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Swenson ER, Maggiorini M, Mongovin S, et al. Pathogenesis of High-Altitude Pulmonary Edema: Inflammation Is Not an Etiologic Factor. JAMA. 2002;287(17):2228–2235. doi:https://doi.org/10.1001/jama.287.17.2228
Author Affiliations: Medical and Research Services, Veterans Affairs Puget Sound Health Care System, University of Washington, Seattle (Dr Swenson and Mr Mongovin); Medical Intensive Care Unit, Department of Internal Medicine, University Hospital, Zurich, Switzerland (Drs Maggiorini and Greve); National Heart and Lung Institute, Imperial College School of Science, Technology, and Medicine, London, England (Dr Gibbs); and Division of Sports Medicine, Department of Medicine, University Clinic, Heidelberg, Germany (Drs Mairbäurl and Bärtsch).
Context The pathogenesis of high-altitude pulmonary edema (HAPE) is considered
an altered permeability of the alveolar-capillary barrier secondary to intense
pulmonary vasoconstriction and high capillary pressure, but previous bronchoalveolar
lavage (BAL) findings in well-established HAPE are also consistent with inflammatory
Objectives To determine whether inflammation is a primary event in HAPE and to
define the temporal sequence of events in HAPE.
Design, Setting, and Participants Case study from July through August 1999 of 10 subjects with susceptibility
to HAPE and 6 subjects resistant to HAPE, all of whom are nonprofessional
alpinists with previous mountaineering experience above 3000 m.
Main Outcome Measures Pulmonary artery pressure measurements and BAL findings at low altitude
(490 m) and shortly before or at the onset of HAPE at an altitude of 4559
Results Subjects who were HAPE susceptible had higher mean (SD) pulmonary artery
systolic blood pressures at 4559 m compared with HAPE-resistant subjects (66
vs 37 mm Hg; P = .004). Despite development of HAPE
in the majority of HAPE-susceptible subjects, there were no differences in
BAL fluid total leukocyte counts between resistant and susceptible subjects
or between counts taken at low and high altitudes. Subjects who developed
HAPE had BAL fluid with high concentrations of plasma-derived proteins and
erythrocytes, but there was no increase in plasma concentrations of surfactant
protein A and Clara cell protein. The chest radiograph score was 12.7 for
the 3 HAPE-susceptible subjects who developed HAPE before BAL was performed;
they were lavaged within 3 to 5 hours. The remainder of the HAPE-susceptible
group was lavaged before edema was apparent on radiographs. However, 6 subjects
from the HAPE-susceptible group who developed HAPE on the following day had
a score on bronchoscopy of 1.5, which increased to 4.6, reflective of mild
pulmonary edema. In HAPE cases, there were no elevations in a number of proinflammatory
cytokines and eicosanoid and nitric oxide metabolites.
Conclusions Early HAPE is characterized by high pulmonary artery pressures that
lead to a protein-rich and mildly hemorrhagic edema, with normal levels of
leukocytes, cytokines, and eicosanoids. HAPE is a form of hydrostatic pulmonary
edema with altered alveolar-capillary permeability.
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