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Biomedical subjects

P Sauder

Publications and source records attributed to P Sauder.

44 records · Page 3Linked to original sources
PubMedDate not supplied

Toxicokinetics of lithium intoxication treated by hemodialysis.

A 66-year old female on long-term lithium therapy, developed neurologic toxicity with coma and convulsions. The treatment consisted artificial ventilation, fluid and electrolyte infusions and a six hour hemodialysis (HD) on days 2, 3 and 4. The convulsions disappeared on day 4; the patient regained consciousness on day l2 and recovered with slight sequelae. Toxicokinetic studies were conducted for a period of 12 days. The lithium (Li) serum concentration fell from 4.4 mmol/l on admission to 2.16 before HD and 0.35 after three HD. Li serum half life was 54 hours before HD, 25 hours during the three days on which HD was carried out and 106 hours thereafter. The Li cerebrospinal fluid/Li serum ratio ranged between 0.4 and 0.6 and was not influenced by HD. Mean renal clearance was 10.6 ml per min. During hemodialysis, Li serum half life decreased to 3.5 - 4.9 hours and clearance was 108 ml/min. A total amount of l28.6 mmol lithium was excreted; 84.3 mmol by HD and 44.3 mmol in urine. Patient's clinical course and electroencephalographic signs were correlated with the calculated cellular pool of Li but not with Li serum concentrations. This study confirms the effectiveness of HD to decrease the cellular pool of lithium. However, rather than considering only the absolute Li serum concentration, the presence of a rebound peak after HD may be viewed as indication for further hemodialysis.

Aged↗
PubMedDate not supplied

[Toxicity of calcium inhibitors].

Calcium antagonists decrease the intracellular concentration of calcium ions. They act essentially on the smooth vascular muscle, on the cardiac muscle and on the automatic and conducting cells in the heart. At toxic doses these effects induce hypotension, shock and disturbances of sinusal automatism and atrio-ventricular conduction. The toxicity of the different calcium antagonists varies according to their tissue specificity. The treatment of overdose includes gastric lavage, oral activated charcoal, cardiorespiratory support, especially alphamimetic vasopressors for shock or hypotension, adrenaline or cardiac pacing for atrio-ventricular block.

Animals↗
PubMedDate not supplied

[Acute diltiazem poisoning: kinetic and hemodynamics study].

The authors report three cases of diltiazem overdose with hypotension and atrio-ventricular conduction disturbances. Hemodynamic study in 2 cases showed a hyperkinetic state with a decrease of systemic vascular resistances. Diltiazem kinetics studied in 2 cases showed a plasma half life of 5.4 and 8.3 hours, a prolonged absorption until the 28th hours in one case. Treatment included gastric lavage, oral activated charcoal (2 cases), plasma expanders and in 2 cases vasopressors with alpha effects. All three patients recovered.

Acute Disease↗
PubMedDate not supplied

[Acute verapamil poisoning. 6 cases. Review of the literature].

Six cases of acute verapamil poisoning are reported. The dose ingested ranged between 1.2 and 9.6 g. In all cases other drugs had also been ingested and especially betablockers in two cases. Symptomatology included a cardiogenic shock in two cases and an atrioventricular block in four cases. A hemodynamic study in one case showed a cardiogenic shock with increased systemic vascular resistances. The treatment of cardiogenic shock included artificial ventilation, several vasopressors and inotropic agents and cardiac pacing in one case. All patients recovered without sequelae. A toxicokinetic study performed in two cases showed plasma half lives of 7.9 and 13.2 hours, total body clearances of 425 and 298 ml/min. Only 2 to 4.2 per cent of the dose ingested were eliminated in urine. These results confirm the severity of verapamil overdose and the efficacy of symptomatic treatment by inotropic agents. The high rate of spontaneous elimination by hepatic metabolism does not justify drug removal by extra-corporeal methods.

Acute Disease↗
PubMedDate not supplied

[Hepatitis secondary to a gold salt overdose].

The authors report the case of a 51-year-old woman who developed cholestatic and cytolytic hepatitis after an overdose of sodium aurothiopropanol sulfonate 1.1 g, namely 300 mg gold metal. Liver biopsy demonstrated cholestasis, centrolobular steatosis and portal fibrosis. Electron microscopy showed abundant lipo-pigments in the hepatic and cellular cells, as well as myelinic bodies. Gold analysis by atomic absorption spectroscopy showed a level of 22.76 micrograms per ml in the plasma and a level of 2.16 micrograms per g in the liver. Chelating agents increased the urinary gold excretion, but were without effect on the course of hepatitis. Dimercaptopropanol seemed to favor the occurrence of other gold salt side-effects and penicillamine increased the hepatic cytolysis. The patient recovered without sequelae.

Anti-Inflammatory Agents↗
PubMedDate not supplied

Soybean oil, blackcurrant seed oil, medium-chain triglycerides, and plasma phospholipid fatty acids of stressed patients.

Thirty-six adult severe head injury and cerebral stroke patients in four intensive-care units were randomized to receive one of three enteral diets for 21 days. These diets, which supplied 45% of calories from fat, differed only in lipid composition. Diet A was comprised of 100% soybean oil, diet B contained a 50:50 (wt/wt) mixture of soybean oil and medium-chain triglycerides (MCTs), and diet C contained 42.5% MCT, 50% soybean oil, and 7.5% blackcurrant seed oils. Plasma phosphatidylcholine and fatty acid composition of plasma total phospholipids were determined before initiating treatment (day 0) and weekly throughout the study. Results indicated that at the start of the study, all patients had low linoleic acid (18:2 omega 6) levels compared with healthy subjects. Emulsion A disturbed the balance between several fatty acids of the omega 6 series, as exemplified by the significant increase in 18:2 omega 6 proportions. In contrast, both emulsions B and C introduced a less-pronounced rise in 18:2 omega 6 associated for emulsion C with a significant increase in dihomo-gamma-linolenic acid (20:3 omega 6) and docosapentaenoic acid (22:5 omega 3) in plasma phospholipids. Furthermore, 18:3 omega 6 change was significantly different between groups A and C and that of 20:3 omega 6 between group A and both groups B and C. Throughout the study, arachidonic acid (20:4 omega 6) exhibited remarkable steady-state levels regardless of the diet. This study shows that providing the injured body with high amounts of 18:2 omega 6 does not lead to high levels of its upper derivatives in plasma phospholipids.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