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{{short description|Human disease}}
{{Infobox medical condition (new)
| name = High-altitude pulmonary edema
| synonyms = High-altitude pulmonary oedema (HAPO)<ref>{{cite journal |last1=Oelz |first1=O |last2=Maggiorini |first2=M |last3=Ritter |first3=M |last4=Waber |first4=U |last5=Jenni |first5=R |last6=Vock |first6=P |last7=Bärtsch |first7=P |title=Nifedipine for high altitude pulmonary oedema. |journal=Lancet |date=25 November 1989 |volume=2 |issue=8674 |pages=1241–44 |doi=10.1016/s0140-6736(89)91851-5 |pmid=2573760|s2cid=30715338 }}</ref>
| image = Chest_XR_of_HAPE.png
| caption = Chest x-ray of HAPE showing characteristic patchy alveolar infiltrates with right middle lobe predominance.
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| field = [[Emergency medicine]], [[wilderness medicine]]
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'''High-altitude pulmonary edema''' ('''HAPE''') is a life-threatening form of non-cardiogenic [[pulmonary edema]] that occurs in otherwise healthy people at altitudes typically above {{Convert|2500|m|ft|sp=us|sigfig=2}}.<ref name=Borden>{{cite book |last1=Roach |first1=James M. |last2=Schoene |first2=Robert B. |editor1-first=Kent B. |editor1-last=Pandolf |editor2-first=Robert E. |editor2-last=Burr |title=Medical Aspects of Harsh Environments |volume=2 |chapter=High-Altitude Pulmonary Edema |publisher=Borden Institute|location=Washington, DC |year=2002 |pages=789–814 |chapter-url=https://ke.army.mil/bordeninstitute/published_volumes/harshEnv2/HE2ch25.pdf |oclc=64437370}}</ref> However, cases have also been reported between {{convert|1500|-|2500|m|ft|disp=or}} in more vulnerable subjects.

Classically, HAPE occurs in persons normally living at low altitude who travel to an altitude above 2,500 meters (8,200 feet).<ref name=":0" /> Re-entry HAPE is also an entity that has been described in persons who normally live at high altitude but who develop pulmonary edema after returning from a stay at low altitude, this has been called re-entry HAPE.<ref name=":0" /> It is severe presentation of [[altitude sickness]].

There are many factors that can make a person more [[Susceptible individual|susceptible]] to developing HAPE, including genetic factors, but detailed understanding is lacking and currently under investigation. HAPE remains the major cause of death related to high-altitude exposure, with a high mortality rate in the absence of adequate emergency treatment.<ref name=":0" />

==Signs and symptoms==
{| class="wikitable" style="float:right; margin:1em 1em;"
|+Defining altitude<ref>{{cite web | title=Non-Physician Altitude Tutorial | publisher=International Society for Mountain Medicine | url=http://www.ismmed.org/np_altitude_tutorial.htm | archive-url=https://web.archive.org/web/20110624013438/http://www.ismmed.org/np_altitude_tutorial.htm | archive-date=2011-06-24 | url-status=dead | access-date=22 December 2005}}</ref>
|-
|High altitude
|{{convert|1500|to|3500|m|ft}}
|-
|Very high altitude
|{{convert|3500|to|5500|m|ft}}
|-
|Extreme altitude
|{{convert|5500|to|8850|m|ft|-2}}
|}
Physiological and symptomatic changes often vary according to the altitude involved.<ref>{{cite web|url=http://www.altitude.org/home.php|publisher=Altitude.org|title=Why do low oxygen levels cause altitude sickness?|access-date=2010-04-09|archive-url=https://web.archive.org/web/20100416170609/http://www.altitude.org/home.php|archive-date=2010-04-16|url-status=dead}}</ref>

The Lake Louise Consensus Definition for high-altitude pulmonary edema has set widely used criteria for defining HAPE symptoms.<ref>{{cite web|title=The Lake Louise Consensus on the Definition of Altitude Illness|work=High Altitude Medicine Guide|publisher=Thomas E. Dietz|access-date=2012-11-10|url=http://www.high-altitude-medicine.com/AMS-LakeLouise.html}}</ref>

In the presence of a recent gain in altitude, the presence of the following:

Symptoms: at least two of:
* [[dyspnea|Shortness of breath]] at rest
* Cough
* Weakness or decreased exercise performance
* Chest tightness or congestion

Signs: at least two of:
* Crackles or wheezing (while breathing) in at least one lung field
* Central [[cyanosis|blue skin color]]
* [[Tachypnea]] (rapid breathing)
* [[Tachycardia]] (rapid heart rate)

Acute mountain sickness and high altitude cerebral edema may also be present in conjunction with HAPE, however these symptoms may be subtle or not present at all. The most reliable sign of HAPE is severe fatigue or exercise intolerance, especially in a climber that was previously not displaying this symptom.<ref name=":3">{{Cite web|title=Altitude Illness Clinical Guide For Physicians|url=http://www.high-altitude-medicine.com/ams-medical.html#HAPE|website=www.high-altitude-medicine.com|access-date=2020-04-30}}</ref>

==Risk factors==
There are multiple factors that can contribute to the development of HAPE, including sex (male), genetic factors, prior development of HAPE, ascent rate, cold exposure, peak altitude, intensity of physical exertion, and certain underlying medical conditions (e.g., pulmonary hypertension).<ref name=":0" /><ref name=":1" /> Anatomic abnormalities that are predisposing include [[Pulmonary atresia|congenital absence of pulmonary artery]], and left-to-right [[Acyanotic heart defect|intracardiac shunts]] (e.g., atrial and ventricular septal defects), both of which increase pulmonary blood flow.<ref name=":0" /><ref name=":1" /> HAPE-susceptible (HAPE-s) individuals were also found to be four times more likely to have a [[Foramen ovale (heart)|patent foramen ovale]] (PFO) than those who were HAPE-resistant.<ref name=":1" /> There is currently no indication or recommendation for people with PFO to pursue closure prior to extreme altitude exposure.<ref name=":1" />

In studies performed at sea level, HAPE-s people were found to have exaggerated circulatory response to both hypoxia at rest and during exercise.<ref name=":1" /> In these individuals, the [[pulmonary artery pressure]] (PAP) and [[pulmonary vascular resistance]] (PVR) were shown to be abnormally high.<ref name=":1" /> [[Microneurography|Microneurographic]] recordings in these individuals developed a direct link between PAP rise and [[sympathetic nervous system]] over-activation, which could explain the exaggerated response to hypoxia in these persons.<ref name=":1" />

[[Endothelium|Endothelial tissue]] dysfunction has also been linked to development of HAPE, including reduced synthesis of [[Nitric oxide synthase|NO]] (a potent [[Vasodilation|vasodilator]]), increased levels of [[endothelin]] (a potent [[Vasoconstriction|vasconstrictor]]), and an impaired ability to transport sodium and water across the [[epithelium]] and out of the [[Pulmonary alveolus|alveoli]].<ref name=":1" />

Data on the genetic basis for HAPE susceptibility is conflicting and interpretation is difficult. Genes implicated in the development of HAPE include those in the [[Renin–angiotensin system|renin-angiotensin system]] (RAS), [[Nitric oxide synthase|NO pathway]], and [[Hypoxia-inducible factors|hypoxia-inducible factor pathway]] (HIF).<ref name=":1" /> Future [[Genetic testing|genomic testing]] could provide a clearer picture of the genetic factors that contribute to HAPE.<ref name=":1" />

==Pathophysiology==
[[File:HAPEPathophys.png|thumb|upright=1.3|Currently proposed pathophysiology of HAPE.]]
Though it remains a topic of intense investigation, multiple studies and reviews over the last several years have helped to elucidate the proposed mechanism of HAPE. The inciting factor of HAPE is the decrease in partial pressure of arterial [[oxygen]] caused by the lower air pressure at high altitudes ([[pulmonary gas pressures]]).<ref name=Borden/><ref name=":1">{{Cite book|title=Wilderness Medicine|last=Auerbach|first=Paul S.|publisher=Elsevier|year=2017|isbn=978-0-323-35942-9|pages=20–25}}</ref><ref>{{cite web | author1=Kenneth Baillie | author2=Alistair Simpson | title=Barometric pressure calculator | url=http://www.altitude.org/high_altitude.php | publisher=Apex (Altitude Physiology EXpeditions) | access-date=2006-08-10 | archive-url=https://web.archive.org/web/20190502074315/http://www.altitude.org/high_altitude.php | archive-date=2019-05-02 | url-status=dead }}</ref> The resultant [[hypoxemia]] is then thought to precipitate the development of:

# Increased pulmonary arterial and capillary pressures ([[pulmonary hypertension]]) secondary to [[hypoxic pulmonary vasoconstriction]].<ref name=":1" /><ref>{{cite journal |doi=10.1056/NEJM199110313251805 |last1=Bärtsch|first1=P|last2=Maggiorini|first2=M|last3=Ritter|first3=M|last4=Noti|first4=C|last5=Vock|first5=P|last6=Oelz|first6=O|display-authors=4 |title=Prevention of high-altitude pulmonary edema by nifedipine |journal=The New England Journal of Medicine |volume=325 |issue=18 |pages=1284–89 |date=October 1991 |pmid=1922223}}</ref>
# Increased capillary pressure ([[hydrostatic pressure]]) with over-distention of the capillary beds and increased [[Vascular permeability|permeability]] of the vascular [[endothelium]], also known as "stress failure."<ref name=":1" /><ref>{{cite journal |last1=Swenson|first1=ER|last2=Maggiorini|first2=M|last3=Mongovin|first3=S|title=Pathogenesis of high-altitude pulmonary edema: inflammation is not an etiologic factor |journal=JAMA |volume=287 |issue=17 |pages=2228–35 |date=May 2002 |pmid=11980523 |doi=10.1001/jama.287.17.2228|display-authors=etal|doi-access=free}}
</ref> This leads to subsequent leakage of cells and proteins into the [[Pulmonary alveolus|alveoli]], aka pulmonary edema.<ref name=":1" />

Hypoxic pulmonary vasoconstriction (HPV) occurs diffusely, leading to arterial vasoconstriction in all areas of the lung. This is evidenced by the appearance of "diffuse," "fluffy," and "patchy" infiltrates described on imaging studies of climbers with known HAPE.<ref name=":1" />

Although higher pulmonary arterial pressures are associated with the development of HAPE, the presence of [[pulmonary hypertension]] may not in itself be sufficient to explain the development of [[edema]]; severe pulmonary hypertension can exist in the absence of clinical HAPE in subjects at high altitude.<ref name=":1" /><ref>{{cite journal |last1=Maggiorini|first1=M|last2=Mélot|first2=C|last3=Pierre|first3=S|title=High-altitude pulmonary edema is initially caused by an increase in capillary pressure |journal=Circulation |volume=103 |issue=16 |pages=2078–83 |date=April 2001 |pmid=11319198 |doi=10.1161/01.cir.103.16.2078|display-authors=etal|doi-access=free}}</ref>

==Diagnosis==
{| class="wikitable" style="float:right; margin:0 1em;"
|+Expected SpO2 and PaO2 levels at altitude<ref name=":0" />
|-
!Altitude
!SpO2
!PaO2 (mm Hg)
|-
|{{convert|1500|to|3500|m|ft|disp=br|abbr=on}}
|style="text-align: center;"|about 90%
|style="text-align: center;"|55–75
|-
|{{convert|3500|to|5500|m|ft|disp=br|abbr=on}}
|style="text-align: center;"|75–85%
|style="text-align: center;"|40–60
|-
|{{convert|5500|to|8850|m|ft|-2|disp=br|abbr=on}}
|style="text-align: center;"|58–75%
|style="text-align: center;"|28–40
|}
The diagnosis of HAPE is entirely based on symptoms and many of the symptoms overlap with other diagnoses.<ref name=":0" /><ref name=":1" /> Before HAPE was understood it was commonly confused with pneumonia which resulted in inappropriate treatment.{{citation needed|date=November 2020}}

HAPE generally develops in the first 2 to 4 days of hiking at altitudes >2,500 meters (8,200 ft), and symptoms seem to worsen most commonly on the second night.<ref name=":1" /> Initial symptoms are vague and include [[shortness of breath]], decreased exercise ability, increased recovery time, fatigue, and weakness, especially with walking uphill.<ref name=":0" /><ref name=":1" /> People then develop a dry, persistent cough, and often [[cyanosis]] of the lips. Another cardinal feature of HAPE is the rapid progression to dyspnea at rest.<ref name=":0" /><ref name=":1" /> The development of pink, frothy, or frankly bloody [[sputum]] are late features of HAPE.<ref name=":0" /><ref name=":1" /> In some cases, people will develop concomitant neurological features such as [[Ataxia|poor coordination]], altered consciousness, or cerebral edema ([[High-altitude cerebral edema]]).<ref name=":0" /><ref name=":1" />

