CONTENTS
- Rapid Reference 🚀
- Core topics in ICU stroke management
- Specific management situations
- Background information
- Goals of this chapter
- Stroke anatomy
- Physiology: Core infarct vs. ischemic penumbra
- Diagnosis: Stroke mimics
- Basic workup
- Imaging & interventional radiology
- Podcast
- Questions & discussion
- Pitfalls
thrombolysis/endovascular therapy
- If potential candidate, activate a stroke code.
labs to consider
- STAT fingerstick glucose.
- Complete blood count.
- Electrolytes including Ca/Mg/Phos.
- Liver function tests.
- Coagulation studies:
- Generally PT, PTT, fibrinogen.
- Anti-Xa for patients on oral Xa inhibitors (e.g., apiXaban).
- Blood cultures x2 if concern for endocarditis (e.g., fever or history of IV drug use).
- Pregnancy test as appropriate.
blood pressure control 📖
- Hypertension:
- No intervention: permissive HTN (<220/<120).
- Status post thrombolysis: <180/<105.
- Status post endovascular therapy:
- TICI 0-2a flow: SBP 120-180 mm.
- TICI 2b-3 flow: SBP 120-160 mm.
- May use labetalol boluses PRN, or clevidipine/nicardipine infusion.
- Maintenance IV fluid may be considered for patients who are NPO with minimal fluid inputs, but I/O balance should be followed carefully with avoidance of volume overload.
antiplatelet therapy 📖
- Antiplatelet therapy with aspirin (or clopidogrel, if aspirin allergy).
- Start with a loading dose (325 mg aspirin, or 300 mg clopidogrel).
- Contraindications include:
- (1) Status post thrombolysis (generally delayed until 24 hours after thrombolysis and review of post-thrombolysis CT scan).
- (2) Decompressive craniectomy is possible.
DVT prophylaxis 📖
- Enoxaparin is preferred, if renal function allows (GFR >30 ml/min).
- Hold chemical DVT prophylaxis for 24 hours following thrombolysis (use sequential compression devices).
other
- If febrile (>38C), investigate for infection and start scheduled acetaminophen 💉 (e.g., 1 gram q6hrs for most patients).
- Consider atorvastatin 80 mg daily (if no contraindication and stroke is thought to be atherosclerotic in origin).
management of hypertension
Bp for patients not receiving any intervention
- Hypertension is a normal, physiologic response to improve perfusion of the brain. This should generally be left alone for the first ~24-48 hours. Reduction in blood pressure is indicated only if:
- Systolic >220 mm.
- Diastolic >120 mm.
- Hypertensive emergency with target organ damage caused by hypertension (e.g., myocardial ischemia, hypertensive nephropathy, pulmonary edema). Hypertensive emergency is discussed further here 📖.
- If blood pressure reduction is needed, this should be gentle (e.g., ~15% reduction during the first 24 hours, unless there is target organ damage).(33512282)
Bp for patients receiving thrombolysis
- Before thrombolysis: Target Bp <185/<110.(31662037)
- After thrombolysis: Target Bp <180/<105 for 24 hours.(31662037)
Bp control for patients receiving endovascular therapy
- Peri-procedural period: For patients undergoing intubation prior to endovascular therapy, avoid hypotension. Even small blood pressure reductions (e.g., >10% decrease) may correlate with worse outcomes. A reasonable blood pressure target for most patients in the periprocedural period might be a systolic BP of ~140-180 mm.(31346678)
- Following thrombectomy:
- Most guidelines recommend <180/105 (similar to post-thrombolysis patients).(31662037)
- However, blood pressure targets may vary depending on the success of revascularization. Common targets are:
- The neurointerventionalist will often recommend an individualized blood pressure target.
preferred agents for lowering blood pressure
- Nicardipine 💉 or clevidipine 💉 infusions are highly effective. 📖
- PRN labetalol boluses may be used if the blood pressure is only slightly above target (the dosing and strategy for labetalol use are discussed further here 💉).
management of hypotension
- Hypotension is potentially dangerous in this situation, since it may promote cerebral hypoperfusion. Several studies have found an association between hypotension and worse neurological outcomes.(36333037)
- Evaluate for the etiology of hypotension and treat any causes (e.g., hypovolemia).
- Discontinue any antihypertensives.
- The use of vasopressors here is not evidence-based, but could be reasonable within specific patient scenarios (e.g., the perfusion-dependent patient whose neurological exam worsens due to hypotension, so vasopressors are started and this causes an improvement in the neurological exam).
volume management
- Avoiding hypotension is important, as this could compromise perfusion of ischemic tissue.
- A euvolemic state should be targeted.
- Indications to consider IV fluid may include:
- (1) Hypotensive patients, especially if examination or clinical history suggests hypovolemia.
- (2) Patients who are NPO for extended periods.
- (3) Patients with widely labile blood pressure and evidence of hypovolemia (the combination of hypovolemia plus variable systemic vasoconstriction may cause wide blood pressure swings). 📖
- Follow input/output balance and ensure that patients don't become hypervolemic.
anticoagulation for cardioembolic infarction in context of atrial fibrillation
- Two main considerations apply here:
- (a) Anticoagulation may increase the risk of hemorrhagic conversion.
- (b) Anticoagulation may decrease the risk of another stroke.
- General recommendations are to start oral anticoagulation with warfarin 4-14 days after the stroke.(31662037)
- Warfarin may be preferable to a direct oral anticoagulant (DOAC), since warfarin can be rapidly reversed if hemorrhagic transformation occurs. Bridging with heparin is not generally beneficial.
- For larger strokes with a higher risk of hemorrhagic transformation, it makes sense to delay anticoagulation initiation towards closer to the ~14 day mark.
antiplatelet therapy
- Aspirin is one of the most strongly evidence-based therapies for acute stroke (demonstrated to reduce recurrence and mortality).(10835439)
- For patients not undergoing thrombolysis:
- Start aspirin with a loading dose of 325 mg orally or 300 mg rectally, followed by 81 mg daily.
- In patients with aspirin allergy: use clopidogrel instead (beginning with a 300-mg loading dose).
- For patients treated with thrombolysis: delay initiation of antiplatelet therapy until after reviewing the CT scan performed ~24 hours after thrombolysis.
dual antiplatelet therapy
- Dual antiplatelet therapy has shown benefit in acute ischemic stroke, but this has been studied only in high-risk TIA and minor stroke. As such, this data will not apply to most critically ill patients with acute ischemic stroke.
- Dual antiplatelet therapy is not generally recommended for patients with moderate or large strokes.
DVT prophylaxis
- Low-molecular-weight heparin is preferred for DVT prophylaxis.(17448820)
- Patients treated with thrombolysis or successful endovascular thrombectomy: delay chemical DVT prophylaxis for 24 hours.
- Patients unable to receive chemical DVT prophylaxis should be managed with intermittent pneumatic compression.(26418530)
management of hypoxemia
- Guidelines recommend targeting an oxygen saturation >94%.(31662037)
- Supplemental oxygen is not recommended for patients who are not hypoxemic.
- Ischemic stroke by itself shouldn't generally cause hypoxemia. Thus, hypoxemia should be investigated to determine an underlying cause (e.g., aspiration pneumonitis).
intubation & mechanical ventilation
- Indications for intubation include:
- Respiratory failure (especially hypercapnia that may be exacerbating elevated intracranial pressure).
- Bulbar dysfunction with inability to protect the airway.
- To facilitate procedural sedation (e.g., endovascular therapy).
- Impaired consciousness with ongoing neuroworsening.
- Anterior territory strokes usually don't impair airway protection, unless there is edema compressing other areas of the brain (i.e., malignant MCA syndrome). Thus, the need for airway protection in an anterior stroke should trigger consideration for whether a decompressive craniectomy is indicated (more on this below 📖).
