Neuro-clinics 21

Dr Pratyush Chaudhuri

Supported by Nirmal clinics & Mankind Pharmaceuticals

CASE DISCUSSIONAcute Ischemic StrokeIntra-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

BotulismEncephalitisHyperglycemiaHypertensive urgency/emergencyHypoglycemiaPsychiatric disorders/conversion disorderSeizureSpinal injuryUremiaIngestions (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 1st 24 hrs even though BBB brokenEnhancement 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 normal31 % 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 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

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 ?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 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

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

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 / mm³

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

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

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

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

Intensive care management 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

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

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

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 !