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

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

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

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

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

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 exchange Poor prognostic sign Beware hypotension and raised ICP during induction for intubation Keep pO2 ~100 and PCO2 ~ 35 PEEP 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 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

Neuro clinics 21- stroke case discussion

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