Stroke Syndromes
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Texts taken from several sources, mainly from Tintinalli's Emergency Medicine: A Comprehensive Guide, 9th Edition
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Stroke Syndromes
- 1. TINTINALLI’S HOUR: NEUROLOGY SECTION “STROKE SYNDROMES” Jo Anne N. Ramos, MD Emergency Medicine BATAAN GENERAL HOSPITAL AND MEDICAL CENTER DEPARTMENT OF EMERGENCY MEDICINE
- 2. INTRODUCTION • Globally 1 in 4 adults over the age of 25 will have a stroke in their lifetime. • 13.7 million people worldwide will have their first stroke this year and five and a half million will die as a result. • Current trends suggest that the number of annual deaths will climb to 6.7 million annually without appropriate action. https://www.world-stroke.org/world-stroke-day-campaign/why-stroke-matters/learn-about-stroke
- 3. INTRODUCTION • From 2009 to 2019, stroke remains the second leading cause of death and one of the top five leading causes of disability in the Philippines. • Based on types of stroke, 7 out of 10 cases are diagnosed as ischemic while the other three are considered hemorrhagic. • Thirty six percent (36%) of the total stroke deaths are not attended by any medical personnel. Institute of Health Metrics. GBD Compare. Available online at: http://vizhub.healthdata.org/gbd-compare (accessed February 5, 2021). Department of Health. Philippine Health Statistics 2018. Available online at: https://doh.gov.ph/node/24432
- 4. INTRODUCTION • There is no established unified national stroke registry thus, determining the local burden of stroke remains a challenge. Front. Neurol., 17 August 2021 https://doi.org/10.3389/fneur.2021.665086
- 5. PATHOPHYSIOLOGY • Stroke is generally defined as any disease process that interrupts blood flow to the brain. • Injury is related to the loss of oxygen and glucose substrates necessary for high-energy phosphate production and the presence of mediators of secondary cellular injury. Tintinalli’s Emergency Medicine 9th Ed.
- 6. VASCULAR SUPPLY OF THE BRAIN
- 8. PATHOPHYSIOLOGY Tintinalli’s Emergency Medicine 9th Ed. 2 MAJOR MECHANISMS ISCHEMIA (87%) HEMORRHAGE (10%) THROMBOTIC EMBOLIC HYPOPERFUSION INTRACEREBRAL NT SAH (3%) Altered neuronal perfusion
- 9. STROKE CLASSIFICATION STROKE TYPE MECHANISM CAUSE CLINICAL NOTES ISCHEMIC THROMBOTIC Narrowing of the vascular lumen Atherosclerosis and etc Gradual onset, wax and wane; Common cause of TIA EMBOLIC Obstruction of a normal vascular lumen from a remote source Mural thrombi, vascular vegetations Abrupt in onset; 20% of all ischemic strokes HYPOPERFUSION Low blood flow state Heart failure, systemic hypotension Diffuse pattern in “watershed regions”; Wax and wane (hemodynamic factor) Tintinalli’s Emergency Medicine 9th Ed.
- 11. STROKE CLASSIFICATION STROKE TYPE MECHANISM CAUSE CLINICAL NOTES HEMORRHAGIC ICH Intraparenchymal hemorrhage Hypertension, vascular malformations, etc ICP riseneuronal damage MC in African, Asian descent NT SAH Hemorrhage into SA space Berry aneurysm, vascular malformation ruptures May be preceded by a warning leak (sentinel HA) Tintinalli’s Emergency Medicine 9th Ed.
- 12. CLINICAL FEATURES Tintinalli’s Emergency Medicine 9th Ed. HISTORY • The timing of symptom onset, the presence of associated symptoms, and the medical history may point toward a particular mechanism of stroke. • STROKE MIMICS: – a situation in which a diagnosis of stroke at admission is not confirmed
- 14. CLINICAL FEATURES Tintinalli’s Emergency Medicine 9th Ed. PHYSICAL EXAMINATION • Assessment of ABCs is top priority • Next goals are to: –Confirm the diagnosis –Exclude stroke mimics –Identify comorbidities
- 15. STROKE SEVERITY SCALE (validated) The NIH Stroke Scale (NIHSS) is a common diagnostic method for quickly assessing the severity of a stroke experienced by a patient.