- Brainstem and thalamic strokes may directly affect both level of consciousness and respiratory centers, which may necessitate intubation.(36333037)
- Erratic breathing patterns may associate with certain strokes (discussed further here 📖 ).
epidemiology
- Overall, there is a <10% incidence of seizure. Risk factors include:
- Higher stroke severity.
- Cortical involvement, especially involvement of multiple lobes.
- Hemorrhagic conversion.
- In the context of acute ischemic stroke, seizure may reflect hemorrhagic transformation.
possible indications for continuous EEG monitoring (LaRoche 2018)
- Fluctuating neurologic deficits.
- Unexplained coma or altered level of consciousness.
- Following a seizure or status epilepticus, if the patient has a persistently abnormal mental status.
- Seizures or status epilepticus that requires active therapy.
- Treatment precludes reliable neurologic examination (e.g., paralysis).
- Clinical suspicion of seizure (e.g., twitching).
management
- Seizure prophylaxis is not recommended.(31662037)
- If seizures occur, they should be treated in the usual fashion. Ongoing use of a maintenance antiepileptic agent is generally continued to prevent recurrence (at least in the short term). 📖
dysphagia evaluation
- Dysphagia is common following ischemic stroke.
- All patients should receive a bedside dysphagia screening examination prior to initiation of a diet (e.g., supervised ability to drink a glass of water by a bedside nurse or speech and language therapist).
- Patients who fail the bedside screening examination may require more comprehensive dysphagia evaluation.
early enteral nutritional support
- Patients who are intubated should have enteral nutrition started within 24-48 hours, as is standard for any critically ill patient.📖
- Patients who are not intubated and have substantial dysphagia should have enteral nutrition started within <7 days.(31662037) Feeding may be provided via a small-bore, flexible feeding tube.📖 A small-bore feeding tube is often adequate to provide nutritional support and enteral medication access for some weeks, during which the patient's ability to swallow would hopefully recover.
- If patients have persistent dysphagia for >2-3 weeks, then the utility of a percutaneous gastrostomy tube (PEG tube) may be considered.
statin
- High-intensity statin (e.g., atorvastatin 80 mg) is often recommended based on the SPARCL trial.(16899775)
fever investigation & treatment 📖
- Elevated temperature (>38C) should be investigated and treated aggressively.(31662037) For example, this might include an infection workup 📖 followed by scheduled acetaminophen to suppress fever (e.g., 1 gram q6hr scheduled). Simply providing individual doses of acetaminophen PRN for every fever spike is less likely to achieve consistent temperature control. If acetaminophen fails to achieve normothermia, physical cooling should be initiated (e.g., cooling blankets).(31346678)
- Note that the cutoff of an actionable temperature here (>38 C) is less than the usual definition of fever in the ICU (>38.3 C).
- Unlike intracranial hemorrhage, ischemic stroke is unlikely to cause a neurogenic fever. 📖
glycemic control
- Hyperglycemia correlates with worse outcomes in stroke, as is generally true within critical care. However, the risks-vs-benefits of lowering glucose remain unclear. Hypoglycemia is certainly quite detrimental to an injured brain.
- The SHINE trial of tight glycemic control (targeting a glucose of 80-130 mg/dL) found that tight glycemic control actually caused harm (in terms of an increased risk of severe hypoglycemia).(31334795)
- The usual approach to glycemic control among critically ill patients may be reasonable for these patients. 📖
differential diagnosis: more common considerations
- Hypoglycemia.
- Infarct extension, reocclusion, or additional infarctions (e.g., due to additional embolic events).
- Hemorrhagic transformation (may occur even without thrombolysis or endovascular therapy).
- Edema (e.g., malignant MCA syndrome).
- Elevated intracranial pressure (e.g., due to a cerebellar stroke that obstructs the cerebral aqueduct).
- Blood pressure:
- Hypertension causing PRES (posterior reversible encephalopathy syndrome).
- Excessive drop in blood pressure causing brain malperfusion.
- Medication effects (e.g., procedural sedation).
- Seizure (including nonconvulsive seizures and postictal state).
approach: tests to consider
- STAT fingerstick glucose.
- If relative hypotension causing brain malperfusion is suspected, may elevate the blood pressure using vasopressors and repeat the clinical examination.(Albin 2022)
- STAT CT scan (evaluate for hemorrhage, edema, or elevated intracranial pressure).
- EEG (especially consider for altered mental status that remains unexplained despite neuroimaging).
basics
- Angioedema is a rare complication of thrombolysis that occurs with a frequency of ~2%. It usually begins 30-120 minutes after tPA infusion.(Louis 2021) This is a physiological class effect that results from augmenting plasmin activity, so it may result from the use of any thrombolytic (e.g., tPA or tenecteplase).
- Thrombolytic-induced angioedema is a form of bradykinin-mediated angioedema, based on the mechanism shown above.(30215283) Clinically, bradykinin-mediated angioedema is often asymmetric angioedema that frequently involves the tongue or lips without involving other organ systems (e.g., absence of pruritus, hypotension, bronchospasm). 📖
- The risk of angioedema is increased in patients taking ACE inhibitors or patients with C1-esterase deficiency (as expected, since these cause increased bradykinin levels).(26288671)
management
- There is no high-quality evidence on this topic.
- If thrombolytic is still being infused, the infusion should be discontinued immediately. Discontinue any ACE inhibitors as well.
- In many cases, angioedema may be mild and self-limited, so close observation may be all that is necessary. Given that thrombolytics have a short half-life, most cases may be expected to improve over time. However, if angioedema is rapidly enlarging and threatening the airway, then intubation may be necessary.
- Tranexamic acid would theoretically be beneficial here, but lacks evidentiary support. Additionally, tranexamic acid could abrogate any therapeutic benefits of thrombolysis on the stroke.
- Mechanistically, C1 inhibitor concentrate might be expected to be the best therapy here, with success reported in one case.(27174372) The use of icatibant for thrombolytic-induced angioedema has been described, but this medication is not widely available.(29653785)
- ⚠️ Patients with angioedema following thrombolysis that is clinically consistent with bradykinin-mediated angioedema are not expected to respond to treatments directed at histamine-mediated angioedema (e.g., epinephrine, steroid, and antihistamines).
basics
- Hemorrhagic transformation may result from the natural evolution of ischemic stroke, usually within the first week.
- “Hemorrhagic transformation” is a very broad term, which encompasses roughly three entities:
- (#1) Petechial hemorrhages: Most hemorrhagic transformations are small, petechial hemorrhages of little clinical significance.
- (#2) Asymptomatic hematomas: Small hematomas can occur within infarcted brain. If the hematoma is small and it occurs in a region of brain tissue which is already nonfunctional, this may not affect clinical outcome.
- (#3) Symptomatic hematomas: Large hematomas may exert mass effect, cause vasogenic edema, and worsen clinical outcomes. Symptomatic hematoma formation occurs in ~2% of patients without thrombolysis, or up to ~6% of patients treated with thrombolysis.(32668115)
- Radiographically, hemorrhagic transformation may be classified as follows:
- Hemorrhagic infarct type 1 (HI-1): Petechial hemorrhages at the margins.
- Hemorrhagic infarct type 2 (HI-2): Petechial hemorrhages throughout the infarct, no mass effect.
- Parenchymal hematoma type 1 (PH-1): Hemorrhage of <30% of the stroke volume with mild mass effect.
- Parenchymal hematoma type 2 (PH-2): Hemorrhage of >30% of the stroke volume with substantial mass effect, or hemorrhagic extension beyond the infarct.
risk factors for hemorrhagic transformation
- Large infarct size (e.g., hypodensity in more than a third of the MCA territory).
- Coagulopathy (e.g., therapeutic anticoagulation or thrombolysis).
- Older age.
- Diabetes mellitus, hyperglycemia.
