NTSB investigators either traveled in support of this investigation or conducted a significant amount of investigative work without any travel, and used data obtained from various sources to prepare this aircraft accident report.
The commercial rated pilot was landing the airplane at the end of a personal local flight. The airport manager saw the airplane very low on final approach for runway 18. As the airplane continued toward the airport, it collided with power lines about 0.5 mile north of the runway's approach end. Weather conditions at the time of the accident included a clear sky with no obstructions to visibility. Examination of the airframe and engine did not reveal any anomalies that would have contributed to the accident. The pilot was familiar with the airport and was likely aware of the location of the power lines, which were well below a normal glideslope to the runway.
The pilot did not hold a medical certificate. An autopsy of the pilot revealed coronary artery disease and significant brain pathology. It is unlikely that the pilot's coronary artery disease contributed to the accident as it would not have impaired the pilot's judgment, vision, or decision-making. The pilot had scarring from a previous brain injury and severe damage to his left optic nerve to the extent that he was nearly blind in that eye. Given that the pilot failed to maintain proper altitude while operating in visual conditions and struck a potentially visible hazard, it is likely that his vision deficiency contributed to the accident.
Toxicology test results indicated that the pilot had used multiple psychoactive drugs before the accident, including cocaine, methamphetamine, clonazepam, and diphenhydramine. In addition to their psychoactive effects, these drugs are potent vasoconstrictors and can cause small arteries to spasm, cutting off blood flow to portions of vital organs. Although the neuropathologist who examined the pilot's brain believed the degree of cerebral hypoxic/ischemic damage he identified would take several hours to develop, the pilot was deceased by the time first responders arrived about 10 minutes after the witnessed crash. Therefore, this hypoxic/ischemic damage had to have begun before the accident and was likely caused by the pilot's misuse of cocaine and methamphetamine. This evolving brain ischemia may have played a role in the circumstances of the accident, but without specific information regarding the pilot's symptoms, its exact role cannot be determined. Although the pilot's stage of intoxication with methamphetamine or cocaine at the time of the accident is unknown, it is very likely that he was impaired by the combined effects of these drugs.