Computed tomography assessment of exogenous surfactant-induced lung reaeration in patients with acute lung injury

Multidisciplinary Intensive Care Unit, Department of Anesthesiology and Critical Care Medicine, Assistance Publique-Hôpitaux de Paris, La Pitié-Salpêtrière Hospital, UPMC Univ Paris 06, 47-83 boulevard de l'hôpital, 75013 Paris, France.
Critical care (London, England) (Impact Factor: 4.48). 07/2010; 14(4):R135. DOI: 10.1186/cc9186
Source: PubMed


Previous randomized trials failed to demonstrate a decrease in mortality of patients with acute lung injury treated by exogenous surfactant. The aim of this prospective randomized study was to evaluate the effects of exogenous porcine-derived surfactant on pulmonary reaeration and lung tissue in patients with acute lung injury and acute respiratory distress syndrome (ALI/ARDS).
Twenty patients with ALI/ARDS were studied (10 treated by surfactant and 10 controls) in whom a spiral thoracic computed tomography scan was acquired before (baseline), 39 hours and 7 days after the first surfactant administration. In the surfactant group, 3 doses of porcine-derived lung surfactant (200 mg/kg/dose) were instilled in both lungs at 0, 12 and 36 hours. Each instillation was followed by recruitment maneuvers. Gas and tissue volumes were measured separately in poorly/nonaerated and normally aerated lung areas before and seven days after the first surfactant administration. Surfactant-induced lung reaeration was defined as an increase in gas volume in poorly/non-aerated lung areas between day seven and baseline compared to the control group.
At day seven, surfactant induced a significant increase in volume of gas in poorly/non-aerated lung areas (320 ± 125 ml versus 135 ± 161 ml in controls, P = 0.01) and a significant increase in volume of tissue in normally aerated lung areas (189 ± 179 ml versus -15 ± 105 ml in controls, P < 0.01). PaO2/FiO2 ratio was not different between the surfactant treated group and control group after surfactant replacement.
Intratracheal surfactant replacement induces a significant and prolonged lung reaeration. It also induces a significant increase in lung tissue in normally aerated lung areas, whose mechanisms remain to be elucidated.

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