A 28-year-old trekker presents with acute dyspnea, pink frothy sputum, and bilateral crackles after rapid ascent to 4500 m in Ladakh on day 2. SpO₂ is 64% on room air. Chest X-ray shows patchy asymmetric alveolar infiltrates. After emergency descent and recovery, spirometry is repeated. The pattern marked **A** in the diagram — a restrictive pattern with reduced DLCO that normalises after descent — is observed. Which of the following best explains the reversibility of this spirometric abnormality in high-altitude pulmonary edema (HAPE)?
A. Permanent alveolar damage from barotrauma during rapid decompression, necessitating lifelong supplemental oxygen
B. Reversible interstitial edema from capillary stress failure due to patchy hypoxic pulmonary vasoconstriction, with normalisation of fluid resorption upon descent and reoxygenation
C. Chronic interstitial fibrosis from repeated altitude exposure, requiring long-term immunosuppressive therapy
D. Fixed airway obstruction from bronchial wall thickening and smooth muscle hypertrophy secondary to sustained hypoxia
Explanation
Why "Reversible interstitial edema from capillary stress failure due to patchy hypoxic pulmonary vasoconstriction, with normalisation of fluid resorption upon descent and reoxygenation" is right
The clinical anchor is that HAPE produces a restrictive spirometric pattern with reduced DLCO that normalises on descent, reflecting the underlying pathophysiology: exaggerated, patchy hypoxic pulmonary vasoconstriction causes capillary stress failure and a non-cardiogenic, low-protein alveolar leak. The fluid is interstitial and alveolar edema, not structural lung damage. Upon descent and reoxygenation, pulmonary artery pressures fall, capillary stress resolves, and fluid is resorbed, restoring normal spirometry and DLCO. This reversibility is the diagnostic hallmark that distinguishes HAPE from chronic interstitial disease (Wilderness Medical Society Practice Guidelines 2024; Bartsch & Swenson, NEJM 2013).
Why each distractor is wrong
Chronic interstitial fibrosis from repeated altitude exposure, requiring long-term immunosuppressive therapy: HAPE is acute and reversible; it does not cause permanent fibrosis. Spirometry normalises completely on descent, ruling out chronic structural disease. Immunosuppression is not indicated.
Fixed airway obstruction from bronchial wall thickening and smooth muscle hypertrophy secondary to sustained hypoxia: This describes a chronic obstructive pattern (like COPD), not the restrictive pattern with reduced DLCO seen in HAPE. Fixed obstruction does not reverse with descent.
Permanent alveolar damage from barotrauma during rapid decompression, necessitating lifelong supplemental oxygen: HAPE is not caused by barotrauma; it results from hypoxic pulmonary vasoconstriction and capillary stress failure. Permanent damage does not occur if descent is timely, and supplemental oxygen is a temporary bridge, not lifelong therapy.
High-YieldNEET PG
HAPE spirometry is reversible because the pathology is acute interstitial edema from capillary stress failure, not structural lung damage—normalisation on descent is diagnostic and prognostically reassuring.
Wilderness Medical Society Practice Guidelines 2024; Bartsch & Swenson, NEJM 2013; Harrison 21e Ch. on Altitude Illness
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