PubMed Health⌕ Search

Biomedical subjects

D Jacobsen

Publications and source records attributed to D Jacobsen.

At least 91 records · Page 5Linked to original sources
PubMed1984

Clinical course in acute self-poisonings: a prospective study of 1125 consecutively hospitalised adults.

The clinical course in an unselected group of 1125 consecutively hospitalised self-poisonings was studied during 1 year in Oslo. Mortality was 0.5%, but only 0.3% in those admitted without cardiac and respiratory arrest. Mortality among those in grade IV coma was 4.2%. The deepest comas (grade III or IV) occurred in 25.1% of the admissions with a mean duration of the coma of 5.8 h (range 1-80). Complications occurred in 21.7% of the admissions and 6.9% suffered more than one complication of which the most frequent were respiratory depression (13.5%), hypotension (5.3%), pneumonia (4.4%), and hypothermia (1.6%). The complication rate was highest in poisonings with opiates (60.7%), meprobamate (37.5%) and antihistamines (30.0%). Arrhythmias and respiratory depression were closely associated with poisonings with antidepressants and opiates, respectively. Owing to frequent polydrug overdoses it was difficult to associate other complications with other main toxic agents. Administration of antidotes (20.6%), cuffed intubation (4.4%) and forced alkaline diuresis (3.4%) were the most frequent special therapeutic measures taken. The change in pattern of self-poisonings in Oslo focuses on antidote therapy and intensive care, especially outside hospital, but limits the need for haemodialysis and haemoperfusion which were performed in only 1.0% of the admissions.

Acute Disease↗
PubMed1984

Resin haemoperfusion in levomepromazine poisoning: evaluation of effect on plasma drug and metabolite levels.

Plasma levels of levomepromazine and two of its major metabolites N-desmethyl-levomepromazine and levomepromazine sulphoxide were studied in two poisoned patients treated with resin haemoperfusion at a constant blood flow of 200 ml/min. The mean haemoperfusion clearance of levomepromazine, N-desmethyl-levomepromazine and levomepromazine sulphoxide was 114, 123 and 151 ml/min, respectively, in patient no. 1, and 153, 148 and 184 ml/min, respectively, in patient no. 2. Patient no. 2 had also ingested amitriptyline, and the mean haemoperfusion clearance of amitriptyline and its metabolite nortriptyline was 183 and 183 ml/min respectively. Haemoperfusion did not seem to alter the elimination profile of levomepromazine or the two metabolites in either patient. We conclude that haemoperfusion is of little value in removing levomepromazine, N-desmethyl-levomepromazine or levomepromazine sulphoxide from the body. This is probably due to the large apparent volume of distribution and the high intrinsic hepatic metabolic clearance of these compounds.

Adult↗
PubMed1984

Glycolate causes the acidosis in ethylene glycol poisoning and is effectively removed by hemodialysis.

Six male patients with severe ethylene glycol poisoning were studied with respect to the origin of the metabolic acidosis. The plasma concentrations of ethylene glycol were 4-41 mmol/l and treatment included alkali, ethanol and hemodialysis. Plasma analysis by isotachophoresis and whole blood lactate determinations showed that glycolate (17.0-29.3 mmol/l), lactate (1.4-6.2 mmol/l) and beta-hydroxybutyrate (less than or equal to 1.8 mmol/l) were present in elevated concentrations contributing to the acidosis. Oxalate (less than or equal to 0.33 mmol/l), glyoxylate (less than 0.2 mmol/l) and formate (less than 0.4 mmol/l) concentrations were negligible and did not contribute to any significant degree to the acidosis. The elevated plasma glycolate concentration was highly correlated to the anion gap (r = 0.923) and the glycolate made up for 96.1% (n = 6, range 84.7-108.8) of the increased anion gap. We conclude that glycolate accumulation is the main reason for the metabolic acidosis in ethylene glycol poisoning. The mean dialysator (1.6 m2) clearances of glycolate at a blood flow of 200 ml/min in two patients were 137 ml/min (n = 9, SD +/- 8, range 125-149) and 144 ml/min (n = 11, SD +/- 8, range 133-158). By applying first order kinetics during hemodialysis a volume of distribution of glycolate of 0.55 l/kg was found, assuming that the dialysator clearance equals the total body clearance of glycolate. Thus glycolate, the probable main metabolite of ethylene glycol, is efficiently removed by hemodialysis.

