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Biomedical subjects

K Hruby

Publications and source records attributed to K Hruby.

At least 19 recordsLinked to original sources
PubMed1995

[Dangerous intoxication from extreme serum concentrations of methaqualone metabolites. Detection and quantification of biosynthesis with gas chromatography-mass spectrometry].

CLINICAL COURSE: We present a potentially fatal case of acute methaqualone (M) poisoning with very low serum concentrations of M but extremely high levels of its metabolite, 2-methyl-3-(2-hydroxymethyl-phenyl)-4 (3H)-chinazoline (Met-1). A 23-year-old man was admitted to the intensive care unit 2 days after ingestion of 4-5 g M in an suicidal attempt. On admission he was somnolent and poorly responsive to painful stimuli. Physical examination revealed a heart rate of 95 bpm, a blood pressure of 125/65 mmHg, and a normal body temperature. His chest was clear to auscultation, respirations were shallow, and the skin was cyanotic. The electrocardiogram was unremarkable. The chest radiograph showed a normal heart size without pulmonary infiltrates or venous congestion. The pupils were dilated but reactive to light. The neurologic examination was further remarkable for increased limb reflexes, myoclonia, and positive pyramidal signs. During the next 2 days the patient became comatose and developed respiratory insufficiency due to non-cardiogenic pulmonary oedema, which was confirmed by chest radiograph and haemodynamic investigations by means of right heart catheterisation. He required mechanical ventilation for 6 days. Finally, he recovered completely and was discharged in good condition. DIAGNOSTICS: A lumbar puncture revealed neither blood nor pleocytosis in the cerebrospinal fluid. Cranial computed tomography was carried out on an emergency basis, but no abnormality was disclosed. An electroencephalogram did not exhibit any significant pathological findings. Testing for infectious diseases or porphyria gave negative results. Toxicological screening based on enzyme immunoassays (ELISA) was negative for alcohol, tricyclic antidepressants, benzodiazepines, barbiturates, and morphine, but gave a positive result for M. From the moment of admission daily blood samples were taken and analysed by combined gas chromatography and mass spectrometry. These showed very low levels of M but extremely high levels of Met-1. THERAPY: After gastric lavage, continuous enteric lavage with activated charcoal and mannitol was initiated to minimise intestinal absorption. Since M was hardly detectable in the serum, haemoperfusion was not regarded as indicated for drug elimination and treatment was restricted to general supportive measures. To rule out a central anticholinergic syndrome, an anticholinesterase drug (physostigmine) was administered but remained without therapeutic effect. CONCLUSIONS: The presented case is the first report of a life-threatening intoxication after M ingestion primarily caused by Met-1. It supports the significance of this metabolite for the toxic effects of the drug. A toxicological screening test based on ELISA proved helpful due to its cross-reactivity with metabolites. In cases similar to ours, resin haemoperfusion may be indicated to remove the metabolites despite low detectable concentrations of the parent substance in the serum.

Adult↗
PubMed1990

Upregulation of a lymphoid serine protease in kidney allograft recipients.

The presence of a putative, cytotoxicity-linked lymphoid serine esterase (SE) has been studied in 79 kidney graft recipients. Peripheral blood lymphocytes (PBL) bearing an N-alpha-benzyloxy carbonyl-L-lysine thiobenzyl ester (BLT)-specific SE were evaluated by a novel cytochemical staining method. A characteristic of post-allograft patients was an increased presence of SE containing granules in PBL. In 46 patients with stable graft function SE + PBL were 33.41 +/- 10.34% (controls: 26.30 +/- 5.22%, P less than 0.0025), SE + CD4+ 4.32 +/- 3.85% (controls 2.13 +/- 1.52%, P less than 0.0025) and SE + CD8+ T cells 47.68 +/- 18.64% (controls: 28.50 +/- 6.50%, P less than 0.0005). In those graft recipients undergoing a rejection episode a marked upregulation of SE activity could be observed when compared to the stable graft group: SE + PBL were 59.91 +/- 10.89% (P less than 0.0005), SE + CD8+ 74.30 +/- 10.79% (P less than 0.0005) and SE + CD4+ T cells 28.56 +/- 13.50% (P less than 0.0005). In 10 cases this increase of SE activity was observed with a time lag of up to 37 days prior to the onset of clinical or biopsy proven rejections, promptly decreasing in response to methylprednisolone antirejection therapy. In patients with recurrent rejection episodes and subsequent graft loss, a repeating increase of SE activity indicated a failure of therapeutic agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

[Is retinitis pigmentosa absolutely incurable?].

