Writes a longtime friend and colleague (some details changed for privacy):
43yo man with right MCA stroke, found to have right ICA extracranial dissection with possible pseudoaneurysm right below petrous portion. Given the stroke, I put him on Coumadin and was going to watch and reimage in a month or so.
He went back home . . . saw another [academic neurologist], and he was scheduled for a stat angio and stent of the pseudoaneurysm.
He also thought that his dissection was secondary to migraines…not the kickboxing class he was taking here.
Clinically, he has had no TIAs or other issues since his initial event. Am I totally out of line here in my thinking? Have you heard of migraines causing dissection?
I don’t think my colleague is out of line at all. In fact, I usually treat such patients even more conservatively, with aspirin instead of anticoagulation. Current guidelines don’t recommend one over the other (emphasis added):
1. For patients with ischemic stroke or TIA and extracranial carotid or vertebral arterial dissection, antithrombotic treatment for at least 3 to 6 months is reasonable (Class IIa; Level of Evidence B).
2. The relative efficacy of antiplatelet therapy compared with anticoagulation is unknown for patients with ischemic stroke or TIA and extracranial carotid or vertebral arterial dissection (Class IIb; Level of Evidence B). (New recommendation)
The guidelines are clear about not jumping to stent these lesions:
3. For patients with stroke or TIA and extracranial carotid or vertebral arterial dissection who have definite recurrent cerebral ischemic events despite optimal medical therapy, endovascular therapy (stenting) may be considered (Class IIb; Level of Evidence C).
The medical questions here are almost trivial; you residents could field them in your sleep. I chose to blog about this to highlight two additional points: First, here’s another possible example of the relationship between migraine and stroke. I’m skeptical of the claim that the patient’s migraines caused his dissection, but as I’ve written here before, there are many cases where migraines are associated with vascular lesions; it may be that there’s a genetic susceptibility common to both.
The bigger issue that I wanted to explore, however, is the psychology of “doing more”. It seems that doing more is much easier than doing less. Doing more testing and doing more treatment provides the patient with the sense that you’re working tirelessly for him. You’re not going to let him have a stroke on your watch; no, you’re going to find the problem and you’re going to fix it. And if something goes wrong–if the patient has a stroke as a complication of angiography–well, sir, we did everything we could.
Contrast this with doing less: You have to tell the patient that you’re making an explicit recommendation not to image the lesion in more detail, not to “fix” it, and in many of my own dissection cases, not even to re-image in a few months. Doing less might also mean:
- Not fixing that PFO
- Not adding clopidogrel to aspirin
- Not imaging the carotids in a very old TIA patient
The patient might ask, “What? You’re going to wait for me to have another stroke before doing anything about it?” Your own colleagues might ask the same thing. So you carefully explain the current evidence base, the guidelines, the uncertain risk/benefit ratios, etc., but the patient may remain skeptical. And then he gets a second opinion from someone who’s much more aggressive. If consultant #2 is careful, he explains that these matters aren’t settled, that there is a range of practice, etc. But if he’s not, then you get the kind of feedback that makes you want to email your old buddies just to make sure you haven’t missed something.
No, my friend, you haven’t missed anything. Your patient and his other physician have simply fallen victim to gizmo idolatry.