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Klinik für Anästhesiologie und Intensivmedizin Klinik für Allgemeine Psychiatrie und Psychotherapie, Universitätsklinikum Essen, Essen, Germany
To the Editor:
We read with interest Ma et al.’s article (1) reporting beneficial effects of clonidine on gastrointestinal stimulation occurring during ultra-rapid opioid detoxification.
Although not quoted by the authors, we also observed clinically relevant withdrawal symptoms in opioid-addicted patients when a large dose of the opioid receptor antagonist naloxone was administered for antagonist-supported detoxification despite deep general anesthesia (2,3) contrasting earlier enthusiastic reports (4). This withdrawal syndrome includes neurohumoral, cardiovascular, and gastrointestinal stimulation as well as restlessness and muscle cramps usually lasting several days if not pharmacologically relieved (2,3). Sympathetic activation is likely to contribute to this withdrawal syndrome as indicated by increased muscle sympathetic activity and plasma catecholamine concentrations in these patients during detoxification (2,5). However, increased sympathetic neural outflow in response to opioid receptor blockade can both be prevented as well as rapidly normalized by administration of a large dose of the 
2-adrenoceptor agonist clonidine (5 µg · kg-1 IV + 2–5 µg · kg-1 · h-1 IV) (6). The prevention of sympathetic withdrawal symptoms in our patients was associated with an inhibition of both cardiovascular and gastrointestinal stimulation. Accordingly, none of our patients experienced diarrhea when treated by a large dose of clonidine guided by a target heart rate of 50 min-1 (6). Therefore, coadministration of various drugs to control withdrawal symptoms, e.g., glycopyrrolate, ondansetron, droperidol, somatostatin, and/or other drugs, (1) can be avoided, decreasing the risk of potential pharmacological interactions and expenses.
In summary, we can accept Ma et al.’s notion that during antagonist supported opioid detoxification additional drugs administered for control of withdrawal symptoms are not needed when 2-adrenoceptor agonists are given in sufficient doses.
References
Department of Anesthesiology & Pain Management, University of Texas Southwestern Medical Center at Dallas, Dallas, TX Department of Anesthesiology, Cedars Sinai Medical Center in Los Angeles, Los Angeles, CA
In Response:
It is very gratifying to know that Kienbaum and his colleagues have also found that gastrointestinal stimulation evoked by µ-opioid receptor blockade in patients addicted to opioid analgesics was reduced by intravenous clonidine (1,2). The article by these investigators on intravenous clonidine in Anesthesiology (1) was published after our manuscript had already been submitted for publication in Anesthesia & Analgesia. Further studies are clearly needed to verify the authors’ suggestion that no additional adjunctive drugs are needed to control the numerous side effects associated with ultra-rapid opioid detoxification. Hopefully, our publication will stimulate further research to determine the optimal anesthetic technique for opioid detoxification.
References
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