RESUMEN
A man in his early 60 s who worked at a waste disposal plant had fallen into the refuse pit and was immediately taken to the emergency department for treatment. After 8 days without recovering consciousness, the man died. Antemortem contrast-enhanced computed tomography at the emergency department indicated Stanford type B/DeBakey type IIIb aortic dissection. The autopsy showed a sharp and transverse intimal tear 0.6 cm in length in the aortic isthmus and fractures in the 5th-6th thoracic vertebrae. No structural abnormalities in arterial walls were noted on histopathological examination. The traumatic aortic dissection induced by falling is rare, compared with vehicle crash. Although the verification process was challenging, the cause of death was ultimately concluded as traumatic aortic dissection due to falling into the refuse pit. The following observations were cited as evidence: (1) the location and feature of the intimal tear, (2) the positional relationship between the impact site and the entry tear, and (3) the circumstance of clash impact onto the "cushion" of accumulated waste in the refuse pit. Inquiries into the cause of death, such as those made in this report, are required to provide detailed information on the circumstances of the accident, postmortem examinations, and careful consideration.
Asunto(s)
Disección Aórtica , Laceraciones , Heridas no Penetrantes , Humanos , Autopsia , Aorta Torácica/lesiones , Tomografía Computarizada por Rayos XRESUMEN
The deceased was a 44-year-old male who was treated for a suspected Ebstein's anomaly observed using transthoracic echocardiogram. He was found dead in his bed at home. Autopsy revealed that the septal tricuspid leaflet was intact; however, a large anterior tricuspid leaflet cleft and right atrioventricular cavity dilation were observed. Pathological examination revealed a normal tricuspid valve, except for the presence of a cleft with local fibrosis of the left ventricle papillary muscle and hemosiderin-containing macrophages at both lungs. There were no other abnormalities that may have led to death. It was concluded that he died a cardiac death based on the right heart overload associated with the anterior tricuspid leaflet cleft. This case indicates the possibility that the anterior tricuspid leaflet cleft can cause death and also highlights the necessity of a detailed autopsy to accurately diagnose the cause of death.
Asunto(s)
Válvula Tricúspide/anomalías , Válvula Tricúspide/patología , Adulto , Proteína C-Reactiva/análisis , Diagnóstico Diferencial , Anomalía de Ebstein/diagnóstico , Fibrosis , Patologia Forense , Insuficiencia Cardíaca/etiología , Ventrículos Cardíacos/patología , Hemosiderina/metabolismo , Humanos , Pulmón/metabolismo , Macrófagos/metabolismo , Masculino , Péptido Natriurético Encefálico/sangre , Músculos Papilares/patología , Fragmentos de Péptidos/sangre , Insuficiencia de la Válvula Tricúspide/complicacionesRESUMEN
The plant species Gloriosa superba and Colchicum autumnale produce extremely poisonous colchicine as a major toxic metabolite. Almost all previous studies on colchicine poisoning have focused on drug analysis and clinical and pathological aspects. In this study, we developed a rapid, highly sensitive method to identify G. superba and C. autumnale. This method, which can distinguish between G. superba and C. autumnale using even minute amounts of plant material, is based on duplex real-time PCR in combination with melting curve analysis. To discriminate between the two genera of colchicine-containing plants, we designed new primer pairs targeting the region of the ycf15 gene, which is present in C. autumnale but not G. superba. By producing PCR amplicons with easily distinguishable melting temperatures, we were able to rapidly and accurately distinguish G. superba from C. autumnale. The new primer pairs generated no PCR amplicons from commercially available human DNA or various plant DNAs except for G. superba and C. autumnale. Sensitivity testing indicated that this assay can accurately detect less than 0.031 ng of DNA. Using our method in conjunction with colchicine drug analysis, we successfully identified G. superba in the stomach contents of a suicide victim who ingested massive quantities of a colchicine-containing plant. According to these results, duplex real-time PCR analysis is very appropriate for testing forensic samples, such as stomach contents harboring a variety of vegetables, and enables discrimination between G. superba and C. autumnale in forensic and emergency medical fields.
