STROKE BY DR. NITHA THOMAS 2024 .pptx

STROKE- ACUTE ISCHEMIC STROKE AND INTRACRANIAL HEMORHAGES

1. STROKE By Dr.Nitha Thomas 1st year MEM

2. TOPICS COVERED ANATOMY AND PHYSIOLOGY DEFINITION AND ETIOLOGY TYPES AIS STROKE MIMICS STROKE CHAMELEONS ICH/SAH

3. LOBES

4. DEFINITION Stroke is defined as any disease process that interrupts blood flow to the brain. Injury occurs due to loss of oxygen and glucose substrates necessary for high-energy phosphate production and the presence of mediators of secondary cellular injury. Acute onset of focal neurological deficit of vascular origin which lasts for more than 24 hours.

5. ETIOLOGY

6. CLASSIFICATION

7. ISCHEMIC STROKE :CAUSES 1 . THROMBOTIC Large Vessel Disease - atherosclerosis, arterial dissection , art- art embolism Caused by above risk factors - HTN, DM, HLD, smoking and age Pathophysiology: 1) Plaque in vessel wall ruptures 2) Thrombus develops over plaque decreasing lumen 3) Decreased blood flow beyond thrombus 4) Ischemia → Infarction Most common sites: o ICA after bifurcation of common carotid artery o Vertebrobasilar System o Stem of the MCA or just prior to its first bifurcation

8. Small Vessel Disease - Lacunar stroke A ssociated with lipohyalinosis and atherosclerosis Lipohyalinosis - concentric hyaline thickening of small cerebral vessels leading to the occlusion of penetrating arteries Atherosclerotic plaques in parent arteries causing occlusion. Most common sites: ( deep perforating arteries) Lenticulostriate vessels supply basal ganglia, internal capsule and corona radiata Small pontine penetrating vessels ostium of perforating branches

9. 2.EMBOLIC - commonly affect the MCA, PCA or smaller cortical vessels Cardiac Emboli Atrial Fibrillation Left ventricular thrombus CHF with low ejection fraction - increases stasis of blood flow and risk of clots Septic emboli from infective endocarditis vegetations on mitral or aortic valve Fibrinous material on mitral or aortic valves from rheumatic heart disease Mechanical heart valve (highly thrombogenic)

10. Arterial Emboli From plaque on Aortic or Internal Carotid Artery Plaque or piece of it is dislodged Embolus gets stuck in downstream cerebral vessel Decreased blood flow beyond embolism Ischemia → Infarction Paradoxical Emboli From DVT in patients with Patent Foramen Ovale (PFO) or Atrial Septal Aneurysm

11. OTHER CAUSES Hypercoagulable states Vasculitis Arterial dissection Global Cerbral ischemia - occurs in Shock, carotid artery stenosis, acute respiratory failure. Systemic Hypoperfusion

12. ISCHEMIC STROKE :pathophysiology insufficient blood supply to a focal area of brain tissue. —> imbalance between the consumption and production of ATP —> diminished energy stores —> ionic imbalances, electrical disturbances and cascade of ischemic changes —> Increase in prodn of reactive oxygen species ( ROS) and Nitric oxide ( NO) —> cell membrane destruction, cell lysis and death —> Within minutes, the central core of tissue in this affected area progresses toward irreversible damage, —> infarction. However, the penumbra, does not experience immediate cell death and has the potential for recovery if early reperfusion is achieved. The intricate ischemic cascade triggered by acute stroke ultimately leads to the loss of neurons and supporting structures.

13. Stroke classification

14. AIS Divisions

15. ANTERIOR CIRCULATION STROKE 70% of strokes Middle cerebral artery Anterior cerebral artery Internal carotid artery stroke Lenticulostriate arteries FAST : facial asym, any limb weakness, speech, time of onset POSTERIOR CIRCULATION STROKE 30% of strokes Posterior cerebral artery Basilar artery and AICA 5D-A : Dysarthria, dysphagia, dizziness, diplopia , deterioration of decreased consciousness, ataxia

16. STROKE LOCALISATION

17. Vessel Symptoms Vessel Symptoms MCA Contralateral weakness/paralysis and sensory loss of upper limbs, face and upper trunk Ipsilateral gaze deviation Aphasia (expressive, receptive or both) Contralateral Homonymous hemianopia without macular sparing Apraxia + Hemineglect if infarct on nondominant hemisphere PICA (Lateral Medulla) Ataxia Dysphagia, Dysphonia, ↓ gag and cough reflexes Contralateral uvular deviation Vertigo, N/V, Nystagmus Ipsilateral Horner’s Syndrome Loss of pain and temperature on ipsilateral face and contralateral whole side ACA Contralateral weakness/paralysis and sensory loss of lower limbs and lower trunk Urinary and fecal incontinence Abulia or Akinetic mutism Transcortical motor aphasia (able to repeat phrases) Vertebral Artery/ASA (Medial Medulla) Contralateral weakness/paralysis and sensory loss (fine touch, vibration + proprioception) of whole side Ipsilateral tongue deviation

