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INTRODUCTION

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Postobstructive pulmonary edema, also known as negative-pressure pulmonary edema (NPPE), is a serious, potentially fatal condition which commonly results from upper airway obstruction. More specifically, forced inspiration against an obstructed upper airway generates a large intrathoracic pressure gradient, an increased pulmonary vascular volume, and subsequently a significant increase in the pulmonary capillary transmural pressure, which produces a significant disruption of the capillary alveolar membrane. The movement of fluid across the pulmonary capillary bed can be further summarized by the Starling equation: Q = K × [(Pc– Pi) – σ (πc πi)] (Q, flow across the pulmonary capillary bed; Pc, capillary hydrostatic pressure; Pi, interstitial hydrostatic pressure; πc, capillary oncotic pressure, and πi, interstitial oncotic pressure).

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Negative-pressure pulmonary edema has been reported in the literature to occur in approximately 0.1% of anesthetic cases. NPPE can be further classified as either Type I or Type II. Generally, Type I NPPE results immediately after an episode of acute airway obstruction, most often caused by laryngospasm. Other causes of Type I NPPE include upper airway tumors, foreign bodies, drowning, endotracheal tube obstruction, epiglottitis, and croup. Type II NPPE usually develops as a delayed response, following the relief of chronic upper airway obstruction, commonly caused by tonsillar, adenoid, or uvular hypertrophy (Table 107-1).

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Table Graphic Jump Location
TABLE 107-1Types of Negative-Pressure Pulmonary Edema
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PATHOPHYSIOLOGY

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The mechanism underlying NPPE is usually triggered following an obstruction of the upper airway, which generates a negative intraalveolar pressure with the resultant transmural pressure gradient causing a fluid shift from the pulmonary capillary bed into the interstitial and alveolar spaces.

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There are four basic mechanisms that account for an increased level of pulmonary fluid in the interstitial compartment: (1) increased hydrostatic pressure in the capillary bed; (2) decreased plasma oncotic pressure; (3) capillary alveolar membrane disruption leading to increased permeability; and (4) decreased lymphatic return to the venous circulation.

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Under normal physiologic conditions, intrathoracic pressure ranges from –3 to –10 cm H2O, but highly negative intrathoracic pressures (> –50 cm H2O) can produce a significant increase in venous return of blood, thus substantially increasing the left ventricular end-diastolic volume and subsequently the end-diastolic pressure. The combination of low intrathoracic pressure and high left ventricular end-diastolic pressure favors the formation of a transmural pressure gradient. This pressure gradient results in the accumulation of fluid in the alveolar and interstitial compartments, with concomitant significant pulmonary edema. The sudden ...

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