Reascent Following Resolution of High Altitude Pulmonary Edema (HAPE)

Litch, James A.; Bishop, Rachel A.

doi:10.1089/152702901750067927

Cited by 19 publications

(18 citation statements)

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“…Large clinical series of HAPE treatment at 2500 to 2928 m in Colorado have been reported in which selected patients were treated at that altitude (Sophocles, 1986;Hultgren et al, 1996;Zafren et al, 1996). Effective treatment of HAPE has been reported above 4240 m in isolated cases (Litch and Bishop, 2001) and under experimental, rather than clinical, circumstances at the Capanna Regina Margherita at 4559 m (Oelz et al, 1989). It should be noted that Capanna Regina Margherita studies typically monitor research subjects continuously and initiate treatment as soon as a HAPE diagnosis is established (Oelz et al, 1989;Sartori et al, 2002;Maggiorini et al, 2006), a scenario very different from the one we encountered in which sometimes critically ill patients presented for treatment, often many hours to several days into the course of their disease and without treatment having been initiated.…”

Section: Discussionmentioning

confidence: 99%

Treatment of High Altitude Pulmonary Edema at 4240 m in Nepal

Fagenholz

Gutman

Murray

et al. 2007

High Altitude Medicine & Biology

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High altitude pulmonary edema (HAPE) is the leading cause of death from altitude illness and rapid descent is often considered a life-saving foundation of therapy. Nevertheless, in the remote settings where HAPE often occurs, immediate descent sometimes places the victim and rescuers at risk. We treated 11 patients (7 Nepalese, 4 foreigners) for HAPE at the Himalayan Rescue Association clinic in Pheriche, Nepal (4240 m), from March 3 to May 14, 2006. Ten were admitted and primarily treated there. Seven of these (6 Nepalese, 1 foreigner) had serious to severe HAPE (Hultgren grades 3 or 4). Bed rest, oxygen, nifedipine, and acetazolamide were used for all patients. Sildenafil and salmeterol were used in most, but not all patients. The duration of stay was 31 +/- 16 h (range 12 to 48 h). Oxygen saturation was improved at discharge (84% +/- 1.7%) compared with admission (59% +/- 11%), as was ultrasound comet-tail score (11 +/- 4 at discharge vs. 33 +/- 8.6 at admission), a measure of pulmonary edema for which admission and discharge values were obtained in 7 patients. We conclude it is possible to treat even serious HAPE at 4240 m and discuss the significance of the predominance of Nepali patients seen in this series.

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Section: Discussionmentioning

confidence: 99%

Treatment of High Altitude Pulmonary Edema at 4240 m in Nepal

Fagenholz

Gutman

Murray

et al. 2007

High Altitude Medicine & Biology

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“…Although reports document successful ascents of Mount Everest following episodes of HAPE [138,139], the safety of continuing ascent after resolution of HAPE or HACE remains controversial. If ascent is pursued in such circumstances, the individual should be symptom-free and off any medications for at least several days before initiating further ascent and should strongly consider pharmacological prophylaxis for their ascent, including a pulmonary vasodilator for individuals who had HAPE and dexamethasone for individuals who had HACE.…”

Section: Re-ascent Following Resolution Of Acute Altitude Illnessmentioning

confidence: 99%

Acute high-altitude sickness

2017

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At any point 1-5 days following ascent to altitudes ⩾2500 m, individuals are at risk of developing one of three forms of acute altitude illness: acute mountain sickness, a syndrome of nonspecific symptoms including headache, lassitude, dizziness and nausea; high-altitude cerebral oedema, a potentially fatal illness characterised by ataxia, decreased consciousness and characteristic changes on magnetic resonance imaging; and high-altitude pulmonary oedema, a noncardiogenic form of pulmonary oedema resulting from excessive hypoxic pulmonary vasoconstriction which can be fatal if not recognised and treated promptly. This review provides detailed information about each of these important clinical entities. After reviewing the clinical features, epidemiology and current understanding of the pathophysiology of each disorder, we describe the current pharmacological and nonpharmacological approaches to the prevention and treatment of these diseases.

