Hepatic Relaxation Times from Postmortem MR Imaging of Adult Humans.

PURPOSE: To measure T1 and T2 values of hepatic postmortem magnetic resonance (PMMR) imaging. MATERIALS AND METHODS: We performed hepatic PMMR imaging of 22 deceased adults (16 men, 6 women; mean age, 56.3 years) whose deaths were for reasons other than liver injury or disease at a mean of 27.7 hours after death. Before imaging, the bodies were kept in cold storage at 4°C (mean rectal temperature, 17.6°C). We measured T1 and T2 values in the liver at two sites (the anterior segment of the right lobe and the lateral segment of the left lobe). We also investigated the influence of the body temperature and postmortem interval on T1 and T2 values. RESULTS: In the anterior segment of the right lobe and the lateral segment of the left lobe, T1 values of PMMR imaging were 524 ± 112 ms and 472 ± 104 ms (mean ± standard deviation), respectively; while T2 values were 42 ± 6 ms and 43 ± 8 ms, respectively. T1 and T2 values did not differ significantly between the two sites (P ≧ 0.05). Regarding temperature, the T2 values of hepatic PMMR imaging were linearly correlated with the body temperature, but the T1 values were not. The T1 and T2 values of the two sites in the liver did not correlate with the postmortem interval. CONCLUSION: Reduction in body temperature after death is considered to induce T1 and T2 value changes in the liver on PMMR imaging.

Possibility of visualization of gastrothorax based on unenhanced postmortem computed tomography/PMCT.

We present a fatal case of a gastrothorax due to an acute gastric volvulus resulting from a Bochdalek hernia. A 5-year-old boy without previous medical history was brought to our institution in a state of cardiopulmonary arrest and was subsequently pronounced dead. Postmortem computed tomography (PMCT) of the torso showed abdominal organs involving the lower section of the esophagus up to the entire stomach, the left side of the transverse colon, the entire spleen, and the tail of the pancreas herniated into the left thoracic cavity. The stomach was markedly expanded and a mesentero-axial (rotation along the short axis) volvulus was observed, displacing mediastinal structures to the right side and depressing the diaphragmatic contour. A PMCT of the thorax at the lung window setting revealed displacement of bilateral lungs. The bilateral lungs were severely atelectatic and congested. The PMCT findings mentioned above were consistent with the autopsy findings. PMCT can provide useful information for the diagnosis in cases we initially cannot predict any significant changes, for example, organ displacement.

Optimization of Inversion Time for Postmortem Fluid-attenuated Inversion Recovery (FLAIR) MR Imaging at 1.5T: Temperature-based Suppression of Cerebrospinal Fluid.

PURPOSE: Signal intensity (SI) and image contrast on postmortem magnetic resonance (MR) imaging are different from those of imaging of living bodies. We sought to suppress the SI of cerebrospinal fluid (CSF) sufficiently for fluid-attenuated inversion recovery (FLAIR) sequence in postmortem MR (PMMR) imaging by optimizing inversion time (TI). MATERIALS AND METHODS: We subject 28 deceased patients to PMMR imaging 3 to 113 hours after confirmation of death (mean, 27.4 hrs.). PMMR imaging was performed at 1.5 tesla, and T1 values of CSF were measured with maps of relaxation time. Rectal temperatures (RT) measured immediately after PMMR imaging ranged from 6 to 32°C (mean, 15.4°C). We analyzed the relationship between T1 and RT statistically using Pearson's correlation coefficient. We obtained FLAIR images from one cadaver using both a TI routinely used for living bodies and an optimized TI calculated from the RT. RESULTS: T1 values of CSF ranged from 2159 to 4063 ms (mean 2962.4), and there was a significantly positive correlation between T1 and RT (r = 0.96, P < 0.0001). The regression expression for the relationship was T1 = 74.4 * RT + 1813 for a magnetic field strength of 1.5T. The SI of CSF was effectively suppressed with the optimized TI (0.693 * T1), namely, TI = 0.693 * (77.4 * RT + 1813). CONCLUSION: Use of the TI calculated from the linear regression of the T1 and RT optimizes the FLAIR sequence of PMMR imaging.

