Morio Iino

Postmortem Computed Tomography Findings of Upper Airway Obstruction by Food

Abstract:  This study is a retrospective analysis of 14 cases with food bolus upper airway obstruction as the defined cause of death where both postmortem computed tomography and autopsy were performed. Three groups were defined by the images i.e., Type 1: foreign body situated between the oral cavity and oropharynx, while the epiglottis sits in normal position, Type 2: foreign body situated in the oropharynx just above the epiglottis pushing it posteriorly and obstructing the airway, and Type 3: foreign body obstructing the laryngeal inlet while pushing the epiglottis anteriorly. At the time of autopsy, foreign bodies were detected by pathologists, occasionally in a different position, presumably being dislodged in the act of organ removal especially for the “Type 1” pattern. CT imaging provides accurate interrogation of upper airway bolus obstruction prior to autopsy.

Latent adrenal Ewing sarcoma family of tumors: A case report.

Ewing sarcoma family of tumors (ESFT) is derived from the neural crest, which originates from basal embryo cells in the primitive neural tube. ESFT often arises at the bone, chest wall, and soft tissues of the thoracic region. However, ESFT that arises from the adrenal gland is much rarer and it is usually revealed by clinical symptoms. We report an autopsy case of suicidal hanging, in which adrenal ESFT was incidentally revealed. To our knowledge, this is the first case of latent ESFT arising from the adrenal gland. Autopsy can sometimes reveal latent disease. Some of these latent diseases are very rare and we would not be able to detect them without a complete autopsy. As forensic pathologists, we should attempt to perform a complete autopsy and report new discoveries for the development of medicine.

Obesity and sudden unexpected deaths in Osaka, Japan

Obesity and cardiomegaly/hypertension may be strongly associated with sudden unexpected deaths (SUD) due to circulatory diseases. Six hundred and forty-nine SUD involving 402 postmortems, aged between 10 and 59 years in Osaka in 1997 were analyzed using the calculated body mass index (BMI) and the calculated degree of cardiac hypertrophy (DCH) by Hitosugi (Legal Med 1999;1:80). The percentage of individuals who died due to circulatory diseases was 54% in men and 64% in women, and at ages 50-59 years, 60% in men and 75% in women. It was 80% with DCH>/=20%, 84% for individuals with hypertension as a past illness and 80% with BMI>/=24. Thirty-four percent of all SUD have cardiomegaly more than 20%, 41% have BMI more than 24, and 17% have at least hypertension as a past illness.

Simultaneous determination of flunitrazepam and 7-aminoflunitrazepam in human serum by ion trap gas chromatography–tandem mass spectrometry

A method for the determination of flunitrazepam (FNZ) and 7-aminoflunitrazepam (7-AFNZ) in human serum was developed with ion trap gas chromatography (GC)-tandem mass spectrometry. The 7-AFNZ was derivatizated with 50 microl trifluoroacetic anhydride (TFAA), 60 degrees C-20 min. EI mass spectra and tandem mass spectra of FNZ and 7-AFNZ-TFA were m/z 238, 239, 266, 286, 294, 312, 313(M(+)), m/z 350, 351, 360, 378, 379(M(+)), m/z 238, 239, 240 (precursor ion m/z 286, collision energy 1.5 V), and m/z 239, 254, 264, 336 (precursor ion m/z 351, collision energy 1.8 V), respectively. The detection limits of full scan EI mass spectrometry and tandem mass spectrometry for FNZ and 7-AFNZ in human serum were ca. 200 ng/ml, 60 ng/ml, 15 ng/ml and 1 ng/ml, respectively.

