Breath/Blood Alcohol Concentration as an Indicator of Alcohol Use Problems.

INTRODUCTION: The Federal Aviation Administration Office of Aerospace Medicine (AAM) is required by law to identify pilots who have driving under the influence (DUI) convictions. It is the responsibility of AAM to determine, based on the DUI, if the pilot has a drinking problem and needs follow-up treatment. Pilots with alcohol problems are at risk to themselves and the public and need to have treatment to reduce the extent of the risk. It has been suggested by some that a blood alcohol concentration (BAC) of 0.15 g · dL-1 is evidence of tolerance and the pilot should be placed in an alcohol treatment program.METHOD: The National Institute on Alcohol Abuse and Alcoholism (NIAAA) Clinician's Guide considers a person at risk for a drinking problem when a man drinks 5 or more drinks or a woman drinks 4 or more drinks in a day and reaches a 0.08 g · dL-1 of ethanol in the blood. It is possible to estimate from a BAC or breath alcohol concentration (BrAC) the number of drinks consumed using the volume of distribution for ethanol and the weight of the individual. A spread sheet tool was developed to estimate the number of drinks consumed.RESULTS: It was determined that DUI/DWI concentrations could be used to determine the minimum number of drinks consumed. Overweight people reach binge drinking levels and higher Hingson levels at lower DUI/DWI concentrations than people with an average weight or lower.DISCUSSION: Using this tool there is a high probability (99.7%) of identifying a true binge drinker.Canfield DV, Forster EM, Cheong Z-I, Cowan JM. Breath/blood alcohol concentration as an indicator of alcohol use problems. Aerosp Med Hum Perform. 2019; 90(5):488-491.

Pilot-Reported Beta-Blockers Identified by Forensic Toxicology Analysis of Postmortem Specimens.

INTRODUCTION: This study compared beta-blockers reported by pilots with the medications found by postmortem toxicology analysis of specimens received from fatal aviation accidents between 1999 and 2015. Several studies have compared drugs using the standard approach: Compare the drug found by toxicology analysis with the drug reported by the pilot. This study uniquely examined first the pilot-reported medication and then compared it to that detected by toxicology analysis. This study will serve two purposes: (i) to determine the capability of a toxicology laboratory to detect reported medications, and (ii) to identify pilots with medications below detectable limits. METHOD: All information required for this study was extracted from the Toxicology Data Base system and was searched using ToxFlo or SQL Server Management Studio. The following information was collected and analyzed: pilot-reported trade and/or generic drug, date specimens received, time of accident, type of aviation operations (CFR), state, pilot level, age, class of medical, specimen type, specimen concentration, dose reported, frequency reported associated with the accident, quantity reported, National Transportation Safety Board (NTSB) accident event number, and all NTSB reports. RESULTS: There were 319 pilots that either reported taking a beta-blocker or were found to be taking a beta-blocker by postmortem toxicology analysis. DISCUSSION: Time of death, therapeutic concentration and specimen type were found to be factors in the ability of the laboratory to detect beta-blockers. Beta-blockers taken by pilots will, in most cases, be found by a competent postmortem forensic toxicology laboratory at therapeutic concentrations. The dose taken by the pilot was not found to be a factor in the ability of the laboratory to identify beta-blockers. Time of dose, route of administration, specimen tested and therapeutic concentration of the drug were found to be factors in the ability of the laboratory to identify beta-blockers in postmortem specimens.

The first sign of loss of consciousness.

