Biomedical subjects

K E Hovda

Publications and source records attributed to K E Hovda.

6 recordsLinked to original sources

PubMed2006

Clinical vs. laboratory identification of drugs of abuse in patients admitted for acute poisoning.

OBJECTIVE: The extent of drug abuse in patients admitted for self-poisonings is uncertain. The aim of this study was to assess the pattern of drugs of abuse among patients admitted for acute poisoning according to age and gender, and to study the concordance between the clinical assessments by the physicians on duty and the drug analyses. METHODS: Prospective cross sectional study of all patients (n = 405, 52% males, median age 31 years) treated for acute poisoning in our department during one year (2001). The physician on-call classified type of drug of abuse by history and clinical assessment. This was later compared to urine and blood samples analysed for ethanol, benzodiazepines, opiates, cocaine, ecstasy, GHB, amphetamine and cannabis. RESULTS: In 320 admissions (79%), the comparison between clinical diagnosis and laboratory analyses could be performed. A total of 478 drugs were suspected and 621 were found. The main toxic agents found were benzodiazepines (49.7%), ethanol (40.3%), opiates (35.3%), cannabis (23.8%) and amphetamine (21.3%). Ninety-two had used drugs of abuse. The agreement between clinical assessments and laboratory findings was best for GHB and ethanol (kappa = 0.43), and for opiates (k = 0.38). For benzodiazepines and cannabis, the concordance was poor (k = 0.18 and 0.10, respectively). However, the correct clinical evaluation for these substances was 59% and 77%, respectively. CONCLUSIONS: Drugs of abuse were more frequently found than suspected clinically. Benzodiazepines, ethanol and opiates were most common. The agreement between clinical assessment and drug analyses was moderate to low. Physicians seem to underestimate the use of these drugs.

Acute Disease↗

PubMed2005

Methanol outbreak in Norway 2002-2004: epidemiology, clinical features and prognostic signs.

OBJECTIVES: Knowledge on methanol poisoning does mainly come from clinical studies. We therefore report epidemiological, clinical and prognostic features from the large methanol outbreak in Norway in 2002-2004 where the new antidote fomepizole was the primary antidote in use. DESIGN AND SUBJECTS: Combined prospective and retrospective case series study of 51 hospitalized patients who were confirmed poisoned with methanol, of whom nine died. In addition, eight patients died outside hospital. Most patients were admitted in a late stage and because of symptoms. Treatment consisted of alkali, fomepizole (71%) and haemodialysis (73%). RESULTS: The median serum methanol was 25.0 mmol L-1 (80 mg dL-1) (range 3.1-147.0 mmol L-1), median pH was 7.20 (6.50-7.50), and median base deficit 22 mmol L-1 (range 0-31). The most frequent clinical features reported were visual disturbances (55%), dyspnoea (41%), and gastrointestinal symptoms (43%). Twenty-four per cent were comatose on admission, of whom 67% died. There was a trend towards decreasing pCO2 with decreasing pH amongst the patients surviving. The opposite trend was demonstrated in the dying; the difference was highly significant by linear regression analyses (P<0.001). CONCLUSIONS: Methanol poisoning still has a high morbidity and mortality, mainly because of late diagnosis and treatment. Respiratory arrest, coma and severe metabolic acidosis (pH<6.90, base deficit>28 mmol L-1) upon admission were strong predictors of poor outcome. Early admission and ability of respiratory compensation of metabolic acidosis was associated with survival.

Adult↗

PubMed2005

Fomepizole may change indication for hemodialysis in methanol poisoning: prospective study in seven cases.

BACKGROUND: Treatment of methanol poisoning includes administration of buffer, antidote and hemodialysis. The role of hemodialysis using the new antidote fomepizole has not been studied. We studied the kinetics of methanol and formate during hemodialysis, and the possibility for delayed hemodialysis in the methanol poisoned patients without severe metabolic acidosis or visual disturbances. PATIENTS AND METHODS: Prospective case series study on methanol, formate and dialysis kinetics in 7 cases of severe methanol poisoning treated with buffer, fomepizole and hemodialysis (average 7 hours, range 5 - 8). Four patients were dialyzed early after diagnosis was obtained, while three were dialyzed "electively" the next day. RESULTS: The median pH upon admission was 6.9 (range 6.6 - 7.5) and median base deficit 20.4 mmol/l (range 5.1 - 30.0). Their median S-methanol was 76.3 mmol/l (range 15.6 - 140.6) and S-formate 13.6 mmol/l (range 3.3 - 21). The median half-life of methanol during fomepizole treatment before dialysis was 71.2 hours (range 69.3 - 77); compared to 2.5 hours (range 1.7 - 3.3) during procedure. The median half-life of formate during dialysis was 1.7 hours (range 1.5 - 1.9). The median dialysis clearance of methanol was 222 ml/min (range 204 - 232) and for formate 225 ml/min (range 220 - 229) at a blood flow of 250 ml/min. One patient died and 2 were discharged with permanent visual and cerebral sequelae, whereas one died one year later. All three patients, in whom "elective" hemodialysis was performed, were discharged without sequelae. CONCLUSION: The efficacy and side effect profile of fomepizole may change the role of hemodialysis in methanol poisoning. More patients may be stabilized in local hospitals and transferred for "elective" dialysis, if methanol removal is still indicated after correction of metabolic acidosis.

Acidosis↗

PubMed2003

Conventional and diffusion-weighted MRI in the evaluation of methanol poisoning.

Cerebral lesions were studied in 2 methanol-poisoned patients using conventional magnetic resonance imaging (MRI). In 1 patient, diffusion-weighted MRI (DWI) was also performed. In this patient, conventional MRI showed symmetrical, bilateral increased signal in the lentiform nuclei, involving predominantly putamina, but also extending into the corona radiata, centrum semiovale and subcortical white matter. DWI showed decreased diffusion, which most probably reflects cytotoxic edema. In the other patient, fluid attenuated-inversion recovery (FLAIR) and T2-weighted images showed hyperintensity in the putamina, characteristic of post-necrotic changes.

Adult↗

PubMed1998

[Ecstasy--cool dope with long-lasting effects?].

The amphetamine derivative MDMA (3,4-methylenedioxymethamphetamine) was first synthesised in 1914 as an appetite suppressant, but was never used as such. MDMA is commonly known as "ecstasy" and has become a popular recreational drug of abuse at dance-clubs and rave parties, where it is combined with all-night dancing, crowded conditions, poor hydration and loud sound. This combination is probably the main reason why we have seen an upsurge in toxicity problems at rave parties, since all these factors are thought to promote or increase the toxicity of MDMA. The desired effects of MDMA are euphoria, increased energy and enhanced communication with others. Adverse effects are hyperthermia, rhabdomyolysis, acute renal failure, hepatotoxicity, depression and psychosis.

3,4-Methylenedioxyamphetamine↗

PubMed1998

[Gamma-hydroxybutyrate--an endogenous substance and an intoxicant].

Gamma-hydroxybutyrate (GHB), a compound found in the mammalian brain, meets many criteria of a neurotransmitter. Experimentally, GHB has been used as a model for petit mal epilepsy; clinically it has been used as a general anaesthetic, to treat certain sleep disorders and alcoholism. Lately GHB has been abused for its euphoric, sedative and anabolic effects. Coma and seizures following abuse of GHB have been reported, but dependency has received little attention. Adverse effects of GHB include seizure activity and a withdrawal syndrome characterised by insomnia, anxiety and tremor. The present paper reviews the neuropharmacology, potential therapeutic uses and acute adverse effects of GHB, together with a presentation of three cases.

Adult↗