Hemodynamic and Pulmonary Edema Protein Measurements in a Case of Reexpansion Pulmonary Edema

doi:10.1378/chest.81.2.250

Chest

Volume 81, Issue 2, February 1982, Pages 250-251

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We describe a patient with unilateral reexpansion pulmonary edema following thoracocentesis of a right pleural effusion. The pulmonary edema-serum total protein ratio was 0.85. Right heart catheterization revealed a normal pulmonary wedge pressure. The pulmonary edema cleared quickly. This is the first case to our knowledge in which pulmonary hemodynamics and lung fluid total protein levels have been monitored in reexpansion pulmonary edema.

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Case Report

A 49-year-old woman was admitted for shortness of breath. Her past history included multiple bouts of alcohol-induced pancreatitis, biopsy-proved alcoholic cirrhosis, and status-post portocaval shunt. Seven months before admission, an abdominal sonogram (by serendipity) disclosed a small right pleural effusion and ascites. Four months later, a chest roentgenogram showed a moderate-sized right pleural effusion, with partial right lower lobe collapse. The patient refused any workup at that time.

Discussion

This is the first case to our knowledge of REP edema in which hemodynamic monitoring and evaluation of the pulmonary edema fluid is available. The finding of a pulmonary edema-serum protein ratio of 0.85 strongly suggests an increase in permeability, either pulmonary microvascular or alveolar epithelial or both, as a factor in the pathogenesis of REP.⁷ In addition, the presence of normal pulmonary artery and pulmonary wedge pressure readings in our patient eliminates a sustained increase in

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Cited by (35)

