Over the past 4 years, 7.4% of deaths caused by strangulation in Peoria County, Ill., involved children under 18 years of age. Clinical review of a consecutive series of 13 children treated from 1985 through 1994 revealed an incidence of 32 of 10,000 intensive care unit admissions with a 5.5:1 male bias. Accidental causes were seen in six children, with suicide or autoerotic causes prevalent in older children and adolescents. Five children had behavioral disorders before injury. The initial Glasgow Coma Scale score was 8 or below in seven children. Cervical roentgenograms in all patients and computed tomographic examinations performed in seven children were interpreted as normal. Seven children required ventilatory assistance, and four had pneumonia or acute lung injury. Intracranial pressure monitoring in three children failed to reveal sustained elevations of pressure. Serial changes in electroencephalograms in five patients paralleled improvements in their clinical examinations. Ten children were normal on follow-up; one adolescent reported mild neurologic sequelae and one adolescent showed severe disability. One adolescent died 2 days after injury. Comparison of this series with previous reports of 26 children indicated that the extent of the initial injury and effectiveness of resuscitation were major determinates for outcome. Pulmonary complications were common, whereas the development of elevated intracranial pressure indicated a poor prognosis and suggested the use of telemetry in children, with clinical evidence of severe injury. Continued awareness of preventative measures for accidental strangulation in infants and intentional hanging in children with behavioral disorders may reduce the incidence of these injuries.
The cerebrovascular hemodynamics were recorded in two children with comparable hypoxic-ischemic injuries after strangulation. Monitoring was initiated within 13 hours of injury and continued for at least 38 hours. The profile included continuous measurements of cortical regional cerebral blood flow (rCBF) with a subdural thermal diffusion probe, intracranial pressure, mean arterial pressure, and expired CO2 tension. Data sets were obtained every 15 minutes or every 5 minutes during epochs of hyperventilation and inotropic support. Arterial CO2 and oxygen content and pH and, in the second patient, cardiac output (and cardiac index) were determined every 3 to 6 hours. Both children showed cortical hyperemia with a gradual rise of rCBF during the study; neither child showed elevated intracranial pressure. Mean CO2 reactivities were 1.8 and 2.1 mL/100 g/minute/mm Hg, with gradual elevations during the study. Mean cerebrovascular resistances were 0.7 and 0.9 mL/100 g/minute/mm Hg, respectively. Dissociative vasoparalysis with loss of autoregulation and preservation of CO2 reactivity was observed in both children. In the second child, during two periods of hyperventilation, an inverse steal occurred with rCBF indirectly related to expired CO2 tension; the rCBF was not related to changes in cardiac output or cardiac index. Neurologic outcome was not related to mean levels of rCBF, CPP, and CO2 reactivity, or clinical dissociative vasoparalysis. Lower initial and mean values of rCBF and an inverse steal after hyperventilation were associated with a poor outcome in the second patient.
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