Stroke Presentation & Management PDF

STROKE Supervisor. Dr. Razan Alshaheen. PGY-4, SFH  Fifth leading cause of death in the US. In-hospital mortality rate of 5% to 10% for ischemic stroke and 40% to 60% for hemorrhagic Only 10% of stroke survivors will recover completely. 87% of all strokes are ischemic in origin,...

STROKE Supervisor. Dr. Razan Alshaheen. PGY-4, SFH  Fifth leading cause of death in the US. In-hospital mortality rate of 5% to 10% for ischemic stroke and 40% to 60% for hemorrhagic Only 10% of stroke survivors will recover completely. 87% of all strokes are ischemic in origin, 13% are hemorrhagic strokes.  Stroke can be defined as any vascular injury that reduces cerebral blood flow (CBF) to a specific region of the brain, retina, or spinal cord, causing neurologic impairment TIA: A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.  A 61-year-old woman presents with a gradual onset weakness and lightheadedness. Prior to arrival she had right arm weakness that lasted approximately 20 minutes and has now resolved. No nuchal rigidity is present. Which of the following is the most likely diagnosis? A)Classic migraine B)Epidural hematoma C)Todd paralysis D)Transient ischemic attack Risk factors for having a stroke after a TIA :- hypertension, diabetes mellitus, symptoms lasting ≥ 10 minutes, motor deficits, and speech impairment. 10% of TIA patients will have a stroke within 90 days Low-risk TIA (ABCD2 score < 4) or moderate to major ischemic stroke (National Institutes of Health Stroke Scale (NIHSS) > 3) Treatment with aspirin alone High-risk TIA (ABCD2 score ≥ 4) or minor ischemic stroke (NIHSS score ≤  How to read CT head on emergency Mnemonic : Blood Can Be Very Bad. Blood = blood Can = cisterns Be = brain Very = ventricles Bad = bone B(LOOD) IS FOR BLOOD Subarachnoid Subdural Intraventricu Intraparenchy Hemorrhage Hematoma lar mal Blood in the Crosses Hemorrhage Hemorrage cisterns/cortical sutures but (IVH) (IPH) gyral surface does not  C(AN) IS FOR CISTERNS four key cisterns (Circummesencephalic, Suprasellar, Quadrigeminal and Sylvian) Is there blood (subarachnoid hemorrhage)? Are the cisterns open/is there high intracranial pressure? B(E) IS FOR BRAIN SYMMETRY Make sure sulci and gyri appear the same on both sides. Check for effacement of sulci (unilateral or bilateral). GREY-WHITE DIFFERENTIATION SHIFT HYPER/HYPODENSITY  V(ERY) IS FOR VENTRICLES/VESSELS Examine the ventricles for dilation or compression/shift. vessels for signs of clot (hyperdense vessel) B(AD) IS FOR BONE Thrombosed ophthalmic artery :- amaurosis fugax  Anterior Circulation Posterior Circulation progress within the first 24 progress for up to 3 days hours rarely includes LOC LOC + N/V frontal lobe function: AMS Brain stem + cerebellar: coupled with impaired Vertigo, dysphagia, spasticity, judgment and insight ataxia, or nystagmus Bowel and bladder incontinence (ACA) Paralysis and hypesthesia of Crossed deficits the lower limb contralaterally Ipsilateral Hemianopsia homonymous hemianopsia Agnosia (dominant stroke) Visual agnosia Aphasia (dominant stroke) Alexia + dysarthria Hemmorhagic stroke The clinical presentation can be identical with sichemic stroke 30-day mortality rate of up to 50% HTN and cerebral amyloid angiopathy are most common risk factor PRE-HOSPITAL STROKE ASSESSMENT Transportation For pts. with suspected large vessel occlusion stroke, the mission: Lifeline Severity– based Stroke Triage Algorithm for EMS recommends transport to a comprehensive stroke center if travel time is < 15 additional minutes compared to the closest primary stroke center  STROKE CENTERS ASRH  can establish initial stroke diagnosis + CLASSIFCATION provide initial care PSC  offers stroke infrastructure (stroke team, stroke unit, pt. care protocols & support services, including CT & lab testing availability) CSC  offer advanced imaging modalities, perform surgical & endovascular interventions & having stroke unit & stroke registry  ABCD AND NEUROLOGICAL ASSESSMENT IN ED DDX: STROKE MIMICS  DIAGNOSIS CBC CT scan can identify the vast majority of parynchimal Urea and electrolytes (U&E) hemmorrhage more than 1 cm KFT, LFT Has limited sensitivity for RBS posterior stroke ECG Most ischmic stroke will appear on routine CT at least 6-12 CT head and CT contrast hours , however early ischmic changes have been noted in up to 67%. In the first 3 hours. Exclude intracranial bleeding, NIHSS Scoring (National Institutes of Health Stroke Scale)  useful & rapid tool  assesses neuro-deficit  determines Tx. options - fibrinolytic Tx. vs. null  identifies those at risk for hemorrhage  - subtle, early ischemic changes include: “have been noted in 67% of non- contrast CT scans within 1st 3 hrs” 1. hyperdense artery sign (acute thrombus in a vessel) 2. sulcus effacement 3. loss of the insular ribbon CT BRAIN 4. loss of gray-white interface 5. mass effect 6. acute hypodensity Only acute hypodensity & mass effect are associated with increased risk of ICH insular ribbon sign Managementement Airway always first Avoid dehydration and be cautios to avoid fluid overload Avoid hypothermia 