Intensive care medicine
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Intensive care medicine · Jun 1998
Estimation of direct cost and resource allocation in intensive care: correlation with Omega system.
An instrument able to estimate the direct costs of stays in Intensive Care Units (ICUs) simply would be very useful for resource allocation inside a hospital, through a global budget system. The aim of this study was to propose such a tool. ⋯ The Omega system appears to be a simple and relevant indicator with which to estimate the direct costs of each stay, and then to organise nursing requirements and resource allocation.
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Intensive care medicine · Jun 1998
Clinical TrialThe effects of low-dose dopamine infusions on haemodynamic and renal parameters in patients with septic shock requiring treatment with noradrenaline.
To investigate whether low-dose dopamine (LDD) has a significant effect on systemic haemodynamic variables and renal function when used in conjunction with high-dose noradrenaline in optimally volume-resuscitated patients with septic shock. ⋯ Low-dose dopamine causes significant increases in SBP SV, cardiac output and urine flow during treatment with noradrenaline.
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Intensive care medicine · Jun 1998
Case ReportsRecovery from circulatory shock in severe primary pulmonary hypertension (PPH) with aerosolization of iloprost.
The treatment of decompensated right ventricular failure with vasodilators is difficult due to reduced systemic pressure and/or ventilation/perfusion (V/Q) mismatch with hypoxemia. In a recent study we demonstrated that inhaled vasodilatory prostanoids may offer a new strategy to achieve pulmonary selective vasodilatation and improvement of right ventricular function. We applied this new approach to a patient with circulatory shock due to primary pulmonary hypertension (PPH), complicated by a pulmonary infiltrate, who did not tolerate intravenous prostacyclin. ⋯ Inhalation of aerosolized iloprost may offer a new life-saving strategy in near desperate cases of pulmonary hypertension in which intravenous prostacyclin cannot be applied due to severe side effects.
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Intensive care medicine · Jun 1998
Case ReportsRescue therapy with C1-esterase inhibitor concentrate after emergency coronary surgery for failed PTCA.
Administration of C1-esterase inhibitor (C1-INH) attenuates myocardial necrosis and sustains normal cardiac performance after myocardial ischemia and reperfusion in animal experiments. We report on our first experience of C1-INH application as rescue therapy in patients undergoing emergency surgical revascularization after failed percutaneous transluminal coronary angioplasty. Three patients were treated, because post-operative hemodynamic stabilization could not be achieved despite prolonged reperfusion periods, high-dose inotropic support, inodilators and aortic counterpulsation. ⋯ All patients survived and were discharged from hospital. In this group of patients suffering from severe reperfusion injury after coronary surgery, C1-INH seemed to be an effective adjuvant therapy to restore myocardial function by blocking the complement cascade. These results should encourage the performance of controlled studies on the effects of prophylactic C1-INH substitution therapy in patients undergoing coronary surgery at high risk conditions.
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Intensive care medicine · Jun 1998
Reduction of NO-induced methemoglobinemia requires extremely high doses of ascorbic acid in vitro.
The objective of the present study was to investigate the treatment of nitric oxide (NO)-induced methemoglobinemia by ascorbate and its consequences on red blood cell (RBC) glutathione in vitro. RBC were obtained from five healthy volunteers. The following experiments were carried out: (1) After methemoglobin generation by NO, ascorbate was added (2) RBC were simultaneously exposed to NO and ascorbate (3) Methemoglobin was generated by NO, ascorbate was added and incubation with NO continued. (1) After discontinuation of NO, the mean half life for methemoglobin was reduced from 195 min (controls) to 60 min (10 mM ascorbate) in a dose-dependent manner. (2) Methemoglobin formation after 3 h of NO exposure was 2.7 +/- 0.3% in controls and 1.8 +/- 0.1% with 10 mM ascorbate (p < 0.01). (3) Further methemoglobin formation was inhibited only by 10 mM ascorbate (p < 0.001). ⋯ Treatment with 10 mM ascorbate significantly decreased glutathione (p < 0.002). In vitro, NO-induced methemoglobin formation is significantly decreased only by a high (10 mM) ascorbate concentration. Glutathione, critical for ascorbate activity, is not influenced by NO.