The importance of phosphatides in the biochemistry of the retina and in visual function provided a basis for therapeutic administration of these substances in cases of senile maculopathy and retinitis pigmentosa. In cases of dry senile maculopathy, good results were only obtained by administering (n-3)-docosahexaenacid to the retina as the active component of intramuscular injections of Etaretin. So far only one report of a convincing therapeutic success in a case of retinitis pigmentosa has been published.

Adolescent↗
PubMed1987

[Specific therapy of acute benzodiazepine poisoning using flumazenil (Ro 15-1788)].

In 20 patients with coma (grade 4: n = 7, grade 3: n = 8, grade 2: n = 2, grade 1: n = 3) due to benzodiazepine intoxication, solely or combined with alcohol or other psychoactive drugs, the effect of a specific benzodiazepine antagonist, Flumazenil (Ro 15-1788), was evaluated. In terms of coma depth, 80% of the patients responded to application of 1.96 mg Flumazenil as a mean with immediate awakening or improvement of at least two steps in coma grading. In those 3 patients, who failed to respond to Flumazenil, the history revealed amitriptyline or barbiturates to be responsible for the comatose state. The observed side-effects of Flumazenil included increase (n = 4) or decrease (n = 3) of blood pressure, increase of heart rate (n = 7), cutaneous flush (n = 1) and ventricular extrasystoles (n = 1). Agitation and generalized convulsions, each observed in 1 patient, presumably were due to an acute benzodiazepine-withdrawal rather than an intrinsic side effect of the antagonist. In conclusion, Flumazenil proved to be a potent antagonist of benzodiazepines in patients with severe coma and even may serve as a valuable diagnostic in cases of suspected benzodiazepine intoxication.

Adult↗
PubMed1986

[Was Dr. Carl Koller driven from Vienna in 1885?].

In this article the principal reason for the emigration of Dr. Carl Koller is examined on the basis of the available literature. In fact, antisemitism did not play a crucial role. After his colleague, Dr. Fritz Zinner, called him an impudent Jew in public in the General University Hospital of Vienna, Koller reacted by hitting the man in the face. A duel with heavy sabres was the outcome; Koller was unharmed, whilst his opponent received two deep gashes. Such duels were strictly forbidden at that time already, but were nonetheless still executed. In consequence, Koller's hopes of obtaining a position in the Eye Department, for which he was very well qualified, and of an academic career in Vienna were dashed and he had to emigrate. Koller eventually settled in New York in 1888, where he received many distinctions during his life span. The Medical Association of Vienna also honoured him in 1930. Dr. Koller was proposed several times for the Nobel prize in Physiology and Medicine, since his discovery of cocaine as local anaesthetic in ophthalmology was undoubtedly worthy of this prize, but his discovery had been published too long previously, so that according to the statutes of the Nobel prize this distinction could not be granted. Hence, it can be concluded that although Dr. Koller was forced to leave Vienna in 1885, it was not principally for antisemitic reasons. There were Jewish professors in the Medical Faculty of Vienna University at the time and, indeed, when the author studied medicine in 1931 to 1936, four Jewish professors held chairs in Vienna and one of his predecessors as chief of the First Department of Ophthalmology, Isidor Schnabel, was Jewish.

Anesthesia, Local↗
PubMed1985

[Rise and fall of the German University Eye Clinic in Prague].

The German University in Prague was founded in 1348 by the German Emperor Karl IV. However, it was not until 1808 that an eye clinic was established there, by Johann Nepomuk Fischer; the clinic was incorporated into the university in 1820. Fischer retired in 1847 and was succeeded by Ferdinand Arlt, though not as professor in ordinary. Fortunately, the chair in Prague was offered to Arlt before he had definitively accepted a call to Leipzig. During the period 1856 to 1883 Ferdinand Ritter von Arlt held the chair of ophthalmology in Vienna, an ophthalmic center of high repute. One of his most famous pupils was Albrecht von Graefe, of Berlin. Josef von Hasner directed the Prague Eye Clinic from 1856 to 1883, followed by Hubert Sattler (1886-1891). Isidor Schnabel was professor in Prague from 1891 to 1895, before going to Vienna. His successor, Wilhelm Paul Czermak, directed the Prague Eye Clinic from 1895 to 1906. He was followed by Isidor Schnabel's most outstanding pupil, Anton Elschnig, a Styrian by birth, who held the chair from 1907 to 1933. Under Elschnig's guidance the Prague University Eye Clinic reached a high international standard. Professor Elschnig retired in 1933 and died in Vienna in 1939 following a street accident. Elschnig's successor was his former assistant Jaroslav Kubik; he had to relinquish the chair after the Germans occupied Czechoslovakia because his wife was Jewish.(ABSTRACT TRUNCATED AT 250 WORDS)

Austria↗
PubMed1985

[The first description of the Irvine syndrome].

