[Asphyxia by drowning].

The differentiation of SIDS from accidental or inflicted suffocation may be impossible without corroborating findings from the death scene or autopsy or in the absence of a confession from a perpetrator. Pulmonary intra-alveolar hemorrhage (PH) has been proposed as a potential clue to suffocation, but none of the previous studies on this topic have limited SIDS cases to those who were in a safe sleep environment, in which all were found supine and alone on a firm surface with their heads uncovered. Our aims are to: (1) compare PH in SIDS cases found in a safe sleep environment to a control group comprised of infants whose deaths were attributed to accidental or inflicted suffocation and (2) assess the effect of age, CPR, and postmortem interval (PMI), with regard to the severity of PH in this subset of safe-sleeping SIDS cases. We conducted a retrospective study of all postneonatal cases accessioned by the Office of the Medical Examiner in San Diego County, California who died of SIDS or suffocation between 1999 and 2004. A total of 74 cases of sudden infant death caused by SIDS (34 cases as defined above, comprising 8% of the total SIDS cases), accidental suffocation (37), and inflicted suffocation (3) from the San Diego SIDS/SUDC Research Project database were compared using a semiquantitative measure of pulmonary intra-alveolar hemorrhage. The most severe (grade 3 or 4) PH occurred in 35% of deaths attributed to suffocation, but in only 9% of the SIDS cases. Age, duration of CPR attempts and PMI had no effect on the severity of PH in SIDS. Our results indicate that the severity of PH cannot be used independently to differentiate SIDS from suffocation deaths. Each case must be evaluated on its own merits after thorough review of the medical history, circumstances of death, and postmortem findings.

Asphyxia↗

PubMed2007

Postmortem determination of concentrations of stress hormones in various body fluids--is there a dependency between adrenaline/noradrenaline quotient, cause of death and agony time?

To find out whether a certain cause of death or a certain length of an agonal period shows specific adrenaline or noradrenaline profiles, heart blood, femoral vein blood, liquor, urine and vitreous humour were taken from corpses (n = 98) at the Medical School Hannover, and noradrenaline and adrenaline were determined using high-performance liquid chromatography (HPLC). Corpses were classified according to the following five categories: short agony, long agony, state after hanging, state after asphyxiation and state after CPR with documented administration of epinephrine. Once results were collected the adrenaline/noradrenaline quotient was determined. It became clear that there were no significant differences regarding the concentration of adrenaline and noradrenaline in the various body fluids in relation to the above-mentioned categories. The means adrenaline/noradrenaline quotients in femoral vein blood were 0.21 +/- 0.29 for hanged persons, 0.38 +/- 0.47 for asphyxiated persons, 0.17 +/- 0.19 for those with short agony and 0.42 +/- 0.43 for those with long agony, significantly below 1 (p < 0.001; p = 0.001; p = 0.003). For condition after CPR we found an adrenaline/noradrenaline quotient of 2.81 +/- 5.8. In liquor the adrenaline/noradrenaline quotients for short agony was 0.17 +/- 0.17, for hanged persons 0.18 +/- 0.19 and for asphyxiated ones 0.30 +/- 0.38, significantly lower than 1 (p < 0.001). In urine the adrenaline/noradrenaline quotients for all categories are lower than 1 (p < 0.001); short agony (0.13 +/- 0.09), long agony (0.21 +/- 0.16), hanged (0.15 +/- 0.16), asphyxiated (0.14 +/- 0.08) and CPR (0.14 +/- 0.06). In vitreous humour the quotients for short agony (0.14 +/- 0.28), long agony (0.13 +/- 0.12), hanged (0.07 +/- 0.09) and asphyxiated (0.09 +/- 0.11) are lower than 1 (p < 0.001). The spread of data for the adrenaline/noradrenaline quotient did not allow for any conclusions about cause of death and length of agony in individual cases.

Asphyxia↗