidine might cause permanent damage to the noradernaline reuptake system, as guanethidine accumulates in nerves for a prolonged time.2Hanington-Kiff J.B. Sympathetic nerve blocks in painful limb disorder.in: Wall P.D. Melzack R. Textbook of pain. Churchill Livingstone;, London1994: 1035-1052Google Scholar The clinical effect of guanethidine in cases of SMP has been reported to last days to weeks,2Hanington-Kiff J.B. Sympathetic nerve blocks in painful limb disorder.in: Wall P.D. Melzack R. Textbook of pain. Churchill Livingstone;, London1994: 1035-1052Google Scholar but others failed to observe a long-term pain relief.3Blanchard J. Ramamurthy S. Walsh N. et al.Intravenous regional sympatholysis a double-blind comparison of guanethidine, reserpine, and normal saline.J Pain Symptom Manage. 1990; 5: 357-361Abstract Full Text PDF PubMed Scopus (107) Google Scholar, 4Ramamurthy S. Hoffman J. Guanethidine Study Group. Intravenous regional guanethidine in the treatment of reflex sympathetic dystrophy/causalgia a randomized, double blind study.Anesth Analg. 1995; 81: 718-723Crossref PubMed Google Scholar, 5Kaplan R. Claudio M. Kepes E. Gu X.F. Intravenous guanethidine in patients with reflex sympathetic dystrophy.Acta Anaesthesiol Scand. 1996; 40: 1216-1222Crossref PubMed Scopus (28) Google Scholar Reserpine has also been used for Bier block in cases of SMP. This is a false precursor for dopamine and norepinephrine in the nervous system. Injectable guanethidine and reserpine are not clinically available in the USA and bretylium has been used instead.6Ford S.R. Forrest W.H. Eltherington L. The treatment of reflex sympathetic dystrophy with intravenous regional bretylium.Anesthesiology. 1988; 68: 137-140Crossref PubMed Scopus (29) Google Scholar, 7Hord A.H. Rooks M.D. Stephens B.O. et al.Intravenous regional bretylium and lidocaine for treatment of reflex sympathetic dystrophy a randomized, double-blind study.Anesth Analg. 1992; 74: 818-821Crossref PubMed Google Scholar Initially, bretylium releases norepinephrine from sympathetic ganglia and terminal endings of postganglionic adrenergic neurons. Subsequently, the drug inhibits the release of norepinephrine from adrenergic nerve endings and blocks its reuptake. Bretylium was found effective in the treatment of CRPS.6Ford S.R. Forrest W.H. Eltherington L. The treatment of reflex sympathetic dystrophy with intravenous regional bretylium.Anesthesiology. 1988; 68: 137-140Crossref PubMed Scopus (29) Google Scholar, 7Hord A.H. Rooks M.D. Stephens B.O. et al.Intravenous regional bretylium and lidocaine for treatment of reflex sympathetic dystrophy a randomized, double-blind study.Anesth Analg. 1992; 74: 818-821Crossref PubMed Google Scholar For our patient, the standard bretylium combined with lidocaine did not provide significant pain relief. Ischemic tourniquet block caused an exacerbation of pain, and, therefore, it is unlikely that the pain relief during his numerous Bier blocks was caused by A beta conduction block. Administration of normal saline and local anesthetic alone did not provide long-lasting pain relief. Phentolamine infusion and lumbar sympathetic blocks were ineffective. There are very few reports about the use of drugs with nonselective beta-blocker properties (propranolol) or with combined alpha and beta-blocker potency (labetalol) for CRPS pain. Several patients with causalgia were successfully treated with propranolol.8Simson G. Propranolol for causalgia and Sudeck's atrophy.JAMA. 1974; 227: 327Crossref PubMed Scopus (18) Google Scholar, 9Magee C.P. Grosz H.J. Propranolol for causalgia.JAMA. 1974; 228: 826-827Crossref PubMed Scopus (3) Google Scholar Successful use of IV and PO labetalol for pain was reported in one patient with algodystrophy, a term synonymous with CRPS.10Churcher M.D. Algodystrophy after aortic bifurcation surgery.Lancet. 1984; 2: 131-133Abstract PubMed Scopus (17) Google Scholar Labetalol was also given into the epidural space for treatment of pain in gynecologic cancers.11Margaria E. Gagliardi M. Palieri L. et al.Analgesic effect of peridural labetolol in the treatment of cancer pain.Int J Clin Pharmacol Ther Toxicol. 1983; 21: 47-50PubMed Google Scholar The efficacy of epidural labetalol in pain control was attributed to membrane stabilizing activity (also known as quinidine-like effect or local anesthetic activity), and to beta-blocking effect.11Margaria E. Gagliardi M. Palieri L. et al.Analgesic effect of peridural labetolol in the treatment of cancer pain.Int J Clin Pharmacol Ther Toxicol. 1983; 21: 47-50PubMed Google Scholar However the use of labetalol in the Bier block was never reported. Labetalol is a competitive antagonist of alpha-1 receptors as well as beta-1 and beta-2 receptors. Labetalol's affinity for alpha-receptors is 10 times less than that of phentolamine, but labetalol is alpha-1 selective. Its beta blocking potency is 3 times lower than that of propranolol. The ratio of beta- to alpha-adrenergic blocking potency of labetalol is 3:1 with oral administration and 7:1 with parenteral administration. It is not clear by which mode of action labetalol provided pain relief in our patient. Beta-1 receptors are located in presynaptic adrenergic nerve terminals, whereas beta-2 and alpha-1 receptors are not present in peripheral nerves. Alpha-1 receptors are present on postsynaptic effector cells, especially smooth muscle, and under the pathological condition of SMP, they can be expressed on the peripheral nociceptors. Therefore, a possible explanation of labetalol's efficacy in this patient could be related to the fact that labetalol's beta-1 presynaptic effect inhibits the reuptake of norepinephrine into adrenergic nerve terminals. The inhibition of norepinephrine uptake by labetalol suggests a mechanism somehow similar to that of guanethidine and bretylium, and may account for labetalol's longer lasting analgesic properties. Nevertheless the alpha-1 blocking effect may also provide pain relief by blocking the ongoing activity in peripheral sensitized nociceptors. Another possible explanation might be the local anesthetic activity of labetalol, also known as “membrane stabilizing” effect. This action is the result of sodium channel blockade. The local anesthetic blockade is usually not evident after systemic administration because the plasma concentration is too low. During the Bier block, the concentration of labetalol in the treated extremity is significantly higher, making it possible for labetalol to be clinically effective as sodium channel blocker without eliciting systemic side effects. However, this action alone is unlikely to account for long-lasting pain relief. In summary, this case illustrates the successful and unusual use of labetalol with Bier blocks for CRPS refractory to conventional treatment. The case supports the safety of repeated treatment with Bier blocks in patients with CRPS and also demonstrates a lack of tolerance to this treatment modality. The authors would like to thank the MGH Pain Center, Department of Anesthesia and Critical Care Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts." @default.
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• W2065859920 title "Multiple Bier Blocks with Labetalol for Complex Regional Pain Syndrome Refractory to Other Treatments" @default.
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