- Uncontrolled hypertension.(32224752)
clinical presentation of symptomatic hemorrhagic transformation
- Neurological deterioration (may have focal symptoms, depending on the location of the stroke).
- ⚠️ It may be very difficult to differentiate neurological deterioration due to progression of acute ischemic stroke versus superimposed hemorrhage. When in doubt, there should be a low threshold to obtain a CT scan.
- Headache, nausea/vomiting.
- Acute spike in blood pressure.
management of symptomatic hemorrhagic transformation
- Coagulation management:
- Immediately stop thrombolytic if this is still infusing. Discontinue any other anticoagulating medications.
- Reverse any relevant coagulopathies. Especially if the patient recently received thrombolysis, this should be aggressively reversed.📖
- Measure coagulation labs as a baseline (INR, PTT, fibrinogen, complete blood count, type & cross-match). This shouldn't delay the administration of blood products to reverse known coagulopathies (e.g., thrombolysis), but it may help guide ongoing coagulation optimization.(33952393)
- Additional aspects of intracranial hemorrhage management here: 📖.
basics
- Proximal MCA infarction may lead to marked edema causing herniation and death (e.g., malignant MCA syndrome). Edema usually peaks after 3-4 days, but reperfusion may accelerate this.(Shutter 2019)
- Decompressive craniectomy may prevent herniation and death, by opening of a generous bone window.
- Patients with malignant MCA syndrome can have a normal intracranial pressure (ICP). Deterioration results from tissue shifts, rather than having a globally elevated intracranial pressure.(Nelson, 2020)
risk factors for malignant MCA syndrome
- Younger patients (who have less underlying atrophy and thus less space to accommodate edema).
- Dense MCA sign indicates a proximal MCA infarction with a large territory at risk.
- Large amount of territory involved, for example:
- >50% of MCA territory shows hypodense edema on CT scan.
- Involvement of multiple vascular territories (e.g., combined infarction of ACA plus MCA territories).
- MRI diffusion weighted imaging (DWI) volume >82 ml if performed within six hours of stroke onset.(36333037)
- Mass effect is seen on imaging (e.g., midline shift, effacement of the ipsilateral sulci and lateral ventricles), especially if this occurs rapidly.
- Rapid edema development:
- Frank hypodensity on CT scan within the first six hours.(Nelson, 2020)
- Early development of encephalopathy.(36333037)
initial management of MCA edema
- There is usually no role for invasive ICP monitoring, since the global ICP may not necessarily be elevated.(Louis 2021) Clinical examination as well as interval CT scanning (e.g., q24 hours plus PRN) is used to track the patient's progress.
- AHA guidelines indicate that it's reasonable to use a decrease in level of consciousness attributed to brain swelling as a trigger for decompressive craniectomy.(31662037)
- Medical therapies for ICP elevation (e.g., hypertonic therapy) should be used to treat edema. Medical management alone will usually fail. However, medical therapies can be used as a temporizing measure, to help bridge the patient to craniectomy. 📖
craniectomy for MCA syndrome
- For malignant MCA syndrome, craniectomy is undoubtedly a life-saving procedure. The thorny issue is what quality of life would patients subsequently be left with. Surviving patients are likely to be left with severe disability.(Nelson, 2020)
- The best surgical candidates will have the following characteristics:
- Younger age (<60 years old).
- Earlier surgery (within <24-48 hours of stroke onset, and prior to any herniation symptoms).(36333037)
- Surgical intervention prior to irreversible secondary brain injury.
- The value of decompressive craniectomy among patients >60 years old is questionable. The DESTINY-II trial involved 112 patients over 60 years old with large MCA infarctions (inclusion required involvement of more than two thirds of the MCA territory, reduced level of consciousness, and NIH Stroke Scale scores of >14 or >19 in nondominant or dominant infarctions, respectively). Regardless of whether patients were randomized to medical therapy or decompressive craniectomy, no patients in either group achieved functional independence (Modified Rankin Scale 0-2). There were no differences in the number of patients with moderate disability after a year (Modified Rankin Scale 3). Craniectomy prevented death by increasing the number of patients with moderately severe or severe disability. 🌊 (24645942)
- For a discussion of patient management status following craniectomy: 📖
potential danger
- Cerebellar infarction is problematic due to the limited space within the posterior fossa. Consequences of swelling include:
- (#1) Noncommunicating hydrocephalus could result from compression of the cerebral aqueduct or the fourth ventricle.
- (#2) If more severe, swelling could compress the adjacent brainstem.
- Risk factors:
- Occlusion of the posterior inferior cerebellar artery (PICA) is the most worrisome, since it supplies the largest portion of the cerebellum.(Nelson, 2020)
- Involvement of the cerebellar vermis is associated with increased likelihood of deterioration.
management
- Cerebellar edema with clinical deterioration is generally regarded as an indication for suboccipital craniectomy.(Shutter 2019)
- ⚠️ Note that among patients with noncommunicating hydrocephalus, treatment with an external ventricular drain alone (without suboccipital craniectomy) may lead to upward transtentorial herniation of the cerebellum.
- Patients undergoing decompressive suboccipital craniectomy for cerebellar infarction tend to have better outcomes than patients undergoing decompressive craniectomy for MCA infarction, because the underlying stroke is smaller and involves less eloquent areas of the brain (with 35-40% of patients achieving functional independence).(Nelson, 2020)
- For a discussion of patient management following posterior fossa surgery: 📖
basics
- Moyamoya disease is a chronic, progressive, idiopathic, occlusive disease involving the internal carotid artery, proximal ACA (anterior cerebral artery), and proximal MCA (middle cerebral artery). Disease may be bilateral or unilateral. Hypertrophied small collateral vessels generate a characteristic “puff of smoke” appearance on angiography.
- Moyamoya syndrome refers to vessel stenosis with collateralization that resembles Moyamoya disease, but it is due to a known underlying cause. Such causes include: (Louis 2021)
- Genetic diseases (Sickle cell disease, trisomy 21, pseudoxanthoma elasticum, glycogen storage disease type 1a, Fabry disease, neurofibromatosis type I, polycystic kidney disease, tissue plasminogen activator deficiency).
- CNS infections (tuberculosis, EBV infection).
- Inflammatory diseases (eosinophilic angiitis, Kawasaki syndrome, Sjogrens disease, lupus).
- Postradiation vasculopathy.
- Fibromuscular dysplasia.
epidemiology
- Women of East Asian descent seem to be most often affected.
- Among adults, the peak incidence occurs among patients in their 40s.
clinical manifestations include:
- (1) Acute ischemic stroke: Moyamoya disease most often presents with an ischemic event.
- (2) Intracerebral hemorrhage:
- About a third of patients present with an intracranial hemorrhage resulting from fragile collaterals and/or false aneurysms.(34618759)
- Hemorrhage is most commonly located in the basal ganglia.
- Subarachnoid hemorrhage may occur.
- (3) Recurrent headaches.
radiology
- CT scan may show evidence of ischemic stroke and/or hemorrhage.
- MRI: (Tang 2015)
- T2 may show collateral flow voids in the basal ganglia and basilar cistern.
- FLAIR may show sulcal brightness, due to slow flow via pial collaterals.
- Angiography:
- Stenosis/occlusion of distal internal carotid artery or proximal arteries within the circle of Willis.
- Hypertrophy of collateral capillaries occurs as a compensatory mechanism, which may resemble a “puff of smoke” on angiography.
- (Going further: Momoya disease in Radiopaedia 🌊)
management
- Surgical revascularization may be indicated (e.g., bypass from the superficial temporal artery to the middle cerebral artery). Revascularization may run the risk of cerebral hyperperfusion syndrome, due to rapid restoration of blood flow.
- Hypertrophied, fragile collateral arteries have a tendency to bleed. Therefore, some caution should be exercised with anticoagulation. Nonetheless, aspirin is commonly prescribed to patients with ischemic symptoms. (Louis 2021)
Acute ischemic stroke is an enormously broad topic, which alone is the subject of many textbooks. It would be impossible to provide detailed information about all aspects of ischemic stroke within a single chapter.
