High-altitude pulmonary edema: Difference between revisions

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=":1" /><ref name=":0" /> 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=":1" /><ref name=":0" /> 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" />

The diagnosis of HAPE is entirely based on symptoms and many of the symptoms overlap with other diagnoses.<ref name=":1" /><ref name=":0" /> 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&nbsp;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=":1" /><ref name=":0" /> 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=":1" /><ref name=":0" /> The development of pink, frothy, or frankly bloody [[sputum]] are late features of HAPE.<ref name=":1" /><ref name=":0" /> 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=":1" /><ref name=":0" />

On physical exam, increased breathing rates, increased heart rates, and a low-grade fever 38.5^o (101.3^o F) are common.<ref name=":1" /><ref name=":0" /> [[Auscultation|Listening]] to the lungs may reveal [[crackles]] in one or both lungs, often starting in the right middle lobe.<ref name=":1" /><ref name=":0" /> Imaging studies such as [[X-ray]] and [[CT imaging]] of the chest may reveal thoracic infiltrates that can be seen as opaque patches.<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><ref name=":1" /><ref name=":0" /> 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=":1" /><ref name=":0" /> 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" />

Differential diagnosis:<ref name=":1" /><ref name=":0" />

The most studied and preferred medication for prevention of HAPE is [[nifedipine]],<ref name="WMS" /><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> 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&nbsp;ft).<ref name="WMS" /><ref name=":0" />

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="WMS" /><ref name=":0" /><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="WMS" /><ref name=":0" /> 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" />