Dyspnea, Cough, and Extreme Fatigue in a Hiker

Medscape

2 days ago

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Background and Initial Presentation
A 32-year-old man presents to an emergency department in a remote mountain town after being rescued from a solo hiking expedition at 12,500 feet. He had been hiking for 3 days at high altitude with minimal acclimatization. Over the past 24 hours, he has developed progressive shortness of breath, a persistent dry cough, and extreme fatigue. The symptoms worsened overnight, and he was unable to continue hiking. He activated his personal emergency beacon and was airlifted to safety. Upon arrival at the hospital, he appeared dyspneic, with a resting oxygen saturation of 82% on room air.
Physical Examination and Workup
On examination, the patient was tachypneic (respiratory rate, 28 breaths/min) and tachycardic (heart rate, 112 beats/min). He was afebrile. Auscultation revealed bilateral inspiratory crackles, most prominent in the lower lung fields. There was no peripheral edema or jugular venous distension.
Chest radiography is the most important initial test of those listed above because it provides rapid, noninvasive imaging to assess for pulmonary pathology and can help differentiate between potential causes of hypoxemia. Although ECG can help rule out cardiac causes, it is neither sensitive nor specific for the likely causes of this patient's symptoms. Similarly, although arterial blood gas analysis provides useful information about oxygenation and acid-base status, it does not identify the underlying cause of hypoxemia. CT pulmonary angiography is primarily used to evaluate for pulmonary embolism; however, given the low pretest probability based on the patient's history, a D-dimer should be obtained first.
Initial workup included chest radiography, which demonstrated patchy alveolar infiltrates (Figure). Arterial blood gas analysis revealed hypoxemia (partial pressure of arterial oxygen, 58 mm Hg) and respiratory alkalosis (pH, 7.48). Bedside lung ultrasonography, performed shortly after presentation, showed diffuse B lines bilaterally. Cardiac biomarkers (troponin and B-type natriuretic peptide) were within normal limits, and ECG showed sinus tachycardia without ischemic changes. D-dimer was 0.3 mg/L (low probability).
Figure. Chest radiograph showing patchy alveolar infiltrates.
Discussion
High-altitude pulmonary edema (HAPE) is a noncardiogenic pulmonary edema caused by hypoxia-induced pulmonary vasoconstriction at high altitudes.[1,2] It typically occurs above 8000 feet and is a leading cause of altitude-related mortality.[1] Risk factors include rapid ascent, lack of acclimatization, and strenuous physical exertion.[1-3]
The diagnosis of HAPE is clinical and based on a history of recent ascent in an unacclimatized individual. Diagnosis, particularly in the field, relies primarily on characteristic reported symptoms such as dyspnea on exertion disproportional to previous experience, nonproductive cough, fatigue, and weakness, which can progress to dyspnea at rest. Objective findings, when available, aid in confirming the diagnosis and ruling out alternatives.[1] In well-resourced facilities, the presence of hypoxemia and either unilateral or diffuse bilateral alveolar opacities on plain chest radiography is sufficient to confirm the diagnosis in the appropriate clinical context. Objective findings include radiographic findings of pulmonary edema, often seen as patchy alveolar infiltrates on chest radiographs, and diffuse B lines on lung ultrasound, consistent with pulmonary congestion.[4]
Arterial blood gas analysis frequently shows hypoxemia with respiratory alkalosis, and pulse oximetry can confirm hypoxemia, a key feature that distinguishes HAPE from other sources of dyspnea. The case patient had hypoxemia and respiratory alkalosis. This distinction can help differentiate between inflammatory and infectious causes of pulmonary infiltrates at altitude. Although HAPE can present with a low-grade fever, it typically lacks the high-grade fever, leukocytosis, and purulent sputum often associated with pneumonia. Differentiation from other conditions presenting with pulmonary edema is important.[1] Acute respiratory distress syndrome, while also a non-cardiogenic pulmonary edema, usually occurs in response to a systemic insult rather than altitude exposure. Pulmonary embolism is less likely given the absence of pleuritic chest pain, focal findings on imaging, and a normal D-dimer value but should not be excluded solely on clinical grounds.
Treatment of HAPE
The mainstay of HAPE treatment is immediate descent to lower altitude, which often leads to rapid improvement. Supplemental oxygen is highly effective in reversing hypoxemia. When descent is not possible, pharmacologic treatment with nifedipine (a pulmonary vasodilator) can reduce pulmonary hypertension and improve oxygenation. Portable hyperbaric chambers may also be used in remote settings. Beta-blockers are not recommended because they blunt the sympathetic response needed to maintain adequate cardiac output and oxygen delivery during hypoxia.[5] In addition, they do not address the underlying pulmonary hypertension that contributes to HAPE.[5]
The patient was placed on high-flow oxygen, given oral nifedipine, and observed for 24 hours. He demonstrated significant improvement, with normalization of his oxygen saturation and resolution of dyspnea. He was advised to avoid rapid ascents in the future, which is a primary method for preventing HAPE. He was also advised to consider prophylactic nifedipine for future high-altitude activities. Tadalafil may be used in patients who are not candidates for nifedipine. Acetazolamide should not be used for HAPE prevention in those with a history of the disease, although it can be considered for prevention of reentry HAPE, which affects individuals who reside at high altitudes, travel to a lower elevation, and then develop HAPE upon rapid return to their residence.[1]
Proper prevention strategies for altitude sickness include gradual ascent, often achieved through staged ascent and limiting daily altitude gain. For HAPE prevention in individuals with a history of the condition, nifedipine is the preferred medication, with tadalafil as an alternative.[1-3] The patient was discharged with instructions to avoid further high-altitude exposure until fully recovered and to seek medical guidance for future expeditions.
HAPE is a potentially life-threatening condition, but with prompt recognition and treatment, the prognosis is generally excellent. When treated early with interventions including immediate descent to a lower altitude, supplemental oxygen, and sometimes medications such as nifedipine, most patients recover fully, without long-term complications.[1,2] The condition is typically self-limiting once altitude exposure is reduced, and most patients do not develop chronic lung disease. However, if left untreated or reexposure occurs without proper acclimatization, the condition can be fatal or lead to complications.
Patients who experience HAPE should be educated on proper acclimatization strategies to prevent recurrence in future high-altitude activities, but with appropriate treatment, full recovery is common and long-term effects are rare.