Cardiogenic shock caused by disulfiram

Cardiogenic shock caused by disulfiram


Ana Jerónimo; Carla Meira; Augusta Amaro; Glória Cabral Campello; Cristina Granja
Serviço de Cuidados Intensivos, Hospital Pedro Hispano, Matosinhos - Portugal
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SUMMARY
Drug intoxication with disulfiram is a rare condition that may lead to severe and potentially fatal cardiovascular manifestations such ascardiogenic 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.
Key Words:Shock, cardiogenic; disulfiram/poisoning, adverse effects.
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Introduction
Deliberate self-poisoning is an important health problem worldwide, with a substantial number of patients requiringadmission in Intensive Care Units (ICU) due to coma or hemodynamic instability. Antidepressants, benzodiazepines and organosphosphates are the most frequently used drugs, commonly associated with each other or with alcoholic beverages1. Deliberate self-poisoning with disulfiram is uncommon, but the severity of the acute complications requires that its toxic effects be recognized.
Disulfiram, whichis used for the treatment of alcoholism, exerts its action when taken concomitantly with alcohol. It irreversibly inhibits the aldehyde dehydrogenase enzyme which is responsible for ethanol metabolization, thus leading to increased serum concentration of the metabolite acetaldehyde, whose toxicity results in the "acetaldehyde syndrome". The typical reaction is self-limited, with headache, flushing,dizziness, nausea, blurred vision, tremor and dyspnea2. When not associated with alcohol ingestion, its effects are scarce at usual daily doses. Acute intoxication at doses higher than 500 mg/day, in turn, may result in severe collateral effects, and can be lethal at doses between 10-30g/day3.

Case Report
A 49-year-old female patient with major depression and chronic alcoholism was admittedto the emergency room four hours after deliberate ingestion of 60 disulfiram tablets (15g), 16 clonazepam tablets (8mg) and six maprotiline tablets (450mg), in association with alcohol.
Her clinical examination was notable for sleeplessness, tachypnea, and poor peripheral perfusion. Blood pressure: 68 x 35mmHg; heart rate: 105 bpm. Pulmonary auscultation revealed diffuse coarse crackles.Laboratory studies were significant for increased C-reactive protein (CRP) - 31 mg/dL. Her blood gas showed severe hypoxemia (PaO2 66 mmHg, with FiO2 85%).
Markers of myocardial ischemia resulted negative. Electrocardiography showed sinus tachycardia, with no changes consistent with acute ischemia. Chest radiography showed alveolar opacities bilaterally (Figure 1).
Volume resuscitation measures wereintroduced immediately, followed by dopamine. Blood cultures were collected and broad-spectrum antibiotic therapy was started. Despite these measures, the patient remained in refractory shock and progressed with worsening of the respiratory distress and increasing desaturation. Orotracheal intubation was required and mechanical ventilation was started. The patient was transferred to the ICU.
Theclinical picture was initially interpreted as mixed - cardiogenic and septic - shock. Sepsis was assumed as the major component, having possibly originated from aspiration pneumonia due to prostration. The cardiogenic component could result from the collateral effects of the medications taken.
In order to clarify the degree of cardiac involvement, an echocardiography was performed, showing...