Asunto(s)
Colchicina/envenenamiento , Sobredosis de Droga/diagnóstico , Plantas Tóxicas/envenenamiento , Suicidio , Humanos , Reacción en Cadena en Tiempo Real de la Polimerasa/métodosRESUMEN
A crossbow is a bow that shoots an arrow when a gun-like trigger is pulled. Deaths caused by accidental crossbow shootings are extremely rare. Here we describe an autopsy case of a penetrating wound to the left cerebral hemisphere caused by an accidental shooting with a crossbow. A man in his early 60s who lived with his wife and had used crossbows for 20 years as his hobby was found one early morning in the shed of his house, collapsed and bleeding from the head and neck. He was taken to a hospital and died after approximately 3 days of conservative treatment. At autopsy, a penetrating wound between the upper part of the left anterior neck and the left frontoparietal region was evident. Traumatic intracerebral hematoma was observed in the left frontal lobe, and severe traumatic subarachnoid hemorrhage was present throughout the brain. Cerebral contusion and hematoma without any organization were noted around the penetration. The cause of death was determined to be cerebral contusion and intracerebral hematoma due to the penetrating wound by the crossbow arrow. He was probably trying to load an arrow into the crossbow by placing it on the floor, pointing upward, and made a mistake in its operation that resulted in the shooting of the arrow. This case is unique because it was a rare accidental death caused by a crossbow arrow, and a detailed histopathological examination was performed.
Asunto(s)
Accidentes , Cerebro/lesiones , Traumatismos Penetrantes de la Cabeza/etiología , Armas , Edema Encefálico/diagnóstico por imagen , Edema Encefálico/patología , Infarto Encefálico/diagnóstico por imagen , Infarto Encefálico/patología , Cerebro/diagnóstico por imagen , Cerebro/patología , Traumatismos Penetrantes de la Cabeza/diagnóstico por imagen , Traumatismos Penetrantes de la Cabeza/patología , Hematoma/patología , Humanos , Masculino , Persona de Mediana Edad , Arteria Cerebral Media/diagnóstico por imagen , Arteria Cerebral Media/lesiones , Hemorragia Subaracnoidea/diagnóstico por imagen , Hemorragia Subaracnoidea/patologíaRESUMEN
Environmental factors such as outside temperature at the time of death are very important for forensic diagnoses and police investigations. In particular, death in a cold environment is associated with factors of forensic interest, including hypothermia, drowning in cold water, or postmortem body movement by a suspect. Hypothermia raises a special problem because of the difficulty of evaluation during autopsy. We describe here a unique method of estimating antemortem environmental temperature, involving the immunohistochemical analysis of HSP70 expression patterns in glomerular podocytes. Using this method, we found that HSP70 was present in glomerular podocytes at autopsy and that HSP70 was highly expressed, mainly in the nucleus of podocytes, in deaths associated with exposure to cold. Interestingly, this expression pattern was specific to death in a cold environment, including hypothermia and drowning in cold water. Analysis of the pattern of HSP70 expression in glomeruli may therefore be very useful in forensic diagnosis, for determining whether the antemortem environmental temperature was low. Moreover, immunohistochemical and real-time PCR assays of the molecular mechanism of HSP70 and HSF1 expression in glomeruli following exposure to cold indicated that HSP70 was rapidly translocated to the nucleus of podocytes following exposure to cold, but without new protein synthesis.
