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

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 degrees C or to 50 degrees 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 degrees C group [10% (quartiles 1.0%-7.8%); n = 20] exceeded that in the 30 degrees 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.