The first clinically observable sign of an unconsciousness episode (UNCE) serves as the temporal sequence (kinetics) onset point for neurological events occurring during the loss of consciousness, unconsciousness and recovery of consciousness phases of the UNCE. The initial neurologic signs of 212 individuals exposed to gradual (N=114) and rapid (N=98) onset +Gz acceleration stress, inducing the ischemic LOC phase in 83.3±18.6s and 8.89±1.52s; p<0.001 respectively, were determined. The duration of the unconscious phase (considered absolute incapacitation) was 10.42±5.3s and 9.36±3.99s; p>0.1 for gradual and rapid onset +Gz-stress, respectively. Cerebral autoregulation may play a role in determination of ischemic UNCE induction and recovery. Five signs: loss of muscle control, eyelid closure, eye fixation, upward eye deviation, and muscular twitching occurred at LOC phase onset. The most frequent initial sign of LOC phase onset was loss of muscle control (84% of the episodes), followed by eye fixation (8.5%), and upward eye deviation (6.1%). Signs play a key role in differential diagnosis of syncopal, epileptic, psychogenic and other causes of UNCEs. Sign kinetics may provide insight into localization of the essential components and networks within the cephalic nervous system associated with UNCEs.

Neurologic state transitions in the eye and brain: kinetics of loss and recovery of vision and consciousness.

Visual alterations, peripheral light loss (PLL) and blackout (BO), are components of acceleration (+Gz) induced loss of consciousness (LOC) and recovery of consciousness (ROC). The kinetics of loss of vision (LOV) and recovery of vision (ROV) were determined utilizing ocular pressure induced retinal ischemia and compared to the kinetics of LOC and ROC resulting from +Gz-induced cephalic nervous system (CPNS) ischemia. The time from self-induced retinal ischemia in completely healthy subjects (N = 104) to the onset of PLL and complete BO was measured. The time from release of ocular pressure, with return of normal retinal circulation, to the time for complete recovery of visual fields was also measured. The kinetics of pressure induced LOV and ROV was compared with previously developed kinetics of +Gz-induced LOC and ROC focusing on the rapid onset, vertical arm, of the +Gz-induced LOC and ROC curves. The time from onset of increased ocular pressure, immediately inducing retinal ischemia, to PLL was 5.04 s with the time to BO being 8.73 s. Complete recovery of the visual field from BO following release of ocular pressure, immediately abolishing retinal ischemia, was 2.74 s. These results confirm experimental findings that visual loss is frequently not experienced prior to LOC during exposure to rapid onset, high levels of +Gz-stress above tolerance. Offset of pressure induced retinal ischemia to ROV was 2.74 s, while the time from offset of +Gz-induced CPNS ischemia to ROC was 5.29 s. Recovery of retinal function would be predicted to be complete before consciousness is regained following +Gz-induced LOC. Ischemia onset time normalization in neurologic tissues permits comparison between different stress-induced times to altered function. The +Gz-time tolerance curves for LOV and LOC provide comparison and integration of neurologic state transition kinetics in the retina and CPNS.

The +Gz recovery of consciousness curve.

BACKGROUND: The limiting physiological envelope to extreme gravitational stress is defined by neurologic symptoms and signs that result from exceeding neurologic tolerance. The edge of the limiting envelope is defined by the complete incapacitation associated with acceleration (+Gz) induced loss of consciousness. Should + Gz-induced loss of consciousness occur in-flight, brisk recovery of conscious function is essential for aircraft recovery. If recovery does not occur, accident investigation aimed at preventing such accidents is enhanced by understanding the temporal aspects of the resulting incapacitation. The mechanistic basis of neurological reintegration leading to consciousness recovery is of broad medical and scientific interest. METHODS: Recovery of consciousness episodes from a prospectively developed +Gz-induced loss of consciousness repository of healthy individuals was analyzed to define variables influencing recovery of consciousness. The time from loss to recovery of consciousness as measured by observable signs, is defined as the absolute incapacitation period. The absolute incapacitation period from 760 episodes of loss and recovery of consciousness in healthy humans was analyzed to define +Gz-profile variables that determine the duration of functional neurologic compromise. RESULTS: Mean time from loss to return of consciousness for 760 episodes of consciousness recovery was 10.4 ± 5.1 s; minimum 1 s; maximum 38 s. Offset rate for the +Gz-exposure deceleration profiles varied from a minimum of 0.17 Gs(-1) to a maximum of 7.93 Gs(-1).The curve produced by plotting +Gz-offset rate (Gs(-1); y) versus absolute incapacitation period (s; x) described a hyperbolic relationship. The hyperbolic relationship indicates there is a minimum time (mean 8.29 ± 3.84 s) required for recovery of consciousness when complete loss of consciousness occurs. CONCLUSIONS: Mean recovery time from +Gz-induced unconsciousness is dependent on the deceleration profile's offset rate from the point of loss of consciousness. This relationship is described by a curve plotting offset rate and time for recovery of consciousness. This curve predicts when conscious function should return following exposure to +Gz stress sufficient to cause unconsciousness. The maximum +Gz level of the recovery exposure profile was found to be inadequate for predicting variations in the time for recovery of consciousness.

