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Biomedical subjects

C Köppel

Publications and source records attributed to C Köppel.

At least 37 records · Page 2Linked to original sources
PubMed1991

Acute poisoning with bromofosmethyl (bromophos).

One hour after suicidal ingestion of about 20 mL of a 38% solution of bromofosmethyl, CAS: 2104-96-3 (bromophos), a 52 year-old female was admitted to the hospital with extreme miosis, hypersalivation, hyperperistalsis and muscular fibrillation. Gastric lavage was performed and activated charcoal administered. Cholinergic symptoms were antagonized by repeated doses of 0.5 mg atropine. Because of the high dose of bromophos, hemoperfusion was performed with amberlite XAD4. The bromophos clearance during hemoperfusion was 95 mL/min (flow 200 mL/min). The patient received two doses of 500 mg obidoxime for recurrent muscular fibrillation. The further clinical course was uneventful. On day 4, the patient was transferred to a psychiatric ward because of persistent suicidality. In contrast to poisoning by most organophosphates, red blood cell acetyl cholinesterase was only minimally depressed but the plasma butyryl cholinesterase was initially decreased and normalized within a few days. The records of 25 patients reported to our Poison Control Center with ingestion of more than 1 g bromophos were also evaluated. The most frequent symptoms were miosis, hyperperistalsis, hypersalivation, agitation, nausea/vomiting and convulsions. Nine of the patients had no symptoms. Bromophos is relatively less toxic than its phosphate derivative, parathion.

Adolescent↗
PubMed1990

Suicidal ingestion of formalin with fatal complications.

After ingestion of an unknown amount of formalin with suicidal intent, a 55-year-old female and a 34-year-old male were admitted to the hospital with extensive gastrointestinal corrosive damage, circulatory shock, metabolic acidosis, respiratory insufficiency and impairment of renal function, which rapidly progressed to acute renal failure. Metabolic acidosis was in part due to high plasma levels of formic acid, the main metabolite of formaldehyde, and hyperlactatemia. Both patients underwent hemodialysis and hemofiltration treatment. In the male patient, a gastrectomy had to be performed. The further clinical course in the patients was characterized by sepsis and protracted pulmonary complications. Both patients died after developing adult respiratory distress syndrome and global cardiac insufficiency. In vitro experiments on formaldehyde reactivity to proteins yielded evidence for almost complete but reversible binding to plasma and blood. Formaldehyde probably exerts systemic toxicity in the form of its labile Schiff's base with proteins, but not as free formaldehyde.

Adult↗
PubMed1990

Clinical experience with the benzodiazepine antagonist flumazenil in suspected benzodiazepine or ethanol poisoning.

The clinical efficacy of different doses of the specific benzodiazepine antagonist flumazenil was studied in a total of 72 patients with benzodiazepine or ethanol overdose. In a randomized double-blind study, 18 patients (group 1) and eight patients (group 2) with suspected benzodiazepine overdose received 5 mg (group 1) or 1 mg (group 2) flumazenil or placebo, respectively. The stage of coma, heart rate, blood pressure and respiratory rate were monitored within the following 15 min. If no change in the stage of coma was observed, 5 mg (group 1) or 1 mg (group 2) flumazenil were given, and the stage of coma, heart rate and blood pressure were again monitored. In a similar way, the effect of 5 and 1 mg flumazenil was investigated in 13 patients (group 3) and four patients (group 4) with ethanol intoxication. In an open trial, the clinical efficacy of flumazenil for the diagnosis of benzodiazepine or ethanol overdose was studied in 29 patients (group 5). In all patients, a toxicological screening confirmed benzodiazepine or ethanol overdose. None of the patients receiving placebo showed effects on stage of coma, heart rate, blood pressure or respiratory rate. Patients with benzodiazepine overdose who received 5 mg flumazenil regained consciousness about 1-2 min after the end of injection. The effect of 1 mg flumazenil (group 2) on benzodiazepine-induced coma was less pronounced. In patients with ethanol overdose (group 3), ethanol-induced coma was reversed after 5 mg flumazenil more slowly than in patients of group 1. No effect of flumazenil on ethanol-induced coma was observed in group 4. In group 5, flumazenil proved to be useful for diagnosing benzodiazepine or ethanol intoxication. In one patient with coma due to carbamazepine overdose, flumazenil was also found to be effective. Additionally, a possible analytical interference of flumazenil and its metabolites with the identification of other benzodiazepines by a toxicological screening procedure was studied. Even after an oral dose of 200 mg flumazenil, no interference with immunological benzodiazepine assays (EMIT, TDX, and RIA) was found. A metabolite and an artifact of flumazenil could be identified in urine by gas chromatography/mass spectrometry.

