Negative pressure pulmonary edema (NPPE) describes the phenomenon of alveolar-capillary membrane injury after the exposure of alveoli to subatmospheric pressures (1). Multifactorial in origin, it results in a capillary leak, often leading to respiratory failure requiring mechanical ventilation (2). Usually, NPPE follows an episode of vigorous inspiration attempts in association with acute airway obstruction (3). We report a case of NPPE occurring after suction was applied to the pleural space via chest tube for the evacuation of a pneumothorax in a lung transplant patient with bilateral anastomotic bronchial strictures.
A 29-yr-old male with a medical history of bilateral lung transplantation for cystic fibrosis 2 mo previously was hospitalized after fiberoptic bronchoscopy and attempted dilation of bilateral bronchial anastomotic strictures. A postoperative chest radiograph revealed a left-sided apical pneumothorax, presumably secondary to a small anastomotic disruption caused during the dilation attempt. A chest tube was placed into the left pleural space and connected to −20 cm H2O suction, resulting in successful evacuation of the pneumothorax. A moderate air leak was noted for several days. The patient’s postoperative course was further complicated by intermittent right upper lobe collapse, which was attributed to mucous plugging and the proximity of the right upper lobar bronchus orifice to the stenotic anastomotic site. These episodes were associated with dyspnea requiring oxygen supplementation. Although repeated bronchoscopic suctioning alleviated these symptoms temporarily, it was obvious that the attempts to dilatate the bronchial strictures were not successful, and the patient continued to manifest airway obstruction aggravated by mucous secretions collecting at the stenotic sites. On day 7 of his hospitalization the patient was noted to be febrile, and once again a collapsed right upper lobe was noted on the chest radiograph. In addition, a recurrence of the pneumothorax on the left side was seen (Fig. 1a). With oxygen requirements increasing, a respiratory rate of 35, and an Spo2 of 88%–91% on an Fio2 of 0.7–0.8 via non-rebreathing face mask, the patient was transferred to the intensive care unit with presumed diagnosis of right-sided pneumonia. Chest auscultation revealed distant breath sounds bilaterally and absence of air movement in the right upper lobe. At this time arterial blood gas (ABG) revealed a pH of 7.38, a Pco2 of 39, and a Po2 of 66. Antibiotics were started, and, in an attempt to evacuate the left-sided pneumothorax more effectively, the suction applied to the chest tube was increased to −40 cm H2O. Shortly thereafter, the patient’s condition deteriorated, and tracheal intubation followed by mechanical ventilation with an Fio2 of 1.0 and positive end-expiratory pressure of 10 mm Hg was required. Immediately, copious blood-tinged secretions were suctioned. Fiberoptic bronchoscopy revealed frothy secretions originating mainly from the left lung. A chest radiograph showed complete opacification of the left field (Fig. 1b). The chest tube suction was decreased to −20 cm H2O. A chest computed tomographic scan confirmed a picture consistent with left-sided pulmonary edema. Over the next 12 h the patient’s respiratory status improved without further intervention, and the Fio2 requirement and the secretions diminished dramatically. A chest radiograph 24 h later showed improvement of pulmonary edema. ABG on an Fio2 of 0.4 showed a pH of 7.35, a Pco2 of 37, and a Po2 of 101.
Despite this initial improvement, the patient’s course was further complicated by sepsis, presumably from a pulmonary source. A tracheostomy was performed to provide access for frequent pulmonary toilet and bronchoscopy. Over the next several weeks the patient’s condition improved and bronchial stents to alleviate the anastomotic obstructions were successfully placed. With patent airways the patient was successfully weaned off the ventilator.
The usual clinical scenario leading to NPPE involves forceful inspiration against an obstructed artificial or physiologic airway (4,5). Excessive suction applied directly to the tracheobronchial tree via a tracheostomy adapter or during bronchoscopy has also been described as a contributory factor (6,7). Although rare, the unilateral presentation of NPPE has been reported (6,8), suggesting that localized exposure to negative pressure is responsible for its occurrence.
A unilateral appearance of pulmonary edema reduces the large list of possible differential diagnoses (9), which can be narrowed to include localized insults, such as unilateral gastric content aspiration, bleeding, or trauma. In this context, reexpansion pulmonary edema (RPE) has been described as a possible cause (3). RPE is a rare complication of reexpansion of collapsed lung after drainage of large pleural effusions or, rarely, after pneumothoraces (3).
Various pathophysiologic mechanisms have been proposed for development of NPPE. Enhancement of venous return and increase in pulmonary hydrostatic pressure, hypoxia-induced cardiac dysfunction, and pressure-induced, mechanical alveolar-capillary disruption promoting capillary permeability and favoring transudation of fluid into the lung tissue have been postulated (10). Although these mechanisms may contribute to the development of NPPE and RPE, altered capillary membrane permeability in the hypoxic, previously atelectatic lung segment after reexpansion has been proposed as an additional factor in RPE (3).
In the presented case, the unilaterality of the findings and the temporal proximity to the increase in chest tube suction suggests that the application of increased negative intrapleural pressure was the inciting factor leading to the picture of respiratory distress, the formation of copious serosanguinous pulmonary secretions, and radiographic evidence of pulmonary congestion—the hallmark of NPPE (11).
Although it may be impossible to distinguish with absolute certainty between NPPE and RPE, Woodring (3) identifies a short duration of involved collapsed lung, as present in our case, as an unlikely factor leading to RPE. In addition, the author points out the lack of evidence that conventional intrapleural suctioning, per se, is associated with RPE. He further concludes that RPE is associated with a focal appearance of edema localized to previously collapsed lung tissue (3). This is in contrast to our case, in which the whole lung was involved.
Negative pressure applied to the intrapleural space in a post-lung transplant patient has not been described as a mechanism of alveolar-capillary lung injury.
In our patient, the negative pressure on the chest tube was increased from −20 to −40 cm H2O in an attempt to evacuate the persistent pneumothorax. The presence of a bronchial stenosis, which was aggravated by further compromise of the bronchial lumen diameter by mucous secretions, may have precluded adequate equilibration of atmospheric and alveolar pressures, thus acting as a partial obstruction to airflow and allowing the creation of a subatmospheric alveolar pressure milieu.
Increased negative pressure distal to the stenosis may have added a dynamic component of airway collapse at or proximal to the obstruction by virtue of a Bernoulli effect across the stenosis, causing the phenomenon of flow limitation.
A contributing factor to NPPE in this case may be the limited ability of the transplanted lung to handle increased interstitial fluid loads, secondary to disrupted lymphatic drainage. Kline and Thomas (12) showed that in canines undergoing lung transplantation “the pulmonary lymphatics seemed to be ineffectual in clearing the allograft of the accumulating cellular infiltrates and fluid.”
In conclusion, NPPE may occur secondary to high levels of negative pressure applied to the intrapleural space via chest tubes in the setting of partial large airway obstruction. After lung transplant patients may be especially at risk because of compromised lymphatic drainage. We recommend the avoidance of application of excessive negative pressure to chest tubes in this patient population.
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