Understanding negative pressure pulmonary edema
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KeywordsPulmonary Edema Noninvasive Positive Pressure Ventilation Pulmonary Capillary Alveolar Fluid Clearance Negative Intrathoracic Pressure
Negative pressure pulmonary edema
Upper airway obstruction
Intensive care unit
Acute respiratory distress syndrome
Noninvasive positive pressure ventilation
Negative pressure pulmonary edema (NPPE) is a form of noncardiogenic pulmonary edema (PE) that results from the generation of high negative intrathoracic pressure (NIP) needed to overcome upper airway obstruction (UAO). NPPE is a potentially life-threatening complication that develops rapidly after UAO in otherwise healthy young persons who are capable of producing large markedly NIPs. The incidence of NPPE, in patients developing acute UAO, has been estimated to be up to 12 % . The true incidence, however, is not known and may be higher than has been suggested, since many cases may have been misdiagnosed because of a lack of familiarity with the syndrome. All causes of obstructed upper airway may lead to NPPE . However, the most commonly reported etiology of NPPE in adults is laryngospasm during intubation or in the postoperative period after anesthesia (50 % of cases of NPPE) . Nevertheless, NPPE may be more common in ICU patients than is thought; For instance, ventilation with low tidal volume during the acute phase of ARDS in patients with increased respiratory drive can lead to patient–ventilator asynchrony that causes increased breathing effort and the generation of high NIPs that will further worsen PE. Also, strong inspiratory efforts in the presence of increased resistive work of breathing will lead to negative alveolar pressures mimicking the cardiothoracic relationships present during NPPE, and may contribute to extubation failure in some patients.
Understanding the pulmonary fluid homeostasis is crucial to comprehend the mechanisms responsible for pulmonary edema formation. In the normal lung, the net fluid transfer across the pulmonary capillaries depends on the net difference between hydrostatic and colloid osmotic pressures, as well as on the permeability of the capillary membrane (Starling’s law). Under normal conditions, most of this filtered fluid is removed from the interstitium through the lymphatic system to return to the systemic circulation . The alveolar epithelium, because of its tight intercellular junctions, acts as an effective barrier limiting water intrusion into alveolar spaces. However, when the hydrostatic pressure in the pulmonary capillary bed increases and/or the lung interstitial pressure decreases, the rate of transvascular fluid filtration rises, causing edema in the perimicrovascular interstitial spaces, and maybe alveolar flooding if a critical quantity of edema fluid in the interstitial space has been reached [4, 5].
The second suggested mechanism is that the mechanical stress developed from respiration against an obstructed upper airway may induce breaks in the alveolar epithelial and pulmonary microvascular membranes, resulting in increased pulmonary capillary permeability and protein-rich PE [7, 10]. This theory is based on the concept of wall stress failure developed more than 20 years ago by West et al. , in which increasing transmural pulmonary capillary pressures cause disruption of the alveolar–capillary membrane with resultant high-permeability PE. In animals, when pulmonary capillaries are subjected to increased transmural pressure, ultrastructural damage of the walls of the capillaries and alveolar epithelium is observed under scanning electron microscope . Stress failure of pulmonary capillaries has been suggested to be involved in several conditions causing PE and hemorrhage, including neurogenic and high-altitude PE , and following intense exercise in elite human athletes . This indicates that acute increases in transmural pulmonary capillary pressures as observed in NPPE may lead to high-permeability PE . However, Fremont et al. , in 10 NPPE patients, found a low PE fluid-to-serum protein ratio with normal alveolar fluid clearance, further supporting a hydrostatic mechanism for edema fluid formation. Nevertheless, we believe that the pathogenesis of NPPE is probably multifactorial, ranging from transudative to high-permeability edema when a very high transmural pulmonary capillary pressure has been produced.
Treatment of NPPE generally includes maintaining a patent airway, and oxygen supplementation with addition of positive end-expiratory pressure or noninvasive positive pressure ventilation (NIV) as guided by physical examination and arterial blood gas analysis. Mechanical ventilation should be reserved for severe patients who do not respond to NIV. Diuretics are often used; however, there is no evidence of their utility, and they may exacerbate hypovolemia and hypoperfusion. Ultimately, NPPE usually has a rapidly resolving clinical course in 12–48 h when recognized early and treated immediately.
Understanding the pathophysiological mechanisms contributing to PE can help in distinguishing NPPE from other causes of noncardiogenic PE, thus preventing use of inappropriate and dangerous treatment for patients with NPPE.
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