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Biomedical subjects

A Jaeger

Publications and source records attributed to A Jaeger.

At least 73 records · Page 4Linked to original sources
PubMed1983

[Pulmonary edema caused by heroin. Hemodynamic study of 2 cases].

The authors report two cases of heroin induced pulmonary edema. In both cases the severity of respiratory failure, attested by a deep hypoxemia (paO2 28 and 32 mmHg) and a metabolic and respiratory acidosis (pH 7.07 and 7.14) imposed an artificial ventilation with positive end expiratory pressure (PEEP). Hemodynamic study revealed a noncardiogenic edema. In both cases, a cardiac insufficiency was also present : in the first case it's etiology remained unclear, in the second it was a complication of hyperkalemia.

Acidosis↗
PubMed1983

[Acute poisoning by inhalation of metallic vapors].

Seven cases of acute intoxications by inhalation of metallic vapors are reported. The metals involved were zinc in three cases, tin in one case and mercury in three cases. The severity of the respiratory symptoms was dependent from the inhalated metal. The inhalation of zinc or tin vapors produced an acute limited pneumonitis. A lesional pulmonary oedema and acute interstitial fibrosis with lethal outcome was observed in two cases of intoxication by mercury vapors. The treatment by dimercaptopropanol used in mercury intoxications, increased urinary mercury excretion, but did not improve the pulmonary symptoms.

Adult↗
PubMed1983

[The pulmonary toxicity of mercury vapors in the rat].

Rats have been exposed for periods of 120 to 240 minutes to an atmosphere containing 6 +/- 0.7 mg per cu.m mercury vapor. All rats developed an acute respiratory distress which lead to death within 2 to 210 hours (mean 53.5 h). Microscopical examination of the lungs showed an oedema rich in fibrin, an epithelial necrosis, hyaline membranes and in two cases an interstitial fibrosis. Mercury levels in the lungs ranged between 0.5 and 9.37 micrograms per gramme wet weight. The activity of pulmonary superoxide dismutase was decreased to 1.57 +/- 0.66 micrograms per mg of soluble proteins, compared with the level of 5.01 +/- 0.76 micrograms per mg in control rats. This study confirm the pulmonary toxicity of mercury vapors observed in human intoxication.

Animals↗
PubMed1982

[Acute nadoxolol poisoning. A multicentric study of 35 cases].

Between 1976 and 1980, 35 cases of nadoxolol poisoning were collected from french antipoison centers. Acute intoxication was voluntary (50%) or accidental (50%). The ingested dose ranged between 0,25 and 22,5 g. Clinical symptoms appeared three hours after ingestion and consisted of cardio-vascular disorders which were present in 10 patients: bradycardia (7 cases), cardiogenic shock (6 cases), intraventricular block (5 cases), increase of P.R. interval (4 cases) and Q.T. interval (3 cases). The toxic dose in otherwise healthy adults was 5 g. The treatment consisted of gastric lavage and correction of cardiovascular disorders with sodium lactate (4 cases) or dopamine (1 case). All the patients recovered.

Acute Disease↗
PubMed1981

[Acute voluntary or accidental disopyramide poisoning. A multicentric study of 106 cases (author's transl)].

Between 1972 and 1978, 106 case-records of disopyramide poisoning were collected from French anti-poison center. Acute intoxication was voluntary in 90% of the cases and occurred in young adults. Clinical symptoms appeared early and consisted mostly of cardiovascular disorders, which were present in 60 patients: cardiogenic shock (24 cases), circulatory arrest (17 cases), atrio-ventricular block (21 cases), intraventricular block (24 cases) and severe ventricular arrhythmia (12 cases). The toxic dose in otherwise healthy adults was 1,5 g and the mortality rate was high (12,2%). An analysis of therapeutic measures and outcome indicated that the best treatment consists of early gastric lavage, cardiorespiratory manoeuvres, electric heart stimulation, administration of sodium lactate in cases with intraventricular conduction disturbances and isoprenaline in cases with cardiogenic shock.

Acute Disease↗
PubMed1981

[Mild spontaneous course of a case of pseudomembranous colitis. Case report and literature review].

Pseudomembranous colitis (PMC) caused by a toxin produced by Clostridium difficile is described in the literature as a severe diarrheal disease with a high mortality rate. A case which tends to absolve PMC from this reputation is reported involving an outpatient who developed well documented PMC subsequent to ampicillin therapy but required no treatment. The number of unreported cases of antibiotic-associated colitis with and without pseudomembrane formation is probably very high, since only severe cases of diarrhea are thoroughly investigated. In a chronological literature review an attempt is made to update the nomenclature of antibiotic-associated colitis. There are recent reports of a connection between the Clostridium difficile toxin and the chronic inflammatory "non-bacterial" intestinal diseases ulcerative colitis and Crohn's disease. The authors finally consider whether in cases of antibiotic-associated diarrhea efforts should be made to isolate Clostridium difficile and/or demonstrate the presence of its toxin, for the purposes of prognosis and therapy.

Ampicillin↗
PubMed1981

Light and electron microscopic study of ear cartilage in a case of relapsing polychondritis evolving under corticoid treatment.

Light and electron microscope studies of the ear cartilage in a patient with relapsing polychondritis (RP) under corticoid treatment are reported. Unilateral auricular deformation evolved without inflammatory epidoses and the lesions consisted mainly of marginal erosions filled with fine collagen fibrils and containing degenerating perichondrial cells in their basal parts. Degenerative cells were scattered throughout the perichondrium, but cartilage erosions only occurred when numerous cells were affected in a same area. Cartilage outside the eroded zones did not seem to be modified. Cartilage lesions thus appear to be a result of a chondrocyte renewal defect leading to loss of proteoglycans and elastic fibers, with only collagen remaining. These data suggest that inflammation is probably not the initial pathogenic process responsible for cartilage injury in RP, but that a metabolic defect in perichondrial cells might be involved.

Adrenal Cortex Hormones↗
PubMed1981

[Acute post-operative peritonitis in gastro-enterological surgery. Opinion of the intensive care unit (author's transl)].

Acute purulent post-operative peritonitis is highly severe and difficult to diagnose. Six symptoms have a real prognostic value: shock, acute renal insufficiency, respiratory failure, jaundice, acidosis and septicaemia. If more than three of these signs of severity coexist, the mortality rate reaches nearly 100%. A patient with evidence of acute diffuse post-operative peritonitis must be operated on after a short preoperative treatment to restore a situation altered by shock, renal failure and pulmonary edema. Antibiotic agent alone, though necessary, cannot bring recovery. The maintenance of high nutritional intake for excess caloric expenditure is essential. The effects of the early decision of a surgical reintervention are studied in 27 patients with only two recoveries.

Acute Disease↗