An unusual death involving a sensory deprivation tank.

Deaths involving sensory deprivation tanks are very rare. We describe a unique case in which a previously healthy 50-year-old woman apparently died while floating in a sensory deprivation tank at her residence. Autopsy failed to reveal definitive anatomical abnormalities pointing to the cause of death. A thorough scene investigation, full medicolegal autopsy to include toxicological analyses, and a complete investigation into the equipment at the scene, were conducted. Blood toxicologic studies were significant for the presence of ethanol (0.27%) and a mixture of over-the-counter sedating medications and prescription drugs. The cause of death was ruled as acute mixed drug and ethanol toxicity combined with probable environmental hyperthermia; manner was accident. This case report will help the forensic community understand the intended use of flotation tanks, as well as possible risks associated with improper use.

Acute hemorrhagic leukoencephalitis: a critical entity for forensic pathologists to recognize.

Acute hemorrhagic leukoencephalopathy (AHLE) is a rare, acute disorder characterized by perivenular demyelination and diffuse hemorrhagic necrosis of the central nervous system. AHLE is thought to represent a hyperacute form of acute disseminated encephalomyelitis. AHLE is associated with a greater morbidity and mortality and, fortunately, is much less common than acute disseminated encephalomyelitis. Since most cases of AHLE result in patient demise, forensic pathologists should be cognizant of this entity and consider it in their differential diagnosis.Here we describe an interesting case of a previously healthy 11-year-old boy who initially complained of vague gastroenteritis-like symptoms while visiting a mountain lake. The boy's symptoms evolved to include severe headache and dizziness, necessitating a visit to a rural emergency department. He presented with focal neurologic findings, and head computed tomography (CT) scan confirmed thalamic edema. Cerebrospinal fluid analysis was suggestive of infectious etiology, and multiple empiric therapies were initiated. He was transferred to our institution, and his clinical status continued to worsen. Given the poor prognosis, the family requested withdrawal of supportive care. On day 14 of symptoms the boy succumbed to his illness. An autopsy was requested to further characterize the proximate cause of death.AHLE often presents with abrupt onset of fever, neck stiffness, seizure, and/or focal neurologic signs several days following a viral illness or vaccination. Thus, AHLE can clinically mimic a direct central nervous system infection or a toxic ingestion. AHLE has a very poor prognosis, with rapid deterioration and death usually occurring within days to one week after onset of symptoms. The cause for AHLE is unclear. An autoimmune pathophysiology is likely, with immune cross-reactivity between myelin basic protein moieties and various infectious agent antigens. Treatment for AHLE is not well-established; some authors describe in recent literature that a combination of immunosuppressant medications and/or therapeutic plasma exchange may be of benefit in treating AHLE.

A fatal case of benzodiazepine withdrawal.

Medical examiners often receive cases with limited medical history. Sometimes the medical history received is slightly skewed, or even incorrect. Here we describe a case which was initially referred to the Bexar County Medical Examiner's Office from a large community hospital as a case of zolpidem overdose. The deceased presented to the hospital with hypertension, elevated temperature, worsening bizarre behavior, and movement irregularities. While in the hospital, the decedent developed seizure-like activity and died approximately 15 hours after admission. A complete autopsy was performed and yielded no significant gross or histologic abnormalities. A full toxicologic analysis revealed therapeutic levels of citalopram and phenytoin. Zolpidem was not present. Further review of the decedent's medical history as well as information provided by the next of kin revealed that the deceased had been taking diazepam for several years but had recently been switched to alprazolam. The decedent had abruptly stopped taking the alprazolam approximately 4 days before admission when she ran out of the medication, after taking approximately 200 mg in a 6-day period. Given the inconsistent clinical presentation and the findings at autopsy, we suspect that she suffered from benzodiazepine withdrawal and not an overdose as initially reported. Although it is possible that the zolpidem, reportedly taken in the 12 hours before admission, masked the initial symptoms of withdrawal, the constellation of symptoms and signs at presentation are more consistent with benzodiazepine withdrawal than of zolpidem overdose. In this report, we emphasize to the forensic community that one must maintain a high index of suspicion for alternative explanations if the initial report does not seem to fit the presentation or autopsy findings. This case illustrates that although it may take some extra time and effort, further investigation into clinical history can prove crucial to obtaining the correct cause of death and manner of death. This is only the second case within the English literature of death because of benzodiazepine withdrawal.

Diabetic (lymphocytic) mastopathy with exuberant lymphohistiocytic and granulomatous response: a case report with review of the literature.

We report a case of a 66-year-old woman who presented with multiple painless masses in both breasts. Prior bilateral biopsies were diagnosed as Rosai-Dorfman disease (Sinus Histiocytosis with Massive Lymphadenopathy). A recent lumpectomy specimen revealed a gray-white smooth cut surface with a discrete masslike lesion. The histopathology demonstrated a fibrotic breast parenchyma with foci of dense fibrosis and scattered inconspicuous breast epithelium surrounded by lymphocytes that formed aggregates and follicles with germinal centers. The inflammation was in a periductal, perilobular, and perivascular distribution. In addition, an exuberant inflammatory response with histiocytes and fibroblasts was present. This inflammatory response focally surrounded areas of fat necrosis and formed noncaseating granulomas with rare multinucleated giant cells. This process had infiltrative, ill-defined edges and involved the subcutaneous tissues. The overlying epidermis was normal. The final diagnosis was diabetic mastopathy with an exuberant lymphohistiocytic response. The differential diagnosis included Rosai-Dorfman disease, inflammatory myofibroblastic tumor, granulomatous mastitis, sclerosing lipogranulomatous response/sclerosing lipogranuloma, lupus panniculitis, and rheumatoid nodules. Immunohistochemical studies and flow cytometry confirmed the polyclonal nature of the lymphoid infiltrate. After the histologic evaluation, we inquired if the patient had a history of diabetes mellitus, and learned that she did have type 2 noninsulin-dependent diabetes mellitus. In conclusion, we report a case of diabetic mastopathy that presents with bilateral tumorlike masses and an unusual exuberant lymphohistiocytic response with granuloma formation. The pathologist may not be provided with a history of diabetes mellitus, but the characteristic fibrosis, lymphocytic ductitis/lobulitis, and sclerosing lobulitis with perilobular and perivascular lymphocytic infiltrates should provide clues for an accurate diagnosis, even when an exuberant and an unusual lymphohistiocytic response is present. A timely accurate diagnosis can help limit repeat surgeries in this vulnerable group of patients.