A fluvoxamine-related fatality: Case report with postmortem concentrations.

Fluvoxamine is a selective serotonin reuptake inhibitor that has been considered relatively safe in overdose. At therapeutic and supratherapeutic concentrations, fluvoxamine affects cardiac conduction, prolongs QTc interval, causes hypotension, obtundation, and can increase propensity for seizures. A man in his 60s was found dead at his home with a postmortem fluvoxamine peripheral blood concentration of 4.9 mg/L, and a liver concentration of 440 mg/kg. His cause of death was determined to be acute fluvoxamine toxicity.

Cerebral Paragonimiasis Presenting with Sudden Death.

A 58-year-old Korean-born woman with a history of seizures and psychiatric issues was found dead at home. Autopsy was notable for large, calcified nodules that had nearly replaced her right temporal lobe. Histologic examination revealed the presence of Paragonimus eggs. This case demonstrates a rare manifestation of an aberrantly migrated lung fluke that resulted in epilepsy and sudden death years after the initial infection.

Acute benztropine intoxication and fatality.

A woman was found unresponsive with an empty bottle of Cogentin(®) prescribed to another. Admitted to an area hospital, her condition steadily declined until death 29 h after admission. Following toxicological screening on hospital (admission) whole blood, the only significant compound detected was benztropine. Benztropine was confirmed at 0.28 mg/L - the highest antemortem blood concentration recorded in a case of toxicity or fatality uniquely associated with benztropine. A second serum antemortem specimen showed a benztropine concentration of 0.19 mg/L. Despite over 24 h in the hospital, benztropine was also found in the postmortem specimens collected at autopsy. Peripheral blood, central blood, liver, and gastric concentrations were 0.47 mg/L, 0.36 mg/L, 9.6 mg/kg, and 44 mg, respectively. These results indicate that benztropine exhibited a potential difference between whole-blood and serum (plasma) concentrations. Additionally, in consideration of literature data, benztropine was found indicative of a compound prone to at least some postmortem redistribution.

Hydroxyzine distribution in postmortem cases and potential for redistribution.

Hydroxyzine is an antihistaminic with sedative properties used in the control of anxiety and emesis. Peripheral blood hydroxyzine concentrations are compared to central blood and liver concentrations in 10 medical examiner cases. Specimens were initially screened for alcohol and simple volatiles by GC-FID headspace analysis, ELISA for drugs of abuse, and alkaline drugs by GC/MS. Hydroxyzine, when detected by the alkaline drug screen, was subsequently confirmed and quantified by a specific GC-NPD procedure. Data suggest that postmortem peripheral blood hydroxyzine concentrations may be considered therapeutic to at least 0.24 mg/L and corresponding liver concentrations to at least 4.9 mg/kg. Hydroxyzine concentrations ranged 0.07-3.0mg/L in peripheral blood, 0.04-3.8 mg/L in central blood, and 0.88-55 mg/kg in liver. Hydroxyzine central blood to peripheral blood ratios averaged 0.92±0.25 (±standard deviation; N=6). Liver to peripheral blood ratios, on the other hand, were higher and averaged 13.8±6.2 (±standard deviation; N=10). Given that a liver to peripheral blood ratio less than 5 is consistent with little to no postmortem redistribution while exceeding 20-30 is indicative of propensity for significant postmortem redistribution, these data suggest that hydroxyzine is prone to a moderate degree of postmortem redistribution.

Delayed homicides due to infant head injury initially reported as natural (cerebral palsy) deaths.

A spectrum of neuropathology occurs in infants who sustain traumatic brain injury. Because of a prolonged survival interval, there is a risk that these deaths may not be recognized as a sequel of trauma. We reviewed the records in New York City of 5 delayed fatalities due to nonaccidental infant head injury that had survival intervals from 2.5 to 17 years. The head injuries occurred at 2 to 3 months of age, and death occurred at 2.5 to 17 years of age. Initially, they were reported as natural deaths by treating physicians, families, and/or police. All 5 infants had unexplained or poorly explained remote traumatic head injury that included subdural hematomas. At autopsy, the neuropathologic exam demonstrated remote subdural hemorrhages and lesions related to chronic hypoxic-ischemic injury including atrophy, arterial infarcts, border-zone infarcts, and cystic encephalomalacia. Each child survived the initial injury but later succumbed to the delayed effects of secondary hypoxic-ischemic encephalopathy. These 5 deaths highlight the need to investigate independently the medical history of any child (or adult) who dies with a clinical diagnosis of "cerebral palsy." The term cerebral palsy often is used as a catchall for any patient who has had neurologic impairment since infancy or childhood. If there is a direct link between the initial injury and the death, even if the injury occurred many years before death, then the injury is the proximate cause of death and dictates the manner of death. All 5 deaths were certified as homicides.

Disappearance of meconium pigment in placental specimens on exposure to light.

CONTEXT: Meconium discharge has been associated with fetal distress and poor neonatal outcome; thus, its presence is of clinical importance. OBJECTIVE: Loss of meconium pigment in histologic sections from light exposure has been described. We sought to confirm this finding and to measure this loss quantitatively. DESIGN: Sections of umbilical cord, fetal membranes, and fetal surface from 11 grossly meconium-stained placentas were processed swiftly to minimize light exposure. Two serial sections from each block were cut and stained; one set was reviewed immediately, and the other was exposed to 8 hours of direct fluorescent lighting. Each site and exposure was scored for pigment intensity (0, no staining; 1, weak expression; and 2, moderate/strong expression) and number of meconium-laden macrophages per 10 high-power fields (HPF). Results were compared on the same specimen using the chi(2) and the paired-samples t test. RESULTS: The maximum meconium macrophage count was 13.2/10 HPF in the unexposed sections versus 6.1/10 HPF in the exposed sections (P <.001). Unexposed sections varied from 1+ to 2+ intensity, while exposed sections were all 1+ or negative (P <.001). CONCLUSION: Exposure to fluorescent laboratory lights for 8 hours resulted in a significant loss in the intensity and number of identifiable meconium macrophages in histologic sections. These findings have important implications in the handling of placental specimens, and we recommend that care be taken to minimize exposure to laboratory lights during processing.