Dr. Nguyen Anh Tuan

Goals

 Work up for TIA and stroke  Window time for TPA, recommendation  Treatment of hemorrhagic stroke  BP control in ICH  SAH: emergency treatment

Stroke – incidence and prevalence

Cause of death

1. Cardiovascular disease 2. Cancer 3. Stroke

531.000 new cases of stroke and 200.000 recurrences of stroke each year in the US

In 22 European countries with a combined population of approximately 500 million, almost one million strokes are estimated to occur each year

Sorelle R. Circulation 2000;102:E9047-9 Brainin M et al. Eur J Neurol 1999;7:5-10

Stroke – definitions

An injury to the brain caused by:

(ischaemic stroke)

or

 Interruption of blood flow

(haemorrhagic stroke)

 Bleeding into or around the brain

Risk factor  Hypertension  Diabetes Mellitus  Cardiac disease  Hyperlipidaemia  Smoking  Family history  Obesity

ANATOMY: Blood supply to the brain

Circle of Willis

Stroke – diagnosis

Stroke

Common symptoms  Weakness and sensory loss down one side of the body

 Disturbances of

consciousness and confusion

 Impariment of speech,

vision and co-ordination of movement

Computed tomography (CT)

 Principle: differential absorption of x-ray

beams by different tissues

 Less time  Less expensive  More available in emergency rooms  Not reliable if done too early

CT scan

CT

Easily detects  Blood products (haemorrhages larger than 1 cm diameter)

Blood

 Hydrocephalus  Brain oedema  Herniation

Brain tissue

Magnetic resonance imaging (MRI)

Cerebral infarction

 High-resolution neural imaging technique  Different parts of the brain have different signal intensities on T1- or T2-weighted images

MRI scan

Diffusion-weighted imaging (DWI) MRI

 Best way to image acute stroke  Ischemia can be visualised as early as within

30 minutes of stroke

 Relies on reduction of random diffusion

(Brownian motion) of water after acute stroke

MRI scan

Features of ischaemic region  Swollen cells  Reduced extracellular

space

 Decrease in diffusion of

water molecules

Ischaemic region

Case  At 6.30pm, a female collapsed at a shopping mall  At 6.40 you find a woman sitting on the bench, she

is confuse but response to verbal stimuli

 Summary signs and symptoms:

 Regular heart rate and adequate perfusion  No chest pain  Right-side paralysis  Dysarthria What additional assessment do you need?

Case

 63-y –o woman  Facial drop (ask patient to show teeth and smile)  Arm drift  Speech  Patient demonstrate a right-side facial drop, right

arm weakness and slurred speech

What is your conclusion from your exam?

Clinical syndrome: occlusion  MCA infarction:

 Dominant hemisphere: speech affected, comprehension

and expression speech. The other side: hemianopia

 Limbs are flaccid and areflexic

Clinical syndrome: occlusion

cortical sensory loss in the leg  PCA occlusion: cortical bliness  Lacunar infarct: occlusion of small perforating

vessels, internal capsule, basal ganglia, thalamus, pons  Brainstem stroke

 ACA occlusion: contralateral weakness and

Cerebral ischaemia Duration of ischaemia

 Cerebral ischaemia can produce

irreversible injury to highly vulnerable neurons in 5 minutes

 If cerebral ischaemia persists for

>6 hours, infarction of part or all of the involved vascular territory is completed

 Clinical evidence depends on the

location of stroke

Strokes are an EMERGENCY

right away – CALL 9-1-1 in US (115 in Vietnam)

 If patients are having a Stroke come to the hospital

Case (continue…)

 What is the next step?

 7.15pm (45munutes after symptom onset)  Patient arrives in the ED, the nurse immediately triage the patient to the critical area of the ED and notifies the physician of the arrival and that she is a possible thrombolytic candidate

Once patients are at the Hospital

 CT or MRI of the brain

 ECG

 Diagnostic Testing

Thrombolytics (t-PA)

Some criteria for thrombolytics  Should preferably be given within 3 hours of symptom

onset

 No other likely explanation for the neurologic symptoms  No significant risk of bleeding  No evidence of bleeding on head CT scans  No evidence of early infarct sign on head CT scan Benefit  30% likely to have minimal or no disabilities after 3 or 12

months

Adverse effects (5%)  Significant brain hemorrhage

Recomemdation for TPA

treatment can be initiated within 3 h of symptom onset, we recommend IV recombinant tissue plasminogen activator (r-tPA) over no IV r-tPA (Grade 1A).  In patients with acute ischemic stroke in whom

treatment can be initiated within 4.5 h but not within 3 h of symptom onset, we suggest IV r-tPA over no IV r- tPA (Grade 2C)

 In patients with acute ischemic stroke in whom

IV TPA vs IA TPA

 In patients with acute ischemic stroke in whom treatment cannot be initiated within 4.5 h of symptom onset, recommend against IV r-tPA (Grade 1B).

