[Intoxication of female patient with generalised cancer in hospital--a case report]. / Zatrucie pacjentki z uogólniona choroba nowotworowa w szpitalu--opis przypadku.

Medical errors are crucial factors influencing hospital mortality. We present a case of 79-year-old female, who was admitted to the hospital due to complications associated with advanced cancer disease. After several days of hospitalization, the woman died as a result of cancer as well as severe drugs intoxication. The investigation showed extremely high concentrations of chlorprothixen and tramadol in the. blood of the patient. This paper describes a number of medical errors made by hospital staff, of which the most significant was an inappropriate drugs policy.

Black esophagus: acute esophageal necrosis in fatal haloperidol intoxication.

Herein, we present a case of 53-year-old psychotic woman with acute esophageal necrosis (black esophagus), who was found lying on the floor in the living room of her flat. Pillboxes of antipsychotic drugs were located in the bin. External examination of the body was unremarkable. On internal examination, we found acute esophageal necrosis. Histologically, there was complete epithelial necrosis with focal involvement of muscularis mucosae, dense infiltrate of leukocytes, and ulcerations without any viable cells. There was no evidence of underlying organic diseases or trauma. Toxicological analysis revealed a fatal blood level of antipsychotics (haloperidol, zotepine, and chlorprothixene). Death of the deceased was attributed to fatal intoxication with three various types of antipsychotics. As far we know, this is the first described association between so-called black esophagus and fatal blood level of neuroleptics.

Acute oliguria associated with chlorprothixene overdosage.

The occurrence of acute reversible oliguria is described in a 23-year-old male after ingestion of 1,500 mg of chlorprothixene in a suicidal attempt. In contrast to earlier reports hypothesizing that the pathophysiology of the renal insufficiency associated with chlorprothixene intoxication may be attributed to direct nephrotoxic effects of the compound or to ischaemia owing to transitory unrecognized shock, a careful diagnostic work-up including renal biopsy, disclosed the presence of acute interstitial nephritis.

Hemoperfusion in severe chlorprothixene overdose.

Two to twelve hours after suicidal ingestion of an estimated dose of 10 g chlorprothixene, a 31-year-old female was admitted to the emergency ward of the clinic with cardiorespiratory arrest. After successful resuscitation, the further clinical course was complicated by persistent ventricular extrasystoles and ventricular fibrillation which necessitated repeated defibrillation. Since the patient did not respond satisfactorily to supportive treatment, a combined hemoperfusion/hemodialysis was performed. Under extracorporeal detoxication, elimination of chlorprothixene from plasma was accompanied by substantial improvement of the patient's clinical condition, although only about 1.6% of the estimated dose had been removed. This case seems to indicate that evaluation of the therapeutic efficacy of hemoperfusion should not be based exclusively on the relation of the amount of the eliminated drug to total absorbed dose.

Determination of chlorprothixene and its sulfoxide metabolite in plasma by high-performance liquid chromatography with ultraviolet and amperometric detection.

This communication describes a rapid, sensitive and selective method for the assay of chlorprothixene and its sulfoxide metabolite in human plasma, using reversed-phase high-performance liquid chromatography. Alkalinized plasma was extracted with heptane--isoamyl alcohol (99:1), after addition of thioridazine as the internal standard. The residue obtained after evaporation of this extract was chromatographed on a cyano column, using acetonitrile--0.02 M potassium dihydrogen phosphate pH 4.5 (60:40) as the mobile phase with ultraviolet (229 nm) detection. Quantitation was based on peak height ratios over the concentration range of 5.0-50.0 ng/ml for both compounds with 85% and 90% recovery for chlorprothixene and its sulfoxide metabolite, respectively, using a 1.0-ml plasma sample. The assay chromatographically resolves chlorprothixene and the sulfoxide metabolite from the N-desmethyl metabolite, which can only be semi-quantitated owing to low and variable recoveries. The method was used to obtain plasma concentration versus time profiles in two subjects after oral administration of 100 mg of chlorprothixene suspension and in two additional subjects following overdosages of chlorprothixene estimated to exceed several hundred milligrams. These analyses demonstrated that the sulfoxide metabolite is the predominant plasma component following therapeutic administration and overdosages. High-performance liquid chromatography with oxidative amperometric detection with the glassy carbon electrode was also evaluated. Although this procedure demonstrated comparable sensitivity and precision to ultraviolet detection for the analysis of chlorprothixene and N-desmethyl chlorprothixene, the sulfoxide metabolite could not be measured with high sensitivity (less than 100 ng/ml) owing to endogenous interferences. Hence the utility of this alternative assay technique is limited.

