RESUMEN
Spinal cord injury is difficult to detect directly on postmortem computed tomography (PMCT) and it is usually diagnosed by indirect findings such as a hematoma in the spinal canal. However, we have encountered cases where the hematoma-like high-attenuation area in the cervical spinal canal was visible on PMCT, while no hematoma was observed at autopsy; we called it a "pseudo hematoma in the cervical spinal canal (pseudo-HCSC)." In this retrospective study, we performed statistical analysis to distinguish true from pseudo-HCSC. The cervical spinal canal was dissected in 35 autopsy cases with a hematoma-like high-attenuation area (CT values 60-100 Hounsfield Unit (HU)) in the spinal canal from the first to the fourth cervical vertebrae in axial slices of PMCT images. Of these 22 had a hematoma and 13 did not (pseudo-HCSC). The location and length of the hematoma-like high-attenuation and spinal cord areas were assessed on reconstructed PMCT images, true HCSC cases had longer the posterior hematoma-like area and shorter the spinal cord area in the midline of the spinal canal (P < 0.05). Furthermore, we found that true HCSC cases were more likely to have fractures and gases on PMCT while pseudo-HCSC cases were more likely to have significant facial congestion (P < 0.05). We suggest that pseudo-HCSC on PMCT is related to congestion of the internal vertebral venous plexus. This study raises awareness about the importance of distinguishing true HCSC from pseudo-HCSC in PMCT diagnosis, and it also presents methods for differentiation between these two groups.
Asunto(s)
Hematoma , Imágenes Post Mortem , Humanos , Estudios Retrospectivos , Hematoma/diagnóstico por imagen , Cuello , Canal Medular/diagnóstico por imagenRESUMEN
Respiratory viruses can cause fatal systemic infections; therefore, post-mortem diagnosis is essential in forensic autopsy cases. However, little is known regarding the distribution of respiratory viruses in the body. In this study, we investigated the anatomical distribution of respiratory viruses in 48 forensic autopsy cases suspected of viral infections at our institute. Fast Track Diagnostics (FTD) Respiratory Pathogens 21 was used as a screening test for 20 respiratory viruses in nasopharyngeal swabs. In cases with positive results for virus detection by the screening test, the detected viruses were quantified in body fluid and organ specimens by virus-specific real-time reverse transcription polymerase chain reaction (RT-PCR) and digital PCR. Viruses were detected in 33 cases, with the viral distribution and load differing among the cases. Since various respiratory viruses were detected from the nasopharyngeal swab and its viral load was higher than those of other body fluid specimens, the nasopharyngeal swab was suggested as a useful specimen for the post-mortem detection of respiratory viruses. Viruses were detected in almost all specimens including the serum in six cases. Considering the viral distribution in the body, pathological findings, and ante-mortem symptoms, these cases were presumed to be systemically infected, having died in the acute infection phase. In conclusion, the anatomical distribution of respiratory viruses can help indicate ante-mortem systemic conditions and the cause of death.
Asunto(s)
Infecciones del Sistema Respiratorio , Virosis , Virus , Autopsia , Humanos , Reacción en Cadena en Tiempo Real de la Polimerasa , Infecciones del Sistema Respiratorio/diagnóstico , Virosis/diagnóstico , Virus/genéticaRESUMEN
Benzalkonium chloride is widely used in disinfectants. Several toxicological and fatal cases have been reported; however, little is known about its kinetics and distribution. We investigated the kinetic characteristics and distribution of benzalkonium cation (BZK) based on the length of the alkyl chains C12, C14, and C16. Rats were treated intravenously with BZK solution (dose, 13.9 mg/kg) containing equal amounts of the three homologues. Kinetic parameters in the blood were assessed, and BZK distribution in the blood and tissues was examined both in rapid intravenous (IV) and drip intravenous (DIV) administrations. BZK concentrations were analysed by liquid chromatography-tandem mass spectrometry (LC-MS/MS). BZK with longer alkyl chains showed lower elimination tendencies and remained in the blood for a longer duration. Concentrations of BZK were higher in the heart, lung, spleen, and kidney than those in the blood, and lower in the brain and fat. In both the IV and DIV groups, the lung, liver, spleen, and fat samples showed higher concentrations of the longer alkyl chains (BZK-C12 < -C14 < -C16), and the opposite trend was observed in the kidney (BZK-C16 < -C14 < -C12). Only the heart and muscle samples displayed the homologues in ratios comparable to the original administered solutions. Differences between IV and DIV groups could be identified by comparing concentrations of BZK homologues in the heart, lung, spleen, and kidney samples. We found that the kinetics and distribution of BZK were influenced by the alkyl chain length, and analysing each BZK homologues in blood and tissue samples may provide useful information.
Asunto(s)
Compuestos de Benzalconio/metabolismo , Compuestos de Benzalconio/farmacocinética , Animales , Compuestos de Benzalconio/administración & dosificación , Compuestos de Benzalconio/química , Infusiones Intravenosas , Riñón/metabolismo , Pulmón/metabolismo , Masculino , Miocardio/metabolismo , Ratas Wistar , Soluciones , Bazo/metabolismo , Relación Estructura-Actividad , Distribución TisularRESUMEN
Ataxia telangiectasia mutated (ATM) is a tumor suppressor gene, and its somatic inactivation plays a role in the pathogenesis of lymphoid malignancies. However, the role of ATM in patients with myeloid malignancies is still unknown. We herein report a case of acute megakaryoblastic leukemia (AMKL) with ATM gene deletion. An 84-year-old Japanese woman presenting with a pale face and pancytopenia was admitted to our institution and diagnosed to have AMKL with ATM gene deletion. She was treated with intravenous azacitidine. The azacitidine treatment was effective for approximately 1 year. Somatic inactivation of the ATM gene may therefore be involved in the pathogenesis of AMKL.