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INTRODUCTION

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).

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).

TABLE 107-1Types of Negative-Pressure Pulmonary Edema

PATHOPHYSIOLOGY

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.

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.

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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