Autopsy case of sudden maternal death from thrombotic thrombocytopenic purpura

A 31‐year‐old pregnant woman was transferred to the emergency room at 27 weeks of gestation. She had one‐day history of fever and upper abdominal pain. Soon after admission, she underwent cardiopulmonary arrest. Autopsy was performed and multiple microthrombi were seen within the small‐caliber vessels of many organs, but not in the lungs. Immunohistochemical staining revealed that the thrombi were rich in von Willebrand factor. We also obtained results which showed severely deficient plasma a disintegrin‐like and metalloprotease with thrombospondin motifs (ADAMTS) 13 activity and positive ADAMTS13 inhibitor, confirming a diagnosis of thrombotic thrombocytopenic purpura. As far as we know, in Japan, this is the first autopsy report of sudden maternal death from thrombotic thrombocytopenic purpura. We expect that the routine laboratory application of ADAMTS13 assays for unknown thrombocytopenic patients during pregnancy may help in differential diagnosis at an earlier stage of the disease and facilitate tailor‐made therapeutic intervention.

A case of diffuse axonal injury in violent death

A 59-year-old man was carried to the hospital by three men. The deceased was unconscious at admission and his face was severely swollen with many subcutaneous hemorrhages and extensive edema. His death was confirmed 17 min after resuscitation. A judicial autopsy was performed the next day. Findings showed that the victims face and head were reddish and swollen, and that subscalp bleeding was ubiquitous, but no skull fracture, epi- and subdural hematoma or subarachnoidal bleeding was observed. The brain itself was severely edematous but no bleeding was found. Although small hemorrhages were seen in the limbs and back, there were no marked wounds except to the head. To determine the cause of death, we performed a microscopic histochemical examination. Conventional H.E. staining disclosed eosinophilic change, concentration of nuclei, edema, gliosis, and oozing at the corpus callosum. To identify further details of the cause of death, we used Bodian staining, Kluver-Barrera staining, anti-beta amyloid immunostaining, and anti-neurofilament immunostaining. We found sinusoidal swelling of axons and waving axons, which are typical findings of Diffuse Axonal Injury (DAI), but no positive staining of beta amyloid. Focal lesions of the corpus callosum and of the dorsolateral quadrant of the rostral brain stem, and diffuse damage to axons are considered to constitute the DAI triad. We therefore diagnosed the cause of death as DAI. Our experience shows that it is important to use several staining methods for diagnosis of a variety of neuronal degenerative disorders. Several days later, we were informed by the police that several men had hit and kicked the victim in an attempt to lynch him. To compare with this case, we also report two other cases in which DAI was observed.

Response to 'Death during pregnancy: thrombotic thrombocytopenic purpura or septic shock?'.

We very much welcome the interest shown in our paper and appreciate the comment. Pourrat suggests that our case may have died from some cardiac diseases. We neither had the clinical data that suggested a cardiovascular disease, nor the pathological change of cardiac involvement. We could not make a diagnosis of cardiac disease from the autopsy alone. He also suggests that disseminated intravascular coagulation (DIC) caused by severe sepsis may have occurred in the present case. It is true that low ADAMTS-13 activity has been observed in severe sepsis. Some cases have also been reported in which severe low ADAMTS-13 activity and positive inhibitor were observed, while Kremer-Hovinga et al. reported that no severe (<5%) or borderline severe (<10%) ADAMTS-13 deficiency was detected. We suppose that one of the reasons for this discrepancy is due to the difference of ADAMTS-13 activity assays. The assay of VWFM and FRETS-VWF73 are less sensitive than those of chromogenic enzyme linked immunosorbent assay or surface-enhanced laser desorption/ionization time-of-flight mass spectrometry. In our data, using these methods, no severe sepsis case with <0.5% activity has been observed. In the present case, we reached a diagnosis of thrombotic thrombocytopenic purpura because ADAMTS-13 activity was within 0.5% and inhibitor was positive. As Pourrat suggests, there is no doubt that DIC with severe sepsis is an important differential diagnosis in our case and we have to pay close attention when interpreting the results of ADAMTS-13 assay. We also need to confirm that the inhibitor is immunoglobulin G. Disclosure