The main reason for getting a TEE in a patient with ischemic stroke is to find out if that patient has an indication for warfarin anticoagulation. You can begin the selection process by excluding patients who already have an obvious indication for warfarin (e.g. atrial fibrillation) and those who have a contraindication for warfarin.
Among the remaining patients only those with cryptogenic stroke are likely to need a TEE. This is an old paper demonstrating a high yield for TEE in finding an indication for warfarin in such patients. Here is a new study documenting similar findings:
The TOAST classification may be helpful in the determination of cryptogenic stroke.
Showing posts with label Stroke. Show all posts
Showing posts with label Stroke. Show all posts
When will you request TEE in Ischemic Stroke?
June 14, 2009
Stroke and Imaging
November 14, 2008
Early diagnosis of stroke is essential to intervene before irreversible damage happens to brain tissue. Imaging is an important tool before even thrombolytic therapy can be considered. Read more..
Thrombolytics in Acute Stroke? Time is brain
September 28, 2008
According to this article in the September 25th edition of the New England Journal of Medicine, alteplase improves the outcomes in stroke patients up to 4.5 hours after symptom onset. Previously, the “window” of effectiveness was only three hours. The clinical trial criteria are here.
The percentage of patients having a favorable outcome at 90 days in this study wasn’t huge, but was statistically significant - 52% of patients receiving alteplase had good outcomes compared with 45% of patients who received placebo. At the same time 27% of patients had some type of bleeding after receiving thrombolytics compared with only 17% of patients who had bleeding after receiving placebo. The rate of symptomatic bleeding in the brain was 2.4% for thrombolytics versus 0.2% for placebo.
So while you may have an overall improvement in your outcome at 90 days if you get the medication, more than 1 in 4 patients who receive the medication will have bleeding and 1 in 40 patients will have symptomatic bleeding.
Is it worth the risk?
In the editorial article accompanying the study, one of the study authors states that “one cannot help wondering why thrombolytic therapy has traveled such a long, difficult path to wider clinical use.”
I can help wondering.
Thrombolytics are one of the few things that physicians can give that will have an immediate and significant harm on patients. Sure, patients may occasionally have bad outcomes from allergic events or they may have undesirable side effects from some medications. But 2.4% of patients will have symptomatic bleeding in their brains when they get thrombolytics. Some of those patients will die.
I like to pose this scenario to my trainees: a patient presents to you 30 minutes after the onset of a left hemispheric stroke; how long do you have to initiate thrombolytic therapy?
The correct answer is 1 minute, not 2.5 hours, and ECASS III does not now justify an answer of 4 hours. From the moment the patient arrives at the door, every minute counts, and the only justifiable delays would be for performing brain imaging studies to exclude hemorrhage and for obtaining the results of a few simple laboratory tests. In fact, the very real peril of the ECASS III data is that some may take an even more leisurely approach to treating acute stroke. Nothing could be more wrong, for as we look back on the past decade of thrombolytic therapy for stroke, it is very clear that our focus must remain on the door-to-needle time. Every minute matters during a stroke.
So the choice is …
1. Let patient continue with the stroke symptoms they have already presented with and follow the doctrine of “primum non nocere.” After all, even this study shows that if doctors do nothing, 45% of the patients will get better on their own.
-or-
2. Give a medication that may improve clinical outcome in 7% more of the patients … at the risk of getting a bad outcome from the medication.
What would you choose?
Want a simple way to immediately expand the use of thrombolytic therapy?
If an On Call physician gets a CT report from a radiologist that says “no bleed,” the patient meets the criteria for thrombolytic therapy and doesn’t have any exclusion criteria, then the Physician cannot be held liable for any bad outcomes for giving thrombolytics.
There will still be some that philosophically disagree with giving patients a medication that could kill them. Nevertheless, there would be an instant spike in thrombolytic use. I guarantee it.
Stroke Prevention- Still Confusion?
August 29, 2008
Recurrence of stroke is disabling event and prevention of such event is important. S MATCH trial showed increased bleeding in patients taking combination of aspirin with Clopidogrel . This study looked at combination of aspirin plus extended release Dipyridamole compared to clopidogel. Study concludes that there is no difference in using either drugs. Aspirin dose used is only 50 mg daily. What do we do with our stroke patient?"For stroke prevention,/ use an antiplatelet drug./ Treat hypertension" Read more.
