English

Abstract

We report a case of an ipsilateral re-expansion pulmonary edema occurring after the insertion of an intercostal drainage tube in a young male patient with spontaneous pneumothorax. The patient was managed with oxygen via a non-rebreathing face mask to compensate for his hypoxemia. In about 24 hours after the event, the patient gradually improved and recovered completely without any residual hypoxemia. Re expansion pulmonary edema occurring after the insertion of an intercostal drainage tube for pneumothorax or pleural effusion is a rare complication with a high mortality rate up to 20%. This condition should be considered if the patient develops cough, dyspnea and hypoxemia following the insertion of a chest tube. The exact pathophysiology leading to this complication is still unknown. The risk factors for re-expansion pulmonary edema should be evaluated and considered prior to the insertion of chest tubes. Treatment remains supportive only. INTRODUCTION: In 1853, Pinault (1) described REPE following pleural effusion in a patient who had a large volume of pleural fluid rapidly removed by thoracentesis. This is probably the first report of REPE. In 1958, re expansion pulmonary edema (REPE) was first reported following pneumothorax by Carlson and colleagues(2) and was comprehensively reviewed by Ziskind and colleagues(3) in 1965. In 1991 Matsuura in his clinical analysis of 146 patients and summarized that 21 of 146 cases of spontaneous pneumothorax which were treated by Thoracentesis and continuous low negative pressure suction drainage (- 12cm H20) of the pleural space developed REPE, The rate of REPE was higher in patients 20 to 39 years of age than in those over the age of 40. (4) REPE can occur on the ipsi- or contralateral side, can be bilateral and can even be asymptomatic.(5-9) The exact pathophysiology for this complication is unknown. Factors that have been implicated in the pathogenesis of this complication include chronicity of collapse, technique of re-expansion, increased pulmonary vascular permeability, airway obstruction, loss of surfactant and pulmonary artery pressure changes. (10) Oxygen radicals are produced during the hypoxemia in the collapsed lung. Moreover, the activity of different cytokines such as interleukin 8 and monocyte chemo attractant protein 1 (MCP-1),(11) or the activity of xanthine oxidase(12) have been implicated in the pathogenesis of REPE. Additionally, the GJP-binding protein Rho and its target Rho-Kinase (ROCK) identified by Sawafuji et al. has been implicated in permeability changes causing RPE as well. (13)