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“…On the other hand, susceptible mountaineers can ascend up to 7,000 m without developing HAPE when ascent rate is slow, with an average gain of altitude of 300 -350 m/day above 2,000 m (9). Even more astonishing is the fact that a mountaineer who develops HAPE and descends to recover can reascend to even higher altitudes a few days after recovery without developing HAPE again (66). There is most likely no complete "resistance" to HAPE.…”

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confidence: 99%

Physiological aspects of high-altitude pulmonary edema

Bärtsch

Mairbäurl²,

Maggiorini³

et al. 2005

Journal of Applied Physiology

295

216

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High-altitude pulmonary edema (HAPE) develops in rapidly ascending nonacclimatized healthy individuals at altitudes above 3,000 m. An excessive rise in pulmonary artery pressure (PAP) preceding edema formation is the crucial pathophysiological factor because drugs that lower PAP prevent HAPE. Measurements of nitric oxide (NO) in exhaled air, of nitrites and nitrates in bronchoalveolar lavage (BAL) fluid, and forearm NO-dependent endothelial function all point to a reduced NO availability in hypoxia as a major cause of the excessive hypoxic PAP rise in HAPE-susceptible individuals. Studies using right heart catheterization or BAL in incipient HAPE have demonstrated that edema is caused by an increased microvascular hydrostatic pressure in the presence of normal left atrial pressure, resulting in leakage of large-molecular-weight proteins and erythrocytes across the alveolarcapillary barrier in the absence of any evidence of inflammation. These studies confirm in humans that high capillary pressure induces a high-permeability-type lung edema in the absence of inflammation, a concept first introduced under the term "stress failure." Recent studies using microspheres in swine and magnetic resonance imaging in humans strongly support the concept and primacy of nonuniform hypoxic arteriolar vasoconstriction to explain how hypoxic pulmonary vasoconstriction occurring predominantly at the arteriolar level can cause leakage. This compelling but as yet unproven mechanism predicts that edema occurs in areas of high blood flow due to lesser vasoconstriction. The combination of high flow at higher pressure results in pressures, which exceed the structural and dynamic capacity of the alveolar capillary barrier to maintain normal alveolar fluid balance. pulmonary artery pressure; hypoxic pulmonary vasoconstriction; nitric oxide; inflammation; alveolar fluid clearance; pathophysiology; review CLINICAL PICTUREHigh-altitude pulmonary edema (HAPE) is noncardiogenic pulmonary edema that usually occurs at altitudes above 3,000 m in rapidly ascending nonacclimatized individuals within the first 2-5 days after arrival. It may also occur in high-altitude dwellers who return from sojourns at low altitude. The first medical description of HAPE was published in Peru and recognized the latter form, also called reentry HAPE, as a pulmonary edema associated with electrographic signs of right ventricular overload (67). The first cases of HAPE in unacclimatized lowlanders climbing to high altitude were reported from the Rocky Mountains (53). The two forms very probably share the same pathophysiology.The reader is referred to other reviews (9,41,96,97) for an extensive presentation of the clinical picture. In this review, we point out some particular characteristics that might elucidate the underlying pathophysiology and are revealed by classical and newly evolving pathophysiological concepts.The prevalence of HAPE depends on the degree of susceptibility, the rate of ascent, and the final altitude. At an altitude of 4,500 m, the prevalence may ...

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Reascent Following Resolution of High Altitude Pulmonary Edema (HAPE)

Cited by 19 publications

References 5 publications

Treatment of High Altitude Pulmonary Edema at 4240 m in Nepal

Treatment of High Altitude Pulmonary Edema at 4240 m in Nepal

Acute high-altitude sickness

Physiological aspects of high-altitude pulmonary edema

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