You go to examine the patient. She has some mild conversational dyspnea. Mental status is intact. She has no ocular movement abnormalities, including no fatigable ptosis. There's no facial weakness, nor any dysarthria. She has subtle shoulder abduction weakness bilaterally. Looking back at her last neuromuscular clinic note from six months ago, it looks like these findings are similar. The ED pages you and asks if you're going to admit this patient.
At this point, it doesn't quite look like it. Setting aside her neurologic exam findings, we know she's hypoxemic, as per her oxygen requirement (improved with nasal cannula) and as supported by her ABG. She also lacks hypercapnia. With myasthenia, if there were respiratory difficulties, we'd expect hypercapnia first (from respiratory muscle weakness reducing effective tidal volumes). In the advanced stages of hypoventilation/hypercapnia, you can then get hypoxemia from the CO2 molecules taking up so much volume so as to displace the O2 molecules (Dalton's law of partial pressures). It'd be highly unusual to get pure hypoxemia from neuromuscular respiratory weakness, at least without the presence of other findings. In this patient's case, her neurologic exam is roughly stable. So, overall, this is less likely to be myasthenia.
So what could this be? This patient has isolated hypoxemia. She has an elevated A-a gradient, so we're thinking V/Q mismatch, shunt, or a diffusion problem. In the context of her clinical history, as well as baseline immunosuppression, a community-acquired pneumonia-- perhaps with an atypical organism, which wasn't covered by the amoxicillin-- could be to blame. Pulmonary embolism is a good consideration as well. Her hypoxemia improved well to low-flow oxygen, so a florid right-to-left shunt seems less likely. Nothing is suggesting interstitial lung disease.
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