18. ICA Mixture of MCA and ACA symptoms May have PCA symptoms if fetal variant present Amaurosis Fugax – Transient ipsilateral mono-ocular vision loss that may become permanent if not treated AICA (Lateral Pons) Ataxia Vertigo, N/V, Nystagmus Hearing loss + tinnitus Ipsilateral Horner’s Syndrome Ipsilateral loss of sensation to face, loss of corneal reflex and weakness of mastication and facial muscles Contralateral loss of pain and temperature on whole side PCA Homonymous Hemianopia with macular sparing Variable or contralateral sensory loss/paresthesia of whole side (thalamus) Weber, Claude or Benedikt Syndromes (midbrain) Basilar Artery (Medial Pons) Contralateral weakness and loss of fine touch, proprioception and vibration Ipsilateral loss of eye abduction→ Medial gaze deviation Intranuclear ophthalmoplegia

19. STROKE MIMICS - false positive TRANSIENT ISCHEMIC ATTACK ( MANAGED DIFFERENTLY THOUGH RELATED HYPOGLYCEMIA POST ICTAL PARALYSIS ( TODD’S PARALYSIS) HEMIPLEGIC MIGRAINE BRAIN TUMORS/ABSCESS CEREBRAL VENOUS THROMBOSIS POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME ( PRES)

20. STROKE CHAMELEONS - false negative HYPERTENSIVE EMERGENCY ALTERED SENSORIUM ACUTE PSYCHOSIS PERCEIVED DELIRIUM AND MEMORY DEFICITS GENERALISED ENCEPHALOPATHY

21. MANAGEMENT IN AIS

22. NATIONAL INSTITUTE OF HEALTH STROKE SCALE

23. CT/CTP/CTA CT :gold standard to r/o ICH , but if its AIS , CT may be normal in the first 6h Earliest changes : loss of gray and white matter/differentiation of sulci and gyri Insular ribbon sign - hypodensity + swelling of insular cortex Dense MCA sign MCA dot sign Dense basilar sign ASPECTS score for early ischemic changes CTA: large vessel occlusion +/- CTP: volume of core of penumbra,matched or mismatched perfusion

24. INSULAR RIBBON SIGN

25. Dense MCA sign MCA dot sign

26. Hyper dense basilar tips sign

27. ASPECT SCORE - quantitate score that measures the extent of early ischemic changes in anterior circulation hyperacute ischemic stroke - volumetric estimate of the size of cerebral infarction of the MCA -for each area involved one point is given which is subtracted from 10 . Less than or equal to 7 predicts a worse functional outcome at 3 months as well as symptomatic haemorrhage .

28. MRI/MRA Sequences : T1-weighted imaging (T1-W1) - CSF has low intensity * brain tissue T2 - weighted imaging ( T2-W2) - CSF has high signal intensity * brain tissue Diffusion-weighted imaging (DWI): Most sensitive to reliably demonstrate small and early infarcts within the first minutes to hours after onset. An acute infarct appears as a hyperintensity in DWI. DWI with apparent diffusion coefficient (DWI/ADC): The appearance of DWI/ADC depends on the timing. An acute infarct, which is seen as a hyperintensity on DWI is seen as a hypointensity on DWI/ADC.

29. T2-weighted fluid-attenuated inversion recovery (FLAIR) FLAIR is a T2-weighted sequence in which the CSF signal is suppressed. On traditional T2-weighted MRI, CSF appears bright, whereas on FLAIR this fluid appears dark. This is very useful in identifying subarachnoid hemorrhage (SAH) and subdural hemorrhage (SDH). Acute ischemic stroke produces no signs on FLAIR in the first 6 hours from onset with areas of hyperintensity evolving thereafter. In those with unwitnessed onset/wake-up strokes, a DWI lesion without a matching hyperintensity on FLAIR suggests that the stroke occurred less than 6 hours previously.

