Reexpansion pulmonary edema: a case report and review of the current literature

Introduction 

Reexpansion pulmonary edema (REPE) is a rare and potentially lethal complication of thoracostomy tube placement for pneumothorax, pleural effusion and severe atelectasis. Its onset is sudden and dramatic. One author estimated it occurred once every 2 years at his institution (1). REPE is potentially lethal with mortality estimates as high as 20% (2). Identification of these risks for this complication may help to avoid its onset.

Case report 

A 28-year-old man presented complaining of dypnea on exertion and cough for the prior 4 days. He denied any chest pain and stated that he had first noted the symptoms upon awakening. The cough was non-productive, and he had no fevers or chills.

The patient denied any significant past medical or surgical history. He took no medications and reported no drug allergies. He reported 1 pack per day (PPD) smoking history and occasional alcohol consumption. He denied illicit drug use.

Triage vital signs were: temperature of 36.4°C (97.6°F), pulse of 100 beats/min, blood pressure 129/95 mm Hg, respiratory rate of 20 breaths/min with a pulse oximeter reading of 93–96%. He seemed comfortable and was in no respiratory distress. He spoke in complete sentences. The trachea was midline and there was no jugular venous distension. The heart rate was regular, and there were no murmurs. No breath sounds could be heard in the right hemithorax. The left lung fields were clear. No other abnormalities were noted on physical examination.

Complete blood count, electrolytes and coagulation studies were within normal limits. A chest X-ray study showed a total pneumothorax on the right (Figure 1).

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Figure 1. Total pneumothorax of the right lung.

A 24 French thoracostomy tube was placed, with a resultant “gush of air” upon entering the chest cavity. The tube was connected to a pleuravac device and set to negative 20 cm H2O pressure. The patient tolerated the procedure well with a minimal amount of pain and coughing. Pulse oximetry was measured at 100% on 2 L nasal cannula approximately 30 min after the procedure.

One hour after chest tube insertion the patient’s condition deteriorated. He became tachycardic, tachypneic, and began to cough more vigorously. Pulse oximetry reading on 2 L NC was now 83%. A 100% non-rebreather was placed on the patient but his pulse oximeter remained low at 84%. Re-examination revealed unilateral crackles on the right. A repeat chest X-ray study (Figure 2) demonstrated pulmonary edema on the right. The patient was intubated secondary to worsening respiratory distress and admitted to the surgical intensive care unit.

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Figure 2. Repeat chest X-ray study approximately 1 h after thoracostomy tube insertion demonstrating unilateral pulmonary edema.

Hospital course included improving oxygenation with lower requirements of FiO2 over the next 24 h. Thirty-six hours after mechanical ventilation was instituted the patient was extubated. He was transferred to the surgical floor on hospital day #2 and discharged without further complication on hospital day #6.

Discussion 

Reexpansion pulmonary edema (REPE) after spontaneous pneumothorax is a rare complication of tube thoracostomy. The single largest retrospective study of individuals with REPE (n = 21) who were treated for spontaneous pneumothorax reported an incidence of 14% (3). Earlier studies of spontaneous pneumothorax do not report this complication at all 4, 5.

The mortality of this complication is not well defined. A case series by Mahfood et al. suggests that REPE may be more lethal than one might expect (2). They report a mortality rate of 20% in the 53 cases they reviewed. These results likely represent an inflated mortality rate secondary to the inherent selection bias present in case series. Other studies report no fatalities from REPE 2, 4, 5.

The clinical picture of REPE is dramatic. Onset is often immediate, with 64% of patients exhibiting symptoms within 1 h. All patients are symptomatic within 24 h (2). Severe coughing often heralds the development of pulmonary edema. The patient becomes tachypneic and tachycardic as hypoxia increases. The patient does not respond to oxygen therapy as blood is shunted past fluid-filled alveoli. Rarely, bilateral or contralateral edema develops (6). If third spacing within the lung is significant enough, hypotension can occur (7). Symptoms usually resolve within 24 to 72 h.

The pathophysiology of REPE is complex and still not completely understood. Multiple factors contribute to a capillary bed with increased permeability. An inflammatory response occurs when the lung re-expands. This response is believed to be secondary to expansion-related mechanical injury to the alveolar-capillary membrane and reperfusion injury as blood flow returns to the now fully expanded lung (1). Recent studies in rabbits implicate inflammatory mediators (IL-8 and monocyte chemoattractant protein) in the pathogenesis. Both of these inflammatory mediators are found in the affected lung and, to a lesser degree, in the contralateral lung, possibly adding explanation to the bilateral nature sometimes present in REPE 8, 9.

A subset of patients with spontaneous pneumothorax seem to be more susceptible to developing REPE. Matsuura et al. reviewed 146 cases of spontaneous pneumothorax treated by thoracentesis or continuous low negative pressure at their institution. They found no significant difference in the rate of development of REPE when classified by gender, side of collapse, pulmonary co-morbidities, history of pneumothorax, or signs and symptoms of pneumothorax. However, they did report a statistically significant increased incidence of REPE in patients aged 20–39 years in their series (3).

