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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.

Unlabelled: Aim of the study was the clinical investigation of sevoflurane degradation when using water-free lithiumhydroxide versus moist Drägersorb 800 for carbon dioxide absorption., Methods: Concentrations of Compound A in the inspiratory gas mix and serum fluoride levels were measured in two groups of 8 patients each., Results: When water-free lithiumhydroxide was used for carbon dioxide absorption, concentration of Compound A in the inspiratory gas mix was ca. 1 ppm (near minimal level of detection) as compared to ca. 20 ppm for moist Drägersorb 800. The concentration of fluoride increased during sevoflurane anesthesia (15.0 +/- 4.8 mumol/l with lithiumhydroxide versus 21.9 +/- 4.0 mumol/l with Drägersorb 800 after 60 mins)., Conclusions: When lithiumhydroxide is used, there is only minimal formation of compound A from sevoflurane degradation. Since serum fluoride levels increased in both patient groups, we conclude that this is caused mainly by metabolism of sevoflurane. Capacity of lithiumhydroxide for carbon dioxide absorption is similar to that of Drägersorb 800. Therefore, the use of lithiumhydroxide increases patient safety.

The various components of commercial soda lime (sodium hydroxide, potassium hydroxide, calcium hydroxide, barium hydroxide) were studied in terms of their reactivity with sevoflurane at its boiling point (59 degrees C). A simple closed system, a reflux cooler, served as a model. Analyses were performed by GC/MS. Besides sevoflurane, we identified four compounds: A, B, C, and D. Free methanol, formaldehyde and formic acid could not be found. Presumably methanol is transferred from an intermediate formalin-semiacetal of the hexafluorisopropanol. Calcium hydroxide and barium hydroxide showed little reaction with sevoflurane, whereas larger amounts of reaction products were observed with sodium hydroxide and potassium hydroxide. The alkali hydroxides of sodalime are presumably responsible for its reaction with halogenated inhalation anaesthetics. We therefore conclude that decomposing reactions of halogenated inhalation anesthetics with dry soda lime could be prevented by using a newly developed soda lime.

In the case of the biodegradable cryoprotectant hydroxyethyl starch (HES) no deglycerolization process is required prior to the transfusion of frozen red blood cells (RBC). In a first study the elimination of an HES 200,000/0.62 from the plasma of 6 dogs was investigated by means of a novel HPLC-GFC method. 16% of the blood volume were replaced by autologous HES protected frozen/thawed RBC. In a second study the HES concentration in the plasma of 7 healthy volunteers was determined following the substitution of 8% of the blood volume, but a washing step has been performed to reduce the concentration of the cryoprotectant (HES 200,000/0.5). In a third study, however, this step was omitted. The elimination of the HES followed always first order kinetics. In the case of the transfusions without postthaw washing in dogs and humans, the initial plasma concentrations amounted to 2.11 +/- 0.15 g/dl and 0.75 +/- 0.26 g/dl, respectively. The corresponding value for the washed preparations was less than 0.03 g/dl. Within 4-5 h the concentrations dropped to less than 50% of the initial values. The 9-hour value was less than 35% (dogs), the 20-hour value about 15% (humans) of the initial concentration. As HES is primarily eliminated via the kidneys, within this period the concentrations of HES in the urine dropped from 4.3 +/- 2.11 g/dl to less than 0.03 g/dl (humans, no washing step). In conclusion, the elimination of the accompanying cryoprotectant HES was no problem in the concentrations applied. A simple washing step with isotonic saline, however, effectively reduced the concentration of the extracellular cryoprotectant HES far below critical levels.