The intensivist's role in stroke care is a humble one – predominantly to assist with supportive management. Most strokes will already be diagnosed prior to ICU arrival. Likewise, major treatment decisions regarding thrombolysis and endovascular therapy have generally already been made (or will be determined by neurology and neuroradiology teams).
The goal of this chapter is to provide a foundation for understanding stroke care, with an emphasis on supportive therapies. Some aspects (e.g., when to pursue thrombolysis and/or endovascular therapy) are omitted since they are beyond the scope of practice of most intensivists. The stroke neurology team will typically focus on issues surrounding neuroimaging, thrombolysis, and endovascular therapy. Meanwhile, the ICU team may simultaneously focus on supportive care (e.g., airway assessment, blood pressure control, hemodynamic optimization, vascular access, electrolyte and glucose management). Dividing up the tasks with ongoing close communication may allow for rapid and comprehensive patient management.
anterior cerebral artery syndromes
- Either side:
- Contralateral leg weakness and sensory loss.
- Frontal lobe dysfunction:
- Poor judgement, apraxia.
- Flat affect, abulia = apathy and reduced speech.
- Imitation behavior: automatic and involuntary imitation of the examiner's movements.(Louis 2021)
- Incontinence.
- “Alien hand sign” or hemiballism – one hand acts involuntarily.
- Nondominant hemisphere:
- Acute confusional state.
- Contralateral hemineglect may occur (particularly when that is the left).
- Dominant hemisphere:
- Transcortical motor aphasia (due to involvement of the supplementary motor area). This is similar to Broca's aphasia, but with preservation of repetition.
bilateral anterior cerebral artery occlusion
- Some patients have an anatomic variant where the proximal anterior cerebral arteries share a common trunk (A1) (this variant is called an “Azygous ACA”).
- Occlusion of this shared artery will cause bilateral anterior cerebral artery occlusion. The combination of bilateral leg weakness and incontinence may mimic a spinal cord lesion. Other clinical findings may include executive dysfunction with abulia (paucity of spontaneous behaviors) or even akinetic mutism (awake unresponsiveness).(Louis 2021)
anatomy of the anterior cerebral artery (ACA)
- The recurrent artery of Huebner comes off the proximal ACA, providing blood to parts of the internal capsule, globus pallidus, putamen, and caudate head (figure below). Infarction of this artery may cause contralateral hemiparesis and/or movement disorder, abulia, incontinence, and dysarthria. (Louis 2021)
- Nomenclature:
- A1 = ACA proximal to the anterior communicating artery.
- A2 = ACA distal to the anterior communicating artery.
effects of superior MCA trunk occlusion
- Either side:
- Contralateral hemiparesis of face and arm.
- May have contralateral hemisensory loss involving face and arm.
- Conjugate ipsilateral eye deviation.
- Nondominant hemisphere:
- Neglect of the contralateral side of space (including visual, auditory, and tactile stimuli).
- Anosognosia (lack of insight into neurological deficits).
- Dominant hemisphere:
- Broca's aphasia.
- Bilateral apraxia (inability to perform purposeful movements such as brushing teeth).
effects of inferior MCA trunk occlusion
- Either side:
- Contralateral superior quadrantanopia.
- Nondominant side:
- Severe left hemineglect.
- Anosognosia (unawareness of deficits).
- Motor neglect (not moving left side, yet strength is intact – for example, may be able to withdraw from pain).
- Sensory neglect.
- Severe left hemineglect.
- Dominant side:
- Wernicke's aphasia.
- ⚠️ Patients may appear confused or psychotic. Given intact sensation and motor function, this can be difficult to sort out from a primary psychiatric event or diffuse metabolic encephalopathy.
proximal MCA syndromes (occlusion near the base of M1)
- Either side:
- Contralateral hemiplegia involving the face and arm > leg.
- Contralateral hemisensory loss.
- Contralateral hemianopia.
- Ipsilateral conjugate eye deviation.
- Nondominant hemisphere:
- Hemispatial neglect (generally of the left side).
- Anosognosia.
- Drowsiness and eyelid-opening apraxia (less common).
- Dominant hemisphere:
- Global aphasia.
occlusion of the deep territory (lenticulostriate arteries supplying the basal ganglia and internal capsule)
- Primary effect: Contralateral hemiparesis (may mimic a lacunar syndrome).
- Larger infarcts may mimic cortical deficits, by functionally cutting off the cortex from the rest of the brain. For example:
- Nondominant hemisphere: Mild hemineglect.
- Dominant hemisphere: Dysarthria, with sparing of repetition (similar to transcortical aphasia).
anatomy of the MCA
- M1 = Horizontal portion which gives off lenticulostriate arteries.
- M2 (aka, insular segment) = Short portion of MCA running within the Sylvian fissure.
- M2 occurs before the MCA splits into superior vs. inferior divisions.
- M2 occlusions may be amenable to endovascular therapy.
- M3 (inferior)= Cortical branches of the MCA that run along the temporal lobe. This supplies the lateral surface of the temporal lobe and the inferior parietal lobe.
- M4 (superior) = Cortical branches of MCA that run along the parietal lobe. This supplies the frontal and superior parietal lobes.
clinical consequences of infarction may include:
- Triple H:
- Contralateral hemiparesis.
- Contralateral hemisensory loss.
- Contralateral hemianopia.
- “Cortical signs” (e.g., hemineglect) may or may not be seen. An absence of cortical signs may point towards a choroidal infarction (as opposed to an MCA infarct).
anatomy
- The anterior choroidal artery originates directly from the internal carotid artery.
- Structures supplied by this artery:
- Posterior thalamus (including the lateral geniculate nucleus, which relays sensory information to the cortex).
- Internal capsule (including descending motor and ascending thalamocortical pathways).
posterior cerebral artery syndromes
- Either side:
- Hemianopia or superior quadrantanopia.
- Thalamic involvement may cause contralateral sensory loss (ventroposterolateral nuclei) or reduced arousal.
- Uncommonly, may cause contralateral hemiplegia (due to involvement of the internal capsule).
- Dominant hemisphere:
- Alexia without agraphia (patients are able to write but not read). This results from infarction of the splenium of the corpus callosum, thereby cutting off visual information from the language processing centers.
- Difficulty naming objects (transcortical sensory aphasia).
- Visual agnosia (inability to describe what an object is used for).
- Inferomedial temporal lobe infarction may cause global amnesia or agitated delirium.(Louis 2021)
- Thalamic aphasia (if the thalamus is involved).
- Nondominant hemisphere:
- Prosopagnosia (inability to recognize faces).
- Bilateral infarctions
- Anton syndrome: cortical blindness that is unrecognized by the patient, who may confabulate what they are seeing.
- Charles Bonnet syndrome: release visual hallucinations.
- Agitated delirium may occur. (Louis 2021)
anatomy of the posterior cerebral artery (PCA)
- PCA supplies the posterior thalamus via small thalamoperforator arteries coming off the proximal PCA, as well as longer arteries (posterior choroidal artery and thalamogeniculate arteries).
- Branches of the PCA supply the midbrain, inferomedial temporal lobe, and occipital lobe
The thalami are critical relay and processing centers involved in connections between the cortex, basal ganglia, midbrain, and cerebellum. The thalami consist of about two dozen nuclei that are closely packed together. The discussion below highlights some key clinical aspects of the more common thalamic infarctions.
anterior thalamic infarct (12%)
- Vascular supply: tuberothalamic arteries originate from the posterior communicating artery.
