The clinical presentation and chest radiograph obtained in the ED immediately after the patient's arrival allowed diagnosis of left-sided tension pneumothorax. This condition rapidly improved after drainage via a tube thoracostomy.
Tension pneumothorax is a clinical diagnosis; the combination of severe hypoxia and hemodynamic instability is typically sufficient clinical evidence to institute needle decompression without a confirmatory chest radiograph. Delays in getting a chest radiograph can result in increases in morbidity and mortality when treating tension pneumothorax, which is one of the true clinical emergencies.
The sudden, dramatic worsening of the clinical picture 10 minutes postprocedure was unexpected. The second chest radiograph (Figure 2) showed florid left-sided pulmonary edema consistent with reexpansion pulmonary edema. This is a rare complication of the treatment of lung collapse secondary to atelectasis, pleural effusion, or pneumothorax.[1,2,3]
This case demonstrates that reexpansion pulmonary edema is a risk and should be kept in mind when treating a patient requiring tube thoracostomy. Many cases of unilateral reexpansion pulmonary edema have been reported, and the condition is associated with high mortality. It seems to be a relatively rare complication, but the actual incidence is unknown because many cases do not manifest clinically.
Reexpansion pulmonary edema generally occurs after a prolonged period of total lung collapse, or when the reexpansion treatment occurs too rapidly. This complication generally manifests early after reexpansion.[1,3]
The pathogenesis of reexpansion pulmonary edema is controversial because the causes are unclear and probably multifactorial. A relative lack of surfactant has been suggested as a causative factor, which could account for unilateral pulmonary edema occurring after long-standing total collapse of the lung. The condition can also develop after a very short time of lung collapse. Some evidence suggests other possible mechanisms, but increased pulmonary microvascular permeability is the only pathogenesis that has actually been studied and proven.
Another potential factor in the pathogenesis of reexpansion pulmonary edema is the speed of reexpansion after chest tube insertion. The thought is that rapid reexpansion perhaps enhances the inflow of fluid from the capillaries. This theory is debatable because case reports have demonstrated pulmonary edema occurring in lungs that have reexpanded without suction or in episodes of atelectasis that have reexpanded spontaneously. For pleural effusions, some evidence suggests no more than about 1.5 L should be drained at one time, or extreme caution should be exercised if removal of more than 1.5 L is planned; however, other evidence suggests that much larger volumes of fluid can be safely drained.
Cases of reexpansion pulmonary edema occurring with less than 1.5 L that have been caused by unknown factors have also been documented; these factors could possibly be negative intrapleural pressure, the amount of time that the lung has been down, and the age of the patient. Some evidence suggests that only underwater seal and not suction should be used in larger pneumothoraces that last longer than 3 days.
Caution should be applied irrespective of the amount of fluid drained, and the patient must be monitored for the development of respiratory symptoms. This could be accomplished, for example, by avoiding excessively negative intrapleural pressures. If no symptoms occur, then little evidence contraindicates draining an effusion to dryness.[1,3,5,6,7] Tarver and colleagues also suggest stopping air or fluid removal when the patient coughs, which is the first sign of reexpansion pulmonary edema.
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Cite this: Giovanni Volpicelli. A 75-Year-Old Man With Dyspnea and Chest Pain - Medscape - Nov 30, 2016.