DAUBERT/ROBINSON HEARING TO EXCLUDE ALCOHOL TESTIMONY
A motorcycle driver and his passenger veered off the road at 11:30 p.m. resulting in the ejection of the passenger. An unlighted back road in poor condition was selected by the driver because "since I was drinking, I didn't want to get a ticket." Records revealed nine prior alcohol-related arrests. The driver gained control of the motorcycle to return to find the passenger unconscious but breathing. His helmet was fractured but held on by the chin strap. Both had been drinking beer during the preceding eight hours while engaged in heavy physical activity. The driver refused a breathalyzer test. Blood alcohol concentration of the driver three hours after the accident was 0.21Gm%. Serum alcohol of the passenger was 0.278 Gm% one and one-half hours after the accident. The passenger survived but sustained significant permanent brain damage. After appropriate adjustments for serum and time, blood alcohol concentration at the time of the accident was estimated to be 0.285 Gm% for the driver and 0.277% for the passenger. The passenger's urine drug screen was positive for "cocaine." The driver admitted that they had sniffed cocaine the night before. Suit was filed against the driver, the helmet manufacturer and others.
PLAINTIFF POSITION: Road defects caused the driver to leave the roadway; helmet failure caused the passenger's brain damage; the driver was not impaired because he could drink 12-18 cans of beer and not feel an effect; heavy physical activity of the driver and passenger increased alcohol clearance; the driver was not impaired because he successfully drove thirty minutes before the accident; the driver's blood alcohol concentration was elevated because of fermentation during the three days before analysis; the passenger's blood was contaminated during collection; cocaine reduced the vasodilator effects of alcohol; there was no credible evidence that alcohol increased the severity of brain injury.
DEFENSE POSITION: Fear of being arrested for DUI caused the use of secondary roads; alcohol impairment contributed to or caused the accident. Alcohol impairment contributed to or caused the ejection of the passenger. Alcohol impairment of homeostasis contributed to the severity of traumatic brain injury.
DISCUSSION: Plaintiffs requested the Court to strike defense expert as a witness since he is not qualified by education, training or experience, and opinions concerning alcohol effects are speculative, arbitrary and unreliable. Defense expert appeared live at hearing to exclude testimony, presenting extensive documentary evidence meeting the requirements under Daubert and showing admission as an alcohol expert in County, State, and Federal jurisdictions in Texas; survival of a Daubert/ Robinson hearing to strike alcohol-related testimony in Brooks County; approval by the State Bars of Texas and Louisiana to provide MCLE credits to attorneys concerning alcohol-related issues; receipt of grants and contracts from County, State and Federal agencies for research and treatment of drug and alcohol-related conditions. Also presented were numerous scientific peer reviewed publications demonstrating opinions which meet requirements for reliability under Daubert and Robinson, and exceed by many times the required odds ratio elucidated in the Havner opinion.
CONCLUSION: Upon exchange of documents and during a pre-hearing conference of plaintiff and defense counsel, the matter was settled for an undisclosed but significantly reduced amount.
Expert for the Defense Eric G. Comstock, M.D. (9366). Mitchell Chaney, Attorney at Law;
Rodriguez, Colvin & Chaney, Brownsville, Texas.
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NOTES AND REFERENCES
The driver maintained that perspiration during the afternoon of heavy labor significantly reduced his alcohol blood level. Perspiration is easily demonstrated to be ineffective for alcohol excretion. Assume a 180-pound (82 kilogram) male contains 65% body water, or 53 liters. At a blood alcohol of 0.2% and assuming blood to be 80% water, the concentration of alcohol in body water is 2.5 grams per liter. Body content of alcohol equals 2.5 x 53, or 132 grams. In order to reduce his blood alcohol to half or 0.1% by perspiration alone, 66 grams of alcohol must be removed, requiring 35 liters of perspiration. It is impossible to sweat yourself sober.
By similar calculations, it can be shown that it is impossible to produce enough urine to significantly influence the concentration of blood alcohol.
