ExploreCME: Diving deep into PANCE Prep!

Stroke, TIA, And The Seconds That Matter

• Phillip

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SPEAKER_01:

Welcome back to the deep dive. Today we are tackling something that is, I mean, truly a critical mission in the clinic.

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Extremely time-sensitive.

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Absolutely. We're doing a custom deep dive into transient ischemic attacks or TIAs and cerebrovascular accidents.

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Or, you know, what everyone just calls a stroke.

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Right, strokes. And if you're currently prepping for the pansy or, you know, heading into your high acuity rotations, this one is really tailored for you. We're not just listing facts.

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Aaron Ross Powell No, we're building a framework following the pansy blueprint categories. We're going from the foundational science to history and physical diagnostics and then uh the huge topic of management.

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Aaron Ross Powell Okay, so let's start with a mental picture, something we can carry through this whole discussion. Think about the brain's blood supply like a like a garden's irrigation system.

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Aaron Ross Powell A network of garden hoses. That works perfectly.

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Trevor Burrus So if you have a transient ischemic attack, a TIA, it's like a hose gets briefly kinked.

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Yeah.

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The water flow slows, the plants in that area start to wilt a little, but then the kink releases and the flow comes back.

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Aaron Powell And no permanent damage. That's the key. Ischemia without an acute infarction.

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Aaron Powell But then you have an ischemic stroke. That accounts for what? Almost 90% of all strokes? With an ischemic stroke, that hose is permanently plugged, maybe a piece of plaque, a rock, whatever. It's blocked for good.

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Aaron Powell And the plants downstream, they die. That's infarction. The tissue is gone.

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Aaron Powell And finally there's the hemorrhagic stroke. This is when the hose actually bursts from high pressure.

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Aaron Powell Right. It floods the whole garden. The damage isn't just from lack of water, it's from the physical force of the bleed, the toxicity.

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The mass effect.

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Exactly. So that analogy really grounds the concepts. And for definitions, remember the timing. A TIA is clinically a deficit that lasts less than 24 hours.

SPEAKER_01:

Aaron Powell But usually it's much faster, right? Like under an hour?

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Oh yeah. Most resolve in under an hour, sometimes just minutes. A stroke means actual tissue death infarction.

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Yeah.

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The TIA is the warning siren.

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Okay. So let's get into the engine room. When that hose is plugged, what is actually killing the cells? What's the uh the microscopic breakdown?

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Aaron Ross Powell It's a pretty brutal cascade, actually. When you cut off oxygen and glucose, the ischemia, the neurons, they just start to panic.

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Aaron Powell And that panic triggers a chemical release.

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A massive one. They start dumping excitatory neuropeptides, mainly glutamate.

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Which is like an internal alarm the cell just can't shut off.

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Precisely. And all that glutamate forces a huge influx of calcium into the cell. Think of it like an internal flood. That calcium overload is what ultimately triggers the enzymes that lead to cell death.

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And that's the infarct core. What about the area around it, the penumbra?

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The penumbra is everything. Those are our wilting plants. That tissue is underperfused, it's struggling, but it's still alive.

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And our whole mission is to save it.

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Our entire mission in acute stroke care is to rescue that penumbra.

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Okay, let's distinguish the hemorrhagic types. Intraserebral hemorrhage, or ICH. That sounds like a problem of chronic poor maintenance.

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It often is. It's typically from years of poorly controlled hypertension. It weakens those tiny deep penetrating vessels until one just ruptures, usually in the basal ganglia or the pons.

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But a subaracnoid hemorrhage, an SAH, that's more of a structural flaw.

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Yeah, that's often a sudden rupture of a sacular aneurysm, the classic berry aneurysm, or maybe an AVM. It's a different mechanism entirely.

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Aaron Powell So where do these plugs even come from in an ischemic stroke? What are the big etiological categories?

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Aaron Ross Powell Okay. So number one is cardioembolic. The clot forms in the heart and travels to the brain.

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Atrial fibrillation is the big one there.

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AFib is by far the biggest culprit. But you also think about heart failure or even a paradoxical embolus that crosses through a patent form and oval PFO.

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Okay. Then category two is large vessel atherosclerosis.

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This is your classic plaque buildup, especially somewhere like the carotid bifurcation in the neck where there's turbulent flow. And that plaque can either grow to block the artery itself or pieces can break off and travel downstream, becoming artery-to-artery emboli.

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And the third type, the very distinct lachinar strokes.

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Right. These are tiny occlusions in those deep, small vessels, almost always a consequence of uncontrolled hypertension or diabetes. And clinically, if you see a pure motor deficit or a pure sensory deficit with no cortical signs.