Adolescent↗
PubMed1990

Clinical course and outcome in class IC antiarrhythmic overdose.

120 cases of class IC antiarrhythmic overdose, including propafenone, flecainide, ajmaline and prajmaline overdose, were evaluated with respect to clinical course, therapy and outcome. Whereas drug overdose in general has an overall mortality of less than 1%, intoxication with antiarrhythmic drugs of class IC was associated with a mean mortality of 22.5%. Nausea, which occurred within the first 30 minutes after ingestion, was the earliest symptom. Spontaneous vomiting probably led to self-detoxication in about half the patients. Cardiac symptoms including bradycardia and, less frequently, tachyrhythmia occurred after about 30 minutes to 2 hours. Therapeutic measures included administration of activated charcoal, gastric lavage and a saline laxative, catecholamines, and in some patients, hypertonic sodium bicarbonate, insertion of a transvenous pacemaker and hemoperfusion. Fatal outcome was mainly due to cardiac conduction disturbances progressing to electromechanical dissociation or asystolia. Resuscitation, which had to be performed in 29 patients, was successful in only two of them. No correlation was found between fatal outcome, the type of antiarrhythmic, and ingested dose. Since a specific treatment is not available and resuscitive procedures including sodium bicarbonate and insertion of a pacemaker are of limited therapeutic value, early diagnosis and primary detoxification are most important for prevention of fatal outcome.

Ajmaline↗
PubMed1989

[Initial experiences with the Reiber 1979 determination of autochthonous IgG production within the scope of clinical and immunologic follow-up studies in multiple sclerosis treated with immunosuppressive therapy].

We carried out clinical and immunological follows-up to 21 patients suffering from multiple sclerosis, 16 of whom had been immunosuppressively treated. A remission in clinical way was possible to point out with 8 of 12 patients (66%) -average remission by 1 score acc. to the Bronx-Scale- and with these patients a local formation of immunoglobulin acc. to Reiber (1979) could be proven. With 40 to 60% of the patients pathological changes were found out by determining of routine parameters by means of liquor examinations (total number of cells, sediment, total protein, electrophoresis) in which the humoral values responded not so sensitively to immunosuppressive therapy than the cellular values. For the present, liquor- and immunodiagnostic is being considered as a solid part of diagnostic programm and therapy control with regard to patients suffering from multiple sclerosis.

Azathioprine↗
PubMed1988

Acute trichloroethylene poisoning with additional ingestion of ethanol--concentrations of trichloroethylene and its metabolites during hyperventilation therapy.

One hour after suicidal ingestion of about 150 g of trichloroethylene, a 32-year-old male was admitted to hospital. On admission, the patient's state of consciousness deteriorated from somnolence to coma. Based on blood level data, an absorbed trichloroethylene dose of at least 35 g was estimated. Additionally, ethanol, which is a strong inhibitor of trichloroethylene metabolism, had been ingested. With respect to the high dose of trichloroethylene, hyperventilation therapy was performed for 28 h. Concentrations of trichloroethylene and its metabolites in blood and urine were determined by gas chromatography. Due to hyperventilation and inhibition of trichloroethylene metabolism, not more than 30% of the absorbed dose was metabolized and excreted via kidneys. Under normal respiratory conditions and in the absence of ethanol, this fraction amounts to about 75%. Obviously, hyperventilation and ethanol-induced inhibition of metabolism led to considerably enforced pulmonary elimination of the absorbed trichloroethylene.

Adult↗
PubMed1988

Hemoperfusion in acute camphor poisoning.