Can ruptured abdominal aortic aneurysm be accurately diagnosed as the cause of death without postmortem computed tomography when autopsies cannot be performed?

PURPOSE: This study aimed to conduct a multicentre retrospective review of cases to clarify how many ruptured abdominal aortic aneurysms (RAAAs) as the cause of death could be diagnosed without post-mortem computed tomography (PMCT) when autopsies cannot be performed. METHODS: We collected consecutive PMCT data from January 2002 to December 2009 from three institutes where PMCT examinations are performed on a routine basis for deceased patients with unknown causes of death. A total of 19 cases were identified where PMCT revealed RAAAs. Ante-mortem clinical presentations, post-mortem external examinations, and peri-mortem ultrasonography findings were assessed for their diagnostic accuracy. RESULTS: The correct diagnosis based on the classic triad of shock, acute abdominal pain, and pulsatile abdominal mass was made in only one of 19 (5.3%) patients. Shock, acute abdominal pain, and abdominal swelling were found in five of 19 (26%) patients. Shock and acute abdominal pain or abdominal swelling were found in two of 19 (10%) patients. Ten of 19 (53%) patients only had shock. Peri-mortem ultrasonography was performed in seven of 19 patients; one was diagnosed with RAAA (14%). No patients had pre-mortem CT examinations. CONCLUSIONS: Post-mortem diagnosis of RAAA is difficult to make based on ante-mortem clinical presentation, post-mortem external examinations, or peri-mortem ultrasonography. PMCT is recommended for diagnosing RAAA as the cause of death if pre-mortem CT examinations are not carried out when autopsies cannot be performed.

Pericardial tear as a consequence of cardiopulmonary resuscitation (CPR) involving chest compression: a report of two postmortem cases of acute type A aortic dissection with hemopericardium.

We present two cases of a pericardial tear as a consequence of cardiopulmonary resuscitation involving chest compressions in fatal acute type A aortic dissection (AoD) with hemopericardium. For each case, postmortem computed tomography revealed a hematoma in the false lumen of the ascending aorta with a slight hemopericardium and a large left hemothorax, as well as focal pericardial dimpling and discontinuity around the left ventricle. At autopsy, we confirmed a convex lens-shape gaping pericardial tear at the left posterolateral site of the pericardium and a massive volume of bloody fluid in the left thoracic cavity. It has been hypothesized that the pericardium ruptured due to chest compressions during resuscitation in these cases of acute type A AoD with hemopericardium and that intrapericardial blood leakage through the pericardial tear resulted in a hemothorax.

Pseudo-Hirschsprung's disease with rectal hypoganglionosis: an autopsied case of circulatory failure due to severe constipation.

We report a 21-year-old female patient who suddenly died of circulatory failure due to pressure from megacolon allied with pseudo-Hirschsprung's disease. Since 3 years before her death, she had exhibited the feeling of abdominal distention, which was diagnosed as constipation. However, her constipation did not respond well to the prescribed oral administration of laxatives and enemas. She was found dead at home in the morning, lying on her back. An autopsy revealed a decreased number of ganglion cells in the rectum, suggesting hypoganglionosis. In cases of intractable chronic constipation, careful investigation of the cause of such symptoms is important.

Cerebral relaxation times from postmortem MR imaging of adults.

