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Negative Pressure Pulmonary Edema Following BronchospasmNegative Pressure Pulmonary Edema and Bronchospasm FREE TO VIEW

David J. Krodel, MD; Edward A. Bittner, MD, PhD, FCCP; Raja-Elie E. Abdulnour, MD; Robert H. Brown, MD, MPH; Matthias Eikermann, MD, PhD
Author and Funding Information

From the Department of Anesthesia, Critical Care, and Pain Medicine (Drs Krodel, Bittner, and Eikermann) and the Pulmonary and Critical Care Unit, Department of Medicine (Dr Abdulnour), Massachusetts General Hospital, Harvard Medical School, Boston, MA; and the Department of Anesthesiology and Critical Care Medicine (Dr Brown); the Department of Environmental Health Sciences, Division of Physiology (Dr Brown); the Department of Medicine, Division of Pulmonary Medicine (Dr Brown); and the Department of Radiology (Dr Brown), Johns Hopkins University, Baltimore, MD.

Correspondence to: David J. Krodel, MD, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, 55 Fruit St, Boston, MA 02114; e-mail: dkrodel@partners.org


Funding/Support: This work was supported entirely by departmental and/or institutional resources.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;140(5):1351-1354. doi:10.1378/chest.11-0529
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Negative pressure pulmonary edema (NPPE) is an important cause of noncardiogenic pulmonary edema but is rarely reported in the setting of bronchospasm. A 43-year-old woman with severe reactive airway disease suffered an episode of severe bronchospasm after endotracheal extubation following an otherwise uneventful general anesthetic. Subsequently, she developed clinical and radiographic signs of pulmonary edema in the absence of other symptoms of acute left-sided heart failure, leading to the diagnosis of noncardiogenic pulmonary edema. She received noninvasive positive pressure ventilation for a few hours, after which her clinical and radiologic signs and symptoms of pulmonary edema were greatly improved. This clinical scenario strongly suggests NPPE. We submit that it is possible to create NPPE by generating highly negative intrathoracic pressures in the setting of severe bronchospasm.

Figures in this Article

Negative pressure pulmonary edema (NPPE) is an important cause of noncardiogenic pulmonary edema that is easily overlooked and is usually suggested by the setting. It often occurs after upper airway obstruction (both acute and after relief of chronic obstruction) but is rarely diagnosed after bronchospasm. Here we report a case of NPPE in the setting of acute bronchospasm upon endotracheal extubation following general anesthesia.

A 43-year-old woman with systemic lupus erythematosus and a 20-year history of severe asthma and COPD presented with abnormal cervical pathology after previous hysterectomy and was scheduled for cervicectomy (excision of the uterine cervix). Preoperative pulmonary function tests revealed an FEV1 of 0.57 L (20% predicted) and FVC of 1.63 L (45% predicted), which increased to 0.66 L and 2.33 L, respectively, a significant bronchodilator response. Her total lung capacity was 6.07 L (120% predicted). She was never a smoker, never had any significant toxic or environmental exposures nor metabolic abnormalities such as α1-antitrypsin deficiency, but did have recurrent respiratory infections in the setting of her severe asthma. She had been on an oral prednisone taper for a COPD exacerbation a few months earlier, currently 7.5 mg daily. A chest CT scan obtained to follow up on previously seen axillary adenopathy during oncologic workup for vaginal/cervical carcinoma in situ performed a week prior to surgery was consistent with chronic bronchitis, emphysema, and bronchiectasis (Fig 1A).

Figure Jump LinkFigure 1. A, Chest CT scan prior to surgery. B, Chest CT scan 2 days postoperatively. Bronchiectasis is apparent on both CT images, but patchy consolidative infiltrates on the postoperative CT scan could be due to diffuse pulmonary edema or, less likely, airway hemorrhage. C, Chest radiograph on admission to the post-anesthesia care unit. D, Chest radiograph after 2 days showing interval improvement of pulmonary edema. The large lung volumes and narrow cardiac silhouette are consistent with the patient’s diagnosis of COPD. Although the infiltrates shown could also represent a diffuse aspiration pneumonitis, the relatively fast improvement is more consistent with pulmonary edema.Grahic Jump Location

On the morning of surgery, she was at her baseline respiratory function and had taken her usual oral prednisone and inhaled fluticasone/salmeterol. Chest auscultation revealed clear breath sounds and a prolonged expiratory phase but no wheezing. She had not taken solids or liquids by mouth for >10 h and had no history of gastroesophageal reflux disease. Induction, intubation, and maintenance of general anesthesia were uneventful, and the patient was hemodynamically stable throughout the case. An uncomplicated cervicectomy was performed with minimal blood loss in 1.5 h.