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Like aphasia or neglect.

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Exactly. You should be thinking lachinar syndrome right away.

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All right, let's move this into the clinic. History taking and physical exam. This is a huge 16% on the pantsy blueprint for a reason. What's the one thing you have to establish first?

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When were they last known to be normal? Not when did the symptoms start, but when was the last time someone saw them acting completely normal?

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Because the entire treatment clock starts from that moment.

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It does. The onset is abrupt, and that timeline for intervention is measured in minutes. If we don't have that last known normal time, we lose options.

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And we immediately have to screen for the big risk factors.

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Hypertension, diabetes, hyperlipidemia, smoking, and aphib. Check those five boxes, you've probably found your cause.

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Let's focus on the subarachnoid hemorrhage history because that one can get missed.

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Oh yeah. It's the thunderclap headache. The key is that it reaches its absolute maximal intensity instantly.

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Not a gradual buildup.

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Zero to ten pain in seconds. Patients will say it's the worst headache of their life. You hear that, you have to rule out SAH.

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Okay, physical exam, clinical localization. Let's start with the big one, the anterior circulation, specifically the middle cerebral artery, the MCA.

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Right. The MCA is the most common site. So you're going to see contralateral hemoplegia and sensory loss. But remember, the homunculus, it's face and arm worse than the leg.

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And what about the eyes?

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You'll see a homonymous hemianopia, and the patient's gaze will deviate toward the side of the lesion.

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Aaron Ross Powell And then there are the high-level cognitive signs.

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Yes. If it's the dominant hemisphere, usually the left, you get aphasia, brochas, verniques. If it's the non-dominant hemisphere.

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Temospatial neglect.

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Exactly. The patient just completely ignores one half of the universe.

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Okay. Contrast that with the anterior cerebral artery, the ACA.

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ACA is the opposite distribution. It's leg worse than arm. And you often see these really interesting behavioral changes like a boolean, which is sort of a profound lack of initiative, and sometimes urinary incontinence.

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Now, the posterior circulation, the vertebasilar system, this always feels tricky. The symptoms can be so vague, vertigo, diplopia.

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It's a huge clinical challenge. But the absolute red flag you have to look for is cross signs.

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Meaning what? Exactly.

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It means you have an ipsilateral cranial nerve palsy, so a facial droop on the same side as the lesion, but contralateral hemoplegia on the opposite side of the body.

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So vertigo plus a facial droop on the opposite side of the weak arm and leg?

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That is posterior circulation until proven otherwise.

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So history and exam point to a stroke. Now we're in diagnostics. Time is brain. What is the very first imaging study? No exceptions.

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Non-contrast CT of the head. Immediately.

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To rule out the burst hose.

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Right. We cannot give a clot buster if there's a bleed. CT is fantastic for splitting acute blood.

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And if that CT is negative, but you're still sure there was a blockage, what's the gold standard?

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MRI, specifically diffusion-weighted imaging, or DWI. It can see the area of ischemia, the restricted water movement, hours before a CT might show anything.

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It's way more sensitive.

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Far more sensitive. And this is critical. We rely on DWI to see if actual tissue damage occurred.

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We also need to look at the vessels themselves, right? To see if there's a big plug we can physically remove.

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Absolutely. A CT angiography, a CTA, or an MRA is essential to look for a large vessel occlusion, an LVO. Finding an LVO changes the entire game.

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It opens the door to thrombectomy.

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And that's a decision that has to be made in minutes.

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While all this imaging is happening, what are the must-have labs?

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You need a finger stick glucose at the bedside immediately to rule out hypoglycemia, which is a great stroke mimic, and then a CVC in coags.

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What if your patient is young, no risk factors?

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Then you have to dig deeper. Think about a toxicology screen, a hypercoagulable workup.

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And don't forget the heart.

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Never. Mandatory ECG looking for AFib, and an echocardiogram, usually with a bubble study, to look for a PFO. And remember, you might not see the AFib right away.

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Right. Up to 20% of these patients have occult AFib you only find later with monitoring.

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Exactly.

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Okay, so that leads us to formulating the diagnosis. We've ruled out the mimics. For the TIA patients, we have to stratify their risk, right?

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This is where the ABCD2 score is absolutely essential. It tells you their immediate risk of having a full-blown stroke.

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And it dictates who gets admitted.

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It does. Let's run through it. A is for age 60 or older, B is for blood pressure of 140 over 90 or higher. C is for clinical features.

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Weakness is two points, speech deficit is one.

