ABSTRACT
Zolpidem is a nonbenzodiazepine sedative hypnotic drug used for the short-term treatment of insomnia. While quite effective in producing sedation, zolpidem has potentially hazardous side effects when put in the context of complex tasks. Therefore, to more fully understand the postmortem concentrations of zolpidem, our laboratory has developed a sensitive method for the quantitation of zolpidem in biological specimens. Additionally, we have evaluated the distribution of zolpidem in various postmortem tissues and fluids from 10 aviation fatalities. This method incorporated a modified acetonitrile 'crash and shoot' extraction and a Waters Xevo TQ-S with an Acquity ultra-performance liquid chromatograph. The linear dynamic range was 0.4-800 ng/mL. The extraction efficiencies ranged from 78 to 87%, depending on the concentration. Postmortem blood zolpidem concentrations in these 10 cases ranged from 7.6 to 76.5 ng/mL. The highest concentrations of zolpidem present in each victim were found in the liver, spleen, lung and kidney tissues. Distribution coefficients for zolpidem were determined for each of the specimen types analyzed. These coefficients are expressed relative to the blood concentration in each case. This method proved to be simple, accurate and robust for the identification and quantitation of zolpidem in postmortem fluids and tissues.
Subject(s)
Chromatography, High Pressure Liquid/methods , Forensic Pathology/methods , Hypnotics and Sedatives/blood , Mass Spectrometry/methods , Pyridines/blood , Humans , Kidney/drug effects , Kidney/metabolism , Liver/drug effects , Liver/metabolism , Lung/drug effects , Lung/metabolism , Spleen/drug effects , Spleen/metabolism , ZolpidemABSTRACT
Blood samples from aircraft accident victims are analyzed for carboxyhemoglobin (COHb) and cyanide ion (CN(-)). Such victims often suffer open wounds near the autopsy blood collection sites. Many aircraft crashes result in fires that fill the victim's atmosphere with smoke that is rich in carbon monoxide (CO) and hydrogen cyanide (HCN). It is important to determine whether pooled blood in those wounds may have absorbed these gases after death, which could lead one to erroneously conclude that the presence of COHb and CN(-) in blood was the result of breathing in these gases. A laboratory desiccator was used as a chamber to establish whether CO or HCN may be absorbed in undisturbed, pooled blood. COHb levels were 4.3-11.0% after exposure to CO (5,532, 8,298, 11,064, 22,129 and 33,193 ppm) for 30 and 60 min. Blood CN(-) concentrations (1.43-5.01 µg/mL) increased with exposure to HCN at 100 and 200 ppm, each at 15, 30, 45 and 60 min. The observed COHb increases do not exclude the possibility for higher COHb levels in blood exposed to highly CO-rich atmospheres, but there is a strong potential for CN(-) levels to increase by the absorption of atmospheric HCN. Thus, postmortem COHb and CN(-) levels should be carefully interpreted.
