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C Köppel

Publications and source records attributed to C Köppel.

At least 19 recordsLinked to original sources
PubMed1996

Carbohydrate-deficient transferrin for identification of drug overdose patients at risk of an alcohol withdrawal syndrome.

BACKGROUND: Chronic alcohol abuse is frequent in patients admitted to the intensive care unit with acute drug overdose. During detoxification, an alcohol withdrawal syndrome may develop in patients with a history of chronic alcohol abuse. Withdrawal or delirium is associated with serious risks, necessitating early identification of patients at risk. Since the information obtained from the patients or their relatives on alcohol consumption is often unreliable, biochemical markers may be helpful. Carbohydrate deficient transferrin is considered a highly specific marker (reported maximum specificity 97%, sensitivity 40-85%) for identifying alcohol abuse. METHODS: In 20 patients with acute drug overdose and suspected alcohol abuse, carbohydrate deficient transferrin was determined by an immunoturbidimetric assay on admission to the intensive care unit. Eight of the patients had carbohydrate deficient transferrin levels above the "positive" threshold and nine in a suspicious range. A "false" negative carbohydrate deficient transferrin was found in three patients who were thought to have changed their drinking habits prior to hospitalization. A "positive" carbohydrate deficient transferrin test is assumed to be associated with ingestion of more than 60-80 g ethanol/d for a period of more than seven days. RESULTS: In all patients, clonidine (30-210 micrograms/h i.v.) was started. None developed delirium. Since alcohol addiction is frequently denied, determination of carbohydrate deficient transferrin may be useful for its early diagnosis but the sensitivity of this parameter requires further evaluation.

Alcohol Withdrawal Delirium↗
PubMed1995

Toxicological and neuropsychological findings in patients presenting to an environmental toxicology service.

Patients presenting to an environmental toxicology service are frequently convinced that their multiple symptoms are caused by exposure to environmental toxicants. In order to evaluate the patients' hypotheses, 120 consecutive patients referred by health care providers to the environmental toxicology service for various symptoms were included in an open prospective study. The basic diagnostic procedure included an environmental toxicology questionnaire, psychological tests, a 45 minute interview, a physical examination and standard biomonitoring for cadmium, mercury, lead, lindane, hexachlorobenzene, DDT, DDE, DDD, and pentachlorophenol and a salivary test for mercury released from amalgam. Allergic disease was found in 42 patients. Nineteen of the 42 patients also had psychosomatic disorders. An unusually high release of mercury from amalgam fillings in the saliva test was found in six patients. An environmental toxic exposure was demonstrated in 19 patients (4 lead, 8 DDE, 6 mercury--most likely from broken thermometers, 1 neurotoxic alkyl naphtol derivatives). Ten of the 19 patients had psychosomatic disorders and six had medical/neurological disorders. Only two patients had symptoms attributable to environmental exposure alone. Rather classical psychosomatic disorders were diagnosed in 83 patients. Of the 37 patients without identifiable neuropsychological dysfunction, 18 had allergic disorders and 12 had other medical diagnoses. The diagnosis of a toxic environmental exposure should be performed in an integrated diagnostic approach covering environmental toxicology and medicine as well as psychosomatic medicine.

Adolescent↗
PubMed1994

Fatal poisoning with detajmium: identification of detajmium and its metabolites and artifacts by gas chromatography-mass spectrometry and quantification by high-performance liquid chromatography.

After ingestion of an unknown dose of detajmium, a 14-year-old female collapsed with asystolia. Resuscitation efforts were not successful. A medicolegal autopsy was carried out, and blood, liver and gastric content were extracted and analyzed by gas chromatography-mass spectrometry (GC-MS). After derivatization with acetic anhydride, detajmium and twelve of its derivatives and metabolites were identified. The main metabolic pathways include hydroxylation and subsequent O-methylation of the indol ring, and oxidation as well as reduction of the C-21 hydroxyl function. Cleavage of the N-alkyl side-chain is a further, possibly non-enzymatic degradation pathway. Artifact formation induced by acetylation included dehydratation of the hydroxyl function of C-21 and the N-alkyl side-chain. The detajmium concentration in blood of the decreased was determined by high-performance liquid chromatography with fluorimetric detection (12 micrograms/ml).

Acetic Anhydrides↗
PubMed1994

Inhaled nitric oxide in advanced paraquat intoxication.

