Negative Pressure Pulmonary Edema (NPPE)

Break the obstruction first - 100% oxygen with positive pressure or CPAP is the earliest and most common treatment. The Larson maneuver, pressure applied slightly cephalad to the earlobe, comes next and should be tried before drugs — but don't wait for desaturation to move on.

Drug sequence for laryngospasm - the pediatric algorithm gives propofol 0.5 mg/kg IV or midazolam 0.03 mg/kg IV; if spasm persists, succinylcholine 1-2 mg/kg IV, or 4 mg/kg IM when there's no line, with atropine 0.02 mg/kg to blunt the bradycardia. Propofol is the choice when succinylcholine is contraindicated — burns, muscular dystrophy, cholinesterase deficiency.

Highest risk is stage 2 - abnormal excitation of the superior laryngeal nerve pathway happens most often during light anesthesia, so induction and emergence are where laryngospasm and therefore NPPE come from.

Preventive options - magnesium 15-30 mg/kg before induction, lidocaine 1-2 mg/kg IV within 5 minutes of extubation, propofol 0.5 mg/kg IV 60 seconds before extubation, and minimizing laryngoscopy attempts.

Type II is the mirror image - exhaling against an obstruction generates positive intrapleural pressure and cuts venous return. When the obstruction is relieved, airway pressure drops, venous return and pulmonary blood volume surge, and hydrostatic pressure drives the same edema. Relieving the obstruction is not the end of the story.

What you'll see - progressively worsening dyspnea, tachypnea, rales on auscultation, and falling saturation.

Prove it isn't the heart - chest film in noncardiogenic edema shows patchy peripheral infiltrates with ground-glass opacities and air bronchograms rather than central edema, Kerley B lines, and cardiomegaly. Echo shows no acute systolic or diastolic dysfunction. Pulmonary capillary wedge pressure under 18 mmHg settles it. Flat neck veins and no peripheral edema fit the same picture.

Treatment is supportive - supplemental oxygen or mechanical ventilation as needed, and address the inciting cause. There is no agent that reverses the capillary leak.

Plan the disposition - the main complication is ventilator-dependent respiratory failure needing intubation and possibly prolonged ventilation, so recognize it early and send the patient somewhere it can be watched.

Negative pressure pulmonary edema (NPPE) is noncardiogenic pulmonary edema that follows forceful inspiratory effort against a closed upper airway — most often laryngospasm at extubation, with an incidence around 0.1%. Young age, male sex, and head or neck surgery are the common risk factors; obstructive sleep apnea (OSA), acromegaly, and difficult intubation are also described.

Inspiring against the obstruction generates intrathoracic pressures as negative as -100 to -140 cmH2O against a normal of roughly -4. That raises left ventricular preload and afterload and drops extramural hydrostatic pressure, while hypoxia adds hypoxic pulmonary vasoconstriction. The right ventricle dilates, the septum shifts left, and left ventricular diastolic function suffers. Transmural pressure across the pulmonary capillary rises and fluid moves out into the interstitium and alveoli. The heart itself is working normally — wedge pressure stays under 18 mmHg.