Journal Logo

Brief Reports

Pulmonary Edema Secondary to Dynamic Tracheal Collapse

Firdose, Romaisa MD; Elamin, Elamin M. MD, MSc, FACP, FCCP

Author Information
  • Free

Abstract

Pulmonary edema is a well-recognized complication of upper airway obstruction. The pathogenesis is multifactorial, with attention primarily focused on excessive negative intrapleural and transpulmonary pressure produced by forceful inspiration against a closed glottis. However, little is known about pulmonary edema secondary to expiratory airway obstruction. A heightened awareness of this poorly recognized and often perplexing syndrome may help reduce the occurrence and facilitate the treatment of this potential complication of airway obstruction.

CASE REPORT

An 80-year-old woman presented with a history of a viral upper respiratory infection associated with a forcible dry cough for about a week. Subsequently she developed rapidly progressing shortness of breath and orthopnea. Her medical history was significant for hypertension and right-side hemiparesis secondary to a ruptured intracranial aneurysm 50 years earlier. She was a nonsmoker. Physical examination revealed bilateral pulmonary crepitations and rales. An arterial blood gas on admission showed the following: pH, 7.5; pCO2, 27.7 mmHg; HCO3, 21 mmoL/L; and PO2, 50 mmHg on room air. Chest radiography revealed bilateral perihilar infiltrates with bilateral pleural effusions consistent with congestive heart failure, whereas an echocardiogram showed normal left ventricular size and systolic function. Subsequently, spiral CT of the chest was performed. Scans were negative for pulmonary embolism; however, they demonstrated irregularities in the entire tracheal contour during respiration. Dynamic CT of the trachea revealed marked collapse of the posterior tracheal wall during expiration (Fig. 1). Further workup by bronchoscopy revealed 75 to 80% expiratory dynamic collapse of the posterior tracheal wall distal to the vocal cord fold (Fig. 2). Similar findings were noted in the posterior wall of the right and left mainstem bronchi as well. Different cough suppressants were tried, with limited improvement in patient respiratory status and pulmonary edema.

FIGURE 1.
FIGURE 1.:
Dynamic CT scan showing fully expanded trachea during inspiration (A) and marked posterior wall collapse during expiration (B).
FIGURE 2.
FIGURE 2.:
Bronchoscopic image showing fully expanded tracheal lumen during inspiration (A) with marked posterior collapse during expiration (B).

An Ultraflex uncuffed tracheal stent (Microvasive, Natick, MA, USA) was placed to support the collapsible trachea. The stent was 6 cm in length and 14 mm in diameter when fully expanded. The patient improved gradually after the procedure, with resolution of the clinical and radiologic manifestations of postobstructive pulmonary edema (POPE) over the following 3 days.

The patient was subsequently discharged home in stable condition. Pulmonary function tests performed before and 3 months after the procedure demonstrated an improvement in FEV1 of 800 mL and in FVC of 1000 mL (Fig. 3). There was no recurrence of pulmonary edema symptoms after 4 years of follow-up.

FIGURE 3.
FIGURE 3.:
Spirometry results before and after tracheal stenting.

DISCUSSION

Pulmonary edema has long been recognized as a complication of upper airway obstruction during inspiration. It has been observed that victims of airway obstruction secondary to strangulation are more prone to develop pulmonary edema compared with victims of rapid hanging, in which the cervical spine is broken. 1,2 POPE has been reported in all ages; however, it occurs more often in the pediatric age group. Underlying mechanisms in children include laryngospasm, epiglottitis, laryngotracheobronchitis, and foreign body aspiration. Although laryngospasm accounts for more than 50% of the reported POPE in adults, 3 other adult etiologies include laryngeal tumors, strangulation, acute epiglottitis, croup, and tracheal obstruction secondary to goiter or neoplasm. 1,2,4–6 Unilateral pulmonary edema can develop after acute obstruction of the contralateral bronchus, such as by a foreign body. 7

Two types of POPE are described in the literature. 8 Type 1 may be associated with any cause of acute airway obstruction, such as postextubation laryngospasm or epiglottitis. Type 2 POPE occurs after surgical relief of chronic upper airway obstruction, such as tonsillectomy and removal of upper airway tumors including thyroid goiter.