No effective treatment is available for adult respiratory distress syndrome, pulmonary hypertension and progressive lung fibrosis in severe paraquat poisoning. A potentially beneficial effect of nitric oxide inhalation on the mean pulmonary artery pressure and gas exchange in a subject with advanced paraquat intoxication is reported. Eight days after the suicidal ingestion of an unknown dose of paraquat, a 52-year-old female had a PaO2 < or = 50 mm Hg despite ventilation with an FiO2 of 1 and a positive end-expiratory pressure of 14 to 18 cm H2O. After administration of 25 ppm nitric oxide, PaO2 increased and the mean pulmonary artery pressure and the right-to-left shunt decreased. Discontinuation of nitric oxide resulted in rapid reversal. Ventilatory function was stabilized for three days during nitric oxide inhalation but the patient developed massive pleural effusions and died on d 11 during an interruption of nitric oxide therapy. The response of serious paraquat intoxications to nitric oxide therapy may merit further study. A remarkable post-mortem finding was extensive myonecrosis supporting prolonged muscular retention of paraquat with toxic myopathy or neuromyopathy as a late manifestation of paraquat toxicity.

Administration, Inhalation↗
PubMed1993

Clinical symptomatology and management of mushroom poisoning.

Among poisonous mushrooms, a small number may cause serious intoxication and even fatalities in man. Humans may become symptomatic after a mushroom meal for rather different reasons: (1) ingestion of mushrooms containing toxins, (2) large amounts of mushrooms may be hard to digest, (3) immunological reactions to mushroom-derived antigens, (4) ingestion of mushrooms causing ethanol intolerance, and (5) vegetative symptoms may occur whenever a patient realizes that there might be a possibility of ingestion of a toxic mushroom after a mushroom meal. Based on the classes of toxins and their clinical symptoms, seven different types of mushroom poisoning can be distinguished: (1) phalloides, (2) orellanus, (3) gyromitra, (4) muscarine, (5) pantherina, (6) psilocybin, and (7) gastrointestinal mushroom syndrome. Two other entities of adverse reactions to mushrooms are (8) coprinus and (9) paxillus syndrome. Phalloides, orellanus, gyromitra and paxillus syndrome may lead to serious poisoning, which generally requires treatment of the patient in an intensive care unit. Diagnosis of mushroom poisoning is primarily based on anamnestic data, identification of mushrooms from leftovers of the mushroom meal, spore analysis, and/or chemical analysis. Therapeutic strategies include primary detoxification by induced emesis, gastric lavage and activated charcoal, secondary detoxification, symptomatic treatment and rarely specific antidotes. Owing to progressing fulminant hepatic failure, lethality associated with phalloides syndrome is still high (5-20%). Basic treatment includes administration of silibinin and penicillin G, although controlled studies on its therapeutic efficacy are still lacking. In serious phalloides syndrome, orthotopic liver transplantation has to be considered. Fortunately, the prognosis in most other mushroom poisonings is excellent.

Animals↗
PubMed1992

Monitoring of ajmaline in plasma with high-performance liquid chromatography.

A rapid, reliable and sensitive assay for routine determination of ajmaline in plasma by high-performance liquid chromatography with fluorimetric detection is presented. A low limit of detection in plasma (less than 1 ng/ml ajmaline) could be achieved by the extraction of plasma samples and the use of fluorimetric detection. Deproteinization of the plasma sample instead of extraction, or the use of an ultraviolet detector, yielded a higher limit of detection (less than 50 ng/ml). Two different eluents were studied. Eluent 1 allowed clear separation of ajmaline from isoajmaline and sandwicine, but did not separate isoajamaline from sandwicine. With eluent 2, separation of isoajmaline and sandwicine was achieved, but separation of ajmaline from sandwicine was less optimal than with eluent 1. Therefore, eluent 1 was used for further clinical studies. No interference was observed from therapeutic doses of other commonly co-administered drugs, such as acetylsalicylic acid, digoxin, digitoxin, ranitidine, dopamine, dobutamine, furosemide, captopril or glycerol trinitrate. In addition, the chemical stability of ajmaline and a possible rearrangement of ajmaline to its stereoisomers isoajmaline and sandwicine was studied in vivo and in vitro. Ajmaline proved to be unusually stable under both in vivo and in vitro conditions.

Ajmaline↗
PubMed1992

Clinical course, therapy, outcome and analytical data in amitriptyline and combined amitriptyline/chlordiazepoxide overdose.