Asunto(s)
Frío , Proteínas HSP70 de Choque Térmico/metabolismo , Hipotermia/diagnóstico , Glomérulos Renales/citología , Podocitos/metabolismo , Anciano , Núcleo Celular/metabolismo , Proteínas de Unión al ADN/genética , Proteínas de Unión al ADN/metabolismo , Exposición a Riesgos Ambientales , Patologia Forense , Factores de Transcripción del Choque Térmico , Humanos , Hipotermia/metabolismo , Inmunohistoquímica , Persona de Mediana Edad , ARN Mensajero/metabolismo , Reacción en Cadena en Tiempo Real de la Polimerasa , Factores de Transcripción/genética , Factores de Transcripción/metabolismoRESUMEN
Vimentin is a type III intermediate filament cytoskeletal protein that is expressed mainly in cells of mesenchymal origin and is involved in a plethora of cellular functions. In this study, myocardial tissues from patients with ischemic heart disease and a mouse model of acute myocardial infarction were subjected to immunohistochemistry for vimentin. We first examined 26 neutral formalin-fixed, paraffin-embedded myocardial tissue samples from autopsies of patients that were diagnosed with ischemic heart disease within 48 h postmortem. Myocardial cells were negative for vimentin, whereas non-myocardial cells, including vascular endothelium, vascular smooth muscle, fibroblasts, nerve fibers, adipocytes and mesothelial cells, showed positivity. Elevated vimentin expression was observed around myocardial cells undergoing remodeling, suggesting fibroblastic and endothelial proliferation in these locations. By contrast, myocardial foci that were completely fibrotic did not show upregulated vimentin expression. Inflammatory foci including macrophages and neutrophils were clearly visualized with vimentin immunostaining. The same vimentin expression phenomena as those found in human samples were observed in the mouse model. Our study indicates that immunostaining of vimentin as a marker for myocardial remodeling and the dynamics of all non-myocardial cell types may be useful for supplementing conventional staining techniques currently used in the diagnosis of ischemic heart disease.
Asunto(s)
Filamentos Intermedios , Isquemia Miocárdica , Animales , Autopsia , Humanos , Ratones , Miocardio , VimentinaRESUMEN
Thiamylal is an ultrashort-acting barbiturate used for intravenous administration or general anesthesia induction. However, some cases of poisoning and suicide with thiamylal administration have been reported. Additionally, there are few reports on its analysis in the organs and adipose tissue, which requires purification by column chromatography and evaporation. A rapid and sensitive method was developed for quantifying thiamylal and its metabolite, secobarbital, in the adipose tissue, serum, and liver using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Samples were prepared using modified QuEChERS extraction. For adipose tissue samples, an acetonitrile-hexane partitioning step was added to the extraction. This method was applied to investigate a suspected self-poisoning autopsy case. The quantitation accuracy for thiamylal added to porcine pericardial fat (0.18 µg/g), human serum (0.015 µg/mL), and porcine liver (0.18 µg/g) was 103%, 113%, and 95.3%, respectively. The quantitation limits calculated for porcine pericardial fat, human serum, and porcine liver at a signal-to-noise ratio of 10 were 0.06 µg/g, 0.005 µg/mL, and 0.06 µg/g, respectively. In addition, the thiamylal and secobarbital levels in the forensic autopsy case were 140 and 1.5 µg/g, respectively, in myocardial fat; 3.5-4.9 and 0.12-0.20 µg/mL, respectively, in serum; and 6.2-42 and 0.58-1.1 µg/g, respectively, in liver tissue. Thiamylal is especially distributed in the adipose tissue. The thiamylal-to-fat ratio may help estimate the time from administration to death. The developed modified QuEChERS extraction method with acetonitrile-hexane partitioning is suitable for analyzing hydrophobic compounds, such as thiamylal, in the adipose tissue.
Asunto(s)
Espectrometría de Masas en Tándem , Tiamilal , Acetonitrilos , Tejido Adiposo , Animales , Cromatografía Liquida , Hexanos/análisis , Humanos , Hígado/química , Secobarbital/análisis , Porcinos , Tiamilal/análisisRESUMEN
von Willebrand factor (VWF) plays a crucial role in hemostasis and thrombosis. VWF is involved in platelet attachment to the subendothelium, serving as a carrier protein for coagulation factor VIII. In this study, myocardial tissues from deceased patients with ischemic heart disease and a mouse model of acute myocardial infarction were subjected to immunohistochemistry to determine VWF expression. We examined 28 neutral formalin-fixed, paraffin-embedded myocardial tissue samples obtained from the autopsies of patients who were diagnosed with ischemic heart disease within 48 h postmortem. Most myocardial cells were negative for VWF, although some cells showed nonspecific positivity. Elevated VWF expression was observed around myocardial cells undergoing remodeling, suggesting that endothelial proliferation occurred at these sites. In contrast, completely fibrotic myocardial foci did not show upregulated VWF expression. Positivity in fibrin deposition and hemorrhagic sites was observed. The same VWF expression characteristics as those observed in the human samples were observed in the mouse model. VWF immunostaining as an endothelial marker may be a useful supplementation to conventional staining techniques that are currently used in the diagnosis of ischemic heart disease in terms of examining the timing of myocardial remodeling in detail and highlighting the remodeling process.
