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Biomedical subjects

M von Clarmann

Publications and source records attributed to M von Clarmann.

At least 19 recordsLinked to original sources
PubMed1991

Clinical and morphological findings on mustard gas [bis(2-chloroethyl)sulfide] poisoning.

In 1984 and 1985, a total of eleven Iranian patients were transferred to hospitals in Munich, Germany, after a reported gas attack in the Iran-Iraq war. The initial symptoms and pretreatment in Teheran, Iran, as well as the admittance examination data, the clinical courses of the patients, and the clinical laboratory data in Germany, are reported. The main injuries were to the skin, the eyes, and the respiratory tract. One patient stopped breathing suddenly on the third day of treatment (eight days after the exposure). A large piece of mucous membrane blocking a bronchus was removed during an immediate bronchoscopy, but attempts at resuscitation failed. The most important autopsy findings in this case were severe pseudomembranous inflammation of the trachea and the bronchial tubes. The histological findings are reported. Chemical proof of the poison (mustard gas) was established. A review of the history of chemical warfare, the physical and chemical properties of mustard gas, and a literature survey of clinical findings (including, especially, experiences from World Wars I and II) contribute to the understanding of the actual cases.

Adult↗
PubMed1990

[Plasma and urine catecholamines in a 7-day survival of parathion poisoning].

During the intensive medical treatment of a finally fatal parathion poisoning (survival time 7 days) with shock symptoms (lung and kidney) the kinetic profiles of both plasma and urinary catecholamines were taken up. In addition the parathion concentrations of the same plasma samples were measured. There could have been found plasma catecholamine profiles exhibiting peak concentrations in the initial phase, followed by a period of 4 days without any detectable plasma epinephrine and finally an extreme elevation of both catecholamines in the last period before death. The excretion patterns confirmed the plasma results. Imaginable pathophysiological mechanisms in consideration of the shock induced renal insufficiency are discussed. The question is raised whether the kinetics of plasma catecholamines may be a possible marker for the prognosis of organophosphate poisoning.

Aged↗
PubMed1989

[Indications for liver transplantation in Wilson's disease with a fulminant course].

In two 19-year-old girls with Wilson's disease the condition took a fulminant course, including a poor general state, marked haemolysis and ascites. In the first patient the diagnosis was histologically confirmed only after three weeks, and onset of treatment with penicillamine was therefore delayed. With this medication the concentrations of alkaline phosphatase, cholinesterase and total bilirubin returned to normal, but again became abnormal after about seven weeks. Despite substitution of clotting factors thromboplastin time remained reduced. She died 82 days after the onset of symptoms. In the second patient, treatment with penicillamine was started at once, without waiting for histological confirmation. All laboratory values became normal and remained so. It is concluded from these observations that liver transplantation is indicated if the abnormal values for cholinesterase, thromboplastin time and bilirubin do not remain normal after six weeks and if the initial suppression of alkaline phosphatase continues or occurs again.

Adult↗
PubMed1989

[The kinetics of plasma catecholamine in alkylphosphate poisoning and their therapy].

In connection with the "endogenous acetylcholine-poisoning" due to organophosphorous compounds beside the clinical important muscarinic and nicotinic symptoms an activation of the sympathetic nervous system (adrenal medulla, sympathetic ganglia) is expected. Therefore a kinetic profile of norepinephrine and epinephrine in the plasma of two patients with severe parathion-poisonings was taken up through the whole period of the intensive-medical treatment. The method used was HPLC with electrochemical detection. The parathion-concentration of the same plasma samples were measured, too. The result were individual different courses with periodically appearing, markedly increased plasma catecholamine values. A direct correlation of catecholamines with the parathion-concentration was not recognizable. A possible influence of the atropine-treatment as well as of stress-factors is discussed but estimated as not responsible for the observed peaks.

Adult↗
PubMed1988

[No Parkinsonian syndrome following acute paraquat poisoning].