Recently G. O. H. Naumann and W. Seibel, while reviewing the literature, stated that A. R. Irvine had not noticed the foregoing biomicroscopic observations of K. Hruby. The name Hruby-Irvine-Gass Syndrome would thus be more appropriate. The article concludes with a discussion of therapeutic problems.

Cataract Extraction↗
PubMed1985

Poisoning with oral antiarrhythmic drugs.

The incidence of poisoning with antiarrhythmic drugs (AAD) is low, but frequently cardiac disturbances cause a high mortality. Clinical and toxicological data on verapamil, quinidine, ajmaline, prajmaliumbitartrate, mexiletine and aprindine as collected by the Austrian Poison Information Center (PIC) are presented in this paper. The drug concentrations of verapamil, mexiletine and quinidine detected in post-mortem specimens are discussed and compared with correspondent data from literature. Clinical experiences with this kind of intoxication are rather poor and therapeutical principles are very inconsistent. To avoid life-threatening symptoms, gastric lavage has to be performed irrespective of the latency period, accompanied by continuous cardiac monitoring. Cardiocirculatory disorders respond well to sympathomimetic drugs. Immediate and adequate cardiopulmonary resuscitation decisively determines the therapeutical success in critical cases.

Administration, Oral↗
PubMed1984

[Goethe's eye disease].

Ophthalmic diseases reported in the age of Goethe are difficult to identify today because the nomenclature used at that time is now antiquated. However, it is not difficult to establish from available documents that Goethe's left eye was seriously affected by an erysipelas (tenonitis? orbital phlegmon?), though it was not permanently damaged. With regard to differential diagnosis, an ophthalmic zoster may also be considered, but this is most unlikely considering the documentary evidence and the absence of lasting ocular damage.

Diagnosis, Differential↗
PubMed1984

Acute oral poisoning with lindane-solvent mixtures.

Six cases of oral intoxication with lindane-solvent mixtures are reviewed. The ingested doses of lindane (mean dosage 120 mg/kg +/- 86 mg/kg) and benzene (mean dosage 366 mg/kg +/- 93 mg/kg) exceeded the toxic level. Symptoms (vomiting, dizziness and hyperreflexia) occurred within 30 min and all patients had epileptiform seizures. Two patients suffered from pulmonary edema and one of them had a severe rhabdomyolysis. Diazepam was sufficient to control convulsions in five cases. Gastric lavage was performed in five patients and activated charcoal, liquid paraffin with saline cathartic, and cholestyramine were used as adsorbents. Recovery was complete in all patients.

Administration, Oral↗
PubMed1983

[Poisoning with andromedotoxin-containing honey].

Two patients poisoned by andromedotoxin-containing honey were treated in Austrian hospitals in 1981 and 1982. The toxin-containing honey had in both cases been obtained in the coastal mediterranean part of Turkey. Both patients had severe arterial hypotension, bradycardic arrhythmias, syncope and CNS symptoms. Symptomatic treatment was fully successful in both patients within 24 hours.

Adult↗
PubMed1983

[Clinical aspects and therapy of acute poisoning by the drug combination melitracen-flupenthixol (Deanxit)].

From 1975 to 1982, the Austrian Poison Information Centre gave medical advice in forty cases of acute melitracenee-flupenthixol poisoning. The case reports were reviewed and analysed in retrospect. 13 patients who either had ingested less than 20 pills (n = 5) or who underwent early gastric lavage (n = 8) showed no symptoms. In 19 patients who had swallowed 20 to 60 (n = 11), 60 to 100 (n = 3) pills respectively, or an unknown dose (n = 5) atropine like symptoms predominated. Five patients developed atropine like and extrapyramidal symptoms. The number of pills taken by these patients ranged from 20 to 60 (n = 4) and in one up to 100. Extrapyramidal reactions were encountered as predominant symptoms in three patients one of which had taken 20, the other 60 and the third an unknown number of pills. Additionally, five patients were unconscious. 21 patients developed ECG changes, 19 of which showing sinus tachycardia. The remaining two patients who had ingested 600 to 1000 mg melitracen atrial premature beats or T-wave inversions were observed. All 40 patients recovered.

Adolescent↗