Before emergence from anesthesia, the oropharynx was suctioned, and the patient was extubated while sedated, spontaneously breathing, and in an upright position. During extubation, the patient coughed and subsequently developed signs and symptoms of severe bronchospasm: wheezing during a prolonged phase of forced exhalation as well as the use of accessory muscles. There was no evidence of stridor during inspiration, as would be consistent with laryngospasm. No gastric secretions were noted in her oropharynx on inspection nor with subsequent suctioning. Despite adequate oxygenation, ventilation with bag-mask remained difficult even after insertion of an oropharyngeal airway and a nasal trumpet. After about 30 min, frothy, pink sputum was noted to be coming from the patient’s mouth. Furosemide was administered for possible pulmonary edema. A 12-lead ECG showed sinus rhythm and no evidence of acute ischemia or infarction. A chest radiograph taken immediately after admission to the post-anesthesia care unit (PACU) showed diffuse bilateral opacities despite net negative intraoperative fluid balance (Fig 1C). Transthoracic echocardiogram demonstrated normal anatomy and function with an estimated right ventricular systolic pressure of 34 mm Hg (assuming right atrial pressure of 10 mm Hg).

Noninvasive positive-pressure ventilation was started with 6 cm H2O of pressure support over 8 cm H2O of positive end expiratory pressure. Consequently, the patient rapidly improved in the PACU, and noninvasive positive pressure ventilation was terminated after 5 h. The following morning the patient was transferred to the gynecology ward and went on to make a full recovery over the next 24 h.

We suspect that NPPE after bronchospasm may occur more frequently than reported but goes unrecognized because pulmonary edema after bronchospasm can often be attributed to other factors, such as aspiration, volume overload, or atelectasis. Many patients require oxygen therapy in the PACU, chest radiographs are not routinely obtained, and often NPPE resolves quickly with conservative measures.

The interaction between airway edema and bronchoconstriction raises many issues. The first is whether bronchoconstriction could be the root cause of the NPPE. There have been a few theories as to this possibility. Large negative pleural pressures have been measured in children with acute asthma, and this has been shown to be correlated with fluid accumulation in the lungs of dogs.1 However, asthma is a very heterogeneous disease and bronchoconstriction is not uniform in either location or extent.2 It is possible to close even large central cartilaginous airways with a large enough stimulus,3 but whether this can happen under clinical conditions is unclear. Although narrowing of large airways occurs in asthma, it is generally believed that it is the additional closure of hundreds or even thousands of small airways leading to air trapping and hyperinflation that causes the clinical signs and symptoms of asthma (Fig 2).2

Figure Jump LinkFigure 2. The pathophysiologic changes in intrapulmonary fluid homeostasis during forced inspiration during peripheral airway obstruction. A, Normal lung. B, Acute bronchial obstruction. Lung and alveolar volumes are increased during obstruction of the terminal bronchi by a variable extent, depending on the amount of air trapping, and ventilation may be impaired. Consequently, respiratory drive is increased from hypercapnia such that highly negative pressure is being generated by the inspiratory respiratory muscles, leading to a net increase in the pulmonary vascular volume and the pulmonary capillary transmural pressure. Even in stable situations, the equilibrium of intravascular/extravascular fluid flux is dynamic and delicately balanced. In patients with asthma, increased vascularity, increased mucosal blood flow, leaky capillaries, inflammatory exudate, and edema may complicate fluid homeostasis. This equilibrium will be disturbed by a change in hydrostatic pressure, such that the markedly negative intrathoracic pressure generated during a deep inspiration would lead to a pressure gradient across the capillary wall and subsequent extravasation of fluid into the interstitial space and airways. PAP = pulmonary artery pressure.Grahic Jump Location

This patient had severe pulmonary disease, a recent decrease in her oral steroid dose, and significant stimulation of her trachea during extubation. This constellation of events could have lead to significant conducting airway narrowing with inadequate airflow during strong inspiratory efforts, leading to the resultant NPPE. A mucus plug could be another inciting factor for the development of her NPPE.

