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High Altitude Pulmonary Edema

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Other Names

  • High Altitude Pulmonary Edema (HAPE)
  • High Altitude Pulmonary Oedema (HAPO)
  • “re-entry” HAPE

Background

History

  • First case English case report by Houston in 1960[1]

Epidemiology

  • It is a relatively rare disease, lacking good epidemiological data
  • Incidence
    • In Peru in the 1970s, estimated to be be 0−6% in adults and 8−9% in children[2]
    • In the early 1980s, estimated to be between 0.01-0.1% in Vail, Colorado[3]
    • Generally thought to represent far less than 1% of all high altitude illness cases (need citation)
    • Incidence increases to 4% to 20% at extreme altitudes (> 5500 m) or extreme rates of ascent (> 600 m/day)[4]

Pathophysiology

  • General
    • HAPE is a pulmonary presentation of acute high altitude illness
    • Onset usually 2–4 days after ascent; rare after 1 week at a constant altitude
    • Most commonly seen above 2500 to 3000 m, less commonly between 1400 and 2400 m[5]
  • Types
    • Most commonly, it occurs in rapid ascension in unacclimatized lowlanders
    • “re-entry” HAPE: rarely, it can occur in inhabitants returning from a trip at "low altitude"

Mechanism

  • Non-cardiogenic Pulmonary edema
    • Alveolar hypoxia causes pulmonary circulation vasoconstriction, subsequent pulmonary hypertension
    • HAPE susceptible individuals have exaggerated pulmonary artery vasoconstriction and pressures with hypoxia or normoxic exercise at sea level[6]
  • Hypoxic pulmonary vasoconstriction
    • Thought to be non-uniform, causing regional overperfusion[7]
    • Endothelial dysfunction may be provoked
    • Impaired nitrous oxide synthesis may confer genetic susceptibility, underlying mechanism
  • Alveolar capillary leak
    • Stress failure secondary to pulmonary artery hypertension
    • Leads to leakage of large molecules into the alveolar space, subsequent high-permeability pulmonary edema
    • Worse/ exacerbated by exercise[8]
  • Impaired clearance of alveolar fluid
    • HAPE susceptible individuals have a defective transepithelial sodium transport in their alveoli
    • Impairment is likely exacerbated at altitude
    • Salmeterol, dexamethasone may improve transepithelial sodium transport[9][10]

Associated Conditions

Risk Factors

Differential Diagnosis

Clinical Features

  • History
    • Early symptoms include exertional dyspnea, dry cough and reduced exercise performance
    • May appear over hours or days, can appear suddenly after a night's sleep at altitude
    • Note that early symptoms are often minimized by individuals but may reflect early HAPE
    • Classic symptoms
      • Dyspnea at rest
      • Cough
      • Decreased exercise tolerance
      • Chest tightness or congestion
    • Other potential symptoms: fatigue, headache, elevated body temperature, generally not exceeding 38.5°C
      • Note that AMS often will overlap
    • Symptoms can worse over time as pulmonary edema progresses
      • Aggravated cough, breathlessness even at rest
  • Physical Exam
    • Classic signs
      • Wheeze on auscultation
      • Central cyanosis
      • Tachypnoea
      • Tachycardia
    • Severe findings include pink frothy sputum, gurgling sounds

Evaluation

Symptom Clinical Signs
Dyspnea at rest Crepitus or wheezing on auscultation
Cough Central cyanosis
Decreased exercise tolerance Tachypnea
Chest tightness Tachycardia
  • Diagnosis is clinical
    • Diagnosis is made by the presence of two clinical symptoms and two clinical signs[12]

Radiographs

  • Chest Radiograph
    • Not required to make diagnosis
  • Findings
    • Peripheral patchy pulmonary oedema in the lower zones, more often right sided
    • Normal cardiac size with prominent pulmonary arteries

Electrocardiogram

  • Not required to make diagnosis
  • Findings[13]
    • Sinus tachycardia
    • Right axis deviation
    • Right bundle branch block or right strain

Laboratory

  • Labs are not required to make the diagnosis
    • Can be useful to confirm, exclude other pathology
  • Blood gas
    • Hypoxemia
    • Respiratory alkalosis