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Correct. D is for duration, 60 minutes or more, gets you two points. And the last D is for diabetes.

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And a score of four or more is considered high risk.

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High risk, and they need to be hospitalized for an expedited workup. The risk of stroke in the next 48 hours is just too high to send them home.

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All right, let's shift into the really acute phase. Clinical intervention. For an ischemic stroke, let's talk thrombolysis.

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Okay. IVRTPA altoplase. The window is within three hours, sometimes extended to four and a half. But before you even think about giving it, blood pressure. Blood pressure. It's the most critical prerequisite. You have to understand that the biggest risk of TPA is causing a bleed.

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A hemorrhagic transformation.

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So you have to get that systolic blood pressure under 185 and the diastolic under 110 before you push the drug. If you can't, you can't give it. End of story.

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Aaron Powell What if the CTA shows that LVO, that big physical blockage?

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Trevor Burrus Then you're thinking beyond just chemical clot busting. You're thinking mechanical thrombectomy.

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Physically going in and pulling the clot out.

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Literally sending an interventionalist to retrieve the clot. And the beauty is the window is much longer, up to six hours, and for some patients, even up to 24 hours if they have salvageable tissue.

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What about BP management for patients who are not getting TPA?

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For them, we actually allow permissive hypertension. Up to 220, overall header to 20 sometimes.

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Why is that?

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Because the brain is trying to perfuse that penumbra through tiny collateral vessels, and it needs high pressure to do that. If you drop the pressure too fast, you can actually extend the infarct.

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And one more critical piece of supportive care.

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A swallow evaluation.

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Oh.

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Always before any food, any pills, any water, you have to prevent aspiration pneumonia.

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Okay, now let's flip the script. Acute hemorrhagic stroke. The BP goal is the complete opposite.

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Completely inverted. For an ICH, you need to aggressively lower that systolic pressure, targeting 140, to try and stop the bleeding, and you have to immediately reverse any coagulopathy.

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And for SAH, there's that specific prophylactic medication.

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Yes, pneumatopene. You have to give it for 21 days to prevent cerebral vasospasm, which is a delayed ischemic complication from the blood irritating the vessels. And of course, you need surgical console for potential decompression or aneurysm clipping.

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Let's move to the long name: health maintenance and therapeutics. After an ischemic stroke, if it wasn't cardioembolic, what's the plan?

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Antiplatelet therapy. Usually aspirin started after 24 hours if they got TPA. But for a high-risk TIA or a very minor stroke, the standard is now dual antiplatelet therapy DAPT.

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Aspirin plus klepinogril.

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Right. For 21 days. That short burst really reduces the early recurrence risk. Then you go to monotherapy.

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And if the cause was cardioembolic from AFib?

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Then they need long-term anticoagulation. A DOAC is now preferred over warfarin for nonvalvular AFib. A key pearl here is we generally don't bridge with heparin in the acute phase. It's too risky.

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And lipid management is a must for anyone with atherosclerosis.

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Oh, non-negotiable. High intensity statin like a torvostatin 80.

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Okay.

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You're not just trying to get the LDL below 100, you're aggressively targeting below 70.

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Okay, final section. Preventive measures beyond medication. What are the surgical options?

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Two main ones. First, carotid endarterectomy or CEA. You're physically cleaning the plaque out of the carotid artery. That's for patients with symptomatic stenosis of 70 to 99%. And the second PFO closure. This is for younger patients, say under 60, who have a cryptogenic stroke, meaning we can't find another cause, and they have a PFO with a documented shunt. You close the hole.

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So what does this all mean? We've gone from the foundational science through the rapid-fire diagnostics all the way to acute interventions and long-term prevention. We've really hit all those critical PNC task areas.

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We have. And I want to leave you with one final thought, something that really revolves around the power of our diagnostic tools.

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Okay.

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Let's say a patient comes in with symptoms that perfectly fit the clinical definition of a TIA. They were weak for five minutes and now they are completely back to normal.

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Okay. Classic TIA presentation.

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But you get an MRI and the DWI sequence is positive. It shows a small acute infarction. What's the diagnosis now?

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It's it's not a TIA anymore. It's a stroke.

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Correct. The imaging overrides the clinical definition. You have to treat that patient as if they had a minor stroke. That subtle finding completely changes your management because their risk of recurrence is dramatically higher.

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The absence of symptoms is not the absence of injury.

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That is a clinical truth you must never ever forget.

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A really powerful way to think about how diagnostics can completely reframe the clinical picture. That is where we will leave our deep dive for today. Integrate this framework, and you'll be ready.