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Miran Brvar

Publications and source records attributed to Miran Brvar.

12 recordsLinked to original sources
PubMed2006

Immediate oxygen therapy prevents brain cell injury in carbon monoxide poisoned rats without loss of consciousness.

In CO-poisoned patients without loss of consciousness no significant long-term functional differences in outcome have been shown in any hyperbaric versus normobaric oxygen studies. Since brain histology changes cannot be studied in CO-poisoned patients we evaluated the efficacy of normobaric and hyperbaric oxygen therapy in preventing brain cell injury in CO-poisoned animals without loss of consciousness. Wistar rats without loss of consciousness after exposure to 3000ppm of CO for 60min were exposed to ambient air (group 1), 100% oxygen at a pressure of 1bar (group 2) and 100% oxygen at a pressure of 3bar (group 3). The rats were sacrificed after two weeks, brain samples were stained with hematoxylin-eosin and a percentage of pyknotic cells in hippocampus was reported. Analyses of differences in percentage of pyknotic cells between different kinds of therapy showed that the percentage of pyknotic cells of the second group (2.3+/-1.2%) treated with normobaric oxygen and the third group (4.5+/-4.0%) treated with hyperbaric oxygen were similar, and both of them were significantly different, with a much lower percentage of pyknotic cells, from the first group left on ambient air (47.7+/-10.0%). In conclusion, immediate normobaric and hyperbaric oxygen therapy equally prevents hippocampal cell injury in CO-poisoned rats without loss of consciousness.

Animals↗
PubMed2006

Prolonged psychosis after Amanita muscaria ingestion.

Amanita muscaria has a bright red or orange cap covered with small white plaques. It contains the isoxazole derivatives ibotenic acid, muscimol and muscazone and other toxins such as muscarine. The duration of clinical manifestations after A. muscaria ingestion does not usually exceed 24 hours; we report on a 5-day paranoid psychosis after A. muscaria ingestion. A 48-year-old man, with no previous medical history, gathered and ate mushrooms he presumed to be A. caesarea. Half an hour later he started to vomit and fell asleep. He was found comatose having a seizure-like episode. On admission four hours after ingestion he was comatose, but the remaining physical and neurological examinations were unremarkable. Creatine kinase was 8.33 microkat/l. Other laboratory results and brain CT scan were normal. Toxicology analysis did not find any drugs in his blood or urine. The mycologist identified A. muscaria among the remaining mushrooms. The patient was given activated charcoal. Ten hours after ingestion, he awoke and was completely orientated; 18 hours after ingestion his condition deteriorated again and he became confused and uncooperative. Afterwards paranoid psychosis with visual and auditory hallucinations appeared and persisted for five days. On the sixth day all symptoms of psychosis gradually disappeared. One year later he is not undergoing any therapy and has no symptoms of psychiatric disease. We conclude that paranoid psychosis with visual and auditory hallucinations can appear 18 hours after ingestion of A. muscaria and can last for up to five days.

Amanita↗
PubMed2006

S100B protein in conscious carbon monoxide-poisoned rats treated with normobaric or hyperbaric oxygen.

OBJECTIVE: To evaluate S100B, an astroglial structural protein, during normobaric and hyperbaric oxygen therapy of conscious carbon monoxide (CO)-poisoned rats. So far, the usefulness of hyperbaric oxygen therapy in conscious CO-poisoned patients has been shown with neuropsychological testing. The S100B protein has been demonstrated as a possible biochemical marker and prognostic parameter in CO-poisoned rats. DESIGN: Randomized, controlled interventional trial. SETTING: University laboratory. SUBJECTS: : Male Wistar rats weighing 254 +/- 14 g. INTERVENTIONS: The rats were exposed to a mixture of 3,000 ppm CO in air for 60 mins. After CO exposure, the first group of eight conscious rats was exposed to ambient air for 30 mins, the second group of six conscious rats was exposed to 100% normobaric oxygen for 30 mins, and the third group of six conscious rats was exposed to 100% hyperbaric oxygen at 3 bars for 30 mins. Blood samples were taken from the jugular vein just before CO exposure and immediately after oxygen therapy. The level of consciousness was evaluated at the end of exposure, and the survival rate was monitored for 14 days. The S100B concentrations were measured with a commercial immunoluminometric assay. MEASUREMENTS AND MAIN RESULTS: Analyses of differences in S100B levels between different kinds of therapy before and after treatment showed a global significant difference (p = .002). The post hoc test results showed that S100B levels after therapy of the first group treated with ambient air (0.16 +/- 0.07 microg/L) and the second group treated with normobaric oxygen (0.19 +/- 0.05 microg/L) were similar (p = .741), and both of them were significantly different, with much higher values of S100B levels after therapy, from the third group treated with hyperbaric oxygen (0.06 +/- 0.03 microg/L; p = .018 and p = .002, respectively). All the rats survived. CONCLUSIONS: S100B is elevated in conscious CO-poisoned rats left on ambient air or treated with normobaric oxygen, but not in conscious CO-poisoned rats treated with hyperbaric oxygen.