Lung Ultrasound Diagnosis and Follow-up in a Case of Reexpansion Pulmonary Edema
2019, Chest
Unilateral postoperative pulmonary edema after minimally invasive cardiac surgical procedures: A case-control study
2015, Annals of Thoracic Surgery
Citation Excerpt :
There are few reports of reexpansion edema in the perioperative patient population, although most programs using minimally invasive cardiac surgical procedures have experienced this problem. The cause of reexpansion edema is incompletely understood; however, the increased hydrostatic force associated with elevated pulmonary capillary wedge pressure has not been implicated [7, 8]. One theory proposes that reperfusion injury is a significant factor in reexpansion pulmonary edema [9–11].
Unilateral postoperative pulmonary edema is an underreported adverse event after a minimally invasive cardiac surgical procedure that combines right minithoracotomy with cardiopulmonary bypass. We sought to characterize its incidence, risk factors, and morbidity.
We conducted a retrospective case-control study of all cardiac surgical procedures that combined right-sided minithoracotomy with cardiopulmonary bypass at our institution over 8 consecutive years. Unilateral postoperative pulmonary edema was defined on the chest radiograph taken on the first postoperative day as relatively increased opacification of the right versus left hemithorax involving at least 20% of the hemithorax, not better explained by atelectasis. Baseline characteristics, potential risk factors, and outcomes were subject to univariable and multivariable analysis.
Radiographs were available for 277 of 278 patients; of those, 68 (25%) met our definition of unilateral postoperative pulmonary edema. Patients with unilateral postoperative pulmonary edema had higher mortality and were more likely to have a lower postoperative PaO₂/F_IO₂ ratio, to require vasoactive medications and mechanical ventilation for longer than 24 hours, and to have longer lengths of stay in the intensive care unit and the hospital. Unilateral postoperative pulmonary edema was independently associated with chronic obstructive pulmonary disease (odds ratio [OR] 4.79; 95% confidence interval [CI] 1.28 to 18.0; p = 0.02); pulmonary hypertension, right-ventricular dysfunction, or both (OR 2.92; 95% CI 1.41 to 6.03; p = 0.004); and increasing cardiopulmonary bypass time (OR 1.019; 95% CI 1.011 to 1.027 per additional minute; p <0.001).
Unilateral postoperative pulmonary edema after minimally invasive cardiac surgical procedures is common, carries significant morbidity, and has identifiable risk factors. Further research is needed to enable a better understanding of the pathophysiology and clinical implications of unilateral postoperative pulmonary edema.
CASE 4-2009 Severe Reexpansion Pulmonary Edema After Minimally Invasive Aortic Valve Replacement: Management Using Extracorporeal Membrane Oxygenation
2009, Journal of Cardiothoracic and Vascular Anesthesia
Citation Excerpt :
Hypoxic pulmonary vasoconstriction preserves arterial oxygenation by shunting blood away from unventilated alveoli, but this compensatory response may render the collapsed lung more susceptible to ischemia-reperfusion injury. Evidence for increased capillary permeability in REPE was first suggested using analysis of colloid osmotic pressure of pulmonary edema fluid and plasma in patients.15,16 Experimental models of lung collapse and reinflation using small mammals (eg, rats and rabbits) have provided additional insight into the pathogenesis of REPE.17,18
Reexpansion Pulmonary Edema
2007, Journal of Cardiothoracic and Vascular Anesthesia
Citation Excerpt :
Despite inotropic support with epinephrine, shock developed, and the patient died. In the other case,25 after the initial episode of RPE after drainage of a right pleural effusion, there was progressive clearing. This was the first case report that included measurements of the pulmonary artery pressures and protein levels in the pulmonary edema fluid.
Association of IL-8 and MCP-1 with the development of reexpansion pulmonary edema in rabbits
2001, Annals of Thoracic Surgery
Background. The aim of this study is to determine the relationships between the cytokines and the inflammatory response in reexpansion pulmonary edema (RPE).
Methods. We examined the cell population, epithelial permeability measured by Evans blue dye (EB), βglucuronidase and cytokine concentrations in bronchoalveolar lavage fluid (BALF) and/or blood using a rabbit RPE model.
Results. We confirmed that RPE is characterized by recruitment of polymorphonuclear leukocytes (PMNs), the release of PMN granular contents into the air spaces, and increased vascular permeability. These findings were highly correlated with increased interleukin-8 (IL-8) and monocyte chemoattractant protein 1 (MCP-1) concentrations in the BALF. Growth related oncogene (GRO) was detected in the BALF from only 2 of the 7 reexpanded lungs while TNFα was not detected in any rabbits. A similar but less severe inflammatory response to the reexpanded lung was found in the contralateral lung.
Conclusions. IL-8 and MCP-1 may play important roles in the development of RPE; the inflammatory response is independent of TNFα and unilateral reexpansion of the lung induces an inflammatory response not only in the reexpanded lung but also in the contralateral lung.
Re-expansion pulmonary oedema after removal of a intrathoracic tumor
1997, Annales Francaises d'Anesthesie et de Reanimation
Une détresse respiratoire aiguë compliquant l'évolution postopératoire immédiate de l'exérèse d'un volumineux fibrome intrathoracique (3,1 kg) chez un enfant de 6 ans est rapportée. Il s'agissait d'un œdème de réexpansion pulmonaire homolatéral (œdème unilatéral, survenant dans l'heure suivant la réexpansion). L'évolution a été rapidement favorable au prix d'un épanchement pleural résiduel. Cette complication a été favorisée par la différence de volume entre un petit poumon et une grande cage thoracique, tous deux remodelés par l'évolution très lente de la tumeur, connue depuis plusieurs années. La physiopathologie particulière de ces œdèmes, où interviennent l'ancienneté et l'importance de la masse intrathoracique retirée, ainsi qu'une forte aspiration pleurale postopératoire nécessite une gestion particulière du drainage thoracique, dont l'aspiration doit être impérativement arrêtée. L'opportunité de la ventilation contrôlée avec pression positive téléexpiratoire est discutée.
We report an acute respiratory insufficiency following the removal of a large intrathoracic fibroma (3.1 kg) in a 6 year-old child, caused by a re-expansion pulmonary oedema (unilateral oedema occurring within one hour after expansion). This oedema improved rapidly and was followed by a well-tolerated pleural effusion. This complication is due to discrepancy between a small lung and a large thoracic cavity, due to the prolonged time course of the tumor growth. These oedemas are caused by rapid lung re-expansion, the volume of the removed tumor and the depth of postoperative pleural suction. The value of positive-end expiratory pressure is discussed.

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Chest

Selected ReportsHemodynamic and Pulmonary Edema Protein Measurements in a Case of Reexpansion Pulmonary Edema

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Case Report

Discussion

Selected Reports
Hemodynamic and Pulmonary Edema Protein Measurements in a Case of Reexpansion Pulmonary Edema