Neuro clinics 21- stroke case discussion

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ischemic and hemorrhagic stroke

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Neuro clinics 21- stroke case discussion

  1. 2. Neuro-clinics 21 Dr Pratyush Chaudhuri Supported by Nirmal clinics & Mankind Pharmaceuticals
  2. 3. CASE DISCUSSION Acute Ischemic Stroke Intra-cerebral hemorrhage Dr Pratyush Chaudhuri
  3. 4. Case 1 <ul><li>A 53-year-old man with a history of hypertension was brought to the hospital after his employer noticed that he had difficulty with speech, ambulation, and vision.  </li></ul><ul><li>The employer told the doctors that the patient usually left his house at 3:40 pm and arrived at work by 4:00 pm; however, no one saw him arrive at work and no time clock is used.  </li></ul><ul><li>The autorickshaw was called at about 5:00 pm.  He was noted to be lethargic on transport.   </li></ul>
  4. 5. <ul><li>Has he had a stroke syndrome ?? </li></ul>
  5. 6. <ul><li>What was the time of onset of the stroke?  </li></ul><ul><li>Before 3.40pm </li></ul><ul><li>3:40 pm </li></ul><ul><li>4:00 pm </li></ul><ul><li>5:00 pm </li></ul>
  6. 7. Stroke - clinical term <ul><li>acute loss of circulation to an area of the brain ischemia corresponding loss of neurologic function. </li></ul><ul><li>Classified </li></ul><ul><li>hemorrhagic </li></ul><ul><li>ischemic </li></ul>
  7. 9. focal neurologic deficits sudden onset <ul><li>weakness </li></ul><ul><li>sensory deficit </li></ul><ul><li>difficulties with language </li></ul>
  8. 10. recognition of stroke <ul><li>in prioritizing - for rapid transport to the hospital </li></ul><ul><li>Cincinnati prehospital stroke scale </li></ul><ul><li>defines 3 major physical findings </li></ul><ul><li>facial droop </li></ul><ul><li>arm weakness </li></ul><ul><li>speech abnormalities </li></ul>
  9. 11. <ul><li>Sudden numbness or weakness of face, arm, or leg, especially on one side of the body </li></ul><ul><li>Sudden confusion, difficulty in speaking or understanding </li></ul><ul><li>Sudden deterioration of vision of one or both eyes </li></ul><ul><li>Sudden difficulty in walking, dizziness, and loss of balance or coordination </li></ul><ul><li>Sudden, severe headache with no known cause </li></ul>
  10. 12. Common signs of stroke <ul><ul><li>Acute hemiparesis or hemiplegia </li></ul></ul><ul><ul><li>Complete or partial hemianopia, monocular or binocular visual loss, or diplopia </li></ul></ul><ul><ul><li>Dysarthria or aphasia </li></ul></ul><ul><ul><li>Ataxia, vertigo, or nystagmus </li></ul></ul><ul><ul><li>Sudden decrease in consciousness </li></ul></ul>
  11. 13. Differential diagnosis <ul><li>Intracranial Abscess Botulism Encephalitis Hyperglycemia Hypertensive urgency/emergency Hypoglycemia Psychiatric disorders/conversion disorder Seizure Spinal injury Uremia Ingestions (eg, ethanol) Intracranial neoplasm </li></ul>
  12. 14. Why is time important? <ul><li>Reperfusion strategies </li></ul><ul><li>improve blood flow and limit size of infarct </li></ul>
  13. 15. <ul><li>What to do ?? </li></ul>
  14. 17. Emergency dept protocol for presumed stroke <ul><li>Monitor and observe vitals every 15 mins </li></ul><ul><li>Cardiac and O2 monitoring </li></ul><ul><li>SOS ABC </li></ul><ul><li>IV access - 2 peripheral lines – start 0.9 % NS at 50ml / hr thru 1 line , block other </li></ul><ul><li>Stat labs – glucose, CBC, platelets, PT, aPTT, urine pregnancy test, toxic screen, chemistry profile </li></ul><ul><li>Wt. of pt. </li></ul><ul><li>Stat CT head – no contrast </li></ul><ul><li>No aspirin, other antiplatelets, heparin or warfarin till further orders </li></ul>
  15. 18. CT <ul><li>Easily available </li></ul><ul><li>Exquisitely sensitive for ICH </li></ul><ul><li>Normal brain – 35 HU </li></ul><ul><li>Grey matter – 39 HU </li></ul><ul><li>White matter – 32 HU </li></ul><ul><li>IV contrast not useful in 1 st 24 hrs even though BBB broken </li></ul><ul><li>Enhancement seen after 72 hrs </li></ul>