The second interaction to consider is the potential effect of the airway edema on subsequent bronchoconstriction. Thickening of the airway wall has been hypothesized to be one of the mechanisms contributing to airway hyperresponsiveness in asthma. Acute changes in thickness can occur from inflammation4 or from local edema caused by vascular leakage in the wall. Such acute airway wall thickening secondary to edema formation has been proposed as a possible cause of wheezing in patients with congestive heart disease in left ventricular failure. As the heart failure improves, pulmonary function also improves.5 Although it cannot be ruled out that airway edema led to bronchoconstriction, given the clinical scenario it remains more likely that in this case the bronchoconstriction indeed came first, perhaps even generating a “downward spiral” of edema, airway narrowing, and bronchoconstriction.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Role of sponsors: The sponsor had no role in the design of the study, the collection and analysis of the data, or in the preparation of the manuscript.

Other contributions: This work was performed at the Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA.

Stalcup SA, Mellins RB. Mechanical forces producing pulmonary edema in acute asthma. N Engl J Med. 1977;29711:592-596 [CrossRef] [PubMed]
 
Venegas JG, Winkler T, Musch G, et al. Self-organized patchiness in asthma as a prelude to catastrophic shifts. Nature. 2005;4347034:777-782 [CrossRef] [PubMed]
 
Brown RH, Mitzner W. The myth of maximal airway responsiveness in vivo. J Appl Physiol. 1998;856:2012-2017 [PubMed]
 
Laitinen LA, Laitinen A, Haahtela T. Airway mucosal inflammation even in patients with newly diagnosed asthma. Am Rev Respir Dis. 1993;1473:697-704 [PubMed]
 
Krodel DJ, Bittner EA, Abdulnour R, Brown R, Eikermann M. Case scenario: acute postoperative negative pressure pulmonary edema. Anesthesiology. 2010;1131:200-207 [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1. A, Chest CT scan prior to surgery. B, Chest CT scan 2 days postoperatively. Bronchiectasis is apparent on both CT images, but patchy consolidative infiltrates on the postoperative CT scan could be due to diffuse pulmonary edema or, less likely, airway hemorrhage. C, Chest radiograph on admission to the post-anesthesia care unit. D, Chest radiograph after 2 days showing interval improvement of pulmonary edema. The large lung volumes and narrow cardiac silhouette are consistent with the patient’s diagnosis of COPD. Although the infiltrates shown could also represent a diffuse aspiration pneumonitis, the relatively fast improvement is more consistent with pulmonary edema.Grahic Jump Location
Figure Jump LinkFigure 2. The pathophysiologic changes in intrapulmonary fluid homeostasis during forced inspiration during peripheral airway obstruction. A, Normal lung. B, Acute bronchial obstruction. Lung and alveolar volumes are increased during obstruction of the terminal bronchi by a variable extent, depending on the amount of air trapping, and ventilation may be impaired. Consequently, respiratory drive is increased from hypercapnia such that highly negative pressure is being generated by the inspiratory respiratory muscles, leading to a net increase in the pulmonary vascular volume and the pulmonary capillary transmural pressure. Even in stable situations, the equilibrium of intravascular/extravascular fluid flux is dynamic and delicately balanced. In patients with asthma, increased vascularity, increased mucosal blood flow, leaky capillaries, inflammatory exudate, and edema may complicate fluid homeostasis. This equilibrium will be disturbed by a change in hydrostatic pressure, such that the markedly negative intrathoracic pressure generated during a deep inspiration would lead to a pressure gradient across the capillary wall and subsequent extravasation of fluid into the interstitial space and airways. PAP = pulmonary artery pressure.Grahic Jump Location

Tables

References

Stalcup SA, Mellins RB. Mechanical forces producing pulmonary edema in acute asthma. N Engl J Med. 1977;29711:592-596 [CrossRef] [PubMed]
 
Venegas JG, Winkler T, Musch G, et al. Self-organized patchiness in asthma as a prelude to catastrophic shifts. Nature. 2005;4347034:777-782 [CrossRef] [PubMed]
 
Brown RH, Mitzner W. The myth of maximal airway responsiveness in vivo. J Appl Physiol. 1998;856:2012-2017 [PubMed]
 
Laitinen LA, Laitinen A, Haahtela T. Airway mucosal inflammation even in patients with newly diagnosed asthma. Am Rev Respir Dis. 1993;1473:697-704 [PubMed]
 
Krodel DJ, Bittner EA, Abdulnour R, Brown R, Eikermann M. Case scenario: acute postoperative negative pressure pulmonary edema. Anesthesiology. 2010;1131:200-207 [CrossRef] [PubMed]
 
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