PURPOSE: We measured T1 and T2 values of cerebral postmortem magnetic resonance (PMMR) imaging and compared the data of cadavers with that of living human subjects. MATERIALS AND METHODS: We performed PMMR imaging of the brains of 30 adults (22 men, 8 women; mean age, 58.2 years) whose deaths were for reasons other than brain injury or disease at a mean of 29.4 hours after death. Before imaging, the bodies were kept in cold storage at 4°C (mean rectal temperature, 15.6°C). We measured T1 and T2 values in the brain bilaterally at 5 sites (bilateral caudate nucleus, putamen, thalamus and gray matter and white matter of the frontal lobe) and compared the data of PMMR imaging with that from MR imaging of the corresponding sites in 24 healthy volunteers (9 men, 15 women; mean age, 51.8 years). We also investigated the influence of body temperature on T1 and T2 values. RESULTS: Compared with MR imaging findings in the living subjects, PMMR imaging showed significantly shorter T1 values in the caudate nucleus, putamen, thalamus and gray matter and white matter of the frontal lobe and significantly longer T2 values in the gray matter and white matter of the frontal lobe; T2 values in the caudate nucleus, putamen, and thalamus showed no such differences. T1 values correlated significantly with body temperature in all 5 brain sites measured, but T2 values did not. CONCLUSION: Compared with findings of cerebral MR imaging in living adult subjects, those of PMMR imaging tended to demonstrate shorter T1 values and longer T2 values. We attribute this to increased water content of tissue, reduced pH, and reduced body temperature after death.

Optimization of inversion time for postmortem short-tau inversion recovery (STIR) MR imaging.

PURPOSE: Signal intensity and image contrast differ between postmortem magnetic resonance (PMMR) images and images acquired from the living body. We sought to achieve sufficient fat suppression with short-tau inversion recovery (STIR) PMMR imaging by optimizing inversion time (TI). MATERIAL AND METHODS: We subjected 37 deceased adult patients to PMMR imaging at 1.5 tesla 8 to 60 hours after confirmation of death and measured T1 values of areas of subcutaneous fat with relaxation time maps. Rectal temperature (RT) measured immediately after PMMR ranged from 6 to 31°C. We used Pearson's correlation coefficient to analyze the relationship between T1 and relaxation time (RT). We compared STIR images from 4 cadavers acquired with a TI commonly used in the living body and another TI calculated from the linear regression of T1 and RT. RESULTS: T1 values of subcutaneous fat ranged from 89.4 to 182.2 ms. There was a strong, positive, and significant correlation between T1 and RT (r = 0.91, P < 0.0001). The regression expression for the relationship was T1 = 2.6*RT + 90 at a field strength of 1.5T. The subcutaneous fat signal was suppressed more effectively with the optimized TI. CONCLUSION: The T1 value of subcutaneous fat in PMMR correlates linearly with body temperature. Using this correlation to determine TI, fat suppression with PMMR STIR imaging can be easily improved.

Antagonistic effects of tetrodotoxin on aconitine-induced cardiac toxicity.

Aconitine, well-known for its high cardiotoxicity, causes severe arrhythmias, such as ventricular tachycardia and ventricular fibrillation, by opening membrane sodium channels. Tetrodotoxin, a membrane sodium-channel blocker, is thought to antagonize aconitine activity. Tetrodotoxin is a potent blocker of the skeletal muscle sodium-channel isoform Na(v)1.4 (IC50 10 nM), but micromolar concentrations of tetrodotoxin are required to inhibit the primary cardiac isoform Na(v)1.5. This suggests that substantial concentrations of tetrodotoxin are required to alleviate the cardiac toxicity caused by aconitine. To elucidate the interaction between aconitine and tetrodotoxin in the cardiovascular and respiratory systems, mixtures of aconitine and tetrodotoxin were simultaneously administered to mice, and the effects on electrocardiograms, breathing rates, and arterial oxygen saturation were examined. Compared with mice treated with aconitine alone, some mice treated with aconitine-tetrodotoxin mixtures showed lower mortality rates and delayed appearance of arrhythmia. The decreased breathing rates and arterial oxygen saturation observed in mice receiving aconitine alone were alleviated in mice that survived after receiving the aconitine-tetrodotoxin mixture; this result suggests that tetrodotoxin is antagonistic to aconitine. When the tetrodotoxin dose is greater than the dose that can block tetrodotoxin-sensitive sodium channels, which are excessively activated by aconitine, tetrodotoxin toxicity becomes prominent, and the mortality rate increases because of the respiratory effects of tetrodotoxin. In terms of cardiotoxicity, mice receiving the aconitine-tetrodotoxin mixture showed minor and shorter periods of change on electrocardiography. This finding can be explained by the recent discovery of tetrodotoxin-sensitive sodium-channel cardiac isoforms (Na(v)1.1, 1.2, 1.3, 1.4 and 1.6).