30. Steps to Identify an Acute Infarct on a MRI Stroke Protocol • DWI: Look for an area of uniform hyperintensity in the suspected territory • DWI/ADC: Look for a hypodensity in the same area as hyperintensity on DWI • MRA: Look for an area of stenosis/cut off • T2W FLAIR: If a hyperintensity is seen, it means that the infarct is greater than 6 hours old and hence beyond the time for thrombolysis • SWI: Look for blooming (hypointensity) which suggests areas of hemorrhage (if present).

31. MRA MRA is very sensitive to flow and is based on the difference in signal between moving blood and stationary brain tissue; angiographic-like images of the cervicocranial vasculature are produced. This is a useful tool in identifying the site of occlusion or dissection. Important to visualise LVO

32. Watch out for ….. ABC Pulse/ECG - Afib, Bradycardia BP - manage HTN RR- tachy, cheyne stokes, Hypoxia, Aspiration pneumonia , pooling of secretions Temp - fever, treat to reduce brain’s metabolic demand GCS - lower the score, larger the infarct/brainstem involvement GRBS- 130-220mg/dl IVF - do not use 5D/DNS ( increases cerebral edema) Ryles/Foleys/ET as needed ( low GCS) DVT prophylaxis ( in low GCS) Seizure as protocol CBC, KFT , VBG , Coagulation - PT PTT INR

33. TREATMENT OF AIS Medical support Thrombolysis Endovascular revascularisation Antithrombotic/anticoagulants stroke rehabilitation

34. HYPERTENSION CONTROL If the pt is a thrombolysis candidate - BP control should be initiated immediately Short acting ,IV , titratable antihypertensives agents Labetalol, 10–20 mg IV over 1–2 min, can double the dose every 10min up to 300mg Contraindications/caution: severe asthma, severe COPD, CHF, DM, myasthenia gravis, concurrent calcium channel blocker use, hepatic insufficiency. Nicardipine infusion, 5 mg/h, titrate up by 2.5 milligrams/h at 5- to 15-min intervals; Maximum dose: 15 MG/h; when desired blood pressure attained, reduce to 3 milligrams/h Caution: MI , concurrent use of fentanyl (hypotension), CHF, hypertrophic cardiomyopathy, portal hypertension, renal insufficiency, hepatic insufficiency (may need to adjust starting dose). Contraindication : severe aortic stenosis. Clevidipine infusion, 1–2 milligrams/h, titrate up by doubling dose every 2–5 min; maximum dose:21 milligrams/h Caution: CHF. Can cause reflex tachycardia atrial fibrillation, and systemic hypotension. Contraindication : severe aortic stenosis. L ipid metabolism disorders (e.g., pathologic hyperlipidemia, lipoid nephrosis, or acute pancreatitis with hyperlipidemia). NTG infusion CCBs

35. THROMBOLYSIS - within 4.5h INDICATIONS AND CONTRAINDICATIONS TO BE NOTED NIHSS SCORE : 4-25 2 iv lines Up to 3-4.5 h after last well known time Weight of pt Mix by swirling movement Time of administration and end to be noted In wake up stroke go by MRI picture ( DWI + and FLAIR - , <6h)

36. WHILE WAITING FOR ICU … Post thrombolysis do a neuro check every 15 min * 2h —-> 30min *6h —>hourly Spo2- 94% BP- <180/105 mmhg Bedside swallow test- 30ml of water , If cough/choking++ keep NPO Maintain grbs 140-180 mmhg , insulin drip if persistently high IVF - NS @1.5ml/kg/h to keep euvolemia Watch for A-fib for around 72 h Check for fever , worse prognosis

37. Avoid indwelling of catheters/tubes to prevent bleeding post tpa atleast 4/nosocomial infections Watch for bleeding from iv sites Head end elevation for 30 degrees to reduce edema DECOMPRESSIVE SURGERY- in LVO , malignant edema / to prevent sudden detoriation due to herniation and massive swelling Do not give anticog/antiplt for 24h post tpa , repeat imaging before administering Watch for complications of tpa —-> angioedema, hemorrhage , severe hypo/hypertension (signs of bleed)

38. If sudden deterioration of sensorium + Stop tpa infusion ?ABC Vitals /GCS/Pupils Treat BP and use non invasive interventions to lower ICP (Head end elevation) Obtain CT scan STAT Notify Neurosurgeon Send samples for PT,PTT, platelets Arrange PRBC 2-4 units, 10U cryoprecipitate IV over 10-30 m ( till fibrinogen level is <200mg/dl) Reverse anticoagulant agents Tranexemic acid 1000mg IV over 10 min and Aminocaproic acid IV 4-5 g over 1 h f/b 1g until bleeding stops Consider 1 SDP : 6-8 RDP

