Abstract
Pharmacological interventions are commonly considered in acute respiratory distress syndrome (ARDS) patients. Inhaled nitric oxide (iNO) and neuromuscular blockers (NMBs) are used in patients with severe hypoxemia. No outcome benefit has been observed with the systematic use of iNO. However, a sometimes important improvement in oxygenation can occur shortly after starting administration. Therefore, its ease of use and its good tolerance justify iNO optionally combined with almitirne as a rescue therapy on a trial basis. Recent data from the literature support the use of a 48-h infusion of NMBs in patients with a PaO2 to FiO2 ratio <120 mmHg. No strong evidence exists on the increase of ICU-acquired paresis after a short course of NMBs. Fluid management with the goal to obtain zero fluid balance in ARDS patients without shock or renal failure significantly increases the number of days without mechanical ventilation. On the other hand, patients with hemodynamic failure must receive early and adapted fluid resuscitation. Liberal and conservative fluid strategies therefore are complementary and should ideally follow each other in time in the same patient whose hemodynamic state progressively stabilizes. At present, albumin treatment does not appear to be justified for limitation of pulmonary edema and respiratory morbidity. Aerosolized β2-agonists do not improve outcome in patients with ARDS and one study strongly suggests that intravenous salbutamol may worsen outcome in those patients. The early use of high doses of corticosteroids for the prevention of ARDS in septic shock patients or in patients with confirmed ARDS significantly reduced the duration of mechanical ventilation but had no effect or even increased mortality. In patients with persistent ARDS after 7 to 28 days, a randomized trial showed no reduction in mortality with moderate doses of corticosteroids but an increased PaO2 to FiO2 ratio and thoracopulmonary compliance were found, as well as shorter durations of mechanical ventilation and of ICU stay. Conflicting data exist on the interest of low doses of corticosteroids (200 mg/day of hydrocortisone) in ARDS patients. In the context of a persistent ARDS with histological proof of fibroproliferation, a corticosteroid treatment with a progressive decrease of doses can be proposed.
Highlights
Dysregulated inflammation, accumulation and activity of leukocytes and platelets, uncontrolled activation of coagulation and altered permeability of alveolar endothelial and epithelial barriers leading to pulmonary edema are key points in the pathophysiology of acute lung injury and acute respiratory distress syndrome (ARDS) [1]
The place of Inhaled nitric oxide (iNO) as a rescue therapy has been clarified by numerous studies that gave practical guidelines on its use
The modest reduction of ventilation duration obtained with a conservative fluid strategy for patients who do not have evidence of tissue hypoperfusion makes impossible to create a “gold standard” for management of the fluid status of every ARDS patient
Summary
Dysregulated inflammation, accumulation and activity of leukocytes and platelets, uncontrolled activation of coagulation and altered permeability of alveolar endothelial and epithelial barriers leading to pulmonary edema are key points in the pathophysiology of acute lung injury and acute respiratory distress syndrome (ARDS) [1]. Four randomized trials investigated early use of high doses of corticosteroids for the prevention of ARDS in septic shock patients [90,91,92] or in patients with confirmed ARDS [93] In these studies, corticosteroids significantly reduced the duration of mechanical ventilation. Another RCT by Meduri evaluated early corticosteroid administration, and showed that methylprednisolone administration (1 mg/kg/d) less than 72 after the onset of ARDS reduced mortality [96] These results should be interpreted with caution, because this study included a large number of patients with septic shock. Another randomized, controlled trial, conducted by the ARDS network, showed no reduction in mortality in the group receiving methylprednisolone [44]. One of the main complications of corticosteroid treatment is ICU acquired weakness [54,55], potentially reversible but often leading to difficulties in weaning from ventilation
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