High Altitude Disorders

Michael Daw

Background

  • Acute Mountain Sickness (AMS), High-Altitude Pulmonary Edema (HAPE), and High-Altitude Cerebral Edema (HACE) o HAPE is the most common cause of death from rapid ascent 
  • Typically occurs with rapid ascents to altitudes >2000-2500m (6500-8000 ft) 
  • Risk factors: Age <50 years, history of migraines, previous altitude illness, impaired circulation or ventilation (pulmonary HTN, COPD, neuromuscular disease, etc.) 
  • Pathophysiology: 
    • Normal acclimatization: 
    • Decreased partial pressure of oxygen -> progressive hypoxemia and tissue hypoxia 
    • Early response: increased minute ventilation -> respiratory alkalosis 
    • Late response: renal bicarbonate excretion -> decreased plasma volume 
    • Hypoxia-inducible factors (HIFs) activate cellular mechanisms to improve oxygen delivery 
    • AMS: acclimatization is inadequate to restore tissue PO2 to sea-level values o HACE: hypoxic vasodilation overrides hypocapnic vasoconstriction -> increased cerebral blood flow and vascular permeability -> high cerebral intravascular pressures -> cerebral edema 
    • HAPE: hypoxic pulmonary vasoconstriction -> pulmonary hypertension -> pulmonary edema

Presentation

  • Onset: 4-72 hours for AMS/HACE versus 2-4 days for HAPE 
  • Headache, dizziness, fatigue/weakness 
  • Anorexia, nausea/vomiting 
  • Peripheral edema 
  • HACE: altered mental status, ataxia, visual impairment, bladder/bowel dysfunction, cerebral edema and/or hemorrhage
  • HAPE: tachypnea, cough, pink/frothy sputum, chest tightness, cyanosis, pulmonary edema, right heart strain with normal LV function

Evaluation

  • Clinical diagnosis based on development of symptoms after ascent to altitude 
  • Exclusion of alternative diagnoses: 
    • Dehydration, exhaustion, hypothermia, glucose or electrolyte disturbances – CMP, EKG 
    • CO poisoning, intoxication – CBC, carboxyhemoglobin, tox screen 
    • Migraine, CNS infection, acute stroke (lack of preceding symptoms or improvement with HACE treatment) – CT or MRI head, LP 
    • Asthma/COPD, CHF, PNA, PE – troponin/BNP, CXR, Cardiac/lung POCUS, CTA chest

Management

  • AMS 
    • Mild AMS: stop further ascent or descend ~1000m, analgesics (ibuprofen) and antiemetics 
    • Moderate to severe AMS: Supplemental O2 (goal SpO2 >90%), PO acetazolamide 250mg Q12H, PO/IV/IM dexamethasone 4mg Q6H 
    • Ascent may be resumed after symptoms resolve, consider acetazolamide ppx 
    • Descend if not improving after 1-3 days 
  • HACE: 
    • Medical emergency - requires immediate descent 
    • High flow O2 (goal SpO2 >92%) 
    • PO acetazolamide 250mg Q12H 
    • PO/IV/IM dexamethasone 8mg once, followed by 4mg Q6H 
    • Hyperbaric oxygen therapy, if available 
  • HAPE: 
    • Immediate descent of at least 1000m 
    • Supplemental O2 >90%; CPAP if in hospital setting 
    • Hyperbaric O2 therapy, if available 
    • If unable to descend: PO nifedipine ER 30mg Q12H (first-line) or PDE5 inhibitors (PO sildenafil 50mg Q8H, PO tadalafil 10mg Q12H)

Prevention

  • Staged/gradual ascent 
  • Supplemental oxygen during sleep 
  • Medication prophylaxis if moderate to high risk of AMS/HACE (prior altitude illness, initial sleeping elevation >2800m, or ascent rate above 3000m of >500m/day): 
    • Start prophylaxis one day prior to ascent. May stop upon descent or 2-4 days after arrival at highest altitude 
    • There is little evidence to support inhaled steroids/beta agonists to treat any altitude illness or diuretics for HAPE 
    • AMS/HACE: PO acetazolamide 125mg Q12H (first line) or PO dexamethasone 2mg Q6H or 4mg Q12H 
    • HAPE: PO nifedipine ER 30mg Q12H or 20mg Q8H or PDE5 inhibitors (PO sildenafil 50mg Q8H, PO tadalafil 10mg Q12H)
Last updated on