- Clinical effects seem to result largely from impacts on the limbic system (dorsomedial nucleus). These may include disorientation, euphoria, apathy, lack of insight or spontaneity, anterograde memory impairment, and transcortical aphasia (for left-sided lesions; this involves halting speech with preserved repetition).(29460331)
paramedian thalamic infarct (35%)
- Vascular supply: paramedian thalamic arteries arising from the P1 segment of the posterior cerebral artery (PCA). Several anatomic variants exist, in some cases with both paramedian thalamic arteries originating from a single PCA artery termed the “Artery of Percheron” (such that a PCA infarction could cause bilateral thalamic infarctions).
- Differential diagnosis of disorders involving the bilateral thalami: 📖.
- Clinical effects include impaired arousal, which may last for hours to days. Chronic impairment may include mood and behavioral changes (e.g., agitation, aggression, disorientation, apathy).
- Bilateral paramedian infarctions cause stupor/coma, amnesia with confabulation, mood changes (including irritability and apathy), and vertical gaze paresis. (29460331)
inferolateral thalamic infarct (45%)
- Vascular supply: thalamogeniculate arteries are 5-10 arteries arising from the P2 segment of the posterior cerebral artery.
- Clinical effects include:
- Central pain syndrome (Dejerine-Roussy syndrome).
- Hemibody sensory loss (potentially including all types of sensation). Small lacunar infarcts that involve the ventral posterior lateral nuclei can cause a pure sensory stroke.
- Impaired extremity movement (especially ataxic hemiparesis).(29460331)
posterior thalamic infarct (rare)
- Vascular supply: posterior choroidal arteries arise from both the P2 segment of the posterior cerebral artery and also some branches from the posterior communicating artery.
- Clinical effects may include homonymous quadrantanopia, hemisensory loss, transcortical aphasia, and memory disturbances.(29460331)
proximal basilar artery syndrome (base of the basilar artery)
- Impaired consciousness (somnolence ranging to coma).
- Quadriplegia. May also have “crossed” paralysis (e.g., left face and right limbs).
- Abnormal movements (e.g., twitching, jerking, tremor, or shivering).
- Oculomotor abnormalities, which may include horizontal gaze palsy (bilateral or unilateral), internuclear ophthalmoplegia (unilateral or bilateral), one and a half syndrome, skew deviation, gaze paretic nystagmus, or bilateral ptosis.
- Pinpoint pupils.
- Bulbar symptoms, which may include: Facial weakness, dysphagia, dysarthria, palatal myoclonus.
- Pseudobulbar affect.
- Sensory loss to light touch.
mid basilar artery (Locked-in syndrome)
- Quadriplegia and facial paralysis, with extensor plantar response.
- Horizontal gaze palsy (vertical gaze and/or blinking may remain intact).
- Anarthria and dysphagia.
- Vertigo.
- Hearing loss can occur.
top of the basilar syndrome
- This results in ischemia of the midbrain, thalamus, and occipital lobes (but not the pons). The cerebellum may also be involved via the superior cerebellar artery.
- Impaired consciousness (somnolence ranging to coma).
- Pupillary abnormalities (may involve afferents to Edinger-Westphal nucleus, CN3 nucleus, or descending sympathetic system). Pupils may be dilated, mid-position, or small.
- Vertical gaze impairment, internuclear ophthalmoplegia, or skew deviation.
- Hemianopsia or complete cortical blindness.
- Amnesia, agitation, and hallucinations (may involve colors and objects).
- Ataxia, tremor, dysarthria (if the cerebellum is involved).
- Homonymous hemianopsia.
management of basilar artery stroke
- Biologically, basilar occlusion may often result from in situ atherosclerotic plaques with superimposed thrombosis. Clinically, this may result in a stuttering process as the clot grows and retracts.
- The natural history of basilar artery occlusion without intervention is very poor.
- Since the biology of basilar occlusions may involve fresher thrombus than most embolic strokes, these patients might be more amenable to thrombolysis than those with other stroke types.
- Recent studies support the use of endovascular therapy for basilar strokes.
pure motor, dysarthria-clumsy hand, or ataxic hemiparesis
- Symptoms:
- Pure motor: Isolated contralateral face/arm/leg weakness.
- Dysarthria-clumsy hand: Dysarthria, facial weakness, slight weakness/clumsiness of the contralateral hand.
- Ataxic hemiparesis: Ipsilateral hemibody weakness and limb ataxia (that is disproportionate to the weakness).
- Localization:
- Corona radiata (small MCA branches).
- Posterior limb of internal capsule (lenticulostriate arteries, anterior choroidal artery, or perforators from the posterior cerebral artery).
- Cerebral peduncle (small proximal posterior cerebral artery branches).
- Anterior pons (basilar perforators).
pure sensory stroke (thalamic lacune)
- Symptoms: Hemibody sensory loss of all modalities.
- Localization: Infarction of the ventral posterior lateral (VPL) and ventral medial nuclei (VPM), supplied by thalamoperforators from the posterior cerebral artery.
sensorimotor stroke (thalamocapsular lacune)
- Symptoms: Combination of thalamic lacune plus pure motor hemiparesis.
- Localization: Posterior limb of the internal capsule plus either thalamic VPL/VPM or thalamic somatosensory radiation. May result from infarction of the thalamoperforator branches of the posterior cerebral artery, or lenticulostriate arteries.
basal ganglia lacune
- Usually asymptomatic, but may cause hemiballismus.
- Localized to caudate, putamen, globus pallidus, or subthalamic nucleus. Due to infarction of lenticulostriate, anterior choroidal, or Heubner's arteries.
The concept of core infarct vs. ischemic penumbra is clinically most relevant for large vessel anterior circulation infarcts, where these can be well defined radiologically. However, the general concepts apply to any ischemic stroke.
core infarct
- The infarct core refers to tissue which has already been irrevocably damaged. Even if the vessel could be immediately opened, the core infarct would not recover.
- The radiological definition of core infarct is based on the development of cytotoxic edema, reflective of neuronal cells swelling. This cytotoxic edema causes a diffusion restriction on MRI, which is the reference standard for defining the core infarct. However, there are also CT techniques to identify the core infarct.
- For anterior hemispheric infarctions, a core infarct volume over ~50-70 ml suggests a poor responsiveness to endovascular therapy.(31485117)
ischemic penumbra
- Ischemic penumbra is tissue which surrounds the core infarct. The ischemic penumbra is malperfused and nonfunctional, but the tissue is still potentially viable if blood supply can be restored. The ischemic penumbra is often maintained by a trickle of blood flow supplied via collateral circulation.
- The entire purpose of revascularization (either with thrombolysis or endovascular therapy) is to resurrect the ischemic penumbra. Alternatively, if the ischemic penumbra is small, then there is little more tissue to salvage: the stroke has already completed.
rapid progressors versus slow progressors
- The natural history of untreated stroke is for the ischemic penumbra to gradually necrose. Thus, over time, the ischemic penumbra will disappear while the core infarct expands.
- The velocity with which the ischemic penumbra necroses varies widely between patients, depending on collateral circulation. Rapid progressors may quickly complete an infarction within hours, due to poor collateral flow. Alternatively, slow progressors may continue to have large ischemic penumbras for many hours (or even days). These slow progressors may remain good candidates for revascularization therapy well beyond traditional thrombolysis time windows (e.g., >>4.5 hours).
moving from time thresholds to tissue thresholds
- The mantra of stroke neurology is that “time is brain.” However, this is only partially true, because different patients progress at different speeds over time. Thus, 4.5 hours could have an entirely different meaning for a slow progressor versus a rapid progressor.
- Applying a rigid time threshold across all patients made sense in the 1990's, when that's all that we had. However, in the modern era of neuroimaging, it is increasingly possible to rapidly determine the amount of salvageable tissue.
- Based on the perpetual evolution of CT and MRI technology, it's possible that tissue viability may largely replace time cutoffs when considering candidacy for interventions.
common stroke mimics
- Migraine with aura, or migraine variant.
