Neuro clinics 21- stroke case discussion

Neuro-clinics 21 Dr Pratyush Chaudhuri Supported by Nirmal clinics & Mankind Pharmaceuticals

CASE DISCUSSION Acute Ischemic Stroke Intra-cerebral hemorrhage Dr Pratyush Chaudhuri

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.

Has he had a stroke syndrome ??

What was the time of onset of the stroke?
Before 3.40pm
3:40 pm
4:00 pm
5:00 pm

Stroke - clinical term
acute loss of circulation to an area of the brain ischemia corresponding loss of neurologic function.
Classified
hemorrhagic
ischemic

focal neurologic deficits sudden onset
weakness
sensory deficit
difficulties with language

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

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

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

Differential diagnosis
Intracranial Abscess Botulism Encephalitis Hyperglycemia Hypertensive urgency/emergency Hypoglycemia Psychiatric disorders/conversion disorder Seizure Spinal injury Uremia Ingestions (eg, ethanol) Intracranial neoplasm

Why is time important?
Reperfusion strategies
improve blood flow and limit size of infarct

What to do ??

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

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

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

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

Loss of gray-white differentiation in the posterior aspect of the right frontal lobe

The scan exhibits subtle, hyperacute ischemic changes, including effacement of the insular ribbon and lentiform nucleus edema of the right hemisphere.

The hyperdense middle cerebral artery sign

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

Would you order an MRI?

MRI
Higher sensitivity for infarcts
Better for posterior fossa, lacunar infarcts and small cortical strokes

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

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

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

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

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

Should we take a break ?

What about a DSA ? Angio??

DSA
Final word - allowing for intraarterial therapy also
But stroke risk 1- 2 %
Needs special facilities
Skilled operator

This is the CT scan picture What now ??

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

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

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

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

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

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 %

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

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

Pt’s BP – 200 / 110 mm Hg

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

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

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

Hemodynamic monitoring – non invasively or invasively
Keep well hydrated
Use saline - no dextrose – avoid hyperglycemia

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

Drugs of choice
Labetalol
Enalapril
Nicardipine

Pt lethargic , but opens eyes to call

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

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

General medical management
Sedation – use short acting agents
Treat fever and infections – avoid hyperthermia
Nutrition - avoid hyperglycemia
DVT prophylaxis

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

Secondary prevention of stroke
Hypertension
Hyperlipidemia
Diabetes mellitus

That’s all folks !

Neuro clinics 21- stroke case discussion

by Pratyush Chaudhuri

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Neuro clinics 21- stroke case discussion Presentation Transcript