The +Gz-induced loss of consciousness curve.

BACKGROUND: +Gz-time tolerance curves were developed to predict when exposure to +Gz stress exceeds human tolerance resulting in neurologic signs and symptoms. The +Gz-induced loss of consciousness (G-LOC) curves were developed to predict when +Gz stress induces G-LOC. The G-LOC curves are based on a theoretical understanding of how acceleration affects underlying physiological mechanisms affording tolerance to acceleration, their limits, and what happens when they are exceeded. The foundation of previous +Gz-time tolerance curves was based on a minimal dataset of sign and symptom endpoints. METHODS: Two G-LOC curves were established from the analysis of 888 centrifuge induced G-LOC episodes in completely healthy humans. The time from the onset of +Gz stress to the onset of unconsciousness was plotted as a function of +Gz level and the G onset rate. RESULTS: The two new G-LOC curves differed significantly from previous curves in temporal characteristics and key aspects underlying neurologic response to acceleration. The new acceleration onset rate curve reveals that for onset rates ≥ 1.0 G/s, G-LOC will occur in a mean time of 9.10 s and is independent of the onset rate. The new +Gz-level curve demonstrates that G-LOC will occur in a mean time of 9.65 s for rapid onset rate exposures to +Gz levels ≥ +7 Gz. The minimum +Gz-level threshold tolerance was defined as +4.7 Gz. When +Gz onset rates are gradual, ≤ 0.2 G/s, G-LOC occurs in a mean time of 74.41 s. G-LOC did not occur earlier than 5 s for any acceleration exposure. CONCLUSIONS: These G-LOC curves alter previous temporal predictions for loss of consciousness and advance the understanding of basic neurophysiological function during exposure to the extremes of acceleration stress. Understanding the acceleration kinetics of the loss and recovery of consciousness provides the characteristics of uncomplicated and purely ischemic causes of LOC for application in medical diagnosis of syncope, epilepsy, and other clinical causes of transient loss of consciousness. The curves are applicable to education, training, medical evaluation, and aerospace operations.

Physiological equivalence of normobaric and hypobaric exposures of humans to 25,000 feet (7620 m).

INTRODUCTION: Skepticism exists about whether normobaric and hypobaric hypoxic exposures are equivalent. We have evaluated if physiological differences between the two environments would translate into actual differences in hypoxia symptoms. METHODS: We exposed 20 subjects to 5-min 25,000-ft (7620-m) equivalent environments in an altitude chami ber and then in a ground-level portable reduced-oxygen training enclosure (PROTE). Heart rate and hemoglobin oxygen saturation (SaO2) were continuously monitored. Alveolar gas samples were collected at 1, 3, and 4 min elapsed time. Subjects completed hypoxia symptom questionnaires at the same time points. RESULTS: Mean fourth minute alveolar oxygen tension (PaO2), alveolar carbon dioxide tension (PaCO2), and respiratory quotient (RQ) differed significantly between the chamber and PROTE. Declines in SaO2 appeared biphasic, with steepest declines seen in the first minute. Rates of SaO2 decline over the 5-min exposure were significantly different. Heart rate was not different, even when indexed to body surface area. Mean number of hypoxia symptoms between hypobaric and normobaric environments after 1 min were significant. However, the temporal pattern of symptom frequencies across subjects between the chamber and PROTE were similar. CONCLUSIONS: Alveolar gas composition and arterial hemoglobin oxygen desaturation patterns differed between a ground level and hypobaric exposure. Differences in mean number of hypoxia symptoms between hypobaric and normobaric environments after 1 min, but not at 3 and 4 min, coupled with similar patterns in symptom frequencies, suggest that ground-level hypoxia training may be a sufficiently faithful surrogate for altitude chamber training.