Read what the editorial has to say..
Central Obesity and Stroke
August 16, 2008
Central Obesity is strongly linked to risk of Stroke. So measurements of central obesity is important in risk assessment of stroke rather than BMI. Read more..
Warfarin for stroke- When and How?
July 16, 2008
With ever increasing number of patients with Atrial Fibrillation we do see patients presenting with cardioembolic stroke. One of the frequent questions that gets asked when to start anticoagulation and how? I have always practiced starting warfarin after 10 days and always bridge with Low molecular weight heparin. After reading this study i should change my practice..
Conclusions:- Anticoagulation of patients with cardioembolic stroke can be safely started with warfarin shortly after stroke. Heparin bridging and enoxaparin bridging increase the risk for serious bleeding.
Read More...
Conclusions:- Anticoagulation of patients with cardioembolic stroke can be safely started with warfarin shortly after stroke. Heparin bridging and enoxaparin bridging increase the risk for serious bleeding.
Read More...
Foreign accent after Stroke
July 9, 2008
Losing speech after a stroke is not uncommon. But acquiring a foreign accent is after stroke is amazing. Brain is known to re wire itself after a stroke but speaking in foreign accent is unheard of. I have not any way..
Foreign accent syndrome (FAS) is a neurological condition that is acquired following a stroke or some other form of brain injury. It occurs as a result of damage to the brain's speech motor centres, so that syllables are mispronounced, making one sound as if they are speaking their native language in a foreign accent.
FAS is extremely rare, with only around 50 reported cases since 1941. Two of these were reported in stroke victims in recent years: Linda Walker, a 62-year-old woman from Newcastle, began speaking in an accent that was described as a mixture of Jamaican, Canadian and Slovakian, whereas Tiffany Roberts, a 63-year-old American, began speaking in what sounds like a British accent.
Neurologists from Toronto now report the first Canadian case study of the condition. Writing in this month's issue of the Canadian Journal of Neurological Sciences, Naidoo et al describe the case of a stroke patient named Rosemary Dore, who previously had a native Southern Ontario accent, but is now speaking with an East Coast Canadian accent, despite never having lived in that part of the country.
This is out in news paper too.
Foreign accent syndrome (FAS) is a neurological condition that is acquired following a stroke or some other form of brain injury. It occurs as a result of damage to the brain's speech motor centres, so that syllables are mispronounced, making one sound as if they are speaking their native language in a foreign accent.
FAS is extremely rare, with only around 50 reported cases since 1941. Two of these were reported in stroke victims in recent years: Linda Walker, a 62-year-old woman from Newcastle, began speaking in an accent that was described as a mixture of Jamaican, Canadian and Slovakian, whereas Tiffany Roberts, a 63-year-old American, began speaking in what sounds like a British accent.
Neurologists from Toronto now report the first Canadian case study of the condition. Writing in this month's issue of the Canadian Journal of Neurological Sciences, Naidoo et al describe the case of a stroke patient named Rosemary Dore, who previously had a native Southern Ontario accent, but is now speaking with an East Coast Canadian accent, despite never having lived in that part of the country.
This is out in news paper too.
NSAIDs use and Strokes
July 3, 2008
In clinical trials involving COX-2 selective NDAIDS is asoociated with increased incidence of strokes. In this European study published in JAMA authors propectively looked at incidence of strokes in over 7000 patients over 10 years. They conclude that Current users of nonselective (HR, 1.72; 95% confidence interval [CI], 1.22-2.44) and COX-2–selective (HR, 2.75; 95% CI, 1.28-5.95) NSAIDs had a greater risk of stroke, but not users of COX-1–selective NSAIDs (HR, 1.10; 95% CI, 0.41-2.97). Hazard ratios (95% CIs) for ischemic stroke were 1.68 (1.05-2.69) for nonselective and 4.54 (2.06-9.98) for COX-2–selective NSAIDs. For individual NSAIDs, current use of the nonselective naproxen (HR, 2.63; 95% CI, 1.47-4.72) and the COX-2–selective rofecoxib (HR, 3.38; 95% CI, 1.48-7.74) was associated with a greater risk of stroke. Hazard ratios (95% CIs) for diclofenac (1.60 [1.00-2.57]), ibuprofen (1.47 [0.73-3.00]), and celecoxib (1.79 [0.52-2.76]) were greater than 1.00 but were not statistically significant.
