High-Altitude Pulmonary Edema and Patent Foramen OvaleHigh-Altitude Pulmonary Edema and Patent Foramen Ovale

To the Editor: In their case-control study, Dr Allemann and colleagues¹ identified an association between patent foramen ovale (PFO) and susceptibility to high-altitude pulmonary edema (HAPE) in mountaineers. In HAPE-susceptible participants, they observed low arterial oxygen saturation that preceded the onset of clinical HAPE. Their study suggests that intracardiac right-to-left shunting through a PFO is partly responsible for this hypoxemia. We believe that subclinical pulmonary edema may also contribute to the early hypoxemia observed in this group and suggest a means of evaluating this in future studies.

The ascent to Capanna Regina Margherita induces subclinical pulmonary edema, even in those persons not developing clinical HAPE.^{2 - 3} Allemann et al describe no attempt to determine the degree of pulmonary edema present when their participants' oxygen saturations were measured. Persons who subsequently developed clinical HAPE may have already incurred significant, if subclinical, pulmonary edema when their oxygen saturations were measured. Correspondingly, a portion of the exaggerated hypoxemia noted in HAPE-susceptible individuals who did not progress to clinical HAPE may share a similar etiology. Chest radiography was only performed at the study's conclusion to confirm or exclude the diagnosis of HAPE and is relatively insensitive for identifying the early pulmonary edema that precedes clinical HAPE.^{2 - 3} Given this, even if radiography had been used to assess for pulmonary edema at the time oxygen saturations were measured, it might not have proven useful.

As an alternative, chest ultrasonography may be more helpful to quantify pulmonary edema.^{4 - 5} The comet-tail technique of chest ultrasonography has been correlated with radiographic and thermodilution measures of pulmonary edema.^{4 - 5} The technique does not require equipment beyond the transthoracic ultrasound equipment usually used for monitoring pulmonary artery pressures in HAPE research.^{1 ,4 - 5} It may help distinguish the relative contributions of edema and intracardiac shunting to the hypoxemia present before and during clinical HAPE.