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Sevoflurane degradation by carbon dioxide absorbents may produce more than one nephrotoxic compound in rats

[La dégradation du sévoflurane par les absorbants de gaz carbonique peut produire plus d’un composé néphrotoxique chez les rats]

Caroline R. Stabernack, MD^*, Edmond I Eger, II, MD, Uwe H. Warnken, MD, Harald Förster, MD, Douglas K. Hanks, MD and Linda D. Ferrell, MD

^* From the Department of Anesthesia and Perioperative Care, and
the Department of Pathology,
University of California, San Francisco, California, USA, and
the Department of Experimental Anesthesiology, University of Frankfurt, Germany.

Address correspondence to: Dr. Edmond I Eger, Department of Anesthesia and Perioperative Care, Box 0464, Science - 455, 513 Parnassus Avenue, University of California, San Francisco, California 94143-0464, USA. Phone: 415-476-6927; Fax: 415-476-9516; E-mail: egere{at}anesthesia.ucsf.edu

Purpose: Degradation of sevoflurane by carbon dioxide absorbents produces compound A, a vinyl ether. In rats, compound A can produce renal corticomedullary necrosis. We tested whether other compounds produced by sevoflurane degradation also could produce corticomedullary necrosis.

Methods: Two groups of rats were exposed for four hours to sevoflurane 2.5% delivered through a container filled with fresh Sodasorb® and heated to 30°C or to 50°C, respectively. Compound A was added to produce an average concentration of 120 ppm in both groups. A third (control) group received 2.5% sevoflurane that did not pass through absorbent, and no compound A was added.

Results: As determined by gas chromatography, the higher temperature produced more volatile breakdown products, including compound A. Median necrosis of the corticomedullary junction in the 50°C group [10% (quartiles 1.0%–7.8%); n = 20] exceeded that in the 30°C group [5% (6.5%–15%); n = 18; P < 0.02], and both exceeded the median necrosis in the control group [0% (0.0%–0.2%); n = 10; P < 0.02]. The respective mean ± SD values for these three studies were: 12.8 ± 16.7%, 5.3 ± 4.4%, and 0.3 ± 0.5%.

Conclusion: Degradation products of sevoflurane other than compound A can cause or augment the renal injury in rats produced by compound A.

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