Animals↗
PubMed2005

Prolonged hypoglycaemia after insulin lispro overdose.

Insulin lispro has a more rapid onset and a shorter duration of hypoglycaemic action than regular insulin. We report a 39-year-old woman, with no previous medical history, who injected 300 U of the insulin lispro (Humalog) in an attempted suicide. Half an hour later, she was found comatose and brought to our emergency department. On arrival, she was comatose, with capillary glucose of 0.4 mmol/L. She awoke after a 50 ml intravenous bolus of 50% glucose. A continuous infusion of 10% glucose was started. Intermittent hypoglycaemia with neurological signs requiring treatment with 50% glucose was recorded three times during subsequent hospitalization, the last episode being 11 h after insulin injection. The plasma insulin level 4 h after injection was 1465 mU/L, and 18 h after injection was 11 mU/L. Hypoglycaemia after an insulin lispro overdose may last for more than 11 h. Repeated hypoglycaemia after an insulin overdose could be avoided with a glucose infusion rate equivalent to the maximal glucose disposal rate.

Adult↗
PubMed2004

Acute poisoning with autumn crocus (Colchicum autumnale L.).

INTRODUCTION: Colchicum autumnale, commonly known as the autumn crocus or meadow saffron, contains the antimitotic colchicine, which binds to tubulin and prevents it forming microtubules that are part of the cytoskeleton in all cells. CASE REPORT: A 71-year-old woman ate a plant she thought to be wild garlic (Allium ursinum). Ten hours later she arrived at the emergency department complaining of nausea, vomiting and watery diarrhea. Ingestion of a poisonous plant was suspected and she was treated with gastric lavage, oral activated charcoal and an infusion of normal saline. Toxicology analysis with gas chromatography and mass spectrometry revealed colchicine in the patient's gastric lavage, blood (5 microg/l) and urine (30 microg/l). She developed arrhythmias, liver failure, pancreatitis, ileus, and bone marrow suppression with pancytopenia. Alopecia began in the third week. Treatment was supportive only. Five months later she had no clinical or laboratory signs of poisoning. DISCUSSION: The patient mistakenly ingested autumn crocus instead of wild garlic because of their great similarity. Colchicine primarily blocks mitosis in tissues with rapid cell turnover; this results in gastroenterocolitis in the first phase of colchicine poisoning, bone marrow hypoplasia with pancytopenia in the second and alopecia in the third, all of which were present in our patient. Colchicine toxicity in tissues without rapid cell turnover caused arrhythmias, acute liver failure and pancreatitis. CONCLUSION: Colchicine poisoning can result in gastroenterocolitis followed by multi-organ dysfunction syndrome. In unexplained gastroenterocolitis after ingestion of wild plants as a salad or spice, especially when wild garlic is mentioned, we should always consider autumn crocus. Diagnosis could be confirmed only by toxicology analyses. Management of colchicine poisoning is restricted to supportive therapy.

Aged↗
PubMed2004

Case report: fatal poisoning with Colchicum autumnale.

INTRODUCTION: Colchicum autumnale, commonly known as the autumn crocus, contains alkaloid colchicine with antimitotic properties. CASE REPORT: A 76-year-old man with a history of alcoholic liver disease and renal insufficiency, who mistakenly ingested Colchicum autumnale instead of wild garlic (Aliium ursinum), presented with nausea, vomiting and diarrhea 12 hours after ingestion. On admission the patient had laboratory signs of dehydration. On the second day the patient became somnolent and developed respiratory insufficiency. The echocardiogram showed heart dilatation with diffuse hypokinesia with positive troponin I. The respiratory insufficiency was further deteriorated by pneumonia, confirmed by chest X-ray and later on by autopsy. Laboratory tests also revealed rhabdomyolysis, coagulopathy and deterioration of renal function and hepatic function. The toxicological analysis disclosed colchicine in the patient's urine (6 microgram/l) and serum (9 microgram/l) on the second day. Therapy was supportive with hydration, vasopressors, mechanical ventilation and antibiotics. On the third day the patient died due to asystolic cardiac arrest. DISCUSSION AND CONCLUSION: Colchicine poisoning should be considered in patients with gastroenterocolitis after a meal of wild plants. Management includes only intensive support therapy. A more severe clinical presentation should be expected in patients with pre-existing liver and renal diseases. The main reasons for death are cardiovascular collapse, respiratory failure and leukopenia with infection.

