Unilateral Pulmonary Oedema following Re-Expansion of Pneumothorax

Shanahan, Mark X.; Monk, Ian; Richards, H. J.

doi:10.1177/0310057x7500300104

Cited by 22 publications

(7 citation statements)

References 11 publications

(6 reference statements)

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“…13 Important factors associated with its development include prolonged lung collapse, the speed of reinflation and application of excessive intrapleural negative pressure. 4 It has also been noted after reinflation by positive pressure 3 ,j and after intubation of the right main bronchus. 6 This last report documented three cases where a tracheal tube was misplaced into the right main bronchus and left-sided pulmonary oedema occurred after correction of the tube position.…”

Section: Discussionmentioning

confidence: 95%

Sudden Onset Unilateral Pulmonary Oedema during Thoracotomy

Vyvyan

Palazzo

1993

Anaesth Intensive Care

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Sudden onset of frank pulmonary oedema intraoperatively is a rare and worrying occurrence. We wish to report a case of unilateral pulmonary oedema that occurred during thoracotomy, and discuss the possible mechanisms. CASE REPORT A 26-year-old previously healthy black male was admitted to hospital for investigation of left-sided pleuritic chest pain, fever and malaise. He was found to have a left pleural effusion and left lower lobe consolidation. Extensive investigation revealed no cause for the effusion which later became infected, possibly as a complication of pleural aspiration and biopsy. The empyema did not resolve with antibiotics and percutaneous chest drainage and he was therefore scheduled for thoracotomy and decortication of the left lung. At the preoperative visit the patient was afebrile and generally well, despite the empyema and extensive collapselconsolidation of the left lung (Figure 1). After induction of anaesthesia, the trachea was intubated with a 41 FG left-sided double-lumen endobronchial tube (Mallinckrodt "Broncho-Cath"). The tube was positioned using the standard sequential clamping technique with inspection of chest expansion and auscultation of breath sounds. This was repeated after positioning the patient on his right side. It was noted that air entry to the consolidated lung was limited to the apex. Both lungs were ventilated with 33% oxygen in nitrous oxide and enflurane. Paralysis was maintained with atracurium, and continuous monitoring included invasive intra-arterial blood pressure and pulse oximetry. Arterial blood gases after twenty minutes'

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Section: Discussionmentioning

confidence: 95%

Sudden Onset Unilateral Pulmonary Oedema during Thoracotomy

Vyvyan

Palazzo

1993

Anaesth Intensive Care

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“…1,[9][10][11][12][13][14][15] The clinical presentation of RPE can be relatively benign or present as a life-threatening event. 1 The pathogenesis of RPE has been shown to be related to an increase in microvascular permeability in clinical and experimental studies.…”

Section: Discussionmentioning

confidence: 99%

Life-threatening Re-expansion Pulmonary Edema

Siddiqi

Huggins

Doelken

et al. 2014

Clinical Pulmonary Medicine

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A 45-year-old woman with a high-grade Burkitt lymphoma developed reexpansion pulmonary edema (RPE) after drainage of 900 mL of pleural fluid. Sequential, bilateral therapeutic thoracenteses with pleural manometry were performed 2 weeks after the initial thoracentesis. Pleural manometry showed increased pleural space elastance in both pleural spaces; air-contrast computed tomography of the chest demonstrated visceral pleural thickening, involving both lungs, consistent with the diagnosis of bilateral, unexpandable lung due to the presence of visceral pleural restriction. The pathogenesis of RPE is unknown, but it is believed to involve a microvascular injury from reperfusion. The pathogenetic role of excessively negative pleural pressures in the development of RPE in humans has never been established. This is the first report utilizing pleural manometry to allow safe removal of pleural fluid in a patient who previously developed life-threatening RPE. (Clin Pulm Med 2014;21:46-49) R eexpansion pulmonary edema (RPE) is a known complication after therapeutic thoracentesis. The clinical ulipresentation of RPE ranges from relatively benign to life threatening. 1 The pathogenesis of RPE is unknown; it is believed that the development of excessively negative pleural pressures with fluid evacuation and microvascular injury from reperfusion are plausible mechanisms. 2-6 Historical guidelines recommend not exceeding 1 to 1.5 L of fluid removal; however, this recommendation is not based on scientific evidence. Multiple studies utilizing pleural manometry during therapeutic thoracentesis have shown a reduction in the incidence of RPE. Termination of drainage in these studies is based on the development of excessively negative pleural pressures. [5][6][7][8] We report a patient with severe, life-threatening pulmonary edema that occurred after a therapeutic thoracentesis, without pleural manometry, of a moderate-size transudative pleural effusion (< 1 L). The possible cause for the development of RPE was discovered 2 weeks later when bilateral therapeutic thoracenteses with pleural manometry were performed, and the patient was noted to have bilateral visceral pleural restriction. This case report suggests a pathogenetic role of the development of excessively negative pleural pressure when attempting to reinflate a trapped lung during thoracentesis and the development of RPE. Furthermore, it is the only documented case where pleural manometry was used to prevent the reoccurrence of RPE in a patient who previously developed life-threatening RPE. CASE REPORTA 45-year-old woman was admitted for induction chemotherapy for Burkitt lymphoma. On day 4, she experienced respiratory failure from tumor lysis syndrome and was noted to have bilateral pleural effusions and pulmonary edema. Prior chest radiographs documented the presence of small, bilateral pleural effusions 2 months before admission. Echocardiogram revealed an ejection fraction of 13% which was attributed to adriamycin. After several days of aggressive diuresis, the patien...

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“…The most eo m mo n eo mp lica tio ns inc1u de pneu mo thorax ( 9) , ate leetasis (5,14) , pleural effusion (I 4), hyp oxem ia (2 ) and pain ( 9) . More serious eomplieations reported are severe emphysema (6), pu lmo nary ede ma ( 2,10,13,15), empye ma (5), pneum onia (I 4) , and a few lethal eases h ave been described (I3 , 15).…”

Section: In Verbal Communication May Have Contributed To a Rnis-mentioning

confidence: 99%