 In patients with acute ischemic stroke due to

proximal cerebral artery occlusions who do not meet eligibility criteria for treatment with IV r-tPA, recommend intraarterial (IA) r-tPA initiated within 6 h of symptom onset over no IA r-tPA (Grade 2C).

 Merci vs Solitaire

Antiplatelets

After first stroke

Acetylsalicylic acid (ASA)  Small benefit within 48 hours of stroke onset  Delay for 24 hours if receiving thrombolytics

After recurrent stroke with taking ASA  Consider clopidogrel or dipyramidole/aspirin

 In patients who do not merit or qualify for aggressive acute thrombolytic treatment, therapy with ASA is warranted.

 ASA should be started within 48 hours of stroke onset  In patients with a contraindication for ASA, dypiridamole or clopidogrel can be used.

Transient ischaemic attack (TIA)

suddenly occur, then disappear; can persist up to 24 hours

 Brief episode in which neurological deficits

brain damage

 Temporary arterial blockage, with no resultant

TIA: Differential diagnosis

PLEASE… Pay Attention to these symptoms

 More that 1/3 of people will go on to have an actual

stroke

 5% of strokes (among TIA) will occur within 1

month of the TIA or first stroke

 12% will occur within 1 year  20% will occur within 2 years  25% will occur within 3 years

 TIA’s should not be ignored

TIA • Aspirin reduces risk of stroke by 15-20% • Carotid endarterectomy (CEA) should be considered for

patients with large vessel atherothrombotic disease in the internal carotid artery that causes low flow or embolic TIAs

• CEA should be done within 2 weeks if no contraindication

with mortality <6%. Very early (within 48h) is not recommended

• Virtually all patients with atrial fibrillation who have a

history of stroke or TIA should be treated with warfarin in the absence of contraindications

HAEMORRHAGIC STROKE

Primary intracerebral haemorrhage

include chronic hypertension

 The most common non-traumatic causes

 Often occurs in the internal capsule and/or basal ganglia, but it can occur in any part of the cortex, in the pons and cerebellum.

 Clinical signs depend on the location  Reduced conscious level due to mass effect.  Difficult to differentiate a haemorrhage from an

infarct.

Emergency Management

 For patients with ICH, emergency management may

include

 Neurosurgical interventions for hematoma evacuation,  External ventricular drainage or invasive monitoring and

treatment of ICP,

 BP management, intubation, and reversal of coagulopathy.

Cooper D, Jauch E, Flaherty ML. Critical pathways for the management of stroke and intracerebral hemorrhage: a survey of US hospitals. Crit Pathw Cardiol. 2007;6:18 – 23.

1- CLOT REMOVAL

 Physical effect of the hematoma (mass effects)  As yet, surgical evacuation has not been shown to be

beneficial

investigation in the STICH II and MISTIE clinical trials, the findings of which could limit adverse surgical effects

 Two potential approaches are currently under

Mendelow AD, Gregson BA, Mitchell PM, Murray GD, Rowan EN, Gholkar AR. Surgical trial in lobar intracerebral haemorrhage (STICH II) protocol. Trials 2011; 12: 124 Morgan T, Zuccarello M, Narayan R, Keyl P, Lane K, Hanley D.Preliminary findings of the minimally- invasive surgery plus rtPA for intracerebral hemorrhage evacuation (MISTIE) clinical trial. Acta Neurochir Suppl 2008; 105: 147–51

2- Hematoma expansion

 A subset of patients with intracerebral haemorrhage undergoes haematoma expansion within the first day after ictus

expansion

 Two types of clinical trial have focused on haematoma

First approach

have been studied: VIIa infusion, platelet infusion

 Agents that alter the coagulation cascade or fibrinolysis

VIIa infusion  Use of factor VIIa is associated with an increased rate

of thromboembolic complications.