The driver maintained that being a heavy drinker allowed him to perform well with elevated blood alcohol levels. Goldberg, 1991, demonstrated that heavy drinkers were slightly less impaired at 0.05% than moderated or occasional drinkers but tolerance acquired by heavy drinking showed no protective effect at a blood alcohol of 0.1% and higher.
The risk of causing a fatal accident by drivers of four-wheeled vehicles at 0.19% blood alcohol is greater than 70 times that of a sober driver under the same or similar circumstances. This places the odds ratio as discussed in Havner at greater than 70 (AMA Council, 1986). Colbert, 1993, showed that experienced motorcycle operators more frequently left a test roadway with alcohol levels of 0.038 to 0.059 grams% and increased risk continued during a sobering up interval. The greater risk of alcohol ingestion to motorcycle operators was shown by Luna, 1984, where mortality among intoxicated drivers with critical head injuries was 80% compared to 43% without alcohol, placing the odds ratio for motorcycle drivers at approximately double that experienced by drivers of four-wheeled vehicles.
The contribution of alcohol to the severity of injury independently of the risk of an accident occurring has been shown both in control animal experiments and in clinical investigations. (Citations follow).
Skin contamination as a factor in blood alcohol determinations was raised as an unknown. McIvor, 1990, performed analyses for alcohol after isopropyl alcohol sponge used in treatment and demonstrated by head space gas chromatography a maximum specimen contamination of 3 mg%. This degree of contamination would not contribute to total alcohol quantitation by the enzymatic procedures because of the relative insensitivity of alcohol dehydrogenase to isopropyl alcohol. Alcohol contamination was thus eliminated as a consideration. In the current case, contact with the laboratory revealed only aqueous disinfectants were used for skin treatment prior to collection of specimens for blood alcohol.
Plaintiff experts asserted cocaethylene must have been present since the urine screen was reported positive for cocaine. Cocaethylene was reported to be many times more potent than cocaine. This assertion was not borne out by the physiologic studies performed by McCance, 1995, where administration to humans demonstrated only a slight difference in potency but a slightly more prolonged duration of action. The role of cocaine in diminishing the effect of alcohol claimed by the plaintiff experts is counterintuitive. Surely no one would claim sobriety because of the recent use of cocaine. The substance identified in urine was not cocaine but benzoylecgonine, an inactive metabolite.
Increased risks of motorcycle drivers applies equally well to pillion passengers with injury to brain and brainstem, a major cause of deaths despite use of helmets (Harrop, 1982).
Albin MS, et al. DMSO Protects Brain Against Experimental Pressure-Induced Focal Ischemia. Crit Care Med 4:251+, 1980.
Albin MS, et al. An Experimental Study of Craniocerebral Trauma During Ethanol Intoxication. Crit Care Med 14(10):841-845, 1986.
AMA Council on Scientific Affairs. Alcohol and The Driver. JAMA 255:522-527, 1986.
Bradbury A. Pattern and Severity of Injury Sustained by Pedestrians in Road Traffic Accidents with Particular Reference to the Effect of Alcohol. Injury 22(2):133-134, 1991.
Colburn N, et al. Should Motorcycles be Operated Within the Legal Alcohol Limits for Automobiles? J Trauma 35(2):183-186, Aug 1993.
Decrescito V, et al. Ethanol Potentiation of Traumatic Cerebral Edema. Neurological Surgery pp. 438-440, 1972.
Desiderio MA. Effects of Acute, Oral Ethanol on Cardiovascular Performance Before and After Experimental Blunt Cardiac Trauma. J Trauma 27:267, 1987.
Evans L, et al. Alcohol's Effect on Fatality Risk from a Physical Insult. J Stud Alcohol 54:441-449, 1993.
Flamm ES, et al. Ethanol Potentiation of Central Nervous System Trauma. J Neurosurg 46:328-335, 1977.
Galbraith S, et al. The Relationship Between Alcohol and Head Injury and Its Effect on the Conscious Level. Br J Surg 63:128-130, 1976.
Garrison HS, et al. Effect of Ethanol on Lactic Acidosis in Experimental Hemorrhagic Shock. Ann Emerg Med 13:26-29, 1984.
