Disulfiram ethanol reaction mimicking anaphylactic, cardiogenic, and septic shock.

Shock is a common reason for medical intensive care unit admission, with septic and cardiogenic accounting for most of the etiologies. However, the potential severity of adverse side effects of drugs indicates that any medication should be carefully scrutinized for potential pharmacokinetic and pharmacodynamic interactions that may result. We herein report the case of a life-threatening shock mimicking successively anaphylactic, cardiogenic, and septic shock, which was finally related to disulfiram ethanol reaction. Indeed, disulfiram ethanol reaction is known to provoke unpleasant symptoms through vasodilatation in various organs. However, extreme manifestations of vasodilatory shock may lead to circulatory failure and lactic acidosis. Because of large prevalence of alcoholism and disulfiram medication, emergency physicians and medical specialists should be aware of this life-threatening condition, with its misleading presentation.

Delayed and prolonged coma after acute disulfiram overdose.

We report the case of a 35-year-old man presenting with a delayed and prolonged coma due to an intentional overdose with disulfiram without simultaneous alcohol ingestion. The clinical features--comprising a severe toxic encephalopathy with coma and convulsions, in combination with a quadriparesis outlasting the loss of consciousness--are summarized, and the physiopathology is reviewed.

Cardiogenic shock caused by disulfiram.

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.

Choque cardiogênico por dissulfiram / Cardiogenic shock caused by disulfiram / Shockcardiogénico por disulfiram

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.

Acute vocal fold palsy after acute disulfiram intoxication.

Acute peripheral neuropathy caused by a disulfiram overdose is very rare and there is no report of it leading to vocal fold palsy. A 49-year-old woman was transferred to our department because of quadriparesis, lancinating pain, sensory loss, and paresthesia of the distal limbs. One month previously, she had taken a single high dose of disulfiram (130 tablets of ALCOHOL STOP TAB, Shin-Poong Pharm. Co., Ansan, Korea) in a suicide attempt. She was not an alcoholic. For the first few days after ingestion, she was in a confused state and had mild to moderate ataxia and giddiness. She noticed hoarseness and distally accentuated motor and sensory dysfunction after she had recovered from this state. A nerve conduction study was consistent with severe sensorimotor axonal polyneuropathy. Laryngeal electromyography (thyroarytenoid muscle) showed ample denervation potentials. Laryngoscopy revealed asymmetric vocal fold movements during phonation. Her vocal change and weakness began to improve spontaneously about 3 weeks after transfer. This was a case of acute palsy of the recurrent laryngeal nerve and superimposed severe acute sensorimotor axonal polyneuropathy caused by high-dose disulfiram intoxication.

Sobredosis de ciamida cálcica (carbimida): descripción de un caso y revisión bibliográfica / Carbimide overdosage: description of a case and review of the literature

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[Imaging in acute toxic encephalopathy]. / Imagerie des encephalopathies toxiques aigues.

Neuroimaging, particularly MR imaging, plays a major role for the diagnosis of many acute toxic encephalopathies. Toxic disorders are related to drugs (immunosuppressive agents, chemotherapeutic agents, anti-epileptic drugs, heroin...), to metals (lead, manganese, mercury...), and to industrial and environmental chemicals (solvent, carbon monoxide...). MR imaging with diffusion and perfusion imaging provides information regarding brain lesions induced by the toxic agents (vasogenic edema, cytotoxic edema, infarction, hemorrhage, demyelination...).

Systemic hemodynamic effects of treatment with the molecular adsorbents recirculating system in patients with hyperacute liver failure: a prospective controlled trial.

The aim of the study is to evaluate the effect of a single treatment with the molecular adsorbents recirculating system (MARS) on systemic hemodynamics and oxygen consumption (VO(2)) in patients with hyperacute liver failure (HALF). In a controlled design, eight patients with HALF were assigned to a 6-hour MARS treatment, and five patients, to a control group that was mechanically cooled to match the MARS group. Systemic hemodynamic variables were determined hourly during the study period. In the MARS group, systemic vascular resistance index increased by 46% from 1,215 +/- 437 to 1,778 +/- 710 dynes x s x cm(-5) x m(-2) (P <.0001), which significantly exceeded a 6% increase in the control group. Mean arterial pressure increased from 69 +/- 5 to 83 +/- 11 mm Hg in the MARS group (P <.0001) and was unchanged in the control group. Cardiac index decreased by 20% from 4.6 +/- 1.8 to 3.7 +/- 1.1 L/min x m(-2) (P =.0007) in the MARS group and by 7% in the control group. Heart rate decreased from 105 +/- 21 to 85 +/- 15 beats/min in the MARS group (P <.0001) and was unchanged in the control group. In the MARS group, oxygen delivery decreased from 621 +/- 198 to 486 +/- 141 mL/min x m(-2) (P <.05), and VO2, from 142 +/- 31 to 112 +/-21 mL/min x m(-2) (P <.05). Arterial lactate and pH levels were unchanged. In conclusion, systemic hemodynamic values tend to normalize, whereas systemic VO(2) decreases during MARS treatment in patients with HALF. These effects cannot be explained by the degree of cooling associated with MARS.