- 21. ISCHEMIC STROKE SYNDROMES ACA infarction: • Rare (0.5% to 3% of all strokes) Tintinalli’s Emergency Medicine 9th Ed.
- 24. ISCHEMIC STROKE SYNDROMES MCA infarction: • MCA most commonly involved in stroke • Mnemonics: “CHANGes” – Contralateral paresis and sensory loss (face and arm) – Homonymous hemianopsia – Aphasia – Neglect – Gaze preference toward the lesion DOMINANT HEMISPHERE (LEFT) (In right-handed patients and in up to 80% of left- handed patients, the left hemisphere is dominant.) Tintinalli’s Emergency Medicine 9th Ed.
- 25. ISCHEMIC STROKE SYNDROMES MCA infarction: • Dominant hemisphere: APAHASIA • Non-dominant: – Inattention – Neglect – Dysarthria without apahasia Tintinalli’s Emergency Medicine 9th Ed.
- 28. ISCHEMIC STROKE SYNDROMES PCA infarction: • Common presenting signs 5 D’s: –Diplopia –Dizziness –Dysarthria –Dysphagia –Dystaxia Tintinalli’s Emergency Medicine 9th Ed. Adam’s and Victor’s Principle of Neurology 11th Ed.
- 30. ISCHEMIC STROKE SYNDROMES BASILAR ARTERY OCCLUSION: • MC presenting symptoms – Unilateral limb weakness – Dizziness – Dysarthria – Diplopia – Headache Tintinalli’s Emergency Medicine 9th Ed.
- 31. ISCHEMIC STROKE SYNDROMES BASILAR ARTERY OCCLUSION: • MC presenting signs: – Unilateral limb weakness – CN VII signs – Dysarthria – Babinski sign – Oculomotor sign • Can also rarely present with “Locked-in Syndrome” Tintinalli’s Emergency Medicine 9th Ed.
- 34. ISCHEMIC STROKE SYNDROMES VERTEBROBASILAR INFARCTION: • MC presenting symptoms: - dizziness - nausea or vomiting - Headache - dysphagia - unilateral limb weakness - unilateral cranial nerve V symptomsoms. Tintinalli’s Emergency Medicine 9th Ed.
- 35. ISCHEMIC STROKE SYNDROMES CEREBELLAR INFARCTION: • MC presenting symptoms: –Non-specific • Mental status: Varies (alert to coma) • 25% shows no lesion on a noncontrast head CT Tintinalli’s Emergency Medicine 9th Ed.
- 36. ISCHEMIC STROKE SYNDROMES CAROTID AND VERTEBRAL ARTERY DISSECTION: • AKA CERVICAL ARTERY DISSECTION • Uncommon • MC in young adults and middle- aged • Risk factor: NECK TRAUMA • Transient or persistent Tintinalli’s Emergency Medicine 9th Ed.
- 37. UNILATERAL HEADACHE (68%) NECK PAIN (39%) FACE PAIN (10%)
- 38. ISCHEMIC STROKE SYNDROMES CAROTID AND VERTEBRAL ARTERY DISSECTION: • Diagnostic of choice ( based on availability and pt’s stability) – CT/ CT angio – MRI/ MRA • Treated similarly to any other stroke patients Tintinalli’s Emergency Medicine 9th Ed.
- 39. “Spontaneous intracerebral hemorrhage may be clinically indistinguishable from ischemic infarction, but the two conditions are distinct clinical entities in terms of management, with higher levels of morbidity and mortality for hemorrhage than for ischemic infarction.” HEMORRHAGIC STROKE SYNDROMES
- 40. Perform a CT to differentiate the two. HEMORRHAGIC STROKE SYNDROMES
- 41. • “TIME IS BRAIN” • Primary goal: – Door to needle time of ≤ 60 mins of ED arrival • Perform brain imaging within 20 minutes of patient’s ED arrival • CT scan should be interpreted by the most expert interpreter available STROKE DIAGNOSIS
- 42. AHA/ASA TIME RECOMMENDATIONS FOR ACUTE ISCHEMIC STROKE PRESENTING IN THE ED INTERVENTION TIME GOAL Activation of stroke team Start of brain imaging Administration of IV thrombolysis Immediately upon arrival ≤ 20 minutes ≤ 60 minutes Nonessential testing and procedures (including IV starts and blood draws) should not delay performing brain imaging within 20 minutes of the patient’s arrival.
