Ischaemic changes in cerebellar Purkinje cells suggest multiple causes of death in bath-related drowning.

Ischaemic changes of cerebellar Purkinje cells from 40 bath-related death cases with aspiration of drowning water and from control cases were examined. Subjects were of three groups: bath-related death by water aspiration and underlying disease (n = 12), bath-related death by water aspiration and alcohol consumption (n = 11), and bath-related death by water aspiration alone (n = 17). The control group comprised deaths by drowning in a river or lake (n = 14), non-drowning deaths by multiple trauma (n = 21), and non-drowning deaths by heart disease (n = 21). Immunohistochemical analysis with anti-calbindin-D28k antibody revealed significantly higher Purkinje cell calbindin-D28k immunoreactivity in all bath-related drowning groups than in river/lake drowning controls (p < 0.05 for underlying disease and water aspiration alone groups; p < 0.01 for alcohol consumption group). Histopathological examination revealed that over 80% of Purkinje cells in bath-related drowning cases were intact (Type I), compared to only 35.7% in river/lake drowning cases. These findings suggest different pathophysiological mechanisms of bath-related and conventional drowning deaths. Maintenance of immunoreactivity of calbindin-D28k in bath-related drowning cases suggests that the deaths are attributable to heat stroke caused by warm bath effects, impaired consciousness caused by arrhythmias or pathological attacks caused by pre-existing medical conditions, or to drinking before bathing, when intoxication-impaired consciousness led to death by bathtub water aspiration. Findings suggest that exposure to ischaemia, which kills neurons and causes death, is of shorter duration in cases of bathing-related death. This distinction presents important implications for forensic investigations and might necessitate re-evaluation of prevention strategies for the approximately 19,000 bath-related deaths which occur annually in Japan.