[Gas embolism after withdrawal of central venous catheters. A little known iatrogenic accident].
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Biomedical subjects
Publications and source records attributed to D Perrot.
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The binding affinities of two steroid anaesthetics, alphaxalone (Alfx) and alphadolone acetate (Alfd), for testosterone-oestradiol-binding globulin (TeBG) and corticosteroid-binding globulin (CBG) were measured in human serum. In 8 male patients, the effect of i.v. administration of Althesin (a mixture of Alfx and Alfd) on the transport of testosterone (T) and cortisol (F) was studied. Both Alfx and Alfd bind to TeBG and CBG with a relatively high affinity (10(6)M-1). A significant change in the percentage of unbound T was observed during Althesin infusion, with no change in total T concentration or in the TeBG binding parameters. The results suggest that by interaction with TeBG binding sites Alfx and/or Alfd displaced T bound to TeBG, and transiently increased the percentage of unbound T. A significant increase in the concentration of F was observed during althesin infusion, while the percentage of unbound F and the CBG binding parameters were unchanged. The dose of Alfx and Alfd used was not sufficient to alter the transport of F during brief althesin anaesthesia in men.
A new case of oxytocin-induced water intoxication is reported in a 30 year old gravid woman. The severe symptoms of this uncommon complication are principally neurological; biological signs are a hyponatraemia with low plasma osmolality. Usually, biological and clinical signs are rapidly cleared up by treatment, but maternal death or neonatal water intoxication may occur. Such accidents must be prevented by clinical monitoring, watching out for alarm signals (oliguria is always found, resulting from the effect of oxytocin on the kidney), minimum fluid and proportional salt intakes, careful monitoring of oxytocin infusion rates, facilitated by the use of a constant flow-rate pump.
A 22-year-old woman had an idiopathic pure red cell aplasia that failed to respond to high doses of corticosteroids. After a series of 10 plasma exchange procedures, bone marrow erythropoiesis and reticulocyte blood count returned to normal; the haematological remission has been now persistent for 12 months. The place of plasma exchange in the management of pure red cell aplasia and its mode of action will be discussed.
A 73 years old patient, treated with Amiodarone for ventricular tachycardia, ingested 6 000 mg of Amiodarone. This did not induce hemodynamic troubles or aggravation of ventricular arrhythmia. Treatment included a gastric lavage and purging at the third hour. Plasma assay revealed a concentration of 3.69 mg/l at the fourth hour. Their evolution can be described as the sum of two exponentials. The half-life of the first exponential is 4.9 hours ; the half-life of the second one is 544 hours. Amiodarone is an antiarrhythmic agent of high safety.
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Between 1977 and 1982, fifty cases of post-traumatic fat embolism were treated in a general intensive care unit. Average age of patients was 25.5 +/- 13 years; there was no male majority. Mean free interval was 39 +/- 27 h. 12 cases (24%) had single fractures and 38 (76%) multiple fractures. Forty-four patients had a fractured femur. Thirty-two patients presented the complete clinical syndrome with general, respiratory, neurological and cutaneous signs. Thrombocytopaenia and hypocholesterolaemia were the biological signs most often seen. In forty-four patients, orthopaedic treatment consisted of immediate immobilization, usually with traction. Twenty-six patients were reoperated on: intramedullary nail for twenty patients, plate for the other six. Fat embolism appeared in spite of surgery in six cases; it worsened after surgery in six others. Seven patients had per- or postanaesthetic problems. Fourteen per cent of patients died. The decrease in mortality was mainly due to an improvement in mechanical ventilation techniques. Early surgical fixation remained the rule if there was no serious respiratory distress or haemodynamic instability, although it did not seem to change the mortality rate in this group of patients.