On physical exam, increased breathing rates, increased heart rates, and a low-grade fever 38.5o (101.3o F) are common.<ref name=":0" /><ref name=":1" /> [[Auscultation|Listening]] to the lungs may reveal [[crackles]] in one or both lungs, often starting in the right middle lobe.<ref name=":0" /><ref name=":1" /> Imaging studies such as [[X-ray]] and [[CT imaging]] of the chest may reveal thoracic infiltrates that can be seen as opaque patches.<ref name=":0" /><ref name=":1" /><ref>{{cite journal |last1=Paralikar |first1=Swapnil |title=High altitude pulmonary edema-clinical features, pathophysiology, prevention and treatment |journal=Indian Journal of Occupational and Environmental Medicine |date=2012 |volume=16 |issue=2 |pages=59–62 |doi=10.4103/0019-5278.107066 |pmid=23580834 |pmc=3617508 }}</ref> One distinct feature of HAPE is that [[pulse oximetry]] saturation levels ([[Oxygen saturation (medicine)|SpO2]]) are often decreased from what would be expected for the altitude. People typically do not appear as ill as SpO2 and chest X-ray films would suggest.<ref name=":0" /><ref name=":1" /> Giving extra oxygen rapidly improves symptoms and SpO2 values; in the setting of infiltrative changes on chest X-ray, this is nearly pathognomonic for HAPE.<ref name=":0" />

===Severity===
The severity of HAPE is graded. The grades of mild, moderate, or severe HAPE are assigned based upon symptoms, clinical signs, and chest x-ray results for individuals.<ref name=":3" /> The symptoms that are taken in to account while evaluation the severity of HAPE are difficulty breathing while exerting or while at rest, the presence of a cough and the quality of that cough, and the level of fatigue of the patient. On physical exam of a suspected HAPE patient the exam findings used to grade the severity are the heart rate, respiratory rate, signs of cyanosis, and severity of lung sounds.<ref name=":3" /> Both symptoms and signs on physical exam can be used to evaluate a patient in the field. Chest X-rays are also used to evaluate the severity of HAPE when they are available.{{citation needed|date=November 2020}}

===Differential diagnosis===
Differential diagnosis:<ref name=":0" /><ref name=":1" />
* [[Pneumonia]]
* [[Bronchitis]]
* Mucous plugging
* [[Pulmonary embolism]]
* [[Acute coronary syndrome]]
* [[Acute decompensated heart failure]]
* [[Asthma]]
* [[Reactive airway disease]]
* [[Exercise-associated hyponatremia]]
* [[Pneumothorax]]

==Prevention==
The primary recommendation for the prevention of HAPE is gradual ascent.<ref name=WMS>{{cite journal |last1=Luks, MD |first1=Andrew M. |last2=McIntosh, MD, MPH |first2=Scott E. |last3=Grissom, MD |first3=Colin K. |last4=Auerbach, MD, MS |first4=Paul S. |last5=Rodway, PhD, APRN |first5=George W. |last6=Schoene, MD |first6=Robert B. |last7=Zafren, MD |first7=Ken |last8=Hackett, MD |first8=Peter H. |display-authors=3 |title=Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Acute Altitude Illness: 2014 Update |journal=Wilderness & Environmental Medicine |volume=25 |date=2014 |issue=24 |pages=S4–S14 |doi=10.1016/j.wem.2014.06.017|pmid=25498261 |doi-access=free }}</ref> The suggested rate of ascent is the same that applies to the prevention of [[acute mountain sickness]] and [[high-altitude cerebral edema]].