The duration of pneumothorax also has been implicated in the incidence of REPE (10). Early case series found that spontaneous pneumothorax was present an average of 14 days with a minimum of 3 days before REPE would develop (11). A study of Rhesus monkeys seemed to confirm the importance of duration of symptoms. None of six animals with experimentally induced total pneumothorax developed REPE if the lungs were re-expanded within 1 h (12). Matsuura’s retrospective review, however, could not find statistical significance for the duration of collapse when controlled for the size of the pneumothorax. There was only a tendency in patients with a pneumothorax > 30% of the lung field to have greater incidence of REPE when the duration of symptoms (and presumably the duration of pneumothorax) was longer (3). Furthermore, REPE has been reported in several patients with a pneumothorax re-expanded only hours after the onset of symptoms 10, 13.

The severity of the pneumothorax may be more predictive than its duration. In Matsuura’s series, no patient with a pneumothorax < 30% of the lung field versus 17% of patients with total collapse and 44% of patients with tension pneumothorax suffered this complication. In addition, in the subset of patients with a large or tension pneumothorax, a duration of < 4 days was more predictive of REPE than duration > 4 days (3). Not coincidentally, when REPE complicated a spontaneous pneumothorax of brief duration, the pneumothorax size was large (13).

The final risk factor for the development of REPE may also help the clinician prevent this complication—the method of re-expansion. Unfortunately, no randomized clinical trials address this question. Some authors suggest that slow re-expansion by low negative pressure would be beneficial, whereas others support the idea that it is not as much the negative pressure as the rate of re-expansion that is important (10).

No human study has been performed prospectively to determine whether the incidence of REPE would be less if the chest tube is put to water seal only. There is one animal study that examined this problem. These authors studied REPE in monkeys and found that after a large pneumothorax of 3 days duration, 6 of 6 monkeys developed REPE if their lungs were re-expanded with −10 cm H20 versus none of the 6 animals who had their lungs re-expanded on water seal alone (12).

Unfortunately, REPE can also occur in patients whose lungs are re-expanded without suction and the clinician is faced with the reality that the development of REPE is related to all three factors—longer duration, greater size and a rapid rate of expansion (2). Controlling for one may not prevent the process if the other two are present.

In lieu of a randomized control trial, the American College of Chest Physicians (ACCP) recently produced a consensus statement on the preferred management of a spontaneous pneumothorax. In clinically stable patients with a large (≥ 30% of the lung field) primary pneumothorax, the ACCP recommends either small-bore (14 F or smaller) catheter or 16–22 F chest tube placement. They recommend these tubes be connected to a Heimlich valve or a water-seal device. However, if the lung fails to re-expand, suction application is deemed appropriate (14).

In general, the ACCP recommends that a patient with a large pneumothorax be admitted. Patients unwilling to undergo hospitalization may be discharged with a small-bore catheter and Heimlich valve if the lung is fully expanded. Follow-up should be arranged within 48 h (14).

The ACCP consensus statement does not specifically address REPE. It does state, however, that in patients with a large pneumothorax and symptoms for > 24 h, their recommendations would not be altered (14). From what is known about REPE, these recommendations seem appropriate. An attempt is made to re-expand the lung without the use of suction, which may increase the incidence of REPE. Admission of patients with a large pneumothorax will detect at-risk patients who may develop REPE up to 24 h after re-expansion. Patients with a small spontaneous pneumothorax may not require admission, and indeed, are not at risk of developing REPE.

Therapy for REPE is generally supportive. Mechanical ventilation with positive end expiratory pressure, and hemodynamic support may be appropriate. Some authors recommend non-steroidal anti-inflammatory agents (NSAIDS) (1). Unfortunately, there are no studies to support the use of NSAIDs. Patient positioning also may be therapeutic when pulmonary edema is unilateral. In these cases, the lateral decubitus position with the affected side up will reduce intrapulmonary shunting and improve oxygenation (1).

Our patient was young, had symptoms for several days and a large pneumothorax on chest X-ray study. The gush of air present upon entering the chest cavity suggests that despite his stable hemodynamics, the pneumothorax was under tension. Additionally, placing the chest tube on suction with a pleuravac system increased the rate of expansion of the lung and further predisposed him to REPE.

In summary, REPE is a rare complication of tube thoracostomy for spontaneous pneumothorax. It most commonly occurs in patients with a large pneumothorax of longer duration. A large pneumothorax seems to be a prerequisite for the development of REPE, whereas a prolonged duration is not always present. There are no randomized control trials to support any preferred method of prevention of this complication. Based on the ACCP consensus recommendations and animal studies, a stable patient with a large pneumothorax should have re-expansion without suction. If REPE does develop, therapy is mostly supportive.