Asunto(s)
Infarto del Miocardio , Isquemia Miocárdica , Animales , Autopsia , Humanos , Ratones , Miocardio , Factor de von WillebrandRESUMEN
CD31, a transmembrane protein expressed on endothelial and hematopoietic cells, plays important roles in leukocyte trafficking, mechanotransduction, angiogenesis, vascular permeability, and regulation of cellular responsiveness. CD31 immunoreactivity is employed as a sensitive and specific endothelial marker in diagnostic pathology. In this study, CD31 expression in myocardial tissues from deceased patients with ischemic heart disease and a mouse model of acute myocardial infarction were examined by immunohistochemical staining. We examined 24 neutral formalin-fixed, paraffin-embedded myocardial tissue samples obtained within 48 h postmortem from the autopsies of patients who were diagnosed with ischemic heart disease. CD31 expression was observed in vascular endothelial and endocardial cells. In necrotic myocardium, diffusion of CD31 antigen was observed. Elevated CD31 expression was observed around myocardial cells undergoing remodeling, suggesting that endothelial proliferation occurred at these sites. In contrast, fibrotic myocardial foci did not show upregulated CD31 expression. The same CD31 expression characteristics as those observed in the human samples were observed in the mouse model. CD31 immunostaining as an endothelial and microvasculature marker may be a useful complement to conventional staining techniques currently used in the diagnosis of ischemic heart disease, and may allow the timing and process of myocardial remodeling to be analyzed in detail.
Asunto(s)
Mecanotransducción Celular , Infarto del Miocardio , Animales , Humanos , Ratones , Autopsia , Biomarcadores , Formaldehído , Miocardio/patología , Molécula-1 de Adhesión Celular Endotelial de Plaqueta/metabolismoRESUMEN
Thrombomodulin is a transmembrane glycoprotein that is ubiquitously expressed on the surface of vascular endothelial cells. Thrombomodulin exerts its anticoagulant effects by combining with thrombin, activating protein C, and inactivating the coagulation factors FVa and FVIIIa. Clinically, thrombomodulin is also known as a marker of vascular injury because it circulates freely in response to endothelial injury. In this study, myocardial tissue from cases of ischemic heart disease was subjected to immunohistochemistry by thrombomodulin. We examined 40 neutral-formalin-fixed, paraffin-embedded myocardial tissue samples from autopsy cases that were diagnosed with ischemic heart disease (within 48 h postmortem). Thrombomodulin expression was observed in vascular endothelial cells between myocardial cells and in mesothelial cells of the epicardium. In necrotic myocardium, diffusion of thrombomodulin, which reflected endothelial injury, was observed. Upregulated thrombomodulin expression was observed around myocardial cells under ongoing remodeling, which suggested endothelial proliferation in these locations. Completed fibrotic foci of the myocardium did not show upregulated thrombomodulin expression. In a mouse model of acute myocardial infarction, the same phenomena as that found in human samples were observed by immunohistochemistry of thrombomodulin. Immunostaining of thrombomodulin, as a marker for endothelial injury or myocardial remodeling, may be useful for supplementing conventional staining techniques in the diagnosis of ischemic heart disease in forensic pathology.
