To the Editor:-We read with interest the article by Kienbaum et al. regarding the hypothesis that u-opioid receptor blockade by naloxone induces cardiovascular stimulation mediated by the sympathoadrenal system.
This study confirms that clinicians who have detoxified heroin addicts for 20 yr have known, i.e., clonidine, an [small alpha, Greek](2-agonist), is essential to avoiding hyperadrengic crisis and pulmonary edema. Riordan and Kleber in 1980 first demonstrated that utility of clonidine in controlling the hemodynamic changes seen in the withdrawal syndrome. Naloxone has also been previously associated with pulmonary edema [3,4]presently because of this sympathoadrenal surge.
It is very dramatic to document the extent of catacholamine secretion. This has been elegantly demonstrated in the study by Kienbaum et al. We also agree with the authors that because of this cardiovascular stimulation secondary to a surge in sympathoadrenal system, the procedure of acute opioid detoxification should be done by trained anesthesiologists in an intensive care setting. However, in order to make this procedure safe, it is imperative to use an [small alpha, Greek]2-agonist, such as clonidine before [micro sign]-opioid receptor blockade, even if the patient is under general anesthesia.
Clifford Gevirtz, M.D.
Dilip V. Subhedar, M.D.
Chang S. Choi, M.D.
Assistant Professor; Metropolitan Hospital Center; New York Medical College; Department of Anesthesiology; New York, New York
(Accepted for publication September 17, 1998.)