The cardiovascular manifestations of tetanus consist of disturbances of heart rate and rhythm, blood pressure instability, arrhythmias, myocardial dysfunction and sympathetic overactivity. It was ...suggested that either a sudden loss of catecholamine stimulation or myocardial damage caused by the direct action of the tetanus toxin, could be involved in cardiac dysfunction described in tetanus. However, histologic evidence of myocardial necrosis in tetanus was demonstrated in few cases. We report a fatal case of tetanus in which we investigated the cardiac morphology and the expression of TNFalpha to elucidate the heart involvement in this case. Since it is well known that myocardial damage caused by catecholamines can induce synthesis of cytokines by myocytes, cytokines, specifically those with known cardiodepressant properties such as TNF-alpha, could be an alternative mechanism involved in cardiac dysfunction in the setting of tetanus.
During the clinical course of dilated cardiomyopathy, arrhythmias, thromboembolism and sudden death are common and may occur at any stage. In patients with dilated cardiomyopathy, elevated plasma ...levels of tumor necrosis factor-alpha are associated with poor prognosis. In animal experiments and clinical trials, myocardial tumor necrosis factor-alpha expression correlates with increased mortality rates. A case of sudden death of a previously asymptomatic young man, having a definitive autoptic diagnosis of dilated cardiomyopathy with endomyoelastofibrosis, is presented. We investigated the cardiac morphology and the expression of tumor necrosis factor-alpha in cardiac tissue specimens to elucidate the role of tumor necrosis factor-alpha expression in this fatal case. Our results demonstrate a strong positive myocytes reaction for tumor necrosis factor-alpha in the heart specimens. The pathogenesis of the fatal event is discussed with particular reference to the histological findings and myocytes expression of tumor necrosis factor-alpha.
Patients with catheter fragments that were entrapped during percutaneous transluminal coronary angioplasty remain a particular challenge because little is known about the clinical outcome. Absolutely ...unique is the partially cutting of the dilator and the pushing of the fragment by the guidewire advancing into the femoral artery to the coronary tree. We describe this exceptionally complication with a complete coronary obstruction and an anterior myocardial infarction sustained by the retained fragment into the left main branch.
Symptoms of cardiac contusion are very greatly and sometimes are non recognized or are masked by associated injury in severe chest trauma. Cardiac contusion clinically presents as a spectrum of signs ...and symptoms of varying severity, ranging from precordial pain, dyspnoea, and non specific ECG changes to increased serum activity of several enzymes, early severe rhythm abnormalities, severe conduction defects and death. We present a fatal case in which the definitive diagnosis of myocardial contusion has proved complex. All clinical data were suggestive of acute myocardial infarction, but the history of chest wall injury and gross and histological examination of the heart and coronary vessels led us to conclude for a cardiac contusion without myocardial infarction. In case of chest blunt trauma, the ECG should be interpreted within the context of the clinical situation, on history of chest wall injury, since a fatal myocardial contusion may occur after apparently mild injury.
Introduction. The severity of ethylene glycol toxicity is related to the metabolic acidosis resulting from the biotransformation of ethylene glycol into toxic metabolites. Glycolic acid causes severe ...acidosis and oxalate precipitates as calcium oxalate in the kidneys and other tissues. Case Report. An adult male was taken to the local hospital by the team rescue and was apparently unconscious; severe metabolic acidosis and renal failure led to death a few hours after the arrival. Confocal laser scanning microscopy demonstrated oxalate crystals deposition within the tubular epithelial cells and widespread necrosis of the tubular epithelium in the proximal tubules. Toxicological examinations revealed ethylene glycol; the blood level was 250 mg/L and in urine the concentration was 0.3%. Discussion. In cases of ethylene glycol poisoning, calcium oxalate may be excreted not only as dihydrate crystals, but also as monohydrate crystals. Direct toxicity, cortical edema, and inhibition of mitochondrial activity, as evidenced by decreased succinate dehydrogenase activity, are possible mechanisms of crystal damage. Since calcium oxalate monohydrate crystals are transported intracellularly by kidney cells, the renal toxicity of ethylene glycol may result from inhibition of mitochondrial respiratory function in proximal tubular cells by calcium oxalate monohydrate crystals. Conclusions. The histologic diagnosis of acute renal failure secondary to ethylene glycol poisoning depends on the recognitions of the changes of acute tubular damage in association with calcium oxalate crystals deposition within the tubular epithelial cells and the widespread necrosis of the tubular epithelium in the proximal tubules.
Authors present the case of the sudden death of a 30-year-old man, 3 h since his hospitalization by the onset of aspecific chest pain. ECG findings revealed the presence of localized ST segment ...elevation in precordial leads (V1-V4) and DII-DII, and aVF mimicking acute antero-inferior myocardial infarction. A diagnosis of acute antero-inferior myocardial infarction was advanced and the patient introduced to thrombolytic therapy. Suddenly, on ECG monitor, conduction abnormalities were early recorded (ventricular extrasystole) followed by ventricular tachycardia degenerating in fatal ventricular fibrillation. An alleged medical malpractice was sued against the cardiologist. A complete immunohistochemical study was performed. Histologically, the heart presented massive interstitial lymphocytic infiltrate and focal myocytes necrosis. The diagnosis of acute lymphocytic myocarditis was established as the cause of death.
Amniotic fluid embolism (AFE) is an uncommon obstetric condition involving pregnant women during labor or in the initial stages after delivery. Its incidence is estimated to be around 5.5 cases per ...100,000 deliveries. Therefore, this paper investigated the pathophysiological mechanism, which underlies AFE, in order to evaluate the role of immune response in the development of this still enigmatic clinical entity. The following databases (from 1956 to September 2014) Medline, Cochrane Central, Scopus, Web of Science and Science Direct were used, searching the following key words: AFE, pathophysiology, immune/inflammatory response, complement and anaphylaxis. The main key word "AFE" was searched singularly and associated individually to each of the other keywords. Of the 146 sources found, only 19 were considered appropriate for the purpose of this paper. The clinical course is characterized by a rapid onset of symptoms, which include: acute hypotension and/or cardiac arrest, acute hypoxia (with dyspnoea, cyanosis and/or respiratory arrest), coagulopathies (disseminated intravascular coagulation and/or severe hemorrhage), coma and seizures. The pathology still determines a significant morbidity and mortality and potential permanent neurological sequelae for surviving patients. At this moment, numerous aspects involving the pathophysiology and clinical development are still not understood and several hypotheses have been formulated, in particular the possible role of anaphylaxis and complement. Moreover, the detection of serum tryptase and complement components and the evaluation of fetal antigens can explain several aspects of immune response.
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