Aged↗
PubMed2004

S100B protein in carbon monoxide poisoning: a pilot study.

Carbon monoxide (CO) poisoning is the most common form of lethal poisoning. The aim of this prospective clinical study was to assess the possible role of S100B, the structural protein in the astroglia, as a biochemical marker of brain injury in carbon monoxide poisoning. Serum S100B determination was performed in 38 consecutive patients poisoned by carbon monoxide who were admitted to the Emergency Department (ED) in Ljubljana. All three unconscious patients had elevated S100B levels. The patient with the highest S100B died. S100B was elevated in two of the six patients with initial transitory unconsciousness at the scene. All 29 patients without loss of consciousness had normal S100B levels. Carbon monoxide poisoning appears to be associated with elevated S100B levels.

Adolescent↗
PubMed2004

Polydipsia as another mechanism of hyponatremia after 'ecstasy' (3,4 methyldioxymethamphetamine) ingestion.

Acute symptomatic hyponatremia after ecstasy (3,4 methyldioxymethamphetamine; MDMA) ingestion is well documented and has been attributed to the syndrome of inappropriate antidiuretic hormone (SIADH). We report the case of an 18-year-old woman who took five tablets of ecstasy in a suicide attempt and drank 1700 ml water at the Emergency Department (ED). The laboratory findings obtained 5 h after ingestion showed a serum sodium concentration of 130 mmol/l, plasma osmolality of 264 mOsm/kg, urinary osmolality of 335 mOsm/kg and natriuresis of 101 mmol/l. The plasma arginine vasopressin level by radioimmunoassay was 33.7 pmol/l 5 h after ingestion. A gas chromatography-mass spectrometry assay confirmed MDMA in blood samples, with serum concentrations of 0.87 mg/l on arrival. This case report strongly suggests that MDMA reduces serum sodium levels through the dual pathways of SIADH and polydipsia. Accordingly, we believe that hyponatremia may be prevented in ED patients after MDMA ingestion by the early restriction of water intake.

Adolescent↗
PubMed2004

Prognostic value of S100B protein in carbon monoxide-poisoned rats.

OBJECTIVE: To assess the possible role of S100B, a structural protein of astroglial cells, as a biochemical marker in acute carbon monoxide-poisoned rats and to compare its prognostic value with consciousness level, which is one of the major parameters for treatment decision in acute carbon monoxide poisoning. DESIGN: Nonrandomized, controlled interventional trial. SETTING: University laboratory. SUBJECTS: Male Wistar rats weighing 263 +/- 18 g. INTERVENTIONS: The rats were exposed to a mixture of 3000 ppm carbon monoxide in air for 60 mins (group 1) and a mixture of 5000 ppm carbon monoxide in air for 30 mins (group 2). Blood samples were taken from the jugular vein just before and immediately after the carbon monoxide poisoning. The level of consciousness was evaluated at the end of the exposure, and the survival rate was monitored for 7 days. The S100B concentrations were measured with a commercial immunoluminometric assay. MEASUREMENTS AND MAIN RESULTS: In the first group, the unconscious rats after carbon monoxide exposure had significantly higher S100B levels compared with the rats without loss of consciousness. In the second group, the unconscious rats that later died had significantly higher S100B levels compared with the unconscious rats that survived. The S100B levels of all conscious and unconscious surviving rats were not significantly different. The serum level of S100B below 0.44 microg/L predicted survival of carbon monoxide-poisoned rats, with a sensitivity of 100% and a specificity of 86%. CONCLUSIONS: Acute carbon monoxide poisoning is associated with elevated S100B levels. S100B is a better predictor of final outcome than the consciousness level, so it could be used as a prognostic parameter for acute carbon monoxide poisoning in rats.

Animals↗
PubMed2003

The potential value of the protein S-100B level as a criterion for hyperbaric oxygen treatment and prognostic marker in carbon monoxide poisoned patients.

Carbon monoxide (CO) poisoning resulting in diffuse tissue hypoxia. Cerebral hypoxia is a major cause of morbidity and mortality after CO poisoning. There are some clinical criteria that could help a physician to make a decision concerning the application of hyperbaric oxygenation therapy. However, it would be convenient to discover an objective biochemical serum marker that could help in the grade evaluation of CO poisoning and indication of therapy in CO-poisoned patients. We present two case reports where the established criteria for the CO poisoning were not optimum for the decision regarding therapy. It seems that the S-100B protein could be used as a biochemical marker of CO induced brain injury. S-100B values could perhaps help us to select patients for hyperbaric oxygen therapy and to predict the short and long term outcome.

Adult↗