- 43. ED CORE INTERVENTIONS (all patients) Cardiac monitoring Oxygen administration if indicated Pulse oximetry Establish IV access ABC’S
- 44. Strict bedrest NPO CBC with APC, coagulation studies, cardiac biomarkers ECG Non-contrast CT or MRI Bedside glucose determination ED CORE INTERVENTIONS (all patients)
- 45. Lumbar puncture Toxicology screen/blood alcohol level Pregnancy test (if child brearing) Urinalysis Chest radiograph ED CORE INTERVENTIONS (selected patients)
- 46. GENERAL TREATMENT FOR ISCHEMIC STROKES • Correct dehydration if present • Keep oxygen saturation to >94% • Fever increases mortality, treat the underlying cause • Admit all stroke patients
- 47. BP CONTROL IN STROKE
- 48. BP CONTROL IN STROKE IV ANTI-HYPERTENSIVE MEDICATIONS before thromboytics or awaiting thrombolectomy Labetolol 10-20mg IV over 1-2 min x 1 Use with caution in certain conditions; may cause dizziness and nausea Nicardipine infusion, 5mg/h titrate up by 2.5mg/h in 5-15 min interval; when desired BP is achieved dec by 3mg/h Max: 15mg/h Contraindicated in patients with severe aortic stenosis. Can cause headache, flushing, dizziness, nausea, reflex tachycardia. Clevidipine infusion, 1-2 mg/h inc by doubling dose every 2-5 min Max: 21mg/h Contraindicated in patients with severe aortic stenosis, allergies to soy or eggs, and lipid metabolism disorders
- 49. BP CONTROL IN STROKE IV ANTI-HYPERTENSIVE MEDICATIONS before thromboytics or awaiting thrombolectomy Labetolol 10-20mg IV over 1-2 min x 1 Use with caution in certain conditions; may cause dizziness and nausea Nicardipine infusion, 5mg/h titrate up by 2.5mg/h in 5-15 min interval; when desired BP is achieved dec by 3mg/h Max: 15mg/h Contraindicated in patients with severe aortic stenosis. Can cause headache, flushing, dizziness, nausea, reflex tachycardia. Clevidipine infusion, 1-2 mg/h inc by doubling dose every 2-5 min Max: 21mg/h Contraindicated in patients with severe aortic stenosis, allergies to soy or eggs, and lipid metabolism disorders
- 50. HYPERGLYCEMIA • The current AHA/ASA guidelines recommend the maintenance of blood glucose between 140 milligrams/dL (7.77 mmol/L) and 180 milligrams/dL (9.99 mmol/L).
- 51. ANTIPLATELET THERAPY • The current AHA/ASA guidelines recommend the administration of oral ASA within 24 to 48 hr after stroke onset. • No antiplatelet should be given within 24 hr after thrombolytic therapy. • ANTIPLATELET THERAPY IS CONTRANDICATED IN ACUTE HEMORRHAGIC STROKE.
- 52. THROMBOLYSIS • The NINDS trial represented the first randomized placebo-controlled trial that showed benefit of IV alteplase in acute stroke. • 3 hours within stroke onset • “Last moment the patient was in his baseline”
- 53. THROMBOLYSIS
- 54. THROMBOLYSIS
- 55. THROMBOLYSIS
- 56. ENDOVASCULAR TREATMENT AHA/ASA Indications for Endovascular Treatment with a Stent Retriever • Prestroke mRS score 0 to 1 • Acute ischemic stroke receiving IV rtPA within 4.5 h of onset according to guidelines from professional medical societies • Causative occlusion of the ICA or proximal MCA (M1) • Age ≥18 y • NIHSS score of ≥6 • ASPECTS of ≥6 • Treatment can be initiated (groin puncture) within 6 h of symptom onset All 7 criteria need to be met for stent retriever endovascular therapy to be indicated.