A total of 103 cases of amitriptyline (AT) overdose (group 1) and 81 cases of overdose with a fixed combination of AT and chlordiazepoxide (CDE) (group 2), treated at our Intensive Care Unit or reported to our Poison Information Center between 1985-1990, were evaluated with respect to clinical course, symptoms and outcome, as well as efficacy of therapy. The mean amount of AT was considerably higher in group 1 compared to group 2 (13 mg kg-1 vs 7.7 mg kg-1). The most frequent symptoms in both groups were impaired consciousness, anticholinergic symptoms, seizures, arrhythmia and hypotension. Respiratory insufficiency necessitated respirator therapy in 63 of the patients. Two patients in group 1 and one patient in group 2 did not survive. Therapy included primary detoxification by gastric lavage and repeated administration of activated charcoal. In four of eight patients with cardiac conduction disturbances, hypertonic sodium bicarbonate led to a significant reduction in QRS duration and AV interval. Physostigmine was effective in eight of 14 patients with pronounced anticholinergic symptoms. No effect was observed in the other six patients. Haemoperfusion, which was performed in five patients, led to rapid improvement of coma after initiation of therapy in four patients. The clinical efficacy of haemoperfusion in AT overdose despite the high volume of distribution of AT deserves further investigation. The rather high average overdose of AT implies that large package sizes of AT were available to the patients. A major step towards prevention of serious AT overdose would be the prescription of package sizes containing a total of less than 500 mg AT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Clinical experience in the therapy of bites from exotic snakes in Berlin.

Since there are nearly no indigenous poisonous snakes in Germany, snake bites by poisonous snakes are rare. Most serious snake bites reported to poison information centres or treated at hospitals are caused by exotic snakes that are kept in private households. Only few types of antivenom are stored in emergency depots in Germany including polyvalent antivenoms from commercial sources. Since experience with the treatment of poisonous snake bites is limited, the records of the Intensive Care Unit and the Poison Information Centre of the Universitätsklinikum Rudolf Virchow from 1980-1991 were evaluated. During this period, 51 snake bites were reported. Eleven patients who had been bitten by exotic poisonous snakes were treated in intensive care. In eight of the cases, ethanol (blood levels on admission 1.2-4.2 g-1) had played an important role in the cause of the bite. A moderate to severe local inflammation at the site of the bite followed by oedema and necrosis was typical. One patient developed respiratory failure, probably because of the neurotoxic effects of the snake venom and a compartment syndrome necessitating fasciotomy. Haemolysis was observed in four patients and coagulopathy in six patients. All patients received polyvalent antivenom within 2-12 h of the snake bite. Despite serious coagulopathy in two of the patients and respiratory arrest in one, all survived without sequelae.

Adult↗
PubMed1991

Plasma level monitoring of D,L-verapamil and three of its metabolites by reversed-phase high-performance liquid chromatography.

A high-performance liquid chromatographic assay was developed for determination of verapamil, norverapamil (M1) and its N-dealkylated metabolites (M2 and M3) in plasma. Plasma samples were vortex-mixed, deproteinized and centrifuged. The analysis was performed on a C18 reversed-phase column with fluorimetric detection. Since the polarity of verapamil and norverapamil differs considerably from that of M2 and M3, two different eluents were used for rapid high-performance liquid chromatographic separation. The eluent for the separation of verapamil and norverapamil was acetonitrile-0.07% orthophosphoric acid (33:67, v/v), and for M2 and M3 acetonitrile-0.07% orthophosphoric acid (25:75, v/v). The high-performance liquid chromatographic assay allowed rapid, sensitive and reliable quantitation of verapamil and three of its metabolites in plasma without an extraction procedure. The limit of detection was less than 5 ng/ml (plasma) for all compounds. No interferences with other commonly co-administered drugs was observed. Plasma concentrations of verapamil and its metabolites were determined in 21 patients receiving a continuous infusion of verapamil for tachyarrhythmia of acute onset. The steady-state plasma concentration data of verapamil and its three main metabolites in these patients gave evidence that the plasma concentration of verapamil and its active metabolite norverapamil was primarily determined by the extent of the formation of M2.

Chromatography, High Pressure Liquid↗
PubMed1991

Formation of formaldehyde adducts from various drugs by use of methanol in a toxicological screening procedure with gas chromatography-mass spectrometry.

Use of methanol as a solvent in a toxicological screening procedure with gas chromatography-mass spectrometry may be associated with artifact formation. Artifacts with a molecular ion of [M + 12]+ are formed from various drugs, such as amphetamine, propafenone, flecainide, beta-blockers and prilocaine. The mechanism of artifact formation was studied by mass spectral techniques, labelling and nuclear magnetic resonance spectroscopy. It was shown that the artifacts were generated by the addition of formaldehyde and subsequent loss of water. Formaldehyde is probably formed by thermal dehydrogenation of methanol in the injection port of the gas chromatograph.

Adrenergic beta-Antagonists↗
PubMed1991

Mass spectral characterization of urinary metabolites of D,L-kawain.

The urinary metabolism of D,L-kawain was studied in humans after an oral dose of 200 mg. Ten metabolites of kawain could be identified by gas chromatography-mass spectrometry with electron impact and chemical ionization. The main metabolic pathways were hydroxylation of the phenyl ring, reduction of the 7,8-double bond, hydroxylation of the lactone ring with subsequent dehydration and opening of the lactone ring. The metabolites were mainly excreted in the form of their conjugates.

Gas Chromatography-Mass Spectrometry↗
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↗