The Wilderness Medical Society (WMS) recommends that, above {{convert|3000|m|ft}}, climbers
* not increase the sleeping elevation by more than {{convert|500|m|ft}} a day, and
* include a rest day every 3–4 days (i.e., no additional ascent).<ref name=WMS/>
In the event that adherence to these recommendations is limited by terrain or logistical factors, the WMS recommends rest days either before or after days with large gains. Overall, WMS recommends that the average ascent rate of the entire trip be less than {{convert|500|m|ft}} per day.<ref name=WMS/>

The most studied and preferred medication for prevention of HAPE is [[nifedipine]],<ref name=":0">{{Cite web|url=https://www.uptodate.com/contents/high-altitude-pulmonary-edema|title=High altitude pulmonary edema|last1=Gallagher, MD|first1=Scott A.|last2=Hackett, MD|first2=Peter|date=August 28, 2018|website=UpToDate|access-date=May 2, 2019}}</ref><ref name="WMS" /> a pulmonary [[Vasodilation|vasodilator]] which prevents the altitude induced pulmonary hypertension.<ref>{{Cite journal|last1=Stream|first1=Joshua O.|last2=Grissom|first2=Colin K.|date=2008|title=Update on high-altitude pulmonary edema: pathogenesis, prevention, and treatment|journal=Wilderness & Environmental Medicine|volume=19|issue=4|pages=293–303|doi=10.1580/07-WEME-REV-173.1|issn=1080-6032|pmid=19099331|s2cid=8799724}}</ref> The recommendation for its use is strongest for individuals with a history of HAPE. According to published data, treatment is most effective if given one day prior to ascent and continued for four to five days, or until descent below 2,500 meters (8,200 ft).<ref name=":0" /><ref name="WMS" />

Additional medications that are being considered for prevention but require further research to determine efficacy and treatment guidelines include [[acetazolamide]], [[salmeterol]], [[tadalafil]] (and other [[PDE5 inhibitors]]), and [[dexamethasone]].<ref name=":0" /><ref name="WMS" /><ref name="Mer2018Pro">{{cite web |title=Altitude Diseases - Injuries; Poisoning |url=https://www.merckmanuals.com/professional/injuries-poisoning/altitude-diseases/altitude-diseases |website=Merck Manuals Professional Edition |access-date=3 August 2018 |date=May 2018}}</ref> Acetazoladmide has proven to be clinically effective, but formal studies are lacking. Salmeterol is considered an adjunctive therapy to nifedipine, though only in highly susceptible climbers with clearly demonstrated recurrence of HAPE.<ref name=":0" /><ref name="WMS" /> Tadalafil was found to be effective at preventing HAPE in HAPE-s individuals during rapid ascent, but optimal dosing and frequency has yet to be established.<ref name=":1" /> Use of dexamethasone is currently indicated for the treatment of moderate-to-severe [[acute mountain sickness]], as well as [[high-altitude cerebral edema]]. It has also been found to prevent HAPE,<ref name="Maggiorini M, Brunner-La Rocca HP, Peth S, et al. 2006 497–506" /> but its routine use is not yet recommended.<ref name=":0" /><ref name=":1" /><ref name="WMS" />

Notably, each of these medications acts to block hypoxic pulmonary hypertension, lending evidence to the proposed pathophysiology of HAPE outlined above.<ref name=":1" />

It is recommended that those who go to high altitude avoid alcohol or sleeping medications.<ref name=":2">{{Cite journal|last=Paralikar|first=Swapnil|date=February 2013|title=High altitude pulmonary edema‐clinical features, pathophysiology, prevention and treatment|journal=Indian Journal of Occupational and Environmental Medicine|volume=16|issue=2|pages=59–62|doi=10.4103/0019-5278.107066|pmid=23580834|pmc=3617508}}</ref>