Asunto(s)
Isquemia Miocárdica , Animales , Autopsia , Células Endoteliales , Ratones , Miocardio , TrombomodulinaRESUMEN
Rosai-Dorfman disease (RDD) is a rare non-Langerhans cell histiocytosis that is characterized histopathologically by accumulation of CD68-positive, S100-positive, and CD1a-negative histiocytes. Cardiac involvement of RDD is rare. We report here an autopsy case of cardiac involvement of RDD presenting as fibrinous pericarditis. A 14-year-old Japanese boy complained of loss of appetite and breathing difficulty when lying down. He was found dead on his back in his bedroom. One year before his death, he was diagnosed with RDD after skin biopsy. At autopsy, the deceased was 153 cm in height and weighed 38 kg with systemic edema. He had flat pigmented light-brown spots, as well as many pale reddish-brown papules on the abdomen and both thighs. Cervical and mediastinal lymphadenopathy was observed. A large amount of pleural and ascitic fluid was observed. The spleen weighed 381.9 g and showed splenomegaly. The heart weighed 620 g and showed acute fibrinous pericarditis with adhesion. Abundant fibrin was observed on the epicardial surface. The infiltrating cells were CD68-positive, S100-positive, and CD1a-negative histiocytes. The skin and spleen showed histiocytic involvement. Systemic edema, large amounts of pleural and ascitic fluid, a high brain natriuretic peptide level in blood, and hemosiderin-laden macrophages in the lungs suggested chronic heart failure. We speculate that the cause of death was extranodal cardiac involvement of RDD with chronic heart failure. This case highlights the need for forensic pathologists to perform a complete autopsy to determine the cause of sudden death when cardiac involvement of RDD is present.
Asunto(s)
Autopsia , Muerte Súbita Cardíaca/etiología , Patologia Forense , Histiocitosis Sinusal/complicaciones , Histiocitosis Sinusal/patología , Miocardio/patología , Pericarditis/etiología , Pericarditis/patología , Adolescente , Enfermedad Crónica , Resultado Fatal , Fibrosis , Insuficiencia Cardíaca/etiología , Humanos , MasculinoRESUMEN
In forensic toxicology studies, drug concentrations must be estimated by the analytical data of formalin-fixed tissues if fresh or frozen tissue specimens are not available. We wished to investigate the stability and time-course of metabolism/degradation of drugs in formalin-fixed tissues using porcine liver homogenates (PLHs) instead of human tissue. Ten psychotropic drugs (amitriptyline, brotizolam, diazepam, diphenhydramine, estazolam, etizolam, levomepromazine, paroxetine, quetiapine and triazolam) were added to PLHs. After the PLHs had been fixed with neutral buffered formalin at room temperature, the concentrations of the drugs in the PLHs were determined by liquid chromatography-tandem mass spectrometry after 3 days, 1 week, 2 weeks, 4 weeks, 2 months, 4 months and 6 months. After 6 months, the residual ratio of amitriptyline, diphenhydramine and quetiapine was 80 %-95 %; that of diazepam, paroxetine and triazolam was 10 %-45 %; and that of brotizolam, etizolam and levomepromazine was 1 %-5 %. Estazolam was not detected from the first day of formalin fixation. These data suggest that the concentrations of drugs in PLHs measured after formalin fixation decreased to varying degrees compared with their initial concentrations. These time-dependent changes in drug concentration were due to degradation during preservation in formalin solution and metabolism by hepatic microsomal enzymes.
Asunto(s)
Estabilidad de Medicamentos , Toxicología Forense/métodos , Hígado/química , Psicotrópicos/análisis , Psicotrópicos/química , Animales , Cromatografía Liquida , Fijadores , Formaldehído , Preservación de Órganos , Manejo de Especímenes , Porcinos , Espectrometría de Masas en TándemRESUMEN
A Japanese woman in her 30s was found dead on a mattress. She had had fever, cough, and dyspnea for about 2â¯weeks. Gross examination at autopsy revealed slight enlargement of the thyroid gland and histopathological examination resulted in a diagnosis of chronic lymphocytic thyroiditis. The concentration of triiodothyronine in the cadaveric blood was extraordinarily high, whereas that of thyroid stimulating hormone was below the detection limit. Autoimmune antibodies against thyroid tissue were positive. The cause of death was assumed to be congestive heart failure caused by thyroid storm associated with chronic lymphocytic thyroiditis. Systemic histopathological examination of tissues and postmortem biochemistry can enable a diagnosis in medicolegal autopsies.