Chlorprothixene and chlorprothixene-sulfoxide in body fluids from a case of drug overdose.

A case of fatal drug overdose involving chlorprothixene is presented. Chlorprothixene and chlorprothixene sulfoxide (CPT-SO) metabolite concentrations (mg/L) in body fluids as determined by spectrophotofluorometry were: blood, 0.10 and 0.60; bile, 3.9 and 7.0; urine, 0.4 and 3.4; and stomach contents, 340 mg and 25 mg total, respectively. Qualitative identification of chlorprothixene and CPT-SO was by thin layer and gas liquid chromatography and spectrophotofluorometry following alkaline permanganate oxidation.

[New aspects of chlorprothixen-poisoning (author's transl)]. / Neue Aspekte der Chlorprothixenvergiftung.

Over the past 8 years the Poison Information Centre of Vienna was confronted 24 times with acute chlorproxithene (CPTX) poisoning. In adults doses of 2 g and more caused severe intoxication, but serious toxic manifestations were observed already at low dosage in children (after the ingestion of less than 5 mg/kg body weight). In one case unexpected death due to cardiac failure occurred as long as 49 hours after CPTX intake. The favorable outcome in one patient treated with gut, as well as gastric lavage indicates that this therapeutic strategy may be of value in the management of CPTX intoxication.

Identification of 2-chlorothioxanthen-9-one in gastric aspirate in a case of chlorprothixene poisoning.

In gastric aspirate from a case of severe chlorprothixene poisoning, large amounts (approximately 30% of the chlorprothixene) of a previously unrecognized compound were found and identified tentatively as 2-chlorothioxanthen-9-one by combined GLC-low-resolution mass spectrometry and high-resolution mass spectrometry. The identity of the unknown compound was verified after synthesis of 2-chlorothioxan-then-9-one by two procedures. Only negligible amounts of 2-chlorothioxanthen-9-one were formed when chlorprothixene, dissolved in acids, bases, chloroform-isopropanol, methanol, or gastric fluid, was stored in the dark. However, large amounts of the drug were converted to 2-chlorothioxanthen-9-one upon exposure to UV light. Moreover, considerable quantities of unidentified degradation products were formed when chlorprothixene was exposed to lamp light as well as to UV light. Therefore, samples from cases of acute drug poisoning should be protected from light until analysis.

The pathophysiology of acute renal failure after chlorprothixene overdosage.

Renal failure after an overdose of chlorprothixene has been attributed to a direct nephrotoxic effect of the drug. We report a carefully investigated case. No evidence of specific nephrotoxicity was revealed and we suggest that the renal failure is due to ischaemia during a transitory syncope, a well known side-effect of chlorprothixene.

[Tricyclic psychotropic drugs: complications and therapy of Choloprothixen-intoxication (author's transl)]. / Intoxikationen mit trizyklischen Psychopharmaka. Komplikationen und Therapie

The broad use of tricyclic psychotropic drugs demands from the physician to take in account the side effects of these drugs. These side effects relate primarily to the cardiovascular system. We describe a suicidal Chlorprothixen(Taractan-)intoxication of a 27 year old female patient. The progress of this intoxication was characterized by severe arrhythmias, mainly ventricular tachycardias. The pathogeneisis of the cardiotoxic reaction is discussed. Since there is no specific antidot against these drugs, therapy of side effects is limited to symptomatic treatment including administration of cholinergic drugs. Severe cardiovascular reaction also can be found, when the drugs are used in therapeutic doses. The cardiodepressive effect of tricyclic psychotropic drugs may lead to considerable complications, especially in older patients.