Immediate non-traumatic postmortem computed tomographic demonstration of myocardial intravascular gas of the left ventricle: effects from cardiopulmonary resuscitation.

An 87-year-old man was found in a state of cardiopulmonary arrest. Despite cardiopulmonary resuscitation (CPR) for over 1 hour by emergency technicians and physicians, the patient died. Immediate postmortem computed tomography showed cardiovascular gas in the right atrium, right ventricle, and left ventricle. Cardiovascular gas in the left ventricle was located in the myocardium and appeared as linear or branch-shaped suggesting the presence of myocardial intravascular gas. This is the first report describing the appearance and significance of myocardial intravascular gas of the left ventricle as a CPR-related change.

Sudden death as a late sequel of Kawasaki disease: postmortem CT demonstration of coronary artery aneurysm.

Kawasaki disease (KD) is an acute, self-limited vasculitis of unknown etiology that primarily affects the coronary artery (CA) and presents during childhood. The characteristic coronary arterial lesion of KD is an aneurysm. Ischemic heart disease derived from a CA aneurysm is experienced approximately two decades after the onset of acute KD. In recent years, the primary issue of concern has been asymptomatic adults with a CA aneurysm caused by undiagnosed KD. We present a case of sudden death as a late KD sequel in a young adult. A postmortem CT scan revealed a coarse calcification of a left anterior descending CA aneurysm, which was confirmed at the time of autopsy. A postmortem CT scan is useful in cases of sudden death where the detection of a calcified CA aneurysm would suggest to the forensic pathologist that the deceased suffered from a late sequel of KD. The use of screening postmortem CT scans for young people may detect cases of unsuspected CA aneurysms, raising the possibility of untreated KD.

A case of fatal cervical discoligamentous hyperextension injury without fracture: correlation of postmortem imaging and autopsy findings.

We present a case of fatal cervical discoligamentous hyperextension injury without fracture. Postmortem computed tomography (PMCT) and postmortem magnetic resonance imaging (PMMRI) disclosed cervical instability and spinal cord injury in the absence of fracture, which was confirmed by autopsy. Cervical discoligamentous injury without fracture may be unnoticeable on PMCT because signs of cervical misalignment change depending on the posture of the neck at the time of postmortem imaging. Because of its greater sensitivity for soft tissue injury, PMMRI is especially useful for detecting pathological changes in cases of death due to cervical discoligamentous injury. In this paper, findings on postmortem imaging for this injury are described in detail and correlated with findings on autopsy.

Postmortem pulmonary edema: a comparison between immediate and delayed postmortem computed tomography.

OBJECTIVE: Postmortem CT (PMCT) findings may change with the passage of time after death. The aim of this study was to investigate time-dependent PMCT findings of the lung in order to aid the interpretation of postmortem images obtained at various times. MATERIALS AND METHODS: Our subjects were three non-traumatically deceased male subjects (25, 44, and 76 years old) who underwent whole body PMCT scan at two time points: one immediately after death and the other several hours after death but before the autopsy. The causes of death of the subjects were acute cardiac insufficiency (so-called sudden manhood death syndrome, 2 subjects), ischemic heart disease (acute coronary syndrome, 1 subject). The immediate and delayed PMCT findings of the lung were compared, and the differences between them were investigated. RESULTS: Compared with immediate PMCT, delayed PMCT showed advanced dependent opacity and consolidation corresponding to congestive pulmonary edema. CONCLUSION: PMCT images of the lung change as the time after death increases due to the natural postmortem changes of the corpse. Immediate PMCT is more suitable than delayed PMCT for discerning cause of death. Delayed PMCT reflects the autopsy findings more accurately than immediate PMCT.

Postmortem magnetic resonance imaging dealing with low temperature objects.