Clinically, patients present with signs of acute respiratory distress that include tachypnea, hypoxia, and production of pink frothy secretions with pulmonary crepitations and rales. In most cases symptoms occur within minutes of relief of upper airway obstruction. However in some patients, the development of pulmonary edema may be delayed for several hours. 9

The incidence of POPE is difficult to assess. It may occur more frequently than is reported. Tami et al 9 reported an incidence of 11% in 27 cases of adult acute upper airway obstruction. Many cases may be missed due to the fact that POPE is not a well-recognized clinical entity. Variable onset of symptoms (ranging from immediate to hours after relief of the obstruction) may contribute to the misdiagnosis.

Pulmonary edema due to upper airway obstruction appears multifactorial in origin. Galvis et al2 reported that POPE occurred secondary to a sudden change in pulmonary homodynamics that took place after release, rather than during, the obstruction. The initiating event in POPE is the markedly negative intrapleural pressure generated by a forceful inspiratory effort against an obstructed extrathoracic airway (modified by the Muller maneuver).3,8,10,11 Relief of the obstruction leads to an abrupt decrease in airway pressure. Such exaggerated negative intrathoracic pressure leads to increased venous return and increased hydrostatic pressure, favoring transudation of fluid from the pulmonary capillary space into the interstitial space of the lung. Other mechanisms may also contribute to the development of edema. Some investigators have suggested that forced inspiration against an obstructed airway may be associated with direct injury to the alveolar–capillary membrane, with subsequent high-permeability pulmonary edema.11

The concept of “stress failure” of pulmonary capillaries, in which increasing pulmonary capillary pressures cause capillary endothelial and alveolar epithelial damage with resultant high-permeability pulmonary edema, may be relevant to this phenomenon as well. 11,12

In addition, the recovery of alveolar fluid with abundant protein and inflammatory cells 4 to 6 hours after the onset of upper airway obstruction may argue against fluid transudation as the only causative factor. 11 However, the rapid resolution of edema that has been observed supports transudation as the dominant mechanism of production of pulmonary edema. This can be explained in part due to the hyperadrenergic state associated with airway obstruction with increased venous return to the heart, which could further contribute to the edema. 9

Goldenberg et al 3 hypothesized that patients with underlying occult cardiac problems are more likely to develop POPE, which could explain why pulmonary edema develops in some individuals, whereas in most it does not, even under similar clinical situations.

The mechanism by which pulmonary edema developed in our patient can be explained by the development of intrinsic positive end-expiratory pressure (PEEPi). During exhalation against a collapsed upper airway, increased intrathoracic pressure impedes venous return. With the onset of inspiration, intrathoracic pressure falls and venous return and right ventricular filling increase abruptly. 13 Because of “ventricular interdependence,” this may shift the septum to the left and compromise left ventricular filling. In addition, increased intrathoracic pressure compresses vascular structures, including pulmonary vessels and the heart itself, increasing pulmonary vascular resistance and pulmonary arterial occlusion (wedge) pressure. The net result is reduced cardiac output, systemic hypotension, and new-onset pulmonary edema.

Fortunately, PEEPi does not develop unless the time needed for complete emptying of the lung exceeds the expiration time. This occurs when the expiratory time is shortened (eg, secondary to tachypnea or frequent cough) or when emptying is delayed (eg, secondary to increased airway resistance or dynamic collapse), or both. Other mechanisms could include hypoxic vasoconstriction, development of a hyperadrenergic state, and direct injury to the capillary membrane, as mentioned earlier.

Management of POPE involves maintaining adequate oxygenation, which may require intubation and mechanical ventilation. However, most of the reported cases were self-limited and resolved rapidly. Early recognition is important, and thus patients who are at risk should be monitored closely. Vigorous diuresis may lead to a significant decrease in mean arterial pressure and shock secondary to worsening of PEEPi-induced hypotension. Finally, because there is some evidence of injury to the microvasculature, theoretically the use of steroids may be helpful. However, this remains strongly controversial.