Acidosis↗
PubMed1983

Pulmonary excretion of methanol in man.

An otherwise healthy methanol-poisoned male was treated with ethanol and forced diuresis. No acidosis or visual symptoms occurred. His blood ethanol concentrations varied between 10.7 and 30.0 mmol/l (0.49-1.38 g/l). His maximal blood methanol concentration was 14.4 mmol/l (0.45 g/l) and his plasma formate levels were within reference range (0.11-0.29 mmol/l). In a 24 h period where methanol metabolism was blocked by ethanol, the total body clearance and renal clearance of methanol were 11.3 and 5.7 ml/min, respectively. The difference, 5.6 ml/min, to a large extent reflects the pulmonary clearance of methanol thus being low in man.

Adult↗
PubMed1983

Formate concentrations in plasma from patients poisoned with methanol.

Formate and methanol were quantified in blood samples from 11 untreated methanol-poisoned subjects. The range for whole blood methanol concentrations was 0-137 mmol/l and for plasma formate concentrations 0.4-17.1 mmol/l. Simultaneously determined acid-base status and serum electrolyte concentrations allowed assessment of the relative importance of formate accumulation for the acidosis. The plasma formate concentration was highly correlated to both the calculated anion gap (r = 0.833), the bicarbonate concentration (r = 0.852) and the negative base excess (r = 0.865). The accumulation of formate fully accounted for the increase in the anion gap and the fall in plasma bicarbonate, whereas the negative base excess values were about 22% higher than the plasma formate concentration. We conclude that formate accumulation is the main or only reason for acidosis in the early, uncomplicated stages of methanol poisoning. Lactate may appear at more advanced stages.

Acid-Base Imbalance↗
PubMed1983

Toxicokinetics of formate during hemodialysis.

During hemodialysis in a methanol poisoned patient, formate elimination followed first order kinetics with a plasma half-life of formate of 165 min. The mean dialysator (1.6 m2) clearance of formate was 148 ml/min (n = 8, SD +/- 11, range 128-161) at a blood flow of 215 ml/min. By applying first order kinetics, a volume of distribution of 0.5 l/kg was found, assuming that the dialysator clearance equals the total body clearance of formate. Formate, the main toxic agent in methanol poisoning, is thus probably more effectively removed by hemodialysis than methanol. This fact, and the very slow endogenous methanol elimination during appropriate ethanol treatment, should be considered when deciding on the treatment of a methanol poisoned patient presenting with metabolic acidosis.

Adult↗
PubMed1983

Acute poisonings of children in Oslo. A one year prospective study.

A one year prospective study of all children under 15 years of age presenting for acute poisoning in Oslo is reported. There were 181 admissions in 179 children, of which 97 (54%) were boys, giving an annual incidence of 2.3%. All children survived without sequelae. Most poisonings were accidental and only two suicidal attempts were recorded. Of all poisonings 68 per cent occurred between the age of 1 and 2 years. The dominating toxic agents were drugs (44%), tobacco (22%) and petroleum products (9%). Most poisonings were mild and only 7 (4%) classified as severe. Seventy-two per cent of all children were admitted within the second hour after the ingestion of the toxic agent. Therapy should therefore be directed towards emptying the stomach with emetics or gastric lavage, unless corrosives or petroleum products are ingested. Childhood poisonings still call for better preventive measures since the toxic agent was found inappropriately stored in 86% of the accidental poisonings.

Accident Prevention↗
PubMed1982

Urinary calcium oxalate monohydrate crystals in ethylene glycol poisoning.

