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Ann Thorac Surg 1997;64:1872
© 1997 The Society of Thoracic Surgeons
Department of Cardiothoracic Surgery, Monash Medical Centre, 246 Clayton Rd, Clayton 3168, Melbourne, Australia
To the Editor:
It is with interest that I read the case report by Zueger and associates [1] on "Dyspnea After Pneumonectomy: The Result of an Atrial Septal Defect." I would like to make the following comments to perhaps place a more sensible onus on this rare, yet in all likelihood under-diagnosed condition.
Zueger and associates described 3 characteristic observations made on their review of published cases of this uncommon, yet very interesting condition of platypnea (dyspnea induced by the upright position and relieved by recumbency). I hasten to add that for completeness the term orthodeoxia (arterial deoxygenization accentuated by the upright position and improved by recumbency) completes the accuracy of this syndrome. These three features are a variable time delay from operation to symptoms, the symptom of platypnea, and the variability of the shunt fraction in regard to blood volume, being greater with hypovolemia.
I would suggest that there is a fourth feature common to all reported cases, from the original description by Burchell and associates [2] in 1949 to the latest case report by Zueger and associates in 1997, and that is that it is seldom if ever initially considered in the differential diagnosis until serendipitously some proceduralist detects that there is a communication between the atria. For example, a nuclear medical specialist looking for evidence of pulmonary emboli eventually notices a delayed uptake of tracer in the systemic circulation (usually kidneys or spleen). In this case two such scans were performed and commented on as clear of pulmonary emboli. Or the echocardiographer (two such tests again performed) or the radiologist (again here a computed tomographic scan, pulmonary angiography and even cardiac magnetic resonance imaging were expected to yield a diagnosis) stumbles across an incidental communication between the atria in the process of establishing other cardiac or pulmonary pathology to account for the patient's dyspnea. Usually in their defense no mention is made that platypnea orthodeoxia rather than dyspnea is the syndrome at hand.
My colleagues and I [3] also had a patient presented to us with a battery of investigations before the serendipitous "penny dropped." Yet the history and physical examination are the absolute and crucial key; even more so than usual because of the interesting strangeness of the history, the opposite of what is expected normally. That is, the patient became profoundly dyspneic and desaturated on standing and symptoms disappeared on lying down! As we point out there are only two clinical possibilities to this syndrome.
Hence I disagree with Zueger and colleagues that the simplest diagnostic test is the arterial blood gas analysis while breathing 100% O2. I would suggest that the diagnosis can be made by the rarity of the history, with the ears! To confirm the diagnosis I would suggest that the recommendations made by Seward and associates from the Mayo Clinic be heeded (incidentally they were the first to surgically treat this condition in 1954). Their recommendation, not surprisingly given the history, is that the initial assessment consist of measurement of arterial blood gases with the patient in the supine and erect positions. The presence of orthodeoxia can then be very easily confirmed either by two-dimensional echocardiography or radionuclide imaging, but only if the examiner is looking for it. Otherwise, in the cynical yet apt words of Samuel Shem [4]: "If you don't take a temperature, you can't find a fever."
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