After ingestion of an unknown dose of a 10% camphor spirit (maximum dose 200 ml), a 54-year-old female was found in coma, having developed grand-mal-like seizures and respiratory failure. For detoxification, gastric lavage and hemoperfusion with amberlite XAD4 were performed. During hemoperfusion, seizures ceased, but no marked influence on the clinical course of the intoxication--especially on grade of coma--was observed. For further evaluation of the efficacy of treatment, camphor plasma elimination kinetics during hemoperfusion were compared to plasma elimination kinetics determined in a volunteer after an oral dose of 200 mg of camphor. Although the plasma compartment was almost completely (89%-95%) cleared of camphor by hemoperfusion, only a total of 35 mg of camphor was removed due to its high apparent volume of distribution (estimated 2-4 l/kg). The plasma elimination half-life was not affected by hemoperfusion, which may be explained by the saturation of metabolizing enzymes, still incomplete absorption, or metabolic interference of isopropanol. In the case presented here, neither the clinical course of the intoxication nor plasma level data gave evidence for a pronounced beneficial effect of hemoperfusion.

Acute Disease↗
PubMed1988

Inadvertent metal loading of critically ill patients with acute renal failure by human albumin solution infusion therapy.

Recent reports on the metal contamination of human albumin solutions (HAS) have raised concern about possible medical implications. Large amounts of HAS are infused to premature babies with respiratory distress syndrome, patients with plasmapheresis treatment or acute renal failure. For assessment of the risk of metal loading in patients with acute renal failure, commercially available HAS were analyzed for aluminium, nickel, chromium, manganese, cobalt, zinc, copper, cadmium, lead, and mercury. A considerable contamination of HAS was found for Al, Ni, Cr, Mn, and in part for Co. Additionally, the influence of 3 weeks of daily HAS infusion on metal blood levels was studied in 8 critically ill patients with acute renal failure, protein catabolism, ventilator therapy and hemodialysis treatment. Since most metals are primarily eliminated with the urine, these patients seemed to be at high risk for metal loading. In all patients, a considerable increase in the blood concentrations of Al, Ni, Cr, and in some patients of Mn and Co was found. In addition, the daily dose of Al, Ni, Cr, Mn, and Co by HAS was calculated for the 21st day after start of HAS infusion. In most patients, the dose of Al, Ni, and Cr considerably exceeded (up to a factor of 10) the average daily metal dose absorbed from the diet by healthy subjects. The increase in Mn and Co blood levels, despite a low dose of Mn and Co with the daily HAS infusion, was most likely caused by depletion of Mn and Co tissue stores due to the catabolic state of the patients. The contamination of HAS probably originated from the use of aluminum hydroxide and from contact of plasma with stainless steel surfaces during the Cohn fractionation process. The high extent of contamination of HAS with Al, Ni and Cr cannot be accepted since it is already technically feasible to produce HAS with metal concentrations comparable to the normal serum level range.

Acute Kidney Injury↗
PubMed1987

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.

Adult↗
PubMed1987

Poisoning with over-the-counter doxylamine preparations: an evaluation of 109 cases.

One hundred and nine cases of monointoxication with doxylamine were evaluated with respect to age distribution, amount ingested, plasma level, and clinical symptomatology. The age of 60% of the patients ranged between 16 and 30 years. In about 60% of the cases 10 to 40 times a single therapeutic dose (25 mg) was ingested. Doxylamine plasma concentrations exceeded the maximum plasma level after a therapeutic dose by a factor of 10 to 40 in two-thirds of cases. The most frequent symptoms included impaired consciousness, seizures, tachycardia, mydriasis and a 'psychosis' similar to that in catatonic stupor. A serious complication may be rhabdomyolysis with subsequent impairment of renal function and acute renal failure. No symptoms were observed in 39% of the patients. No correlation was found between the amount ingested or doxylamine plasma level and the clinical symptomatology. Primary detoxication included gastric lavage, administration of activated charcoal and sodium sulfate. Regarding the high frequency of doxylamine overdose and its possible complications the question arises as to whether doxylamine-containing preparations should be subjected to prescription.

Adolescent↗
PubMed1987

Clinical symptomatology of diphenhydramine overdose: an evaluation of 136 cases in 1982 to 1985.