Paraquat structurally resembles N-methyl-4-phenyltetrahydropyridine (MPTP) and its metabolite 1-methyl-4-phenylpyridine (MPP+). MPTP and MPP+ are neurotoxic chemicals, which induce in exposed humans and in animal-models a Parkinson's disease. A high correlation between the incidence of Parkinson's disease and herbicide use in Canada led to the assumption that paraquat could give rise to parkinsonism. We have therefore carried out a follow-up study with patients having had dermal contact with paraquat or having swallowed paraquat accidentally or in a suicidal attempt. 7 patients took part in the study. Three of them had dermal contact. One had ingested paraquat by accident and three were survivors from suicidal paraquat intake. It was possible to exclude parkinsonism in all patients. One patient exhibited tardive dykinesia most likely due to a long term therapy with neuroleptic drugs.

Accidents↗
PubMed1987

[Treatment guidelines in intestinal burns].

Intestinal burns due to ingestion of acids or alkaline materials still put the physician in a difficult position because until now it is not possible to correlate the amount of ingested material to the extent of damage that can be expected. Furthermore, there are no objective criteria to determine the depth of the burn. Diagnosis is based on endoscopy. Mild, moderate and severe damage can be differentiated endoscopically. Mild and moderate burns are not operated upon primarily. Surgery is indicated with moderate burns whenever complications occur during intensive care treatment, and generally with severe corrosive burns. Operative management depends on intraoperative findings.

Burns, Chemical↗
PubMed1982

[Recent aspects of the treatment of local hydrofluoric acid erosion].

In experimental studies we compared the intraarterial injection of calcium to local infiltration of calcium as treatment of local hydrofluoric acid burns. We showed that intraarterial injection of calcium is the superior therapy in terms of earlier and more effective arrest of destruction. The results are better the earlier the injection is given. There were no local or systemic disturbances due to the intraarterial injection of calcium.

Animals↗
PubMed1979

[Therapy of Amanita phalloides poisoning. Results of clinical and experimental studies].

On the basis of experimental and clinical results evidence accumulates that supportive therapy is still the milestone in the therapy of death cap poisoning. Today the letality is 20%. The main cause of the intoxication are the amatoxines which inhibit DNA dependent RNA Polymerase II or B. Parts of the supportive therapy are: diuresis with 150--200 ml urin/hour, careful corrections of disturbances in electrolyte and acid-base-metabolism, oral administration of charcoal and oral gut sterilization. In spite of a multitude of experimental and clinical reports on the effectivity of Penicillin G, thiocticacid and steroids there are no controlled studies to demonstrate the advantage of one regimen over the other. The time course of resorption and excretion of amatoxines clearly shows that hemoperfusion and/or hemodialysis are only of value if applied within the first 24 hours after poisoning. At this time neither anamnestic nor biochemical data give any clues to the probable course of the disease. Heterologous baboon liver perfusion may be lifesaving in coma hepaticum grade IV, but the small amount of cases so far does not yet allow any comments on its effectivity.

Amanita↗
PubMed1978

The index line as a new aid in clinical and forensic toxicology.

On behalf of the German Federal Ministry for Research and Technology, we investigated the use of electronic data processing for clinical toxicological purposes. Initially, sufficient funds were available for a comprehensive approach to the problem and programs covering the following areas were established: 1. A casuistic data program; 2. an identification program for wild fruits; 3. a program for the identification of tablets by their shapes. Due to a subsequent lack of funds, it was necessary to develop a partial solution: this solution is what we call the Index Line. The Index Line--limited data on poisonings--should enable the user to receive information by telex from the German Institute for Medical Documentation and Information, i.e., information on "who has what, where". As a first step the continuous Index Line registration of all cases of poisoning recorded at the poison control centers in Munich, Freiburg, Hamburg, and Nürnberg as well as at the State Institute for Food, Pharmaceutical and Forensic Chemistry in Berlin was founded in 1975. To participate in the program, complete instructions are necessary.

Computers↗