Acute intoxication with doxazosin.

Experience with overdosage and toxicity with the alpha-adrenoreceptor antagonists remains very limited in the literature. In this paper, the second case in the literature with doxazosin overdosage is reported. Supportive treatment was given to the patient and the patient was discharged 48 hours after admission to the emergency department.

Poisoning with anti-hypertensive drugs: alpha-adrenoceptor antagonists.

Experience with overdosage and toxicity with the alpha (alpha)-adrenoceptor antagonists remains very limited, and all the cases in the literature relate to prazosin overdosage. The selective alpha-blocker appears, however, to have a low acute toxicity. Supportive therapy by the reduction of gastrointestinal absorption, monitoring of vital signs and the correction of hypotension (with intravenous fluids) is indicated.

A fatal case of buflomedil self-poisoning: toxicological data and literature review.

A fatal case of buflomedil (Fonzylane) self-poisoning is presented. Drug identification and quantification in postmortem blood, urine and gastric contents was achieved by means of high pressure liquid chromatography with diode-array detection (HPLC/DAD). Blood concentration was 275 micrograms/ml, > 70 times the usual therapeutic values. Toxicological results are discussed in the light of the existing literature.

Torsade de pointes: a severe and unknown adverse effect in indoramin self-poisoning.

We report the two first cases of torsade de pointes associated with QT interval prolongation following a large ingestion of indoramin.

Acute neurotoxicity after yohimbine ingestion by a body builder.

Yohimbine is an alkaloid obtained from the Corynanthe yohimbe tree and other biological sources. Yohimbine is currently approved in the United States for erectile dysfunction and has undergone resurgence in street use as an aphrodisiac and mild hallucinogen. In recent years yohimbine use has become common in body-building communities for its presumed lipolytic and sympathomimetic effects. We describe a 37-year-old bodybuilder in which severe acute neurotoxic effects occurred in 2 h after yohimbine ingestion. The patient presented with malaise, vomiting, loss of consciousness, and repeated seizures after ingestion of 5 g of yohimbine during a body-building competition in a gymnasium. His Glasgow Coma Score was 3, requiring orotracheal intubation. Two hours after admission, vital signs were blood pressure 259/107 mmHg and heart rate 140 beats/min. Treatment with furosemide, labetalol, clonidine, and urapidil and gastrointestinal decontamination were performed. Twelve hours later the patient was extubated with normal hemodynamic parameters and neurological examination. The yohimbine blood levels at 3, 6, 14, and 22 h after ingestion were 5,240; 2,250; 1,530; and 865 ng/mL, respectively, with a mean half-life of 2 h. Few data are available about yohimbine toxicity and the related blood levels. This is a case of a large ingestion of yohimbine in which severe hemodynamic and neurological manifestations occurred and elevated blood levels of yohimbine were detected.

Carvedilol overdose with quantitative confirmation.

Carvedilol is a non-selective beta-adrenoreceptor antagonist that is also an antagonist at the alpha(1)-adrenoreceptor. This unique pharmacological effect may produce a different toxicodynamic profile compared to other beta-adrenoreceptor antagonists. Only one previous case of carvedilol overdose has been reported. Here, we report massive carvedilol ingestion confirmed by quantitative analysis. The case report deals with an 84-year-old man who chewed a total of 60 (6.25 mg) tablets and rapidly developed symptoms. Vital signs on presentation were systolic blood pressure 70 mmHg; heart rate 45 beats/min.; respirations 18 breaths/min.; temperature 37 degrees . The electrocardiogram showed a junctional rhythm at 49 beats/min. The patient was treated with normal saline boluses, repeated glucagon boluses (2-3 mg each) and a dopamine infusion. At 14 hr after ingestion, he was weaned off vasopressors and was in a normal sinus rhythm. Quantitative confirmation showed a carvedilol serum concentration of 472 ng/ml (steady-state concentration 8.5 ng/ml during 6.25 mg twice daily dosing). Despite its unique pharmacological properties, the clinical manifestations of carvedilol overdose appear similar to other beta-adrenoreceptor antagonists.

[Vasopressin analogue injection as ultimate measure for counteracting severe catecholamine-refractory poisoning by several vasodilators taken with suicidal intent]. / Vasopressinanaloga als Ultima ratio bei einer schweren Intoxikation mit Vasodilatanzien.

HISTORY AND CLINICAL FINDINGS: A 78-year-old woman was admitted to the intensive care unit 9 hours after ingestion of 2 g of isosorbitmononitrate, 430 mg of amlodipine, 250 mg of benazepril and 600 mg of mirtazapin in suicidal intent. INVESTIGATIONS: Clinical findings and invasive monitoring showed signs of a hyperdynamic hemodynamic cardiovascular failure caused by toxic vasodilatation. TREATMENT AND COURSE: Despite of primary detoxication, intravenous volume infusion with calcium gluconate, glucagon and naloxone and administration (norepinephrine up to 2 micro g/kg/min) no hemodynamic stabilization was achieved. Only when the vasopressin-analogue argipressin was given peripheral vasodilatation was overcome and hemodynamic stabilization resulted. 10 hours after discontinuing argipressin and norepinephrine the patient developed a mesenteric ischemia, and she finally died on the third day after admission. CONCLUSION: In circulatory shock due to toxic vasodilatation the use of vasopressin analogue argipressin can be helpful as an ultima therapeutic measure in catecholamine refractory shock caused by vasodilatation. Attention must be paid to overwhelming vasoconstrictor effects resulting in mesenteric ischemia.