Mountain resident high altitude pulmonary edema (MR-HAPE)

For five years I have been writing about children who live above 2500 feet with no history of travel who present with a respiratory illness and hypoxia. Because they do not appear very sick (toxic is the word we use in medical terms), repond to oxygen only, and have inconsistent or poor response to asthma medications, I have decided this is a form of HAPE. Observations by other clinicians support this:

  • Anthony Durmowicz and Ed Noordeweir et al. in Journal of Pediatrics May 1997:
  • “Although no data exists to support or refute the speculation that the presence of an ongoing pulmonary inflammatory process at the time of ascent to high altitude may predispose for the development of HAPE, I have observed that many children visiting high altitude who had HAPE at presentation had evidence of a preexisting inflammation-producing illness, such as a viral URI, OM, or GAS pharyngitis, that had begun before their ascent to high altitude.”
  • “Also noteworthy, the theory of increased endothelial cell permeability in response to hypoxia along with an increase in epithelial cell permeability may result in clinical pulmonary edema and the development of spontaneous HAPE in high altitude residents who acquire relatively mild respiratory tract illnesses seem to support this speculation.”

Careful review of the clinical records for these patients has not shown any factor that can reliably differentiate HAPE from other respiratory diagnoses such as asthma or pneumonia. Physical findings, symptoms, x-ray changes all overlap. The distinguishing feature to me is the clinical picture of a nontoxic patient with a low oxygen at altitude. HAPE is associated with increased pressures in the lungs, which can be diagnosed on an echocardiogram.  I am trying to organize a study to help us understand the causes of hypoxia which will include measuring pulonary pressures during acute episodes.

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