Four patients admitted for ethylene glycol intoxication had massive crystalluria, predominantly of needle-shaped calcium oxalate monohydrate--sometimes referred to as the 'hemp seed' habit. A few 'envelope' type crystals of calcium oxalate dihydrate were observed in one urine sample. Although not a pathognomonic sign, the presence of a large number of calcium oxalate monohydrate crystals (Whewellite) supports the diagnosis of ethylene glycol poisoning in patients having a metabolic acidosis of unknown aetiology. We conclude that the monohydrate form rather than the dihydrate form is the predominant type of calcium oxalate crystal formed in ethylene glycol poisoning.

Adult↗
PubMed1982

Studies on methanol poisoning.

Eleven patients concomitantly poisoned with methanol are described. Their whole blood methanol concentration ranged from 137.2 mmol/l (4.39 g/l) to 7.4 mmol/l (0.24 g/l). The clinical course in most patients was mild, which was attributed to the concomitant and subsequent ethanol ingestion and rapid transport to dialysing units. One patient suffered permanent visual impairment of one eye while the others recovered completely. Symptoms of poisoning were most clearly correlated to the degree of metabolic acidosis. All patients were hemodialysed. In two patients the average dialysator clearance of methanol was 157 and 176 ml/min at blood flows of 200 and 215 ml/min, respectively. In the same patients the average dialysator clearance of ethanol was 149 and 164 ml/min. Assuming a volume of distribution of methanol of 0.7 l/kg, the dialysator represented about 89 and 95%, respectively, of the total body clearance of methanol during ethanol therapy. Ethanol in concentrations even lower than usually recommended may be useful as the only treatment of patients with blood methanol concentrations up to 15 mmol/l (0.5 g/l), provided there is no acidosis or visual impairment.

Adolescent↗
PubMed1982

Studies on ethylene glycol poisoning.

Toxicokinetic studies during hemodialysis are presented in two patients with blood ethylene glycol concentrations of 40 and 41 mmol/l, respectively. Treatment involved bicarbonate, ethanol and hemodialysis with a 1.6 m2 dialysator. Both patients developed acute renal failure and one was discharged with permanent cerebral impairment. The other made an uneventful recovery. The average dialysator clearance of ethylene glycol at a blood flow of 200 ml/min was 145 and 148 ml/min, respectively. Assuming a volume of distribution of ethylene glycol of 0.7 l/kg, the dialysator represented about 92 and 95%, respectively, of the total body clearance of ethylene glycol during ethanol treatment. During hemodialysis a blood ethanol concentration of about 15 mmol/l (0.7 g/l) caused a near complete inhibition of ethylene glycol metabolism at ethylene glycol concentrations up to about 25 mmol/l (1.6 g/l). We recommend prompt hemodialysis in ethylene glycol poisoning to supplement alkali and ethanol treatment.

Acute Kidney Injury↗
PubMed1982

Anion and osmolal gaps in the diagnosis of methanol and ethylene glycol poisoning.

The diagnostic value of determination of the anion and osmolal gaps was studied in 6 patients poisoned with methanol and in 5 poisoned with ethylene glycol. Increased osmolal gap was present on admission in all patients, whereas increased anion gap was present in all except one. In the methanol-poisoned patients the mean blood values were: pH 7.27, anion gap 24 mmol/l, osmolal gap 81 mosmol/kg H2O, methanol 67 mmol/l, ethanol 11 mmol/l and in the ethylene glycol-poisoned patients: pH 6.93, anion gap 38 mmol/l, osmolal gap 35 mosmol/kg H2O and ethylene glycol 24 mmol/l. In the absence of alcoholic acidosis or diabetic coma the finding of a simultaneous increase in both the anion and osmolal gaps indicates methanol or ethylene glycol poisoning. Thus determinations of the anion and osmolal gaps are mandatory whenever facing metabolic acidosis of unknown etiology.

Acid-Base Equilibrium↗