Vitreous fluid and/or urine glucose concentrations in 1335 civil aviation accident pilot fatalities.

During aviation accident investigations, vitreous fluid and urine samples from pilot fatalities are analyzed for glucose and blood for hemoglobin A(1c) (HbA(1c)) to monitor diabetic pilots and to discover other pilots with undiagnosed/unreported diabetes. The prevalence of elevated glucose concentrations in fatally injured pilots was evaluated by searching the Civil Aerospace Medical Institute's Toxicology Database for the period 1998-2005. Out of 1335 pilots involving 363 vitreous fluid, 365 urine, and 607 vitreous fluid and urine analyses, 43 pilots had elevated glucose in vitreous fluid (>125 mg/dL) and/or in urine (>100 mg/dL). Of the 20 pilots whose blood samples were analyzed, nine had >6% HbA(1c)--four were known diabetics, and five were unknown diabetics. Urinary glucose levels were elevated in all 13 known hyperglycemic pilots. A considerable number of pilots (30 of 43) had elevated glucose and HbA(1c) (5 of 20), suggesting undiagnosed/unreported diabetic conditions.

Aircraft-assisted pilot suicides in the United States, 1993-2002.

Our laboratory was interested in epidemiological and toxicological findings from aircraft-assisted pilot suicides. Between 1993-2002 there were 3,648 fatal aviation accidents. The NTSB determined that 16 were aircraft-assisted suicides; 15 from intentional crashing of an aircraft and 1 from exiting the aircraft while in-flight. All pilots involved in these aircraft-assisted suicides were male, with a median age of 40 years. Seven of the 14 pilots for which specimens were available were positive for disqualifying substances. Based on the few cases conclusively attributed to suicide, death by the intentional crashing of an aircraft appears to be an infrequent and uncommon event.

Acceleration-induced near-loss of consciousness: the "A-LOC" syndrome.

BACKGROUND: There is an insidious phenomenon that can occur when aircrew are exposed to +Gz stress even at levels that are insufficient to cause +Gz-induced loss of consciousness (G-LOC). Under these circumstances aircrew exhibit an altered state of awareness that was termed Almost Loss of Consciousness (A-LOC) by the U.S. Navy in the late 1980's. A-LOC is a syndrome that includes a wide variety of cognitive, physical, emotional, and physiological symptoms. While A-LOC has been observed in centrifuge studies and reported in flight for over 15 yr, a definitive description of the syndrome does not exist. METHODS: Nine subjects were exposed to short +6, 8, and 10 Gz pulses of increasing duration until they experienced G-LOC. Instrumentation included two channels of ECG and near infrared spectroscopy (NIRS) to measure relative cerebral tissue oxygenation (rSo2). Subjects indicated +Gz-induced visual symptoms (light loss, LL) by pressing a switch when LL began and releasing it when total vision was restored. Short-term memory loss was assessed using a simple math task. Data analysis included a description and the time course of the physical, physiological, cognitive, and emotional responses. RESULTS: There were 66 episodes of A-LOC that were identified out of a total of 161 +Gz pulse exposures. Many incidents of sensory abnormalities, amnesia, confusion, euphoria, difficulty in forming words, and reduced auditory acuity were documented. Often these responses occurred in multiple subjects and at different +Gz levels. One of the most common symptoms was a disconnection between cognition and the ability to act on it. There was a significant reduction in rSo2 over baseline, greater overshoot in rSo2 (increase in oxygenation above baseline after the +Gz exposure), faster fall in rSo2 during +Gz stress, and prolonged recovery time associated with A-LOC as compared with +Gz exposures without symptoms. CONCLUSION: Evaluation of the range of symptoms associated with A-LOC can lead to a program to increase pilots' awareness of the phenomenon and further our understanding of the relationship between the outward symptoms and the underlying physiological changes.