Haemodialysis clearance of baclofen BRVAR, Miran; VRTOVEC, Matjaz; KOVAC, Damjan ...
European journal of clinical pharmacology,
12/2007, Letnik:
63, Številka:
12
Journal Article
Recenzirano
Baclofen is a centrally acting gamma-aminobutyric acid agonist used for spasticity of spinal origin and mainly excreted unchanged by the kidneys. We report haemodialysis clearance and the ...haemodialysis removal rate constant of baclofen in a comatose patient with baclofen overdose due to acute renal failure.
A 60-year-old man with spastic tetraplegia on chronic baclofen therapy was admitted due to pneumonia and acute renal failure. The patient became comatose and, as a result of the baclofen dosage being left unchanged despite a deterioration leading to renal failure due to hypotension, the concentration of baclofen was determined to be in the toxic range (0.70 mg/L). During a 4-hour-long bicarbonate haemodialysis the patient woke up and became completely orientated and cooperative. Baclofen therapy was subsequently stopped, and the patient remained conscious. The pharmacokinetics calculations revealed a baclofen haemodialysis removal rate constant of 0.152 h(-1) and a haemodialysis clearance of 2.14 mL/s.
Patients on a stable baclofen regime can develop baclofen toxicity due to acute renal failure. Haemodialysis removes baclofen as effectively as normal kidneys, and it would appear that haemodialysis is a reasonable treatment modality in patients with accidental baclofen overdose due to acute renal failure.
Acute ethanol ingestion can prolong the PR interval, but searching Medline, we have found only one report of Wenckebach-type atrioventricular block in ethanol poisoning. We present a high-degree ...atrioventricular block in an ethanol-poisoned patient.
A 17-year-old woman with a non-contributory medical history ingested 3dcl of vodka and was found comatose. On arrival she was somnolent with nausea, tympanic temperature 36.0 degrees C, pulse 70 counts/min, blood pressure 90/60 mmHg, respiratory rate 12 counts/min and SpO(2) 96% on room air. Her blood ethanol level was 130 mg/dL; other blood laboratory test results were normal. ECG revealed sinus rhythm, first-degree atrioventricular block with a PR interval of 0.32 seconds and intermittent second- and third-degree atrioventricular blocks with up to 4-second-long pauses that appeared 15-30 seconds after each vomiting. She was given thiethylperazine and vomiting resolved within an hour. ECG 12 hours after admission revealed a first-degree atrioventricular block with a PR interval of 0.24 seconds. One month later Holter monitor showed a sinus rhythm and first-degree atrioventricular block with a PR interval of 0.21 seconds. Vagal maneuvers did not provoke high-degree atrioventricular block. The echocardiogram was normal.
Acute ethanol poisoning has the potential to prolong the PR interval in adults with first-degree atrioventricular block and provoke intermittent second- and third-degree atrioventricular blocks, possibly by its direct inhibitory action on the conduction system and increasing parasympathetic tone due to nausea and vomiting.
Introduction: The progressive clinical course with delayed neurological damage in carbon monoxide (CO) poisoning may be due to neuron apoptosis. The usefulness of hyperbaric oxygen (HBO) in different ...time periods after CO exposure in neuronal cell apoptosis reduction has not been evaluated thus far. The aim was to evaluate HBO efficacy in reducing neuronal apoptosis in different time periods after CO exposure.
Methods: Wistar rats were exposed to 3000 ppm CO in air for 60 min and 100% oxygen at a pressure of three bar for 30 min 0-12 h after CO exposure. The apoptosis was evaluated by immunohistochemical analysis with antibodies against activated caspase-3 and the percentage of caspase-3 positive hippocampal ganglionic cells was reported.
Results: It was shown that CO poisoning results in ganglionic cell apoptosis. The percentage of apoptotic cells in rats exposed to CO was the highest (32%), whereas the percentage of apoptotic cells in rats exposed to HBO 0 and 1 h after CO was similar with a lower percentage than rats exposed to CO. The percentage of apoptotic cells in rats exposed to HBO 3 and 5 h after CO was similar with a lower percentage than rats exposed to HBO 0 and 1 h after CO. The percentage of apoptotic cells in rats exposed to HBO 7-12 h after CO was similar with a higher percentage than rats exposed to HBO 5 h after CO.
Conclusion: HBO has a time-dependent protective effect on CO-induced neuron apoptosis with the highest efficiency at 3 and 5 h after CO poisoning.
Colchicum autumnale, commonly known as the autumn crocus, contains alkaloid colchicine with antimitotic properties.
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.
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.
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.
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.
Randomized, controlled interventional trial.
University laboratory.
: Male Wistar rats weighing 254 +/- 14 g.
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.
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.
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.
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