- 58. TRANSIENT ISCHEMIC ATTACK • Frequently precedes stroke Can the patient be safely discharged? ABCD2 RISK SCORE
- 59. PARAMETER SCORE AGE >60 yo <60 yo 1 0 BLOOD PRESSURE BP >140/90 BP <140/90 1 0 CLINICAL PRESENTATI ON Unilateral leg weakness Speech impairment 2 1 DURATION ≥60 min 10-59 min <10 min 2 1 0 DIABETES MELLITUS Yes No 1 0 TIA RISK STRATIFICATION SCORE (ABCD2) SCORE: LOW RISK: 0-3 MODERATE RISK: 4-5 HIGH RISK: 6-7 INTERPRETATION: 2-day risks of subsequent stroke is: 1% for scores 0-3 4.1% for scores 4-5 8.1% for scores 6-7 7-day risks for subsequent stroke: 1.2 for scores 0-3 5.9 for scores 4-5 11.7 for scores 6-7 ABCD2 should not be used to identify TIA patients who can be safely discharged home
- 60. SPECIAL POPULATIONS: STROKE OR TIA WITH CONCURRENT MYOCARDIAL INFARCTION • AHA/ASA 2018 RECOMMENDATION treatment with IV alteplase at the dose appropriate for cerebral ischemia followed by PCI and stenting if indicated. • Do not delay thrombolysis if qualified
- 61. SPECIAL POPULATIONS: SICKLE CELL DISEASE • Overall prevalence: 3.8% • MCC of stroke in children • Hemorrhagic stroke in adults 20-29 yo • IV thrombolysis, if qualified • Exchanged PRBC transfusion to reduce S Hgb level by <30%
- 62. SPECIAL POPULATIONS: YOUNG ADULTS • Age 18-50 years • Cardiovascular risk factors • 20% are Cervical Artery Dissection • TREAT AGGRESSIVELY
- 63. THANK YOU!
Editor's Notes
- The true stroke prevalence is uncertain, but reported estimates vary between 0.9% (2005) to 2.6% (2017) of the population.
- An understanding of the diagnosis and treatment of stroke begins with a working knowledge of the relevant vascular supply and neuroanatomy of the brain.
- Neurons are exquisitely sensitive to changes in cerebral blood flow and die within minutes of complete cessation of perfusion—hence, the current treatment emphasis on rapid reperfusion strategies.
- The early detection of stroke must begin with the general public. In general, stroke knowledge among laypersons remains suboptimal, especially in the elderly,2 the poorly educated,2 and minority populations.3 This has led to mass media initiatives to raise stroke awareness4; however, the effectiveness of these initiatives is often short lived. Family members and/ or witnesses to the event should be urged to come to the ED as soon as possible to provide further medical information to the treating physician. Time at the scene should be limited. EMS personnel should rapidly stabilize the patient’s condition and transport the patient to the closest facility best able to emergently and properly treat the patient’s stroke.
- The diagnosis of stroke in the ED rests on the bedrock of a focused, accurate history and physical examination. The time of onset is defined as the last known time when the patient’s condition was at their baseline
- Fever should prompt an investigation for potential infection. CNS infections (meningitis, encephalitis) may mimic a stroke, or an infection such as aspiration pneumonia or a urinary tract infection may be a complication of the stroke. Evaluate for meningismus, signs of emboli (Janeway lesions and Osler nodes), and bleeding diatheses (ecchymoses or petechiae). A funduscopic examination may identify signs of papilledema (suggesting a mass lesion, cerebral vein thrombosis, or hypertensive crisis) or preretinal hemorrhage (consistent with subarachnoid hemorrhage). Assess for findings suggestive of possible cardiac or vascular disease, such as rales, an S3 gallop, or carotid bruit.
- transcortical motor aphasia (a nonfluent aphasia with greatly reduced spontaneous speech, but with retained auditory comprehension and repetition ability), whereas right-sided infarction can result in confusion and motor hemineglect. Bilateral occlusion can cause a combination of the above symptoms but was particularly associated with mutism, incontinence, and poor outcome in one small series.