- Migraine aura is usually marked by positive symptoms (e.g., bright/flashing lights, shimmering scotomas, tingling paresthesias). These positive visual symptoms aren't generally caused by an ischemic stroke. Alternatively, loss of function would be more suggestive of ischemic stroke.
- Migraine headache can be helpful, but migraine aura can occur without headache.
- Seizure with postictal deficit.
- Paralysis (Todd's paralysis) is most classic, but other deficits may occur as well.
- Deficits should improve over minutes-hours. (Louis 2021)
- Recrudescence of a prior focal deficit.(Louis 2021)
- May be triggered by various metabolic derangements (e.g., hypoglycemia, hypoxia, fever, hyponatremia, uremia, or hypercalcemia).(33896525)
- Patients often have a combination of diffuse encephalopathy plus a focal deficit(s).
- Medication effect or intoxication.
- Any focal neurological pathology.
- Examples may include tumor, abscess, viral encephalitis, or autoimmune encephalitis.
- Typically these pathologies may be distinguished on the basis of a more gradual symptom onset compared to ischemic stroke.
- Presyncope or syncope.
- PRES. 📖
transient ischemic attack (TIA)
- Definition:
- Clinical syndrome with abrupt onset of focal neurological symptoms consistent with ischemia, which resolves within 24 hours (and usually much sooner than that, often lasting minutes).
- No abnormality is detected on neuroimaging (e.g., lack of diffusion restriction on MRI scan).
- Significance:
- With improved MRI scans, TIA is becoming less common (as these are often being reclassified as small ischemic strokes based on MRI abnormality). Patients who are unable to receive an MRI scan (e.g., due to a pacemaker) are more likely to be diagnosed with “TIA.”
- Patients are at risk of a recurrent stroke and should receive immediate neurology consultation. Further management of TIA is beyond the scope of this book.
- Last known normal time (which is not necessarily the same as when the symptoms were first noticed).
- Past medical history and medications, with emphasis on:
- Anticoagulants and antiplatelet agents?
- History of atrial fibrillation?
- Risk factors for atherosclerotic disease (e.g., hypertension, diabetes, smoking, coronary artery disease, peripheral artery disease).
- Recent medical history (e.g., recent surgery/procedure? recent head/neck trauma?).
- Pattern of symptoms (stuttering? improving? worsening?).
- Any evidence of seizure (e.g., incontinence, bruising, tongue biting).
NIH stroke scale overview
- The score doesn't necessarily correlate with functional outcomes (e.g., severe aphasia yields two points, which is the same score as would result from bilateral subtle weakness of both arms – although severe aphasia would obviously be more debilitating).
calculating the NIH stroke scale
- Level of consciousness:
- 0 = Alert.
- 1 = Drowsy.
- 2 = Obtunded.
- 3 = Unresponsive.
- Level of consciousness questions: (What month is it? Your age?)
- 0 = Correct.
- 1 = 1 mistake -or- unable to speak, e.g. due to dysarthria.
- 2 = 2 mistakes -or- aphasic.
- Ability to follow two simple commands:
- 0 = Correct.
- 1 = 1 failure.
- 2 = 2 failures.
- Gaze palsy: (follow finger with your eyes)
- 0 = Normal.
- 1 = Partial gaze palsy.
- 2 = Complete gaze palsy.
- Visual fields: (if nonverbal, test with visual threat)
- 0 = Normal.
- 1 = Partial hemianopia (e.g., quadrantanopia).
- 2 = Complete hemianopia.
- 3 = Bilateral hemianopia.
- Facial palsy:
- 0 = None.
- 1 = Minor paralysis (e.g., nasolabial flattening).
- 2 = Partial paralysis (e.g., lower face).
- 3 = Complete unilateral paralysis.
- Limb strength: (repeat for each limb)
- 0 = Normal.
- 1 = Drift.
- In arms: Score if arm drifts down before 10 seconds.
- In legs: Score if leg drifts down before 5 seconds.
- 2 = Some effort against gravity.
- 3 = No effort against gravity.
- 4 = No movement.
- Limb ataxia: (finger-nose & heel-shin)
- 0 = None.
- 1 = One limb.
- 2 = Two or more limbs.
- Sensory:
- 0 = Normal.
- 1 = Mild-moderate sensory loss.
- 2 = Severe sensory loss.
- Best language: (name items)
- 0 = No aphasia.
- 1 = Mild aphasia.
- 2 = Severe aphasia.
- 3 = Mute.
- Dysarthria: (ask to repeat words)
- 0 = Normal articulation.
- 1 = Mild dysarthria.
- 2 = Severe dysarthria (or completely mute).
- Extinction and inattention: (e.g., double simultaneous tactile extinction)
- 0 = Normal.
- 1 = Visual, tactile, auditory, spatial, or personal inattention.
- 2 = Profound hemi-inattention or extinction to more than one modality.
ischemic stroke in elderly patient
- Common causes:
- Thrombosis due to local cerebral atherosclerosis.
- Carotid artery atherosclerosis with embolization or occlusion.
- Cardioembolic stroke due to atrial fibrillation, prosthetic valve thrombus, or ventricular thrombus (in severe left ventricular dysfunction).
- Evaluation rarely has immediate impact on ICU treatment:
- Ultrasonography of carotid arteries.
- Echocardiography.
- Telemetry to evaluate for atrial fibrillation.
ischemic stroke in younger patient
- Causes that also require consideration:
- Septic embolism from endocarditis.
- Paradoxical embolization (DVT passes through a patent foramen ovale).
- Cervical artery dissection.
- Substance use (e.g., cocaine and other sympathomimetics).
- Inflammatory vasculitis (e.g., lupus, primary CNS angiitis).
- Infectious vasculitis, for example: (27695601)
- Meningovascular neurosyphilis. 📖
- VZV.
- Lyme.
- Tuberculosis.
- Acquired thrombophilia (e.g., HITT or antiphospholipid antibody syndrome).
- RCVS (reversible cerebrovascular vasoconstriction syndrome).
- Evaluation for etiology in these patient is more likely to affect immediate management. Tests to consider may include:
- Echocardiography with bubble study, to evaluate for shunt.
- Blood cultures, if endocarditis is possible.
- Evaluation for cervical arterial dissection (e.g. MRA or CTA).
- Evaluation for neurosyphilis (usually with serum VRDL or RPR). 📖
- Inflammatory markers or coagulation studies, depending on clinical context.
- Due to time constraints, CT imaging is generally used as a front-line imaging study.
- Traditionally, this has involved a noncontrast CT scan only. However, the addition of a CT angiogram can rapidly provide a wealth of information. Addition of CT perfusion may help further in determining which patients are candidates for immediate endovascular intervention. CT venography may be considered in patients with features suggestive of cerebral venous sinus thrombosis.📖
- ⚠️ Remember that contrast dye doesn't cause renal failure.📖 Definitive imaging should not be delayed or omitted due to concerns regarding the possibility of “contrast nephropathy.”
(#1) any evidence of intracranial hemorrhage
- Identifying intracranial hemorrhage is of paramount importance, since this changes management entirely. Subdural hematomas 📖 or subarachnoid hemorrhages 📖 may not be obvious on CT scan, so they should be carefully sought.
- Hemorrhage may also represent secondary hemorrhagic transformation following an ischemic stroke.📖 If a hemorrhage is surrounded by an unexpected amount of edema that conforms to an arterial vascular distribution, this may suggest a primary ischemic stroke with secondary hemorrhagic transformation.
(#2) hyperdense vessel sign due to an occluded artery
- As blood clots, it becomes more dense and thus increasingly hyperdense on CT scan.
- The dense MCA sign is encountered most often (with a sensitivity of ~33% and a specificity of 95% for MCA occlusion).(31589578) However, hyperdense vessel signs may also be seen in the anterior cerebral artery, posterior cerebral artery, or basilar arteries. If the thrombus involves the M2 segment of the MCA within the Sylvian fissure, this may cause a “hyperdense dot sign.”