Classification

  • Currently, no classification system exists for HAPE

Management

Prevention

Treatment

  • Sumamry of treatment
    • Increase oxygenation using rapid descent
    • Adjunct: o2 supplementation or portable hyperbaric chamber
    • Adjunct: Nifedipine if oxygen is not available
  • Descent
    • Most effective treatment (as with all forms of AHAI)
    • First line treatment, especially in remote or austere settings
    • Initial descent should be at least 1000 m or until symptms resolve
    • Ideally, with minimal exertion by the patient
  • Hospital
    • Supplementary oxygen
    • Consider positive airway pressure, there are case reports supporting use[15]
    • Consider inhaled nitric oxide
  • Nifedipine
    • Can be used when descent or oxygen not possible
    • Dose: 60 mg modified release divied into 2 or 3 doses (same as prophylaxis)
    • Recommended as a first line adjunct with WMS guidelines
    • However, no benefit if oxygen and descent are available
  • Phosphodiesterase inhibitors
    • Not currently recommended due to increase in AMS severity

Rehab and Return to Play

Rehabilitation

  • Needs to be updated

Return to Play/ Work

  • Little evidence is present to guide team physicians
    • Clinical judgement is paramount
  • Athlete should be completely asymptomatic before considering return
  • Staged ascent is recommended
    • Less than 500 to 600 m/day with rest every 2 days
    • This was effective in one case series to prevent recurrent HAPE in three mountaineers[16]
  • Consider Nifedipine prophylaxis

Complications and Prognosis

Prognosis

  • Death
    • Highest mortality rate of AHAI[17]

Complications

  • Need for hospitalization
  • Death

See Also

References

  1. ↑ Houston CS. Acute pulmonary edema of high altitude. N Engl J Med 1960; 263: 478−80.
  2. ↑ Hultren HN, Marticorena E. High altitude pulmonary edema: epidemiologic observations in Peru. Chest 1978; 74: 372−6.
  3. ↑ Sophocles AM Jr. High-altitude pulmonary edema in Vail, Colorado, 1975–1982. High Alt Med Biol 1986; 144: 569−73.
  4. ↑ Rodway GW, Hoffman LA, Sanders MH. High-altitude related disorders Y part 1: pathophysiology, differential diagnosis, and treatment. Heart Lung. 2003; 33:198.
  5. ↑ Gabry AL, Ledoux X, Mozziconacci M, Martin C. High-altitude pulmonary edema at moderate altitude (<2,400 m; 7,870 feet): a series of 52 patients. Chest 2003; 123: 49−53.
  6. ↑ Hultgren HN, Lopez CE, Lundberg E, Miller H. Physiologic studies of pulmonary edema at high altitude. Circulation 1964; 29: 393–408.
  7. ↑ Hultgren HN. High-altitude pulmonary edema: current concepts. Annu Rev Med 1996; 47: 267–284.
  8. ↑ Eldridge MW, Braun RK, Yoneda KY, Walby WF. Effects of altitude and exercise on pulmonary capillary integrity: evidence for subclinical high-altitude pulmonary edema. J Appl Physiol 2006; 100: 972–980.
  9. ↑ Maggiorini M, Brunner-La Rocca HP, Peth S, et al. Both tadalafil and dexamethasone may reduce the incidence of high-altitude pulmonary edema: a randomized trial. Ann Intern Med 2006; 145: 497–506.
  10. ↑ Sartori C, Allemann Y, Duplain H, et al. Salmeterol for the prevention of high-altitude pulmonary edema. N Engl J Med 2002; 346: 1631–1636.
  11. ↑ 11.0 11.1 Hultgren HN, Honigman B, Theis K, Nicholas D. High-altitude pulmonary edema at a ski resort. West J Med 1996; 164: 222–227.
  12. ↑ Sutton J, Coates G, Houston C. The Lake Louise consensus on the definition and quantification of altitude illness. Hypoxia and Mountain Medicine. 1992. Burlington, Vermont: Queen City Printers, pp. 327–330.
  13. ↑ Maggiorini M. Prevention and treatment of high-altitude pulmonary edema. Prog Cardiovasc Dis 2010; 52: 500–506.
  14. ↑ Wilderness Medical Society Clinical Practice Guidelines for the Prevention and Treatment of Acute Altitude Illness: 2019
  15. ↑ Larson EB. Positive airway pressure for high-altitude pulmonary oedema. Lancet 1985; 1: 371–373.
  16. ↑ Litch JA, Bishop RA. Reascent following resolution of high altitude pulmonary edema (HAPE). High Alt. Med. Biol. 2001; 2:53Y5.
  17. ↑ Maggiorini M. High altitude-induced pulmonary oedema. Cardiovasc. Res. 2006; 72:41Y50.
Created by:
John Kiel on 30 June 2019 23:00:44
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Last edited:
24 April 2022 12:37:46
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