39C as it is increase in hospital mortality Maintain oxygen saturation above >95% Keep blood glucose level at 140-180 mg/dl hyperglycemia during the first 24 hours after stroke is associated with worse outcomes  BP control :- tPA less than 185/110 - No tPA less than 220/120 or MAP 130 Reperfusion therapy IV thrombolytic therapy Mechanical thrombectomy Thrombolytic therapy:- Eligibility Recommendations for IV Alteplase in Pts. with AIS 3 - 4.5 hrs: 1. > 18 & < 80 yrs (for 0-3 hr window  > 80 yrs still candidate for tpA) 2. NIHSS ≤ 25 3. No hx. of both DM & prior stroke 4. Early changes  Contraindications Time of onset > 3 or 4.5 hrs Hx. of or acute ICH Ischemic stroke, head trauma, IC/spinal Sx. within 3 mon SAH BP > 185/110 GI/GU bleed within 21 days Coagulopathy (INR > 1.7, plt < 100,000) Treatment-dose LMWH w/in 24 hrs or DOAC use within 48 hrs -This patient is outside the window for tPA administration as he woke up with weakness and was last seen many symptom-free seven hours prior or patients who are not eligible to receive tPA, current guidelines recommend the administration of aspirin within 24 to 48 hours of symptom onset alteplase tenecteplase. Aspirin Dosage :should not0.25 0.9 mg/kg bemg/kg given if the (maximum 25 mg) given in a patient (maximumhas received dose 90 singletPA. bolus mg) over 60 minutes with initial 10% of Before Endovascular : Ticagrelor  if ASAassociated dose given as bolus is with a over 1 minute higher incidence of contraindicated reperfusion and better functional outcome  ENCHANTED Trial Comparing low dose alteplase (0.6 mg/kg IV) to standard dose (0.9 mg/kg IV) Low dose alteplase was non-inferior to standard dose alteplase with respect to death and disability at 90 days There were significantly fewer symptomatic IC in low dose (1.0%) compared to standard dose (2.1%) Low dose is a current practice is Japan , but still AHA/ASA recommend the standard dose. EXTEND-IA TNK trial Tenecteplase was associated with a higher incidence of reperfusion and better functional outcome complared to alteplase ICH was similar in both groups To give or not to give :- MI YES Pregnancy YES SCA YES Drug abuse YES ESRD YES  therapy (e.g., aspirin and clopidogrel) before stroke on the basis of evidence that the benefit of alteplase outweighs a probable increased risk of ICH Thrombolysis -LMWH: IV alteplase should not be in Patients on administered to patients who have received a full treatment dose of low Anticoagulan molecular weight heparin (LMWH) ts Before the within the previous 24 hours. Stroke - should not be administered to patients taking direct thrombin inhibitors or direct factor Xa inhibitors unless laboratory tests such as activated partial  frequently and usually occurs within 36 hours after t-PA infusion and half of the events are diagnosed within 5 to 10 hours. Current protocols include ICU monitoring for 24 hours with repeat neuroimaging if there is any neurological deterioration. Treatment :- crdiovascular and Symptomatic Intracerebral respiratory support, BP Hemorrhage management, neurological Following monitoring, prevention of Thrombolysis hematoma expansion, control of elevated ICP, and seizure control. Once symptomatic ICH is diagnosed, consider immediately sending a fibrinogen level and empirically transfusing with 10 U cryoprecipitate intravenously over 10 to 30 minutes. RISK FACTORS FOR BLEEDIN G  Patient time of last seen normal is less than 24 hours Proximal LVO M1 branch of Mechanical MCA, ICA, basilar artery Moderate to severe stroke Thrombectom symptoms y Meeting DAWN or candidate DEFUSE3 eligibility criteria Other inclusion criteria as determined by neurology and interventional radiology  Comparing thrompectomy alone VS dual therapy. Dual therapy was associated with higher likelihood of 3- month functional independence and lower odds of 3-month mortality The 2 groups did not differ in symptomatic ICH There are no randomized control trials of mechanical thrombectomy for posterior circulation LVO Hemmorrhagic stroke Evidnece from clinical trials to guide management for spontanous ICH has lagged behined that of ischmic stroke and anyeurysmal SAH. Intensive mornitoring of airway, BP, ICP control, seizure and herniation Refersal of anticougulant Vitamin K antagonist and INR >1.4 : IV Vitamin K or 3,4 PCC, FFP Dapigatrian: Idarucizumab, PCC, FFP Factor Xa inhibitors: Andexanet alfa, 4 PCC COX inhibitors or ADP receptors inhibitors: Desmopressin Platelet transfusion? ICP Treat with HTS or mannitol Some trials showed HTS is more effective that mannitol Avoid hypo or hyperglycemia Avoid fever Corticosteroid is not recommended sedation & seizure control Surgical evacuation Indicated in : supratentorial ICH, neurological deterioration, coma, midline shift or high ICP refractory to medical management. Minimally surgical approach better than open craniotomy and improved in mortality - Agnosia = unability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. - Aphasia = is an inability to comprehend or formulate language because of damage to specific brain regions. - Visual agnosia = the inability to recognize seen