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No Stroke of Luck: What To Do When “Time is Brain”

Strokes! They’re a devastating and very prevalent cause of morbidity and mortality. According to the CDC, they are the fifth leading cause of death in the United States. In your medical school and professional tenure, you will undoubtedly care for a patient who is suffering from an acute stroke, or who is living with the residual consequences of cerebrovascular disease. Obviously, your neurology rotation is where you’ll likely face these brain attacks head-on. But fear not! We’ve prepared a handy guide for you to help make sense of what to do during these stressful, crucial moments where TIME = BRAIN.

“Begin at the beginning and go on till you come to the end: then stop -Lewis Carroll

As a clinician and as a medical student, it’s up to you to identify the signs and symptoms of a suspected stroke.

Like most things in medicine, a focused history and physical exam will give you the information you need. The most important signs to look out for are acute motor or sensory changes in any part of the body (usually the limbs or face), a facial droop, and word-finding/speaking difficulties. Along with this history, it’s crucial to determine the “time last known well.”

When it comes to the physical, this isn’t the time for slow, in-depth bedside teaching. Usually the neurology or emergency medicine resident/fellow will perform the exam, as it must be done quickly and effectively. While this history and physical take place, the CT scanner should be warming up and clearing out any patients to make room for your possible acute stroke.

If time permits, this is the time to obtain some basic lab work, and employ oxygen therapy if the patient is hypoxemic. Important labs include BMP, CBC, and PT/PTT. Glucose levels might have been drawn by EMS, but will be included in your BMP. There are other labs in your stroke workup (e.g. lipid studies), but these aren’t as paramount in the hyperacute setting. You should also obtain an EKG; look for any embolus-generating rhythms like atrial fibrillation.

IMPORTANT: None of this work should delay your upcoming head CT. If the patient has terrible vascular access and labs would take a long time to obtain, defer them until after your CT scan.

After your quick H&P, obtain a non-contrast head CT scan. This will allow you to determine which arm of the treatment algorithm to proceed down by answering whether there’s bleeding in the brain. If there is, you’re dealing with a hemorrhagic stroke, and the last thing you want to do is thin this patient’s blood! Remember, blood on a CT scan will appear bright white (hyperdense), similar to bone (Figure 1). If the patient is bleeding in the brain, and your facility has the capabilities, consult neurosurgery or neuro-interventional radiology for possible intervention.

 

Figure 1. Acute hemorrhagic stroke. NO tPA!!!

If there is no bleeding, look for the findings of an ischemic stroke.

These are often more subtle and difficult for the untrained eye to appreciate. They include loss of gray-white matter differentiation and hypodensities. Take a look at a very non-subtle ischemic stroke (Figure 2) for reference. Just remember not to use the CT to diagnose an ischemic stroke so much as to rule out a hemorrhagic stroke.

 

Figure 2. Ischemic stroke. Muy grande.

If a patient is experiencing an acute ischemic stroke, there’s another necessary question to answer: are they eligible to receive tPA (alteplase)?

Remember from your hematology work that tPA (tissue plasminogen activator) will catalyze the conversion of the inactive plasmin-ogen (-ogens are inactive) to good ol’ clot-busting plasmin, which eats through fibrin clots.

Some caveats to tPA treatment

It’s certainly not without risks! Unsurprisingly, by effectively thinning the blood systematically, the major side effect is bleeding. Therefore, anyone with a bleeding diathesis (disposition) is excluded from receiving it. These include suspected subarachnoid hemorrhage, a history of intracranial hemorrhage, being on anticoagulation (think outpatient warfarin), and active internal bleeding.

Other criteria to exclude tPA treatment are the presence of cerebral blood vessel malformation (arterio-venous malformations or AVMs), aneurysms, seizures, a recent stroke within the last three months, and uncontrolled hypertension (systolic > 185 or diastolic > 110) despite attempts to lower it. A last important exclusion is if the patient’s neuro exam is rapidly improving. In that event, the stroke was more likely a TIA, and the risks of tPA aren’t worth a marginal benefit.

Finally, to administer tPA you need the time last known well to be less than three hours ago (do note that some criteria use a 4.5 hour window in a select group).

Because time equals brain, if the tissue has been ischemic for more than three hours, there will be little to no benefit in reperfusing the tissue it’s likely unsalvageable.

There are a number of other actions to take after these bigger decisions are made. If the patient had an ischemic stroke and you aren’t tPA-ing, you can use a gentler method of “anticoagulation”: 325 mg of oral aspirin. But no matter which type of stroke the patient had, you should gently lower blood pressure with labetalol or nitroprusside. You can afford to leave it a little on the higher side for an ischemic stroke to help with perfusion, but overall, high pressure banging on delicate vessels will cause more bleeding.

You always want to treat the patient’s underlying disease.

If atrial fibrillation caused an embolic stroke, you’ll likely employ rate control therapy and anticoagulation after the acute event. If diabetes mellitus caused vascular damage, aim to control blood glucose levels. Administering a statin is a certain consideration, even in the face of a normal lipid panel. Ensuring adequate nutrition is also key, keeping in mind that these patients may have swallowing difficulties. So is a consult to the speech pathology service to assess for dysphagia.

Lastly, early and aggressive rehabilitation is the most likely way for patients to make strides in retaining higher levels of functional independence.

Most patients will continue either on aspirin or clopidogrel for antiplatelet effects for secondary stroke prevention.

I know all of this material can be a lot to process  we’ll be the first to admit that it’s a bit convoluted  so here are the three key points to take home:

  • Obtain stat head CT without contrast if a stroke is suspected.

  • Decide whether or not the patient would benefit from tPA.

  • Manage any other underlying diseases and rehabilitate as soon as possible.

 

And, last but not least, don’t forget to download MST’s handy-dandy stroke pocket guide. It covers all this information in a much more concise (and aesthetically pleasing) way!