==Treatment==
[[File:Portable hyperbaric chamber.jpg|thumb|Demonstrating the use of a portable hyperbaric chamber.]]
The recommended first line treatment is descent to a lower altitude as quickly as possible, with symptomatic improvement seen in as few as 500 to 1,000 meters (1,640 feet to 3,281 feet).<ref name="Borden" /><ref name=":0" /><ref name=":1" /><ref name="pmid18578641">{{cite journal |last1=Luks|first1=AM |title=Do we have a 'best practice' for treating high altitude pulmonary edema? |journal=High Altitude Medicine & Biology |volume=9 |issue=2 |pages=111–14 |year=2008 |pmid=18578641 |doi=10.1089/ham.2008.1017}}</ref> However, descent is not mandatory in people with mild HAPE and treatment with warming techniques, rest, and supplemental oxygen can improve symptoms.<ref name=":0" /><ref name=":1" /><ref name="WMS" /> Giving oxygen at [[Oxygen therapy|flow rates]] high enough to maintain an SpO2 at or above 90% is a fair substitute for descent.<ref name=":0" /><ref name=":1" /><ref name="WMS" /> In the hospital setting, oxygen is generally given by [[nasal cannula]] or [[Oxygen mask|face mask]] for several hours until the person is able to maintain oxygen saturations above 90% while breathing the surrounding air.<ref name=":0" /> In remote settings where resources are scarce and descent is not feasible, a reasonable substitute can be the use of a [[Portable hyperbaric bag|portable hyperbaric chamber]], which simulates descent, combined with additional oxygen and medications.<ref name=":0" /><ref name=":1" /><ref name="WMS" />

As with prevention, the standard medication once a climber has developed HAPE is [[nifedipine]],<ref>{{cite journal|last1=Bärtsch|first1=P|last2=Swenson|first2=Erik R.|last3=Maggiorini|first3=ER|last4=Maggiorini|first4=M|year=2001|title=Update: High altitude pulmonary edema|journal=Advances in Experimental Medicine and Biology|volume=502|pages=89–106|doi=10.1007/978-1-4757-3401-0_8|isbn=978-1-4419-3374-4|pmid=11950158}}</ref> although its use is best in combination with and does not substitute for descent, hyperbaric therapy, or oxygen therapy.<ref name=":0" /><ref name=":1" /><ref name="WMS" /> Though they have not formally been studied for the treatment of HAPE, [[PDE5 inhibitor|phosphodiesterase type 5 inhibitors]] such as [[sildenafil]] and [[tadalafil]] are also effective<ref name="Maggiorini M, Brunner-La Rocca HP, Peth S, et al. 2006 497–506">{{cite journal|last1=Maggiorini|first1=M|last2=Brunner-La Rocca|first2=HP|last3=Peth S|display-authors=etal|date=October 2006|title=Both tadalafil and dexamethasone may reduce the incidence of high-altitude pulmonary edema: a randomized trial|journal=Annals of Internal Medicine|volume=145|issue=7|pages=497–506|doi=10.7326/0003-4819-145-7-200610030-00007|pmid=17015867|s2cid=2261923}}</ref> and can be considered as add-on treatment if first-line therapy is not possible; however, they may worsen the headache of mountain sickness.<ref>{{cite journal |last1=Bates|first1=MG|last2=Thompson|first2=AA|last3=Baillie|first3=JK |title=Phosphodiesterase type 5 inhibitors in the treatment and prevention of high altitude pulmonary edema |journal=Current Opinion in Investigational Drugs |volume=8 |issue=3 |pages=226–31 |date=March 2007 |pmid=17408118}}</ref> There is no established role for the [[Beta2-adrenergic agonist|inhaled beta-agonist]] salmeterol, though its use can be considered.<ref name=":0" /><ref name=":1" /><ref name="WMS" />

[[Dexamethasone]] has a potential role in HAPE, though there are currently no studies to support its effectiveness as treatment.<ref name="WMS" /> However, as outlined in the 2014 WMS Practice Guidelines, its use is recommended for the treatment of people with concomitant HAPE and [[High-altitude cerebral edema|HACE]] at the treatment doses recommended for HACE alone.<ref name="WMS" /> Additionally, they support its use in HAPE with neurologic symptoms or [[Cerebral hypoxia|hypoxic encephalopathy]] that cannot be distinguished from HACE.<ref name="WMS" />

==Epidemiology==
Rates of HAPE differs depending on [[altitude]] and speed of ascent. In general, there is about a 0.2 to 6 percent incidence at {{convert|4,500|m|ft}}, and about 2 to 15 percent at {{convert|5,500|m|ft}}.<ref name=":0" /> The higher incidence of 6% has been seen when climbers ascend at a rate > 600m/day.<ref name=":2" /> It has been reported that about 1 in 10,000 skiers who travel to moderate altitudes in Colorado develop HAPE; one study reported 150 cases over 39 months at a Colorado resort located at {{convert|2,928|m|ft}}.<ref name=":1" /> About 1 in 50 climbers who ascended Denali [{{convert|6,194|m|ft|disp=or}}] developed pulmonary edema, and as high as 6% of climbers ascending rapidly in the Alps [{{convert|4,559|m|ft|disp=or}}].<ref name=":1" /> In climbers who had previously developed HAPE, re-attack rate was up to 60% with ascent to {{convert|4,559|m|ft}} in a 36-hour time period, though this risk was significantly reduced with slower ascent rates.<ref name=":1" /> It is believed that up to 50% of people suffer from subclinical HAPE with mild edema to the lungs but no clinical impairment.<ref name=":2" />