RESUMEN
An allergic anaphylactic reaction is a potentially fatal cascade consisting of an initial sensitization, antigen exposure, crosslinking of immunoglobulin E (IgE) specific for the antigen, activation of mast cells, and release of bioactive substances. Postmortem diagnosis of anaphylaxis is challenging because of the limited availability of antemortem history and minimal macroscopic evidence at autopsy. The elevated activity of a neutral proteinase, such as tryptase, can be a surrogate marker for the activation and degranulation of mast cells. However, it does not directly indicate the involvement of antigen-specific IgE, which has an important role in IgE-mediated allergic anaphylaxis. In the present study, we examined blood from a case of death following infusion of the antibiotic ceftriaxone (CTRX), with a control case for comparison. The aim was to detect IgE specific for CTRX. A pull-down assay with N-hydroxysuccinimide-activated sepharose identified IgE specific for CTRX only in the serum obtained from the case of CTRX exposure, and not in the control case. The specificity of IgE was confirmed by adsorption to an excess of CTRX, which resulted in the signal for IgE disappearing in the pull-down assay. This antigen-specific IgE is a key molecule in the IgE-mediated allergic anaphylaxis and seldom investigated in postmortem examinations. Its detection can provide support for the postmortem diagnosis of allergic anaphylaxis, especially when combined with an antemortem history of allergen exposure and elevated neutral proteinase levels in serum.
Asunto(s)
Anafilaxia/inducido químicamente , Anafilaxia/diagnóstico , Antibacterianos/inmunología , Inmunoglobulina E/sangre , Anafilaxia/sangre , Anafilaxia/inmunología , Antibacterianos/efectos adversos , Diagnóstico , Humanos , Mastocitos/enzimologíaRESUMEN
A Japanese man in his 30s who had congenital cerebral palsy was found unresponsive in bed. His death was confirmed after resuscitation attempts. He had a history of occasional falling (despite the use of walking sticks and a wheelchair) owing to a slowly progressive gait disturbance, and had a medical examination without full neurological re-examination. Autopsy revealed gangliocytoma in the medulla oblongata, which was diagnosed as the cause of death. Although gangliocytoma is a well-differentiated benign tumor, the almost total replacement of the medulla oblongata by the tumor cells was assumed to result in ataxia via the olivocerebellar tract and secondary cerebellar atrophy, followed by central hypoventilation and death of the patient. The symptoms caused by gangliocytoma may be overlooked owing to long-standing cerebral palsy.
Asunto(s)
Neoplasias Encefálicas/patología , Parálisis Cerebral/patología , Ganglioneuroma/patología , Bulbo Raquídeo/patología , Accidentes por Caídas , Adulto , Autopsia , Neoplasias Encefálicas/diagnóstico por imagen , Causas de Muerte , Parálisis Cerebral/diagnóstico por imagen , Ganglioneuroma/diagnóstico por imagen , Humanos , Masculino , Bulbo Raquídeo/diagnóstico por imagen , Tomografía Computarizada por Rayos XRESUMEN
We report an autopsy case of hemopericardium caused by rupture of a ventricular aneurysm associated with acute myocarditis in an infant boy aged 2 years and 10 months. Three days before his death, the patient developed fever. On the day of death, he described an urge to defecate and attempted to do so in an upright position. While straining to defecate without success for a prolonged period, he stopped breathing and collapsed. On autopsy, his heart weighed 91.7 g and cardiac tamponade was evident, the pericardial cavity being filled with 140 mL of blood that had come from a 1.5-cm-long rupture in a 2.7×1.5 cm ventricular aneurysm in the posterior left ventricular wall. Patchy grayish-white discoloration was noted in the myocardium. Histologically, CD3-positive T lymphocytic infiltration accompanied by pronounced macrophage infiltration was observed in the myocardium. Hemorrhagic necrosis was detected in the area of the ventricular aneurysm. Staining for matrix metalloproteinase (MMP) expression revealed abundant MMP-2, MMP-7, and MMP-9. Polymerase chain reaction to detect viruses failed to identify any specific causative viruses in the myocardium. In this case of lymphocytic (viral) and histiocytic myocarditis with pronounced macrophage infiltration and upregulation of MMP expression, myocardial remodeling and associated wall weakening had resulted in formation and rupture of an aneurysm.