In West Germany, the antihistaminic diphenhydramine is marketed as a non-prescription hypnotic. Results of toxicological screening in cases of drug overdose indicate that poisoning with diphenhydramine represents a substantial part (4.5%) of the total number of intoxications. A total of 136 cases of diphenhydramine poisoning in 1982-1985 were evaluated with respect to age, ingested dose, plasma level, and clinical symptomatology. All patients had taken diphenhydramine with suicidal intent. Two-thirds of the patients were aged 14-30 years. In about 50% of the cases, between 6 and 40 times a therapeutic dose was ingested. Diphenhydramine plasma levels showed a wide range (0.1-4.7/micrograms/ml) due to differences in ingested dose and time between ingestion and admission to hospital. Impaired consciousness was the most common symptom. Psychotic behavior similar to catatonic stupor--often combined with anxiety--was highly specific for diphenhydramine poisoning. Further symptoms included hallucinations, mydriasis, tachycardia, and less frequently diplopia, respiratory insufficiency, and seizures. Primary treatment included gastric lavage, administration of activated charcoal and sodium sulfate. In one case, hemodialysis and ultrafiltration were performed which had only limited effect on diphenhydramine plasma elimination kinetics. This patient died of diphenhydramine overdose and extreme hypothermia. All intoxications except the one mentioned before had an uncomplicated clinical course. In vitro experiments indicate that diphenhydramine may be almost completely removed from the plasma compartment by hemoperfusion. Routine analysis of urine samples in diphenhydramine overdose led to the identification of 4 previously unknown metabolites and artifacts of diphenhydramine.

Adolescent↗
PubMed1987

Urinary metabolism of chlorphenoxamine in man.

After an oral dose of 40 mg of 4-chlorophenyl-methylbenzyloxy-N,N-dimethyl-ethylamine(chlorphe noxamine, Systral) urinary metabolism was studied by gas chromatography/mass spectrometry. Besides the unchanged drug, 8 metabolites and 7 artifacts and derivates could be identified. Metabolism is similar to that of the structurally related antihistaminic drugs diphenhydramine and doxylamine. The main metabolic pathways are: 1. N-demethylation, 2. oxidative desamination and formation of an alcohol and a carbonic acid derivative, 3. cleavage of the ether bond, and 4. hydroxylation of the phenyl ring. For determination of chlorphenoxamine in plasma an assay using gas chromatography was developed. Chlorphenoxamine plasma levels were beyond the limit of detection (10 ng/ml) 30, 60, 120, 240, 480, and 1200 min after oral intake.

Ethylamines↗
PubMed1987

Urinary metabolism of dextromethorphan in man.

After an oral dose of 50 mg of (+)-3-methoxy-N-methylmorphinan (dextromethorphan) to volunteers, urinary metabolism was studied by gas chromatography/mass spectrometry. A total of 15 previously unknown metabolites and derivatives of dextromethorphan could be identified by mass spectrometric techniques. The main metabolic pathways were: O,N-demethylation, O,N-acetylation, hydroxylation of the phenyl ring and the saturated ring system with subsequent further oxidation.

Acetylation↗
PubMed1987

Urinary metabolism of chloroquine.

For reinvestigation of the metabolism of 7-chloro-4-(4-diethylamino-1-methylbutylamino)quinoline (chloroquine, Resochin), urine samples from patients and volunteers with single or repeated chloroquine doses were collected and analyzed by gas chromatography, thin-layer chromatography, and gas chromatography/mass spectrometry. Furthermore, urine samples from two cases of chloroquine overdose were included in the study. Three previously unknown metabolites could be identified in nearly all samples, although they amounted to less than 2% of the concentration of unchanged chloroquine in the urine. However, in those samples with failure of detection, the chloroquine urine levels were already so low that metabolite concentrations were beyond the limit of detection of the analytical method. Altogether, the study gave no evidence for a dose-dependent formation of the three previously unknown metabolites. Besides the new metabolites, an artifact generated from chloroquine-N-oxide could be characterized by gas chromatography/mass spectrometry. However, the formation of a further chloroquine metabolite with an alcohol function which has been described in the literature could not be confirmed.

Adult↗