Journal of forensic and legal medicine
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There has, to date, been no prospective description of the frequency with which police officers encounter individuals who display signs of excited delirium syndrome (ExDS). The ability to document the relationship between signs of excited delirium and subject outcomes and then determine the underlying pathophysiology that results in morbidity and mortality is necessary in order to determine the case definition for ExDS in live individuals. We prospectively evaluated the frequency of signs of ExDS in a cohort of consecutive subjects undergoing use of force by law enforcement officers (LEOs) and determined the frequency with which those features were encountered alone and in combination. Data were collected prospectively for all subjects undergoing use of force (UOF) by LEOs in a single police agency from August 2006 until August 2009. Ten previously published signs of ExDS were prospectively recorded by officers: pain tolerance, constant/near constant physical activity, not responding to police presence, superhuman strength, rapid breathing, not tiring despite heavy physical exertion, naked/inappropriately clothed, sweating profusely, hot to the touch, and attraction to/destruction of glass/reflective surfaces. UOF occurred in 1269 of 1.56 million police-public interactions (0.08%, 95% CI 0.08, 0.086). Of subjects undergoing police use of force, 1101/1269 or 86.8% (95% CI 84.8%, 88.6%) were assessed as having effects of emotional disturbance, drugs, alcohol or a combination of these comorbidities at the scene at the time of the UOF and 837/1269 or 66% (95% CI 63.3, 68.6) were violent at the time of the UOF. Excluding violence, 655/1269 (51.6% 95% CI 48.8, 54.4) had no signs of ExDS at the time of UOF and another 405/1269 (31.9% 95% CI 29.4, 34.6%)) had only one or two signs of ExDS at the time of UOF. The remaining 209/1269 (16.5%, 95% CI 14.5, 18.6) had 3 or more concomitant signs of ExDS at the time of UOF. One person died in our cohort who was experiencing 10 concomitant features of ExDS at the time of the UOF event. With only one death in our 3 year prospective cohort, we cannot comment on causality or correlation between number of Excited Delirium signs and mortality. Further study must be undertaken to determine whether correlation exists between higher numbers of ExDS signs and physiologic measures of acute underlying pathology in live subjects. ⋯ Law enforcement officers and other prehospital care providers can recognize and describe symptoms of ExDS in the field at the time of interaction. Even though police use of force is rare over 15%, or approximately 1 in 6, of individuals undergoing police UoF have 3 or more concomitant signs of Excited Delirium at the time of the UoF event. The single death in our cohort occurred in an individual with 10 concomitant signs of ExDS. Future work including further clinical outcome data will determine whether higher numbers of concomitant signs of ExDS predicts subject morbidity or mortality and whether any specific symptoms or symptom cluster is associated with death. If so, a case definition will be able to be fully described.
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Carbon monoxide (CO) is produced by incomplete combustion of organic compounds. Its intoxication usually results from inhalation of fumes from improper heating stoves, motor vehicles, or smoke from fires. It can reversibly bind various heme-containing proteins such as hemoglobin, myoglobin, cytochrome p450 and cytochrome oxidases. ⋯ To calculate the frequency of CO poisoning within all the autopsies carried out and fatal poisoning cases, the number of cases was divided by the total number of medico-legal autopsies and total fatal poisoning cases. The mean age of cases, the source of CO gas, the most common seasons and months, gender, and blood HbCO levels were also taken into consideration if the data is available. Under the light of the findings, we may suggest that determination of affecting factors in CO poisoning is going to be one of the key subjects for planning preventive interventions.
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This article is to provide insights into the mechanisms underlying chronic pain from whiplash injury. Studies show that injury produces plasticity changes of different neuronal structures that are responsible for amplification of nociception and exaggerated pain responses. There is consistent evidence for hypersensitivity of the central nervous system to sensory stimulation in chronic pain after whiplash injury. ⋯ Spinal hypersensitivity may explain pain in the absence of detectable tissue damage. Whiplash is a heterogeneous condition with some individuals showing features suggestive of neuropathic pain. A predominantly neuropathic pain component is related to a higher pain/disability level.