- The middle cerebral artery is the vessel most commonly involved in stroke, and clinical findings can be quite variable, depending on exactly where the lesion is located and which brain hemisphere is dominant. (In right-handed patients and in up to 80% of left-handed patients, the left hemisphere is dominant.) A middle cerebral artery stroke typically presents with hemiparesis, facial plegia, and sensory loss contralateral to the affected cortex. These deficits variably affect the face and upper extremity more than the lower extremity. If the dominant hemisphere is involved, aphasia (receptive, expressive, or both) is often present. If the nondominant hemisphere is involved, inattention, neglect, extinction on double-simultaneous stimulation, dysarthria without aphasia, and constructional apraxia (difficulty in drawing complex two-dimensional or three-dimensional figures) may occur. A homonymous hemianopsia and gaze preference toward the side of the infarct may also be seen, regardless of the side of the infarction.
- If the dominant hemisphere is involved, aphasia (receptive, expressive, or both) is often present. If the nondominant hemisphere is involved, inattention, neglect, extinction on double-simultaneous stimulation, dysarthria without aphasia, and constructional apraxia (difficulty in drawing complex two-dimensional or three-dimensional figures) may occur. A homonymous hemianopsia and gaze preference toward the side of the infarct may also be seen, regardless of the side of the infarction.
- The classic symptoms and signs of posterior circulation strokes include ataxia, nystagmus, altered mental status, and vertigo, but presentation can sometimes be rather subtle.47 Crossed neurologic deficits (e.g., ipsilateral cranial nerve deficits with contralateral motor weakness) may indicate a brainstem lesion. According to an analysis of a large stroke registry,48 symptoms of posterior cerebral artery involvement include unilateral limb weakness, dizziness, blurry vision, headache, and dysarthria. 48 Visual field loss, classically described as contralateral homonymous hemianopsia and unilateral cortical blindness, is thought to be specific for distal posterior circulation stroke because the visual centers of the brain are supplied by the posterior cerebral artery. Light-touch and pinprick sensation deficits, loss of ability to read (alexia) without agraphia, inability to name colors, recent memory loss, unilateral third nerve palsy, and hemiballismus have also been reported. Motor dysfunction, although common, is typically minimal, which can keep some patients from realizing they have had a stroke.
- The classic symptoms and signs of posterior circulation strokes include ataxia, nystagmus, altered mental status, and vertigo, but presentation can sometimes be rather subtle.47 Crossed neurologic deficits (e.g., ipsilateral cranial nerve deficits with contralateral motor weakness) may indicate a brainstem lesion. According to an analysis of a large stroke registry,48 symptoms of posterior cerebral artery involvement include unilateral limb weakness, dizziness, blurry vision, headache, and dysarthria. 48 Visual field loss, classically described as contralateral homonymous hemianopsia and unilateral cortical blindness, is thought to be specific for distal posterior circulation stroke because the visual centers of the brain are supplied by the posterior cerebral artery. Light-touch and pinprick sensation deficits, loss of ability to read (alexia) without agraphia, inability to name colors, recent memory loss, unilateral third nerve palsy, and hemiballismus have also been reported. Motor dysfunction, although common, is typically minimal, which can keep some patients from realizing they have had a stroke.
- The classic symptoms and signs of posterior circulation strokes include ataxia, nystagmus, altered mental status, and vertigo, but presentation can sometimes be rather subtle.47 Crossed neurologic deficits (e.g., ipsilateral cranial nerve deficits with contralateral motor weakness) may indicate a brainstem lesion. According to an analysis of a large stroke registry,48 symptoms of posterior cerebral artery involvement include unilateral limb weakness, dizziness, blurry vision, headache, and dysarthria. 48 Visual field loss, classically described as contralateral homonymous hemianopsia and unilateral cortical blindness, is thought to be specific for distal posterior circulation stroke because the visual centers of the brain are supplied by the posterior cerebral artery. Light-touch and pinprick sensation deficits, loss of ability to read (alexia) without agraphia, inability to name colors, recent memory loss, unilateral third nerve palsy, and hemiballismus have also been reported. Motor dysfunction, although common, is typically minimal, which can keep some patients from realizing they have had a stroke.