  16. 19. early infarction signs on CT <ul><li>sensitivity is poorer </li></ul><ul><li>than </li></ul><ul><li>the specificity </li></ul><ul><li>in other words </li></ul><ul><li>signs are not generally well detected </li></ul><ul><li>but when seen, they are likely to be present . </li></ul>60% CT’s normal 31 % misinterpreted
  17. 20. <ul><li>Hypoattenuation in thirds of middle cerebral artery territory </li></ul><ul><li>Obscuration of lentiform nucleus </li></ul><ul><li>Cortical sulcal effacement </li></ul><ul><li>Loss of insular ribbon, obscuration of sylvian fissure </li></ul><ul><li>Hyperattenuation of vessel – hyperdense MCA sign – poor outcome </li></ul><ul><li>Loss of gray and white matter differentiation </li></ul><ul><li>Hypoattenuation (measured in Hounsfield units) in basal </li></ul><ul><li>ganglia </li></ul>
  18. 21. Loss of gray-white differentiation in the posterior aspect of the right frontal lobe
  19. 22. The scan exhibits subtle, hyperacute ischemic changes, including effacement of the insular ribbon and lentiform nucleus edema of the right hemisphere.
  20. 23. The hyperdense middle cerebral artery sign
  21. 25. <ul><li>Irreversible injury - Early mass effect and areas of hypodensity -- at higher risk of hemorrhage if given thrombolytics. </li></ul><ul><li>Significant hypodensity on the baseline scan -- question the time of onset </li></ul><ul><li>Hypodensity in an area greater than one third of the MCA distribution - considered a relative contraindication for thrombolytics </li></ul>
  22. 28. <ul><li>Would you order an MRI? </li></ul>
  23. 30. MRI <ul><li>Higher sensitivity for infarcts </li></ul><ul><li>Better for posterior fossa, lacunar infarcts and small cortical strokes </li></ul>
  24. 31. MRI not easily available / need skilled interpretation <ul><li>Subtle signs may not be apparent in 1 st 6 hrs </li></ul><ul><li>Sulcal effacement </li></ul><ul><li>Gyral swelling </li></ul><ul><li>Earliest signal intensity change in grey matter- white matter may be normal for 24 hrs </li></ul><ul><li>FLAIR sequences – optimise conspicuity - only abnormal areas are hyperintense </li></ul>
  25. 32. <ul><ul><li>Diffusion-weighted MRI (DW-MRI) - detects ischemic brain injury earlier than standard T1/T2-weighted MRI images or CT scan </li></ul></ul><ul><ul><li>Perfusion MRI (PW-MRI) – inject contrast material to show areas of decreased perfusion. </li></ul></ul><ul><ul><li>Together yields areas of diffusion-weighted imaging/perfusion-weighted imaging (DW-MRI/PW-MRI) mismatch, -- identifying potentially salvageable tissues . </li></ul></ul><ul><ul><li>MRA - noninvasive / no contrast material. </li></ul></ul><ul><ul><li>shows vascular anatomy and occlusive disease </li></ul></ul>IV contrast (Gado) needed to determine age of infarct
  26. 33. Imaging developments for thrombolytic therapy in stroke magnetic resonance imaging <ul><li>Concept of ischaemic umbra and penumbra translated to diffusion weighted image and perfusion weighted image on MRI. </li></ul><ul><li>DWI= irreversibly damaged infarct core </li></ul><ul><li>PWI=complete area of hypoperfusion </li></ul><ul><li>The volume difference between these two (PWI/DWI mismatch) is a measure of the ischaemic penumbra-- the salvagable ischaemic tissue at risk for infarction </li></ul>
  27. 34. MRI – rule out ICH ?? <ul><li>Conventional spin MRI – good for subacute and chronic haemorrhage </li></ul><ul><li>Not useful in hyperacute ICH </li></ul><ul><li>Gradient recalled echo scans (GRE) very sensitive to fresh blood </li></ul><ul><li>FLAIR also useful </li></ul>
  28. 35. DW - MRI <ul><li>Depends on water molecule diffusability in acute ischemia </li></ul><ul><li>Apparent diffusion constant (ADC) low in area of acute ischemia (upto 10 – 14 days) </li></ul><ul><li>may correleate with final infarct size </li></ul><ul><li>Acute and chronic ischemic changes similar on T2W and FLAIR </li></ul>Returns to normal with time
  29. 36. Should we take a break ?
