[Pathophysiological study of asphyxia and its applications to medico-legal diagnosis]

Asphyxia is commonly defined as "a hypoxic state in the body" which is caused by any one of a wide range of events, starting from an insufficiency of atmospheric oxygen to a failure in oxygen uptake by the cells. The present study outlines a physiopathological study of "mechanical asphyxia" various types of hypoxia caused by mechanical compression of the cervical and thoracic regions and its application to medicolegal diagnosis. We used an animal model in which an actual asphyctic condition was experimentally recreated. By elaborating the asphyctic mechanism through the physiological dynamics of the body fluids and tissues during the fatal process and the succeeding short time span, the study was intended to estimate the causes of death, time lapse after death before the examination, and the time of death in persons who were subjected to investigation, autopsy, or forensic examination. Our intention was also to establish medicolegal indices for the cause of death by examining patients who were resuscitated or expired before arrival (DOA). Our past superimental findings indicate that asphyxia is a state in which arterial blood gas anomalies (hypoxemia and hypercapnia) develop due to a disturbance in the respiratory mechanism, disrupting the maintenance of normal bodily functions by the organism. Among the clinical conditions of respiratory insufficiencies, asphyxia caused by external mechanical, factors (such as external application of pressure to the naso-oral, cervical, or thoracic region, insertion of a foreign body into the airway, and aspiration of fluids) corresponds to acute respiratory insufficiency due to hypercapnia type. In most of these cases with mechanical asphyxia, ventilatory insufficiency due to a lack of O2 in the inhaled air and insufficient removal of CO2 through expiration causes pulmonary alveolar hypoventilation and hyperemia associated with hypercapnia. Consequently, hypoxic hypoxia with systemic disturbances develops. The rapidity of development of the clinical events is correlated with the velocity of the rise in blood CO2 level and the development of acidemia from the early stage. The conditions culminate in non-compensatory (acute) respiratory acidosis. These abnormal physiological changes in turn produce symptoms such as congestion and cyanotic petechia. Asphyxia ensues if no resuscitation or other medical treatment is available during this stage (the so-called early asphctic stage). We believe that an understanding of these physiopathologic changes is useful in the diagnoses of asphyxia. It is also useful in the diagnosis of the above-cited process in cases of DOA and in patients who have received resuscitation or other medical treatment.