- Patients with vertebrobasilar infarction most commonly present with symptoms of dizziness, nausea or vomiting, headache, dysphagia, unilateral limb weakness, and unilateral cranial nerve V symptoms.48 Common presenting signs include unilateral limb ataxia, nystagmus, gait ataxia, cranial nerve V signs, limb sensory deficit, and Horner’s syndrome.
- Obtain early neurosurgical consultation for patients with cerebellar infarction. Cerebellar edema can lead to rapid deterioration with herniation, and consultation is required to determine the need for emergency posterior fossa decompression in these patients. Acute obstructing hydrocephalus or symptomatic mass effect requires rapid treatment of elevated intracranial pressure with hyperosmolar therapy (mannitol or hypertonic saline) and emergent surgical decompression.
- Therefore, consider the administration of IV thrombolytic therapy in all eligible patients with stroke from cervical artery dissection. T anticoagulation or antiplatelet therapy.
- the current AHA/ASA stroke guidelines Class IB recommendation to enact “an organized protocol for the emergency evaluation of patients with suspected stroke” in which the primary goal is to achieve a door-to-needle time of ≤60 minutes of ED arrival in ≥50% of acute ischemic stroke patients who are treated with thrombolytics.1
- The optimal blood pressure for acute ischemic stroke victims is unknown; however, based on consensus opinion, the current AHA/ASA acute stroke guidelines19 recommend that hypotension and hypovolemia be corrected with either colloids or crystalloids128 to maintain organ perfusion; however, there is no specific target blood pressure for patients not eligible for reperfusion therapy. Conversely, based on the blood pressure guidelines used in randomized controlled trials of thrombolytics, blood pressure control is considered essential prior to, during, and after thrombolytic therapy.
- The current AHA/ASA guidelines recommend the maintenance of blood glucose between 140 milligrams/dL (7.77 mmol/L) and 180 milligrams/dL (9.99 mmol/L).19 Avoid and treat hypoglycemia (<60 milligrams/dL [3.33 mmol/L]). Remember that both hypoglycemia and hyperglycemia are important stroke mimics. Hyperglycemia is common in acute stroke,134,135 and glycemic control has been recommended based on data that associate less favorable outcomes with hyperglycemia.136-138 However, data to support improved outcomes with tight glycemic control are lacking,139,140 and hypoglycemia must be avoided because it is associated with brain dysfunction.140
- The current AHA/ASA guidelines recommend the administration of oral (or by rectum if swallowing impairment is present) aspirin within 24 to 48 hours after stroke onset unless thrombolytics have been given within the prior 24 hours. No antiplatelet agent (including aspirin) should be given within 24 hours of receiving thrombolytic therapy.
- The NINDS trial represented the first randomized placebo-controlled trial that showed benefit of IV alteplase in acute stroke.
- The NINDS trial represented the first randomized placebo-controlled trial that showed benefit of IV alteplase in acute stroke.
- The NINDS trial represented the first randomized placebo-controlled trial that showed benefit of IV alteplase in acute stroke.
- The NINDS trial represented the first randomized placebo-controlled trial that showed benefit of IV alteplase in acute stroke.
- Abbreviations: AHA/ASA = American Heart Association/American Stroke Association; ASPECTS = Alberta
- TIA is defined as follows: “a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.”219
- 2-day risks of subsequent stroke as 1% (ABCD2 score 0 to 3), 4.1% (score 4 to 5), and 8.1% (score 6 to 7). The 7-day stroke risks were 1.2% (ABCD2 score 0 to 3), 5.9% (score 4 to 5), and 11.7% (score 6 to 7).
- based on expert consensus, the 2018 AHA/ASA guidelines gave a Class IIa (moderate) recommendation: “For patients presenting with concurrent AIS [acute ischemic stroke] and acute MI [myocardial infarction], treatment with IV alteplase at the dose appropriate for cerebral ischemia, followed by percutaneous coronary angioplasty and stenting if indicated is reasonable.”
- Strokes in young adults (age 18 to 50 years) are increasing in incidence.269,270 Possible causes include an increasing prevalence of some traditional cardiovascular risk factors271 (e.g., hyperlipidemia,272 diabetes,273,274 obesity275), increasing rates of recreational drug use,276 and better awareness and diagnosis of stroke in this age group.