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FORENSIC TOXICOLOGY - Bio Medical Forensics

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illicit drug use increase. Polydrug use further complicates the issue by<br />

making interpretation more difficult, frequently as the result of<br />

insufficient information to support an opinion. Unlike alcohol, drug<br />

concentrations are not correlative to behavioral effects, particularly in<br />

DUI cases. Furthermore, limited literature information is available<br />

correlating drug concentrations with standardized field sobriety tests and<br />

poor driving performance. The following cases are presented to support<br />

the need for more case specific data correlating drug concentrations to<br />

driving performance.<br />

The first case involves a 43-year-old male charged with DWI (2nd<br />

offense) after a witness reported observing the suspect driving erratically<br />

on a major highway. The suspect failed the standardized field sobriety<br />

tests (SFSTs) administered by the arresting officer. The suspect claimed<br />

to suffer from chronic back pain, and several medications were seized<br />

from him including Oxycontin® (40 mg), diazepam (10 mg), Skelaxin®<br />

(metaxalone 800 mg), Lyrica® (pregabalin 75 mg), as well as other<br />

drugs that were not readily identified. The breath alcohol test was<br />

negative, so a DRE was summoned. Upon completion of the DRE<br />

evaluation, the officer opineed that the suspect was under the influence<br />

of a CNS depressant and narcotic analgesic. Blood and urine samples<br />

were tested. The laboratory quantitatively determined diazepam (410<br />

ng/mL), nordiazepam (481 ng/mL), oxazepam (48 ng/mL), and trace<br />

amounts of temazepam, as well as oxycodone (114 ng/mL). The<br />

laboratory did not test for metaxalone or pregabalin. The urine sample<br />

was presumptively positive for benzodiazepines, opiates, cannabinoids,<br />

and cocaine.<br />

The second case involves a 38-year-old male nurse charged with<br />

DUI after a witness complained of his erratic driving to state police. The<br />

arresting trooper was also able to observe the driver’s dangerous<br />

behavior while driving and pulled him over soon after. Upon initial<br />

contact, the driver was observed to be wearing his coat inside out and<br />

upside down. A recently filled prescription for lorazepam (0.5 mg) fell<br />

out of the suspect’s pocket. The suspect failed initial SFSTs and the<br />

breath alcohol was negative, so a DRE was called. The DRE opined that<br />

the suspect was under the influence of a CNS depressant and cannabis.<br />

The suspect admitted to taking lorazepam on an “as needed” basis, but<br />

did not take it regularly. Physician affidavits were obtained verifying<br />

that the suspect was under their medical care and prescribed Ativan®<br />

and Seroquel®. The laboratory’s findings reflected a blood quantitation<br />

of lorazepam (79 ng/mL). The laboratory did not test for the Seroquel®.<br />

The presumptive positive cannabinoids drug screen was subsequently<br />

confirmed negative for both THC and THC-COOH.<br />

The last case involves a subject, who voluntarily participated in an<br />

ongoing study evaluating the applicability of oral fluids to DRE<br />

certifications/DUI investigations. Oral fluid testing is not new to<br />

forensic toxicology; however, the use of oral fluids in DUI cases is being<br />

developed. Oral fluids offer many potential advantages over<br />

conventional blood and urine matrix testing, particularly the ease of<br />

sample collection. Blood, urine, and oral fluid samples are collected<br />

from the volunteer who is under the influence of CNS depressants and<br />

narcotic analgesics. The results of each matrix are compared to one<br />

another and against the DRE’s opinion.<br />

All three cases reflect the laboratories’ limitations in terms of the<br />

types of drugs tested and matrices used. Forensic Toxicology is an everexpanding<br />

field that must consider ways to optimize and standardize<br />

testing through collaborative research and sharing of data.<br />

DRE, Impaired Driving, Forensic Toxicology<br />

K30 Dissociative Driving: Ketamine DUID<br />

Fatality Case Study<br />

Kevin M. Lougee, BS*, Amy L. Lais, BS, Kim G. McCall-Tackett, BS,<br />

Diane J. Mertens-Maxham, BS, R.E. Kohlmeier, MD, and Norman A.<br />

Wade, MS, Maricopa Country <strong>Medical</strong> Examiner, 701 West Jefferson<br />

