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Negative Pressure Pulmonary Edema During Tracheal Dumon Stent Implantation

Sato, Fumitomo MD*; Sato, Nobukazu MD, PhD; Hata, Yoshinobu MD, PhD*; Suzuki, Aika MD*; Goto, Hidenori MD*; Otsuka, Hajime MD*; Ochiai, Ryoichi MD, PhD; Takagi, Keigo MD, PhD*

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Journal of Bronchology & Interventional Pulmonology: October 2012 - Volume 19 - Issue 4 - p 345-348
doi: 10.1097/LBR.0b013e3182732066
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Negative pressure pulmonary edema (NPPE), or acute postobstructive pulmonary edema, is a noncardiogenic condition in which a high, negative intrathoracic pressure generated by an obstructed upper airway results in an accumulation of fluid in the interstitium of the lungs.1 NPPE is generally a benign condition, typically resulting in full recovery in 12 to 48 hours if recognized early and necessary supportive treatment is initiated2; however, several fatal cases attributed to a delay in its diagnosis have been reported.3–5 The most common cause of NPPE is laryngospasm during intubation or after anesthesia in the postoperative period, or epiglottitis and croup in pediatric patients.6,7 NPPE developing after severe bronchospasm may occur more frequently than reported, because of it being unrecognized.8 Here, we present a case of NPPE after tracheal stent placement.


A 39-year-old man presented with lower tracheal and right main bronchial injury caused by a traffic accident in 1995. After intubation, stenosis from granulation tissue formed. Lower tracheal resection (5 rings) was performed but tracheal stenosis with granulation formation persisted. Additional stent implantation was repeated using a Gianturco Z-stent in 1996, an Ultraflex stent in 1999, and a Dumon stent in 2000. After the latter was implanted, airway patency of the lower trachea became stable, although stenosis of the right main bronchus remained (Fig. 1). In 2008, dried secretions inside the Dumon stent were removed under general anesthesia. In 2011, 11 years after its insertion, the Dumon stent was replaced because of dried secretions and foul breath (Fig. 2A). A rigid bronchoscope was inserted under general anesthesia with propofol, fentanil, and a small amount of sevoflurane, without using a muscle relaxant. Percutaneous cardiopulmonary support was available on stand-by. After insertion of the bronchoscope, spontaneous assisted ventilation was maintained. The Dumon stent was pulled out; the resultant bleeding made the patient experience 2 minutes of oxygen deprivation, with the minimum oxygen saturation being 92% (Fig. 2B,C). A new Dumon stent of the same size was substituted without difficulty (Fig. 2D). A few minutes after the reestablishment of central airway patency, oxygen saturation decreased to 88% even with 100% oxygen supplementation. Inspection by means of a flexible bronchoscope showed that the right main bronchus was obstructed by a blood clot. Although this was easily removed, pink frothy sputum production from the right main bronchus resulted and the patient remained hypoxic. Blood pressure was 100/60 mm Hg and heart rate was 80 beats/min. Chest x-ray showed diffuse ground glass opacity in the right lung, normal heart size, and no pleural effusion. This suggested unilateral NPPE (Fig. 3). Noninvasive positive end-expiratory pressure ventilation of 12 cm H2O was performed in the intensive care unit, which, together with steroids and diuretics, resulted in rapid recovery within a couple of hours. The patient recovered fully and by the next morning he was able to participate in the physical therapy.

Chest computed tomography (multiplanar reconstruction) showing 3 types of stents implanted in the lower trachea 11 years ago. Stenosis can still be seen at the right main bronchus.
A, Dumon stent inserted 11 years ago. B, Immediately after removal of the old Dumon stent. C, Bronchoscopic view at the carina showing intact left main bronchus (arrowhead) and stenotic right main bronchus covered by granulation tissue (arrow). D, New stent was replaced without difficulty, but hypoxemia persisted.
A, Chest x-ray after replacement of the Dumon stent showing diffuse ground glass opacity in the right lung. B, Chest computed tomography showing a diffuse infiltrating shadow in the right lung, compatible with unilateral NPPE, which had disappeared by the next morning.