The possible physiological targets of pp60src in chicken embryo fibroblasts transformed by Rous sarcoma virus were looked for by a general screening of the modifications of phosphorylation of the major cell phosphoproteins. These modifications were analyzed quantitatively by SDS-PAGE of total cell proteins on gradient gels, combined with a computerized densitometric evaluation of gel autoradiographies, using cells labeled with either [14C]-amino acids or with [32P]-phosphate. A large numbers of proteins, 37 out of the 68 studied, were found to be more phosphorylated in virally transformed cells. The determination of the phosphoamino acid content of proteins which were more phosphorylated in transformed cells and the study of the kinetics of protein phosphorylation in cells infected by a ts mutant, after a shift from the nonpermissive to the permissive temperature, showed that, among these proteins, five displayed a large increase in phosphotyrosine content and an early increase in phosphorylation after the temperature shift. These proteins of 36 K, 41 K, 46 K, 65 K and 280-300 K doublet are therefore good candidates for being physiological targets of pp60src in the cell.
On the basis of a series of 18 cases of severe eclampsia, the authors analyse the predisposing circumstances for these episodes and the method of delivery. Caesarian section is still the usual method of delivery in severe cases (12/18). There is a high perinatal mortality (4/18), which is principally due to foetal distress which is inevitable during the episodes, to hypotrophy which is present in 3 out of 4 cases and to prematurity. There were no maternal deaths in this particular series. In the second part of the article, the authors consider the management and treatment of the eclamptic episode itself: relieve the maternal and foetal anoxia, stabilize the blood pressure, correct the hypovolaemia and prevent the development of convulsions.
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Thirty-two patients receiving artificial ventilation of the lungs were studied to determine if variations in PACO2 could be reflected in variation in PaCO2. Eleven patients had chronic obstructive lung disease, eight had suffered acute respiratory failure, and 13 had neurological disturbances but normal lungs. PaCO2 and PACO2 were measured concurrently as ventilatory patterns, haemodynamic state or inspired gas concentrations changed. Neither change in inspired oxygen concentration nor change in haemodynamic state had much effect PaCO2 or PACO2. Change in PaCO2 induced by ventilatory change and by change in inspired carbon dioxide concentration were well described by linear regression of PaCO2 on PaCO2. In patients with chronic lung disease, (PaCO2-PACO2) was the same at all values of PACO2 whereas, in the other patients the ratio PaCO2/PACO2 did not change.
Seven cases of acute ajmaline overdose admitted over a 3 year period to a polyvalent intensive care unit are reported. The severity of this condition is related to the membrane stabilising and depolarising effects of ajmaline on the myocardium. The dose ingested varied from 10 to 40 mg/kg. The delay between ingestion and hospital admission ranged from 3 to 6 1/2 hours. The first cardiac disturbances can appear one hour after ingestion. Three cardiac arrests and one hypovolemic shock occurred. Three atrioventricular blocks, six intraventricular blocks, three ventricular tachycardias, and six prolongations of the QT interval were observed. Serum ajmaline levels varied from 0,8 to 6 mg/l. Symptomatic therapy was mainly based on sodium, temporary cardiac pacing, external DC shock, sympathomimetics and external cardiac massage with assisted ventilation. Cardiac bypass should be a part of the therapeutic arsenal. Elimination of the drug is assisted by a complete digestive evacuation. Renal or extrarenal dialysis is not indicated. One of the seven patients died. Prophylaxis is based on the non-prescription of ajmaline for benign cardiac disturbances.
The authors report 7 cases of acute pulmonary edema in acute carbon monoxide poisoning. Hemodynamic data suggest existence of a myocardial failure as a possible cause of these pulmonary edema and indicate caution for volemic expansion during the treatment of shock in carbon monoxide poisoning.
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A 45-year-old man was hospitalized on 3 occasions for recurrent myalgias with paroxysmal myoglobinuria resulting in two episodes of acute renal failure. The second episode was fatal: the patient died of shock and hyperkaliaemia during haemodialysis. The predominant signs and symptoms were muscle pain with functional deficit, signs of renal failure and a rise in serum enzymes. All examinations were negative between attacks. Muscle biopsies showed a major degree of myolysis, and biochemical tests demonstrated severe muscle palmityl transferase deficiency associated with partial deficiency of muscle carnitine. The diagnostic features and physiopathology of the disease are reviewed.