A Case of Aortopulmonary Fistula Caused by a Huge Thoracic Aortic Aneurysm

Aortopulmonary fistula is an uncommon but often fatal condition resulting as a late complication of an aortic aneurysm. The most common cause is erosion of a false aneurysm of the descending thoracic aorta into the pulmonary artery, resulting in the development of a left-to-right shunt and leading to acute pulmonary edema and right heart failure. We report an our experience with aortopulmonary fistula as a rare complication associated with thoracic aortic aneurysm and high output heart failure

Perioperative and anesthetic deaths: toxicological and medico legal aspects

Background: Anesthesia has become safer during decades, though there is still a preventable mortality; the complexity of medical and surgical interventions, increasingly older and sicker patients, has created a host of new hazards in anesthesiology. In this paper, some of these perioperative (PO) fatal adverse events are investigated in terms of health responsibility. Selective literature research in several data bases, concerning perioperative and anesthetic deaths and medical responsibility, was performed. Main text: A generally accepted definition of the anesthesia and perioperatory-related death still remains one of the major concerns in forensic pathology, and the terms “operative deaths” and “anesthetic deaths” are usually applied inaccurately within the medico-legal literature. Such events involve comprehensively PO fatalities and allow for subtle separation of natural and unnatural death, at least from the prospective of forensic pathology. Iatrogenic deaths in this field can be separated into some major categories, as attributable to previous patient’s unfavorable conditions or depending from surgical procedure per se (such as PO cardiac and cerebrovascular events). In this review, the authors carried out syntheses of specific research areas regarding epidemiology, complications of general and spinal anesthetic, failure in airway management and patient’s circulatory homeostasis, and adverse drugs reactions; analysis considering the challenge of anesthetic-related mortality, epidemiology and classifications, by indicating causal chain of death, in respect of both contributing and associated anesthetic and surgery facts. Conclusions: Perioperative quality control programs and its relevance for medico-legal evaluation are emphasized as, although mortality rates have decreased worldwide over the last decades, however, preventable drug-related deaths still happen. Such fatal events have to be considered within the field of forensic pathology experts, with regard of malpractice claims, to implement a strategy for preventing potentially fatal complications

Ventricular androgenic-anabolic steroid-related remodeling: an immunohistochemical study

Background: Several fatal cases of bodybuilders, following a myocardial infarction after long exposure to androgenicanabolic steroids (AAS), are reported. In recent years, evidence has emerged of cases of heart failure related to AAS consumption, with no signs of coronary or aorta atherosclerosis. This study aims to further investigate the pathogenesis of the ventricular AAS-related remodeling performing immunohistochemistry (IHC). Method: In order to examine innate immunity activity and myocytes and endothelial cell apoptosis, IHC analyses were performed on heart tissue of two cases of bodybuilders who died after years of supratherapeutic use of metelonone and nandrolone and where no atherosclerosis or thrombosis were found, using the following antibodies: anti-CD68, anti-iNOS, anti-CD163, anti-CD 15, anti-CD8, anti-CD4, anti-HIF1 α, and in situ TUNEL staining. Results: Results confirm the experimental findings of recent research that, in the absence of other pathological factors, if intensive training is combined with AAS abuse, myocytes and endothelial cells undergo apoptotic alterations. The absence of inflammatory reactions and the presence of an increased number of M2 macrophages in the areas of fibrotic remodeling confirm that the fibrotic changes in the heart are apoptosisrelated and not necrosis-related. Conclusions In conclusion, the study indicates that, in very young subjects with chronic hypoxia-related alterations of the heart, signs of a heart failure in the other organs and a history of AAS abuse, death can be ascribed to progressive heart failure due to the direct apoptotic cardiac and endothelial changes produced by AAS

Fatal heart block from intentional yew tree (Taxus baccata) ingestion: a case report

© The Author(s) 2019. Published by Oxford University Press on behalf of the European Society of Cardiology. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited.Background Taxus baccata, also known as English yew, is a poison that causes cardiac arrhythmias and can result in death from cardiogenic shock.Case summary A 49-year-old gentleman was admitted following yew ingestion with suicidal intent. He was bradycardic at 30 b.p.m. and hypotensive on arrival. Electrocardiography revealed complete heart block with broad complex ventricular escape rate of 30 b.p.m. Bedside echocardiography revealed severe global impairment of right and left ventricular systolic function. Urgent temporary transvenous pacing was instituted, and the patient was considered for veno-arterial extracorporeal membrane oxygenation. Unfortunately, he deteriorated rapidly and cardiorespiratory arrest ensued, and despite prolonged in-hospital resuscitation, the patient died. Post-mortem examination revealed small needle-shaped plant leaves together with seeds found in the stomach. Ante mortem serum sample analysis sent to the Royal Botanical Gardens and revealed the presence of taxine Type B alkaloids in the patient’s blood.Discussion Yew poisoning is a rare occurrence, and there is currently no effective antidote. Treatment involves supportive management, comprising prolonged effective cardiopulmonary resuscitation, pacing, and mechanical cardiac support. This case illustrates the importance of prompt recognition of yew poisoning, alongside early consideration of pacing and mechanical cardiac support. Due to the rarity of this cause of heart block, and since patients may not always volunteer a history of yew ingestion, yew poisoning is something that physicians should be aware of and this should be considered in the differential diagnosis in patients with unexpected heart block. Serum analysis for taxine alkaloids can be used to confirm the diagnosis.Peer reviewe

