High Altitude Pulmonary Edema
- 1 Other Names
- 2 Background
- 3 Pathophysiology
- 4 Risk Factors
- 5 Differential Diagnosis
- 6 Clinical Features
- 7 Evaluation
- 8 Classification
- 9 Management
- 10 Rehab and Return to Play
- 11 Complications and Prognosis
- 12 See Also
- 13 References
- High Altitude Pulmonary Edema (HAPE)
- High Altitude Pulmonary Oedema (HAPO)
- “re-entry” HAPE
- This page refers to high altitude pulmonary edema (HAPE), a pulmonary form of Acute High Altitude Illness
- First case English case report by Houston in 1960
- It is a relatively rare disease, lacking good epidemiological data
- In Peru in the 1970s, estimated to be be 0−6% in adults and 8−9% in children
- In the early 1980s, estimated to be between 0.01-0.1% in Vail, Colorado
- 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)
- 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
- 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"
- 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
- Hypoxic pulmonary vasoconstriction
- Thought to be non-uniform, causing regional overperfusion
- 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
- Impaired clearance of alveolar fluid
- Acute Mountain Sickness
- 50% of patients with HAPE also have AMS
- High Altitude Cerebral Edema
- 14% of patients with HAPE also have HACE
- 50% of autopsies in patients with HAPE had cerebral edema
- Pulmonary Embolism
- Myocardial Infarction
- Heart Failure
- 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
- 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
- Severe findings include pink frothy sputum, gurgling sounds
- Classic signs
|Dyspnea at rest||Crepitus or wheezing on auscultation|
|Decreased exercise tolerance||Tachypnea|
- Diagnosis is clinical
- Diagnosis is made by the presence of two clinical symptoms and two clinical signs
- Chest Radiograph
- Not required to make diagnosis
- Peripheral patchy pulmonary oedema in the lower zones, more often right sided
- Normal cardiac size with prominent pulmonary arteries
- Not required to make diagnosis
- Sinus tachycardia
- Right axis deviation
- Right bundle branch block or right strain
- Labs are not required to make the diagnosis
- Can be useful to confirm, exclude other pathology
- Blood gas
- Respiratory alkalosis
- Currently, no classification system exists for HAPE
- See: Altitude Illness Prevention
- For a more detailed discussion of prevention
- Gradual/staged ascent
- Consider Nifedipine in moderate or high risk individuals
- Sumamry of treatment
- Increase oxygenation using rapid descent
- Adjunct: o2 supplementation or portable hyperbaric chamber
- Adjunct: Nifedipine if oxygen is not available
- 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
- Supplementary oxygen
- Consider positive airway pressure, there are case reports supporting use
- Consider inhaled nitric oxide
- 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
- 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
- Consider Nifedipine prophylaxis
Complications and Prognosis
- Highest mortality rate of AHAI
- Need for hospitalization
- ↑ Houston CS. Acute pulmonary edema of high altitude. N Engl J Med 1960; 263: 478−80.
- ↑ Hultren HN, Marticorena E. High altitude pulmonary edema: epidemiologic observations in Peru. Chest 1978; 74: 372−6.
- ↑ Sophocles AM Jr. High-altitude pulmonary edema in Vail, Colorado, 1975–1982. High Alt Med Biol 1986; 144: 569−73.
- ↑ Rodway GW, Hoffman LA, Sanders MH. High-altitude related disorders Y part 1: pathophysiology, differential diagnosis, and treatment. Heart Lung. 2003; 33:198.
- ↑ 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.
- ↑ Hultgren HN, Lopez CE, Lundberg E, Miller H. Physiologic studies of pulmonary edema at high altitude. Circulation 1964; 29: 393–408.
- ↑ Hultgren HN. High-altitude pulmonary edema: current concepts. Annu Rev Med 1996; 47: 267–284.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 11.0 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.
- ↑ 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.
- ↑ Maggiorini M. Prevention and treatment of high-altitude pulmonary edema. Prog Cardiovasc Dis 2010; 52: 500–506.
- ↑ Wilderness Medical Society Clinical Practice Guidelines for the Prevention and Treatment of Acute Altitude Illness: 2019
- ↑ Larson EB. Positive airway pressure for high-altitude pulmonary oedema. Lancet 1985; 1: 371–373.
- ↑ Litch JA, Bishop RA. Reascent following resolution of high altitude pulmonary edema (HAPE). High Alt. Med. Biol. 2001; 2:53Y5.
- ↑ Maggiorini M. High altitude-induced pulmonary oedema. Cardiovasc. Res. 2006; 72:41Y50.
John Kiel on 30 June 2019 23:00:44
24 April 2022 12:37:46