Abstract
BackgroundReexpansion pulmonary edema (REPE) is known as a rare and fatal complication after tube thoracostomy.ObjectivesWe investigated the risk factors for the development of REPE in patients with spontaneous pneumothorax.MethodsWe selected patients who were diagnosed with spontaneous pneumothorax and were initially treated with tube thoracostomy between August 1, 2003 and December 31, 2011. The patients’ electronic medical records, including operative notes and chest x-ray and computed tomography scans, were reviewed.ResultsREPE developed in 49 of the 306 patients (16.0%). REPE was more common in patients with diabetes (14.3% vs 3.9%, P = 0.004) or tension pneumothorax (46.8% vs 16.2%, P = 0.000). The pneumothorax was larger in patients with REPE than without REPE (57.0 ± 16.0% vs 34.2 ± 17.6%, P = 0.000), and the incidence of REPE increased with the size of pneumothorax. On multivariate analysis, diabetes mellitus [(odds ratio (OR) = 9.93, P = 0.003), and the size of pneumothorax (OR = 1.07, P = 0.000) were independent risk factors of REPE.ConclusionsThe presence of diabetes increases the risk of REPE development in patients with spontaneous pneumothorax. The risk of REPE also increases significantly with the size of pneumothorax.
Highlights
Reexpansion pulmonary edema (REPE) is known as a rare and fatal complication after tube thoracostomy
The presence of diabetes increases the risk of REPE development in patients with spontaneous pneumothorax
After excluding 23 episodes that were treated by oxygen supplementation only, 67 episodes that were operated without tube thoracostomy, and 1 patient who was transferred from another hospital with a tube thoracostomy, 306 episodes of spontaneous pneumothorax that were initially treated with closed tube thoracostomy drainage were included in the study population
Summary
Reexpansion pulmonary edema (REPE) is known as a rare and fatal complication after tube thoracostomy. Reexpansion pulmonary edema (REPE) is generally known as a rare but potentially fatal complication after treatment of pneumothorax, hemothorax and pleural effusion [1,2]. Several factors have been implicated in the pathogenesis of REPE: rapid reexpansion, application of negative intrapleural pressure, decreased surfactant activity, increased pulmonary vascular permeability, airway obstruction, pulmonary artery pressure change, and chronicity of lung collapse [3,4]. Recent studies support increased pulmonary capillary permeability as an important etiologic factor [3,4,5,6]; the pathogenesis of REPE remains unclear.
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