Street, Phoenix, AZ 85007<br />

After attending this presentation, attendees will understand the<br />

pharmacological effects of ketamine and how it may adversely affect<br />

driving tasks.<br />

This presentation will impact the forensic community and/or<br />

humanity by demonstrating the adverse effects of ketamine on driving<br />

skills, motor performance, and behavior in an otherwise healthy individual.<br />

Ketamine came into existence as a safer alternative to PCP. Even<br />

before PCP was withdrawn from the market due to its problematic<br />

adverse reactions in patients, pharmaceutical houses were looking for a<br />

safer alternative that would have less toxic behavioral effects. It was<br />

first synthesized in 1962 and patented in 1966 under the trade name<br />

Ketalar® and received FDA approval in 1970 as a general anesthetic. It<br />

is used as a short-acting induction anesthetic that provides a profound,<br />

rapid, dissociative anesthesia and a short recovery time. Low doses<br />

produce effects similar to PCP but doses in the anesthetic range<br />

(1mg/kg) produce experiences where the individual feels separated from<br />

his body, floating above his body and a near-death experience. This<br />

state, which users call the “K-hole,” can either be spiritually uplifting or<br />

terrifying (heaven or hell). Ketamine is a synthetic, sedative, nonbarbiturate<br />

that acts as a central nervous system depressant and produces<br />

a rapid-acting dissociative effect. It is used in the recreational drug<br />

market by illegally diverting from legitimate suppliers, allowing the<br />

liquid carrier to evaporate. The crystals are scraped into a fine powder<br />

and packaged. The first reports of ketamine abuse occurred in the early<br />

1970s in the San Francisco and Los Angeles areas.<br />

In this case report, a 27-year-old Caucasian male was the driver and<br />

sole occupant of a luxury sedan driving on a dry and clear Arizona<br />

freeway at two thirty AM on an early February morning. He attempted<br />

to exit this freeway for an unknown reason; however, in doing so, he hit<br />

a traffic sign and then continued about 1100 feet until colliding head-on<br />

with a large steel sign post. The force of the collision caused the vehicle<br />

to rotate 180 degrees and caused very extensive front end damage with<br />

major intrusion into the cab area of the automobile. It was reported that<br />

the decedent was not wearing a seat belt and was not exceeding the<br />

posted 65 miles per hour speed limit.<br />

A full autopsy was performed approximately 48 hours after death<br />

was pronounced and cause of death was determined to be massive blunt<br />

force trauma due to head and neck (fractured and dislocated) injuries.<br />

These included transection of the cervical spine, laceration of the<br />

pericardial sac, transection of the thoracic aorta, bilateral rib fractures,<br />

and contusions of all lobes of the lungs and multiple splenic lacerations.<br />

The manner of death was accident. During autopsy the assistant medical<br />

examiner collected pleural blood, bile, vitreous and gastric contents for<br />

complete toxicological testing. Vitreous and blood were analyzed for<br />

volatiles by GC-FID while the pleural blood was assayed by ELISA for<br />

benzodiazepines, barbiturates, benzoylecgonine, opiates, and<br />

methamphetamine with negative results. The blood and bile specimens<br />

were subjected to a qualitative analysis for basic drugs, and ketamine<br />

and its metabolites were confirmed by GC/MS using electron impact<br />

ionization. Quantitation of the ketamine was performed on the pleural<br />

blood with the result being 1.5 mg/L of parent compound. Further<br />

quantitative testing of all tissues submitted will also be presented.<br />

A presentation of this case study will contribute to establishing<br />

guidelines on potential impairment concentrations of ketamine as it<br />

relates to DUID cases. Although this case demonstrates only anecdotal<br />

evidence for DUI impairment, it clearly demonstrates the adverse effects<br />

of ketamine on driving skills.<br />

Ketamine, DUID, Fatality<br />

139 * Presenting Author

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