Clearly, dynamic airway collapse (DAC) is a nonmalignant condition that has “malignant” characteristics. In select patients, DAC will have unrelenting course with progression until there is a near-total collapse of the upper airways during expiration. In this case, when various conservative measures to relieve POPE have failed, placement of a permanent airway stent may be beneficial to avert POPE. However, this decision should be made carefully on a case-by-case basis.

Many of the case series in the literature did not include their mortality rates for POPE secondary to inspiratory effort against an obstructed extrathoracic airway. However, the incidence of severe morbidity or death ranged from 11 to 40%, and this is generally attributed to a delay in diagnosis. 11 Currently, there are no reported data regarding the incidences or mortality secondary to DAC-induced pulmonary edema.

CONCLUSION

Inspiratory airway obstruction is a recognized mechanism for noncardiogenic pulmonary edema. Despite a large number of cases of DAC in everyday clinical practice, to our knowledge there have not been any reported cases of pulmonary edema secondary to expiratory airway obstruction. It is conceivable that a reasonable number of patients with DAC-induced pulmonary edema are treated for cardiogenic pulmonary edema. Hence, a high index of suspicion is required to recognize such an infrequent and unpredictable syndrome in order to provide appropriate treatment and prompt, timely resolution. Tracheal stent placement can be effective in resolving select cases of POPE, but the decision to place one should be made on a case-by-case basis and after various conservative measures have failed.

REFERENCES

1. Oswalt CE, Gates CA, Holstrom FMG. Pulmonary edema as a complication of acute upper airway obstruction. JAMA. 1977;238:1833–1835.
2. Galvis A, Stool SE, Bluestone CD. Pulmonary edema following relief of acute upper airway obstruction. Ann Otol. 1980;899:124–128.
3. Goldenberg JD, Portugal LG, Wenig BL, et al. Negative pressure pulmonary edema in the otolaryngology patient. Otolaryngol Head Neck Surg. 1997;117:62–66.
4. Stradling JR, Bolton P. Upper airway obstruction as cause of pulmonary edema. Lancet. 1982;ii:1353–1354.
5. Leatherman JW. Pulmonary edema due to upper airway obstruction. South Med J. 1983;76:1058–1059.
5a. Zulueta JJ, Gerblich AA. Upper airway obstruction due to inhalation of a tracheal T-tube resulting in pulmonary edema. Chest. 1992;102:644–645.
6. Shikhani AH, Salman SD, Melhem R. Unilateral pulmonary edema as a complication of contralateral bronchial obstruction. Laryngoscope. 1987;97:748–751.
7. Guffin TN, El-Har G, Sanders A, et al. Acute postobstructive pulmonary edema. Otolaryngol Head Neck Surg. 1995;112:235–237.
8. Wilms D, Shure D. Pulmonary edema due to upper airway obstruction in adults. Chest. 1988;94:1090–1092.
9. Tami TA, Chu F, Wildes TO, et al. Pulmonary edema and acute upper airway obstruction. Laryngoscope. 1986;96:506–509.
10. Kollef MH, Pluss J. Noncardiogenic pulmonary edema following upper airway obstruction: 7 cases and a review of the literature. Medicine (Baltimore). 1991;70:91–98.
11. West JB, Mathieu–Costello O. Stress failure of pulmonary capillaries: role in lung and heart disease. Lancet. 1992;340:762–767.
12. Glasser SA, Siler JN. Delayed onset of laryngospasm-induced pulmonary edema in an adult outpatient. Anesthesiology. 1985;62:370–371.
13. Gottfried SB. The role of PEEP in the mechanically ventilated COPD patient. In: Marini JJ, Roussos C, eds. Ventilatory Failure. New York: Springer–Verlag; 1991:392–418.
Keywords:

Post obstructive pulmonary edema; dynamic airways collapse; airway obstruction; airway stent

© 2004 Lippincott Williams & Wilkins, Inc.