  30. 38. <ul><li>What about a DSA ? Angio?? </li></ul>
  31. 39. DSA <ul><li>Final word - allowing for intraarterial therapy also </li></ul><ul><li>But stroke risk 1- 2 % </li></ul><ul><li>Needs special facilities </li></ul><ul><li>Skilled operator </li></ul>
  32. 40. This is the CT scan picture What now ??
  33. 41. Reperfusion strategies improve blood flow and limit size of infarct <ul><li>IV thrombolytics - SK and rt-PA studied </li></ul><ul><li>Intraarterial thrombolytics </li></ul>No benefit More deaths and bleeds Within 3 hrs -Class I recommendation by the American Stroke Association
  34. 43. Establishing time of onset is especially critical <ul><li>Especially if - thrombolytic therapy is an option. </li></ul><ul><li>If the patient awakens with the symptoms, </li></ul><ul><li>then the time of onset is defined as the time the patient was last seen without symptoms. </li></ul>3.40 pm in our pt Arrived at 5 pm
  35. 44. Inclusion criteria for IV rt-PA <ul><li>Age > 18 yrs </li></ul><ul><li>Clinical diagnosis of ischemic stroke with clear symptom onset within 3 hrs </li></ul><ul><li>Non contrast CT without evidence of haemorrhage </li></ul>
  36. 45. Exclusion criteria -- Medical history <ul><li>Prior history of ICH </li></ul><ul><li>h/o IC neoplasm, aneurysm, AV malformation </li></ul><ul><li>Stroke / head trauma – previous 3 months </li></ul><ul><li>Major surgery / biopsy of parenchymal organ – preceding 14 days </li></ul><ul><li>GI / GU bleed – preceding 21 days </li></ul><ul><li>Recent MI - preceding 3 months </li></ul><ul><li>Seizure at onset </li></ul><ul><li>Known hereditary, acquired abnormal hemostasis </li></ul><ul><li>Current use of anticoagulants with PT > 15 secs </li></ul><ul><li>Use of heparin in previous 48 hrs - check aPTT </li></ul>
  37. 46. Exclusion criteria -- Clinical examination <ul><li>Neuro signs that improve rapidly </li></ul><ul><li>Isolated mild neuro deficits – ataxia, dysarthria, sensory loss alone </li></ul><ul><li>SBP > 185 mm Hg or DBP > 110 mmHg </li></ul><ul><li>Aggressive therapy needed to control BP </li></ul>
  38. 47. Exclusion criteria -- CT / lab findings <ul><li>e/o major hypodensity or sulcal effacement </li></ul><ul><li>( > 1/3 of MCA territory) </li></ul><ul><li>Platelet count < 100,000 / mm ³ </li></ul><ul><li>Blood glucose < 50 mg % or > 400 mg % </li></ul>
  39. 48. Protocol for rt-PA administration <ul><li>Informed consent </li></ul><ul><li>Calculate total dose as 0.9mg / kg (not > 90mg ) </li></ul><ul><li>Give 10% as bolus over 1 minute </li></ul><ul><li>Rest ( 90%) over 1 hr as infusion </li></ul><ul><li>Maintain SBP < 185 mmHg and DBP < 110 mmHg </li></ul><ul><li>Be alert for signs of ICH – sudden increase SBP, decline in mental or neuro status, severe headache </li></ul><ul><li>Repeat CT as necessary </li></ul>
  40. 50. Stroke onset>3hours— ( what we routinely see….. ) <ul><li>Role of stroke MRI in selecting patients of unknown onset with PWI>DWI </li></ul><ul><li>Intraarterial and vertebrobasilar thombolysis </li></ul><ul><ul><li>prourokinase for acute M1/M2 occlusion with 9mg/2h within 3-6 hr. of acute MCA infarct </li></ul></ul><ul><ul><li>and upto 12 hrs in vertebrobasilar territory stroke.(PROACT I&II)--survival of 55-70%in successful recanalisation vs.0-10%in untreated/persistent basilar artery occlusion </li></ul></ul><ul><li>Large MCA Territory infarcts-- preemptive craniectomy with duroplasty </li></ul>
  41. 51. <ul><li>Pt’s BP – 200 / 110 mm Hg </li></ul>