 Therefore, studies have focused on ascertaining which patients might benefi t best from factor VIIa admini stration

 Evidence of haematoma expansion with the spot

sign

Mayer SA, Brun NC, Begtrup K, et al. Effi cacy and safety of recombinant activated factor VII for acute intracerebral hemorrhage. N Engl J Med 2008; 358: 2127–37 Mayer SA, Brun NC, Begtrup K, et al. Recombinant activated factor VII for acute intracerebral hemorrhage. N Engl J Med 2005; 352: 777–85

Platelet infusions Use of platelet transfusions for patients on antiplatelet

treatment (PATCH trial)

 Reported some benefi t of early platelet transfusion in patients with intracerebral haemorrhage with low platelet activity or who were known to have received antiplatelet treatment

The Internet Stroke Center. Platelet transfusion in cerebral hemorrhage “PATCH”. http://www.strokecenter.org/trials/ clinicalstudies/platelet-transfusion-in-cerebral-hemorrhage/ description (accessed May 24, 2012)

Second approach

expansion is lowering of blood pressure

 Trial INTERACT (1), ICH ADAPT (2), ATACH (3), reduced hematoma expansion has been reported

 The second approach to prevention of haematoma

(1) Anderson CS, Huang Y, Arima H, et al. Eff ects of early intensiveblood pressure-lowering treatment on the growth of hematoma andperihematomal edema in acute intracerebral hemorrhage: the Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial (INTERACT). Stroke 2010; 41: 307–12 (2) Butcher K, Jeerakathil T, Emery D, et al. The Intracerebral Haemorrhage Acutely Decreasing Arterial Pressure Trial: ICHADAPT. Int J Stroke 2010; 5: 227–33 (3) Qureshi AI, Palesch YY, Martin R, et al. Eff ect of systolic blood pressure reduction on hematoma expansion, perihematomal edema, and 3-month outcome among patients with intracerebral hemorrhage: results from the antihypertensive treatment of acute cerebral hemorrhage study. Arch Neurol 2010; 67: 570–76

Subarachnoid haemorrhage  Causes

 Saccular (‘berry’) aneurysms: 70%.  Arteriovenous malformations (AVMs): 10%.  Not defined: 20%.

 Patients complain of a severe headache the worst

headache they have ever had.

 Nausea and vomiting often occur due to raised

intracranial pressure.

 Clinical features

 The premier symptom is a sudden, severe headache

(97 percent of cases) classically described as the "worst headache of my life."

 The headache is lateralized in 30 percent of patients, predominantly to the side of the aneurysm. The onset of the headache may or may not be associated with a brief loss of consciousness, seizure, nausea or vomiting, and meningismus.

respectively.

 In one series, these occurred in 53, 77, and 35 percent

minor hemorrhage or "warning leak," manifested only by a sudden and severe headache (the sentinel headache) that precedes a major SAH by 6 to 20 days.

 A systematic literature review through September

2002 found that the incidence of sentinel headaches in aneurysmal SAH ranged from 10 to 43 percent

 Approximately 30 to 50 percent of patients have a

Immediate management

(stronger analgesics may depress conscious level and mask deterioration).

 Nimodipine (a calcium-channel blocker): reduces

vasospasm and morbidity/mortality).

 Regular neurological observations.  Bed rest and fluid replacement.  Analgesia for headache: codeine or dihydrocodeine

considered if aneurysm is secured).

 The routine use of prophylactic anticonvulsants is

controversial, but if seizures occur anticonvulsants should be commenced.

 Transfer to neurosurgical unit or intervenist.

 Control of hypertension (triple H should be

stroke by 15-20%, warfarin for AF

• In TIA, carotid endarterectomy should be done within

2 weeks if no contraindication

 TIA should not be ignored, Aspirin reduces risk of

3 hour, may benefit up to 4,5 hour

 Ischemic stroke: Time is brain, window time for TPA is

hour, consider thromboectomy

 Proximal cerebral artery occlusions: IA TPA within 6

Summary

treatment after first stroke, other anti-platelets should be considered

 Aspirin benefit in acute stroke and long-term

110 mmHg, treatment should be started when SBP > 180 mmHg (SBP 140mmg appeared to be save). Look for “spot sign”

 In ICH patient: mean BP should be control around

neurological unit or intervention radiologist

 In SAH: transfer to the hospital which has