- Hyperdense vessels can be mimicked by atherosclerosis, contrasted CT scans, polycythemia, or streak artefact. It's essential to compare the vessel to other vessels seen on the scan (as well as prior CT scans, if available).
- Dense vessels may be more easily detected using thin sections and/or using a maximal intensity projection (MIP) setting.
- Clinical significance of a hyperdense vessel sign:
(#3) signs of cerebral venous sinus thrombosis
- CT signs of cerebral venous sinus thrombosis should be sought, especially in younger patients. (More on the imaging findings of cerebral venous sinus thrombosis 📖)
- (⚠️ If there is substantial concern regarding cerebral venous sinus thrombosis, a CT venogram is needed to exclude the diagnosis.)
(#4) loss of grey-white matter differentiation
- Loss of grey-white differentiation can be seen as soon as an hour after stroke. It is often considered to reflect irreversibly infarcted brain tissue.(32224753) The extent of grey-white differentiation loss provides an early indication of the extent of the infarction.
- In MCA strokes, some useful signs may be:
- Disappearing basal ganglia sign (loss of grey-white differentiation along the edges of the basal ganglia).
- Insular ribbon sign (loss of grey-white differentiation along the insular cortex).
- Cortical ribbon sign (loss of grey-white differentiation along the cortex).
- This can be very subtle.
- ASPECTS score is a systematic approach to define the extent of an MCA or internal carotid artery infarction. A normal score is ten. Points are deducted for loss of grey-white differentiation within ten regions of the anterior circulation (so a score of zero would indicate a catastrophic hemispheric infarction).
(#5) vasogenic edema
- Within ~3-6 hours, infarcted tissue often develops vasogenic edema and becomes hypodense. Frank hypodensity reflects irreversible infarction.(31589578)
- Edema may cause midline shift and compression of ventricles and cisterns (e.g., malignant MCA syndrome). Serial CT scan is essential for patients with large MCA infarctions, as edema may evolve over a period of 2-3 days. 📖
identification of large vessel occlusion & technical feasibility of endovascular therapy
- With increased utilization of endovascular therapy, it's increasingly important to evaluate for the presence of large vessel occlusion. CT angiography is excellent for this.
- Aside from identifying any large occlusions, CTA clarifies vascular anatomy (creating a map to guide IR intervention). In some situations, CTA may reveal patients who are not safe candidates for intervention (e.g., due to highly stenotic vessels or unstable aneurysmal disease).
evaluation of underlying vascular pathology that caused the stroke, e.g.:
- Extracranial carotid or vertebral artery dissection may be the source of thrombi which cause strokes in the brain.
- These cause ~2.5% of all ischemic strokes, with a greater prevalence in younger patients.
- History may include minor neck trauma (e.g. hyperextension or neck manipulation) and neck discomfort.
- Dissection isn't a contraindication to endovascular therapy, but it may make it harder to gain access.
- Carotid atherosclerosis.
- ~10% of strokes are due to carotid atherosclerosis, which carries a high risk of early recurrence.
- Vascular surgery should be consulted to consider followup carotid endarterectomy.
CT perfusion is useful to evaluate for salvageable ischemic penumbra in the context of hemispheric (supratentorial) stroke. However, this isn't generally designed to evaluate posterior circulation strokes. Additionally, CT perfusion only represents a snapshot of blood flow at one point in time – so this may not accurately reflect the status of the brain parenchyma (which depends on an integration of fluctuating blood flow over time).(32224753)
sorting out infarct core versus ischemic penumbra using CT perfusion
- Several parameters can be used to sort out the core infarct versus the ischemic penumbra, as shown above. Different CT systems may use different parameters.
- One common approach is shown below:
- Core infarct is identified based on cerebral blood flow <30%.
- Core infarct plus ischemic penumbra is identified based on elevated maximal transit time >6 seconds.
- The key issue is the degree of mismatch:
- If the two images match up, then the volume of ischemic penumbra is small (completed infarct).
- If the ischemic core is much smaller, then the volume of ischemic penumbra must be large (implying significant salvageable brain tissue).
- Some important parameters:(29364767)
- The ischemic core volume (<50-70 ml suggests a favorable prognosis following intervention).
- The mismatch ratio of penumbra/core (ratios >1.2-1.8 suggest benefit from endovascular therapy).(32947473) A mismatch ratio of >1.2 was used in EXTEND IA, whereas a mismatch ratio >1.8 was used in SWIFT PRIME.
CT perfusion to reach a unique diagnosis
- CT perfusion is typically applied to a patient with known or strongly suspected large ischemic stroke, to determine whether revascularization could be beneficial.
- However, in some situations CT perfusion may yield an unexpected diagnosis:
- (1) Patients with seizure acting as a stroke mimic may have increased regional blood perfusion.
- (2) Occasionally, CT perfusion may reveal a very small ischemic stroke (e.g., one which would have been missed via CT scan with CT angiography alone).
role of MRI
- The use of MRI for hyperacute stroke imaging is often limited by logistic considerations.
- MRI is superior to CT scan for brainstem strokes.
interpretation of various sequences
- Hyperintensity on DWI allows for the diagnosis of stroke within ~10 minutes of symptom onset with high specificity.
- Restricted diffusion is the reference standard for assessment of infarct core (irreversibly damaged tissue at the center of the infarction).(31589578)
- T2/FLAIR may also show hyperintensity, loss of gray-white differentiation, and mass effect.(31485117) However, T2/FLAIR hyperintensity often doesn't emerge until ~4.5-6 hours after the stroke.
- Thus, the combination of hyperintensity on DWI without a corresponding FLAIR hyperintensity identifies a hyperacute stroke.(21978972)
- Absent or sluggish arterial blood flow may be seen as a diminution of normal black arterial flow voids on T2/FLAIR images.
- GRE/SWI: The acute thrombus within an artery has a high concentration of deoxyhemoglobin, which may be visualized as a dark signal on these sequences. Any hemorrhagic transformation will also be detected with GRE/SWI.
endovascular therapy basics
- Endovascular therapy involves mechanical clot removal from a proximal occlusion. Locations which might be amenable to endovascular therapy include the distal internal carotid, MCA (primarily the M1 segment, but possibly also the M2 segment), proximal ACA, or the basilar artery.
- Endovascular therapy is best performed as soon as possible. However, patients with preserved penumbra may be eligible for endovascular therapy up to 24 hours after stroke initiation.
- ⚠️ Patients may be eligible for endovascular therapy well beyond the usual 3-4.5 hour thrombolysis windows.
- Following thrombectomy, the perfusion is described using a Thrombolysis In Cerebral Infarction score (TICI). Scores of 2B or 3 are regarded as successful reperfusion.(32947473)
- TICI Grade 0: No perfusion.
- TICI Grade 1: Penetration with minimal perfusion.
- TICI Grade 2A: Filling of <2/3 of the vascular territory.
- TICI Grade 2B: Complete filling of vascular territory, at a slower rate than normal.
- TICI Grade 3: Normal perfusion.
post-procedure patient management
- (1) Blood pressure management is discussed here: 📖
- (2) The groin puncture site should be followed for any signs of limb ischemia or retroperitoneal hematoma.
- More on the management of retroperitoneal hematoma status post femoral artery instrumentation here. 📖
Follow us on iTunes
To keep this page small and fast, questions & discussion about this post can be found on another page here.
- Hydralazine should be avoided (may cause unpredictable changes in blood pressure).
- For large hemispheric strokes, endovascular intervention may remain a viable therapy even beyond 3-4.5 hours after stroke initiation. Prompt consultation with neurology and/or neurointerventionalists should be obtained even in patients presenting relatively late.
Guide to emoji hyperlinks
- = Link to online calculator.
- = Link to Medscape monograph about a drug.
