Biomedical subjects
Publications and source records attributed to M Rapin.
The authors report three cases. Hemostasis abnormalities and lowering of complement fractions was observed. Severe shock was lethal in two cases associated with severe local lesions. The role of unadapted treatment like corticosteroids and the lack of early penicillino therapy is discussed to explain this evolution.
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To determine the incidence of acute gastroduodenal lesions during severe sepsis, prospective endoscopies were performed in two groups of critically ill patients. The criteria of selection ruled out the incidence of other factors, such as shock, acute renal or respiratory failure. Evaluation of sepsis by clinical and bacteriologic criteria and endoscopic examination were performed in a double blind study. In the group of 14 patients with sepsis, 19 fibroscopies showed abnormalities of mucosa in all of them. In the group of 16 patients with sepsis, 23 fibroscopies showed either superficial lesions or normal mucosa. The difference between the incidence and the severity of acute lesions in the two groups studied was highly significative, p less than 0.001. Besides, gastroduodenal lesions became worse when sepsis prolonged, while they improved dramatically when focal infection and septicemia were eradicated. These data strongly suggest that severe sepsis per se can provoke acute digestive damage.
A pharmacokinetic study with high doses of frusemide has been performed in nine patients with acute tubulopathy, treated by hemodialysis. The patients were studied between 6 and 28 days after the beginning of the disease. Renal function was normal before the episode of acute renal shutdown. The diuretic effect of frusemide was closely related to creatinine clearance (Ccr): no effect in anuric cases, moderate effect if Ccr was lower than 10 ml/mn, marked effect if Ccr was higher than 10 ml/mn. no direct relationship could be demonstrated between drug plasma level and natriuresis. Frusemide half-life in plasma was short even in anuric patients, suggesting the existence of an extra renal excretion and/or inactivation pathway. Hence toxic side effects due to drug accumulation should not appear in the recommended 1 g/day regimen.
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Hemodynamic data were collected in 42 patients with pulmonary edema (P.E.) due to altered permeability of various causes. Pulmonary artery wedge pressure (PWP) was normal, whatever the time of the study and the severity of the P.E. Pulmonary artery hypertension was present in the cases with severe hypoxemia, but disappeared with hypoxemia correction. In some cases, a hyperkinetic or a hypovolemic syndrome was found, being induced by the cause of P.E. Although within normal limits, PWP was significantly higher at the first hours of P.E. than after the 6th hour. Perfusion of colloid solutes worsened P.E., although increasing PWP by only a few mmHg. Dehydration using diuretics markedly improved the venous admixture, although PWP was previously normal. These data document the production of P.E. in many causes-such as severe sepsis, drowning, fat embolism, barbiturate overdose-by impaired alveolo-capillary permeability, PWP and blood protein content remaining within normal limits. They also demonstrate the noxious effects of overperfusion and the efficiency of dehydration in such pulmonary edemas.
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Nosocomial septicemias supervened during the 15 trimesters following the opening of a new built critical care unit were reviewed. During the five first trimesters the incidence of nosocomial septicemias was 5.9 p.cent. It increases to 10.7 p.cent (p smaller than 0.001) during the five following trimesters. Then a drastic restriction in antibiotic administration was performed, including withdrawal of any prophylactic antibiotherapy, preferential use of penicilline G to prevent infection by Clostridium and cocci Gram positive species surinfection, and, in case of bacterial proved infection, use of a narrow spectrum adapted antibiotic for a time as short as possible. During the 5 trimesters following the application of this antibiotic restriction, the incidence of nosocomial septicemias dropped to 5.7 p.cent (p smaller than 0.001). This phenomenon was related to the lowered incidence of the Gram negative bacilli septicemias from 11.1 p.cent to 4.8 p.cent (p smaller than 0.001) while the incidence of Gram positive cocci septicemias remained unchanged. These results strongly suggest the responsibility of the overuse of antibiotics in the determination of nosocomial septicemias and the efficiency of a drastic antibiotic restriction upon the surinfection of patients hospitalized in a critical care unit.
Twenty cases of hypovolemic shock of various etiologies in which initial diagnosis was massive pulmonary embolism are analyzed. The error was due to intensity of respiratory failure symptoms and electrocardiographic changes suggesting acute cor pulmonale. However, although constant, hypoxemia was mild and easily corrected by oxygen administration. Hypovolemia was confirmed by low central venous pressure (CPV EQUALS 1, 3 cm H20); in 7 patients, right heart catheterism showed lowered cardiac output associated to low ventricular filling pressures (VFP). Rapid blood volume expansion simultaneously corrected in all cases both shock and clinical signs of "respiratory failure", while CVP increased only slightly. These findings suggest that CVP must be carefully checked when faced with a clinical picture of massive pulmonary embolism and if low, rapid blood volume expansion must be performed under CVP monitoring, in order to rule out hypovolemic shock.
Right heart catheterisation was undertaken in six patients with accidental deep hypothermia. Studies were carried out before and after rapid blood volume expansion, with and without Isoproterenol infusion, and were repeated at normal body temperatures. The initial haemodynamic pattern indicated a marked hypovolemia with a simultaneous decrease of both cardiac output and ventricular filling pressures, and a decreased measured total blood volume. Rapid correction of the hypovolemia revealed cardiac insufficiency, in part due to the persisting bradycardia. Left ventricular function was depressed in patients with prolonged cold exposure and normal in patients with short exposure. These abnormalities disappeared after Isoproterenol infusion during hypothermia, and spontaneously after return to normothermia. No imbalance existed between the decreased cardiac output and oxygen uptake in hypothermia, arterio-venous oxygen difference being within normal limits.
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Pulmonary edema due to disorders in alveolo-capillary permeability (or lesional) are differentiated from hemodynamic pulmonary edema by the fact that they arise in spite of normal pulmonary capillary pressure (PCP). A hemodynamic study was carried out in 42 cases of lesional P.E. The PCP was normal whatever the date of the examination and the gravity of the P.E. Pulmonary arterial hypertension was only found in the presence of frank hypoxemia and disappeared with the correction of the latter. If there was no hemodynamic profile due to P.E. itself, its etiology sometimes induced a hyperkinetic or hypovolemic syndrome. Finally it was apparent that PCP was significantly higher- although normal- at the initial stage than after 6 hours of P.E.; that an elevation in PCP of only a few mm Hg by the perfusion of colloids aggravated the P.E., that despite the normal value for the PCP dehydration evidently improved hematosis. Thus this study confirms that numerous cases of P.E. can occur while the PCP remains normal. It also confirms the noxious nature of too abundant perfusions in these cases and the effectiveness of dehydration.
Recourse to extra-corporeal oxygenation is legitimate in certain cases of fulminating pulmonary edema, with refractory hypoxemia, particularly when the early onset of the hemodynamic condition and the severity of the hypoxemia do not permit the carrying out of dehydration. Veno-arterial diversion then permits: --the ensuring of half or two thirds of the oxygen consumption; --the restoration of systemic hemodynamics by arterial reinjection; --the very rapid reduction of pulmonary edema by "decompressing" the pulmonary artery.
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