Here is the study report..
Here is the study report..
Biomarkers and Etiology of stroke subtypes
June 11, 2008
Diagnosis of etiology of stroke sub types is not always possible in some patients and this prevents these patients from receiving definitive treatment. In this interesting study authors looked at the diagnostic value of a panel of biochemical markers to differentiate stroke sub types. Is it not wonderful if there is a blood test that will clinch the etiology. Read this article published in Stroke recent issue.
Read Here.
Treating ICH with rTPA?
May 23, 2008
Can you believe you would treat Intra Cranial hemorrhage with Thromolytics. Bleed on CT scan is one of the contraindications for giving rTPA in stroke. If you don't believe me you can see this guideline. It will make them bleed more.
This study is published in Medscape that low dose rTPA safe and effective in treating Intra ventricular hemorrhage, The researchers developed a system where tPA could be delivered directly to the site of the clot with a catheter placed by a neurosurgeon. When patients with intraventricular hemorrhage were given 1mg tPA every 8 hours for 4 days (usual dose for treating ischemic strokes is 100 mg over 90 minutes), their mortality rate dropped from 80% to 15%! In other words, before researchers tried this therapy, 8 out of 10 patients died from intraventricular bleeding. In this study less than 2 out of 10 patients died from intraventricular hemorrhage. In addition, the functional outcomes of the survivors was significantly better (i.e. less people had long-term disability).
More information for the study can be found on the Johns Hopkins web site. The information on inclusion and exclusion criteria is here. Obviously this therapy isn’t ready for prime-time yet, but there’s a lot of promise here.
It must have taken a lot of bravery to give the first patient with recent onset brain bleeding a dose of a thrombolytics, but that type of “outside the box” thinking will save a lot of lives and prevent a lot of disability.
Amazing!!
Management of Carotid stenosis: three to choose from
April 10, 2008
We had a long discussion regarding management carotid stenosis yesterday's internal medicine grand rounds. Eventually we recommended medical treatment and i have suggested same for this case vignette published in NEJM.
Carotid stenting or Surgical endarterectomy in high risk patients: Sapphire Study
This is 3 year follow up study report from SAPPHIRE investigators published in NEJM. They conclude in their patients with severe carotid artery stenosis and increased surgical risk, no significant difference could be shown in long-term outcomes between patients who underwent carotid artery stenting with an emboli-protection device and those who underwent endarterectomy.
How should we manage acute hypertension in stroke? Here comes CHIPPS!
April 8, 2008
Current guidelines for ischaemic stroke stroke do not recommend emergency anti hypertensive therapy until SB 220 or DB 120 unless TPA is given. The guideline for hemorrhagic stroke allow a moderately more aggressive approach to blood pressure lowering depending on the clinician’s estimate or the actual measurement of intracranial pressure.
Results from a small study called CHIPPS presented at the American Stroke Association's (ASA's) International Stroke Conference 2008 demonstrated that immediate antihypertensive treatment targeted to a systolic blood pressure of 145 to 155 mm Hg or a drop in systolic blood pressure of 15 mm resulted in improved stroke outcomes at 3 months.
This small study should not change clinical practice and should be considered preliminary. Moreover, the study population was a mixture of patients with hemorrhagic stroke and ischemic stroke, limiting its applicability to either subgroup.
Is it safe to give thrombolytics to patients already taking antiplatelets?
April 6, 2008
Prior use of antiplatelet (AP) drugs increases the risk of symptomatic intracerebral hemorrhage (SICH) and influences functional outcome in patients with ischemic stroke treated with intravenous thrombolysis.This is a single center prospective cohort study published in Archives in Neurology.
Conclusion Despite a higher incidence of SICH, the net benefit of intravenous tissue plasminogen activator therapy for acute ischemic stroke was greater in patients using AP drugs.
INTERACT: Reducing BP in ICH
In a multicenter open label pilot study published in Lancet Neurology investigators looked at safety and benefit of Intensive BP lowering in patients with ICH.
Methods:The patients, whose elevated systolic blood pressure ranged from 150 to 220 mm Hg, were randomly assigned to early intensive lowering of systolic BP to a target of 140 mm Hg or standard guideline-based management with a target of 180 mm Hg.
Concluson: Early intensive BP-lowering treatment is clinically feasible, well tolerated, and seems to reduce haematoma growth in ICH.
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