[Blood phosphorus on admission to intensive care. Impact of the simultaneous evaluation of arterial pH].
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Biomedical subjects
Publications and source records attributed to A Rimailho.
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The influence of oral amiodarone on the anticoagulant effect of the coumarin derivative acenocoumarol has been investigated prospectively in 10 patients with normal renal, hepatic and haematological function and who were not in cardiac failure. The daily dose of acenocoumarol was sufficient to produce a prothrombin activity of 25 to 35%. When the prothrombin time had become stable amiodarone 600 mg/d was administered for 1 week followed by 400 mg/d for the next 3 weeks. A decrease in prothrombin activity from 30.5 to 20.2% was observed, associated with a decrease in vitamin K coagulation factors, after a mean of 4 days following commencement of amiodarone. In 6 patients a prothrombin activity less than 20% required a 60% reduction in the dose of acenocoumarol after 1 week of amiodarone 600 mg, and a 33% reduction after 3 weeks of amiodarone 400 mg. There was no correlation between the plasma amiodarone and the decrease in prothrombin activity. Inhibition of acenocoumarol metabolism by amiodarone is the most likely explanation of these findings.
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Two cases of Legionnaires' disease proven by seroconversion in indirect immunofluorescence are reported. Creatine phosphokinase (CPK) was increased in both patients, and one had rhabdomyolysis with acute renal failure and acute respiratory distress. A review of the literature brought out 9 other cases of rhabdomyolysis associated with Legionnaires' disease. Myalgias are an inconstant warning symptom; renal impairment is present in more than one half of the cases, and although pulmonary lesions are moderate, respiratory muscle involvement may require mechanical ventilation. In view of the severe complications of rhabdomyolysis, CPK should be systematically assayed in patients with Legionnaires' disease; 57 p. 100 of whom, according to published reports, have high CPK levels. In a retrospective study of bacterial pneumonia caused by common pathogens, we found that CPK was elevated in 31 p. 100 of the cases. The mechanism of muscular involvement is discussed.
Lower respiratory tract secretions (LRS) were sampled during a two year period in patients undergoing mechanical ventilation using a method previously described by Matthew et al. Only those LRS positive for gram-negative bacilli were reported in this study. The patients were separated in two groups: those with nosocomial pneumonia due to gram-negative bacilli (NP+ group) and those without (NP- group). The species most often isolated from LRS were: Pseudomonas aeruginosa (25%), Proteus (20%), Escherichia coli (18%), Klebsiella pneumoniae (10%), Acinetobacter calcoaceticus (8%) and Haemophilus influenzae (7%). The spectrum of gram-negative species was not statistically different in either group of patients. The numbers of gram-negative bacilli isolated from each LRS were more important in the NP+ group (p less than 0.001), but so was the duration of mechanical ventilation before each LRS (p less than 0.01). In this group also, a specific bacteriological diagnosis with only one species was possible in 3 out of the 13 cases; a tentative diagnosis only was possible in 10 cases: in 6 cases, the responsibility of two (or more) species was suggested. The susceptibility to antibiotics of gram-negative bacilli isolated from LRS was moderate. A third generation cephalosporin together with amikacin seemed to be the best choice of antibiotics when no specific bacteriological diagnosis could be made with the LRS.
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A 53 year old man with an anaplastic bronchial carcinoma was hospitalised for septic shock and acute respiratory distress after a cutaneous, probably staphylococcal infection, and died in spite of anti-staphylococcal antibiotherapy. The autopsy showed pulmonary, cardiac, cerebral and renal aspergillosis. A right heart aspergillous endocarditis, very rare in this pathology, was also discovered but there were no cardiac valves lesions. The patient was in an "immunodepressed" state as usually observed in pulmonary aspergillosis. The endocardial localisation of aspergillosis and the "pseudo-miliary" appearances of the pulmonary lesion indicated an extra-pulmonary portal of entry, cutaneous or intravenous which is unusual in this pathology. This hypothesis is supported by previous reports of pulmonary aspergillosis where right heart endocarditis is exceptionally rare and by aspergillous left heart endocarditis after open heart surgery where pulmonary aspergillosis is absent.
Antimicrobial sensitivities, especially trimethoprim-sulfamethoxazole, were studied in all clinical isolates of Escherichia coli in an intensive care unit for over 18 months. Twenty-four per cent of strains were resistant to trimethoprim-sulfamethoxazole. Combined resistance to ampicillin +/- chloramphenicol (+/- tetracycline) and streptomycin (+/- kanamycin) with resistance to trimethoprim-sulfamethoxazole was demonstrated. These data confirm the previously reported increasing trimethoprim-sulfamethoxazole resistance which is probably plasmid-mediated and specify the resistances associated with trimethoprim-sulfamethoxazole resistance. These findings suggest that widespread prophylaxis in granulocytopenic patients with lower urinary tract infection by the trimethoprim-sulfamethoxazole association should be re-examined.
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A 46-year old patient under noramidopyrine treatment was admitted for acute renal failure. Renal biopsy was performed and showed acute interstitial nephritis without staining at immunofluorescent microscopy. In vitro and in vivo immunological tests using noramidopyrine as antigen were all negative. Abnormal serum creatinine levels were still present 4 months later. To our knowledge, noramidopyrine has rarely been the cause of interstitial nephritis (only one other case has been published), but it has frequently been responsible for drug-induced blood diseases, and noramidopyrine-related drugs have previously been involved in drug-induced nephritis. As the renal damage can probably be explained by a delayed hypersensitivity reaction, an early corticosteroid treatment would help in improving renal function.
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A case is reported of acute respiratory distress syndrome occurring during septic shock complicating necrotizing fasciitis of the hand. It is emphasized that, although this kind of evolution is largely unknown, it is logical for this complicated infective pathology. As the presence of septic shock contraindicated the use of positive end-expiratory pressure, the evolution of the respiratory failure could only be of a fulminating nature, and the patient died.