  42. 52. Candidate for thrombolysis - BP control <ul><li>Pretreatment SBP >185 or DBP >110 mm Hg </li></ul><ul><li>Posttreatment DBP >140 mm Hg SBP >230 mm Hg or DBP 121-140 mm Hg </li></ul><ul><li>SBP 180-230 mm Hg or DBP 105-120 mm Hg </li></ul><ul><li>Labetalol 10-20 mg IVP 1-2 doses or Enalapril 1.25 mg IVP </li></ul><ul><li>Sodium nitroprusside (0.5 mcg/kg/min) </li></ul><ul><li>Labetalol 10-20 mg IVP and consider labetalol infusion at 1-2 mg/min or nicardipine 5 mg/h IV infusion and titrate </li></ul><ul><li>Labetalol 10 mg IVP, may repeat and double every 10 min max 150mg </li></ul>
  43. 53. No thrombolysis - BP control <ul><li>DBP >140 mm Hg </li></ul><ul><li>SBP >220 or DBP 121-140 mm Hg or MAP >130 mm Hg </li></ul><ul><li>SBP< 220 mm Hg or DBP 105-120 mm Hg or MAP <130 mmHg </li></ul><ul><li>Sodium nitroprusside 0.5 mcg/kg/min; may reduce approximately 10-20% </li></ul><ul><li>Labetalol 10-20 mg IVP over 1-2 min; may repeat and double every 10 min up to maximum dose of 150 mg or nicardipine 5 mg/h IV infusion and titrate </li></ul><ul><li>Antihypertensive therapy indicated only if AMI, aortic dissection, severe CHF, or hypertensive encephalopathy present </li></ul>
  44. 55. Intensive care management <ul><li>Hemodynamic monitoring </li></ul>No autoregulation so cerebral blood flow dependant on MBP Reduction of BP can increase stroke size and severity Treat only if signs of HT emergencies – encephalopathy, retinal haemorrhage, cardiac ischemia, CHF, rapidly progressive renal dysfunction
  45. 56. Intensive care management <ul><li>Hemodynamic monitoring – non invasively or invasively </li></ul><ul><li>Keep well hydrated </li></ul><ul><li>Use saline - no dextrose – avoid hyperglycemia </li></ul>
  46. 57. Drugs to be avoided <ul><li>NTG – venodilator – raises ICP </li></ul><ul><li>Nifedipine and clonidine – rapid and unpredictable response </li></ul><ul><li>Nitroprusside – can cause vascular steal as normal vessels dilate more than abnormal vessels </li></ul>
  47. 58. Drugs of choice <ul><li>Labetalol </li></ul><ul><li>Enalapril </li></ul><ul><li>Nicardipine </li></ul>
  48. 59. <ul><li>Pt lethargic , but opens eyes to call </li></ul>
  49. 61. Intensive care management <ul><li>Airway – intubation – Inability to protect airway </li></ul><ul><li>Inadequate gas exchange </li></ul>Poor prognostic sign Beware hypotension and raised ICP during induction for intubation Keep pO2 ~100 and PCO2 ~ 35 PEEP as deemed
  50. 62. Intensive care management <ul><li>Elevated ICP - maximum reached in 3 – 5 days </li></ul><ul><li>Clinical signs may precede monitored ICP values – herniation due to local tissue shifts and not global increases in ICP </li></ul>Raise head end 15 – 30 º Osmotherapy Induced coma No steroids
  51. 63. General medical management <ul><li>Sedation – use short acting agents </li></ul><ul><li>Treat fever and infections – avoid hyperthermia </li></ul><ul><li>Nutrition - avoid hyperglycemia </li></ul><ul><li>DVT prophylaxis </li></ul>
  52. 64. Secondary prevention of stroke <ul><ul><li>Aspirin - daily - 50-325 mg - an effective and inexpensive first-choice agent </li></ul></ul><ul><ul><li>Newer antiplatelet agents - clopidogrel and aspirin/dipyridamole combinations – </li></ul></ul><ul><ul><li>also effective in reducing recurrent stroke rate </li></ul></ul><ul><ul><li>may cause adverse effects that must be monitored. </li></ul></ul><ul><ul><li>Warfarin as indicated </li></ul></ul>
  53. 65. Secondary prevention of stroke <ul><li>Hypertension </li></ul><ul><li>Hyperlipidemia </li></ul><ul><li>Diabetes mellitus </li></ul>
  54. 66. That’s all folks !

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