[Acute disulfiram intoxication with severe neurological sequaelae and presenting misleading psychiatric deficiency]. / Intoxication aiguë au disulfirame avec séquelles neurologiques graves et présentation psychiatrique déficitaire trompeuse.

Disulfiram self poisoning is exceptional. The authors report on the case of such an intoxication related to the ingestion of a potentially lethal dose of this drug (30 g) and draw the attention on the following points: 1) The initial signs may be misleading because they include both psychiatrics and neurological signs such as phonation abnormalities, myoclonias and tetraparesia. 2) The evolution is unforseeable with the possible occurrence of severe psychological and motricity sequaelae, associated with bilateral and symetric injuries of the putamen, the palladium and the basal nuclei on CT-scan (or MRI). The pathophysiologic al mechanisms of theses signs are discussed, and the need for disulfiram in the care of alcoholic patients seeking for withdrawal as well.

Differential mechanisms in the effects of disulfiram and diethyldithiocarbamate intoxication on striatal release and vesicular transport of glutamate.

Intoxication with the alcohol-aversive drug disulfiram (Antabuse) and related dithiocarbamates may provoke neuropathies and, in some cases, damage the basal ganglia. Rats received a single administration of disulfiram (7 and 500 mg kg-1 i.p.) and equimolar doses (4 and 290 mg kg-1 i.p.) of its metabolite diethyldithiocarbamate (DDC), roughly corresponding to the daily maximum dose in alcohol abusers or to an estimated nonlethal overdose, respectively. The striatal, extracellular levels of glutamate in freely moving rats previously implanted with a microdialysis probe increased after low and intoxicating doses of disulfiram (126 +/- 3% and 154 +/- 10% of basal values, respectively) and DDC as well (135 +/- 10% and 215 +/- 14%, respectively), a partially Ca++-dependent effect. The prolonged (>7 hr) disulfiram-induced increase in glutamate observed in vivo may reflect the in vitro disulfiram-evoked release of glutamate from striato-cortical synaptic vesicles, where the drug nonspecifically inhibited (Ki approximately 4 microM) the uptake function and abolished the transmembrane proton gradient (DeltapH). In contrast, DDC did not seem to affect DeltapH. The prompt DDC-provoked increase in extracellular levels of glutamate was prevented by 7-nitroindazole, an in vivo specific inhibitor of neuronal nitric oxide synthase, which suggests that the thiol metabolite also acts via the nitric oxide synthesis. At variance, the short-acting 7-nitroindazole did not prevent the sustained in vivo effects of disulfiram and of DDC putatively formed with time. These findings provide new evidence for differential mechanisms underlying disulfiram- and DDC-induced increases in striatal glutamate release. Present glutamatergic changes, although not appearing dramatic enough to represent the only cause for neuronal damage from disulfiram overdose, might contribute to the drug neurotoxicity.

[Acute and reversible myoclonic encephalopathy, extrapyramidal syndrome, polyneuropathy caused by chronic disulfiram poisoning]. / Encéphalopathie myoclonique, syndrome extrapyramidal, polyneuropathie aigus et réversibles par intoxication chronique au disulfiram.

This 44-year woman was admitted for weight loss and global intellectual slowing. She had mild chronic alcoholic neuropathy. She was discontinued alcoholic consumption for 6 months and was given disulfiram (1.5 g/day) since then. She developed over a 5-day period acute neuropathy, confusion and extrapyramidal symptoms with oculo-cephalogyric and dystonic movements and myoclonus. Electromyography revealed a severe polyneuropathy. After disulfiram withdrawal, confusion and extrapyramidal symptoms disappeared within a few days, but sensitivo-motor deficit improved more slowly. Nerve biopsy was suggestive of a pure axonal neuropathy.

Acute encephalopathy and polyneuropathy after disulfiram intoxication.

A chronic alcoholic who had ingested a very high dose of disulfiram (29 g over a 1-week period) without simultaneous alcohol intake developed an acute encephalopathy and a severe flaccid tetraparesis that worsened over the course of several days, even after the intake of the drug had stopped. Recovery was both slow and incomplete. One year after intoxication, the patient still had distal weakness in the arms and legs, and hypesthesia in the hands and feet.