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A fatal suicidal ingestion of drugs, together with activated charcoal, is reported. The death occurred 31 hours after the self-administration. The autopsy revealed a large amount of gastric content that appeared to be a compact mass of black color. Toxicologic analyses showed the presence of toxic levels of desalkylflurazepam and trazodone; metamizole and pridinol were also detected. The obtained results supported the hypothesis of a death due to acute intoxication delayed by the self-administration of activated charcoal, which elimination was probably hindered by the action of pridinol.

A fatality due to ingestion of flurazepam is reported. Flurazepam is a benzodiazepine, a widely prescribed hypnotic drug for use in sleep disorders. There are only few documented reports of the disposition of flurazepam in deaths due to overdose. A 68-year-old woman was found deceased at home with no evidence of trauma or asphyxia. Toxicologic analyses were performed and drug levels measured by means of gas chromatography coupled to mass spectrometry. The flurazepam concentration in each specimen was as follows: heart blood 2.8 microg/mL, bile 323 microg/mL, and urine 172 microg/mL. Presence of flurazepam into gastric content was observed too. Based on the autopsy findings, patient history, and toxicologic results, the cause of death was determined to be acute intoxication of flurazepam and the manner, suicide.

Flurazepam is a benzodiazepine (BZD) derivative and a category IV controlled substance. It is a widely prescribed hypnotic drug for use in sleep disorders. Two dogs were maliciously poisoned with this drug and died. Flurazepam was detected in the urine of 1 dog by thin-layer chromatography. Flumazenil, an antagonist for BZD receptors, is currently used in humans to reverse the effects of intoxication with BZD. It may also be of use in treating companion animals.

A fatality attributed to suicidal ingestion of up to 2.2 grams of flurazepam is described. The deceased was a 52-year old female with a history of depression and suicidal attempts. No significant pathology was found at autopsy. Full toxicological analyses detected only flurazepam and metabolites in her tissues. The concentrations of flurazepam in femoral blood, liver, bile, vitreous humor and urine were 5.5 mg/L, 130 mg/kg, 33 mg/L, 1.3 mg/L and 3.3 mg/L, respectively. Analysis of gastric contents showed 600 mg of flurazepam. Desalkylflurazepam was also detected in blood, liver, bile and vitreous, but at much lower concentrations than the parent compound.

The deliberate ingestion of household 'strong' bleach (NaOCl) caused severe metabolic disturbance. Hyperchloraemic acidosis was probably due to NaOCl reacting with hydrochloric acid in the stomach to form hypochlorous acid and chlorine. 'Strong' household bleach contains 10% NaOCl and this provides a large sodium load. The ingestion of 500 ml contained 673 mmol sodium and caused hypernatraemia.

The interactions between physostigmine and chlordiazepoxide, diazepam, flurazepam were experimentally evaluated in rats and mice by the following test: loss of righting reflex (LRR), acute toxicity, cardiovascular toxicity and EEG pattern. Physostigmine did not modify the duration of LRR produced by chlordiazepoxide. Conversely, the recovery after diazepam was significantly longer. The LD50 of diazepam and chlordiazepoxide were not modified by physostigmine administration, but that of flurazepam was significantly decreased. Heart rate and blood pressure did not change significantly with physostigmine pre-treatment. However, the total lethal dose was lowered for chlordiazepoxide and flurazepam. Only the reversal by physostigmine of the EEG pattern due to benzodiazepines, offers experimental support to the claimed usefulness of physostigmine in benzodiazepine intoxication in humans. Furthermore, the potentiation of flurazepam toxicity must be taken into account in the debate concerning the clinical advantages of physostigmine.

The case of an obtunded elderly woman is presented. The patient initially was thought to have suffered a cardiovascular accident but was discovered to have taken an overdose of flurazepam hydrochloride. Depression is a common and under-recognized problem in the geriatric population. As a consequence, suicide rates are highest in the elderly. Over- and underdosing of both prescription and nonprescription drugs are common means available to the suicidal elderly patient. These overdoses are often attributed to unintentional patient errors and overlooked for what they are, attempted suicides, or they are missed entirely as a cause of the patient's presentation. This case illustrates the need to consider drug overdose in the obtunded elderly patient.

A death case following a suicidal overdose of flurazepam (Dalmadorm) is reported. The body was found after 3 month near a highway. The course of the intoxication is in question as benzodiazepines are believed to be relatively save drugs. The death might have occured rapidly because of the acute toxic actions of the drug overdose as well as after a protracted course involving additional complications like inflammatory alteration of the myocard or hypothermia during a coma. Flurazepam and its major metabolites were analysed in blood and urine. The toxic levels of flurazepam (0.51 mg/l), N1-desalkylflurazepam (0.14 mg/1) and N1-hydroxyethylflurazepam (9.0 mg/1) in the blood amounted to 20--50 times higher than therapeutic levels, with flurazepam and metabolites being in only slight altered relation to each other. The overdose is considered to have been above 2.4 g (80 tablets). The resorption of the drug was complete. The analytical findings in blood and urine as well as in the GI-tract are in satisfactory agreement. The analytical data of flurazepam and its metabolites are discussed in detail, taking metabolic and pharmacokinetic parameters, autopsy findings and case circumstances into consideration. A final decision about the course of the intoxication is not possible. This case shows however the fatal consequences of a flurazepam overdose although alcohol or other drugs were not involved.

Flurazepam hydrochloride is a benzodiazepine derivative marketed for use as a hypnotic agent. Flurazepam is more effective than placebo and is as effective as other hypnotic drugs in most short-term controlled studies. In long-term dosage studies, flurazepam's efficacy persists while other hypnotics become ineffective. Flurazepam has relatively minor effects upon rapid eye movement (REM) sleep and does not lead to REM rebound; this may reduce the likelihood of drug dependence. Flurazepam does not cause enzyme induction and probably presents little hazard of abuse or overdosage. The rational use of hypnotic agents depends as much upon the underlying cause of the sleep disorder as upon the choice of a particular drug. When hypnotic therapy is indicated, flurazepam appears to have advantages over other drugs currently available in the United States.

Eight patients with drug intoxication were hemoperfused on ten occasions at a blood-flow rate of 300 ml/min with a 650gm column of Amberlite XAD-4 resin, which is a macroreticular resin with a specific adsorptive attraction for lipid-soluble organic molecules. Column clearances of glutethimide and a variety of barbiturates ranged from 207 to 300 ml/min for treatment sessions extending from 2 1/2 to ten hours. After ingestion of 75 gm of glutethimide, one patient received hemoperfusion on three successive days for nine, ten, and eight hours, respectively. She recovered after the column removed over 30 gm of drug. The patients demonstrated dramatic clinical responses with no evidence of meaningful toxic reactions. Column hemoperfusion with Amberlite XAD-4 resin was simpler and more effective than any known method of removing barbiturates and glutethimide from the blood of patients with drug overdoses.