Re-expansion pulmonary oedema after spontaneous pneumothorax treatment with chest tube placement
Re-expansion pulmonary oedema after spontaneous pneumothorax treatment with chest tube placement
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DOI:
10.1136/bcr-2021-241734
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发表时间:
2021-03-01
期刊:
影响因子:
0.9
通讯作者:
Costa, Teresa
中科院分区:
文献类型:
--
作者:
Rodrigues, Denny;Valerio, Margarida;Costa, Teresa
Re-expansion Pulmonary oedema (RPE) is a rare but potentially fatal complication, which can arise after a rapid decompressive treatment of pulmonary collapse secondary to pleural effusion, pneumothorax or atelectasis. The pathophysiological mechanism is still poorly understood, admitting a multifactorial aetiology underlying the process of increasing the permeability of the pulmonary microvascular structure secondary to the abrupt re-expansion process. 1 2 A 21-year-old male patient, active smoker (three pack-years), without drug abuse, recent trauma or pathological history. He was admitted to the emergency department after 6 days of sudden onset of dyspnoea, left pleuritic chest pain, palpitations and dry cough, with progressive worsening. The patient had no evident morphological abnormalities, blood pressure was 112/68 mm Hg, heart rate 100 bpm, respiratory rate 22 bpm, peripheral oxygen saturation of 99%(room air) and was apyretic. He presented a hyper-resonant left haemithorax with decreased lung sounds on auscultation. Chest X-ray confirmed left tension pneumothorax (figure 1). Blood samples showed normal haemogram, coagulation and inflammatory parameters. The patient was then treated with oxygen therapy and placement of a chest tube on the fifth left intercostal space, with subaquatic seal (without suction), leading to improved symptoms. One hour after the procedure he developed tachycardia, productive cough, dyspnoea and respiratory distress, unresponsive to oxygen therapy. A repeat chest X-ray confirmed the correctly positioned chest tube, complete left lung expansion, but showed alveolar opacities (figure 2). RPE was assumed and treatment with diuretics, corticosteroids and continuous positive airway pressure was initiated. As a result, the symptoms improved, and clinical stability was achieved. The patient was transferred to intermediate care unit and positive pressure was stopped. One hour after, he underwent in to acute respiratory failure, requiring orotracheal intubation, invasive mechanical ventilation and admission into intensive care unit. He stayed on mechanical invasive ventilation for 6 days. At the 7th day of intensive care unit stay, there was a complete resolution of RPE, but a persistent air leak was noted, so the patient was submitted to surgical pleurodesis (pleural abrasion) via video-assisted-thoracoscopy. He was discharged 10 days later, asymptomatic and with a normal chest X-ray.