In Japan, the medical examiner system is not widespread, the rate of autopsy is low, and many medical institutions therefore perform postmortem imaging using clinical equipment. Postmortem imaging is performed to clarify cause of death, select candidates for autopsy, make a guide map for autopsy, or provide additional information for autopsy. Findings are classified into 3 categories: cause of death and associated changes, changes induced by cardiopulmonary resuscitation, and postmortem changes. Postmortem magnetic resonance imaging shows characteristic changes in signal intensity related to low body temperature after death; they are low temperature images.

Nontraumatic postmortem computed tomographic demonstration of cerebral gas embolism following cardiopulmonary resuscitation.

PURPOSE: The aim of this study was to investigate cerebral gas embolism (GE) on nontraumatic postmortem CT (PMCT), regarding its frequency, location (arterial or venous), and causes. MATERIALS AND METHODS: Our subjects were 404 nontraumatically deceased patients who had been in a state of cardiopulmonary arrest on arrival at our emergency room. PMCT was performed within 2 h of the confirmation of death. RESULTS: Cardiopulmonary resuscitation (CPR) was performed on 387 of the 404 subjects; and of these, cerebral GE was detected in 29 (7.5%) subjects (3 arterial, 25 venous, 1 undeterminable). Cerebral GE was not noted in the other 17 of the 404 subjects who did not undergo CPR. However, there was no significant difference in the incidence of cerebral GE between the subjects who underwent CPR and those who did not. The mechanism of cerebral arterial GE was presumed due to pulmonary barotrauma and/or paradoxical embolism, while the thoracic pump theory was suggested to explain the cerebral venous GE. CONCLUSION: Cerebral arterial/venous GE is found in CPR cases on nontraumatic PMCT.

Characteristic signal intensity changes on postmortem magnetic resonance imaging of the brain.

PURPOSE: We investigated and identified postmortem changes on magnetic resonance imaging (MRI) of the brain to provide accurate diagnostic guidelines. MATERIALS AND METHODS: Our subjects were 16 deceased patients (mean age 57 years) who underwent postmortem computed tomography (CT), MRI, and autopsy, the latter of which showed no abnormalities in the brain. The subjects underwent CT and MRI 6-73 h after confirmation of death (mean 26 h), after being kept in cold storage at 4 degrees C. Postmortem MRI of the brain was performed using T1-weighted imaging (T1WI), T2WI, fluid attenuated inversion recovery (FLAIR) imaging, and diffusion weighted imaging (DWI) with parameters identical to those used for living persons. RESULTS: In all cases, postmortem CT showed brain edema and swelling. Postmortem MRI showed characteristic common signal intensity (SI) changes, including (1) high SI of the basal ganglia and thalamus on T1WI; (2) suppression of fat SI on T2WI; (3) insufficient SI suppression of cerebrospinal fluid on FLAIR imaging; (4) high SI rims along the cerebral cortices and the ventricular wall on DWI; and (5) an apparent diffusion coefficient decrease to less than half the normal value. CONCLUSION: Postmortem MRI of the brain in all cases showed characteristic common SI changes. Global cerebral ischemia without following reperfusion and low body temperature explain these changes.

An accidental case of aconite poisoning due to Kampo herbal medicine ingestion.

An accidental case of aconite intoxication occurred after a patient took a therapeutic dose of Kampo herbal medicine containing Aconiti tuber, Uzu but had used the wrong decoction procedure. The poisoning was likely caused by an increased level of Aconitum alkaloids in the decoction; the patient developed aconite intoxication due to incomplete decoction. Aconitum alkaloid levels in the leftover solution which the patient had drunk and in the decoction extracted from 3g Uzu were determined. It was found that decoction makes the medicine safer to drink. Older individuals, especially those with dementia, have a higher risk of aconite poisoning because they sometimes do not boil the medicine appropriately.

Postmortem computed tomography findings as evidence of traffic accident-related fatal injury.

