Evidence of Acute Inflammatory Response in Reexpansion Pulmonary Edema

doi:10.1378/chest.101.1.275

Chest

Volume 101, Issue 1, January 1992, Pages 275-276

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We analyzed edema fluid in two cases of reexpansion pulmonary edema during thoracotomy. High value of the fluid to plasma protein concentration ratio indicates an increase in pulmonary microvascular permeability. There were marked increases in polymorphonuclear leukocyte (PMN) count and concentration of PMN-elastase in edema fluid. There were also increases in concentrations of thromboxane B₂ and 6-keto-PGF,-alpha in both edema fluid and plasma. These findings strongly suggest that the mechanism of reexpansion pulmonary edema is an inflammatory response and that PMNs in the reexpanded lung may play a role in the increase in permeability.

Section snippets

CASE 1

A 27-year-old woman with a history of hemangioleiomyosarcoma of the right knee was admitted to the hospital for shortness of breath. Initial examination disclosed the following: blood pressure, 120/64 mm Hg; heart rate, 120 beats/min; respiratory rate, 26 breaths/min; and absence of breath sound over the left hemithorax. Chest roentgenograms revealed a large tumor mass and collapsed left lung. Blood flow in the left lung, measured by intravenous administration of Tc-MAA, was 7.8 percent. Left

RESULTS

Total protein concentration in edema fluid increased and resulted in high fluid to plasma ratio (Table 1). Total nucleated cells increased markedly, with PMNs predominating (Table 2). PMN-elastase levels in edema fluid also increased markedly. Thromboxane B₂ and 6-keto-PGF,-alpha levels in both edema fluid and plasma increased (Table 3).

DISCUSSION

In our two cases, chest roentgenograms after the reexpansion of collapsed lungs revealed diffuse parenchymal shadow in the reexpanded lung. This is evidence of pulmonary edema, indicating increase in extravascular lung water.

In these edema fluids, total protein concentrations were high, and the fluid-to-plasma ratios exceeded 0.7. This indicates an increase in pulmonary microvascular permeability.⁴ Measurements of protein concentration in edema fluid have provided evidence of an increase in

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Neutrophils in reexpansion pulmonary edema
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Proinflammatory ischemia-reperfusion injury ensues when normal blood flow is restored with reexpansion. This theory is supported by evidence that reexpansion edema is associated with elevated levels of proinflammatory cytokines and increased vascular permeability [7, 11–14]. In this study, longer CPB, preexisting COPD, and preexisting pulmonary hypertension or significant right ventricular dysfunction independently increased the risk of unilateral postoperative pulmonary edema.
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Restoration of ventilation and increased perfusion to previously collapsed rat lungs were associated with edematous thickening of the alveolar-capillary membrane concomitant with infiltration of polymorphonuclear leukocytes and lymphocytes in the ischemic zone. These findings verified the results of previous studies20-22 and were associated with reduced levels of superoxide dismutase (an important enzyme that metabolizes oxygen-derived free radical intermediates), indirectly suggesting that neutrophil-induced production of reactive oxygen species mediates, at least in part, abnormal microvascular permeability in this form of ischemia-reperfusion injury. Reactive oxygen species produced by endogenous xanthine oxidase also may contribute to REPE by causing apoptosis (programmed cell death) of alveolar and pulmonary vascular endothelial cells.23
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Chest

Selected ReportsEvidence of Acute Inflammatory Response in Reexpansion Pulmonary Edema

Section snippets

CASE 1

RESULTS

DISCUSSION

Am J Med

Am J Med

Chest

Neutrophils in reexpansion pulmonary edema

J Appl Physiol

Selected Reports
Evidence of Acute Inflammatory Response in Reexpansion Pulmonary Edema