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Rituximab is a plausible alternative first-line treatment of ANCA-associated vasculitis. Adverse effects related to its infusion are common and usually have a benign course. However, there have been reports of refractory cardiogenic shock simulating septic shock. We report an 81-year-old male with the diagnosis of ANCA associated vasculitis. Rituximab 500 mg was administered intravenously for a relapse. The infusion proceeded without incident. However, 24 hours after its administration the patient began with fever, chills, coughing and strong malaise. The patient was transferred to the critical patient unit where a septic shock was suspected and resuscitative measures were started. However, the fast response to moderate doses of vasoactive drugs and complementary tests did not support an infectious etiology for the shock. Antimicrobials were discontinued and systemic corticosteroids were maintained, achieving remission of the symptoms. Shock as an unusual adverse reaction to Rituximab was suspected.

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Rituximab is a plausible alternative first-line treatment of ANCA-associated vasculitis. Adverse effects related to its infusion are common and usually have a benign course. However, there have been reports of refractory cardiogenic shock simulating septic shock. We report an 81-year-old male with the diagnosis of ANCA associated vasculitis. Rituximab 500 mg was administered intravenously for a relapse. The infusion proceeded without incident. However, 24 hours after its administration the patient began with fever, chills, coughing and strong malaise. The patient was transferred to the critical patient unit where a septic shock was suspected and resuscitative measures were started. However, the fast response to moderate doses of vasoactive drugs and complementary tests did not support an infectious etiology for the shock. Antimicrobials were discontinued and systemic corticosteroids were maintained, achieving remission of the symptoms. Shock as an unusual adverse reaction to Rituximab was suspected.

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ABSTRACT Kounis syndrome is defined as the coincidental occurrence of allergic reaction and acute coronary syndrome secondary to vasospasm. Anti-inflammatory drugs are included as one of the multiple causes. Current data available about this syndrome come from case reports. We present the case of a patient who suffered Kounis syndrome with cardiogenic shock and asystole after intravenous infusion of Metamizole, and in which no lesions were observed in coronariography.

RESUMO A síndrome de Kounis é definida como a ocorrência concomitante de reação alérgica e síndrome coronariana aguda secundária ao vasoespasmo. Os medicamentos anti-inflamatórios estão incluídos como uma das múltiplas causas. Os dados atuais disponíveis sobre essa síndrome são provenientes de relatos de caso. Relatamos o caso de um paciente que apresentou síndrome de Kounis com choque cardiogênico e assistolia após infusão intravenosa de metamizol e no qual não foram observadas lesões na coronariografia.

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Kounis syndrome is defined as the coincidental occurrence of allergic reaction and acute coronary syndrome secondary to vasospasm. Anti-inflammatory drugs are included as one of the multiple causes. Current data available about this syndrome come from case reports. We present the case of a patient who suffered Kounis syndrome with cardiogenic shock and asystole after intravenous infusion of Metamizole, and in which no lesions were observed in coronariography.

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Drug intoxication with disulfiram is a rare condition that may lead to severe and potentially fatal cardiovascular manifestations such as cardiogenic shock. We report the case of a female patient with refractory shock after deliberate self-poisoning with disulfiram. Clinical, biochemical and echocardiographic assessment, as well as invasive monitoring confirmed cardiogenic shock associated with this drug. The known mechanisms of action of disulfiram are discussed, and the major collateral effects, especially cardiovascular effects, are described. We underscore the importance of suspecting this diagnosis and of adopting prompt and the most adequate therapeutic approach in this context.

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A intoxicação medicamentosa por dissulfiram é uma situação rara, mas, que pode se apresentar com manifestações cardiovasculares graves e potencialmente fatais, como choque cardiogênico. É apresentado o caso de uma paciente com choque refratário, após intoxicação voluntária por dissulfiram. A avaliação clínica e bioquímica, junto à avaliação ecocardiográfica e à monitorização invasiva, confirmaram tratar-se de um choque cardiogênico associado a esse fármaco. São discutidos os mecanismos de ação conhecidos do dissulfiram e descritos os principais efeitos colaterais, especialmente os cardiovasculares, alertando para a importância da suspeição diagnóstica e da abordagem terapêutica imediata mais adequada nesse contexto.

Drug intoxication with disulfiram is a rare condition that may lead to severe and potentially fatal cardiovascular manifestations such as cardiogenic shock. We report the case of a female patient with refractory shock after deliberate self-poisoning with disulfiram. Clinical, biochemical and echocardiographic assessment, as well as invasive monitoring confirmed cardiogenic shock associated with this drug. The known mechanisms of action of disulfiram are discussed, and the major collateral effects, especially cardiovascular effects, are described. We underscore the importance of suspecting this diagnosis and of adopting prompt and the most adequate therapeutic approach in this context.

La intoxicación medicamentosa por disulfiram es una situación rara, aunque puede presentarse con manifestaciones cardiovasculares graves y potencialmente fatales, como el shock cardiogénico. Este relato presenta el caso de una paciente con shock refractario, tras intoxicación voluntaria por disulfiram. La evaluación clínica y bioquímica, junto a la evaluación ecocardiográfica y el monitoreo invasivo, confirmaron tratarse de un shock cardiogénico asociado a ese fármaco. A lo largo del presente relato se discuten los mecanismos de acción del disulfiram conocidos, así como se describen los principales efectos colaterales, específicamente los cardiovasculares. En este sentido, también se alerta para la importancia de la sospecha diagnóstica y del abordaje terapéutico inmediato más adecuado a este contexto.

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A inadvertently administrated high dose of sympathomimetic drug induced cardiogenic shock manifestations in a previously healthy woman. This state was characterized by EKG subendocardial injury, serum cardiac enzymes elevation, extensive regional left ventricular wall motion abnormalities on echocardiogram. Therapeutics included oxygen, systemic vasodilators and diuretics. Clinical recovery occurred over a four days period and parallels the normalization of echocardiogram and EKG alterations.

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UNLABELLED: Nineteen dogs in whom an intent to produce cardiogenic shock due to acute myocardial infarction are studied. The dogs are maintained with closed chest and acute myocardial infarction is produced by injecting a bolus of metalic mercury in the left circumflex coronary artery using two different methods. Comparatively, the results show that a more selective embolism is obtained with the double catheter technique than by the introduction of a single coronary arteriograph catheter. Eight of the 19 dogs died. Six due to accidental introduction of mercury in the anterior interventricular artery together with the left circumflex artery, and 2 due to rupture of the ascending aorta during the maneuvre of placing the coronary arteriograph catheter. In the eleven dogs that survived the following parameters were taken every hour during a period of four to six hours. a) Hemodynamic: Left ventricle pressure, cardiac output by thermodilution, maximum dp/dt and Vmax, central venous pressure, cardiac rate and diuresis; b) Metabolic: Gases and lactate in arterial, venous and coronary sinus blood. Cortisol blood levels. All dogs were anaesthetized with thiobarbital during the venous cutdown and later sedated with morfine. They were maintained breathing atmospheric air. Cardiogenic shock was established when the diuresis fell from 170 cc/hour to an average of 43 cc/hour, the mean arterial pressure fell by 20%, the cardiac output by 58%, Vmax descending 20%, the telediastolic pressure of the left ventricle rose from 2.8 mm. Hg to 19.6 mm. Hg and the presence of acidoses was demonstrated by metabolic studies. CONCLUSION: Since the dog is maintained with a closed chest and breathing atmospheric air, this is an excellent method for the production of cardiogenic shock in conditions similar to the humain without the influence of other variables. In this way a better knowledge of shock is obtained and different terapeutic measures can be studied.

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