What to do in Cardioembolic Stroke with Contraindications to Anticoagulation. In this post, we try to cover what happened if Cardioembolic Stroke with Contraindications to Anticoagulation and how to treat it.
Scenario:
A 74-year-old man with chronic atrial fibrillation was directed to discontinue warfarin therapy3 months ago when he was found to have significant iron deficiency anemia with blood in the stool but negative endoscopic and radiologic workup of his GI tract. Last week he had a transient left visual field loss, and this morning, about 8 hours prior to presenting to the ED, he noticed difficulty with speech after getting out of the shower. In the remote past, he had a left cerebellar stroke which led to transient ataxia and vertigo, at which time the atrial fibrillation was discovered. Today, his heart rate is irregular at approximately 76 beats per minute, atrial fibrillation is identified on ECG, and blood pressure (BP) is 134/76 mm Hg. The general exam is normal, but on the neurological exam there is some difficulty with naming low-frequency objects, and fluency is reduced. Basic labs are normal, including coagulation studies. CT today reveals the old cerebellar stroke and a question of attenuation changes in the cortex near the left Sylvian fissure but is otherwise normal.
What to do?
This patient is likely having recurrent cerebral ischemic events, probably occurring due to cardiac thromboembolic. After confirming this, your next thought should be about ways to prevent further strokes. Anticoagulation is appropriate but there are understandable concerns. First is the fact that this patient was felt to be a risk for serious GI bleeding. The second is that there is likely to be a new area of infarction, which can undergo hemorrhagic conversion, which is more likely if the patient is anticoagulated. He is out of the window for tissue plasminogen activator (tPA). So it is time to assess the risk of anticoagulation versus the risk of a new cardioembolic event while keeping his unique risk factors for bleeding in mind. First, let’s tackle the GI bleeding issue. His blood count is normal and there is no active GI bleeding; his previous GI workup was negative. The ideal timing to restart anticoagulation remains poorly characterized. For patients with a high risk of ischemic stroke from atrial fibrillation estimated with a CHA2DS2-Vasc Score and low risk of rebleeding, resumption of anticoagulation can be considered within a few days (Table 19.1). Patients with a higher risk of bleeding but lower risk of thromboembolism may benefit from a more delayed start. Hematocrit should be followed closely, and the patient should remain vigilant for evidence of rebleeding.
Case Study of Cardioembolic Stroke with Contraindications to Anticoagulation
This patient is likely having recurrent cerebral ischemic events, probably occurring due to cardiac thromboembolic. After confirming this, your next thought should be about ways to prevent further strokes. Anticoagulation is appropriate but there are understandable concerns. First is the fact that this patient was felt to be a risk for serious GI bleeding. The second is that there is likely to be a new area of infarction, which can undergo hemorrhagic conversion, which is more likely if the patient is anticoagulated. He is out of the window for tissue plasminogen activator (tPA). So it is time to assess the risk of anticoagulation versus the risk of a new cardioembolic event while keeping his unique risk factors for bleeding in mind. First, let’s tackle the GI bleeding issue. His blood count is normal and there is no active GI bleeding; his previous GI workup was negative.
The ideal timing to restart anticoagulation remains poorly characterized. For patients with a high risk of ischemic stroke from atrial fibrillation estimated with a CHA2DS2-Vasc Score and low risk of rebleeding, resumption of anticoagulation can be considered within a few days (Table 19.1). Patients with a higher risk of bleeding but lower risk of thromboembolism may benefit from a more delayed start. Hematocrit should be followed closely, and the patient should remain vigilant for evidence of rebleeding. What about the risk of converting an ischemic infarction into a hemorrhagic one? Evidence is controversial here, too. The size of the acute infarction is probably important (i.e., a large infarction is more likely to bleed). Avoiding very high spikes in BP and careful monitoring of coagulation studies will bias the odds against intracerebral hemorrhage. On the other hand, acutely lowering BP in acute stroke can lead to an extension of the infarctions so the risk must be balanced. MRI can help estimate the size of the stroke and can also detect even small amounts of bleeding, which could inform anticoagulation decisions. But, back to the original question: Will the reduction in risk of recurrent infarction be outweighed by the risk of hemorrhagic conversion and resulting morbidity and mortality risks? It turns out that the risks tend to balance out pretty closely. Thus, the evidence here is mixed. Is there any advantage to using low-molecular-weight heparin (LMWH)? No; in fact, there are disadvantages.
The half-life of LMWH is long, and it is inactivated by protamine to a much lesser extent. Therefore, if there is a bleeding complication, heparin is easier to reverse. Also, its activity is not assessable by partial thromboplastin time (PTT), so the degree of anticoagulation is generally inferred. And it is expensive (Table 19.2). So, what to do in terms of attempting to prevent recurrent cerebral ischemia in this patient? Since the evidence does not really help, this becomes a clinical judgment problem. But, you are not alone. This patient and his family can and should be enlisted to weigh the pros and cons. What they need to know is that the next stroke can be devastating, but that it is impossible to know when or if this will happen. Echocardiography can help by ruling out an intracardiac thrombus, but of course, this is just a snapshot, and thrombi can begin to form at any time. The chances of a recurrent stroke happening are generally below 5% in the first several days, so odds are good that this will not occur while they are weighing the options acutely. MRI can help by delineating the size of the stroke. Perhaps it is small but with a penumbra of impending ischemia, therefore less likely to bleed than a large area of infarcted tissue. If the patient and family opt to avoid anticoagulation, this decision can be reassessed over the next few days. Cardiological consultation about acute and long-term plans for dealing with atrial fibrillation with medication, cardioversion, or ablation therapy might help but the success rate of these interventions has not been high enough to obviate the need for anticoagulation.
KEY POINTS TO REMEMBER
- Both systemic bleeding and intracerebral bleeding risks must
be considered before starting anticoagulation in the acute post-stroke setting. - MRI of the brain and echocardiography can help the
neurologist and patient weigh the risks and benefits of starting
anticoagulation.
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