Asunto(s)
Aneurisma Roto/patología , Taponamiento Cardíaco/patología , Ventrículos Cardíacos/patología , Miocarditis/complicaciones , Aneurisma Roto/etiología , Autopsia , Taponamiento Cardíaco/etiología , Preescolar , Humanos , Inmunohistoquímica , Masculino , Miocarditis/diagnóstico , Rotura EspontáneaRESUMEN
A 21-day-old Japanese male infant became inactive and then collapsed unexpectedly. On autopsy, there was no connection between the ascending and descending thoracic aorta. The site of interruption was the aortic isthmus. The heart showed hypertrophy and exhibited intracardiac malformations, including subaortic valve stenosis resulting from posterior deviation of the ventricular outlet septum and ventricular septal defect. The cause of death was diagnosed as prolonged physiological closure of the ductus arteriosus complicated by interrupted aortic arch and followed by assumed ductal shock.
Asunto(s)
Aorta Torácica/anomalías , Autopsia , Causas de Muerte , Conducto Arterioso Permeable/patología , Defectos del Tabique Interventricular/patología , Humanos , Recién Nacido , MasculinoRESUMEN
Coronary artery aneurysm is a fairly uncommon clinical entity, which is defined by a characteristic dilatation that exceeds 1.5 times the width of normal adjacent coronary artery segments. In the present report, we describe a case of rupture of a massive coronary artery aneurysm. A man in his 40s was found dead in his bed. The pericardial cavity contained 270mL of blood with 428.2g of coagulation. Two true aneurysms of the right coronary artery were identified. A proximal aneurysm, adjacent to the right auricle, had ruptured on the right. A distal unruptured aneurysm was identified 5.1cm distal to the proximal ruptured aneurysm. Atherosclerosis of the coronary arteries and aorta was severe. The heart weighed 799.1g and showed concentric ventricular hypertrophy, myocardial thinning, and patchy fibrosis. Histological analysis showed that both aneurysms were purely atherosclerotic true aneurysms without considerable inflammation. The cause of death was determined as cardiac tamponade due to rupture of a giant coronary atherosclerotic aneurysm.
Asunto(s)
Aneurisma Roto/complicaciones , Taponamiento Cardíaco/etiología , Aneurisma Coronario/complicaciones , Adulto , Aneurisma Roto/patología , Causas de Muerte , Aneurisma Coronario/patología , Enfermedad de la Arteria Coronaria/complicaciones , Enfermedad de la Arteria Coronaria/patología , Humanos , Masculino , Persona de Mediana Edad , Miocardio/patologíaRESUMEN
A man in his thirties was found dead in bed. He had undergone repair of a ventricular septal defect in his infancy and had a 2-month history of antemortem chest pain. On autopsy, a ruptured saccular aneurysm of the ascending aorta was identified, and the right thoracic cavity was found to contain coagulated blood. The oval ostium of the aneurysm was smoothly endothelialized and a black suture was found near its edge. Histological analysis revealed a defect of the intimal and medial layers in the wall of the aneurysm and hypertensive changes in several organs. The cause of death was presumed to be the rupture of a pseudoaneurysm at the aortic cannulation site after a long postoperative period. In the present case, preexisting hypertension was suspected as the cause of the formation and rupture of the pseudoaneurysm. In case of unexpected death, it is important to examine the past medical history even after a long postoperative period.