The sudden onset of hypoxemia in the operating room requires a rapid differential diagnosis, but with limited physical findings. The diagnosis of NPPE depends mainly on the clinical feature of pink frothy secretions occurring after treating a central airway obstruction. Other causes of pulmonary edema, particularly those requiring a rapid intervention (fluid maldistribution, anaphylaxis, and cardiogenic pulmonary edema), must be considered before making the diagnosis of NPPE.2 Although many patients with NPPE recover with conservative management, some patients with severe NPPE require temporary intubation and mechanical ventilation with a positive end-expiratory pressure.2,6 Diuretics and steroids are often administered, but their use is controversial.2,6,9 In the case presented, noninvasive positive pressure ventilation was a successful alternative to intubation, which can sometimes be difficult to perform in patients who already have an implanted tracheal stent.

Interventional rigid bronchoscopy is usually performed under general anesthesia with adequate sedation and muscle relaxants.10 Ventilatory support can be provided using spontaneous ventilation, spontaneous assisted ventilation, controlled ventilation with Venturi Jet, high-frequency ventilation, or closed circuit positive pressure ventilation.11 Although there is some discussion about the requirement to preserve and conserve self-ventilation and the securing of compromised central airways without the aid of neuromuscular blocking agents,12 we prefer spontaneous assisted ventilation with intravenous anesthesia.13 Preserving the ability to self-ventilate is especially important in critically unstable patients who might suffer airway collapse if administered muscle relaxants. Communication and coordination between the bronchoscopist and the anesthesiologist is crucial, because preserving self-ventilation is more difficult to manage,12 and shared responsibility for the integrity of the airway is an added risk. Nonetheless, we also need to consider the additional risk of NPPE with spontaneous or spontaneous assisted ventilation during rigid bronchoscopy for patients with central airway obstruction. Under controlled ventilation with muscle paralysis, the potential risk of NPPE could be avoided.

Although the prevalence of postoperative NPPE is low (approximately 0.1%2), young, healthy, athletic patients seem to be at an increased risk because of “their enhanced ability to generate excessive negative intrathoracic pressure.”1 Patton and Baker1 reported NPPE caused by postextubation laryngospasm in 14 patients over a 15-year period in an orthopedic hospital. A total of 16,653 similar surgical procedures were carried out over this period, yielding an overall prevalence of NPPE of <0.1%. Patients with NPPE were significantly younger than those without NPPE (mean age, 28 and 41 y; range, 15 to 54 y and 5 to 93 y, respectively). The case presented here was a healthy 39-year-old patient with benign upper airway disease. During the stent placement in patients with upper airway obstruction, the maintenance of spontaneous breathing is essential for anesthesia management during the procedure. The possible risk of NPPE during this time needs to be taken into consideration, and the depth of anesthesia should be controlled, especially in cases of airway stent implantation in young, healthy patients.

In the case presented, NPPE occurred unilaterally, indicating that the “increased preload theory” is unable by itself to explain the pathophysiology of this presentation. Although its appearance in only 1 lung distinguished it from the classical presentation, some cases of unilateral NPPE have been reported.9 Since 1977, when Oswalt et al14 first described 3 cases of NPPE, the exact pathophysiological mechanism has been debated.1 The most likely mechanism proposed is that high-negative intrathoracic pressures cause significant fluid displacement from the microvessels to the perimicrovascular interstitium.2 A second proposed mechanism involves the disruption of the alveolar epithelium and pulmonary microvascular membranes because of severe mechanical stress, leading to increased pulmonary capillary permeability and protein-rich pulmonary edema.2 Fremont et al7 reported that the edema fluid/plasma protein ratio was normal and alveolar fluid clearance was intact in patients with NPPE. This indicates that the alveolar epithelium remains functionally intact and that hydrostatic forces are the primary mechanism causing NPPE. In contrast, Toumpanakis et al15 reported a potential role for resistive breathing as an inflammatory trigger in rat lung, suggesting that lung inflammation and increased permeability may contribute to NPPE and that airway obstruction can lead to acute lung injury and inflammation. Thus, a potential contribution of cytokine cascades toward the sudden onset of NPPE might be important and needs to be determined in future work.


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negative pressure pulmonary edema; central airway obstruction; airway stent

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