You let the ED know that you're not worried about an acute myasthenia exacerbation. You agree with their concern for pneumonia, but the patient doesn't need to be admitted to your service for this. The ED starts her on IV ampicillin/sulbactam as well as azithromycin and admits her to general medicine.
On day 3 of admission, the general medicine team calls you to see the patient. The patient is more dyspneic now. You examine the patient. She's on 10L NC. She has right-sided ptosis in primary gaze, a moderate flaccid dysarthria, and more neck flexion and shoulder abduction weakness compared with your prior exam. She is tachypneic and using accessory muscles to breathe. She has some pooling of oral secretions.
This patient initially presented with a one-week history of persistent non-productive cough and dyspnea not relieved with an outpatient amoxicillin prescription. She was initially purely hypoxemic, and has been treated with the usual CAP coverage. Her neurologic exam went from stable compared with her baseline to now worse than before, in a pattern of proximal weakness we'd expect from myasthenia. She has cranial nerve deficits referable to myasthenia. Overall, we are now concerned that she has now developed a myasthenia exacerbation.
Does this make sense? Yes. While she didn't have an exacerbation at first, she is having one now, primarily triggered by her pneumonia. It's possible that azithromycin has contributed, though this is a weaker contributor as compared to fluoroquinolones. Pragmatism has to be used when selecting antibiotics for patients with myasthenia. Since she was otherwise neurologically stable, it was reasonable to have chosen it.
In terms of what to do now, it's clear she is experiencing a rapid clinical decline and requires intubation for both acute hypoxemic respiratory failure and airway protection. It's likely she's also developed hypercapnic respiratory failure.
It's important to have considered our course of action here without relying on the crutch of a repeat ABG. You can make the decision on intubation based on the information you already have available. Patients with myasthenia can very abruptly decompensate. Their blood gases can look fine, even up to the point that you see an obvious problem in front of you. (Actually, a "normal" PaCO2 despite tachypnea and increased work of breathing is suspicious in of itself, as you would otherwise expect hypocapnia. The fact that their PaCO2 is normal at that time just means that you've caught them later in their course, just as their PaCO2 is on its rise. Once they can no longer compensate for this respiratory insufficiency, their PaCO2 will become high, and they will crash.)
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