Contralateral Reexpansion Pulmonary Edema

Capt Brian J. Heller, Maj Kurt Grathwohl, USAF, MC, Department of Medicine and the Division of Pulmonary Disease and Critical Care Medicine, Keesler Air Force Base, Biloxi, Miss.

South Med J. 2000;93(8) 

In This Article

Discussion

Reexpansion pulmonary edema is a rare but serious complication of evacuation of pleural effusion or pneumothorax. Mortality as high as 20% has been reported.[1] Although it was first described in 1853, only 60 cases were reported between 1958 and 1999. Contralateral RPE accounted for only four of these cases.[2,3,4] Three occurred with pneumothorax drainage and the fourth with chest tube placement and large volume thoracentesis. Two of these patients had pneumothoraces from attempted insertion of a subclavian vein catheter.[2] Treatment of the pulmonary edema was begun before lung reexpansion. Theoretically, this protected the reinflated lung from edema. Both patients died within 7 days of RPE.[2] The cause of death in each case was multifactorial and could not be attributed solely to RPE. The third patient, who had had an acute anteroseptal myocardial infarction, had a pneumothorax due to attempted insertion of a central venous catheter.[3] This patient had marked right-sided heart failure due to increased pulmonary vascular resistance. She presented with a left-sided pneumothorax and right-sided pulmonary edema. After reexpansion, the left lung began to develop pulmonary edema as well. The fourth patient had unilateral edema followed by contralateral edema after thoracentesis and chest tube placement.[4] He had a possible malignant pleural effusion due to a retroperitoneal sarcoma. More than 4 liters of cytologically negative fluid were drained over 30 minutes with application of more than -50 mm Hg of vacuum. There were no physical or radiologic signs of heart failure. The patient died approximately 3 months after the procedure from causes unrelated to RPE.[4]

After more than 100 years and numerous reports, the pathophysiology of RPE remains poorly understood. There are, however, several theories concerning its etiology. In previous studies, the edema fluid was found to be rich in protein, suggesting capillary leakage.[5] Therefore, some authors suspect that RPE results from increased endothelial permeability and accompanying loss of integrity of the alveolar-capillary membrane. This capillary overflow is purported to be due to mechanical stresses and distention within the reinflated lung.[6] Additionally, the leakage is potentially worsened by increased nitric oxide and inflammatory mediators from neutrophils. Reperfusion injury has also been offered as a potential explanation. With reinflation of the previously nonventilated, nonperfused collapsed lung, oxygen-free radicals may form, with resulting injury. This theory is supported by the finding that increased levels of oxygen and the administration of antioxidants prevents edema formation.[5] Low levels of surfactant in chronically collapsed lungs are another hypothetical cause.[7] The exact cause of RPE, however, has yet to be elucidated.

The physiologic mechanisms of contralateral RPE are even less clear. However, with consideration of our patient's pathophysiology, we have formulated theories of RPE formation. When contrasting our case with cases of high-altitude pulmonary edema (HAPE), interesting comparisons become evident. Hypothetically, HAPE results from the release of a highly cellular and protein-rich fluid in reaction to an increase in microvascular pressure and permeability. This fluid is also abundant in vasoactive and chemotactic mediators.[8] In 1980, Hackett et al[9] reported four cases of HAPE in patients with congenital absence of a right pulmonary artery. This supported the concept of overperfusion of a restricted vascular bed causing pulmonary edema. The overperfusion and leakage are due to both increased pressure and flow. This phenomenon is also seen in unilateral lung transplantation for pulmonary hypertension, with pulmonary edema occurring in the low-pressure transplanted lung. Our patient's partially collapsed right lung due to the large effusion may have similarly resulted in decreased blood flow to the right pulmonary artery. After fluid drainage, blood flow to the right lung may have initially increased. However, intrapulmonary shunting from hepatopulmonary syndrome was potentially worsened, causing hypoxemia and uneven pulmonary vasoconstriction. This may have increased the right pulmonary artery vascular resistance and increased blood flow to the left lung, causing capillary damage with resultant leakage.

There are no definitive guidelines for prevention of RPE, though there are some widely accepted observations and recommendations. It is believed that RPE is more likely to occur in a lung that has been collapsed for more than 3 days. If pleural pressure is not monitored during the procedure, then no more than 1 liter of fluid should be removed. The goal is to keep the pleural pressure above -20 cm of water.[5] The procedure should be halted if the patient has sudden chest tightness or the sudden onset of a cough. Additionally, this case and previous studies show that underlying pulmonary artery hypertension and hypoxemia may be a significant risk factor for the development of RPE. As a result, we recommend supplemental oxygen or close oximetry monitoring in these patients. If RPE occurs, the treatment is mostly supportive, including supplemental oxygen, positive pressure ventilation, and diuresis.[5] However, if there is radiographic evidence of RPE but the patient is asymptomatic, no treatment is necessary.[1]

Reexpanison pulmonary edema is a rare but serious complication of thoracentesis. Physicians should always consider the possibility and varied presentation of this complication. This case was unusual in that RPE developed on the side contralateral to the lung that was drained.

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