Microscopic Examination in Cases of Neck Compression

Microscopy of the furrow reveals abraded or compressed epidermis and dermis (62). Vesicles or blisters filled with serous fluid and fat occur (Fig. 13).

Inflammation associated with hemorrhage is a vital reaction (142). The presence of inflammation is consistent with a period of survival after neck compression with or without resuscitative efforts. An inflammatory reaction has been seen in tongue hemorrhages in cases of strangulation in which the assailant confessed that the victim survived about half an hour (175). The earliest detection of granulocytes has been stated to be 15 min in open and closed skin trauma, and their presence assumes there was no preceding episode of neck trauma (195). Studies of cutaneous or other bodily wounds may not necessarily be applicable to neck compression cases because of variations in perfusion of different tissues (195). Fibrin deposition is an antemortem event, occurring 10 to 30 min after injury (142). Other "vital" reactions, occurring within minutes of compressive and other types of injury, include muscle alterations, such as contraction bands and hyaline change (Zenker's wavy degeneration [142,196]).

Immunohistochemistry has been applied to the study of tissue injuries in strangulation and blunt neck trauma cases (195,197-202).

Longitudinal sections of the superior horns of the larynx, in cases of neck compression, have shown hemorrhage, retraction, and invagination of ruptured and nonrup-tured perichondrium (142). Even without obvious laryngeal damage, laryngeal hemorrhages are observed in cases of manual strangulation and blunt trauma (203,204). Parasaggital sections of formalin-fixed larynges in manual strangulation cases show laryngeal hemorrhages within cartilage, muscle, and epithelium, findings that could be applicable to other types of neck compression (158,192,205).

Typically 5 to 8 min of suspension leads to death, but successful resuscitation is possible even after 30 min of suspension (206). Delayed deaths show hypoxic-ischemic encephalopathy and cerebral edema (3,16,90,125,174,207). Rare cases of delayed encephalopathy are described related to necrotic lesions in the basal ganglia (125). Aspiration and pneumonia are delayed complications (3).

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