39. ENDOVASCULAR THERAPY - within 6 h, Incase of LVO/ failure of thrombolysis due to large clot volume with 8-24 h Probability of LVO increases with increase in NIHSS Up to 8h - MERCI trail Up to 16-24 h - DAWN /DEFUSE-3 trail ANTITHROMBOTIC TREATMENT - Tab. Aspirin 325mg Tab. Clopidogrel 300mg Tab. Atorvastatin 40mg Inj. Heparin 5000IU sc Fondaparinx

40. Approach to AIS https://www.neurocriticalcare.org/Portals/0/Docs/ENLS/ENLS_V_4_0_Protocol_AIS_FINAL.pdf

41. TIA - symptoms last for minutes to hours <24h Ordinal scale that provides risk prediction Of stroke following TIA. Mod to high risk should be admitted and Evaluated and antiplatelets to be started.

42. HEMORRHAGIC STROKE

43. HEMMORRHAGE STROKE - Causes Intracerebral Hemorrhage (ICH) Rupture of small arteries causing bleed within the brain parenchyma due to hypertensive vasculopathy, cerebral amyloid angiopathy. Risk factors :age, hypertension, CAA, smoking, excessive alcohol intake, sympathomimetic drugs, anticoagulants, and antiplatelet drugs Subarachnoid Hemorrhage (SAH)- non traumatic Leakage of blood into the subarachnoid space Risk factors: drug use (such as amphetamines and cocaine), coagulopathy, a ruptured arteriovenous malformation, and vessel rupture due to a dural venous sinus thrombosis ,smoking, hypertension, excessive alcohol consumption, advancing age, personal history of another type of aneurysm or SAH, and family history of an intracranial aneurysm.

44. ICH - Pathophysiology Rupture of small arteries —> expanding hematoma and perihematomal edema. —> elevated intracranial pressure (ICP) —-> reducing cerebral perfusion and ischemic injury.(MONRO-KELLIE DOCTRINE) Sometimes it can lead to intraventricular hemorrhage (IVH) and herniation. Similar to ischemic stroke, ICH also undergoes proinflammatory and anti-inflammatory phases. Secondary mechanisms of injury (such as blood-related cytotoxicity, excitotoxicity, and oxidative stress) disrupt the blood-brain barrier, resulting in significant brain cell death and the development of potentially life-threatening brain edema

45. SAH - Pathophysiology Aneurysm ruptures,--->arterial blood is released into the subarachnoid space —> disseminating through the CSF and increasing ICP. The arterial blood can also extend into the intraventricular space and brain parenchyma. Secondary brain injury can occur due to several factors, including ICH, IVH, ICP, hydrocephalus, subdural hematoma, or delayed cerebral ischemia (DCI)

46. Can occur during routine activities Neurological symptoms tend to worsen over minutes to a few hours progressively. HEADACHE : Blood agitates the meninges → activates sensory fibers of trigeminal nerve (CN V) → sends sensory information to the trigeminal nucleus and trigeminal tract → pain FOCAL NEURO DEFECTS -Aphasia, weakness on one side, gaze preferences , sensory loss RAISED ICP - If you have excess blood, the intracranial pressure increases (monro-kellie doctrine) leading to nausea and vomiting , decreasing level of consciousness, pupillary changes ↑BP, ↓HR, ↓RR (irregular respirations) Decreasing level of consciousness → Altered mental status: when you keep waking up the patient but he/she can’t stop sleeping

47. ICH score

48. ICH TREATMENT Stabilize - ABC Withhold antiplatelets/anticoagulants and administer anticoagulant reversal agents BP management <140/100mmhg Anticonvulsants if Seizure+ , Inj.fosphenytoin 20mg/kg Inj. Levetiracetam 20mg/kg upto 1500mg ICH score ICP Rx: Inj.Mannitol 150 -200 ml 8th hourly , to reduce blood viscosity —-> reflex vasoconstriction Oral Glycerol 15-30ml TID Vasopressor therapy, to MAP++ —----> CCP

49. Neurosurgery interventions → Decompression surgeries : Infratentorial bleed and supratentorial bleed Ventricular drainage : Obstructive hydrocephalus due to intraventricular extension of hemorrhage

50. Approach to ICH https://www.neurocriticalcare.org/Portals/0/Docs/ENLS/ENLS_V_4_0_Protocol_ICH_Final.pdf

51. REFERENCES Tintinalli’s emergency medicine manual 9th edition Oxford handbook of emergency medicine AECTM emergency medicine channel Manipal manual of emergency medicine handbook Medscape NCBI ENLS RADIOPEDIA Ninja nerd

52. Thank you