Goldberg HI, et al. Prevalence of Behavioral Risk Factors in Two American Indian Populations in Montana. Am J Prev Med 7(3):155-160, May-Jun 1992.
Harrop SN, et al. Motorcycle Fatalities in South West Cumbria. Injury 13(5):382-387, 1982.
Huth JH, et al. Effect of Acute Ethanolism on the Hospital Course and Outcome of Injured Automobile Drivers. J Trauma 23:494-498, 1983.
Jagger J, et al. Effect of Alcohol Intoxication on the Diagnosis and Apparent Severity of Brain Injury. Neurosurgery 15(3):303-306, 1984.
Jurkovich GJ, et al. The Effect of Acute Alcohol Intoxication and Chronic Alcohol Abuse on Outcome from Trauma. JAMA 270:51-56, 1993.
Kirn TF. Debunking the Drunk-Driver-And-Survival Myth. JAMA 260: 2480, 1988.
Knott DH, et al. Effects of Alcohol Ingestion on the Production of and Response to Experimental Hemorrhagic Stress. NEJM 269:292-295, 1963.
Luna GK, et al. The Influence of Ethanol Intoxication on Outcome of Injured Motorcyclists. J Trauma 24:695-700, 1984.
McCance-Katz E, et al. Concurrent Use of Cocaine and Alcohol is More Potent and Potentially More Toxic than Use of Either Alone- A Multiple-Dose Study. Biol Psychiatry 44:250-259, 1998.
McIvor RA, et al. Effect of Using Alcoholic and Non-Alcoholic Skin Cleansing Swabs When Sampling Blood for Alcohol Estimation Using Gas Chromatography. Br J Clin Pract 44(6):235-236, Jun 1990.
McQueen JD, et al. Changes in Intracranial Pressure and Brain Hydration During Acute Ethanolism. Surg Neurol 4:375+, 1975.
Merrell Dow Pharmaceuticals vs. Havner, Texas Supreme Court, Cite as No. 953 S.W.2d 706, Texas 1997.
Moss LK, et al. The Effects of Alcohol Ingestion on Experimental Hemorrhagic Shock. Surg Forum 10:390-392, 1959.
Pories SE, et al. Intoxication and Injury. J Trauma 32(1):60-64,Jan 1992.
Soderstrom CA. The Effects of Alcohol on Outcome Among Vehicular Crash Victims Admitted to a Trauma Center. Amer Assoc Auto Med, Sept 28-30, 1997, New Orleans, LA.
Soderstrom CA, et al. Alcohol's Effect on Trauma Outcomes: A Reappraisal of Conventional Wisdom. JAMA 270:93-94, 1993.
Stewart JR. Estimating the Effects Over Time of Alcohol on Injury Severity. Accid Anal Prev 21:575-579, 1989.
Waller PF, et al. Alcohol: A Potentiating Factor in Motor Vehicle Crash Injury. Soc Automotive Engineers, Inc., pp. 53-61, 1986.
Waller PF, et al. The Potentiating Effects of Alcohol on Driver Injury. JAMA 256:1461-1466, 1986.
Waller JA. Methodologic Issues in Hospital Based Injury Research. Amer Assoc Auto Med, Sept. 28-30, 1987, New Orleans, LA.
Waller PF. Alcohol Impairment: What Happens in the Body? Amer Assoc Auto Med, March 12-13, 1987.
Woolf PD, et al. The Adrenocortical Response to Brain Injury: Correlation with the Severity of Neurologic Dysfunction, Effects of Intoxication, and Patient Outcome. Alcohol Clin Exp Res 14(6): 917-921, 1990.
Wool PD, et al. Alcohol Intoxication Blunts Sympatho-Adrenal activation Following Brain Injury. Alcohol Clin Exp Res 14(2): 205-209, 1990
Yersin B, Detrimental Effect of Alcohol Intoxication on Severity of Injuries in Male Traffic Accident Victims: A Cross Sectional Study. Soz Pravent Ivmed 37: 118-123, 1992
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