A chronic effusion was treated by chesttube insertion. The initial drainage rate was kept low by applying a partial clamp to the tubing. After one hour the partial clamp was removed and the remaining fluid drained (without suction) into the collection system. When this system was changed the waterseal was not filled. It is quite probable that the lung collapsed during those 10 minutes, until the water seal had been reestablished. Ten minutes later the patient became agitated, most likely from hypoxia. Many authors describe cough as a fairly early symptom for reexpansion edema. Even with supplemental oxygen his arterial pO2 remained low. A chest X-ray showed bilateral (L>R) pulmonary edema.
Conventional therapy (intravenous morphine, furosemide, nitroglycerine) did not lead to sufficient improvement: the patient required intubation and ventilation. His pulmonary edema resolved within 36 hours, he could be extubated and did well.
The detailed mechanisms of reexpansion pulmonary edema are not well understood. It is believed that people less than 40 years old are more prone to this phenomenon than people older than 40 years. The longer the lung is collapsed the more likely reexpansion edema upon lung reexpansion becomes; but edema has also been observed after very brief periods of lung collapse. The rate of reexpansion does seem to play a role; and it is recommended to not apply suction to chest tubes right after insertion when the probability for reexpansion edema is high. When suction is applied, the pleural pressure should not be made very negative. Experimental studies show, that a more negative intrapleural pressure would increase the chance for edema formation.
Reexpansion edema has been noted to occur after release of a pneumothorax, drainage of a large pleural effusion, removal of an intrathoracic tumor, and release of atelectasis from airway obstruction.
The molecular and cellular mechanisms are also not well understood. A prolonged collapse would lead to a decreased perfusion by autoregulation. Reexpansion will cause reperfusion; edema formation might be a sign of reperfusion damage. Increased levels of mediators of inflammation have been measured (3, 5). Neutrophils get attached during atelectasis (1) and appear to be involved in the edema formation. Oxygen free radicals are being released and they contribute to the damage, but extrinsic catalase has not been useful in preventing the damage (2). An increased permeablity is always seen.
With a prolonged lung collapse the surfactant concentration will be severely diminished. This is an additional factor.
The phaenomenon of bilateral edema formation as we saw it (this has also been described before (4)) lends support to the theory that inflammatory mediators are released during reexpansion/reperfusion, since the contralateral lung could have been affected only by humoral (or neural?) mechanisms. Localized pulmonary edema (confined to just the lobe that had been collapsed) has also been described(6).
The most likely severely disturbed pulmonary lymphatic drainage (due to Hodgkin's disease) in this particular patient could have been an aggravating factor.
The usual therapeutic maneuvers for reexpansion pulmonary edema are borrowed from the standard therapeutic measures for pulmonary edema of different etiologies. Preload reduction, diuretics, afterload reduction (if an increased left ventricular enddiastolic pressure might play a role), positive pressure ventilation (but there are some theoretical and experimental arguments against the use of PEEP in the setting of reperfusion edema), if necessary intubation.
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Copyright Fred Splittgerber.
last update April 3, 2000