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Neuro clinics 21- stroke case discussion

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ischemic and hemorrhagic stroke

ischemic and hemorrhagic stroke

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

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