== History ==
HAPE was recognized by physicians dating back to the 19th century but was originally attributed to “high altitude pneumonia”. The first documented case of pulmonary edema, confirmed by autopsy, was probably that of Dr Jacottet who died in 1891 in the Observatoire Vallot on [[Mont Blanc]]. After participating in a rescue on the mountain, the doctor refused to return. Instead, he spent further two nights at an altitude of {{convert|4300|m|ft}} with obvious AMS symptoms and died on the second night.<ref>{{cite journal |last1=Richalet |first1=J. P. |title=The scientific observatories on Mont Blanc |journal=High Altitude Medicine & Biology |date=2001 |volume=2 |issue=1 |pages=57–68 |doi=10.1089/152702901750067936 |pmid=11252700 |url=https://pubmed.ncbi.nlm.nih.gov/11252700/ |access-date=27 July 2020 |issn=1527-0297}}</ref><ref name="West">{{cite book |last1=West |first1=John |last2=Schoene |first2=Robert |last3=Luks |first3=Andrew |last4=Milledge |first4=James |title=High Altitude Medicine and Physiology 5E |date=2012 |publisher=CRC Press |isbn=978-1-4441-5433-7 |page=310 |url=https://books.google.com/books?id=nS3SBQAAQBAJ&pg=PA310 |access-date=27 July 2020 |language=en}}</ref>
This condition was subsequently noticed in otherwise healthy climbers who would die shortly after arriving at high altitudes.<ref name=":2" /> It was not until 1960 that Charles Houston, an internal medicine physician in Aspen, published a case report of 4 individuals participating in high elevation activities that he had diagnosed with “edema of the lungs”. He described chest X-rays with edema and non-specific changes on EKG. Even though these cases had been termed high altitude pneumonia in the past, Houston indicated that these cases were “acute pulmonary edema without heart disease”.<ref>{{Cite journal|last=Houston|first=CS|date=1960|title=Acute Pulmonary Edema of High Altitude|journal=N Engl J Med|volume=263|issue=10|pages=478–80|doi=10.1056/NEJM196009082631003|pmid=14403413}}</ref>

==Research==
To help understand factors that make some individuals susceptible to HAPE, the International HAPE Database was set up in 2004. The database is administered by [[Apex (altitude physiology expeditions)|APEX]], a high altitude medical research charity.<ref>{{cite web |title=International HAPE database |url=http://www.altitude.org/hape.php |publisher=Apex (Altitude Physiology EXpeditions) |access-date=2006-08-10}}</ref> A few cases support the possibility of reascent following recovery and acclimatization after an episode of HAPE precipitated by rapid ascent.<ref>{{cite journal |last1=Litch |first1=JA |last2=Bishop |first2=RA |title=Reascent following resolution of high altitude pulmonary edema (HAPE). |journal=High Altitude Medicine & Biology |date=2000 |volume=2 |issue=1 |pages=53–55 |doi=10.1089/152702901750067927 |pmid=11252699}}</ref>

==See also==
* [[Hazards of outdoor recreation]]
* [[High-altitude cerebral edema]] (HACE)
* [[High-altitude flatus expulsion]] (HAFE)

==References==
{{Reflist}}

== External links ==
{{Medical resources
| ICD10={{ICD10|T|70|2|t|66}}
| ICD9= {{ICD9|993.2}}
| MedlinePlus=
| eMedicineSubj=
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{{Consequences of external causes}}

{{DEFAULTSORT:High-Altitude Pulmonary Edema}}
[[Category:Lung disorders]]
[[Category:Mountaineering and health]]

High-altitude pulmonary edema - Revision history

CleanupBot at 05:04, 11 December 2022