- = Link to IBCC section about a drug.
- = Link to IBCC section covering that topic.
- = Link to FOAMed site with related information.
- 📄 = Link to open-access journal article.
- = Link to supplemental media.
Guidelines
- AHA/ASA 2019 Guidelines for the early management of patients with acute ischemic stroke (Powers WJ et al.).
Review of seminal studies by The Bottom Line
- DESTINY II trial (2014) – Decompressive hemicraniectomy for malignant MCA infarction in patients >60 years old did not improve the number of patients with good long-term functional outcomes.
References
- 26288671 O'Carroll CB, Aguilar MI. Management of Postthrombolysis Hemorrhagic and Orolingual Angioedema Complications. Neurohospitalist. 2015 Jul;5(3):133-41. doi: 10.1177/1941874415587680 [PubMed]
- Tang, Y., Mukherjee, S., & Wintermark, M. (2015). Emergency Neuroradiology: A Case-Based Approach (1st ed.). Cambridge University Press.
- 27174372 Pahs L, Droege C, Kneale H, Pancioli A. A Novel Approach to the Treatment of Orolingual Angioedema After Tissue Plasminogen Activator Administration. Ann Emerg Med. 2016 Sep;68(3):345-8. doi: 10.1016/j.annemergmed.2016.02.019 [PubMed]
- 27695601 Tipirneni A, Koch S, Romano JG, Malik AM. A 27-Year-Old Man With Right-Sided Hemiparesis and Dysarthria. Neurohospitalist. 2016 Oct;6(4):174-180. doi: 10.1177/1941874416648197 [PubMed]
- 29460331 Li S, Kumar Y, Gupta N, Abdelbaki A, Sahwney H, Kumar A, Mangla M, Mangla R. Clinical and Neuroimaging Findings in Thalamic Territory Infarctions: A Review. J Neuroimaging. 2018 Jul;28(4):343-349. doi: 10.1111/jon.12503 [PubMed]
- 29653785 Brown E, Campana C, Zimmerman J, Brooks S. Icatibant for the treatment of orolingual angioedema following the administration of tissue plasminogen activator. Am J Emerg Med. 2018 Jun;36(6):1125.e1-1125.e2. doi: 10.1016/j.ajem.2018.03.018 [PubMed]
- 30215283 Bar B, Biller J. Select hyperacute complications of ischemic stroke: cerebral edema, hemorrhagic transformation, and orolingual angioedema secondary to intravenous Alteplase. Expert Rev Neurother. 2018 Oct;18(10):749-759. doi: 10.1080/14737175.2018.1521723 [PubMed]
- LaRoche, S. M., & Haider, H. A. (2018). Handbook of ICU EEG Monitoring (2nd ed.). Demos Medical.
- 31346678 Smith M, Reddy U, Robba C, Sharma D, Citerio G. Acute ischaemic stroke: challenges for the intensivist. Intensive Care Med. 2019 Sep;45(9):1177-1189. doi: 10.1007/s00134-019-05705-y [PubMed]
- 31485117 Patra A, Janu A, Sahu A. MR Imaging in Neurocritical Care. Indian J Crit Care Med. 2019 Jun;23(Suppl 2):S104-S114. doi: 10.5005/jp-journals-10071-23186 [PubMed]
- 31589578 Potter CA, Vagal AS, Goyal M, Nunez DB, Leslie-Mazwi TM, Lev MH. CT for Treatment Selection in Acute Ischemic Stroke: A Code Stroke Primer. Radiographics. 2019 Oct;39(6):1717-1738. doi: 10.1148/rg.2019190142 [PubMed]
- 31662037 Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2019 Dec;50(12):e344-e418. doi: 10.1161/STR.0000000000000211 [PubMed]
- Shutter, L. A., Molyneaux, B. J. (2019). Neurocritical care. Oxford University press.
- Wijdicks E.F.M., Findlay, J. Y., Freeman, W. D., Sen A. (2019). Mayo Clinic critical and Neurocritical Care Board Review. Oxford University Press.
- 32054610 Phipps MS, Cronin CA. Management of acute ischemic stroke. BMJ. 2020 Feb 13;368:l6983. doi: 10.1136/bmj.l6983 [PubMed]
- 32224752 Rabinstein AA. Update on Treatment of Acute Ischemic Stroke. Continuum (Minneap Minn). 2020 Apr;26(2):268-286. doi: 10.1212/CON.0000000000000840 [PubMed]
- 32224753 Menon BK. Neuroimaging in Acute Stroke. Continuum (Minneap Minn). 2020 Apr;26(2):287-309. doi: 10.1212/CON.0000000000000839 [PubMed]
- 32668115 Powers WJ. Acute Ischemic Stroke. N Engl J Med. 2020 Jul 16;383(3):252-260. doi: 10.1056/NEJMcp1917030 [PubMed]
- 32947473 Herpich F, Rincon F. Management of Acute Ischemic Stroke. Crit Care Med. 2020 Nov;48(11):1654-1663. doi: 10.1097/CCM.0000000000004597 [PubMed]
- Nelson, S. E., & Nyquist, P. A. (2020). Neurointensive Care Unit: Clinical Practice and Organization (Current Clinical Neurology) (1st ed. 2020 ed.). Springer.
- 33512282 Mullhi RK, Singh N, Veenith T. Critical care management of the patient with an acute ischaemic stroke. Br J Hosp Med (Lond). 2021 Jan 2;82(1):1-9. doi: 10.12968/hmed.2020.0123 [PubMed]
- 33896525 Zubair AS, Sheth KN. Emergency Care of Patients with Acute Ischemic Stroke. Neurol Clin. 2021 May;39(2):391-404. doi: 10.1016/j.ncl.2021.02.001 [PubMed]
- 33947658 Bhalla A, Patel M, Birns J. An update on hyper-acute management of ischaemic stroke. Clin Med (Lond). 2021 May;21(3):215-221. doi: 10.7861/clinmed.2020-0998 [PubMed]
- 33952393 O'Carroll CB, Brown BL, Freeman WD. Intracerebral Hemorrhage: A Common yet Disproportionately Deadly Stroke Subtype. Mayo Clin Proc. 2021 Jun;96(6):1639-1654. doi: 10.1016/j.mayocp.2020.10.034 [PubMed]
- 34010530 Langezaal LCM, van der Hoeven EJRJ, Mont'Alverne FJA, et al.; BASICS Study Group. Endovascular Therapy for Stroke Due to Basilar-Artery Occlusion. N Engl J Med. 2021 May 20;384(20):1910-1920. doi: 10.1056/NEJMoa2030297 [PubMed]
- 34680603 Hasan TF, Hasan H, Kelley RE. Overview of Acute Ischemic Stroke Evaluation and Management. Biomedicines. 2021 Oct 16;9(10):1486. doi: 10.3390/biomedicines9101486 [PubMed]
- Louis ED, Mayer SA, Noble JM. (2021). Merritt’s Neurology (Fourteenth). LWW.
- 34798968 Lyden S, Wold J. Acute Treatment of Ischemic Stroke. Neurol Clin. 2022 Feb;40(1):17-32. doi: 10.1016/j.ncl.2021.08.002 [PubMed]
- 35034076 Sharma D, Smith M. The intensive care management of acute ischaemic stroke. Curr Opin Crit Care. 2022 Apr 1;28(2):157-165. doi: 10.1097/MCC.0000000000000912 [PubMed]
- Albin, C. S. W., & Zafar, S. F. (2022). The Acute Neurology Survival Guide: A Practical Resource for Inpatient and ICU Neurology (1st ed. 2022 ed.). Springer.
- 36333037 Qaryouti D, Greene-Chandos D. Neurocritical Care Aspects of Ischemic Stroke Management. Crit Care Clin. 2023 Jan;39(1):55-70. doi: 10.1016/j.ccc.2022.07.005 [PubMed]