neuro clinics 21- stroke case discussion
DESCRIPTION
ischemic and hemorrhagic strokeTRANSCRIPT
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Neuro-clinics 21
Dr Pratyush Chaudhuri
Supported by Nirmal clinics & Mankind Pharmaceuticals
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CASE DISCUSSIONAcute Ischemic StrokeIntra-cerebral hemorrhage
Dr Pratyush Chaudhuri
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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.
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Has he had a stroke syndrome ??
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What was the time of onset of the stroke?
Before 3.40pm 3:40 pm 4:00 pm 5:00 pm
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Stroke - clinical term acute loss of circulation to an area of the
brain ischemia corresponding loss of neurologic function.
Classified
hemorrhagic ischemic
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focal neurologic deficits sudden onset
weakness
sensory deficit
difficulties with language
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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
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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
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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
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Differential diagnosis Intracranial Abscess
BotulismEncephalitisHyperglycemiaHypertensive urgency/emergencyHypoglycemiaPsychiatric disorders/conversion disorderSeizureSpinal injuryUremiaIngestions (eg, ethanol)Intracranial neoplasm
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Why is time important?
Reperfusion strategies
improve blood flow and limit size of infarct
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What to do ??
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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
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CT Easily available Exquisitely sensitive for ICH
Normal brain – 35 HU
Grey matter – 39 HU
White matter – 32 HU
IV contrast not useful in 1st 24 hrs even though BBB brokenEnhancement seen after 72 hrs
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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 normal31 % misinterpreted
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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
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Loss of gray-white differentiation in the posterior aspect of the right frontal lobe
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The scan exhibits subtle, hyperacute ischemic changes, including effacement of the insular ribbon and lentiform nucleus edema of the right hemisphere.
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The hyperdense middle cerebral artery sign
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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
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Would you order an MRI?
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MRI
Higher sensitivity for infarcts
Better for posterior fossa, lacunar infarcts and small cortical strokes
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MRI not easily available / need skilled interpretation
Subtle signs may not be apparent in 1st 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
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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
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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
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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
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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
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Should we take a break ?Should we take a break ?
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What about a DSA ? Angio??
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DSA Final word - allowing for intraarterial
therapy also
But stroke risk 1- 2 % Needs special facilities Skilled operator
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This is the CT scan picture
What now ??
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Reperfusion strategiesimprove 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
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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 ptArrived at 5 pm
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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
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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
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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
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Exclusion criteria -- CT / lab findings
e/o major hypodensity or sulcal effacement
( > 1/3 of MCA territory)
Platelet count < 100,000 / mm³
Blood glucose < 50 mg % or > 400 mg %
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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
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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
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Pt’s BP – 200 / 110 mm Hg
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Candidate for thrombolysis - BP control
PretreatmentSBP >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 orEnalapril 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
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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 orDBP 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
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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
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Intensive care management Hemodynamic monitoring – non invasively or
invasively
Keep well hydrated
Use saline - no dextrose – avoid hyperglycemia
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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
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Drugs of choice
Labetalol
Enalapril
Nicardipine
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Pt lethargic , but opens eyes to call
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Intensive care management Airway – intubation – Inability to protect airway
Inadequate gas exchangePoor prognostic sign
Beware hypotension and raised ICP during induction for intubation
Keep pO2 ~100 and PCO2 ~ 35PEEP as deemed
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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 ºOsmotherapyInduced coma
No steroids
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General medical management Sedation – use short acting agents
Treat fever and infections – avoid hyperthermia
Nutrition - avoid hyperglycemia
DVT prophylaxis
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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
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Secondary prevention of stroke Hypertension
Hyperlipidemia
Diabetes mellitus
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That’s all folks !