PURPOSE: Most traumatic deaths in Japan are due to nonpenetrating injuries, especially those that result from traffic accidents; however, the autopsy rate of traffic accident-related deaths is only about 5%. We investigated the diagnostic ability of postmortem computed tomography (PMCT) in cases of fatal trauma after traffic accidents. MATERIALS AND METHODS: Our subjects were 78 subjects (59 males, 19 females; mean age 50 years, range 15-87 years) who were brought to our institution in cardiopulmonary arrest on arrival after traffic accidents and died despite resuscitation attempts. PMCT findings of damage to the head, neck, thorax, abdomen, and pelvis were classified into three grades according to the Abbreviated Injury Scale (AIS) severity: A: 1 (minor), 2 (moderate); B: 3 (serious), 4 (severe), 5 (critical); C: 6 (maximum). RESULTS: The percentage ratio of A/B/C in 78 head injuries was 32/60/8, in 41 neck injuries 83/5/12, in 76 thorax injuries 5/38/57, in 76 abdominal injuries 70/24/7, and in 76 pelvic injuries 79/21/0, respectively. CONCLUSION: PMCT can detect or presume fatal trauma when diagnosing the cause of death after traffic accidents.

Presence of beta-linked GalNAc residues on N-glycans of human thyroglobulin.

Hepatic asialoglycoprotein receptor, which may mediate the clearance of circulating thyroglobulin, is known to have a high affinity for GalNAc. Recently, the receptor has been reported to be present also in the thyroid, implicating interaction with thyroglobulin. Here, mammalian thyroglobulins were analyzed for GalNAc termini by Western blotting with GalNAc-recognizing lectins labeled with peroxidase or (125)I. Wistaria floribunda lectin was found to bind human thyroglobulin and, to some extent, bovine, but not porcine thyroglobulin. After desialylation, the lectin bound all of the thyroglobulins tested. The binding was inhibited by competitive inhibitor GalNAc. Peptide N-glycanase treatment of human desialylated thyroglobulin resulted in the complete loss of reactivity with W. floribunda lectin, indicating that the binding sites are exclusively on N-glycans. The binding sites on human desialylated thyroglobulin were partly sensitive to beta-galactosidase, and the remainder was essentially sensitive to beta-N-acetylhexosaminidase. On the other hand, the binding sites of bovine and porcine desialylated thyroglobulins were totally sensitive to beta-galactosidase. Thus the lectin binds beta-Gal termini, as well as beta-GalNAc. GalNAc-specific Dolichos biflorus lectin also bound human thyroglobulin weakly. In contrast to W. floribunda lectin, desialylation diminished binding, suggesting that these two lectins recognize different GalNAc-terminated structures. Again, the binding was inhibited by GalNAc and by treatment with peptide N-glycanase. These results strongly indicate the presence of distinct GalNAc termini of N-glycans on human thyroglobulin.

Effects of long-term administrations of aconitine on electrocardiogram and tissue concentrations of aconitine and its metabolites in mice.

Aconitum alkaloids are well known for their acute and high toxicity, for example, in the causation of severe arrhythmias leading to death. Aconitine, one of the major Aconitum alkaloids, is a highly toxic compound from the Aconitum species. However, there has been no studies reported on the influence of the chronic administration of aconitine. Thus, this study was conducted to investigate the influence of chronic administration of aconitine in experimental animal models. A dose of 1mg/kg per day was administered to the experimental animal models. We determined the concentration of aconitine and its metabolites (benzoylaconine and aconine) in organs and blood with gas chromatography/selected ion monitoring (GC/SIM). In addition, we concurrently recorded the electrocardiogram (ECG). Fifteen minutes after administration on day 0, the early aconitine administered group (acute group) revealed peak organ and blood concentration levels of aconitine with a gradual decrease, thereafter. The concentration of aconitine in organs and blood (from days 0 to 22; 90 min after the last administration of aconitine) gradually decreased according to repeated administration, whereas benzoylaconine and aconine increased. ECG revealed various types of arrhythmias. However, the frequency of arrhythmias remarkably decreased with time and repeated administration of aconitine. These results indicate two possibilities. First, the increase in the activity of aconitine metabolism. Secondly, the decrease of effectiveness to the heart due to long-term (chronic) administration of aconitine.