Cardiac hypertrophy and heart failure: from the case to review of literature

In response to an increased workload due to physiological or pathological stimuli, the heart may undergo a process of growth with increased muscle mass called cardiac hypertrophy. It is a particular mechanism of long term compensation used by the heart to adapt permanently to a greater workload. Although, through its peculiar structural, molecular and metabolic characteristics, in early stage the hypertrophy allows to maintain an adequate cardiac function, after a variable period of time, the same characteristics promote the evolution to contractile dysfunction and heart failure. The latter represents an important cause of death and so the cardiac hypertrophy increases the cardiovascular morbidity and mortality. In this paper we report a rare case of extremely high degree of concentric cardiac hypertrophy, with a heart weight of 1050 g and longitudinal diameter of 16.5 cm, transverse diameter of 16 cm and antero-posterior diameter of 9 cm. The thickness of the left ventricle free wall was 4.2 cm, of the septum 4.3 cm and at the apex level 3.5 cm. These data, compared with those described in scientific literature, indicate the exceptional nature of our necropsy finding of a huge cardiac hypertrophy. The analysis of the pathogenetic mechanisms, which may determinate the fatal event in case of cardiac hypertrophy, shows that in the described case the death cause can be the onset of heart failure in presence of cardiomegaly

Bronchiolitis obliterans.

Bronchiolitis obliterans in the adult patient is a relatively uncommon and vexing clinical entity. This confusion results because this pathologic finding occurs in a variety of diverse clinical settings. Bronchiolitis obliterans is a fibrotic process that primarily affects the small conducting airways. The lesion results from damage to the bronchiolar epithelium and the repair process leads to excessive proliferation of granulation tissue. The alveoli adjacent to the small airway are almost always involved; however, a considerable portion of the interstitium is usually spared. The findings in these patients may physiologically and radiographically mimic chronic obstructive pulmonary disease (COPD). On the other hand, some of the processes associated with bronchiolitis obliterans result in restrictive or mixed restrictive and obstructive ventilatory defects; consequently, they may be confused with other diffuse infiltrative lung disorders. This review will focus principally on bronchiolitis obliterans in adults, which, until recently, was considered rare. There has been heightened interest in this process in adults because of its association with the connective tissue diseases, its development following toxic fume exposure, its occurrence as a result of chronic graft versus host reactions, and the increasing recognition of patients with idiopathic forms of the disease that have an insidious onset often confused with more common problems such as COPD or idiopathic pulmonary fibrosis

Overdose Prevention and Response A guide for people who use drugs and harm reduction staff in Eastern Europe and Central Asia

Provides an overview of the drug overdose problem in Eastern Europe and Central Asia; describes overdose symptoms, factors that affect overdose risk, prevention methods, and step-by-step responses to an overdose. Lists the overdose risks of various drugs

Severe hepatopathy and neurological deterioration after start of valproate treatment in a 6-year-old child with mitochondrial tryptophanyl-tRNA synthetase deficiency

Background: The first subjects with deficiency of mitochondrial tryptophanyl-tRNA synthetase (WARS2) were reported in 2017. Their clinical characteristics can be subdivided into three phenotypes (neonatal phenotype, severe infantile onset phenotype, Parkinson-like phenotype). Results: Here, we report on a subject who presented with early developmental delay, motor weakness and intellectual disability and who was considered during several years as having a non-progressive encephalopathy. At the age of six years, she had an epileptic seizure which was treated with sodium valproate. In the months after treatment was started, she developed acute liver failure and severe progressive encephalopathy. Although valproate was discontinued, she died six months later. Spectrophotometric analysis of the oxidative phosphorylation complexes in liver revealed a deficient activity of complex III and low normal activities of the complexes I and IV. Activity staining in the BN-PAGE gel confirmed the low activities of complex I, III and IV and, in addition, showed the presence of a subcomplex of complex V. Histochemically, a mosaic pattern was seen in hepatocytes after cytochrome c oxidase staining. Using Whole Exome Sequencing two known pathogenic variants were detected in WARS2 (c. 797delC, p. Pro266ArgfsTer10/c. 938 A > T, p. Lys313Met). Conclusion: This is the first report of severe hepatopathy in a subject with WARS2 deficiency. The hepatopathy occurred soon after start of sodium valproate treatment. In the literature, valproate-induced hepatotoxicity was reported in the subjects with pathogenic mutations in POLG and TWNK. This case report illustrates that the course of the disease in the subjects with a mitochondrial defect can be non-progressive during several years. The subject reported here was first diagnosed as having cerebral palsy. Only after a mitochondriotoxic medication was started, the disease became progressive, and the diagnosis of a mitochondrial defect was made