Neurological complications of acute ischemic stroke

NeurologyR5 林念穎

2012/03/22

原由• 在神經內科病房有好多中風病人唷 , 中風病人除了吊吊 IVF, 吃 aspirin, 做復健之外 , 好像就沒再幹嘛了…住院就是在 「觀察」…那那那…到底是在觀察些什麼呢 ????

喔天那…那個中風病人怎麼突然consciousness change了…我是值班醫師 / 主護 , 我要想什麼呢 ?

Introduction

• Mortality after stroke still high– 3nd most common, after ischemic heart

disease and all neoplastic diseases

• Post-stroke complications account for 23~50% of deaths

• Neurological and medical complications

Introduction

• Neurological complications(1) brain edema(2) haemorrhagic transformation(3) seizures and epilepsy(4) recurrent stroke(5) sleep disorders & sleep-

disordered breathing…etc.• Less frequent than medical complications,

but occur earlier– Within 48~72 hours of stroke onset

(1) Brain Edema

• Brain edema: leading cause of death after stroke, in the first week

• Ionic imbalance due to energy depletion• Two types:

– Cytotoxic:• Occurs early, blood-brain barrier intact• High signal in diffusion-weighted MRI (DWI),

low signal in apparent diffusion coefficient (ADC)

– Vasogenic:• Late; blood-brain barrier compromised• High signal in T2-weighted and T2-FLAIR• Increased intracranial pressure, herniation,

additional ischemic injuries

Brain edema

www.thelancet.com/neurology Vol 10 April 2011

(1) Brain Edema

• Younger patients fatal brain edema, malignant MCA syndrome

• Overall risk of cerebral edema in anterior circulation ischemic stroke: 10~20%

• Occurs within first 4 days• Brain edema increased intracranial hypertension

(IICP)– Headache, vomiting– Herniations （腦疝脫）

• Brainstem compression is major cause of mortality!!!!

Herniation:

-Pressure against reticular formation in midbrain consciousness deterioration

- Compression of CN3 pupil dilatation

Malignant MCA Infarction

• MCA territory completely infarction rapidly developing massive swellingbrain herniation as near as 20 hour after onset

• 1~10% of all supratentorial ischemic strokes

• Overall mortality rate estimated 40~80% (compare to 7~23% for acute MCA infarctions)

• Predicted by large hypoattenuation (>2/3 of MCA territory) on brain CT– sensitivity 91%; specificity 94%

Figure 2: CT scans showing cerebral edema after ischemic infarct.

(A) CT scan showing cerebral edema (green arrow) with compression of the left ventricle (red arrow) after infarct of the left middle cerebral artery territory.

Cerebellar Edema

• Common in cerebellar infarctions; 17~54% of cerebellar

• Posterior fossa provides little space for compensation of mass effect

• Usually peaks on the 3rd day• CT scans displacement of 4th

ventricle, obstructive hydrocephalus, obliteration of basal cisterns

• Induce brainstem compression & obstructive hydrocephalus – Gaze palsy– Decline in consciousness level– Sudden apnea, cardiac arrhythmias– Hiccups lesions of lateral medulla,

pontomedullary area of brainstem

Cerebellar Edema

(B) CT scan showing posterior circulation stroke (left-sided posterior inferior cerebellar artery infarct) with involvement of the pons 10 h after onset of stroke (green arrows).

(1) Brain Edema• Treatment- medical

– General: close monitor for neurological worsening

– Osmotherapy: • Glycerol, mannitol, hyperosmolar saline solutions,

corticosteroids, barbiturates; unproven (level 3C)• May be harmfal in CVST

– Hypothermia (32~35 )℃ : • in small RCT (n=25), in addition to

decompressive surgery led to better outcome than surgery alone (level 3C)

(1) Brain Edema

• Surgical– Decompressive surgery

• Early decompressive hemicraniectomy (<48hr) improves survival and functional outcome in patients (aged < 60 years) with malignant cerebral artery infarction (level 1B)

• Suboccipital decompressive craniectomy-- recommended as therapy of choice in malignant cerebellar infarction (level 1B)

– External ventricular drainage (EVD)– • for patients with worsening levels of consciousness and

obstructive hydrocephalus secondary to cerebellar infarction

(2) Hemorrhagic Transformation

• Common; 30~40% of acute ischemic stroke– Symptomatic:

•0.6% in those with supportive care – Aspirin: small increase in bleeding risk, but

non-significant•6% of intravenous alteplase•7% of intra-arterial fibrinolytics and

mechanical embolectomy

(2) Hemorrhagic Transformation

• Risk factors of thrombolysis-related ICH– Old age (>65y/o):

• impaired rate of alteplase clearance, high frequency of cardioembolic stroke, age-associated microangiopathy (cerebral amyloid angiopathy or hypertensive microangiopathy)

– Larger infarct size mass effect on pre-treatment imaging

– High baseline systolic blood pressure– Congestive heart failure– High glucose concentrations/diabetes

mellitus

• Expands brain edema, increase ICP higher mortality

Haemorrhagic transformation

www.thelancet.com/neurology Vol 10 April 2011

ECASS classification of hemorrhagic transformation:Hemorrhagic infarction (HI)

• HI-1: small petechiae along margins of infarcted area

• HI-2: conflent petechiae within infarcted area; no mass effect

Parenchymal hemorrhages (PH)

• PH-1: hematoma less than 30% of infarcted area, with mild mass effect

• PH-2: hematoma in more than 30% of infarcted area with notable mass effect

(2) Hemorrhagic Transformation

• No intervention to reduce risk of hemorrhagic transformation

• Careful selection of suitable patients for thrombolytic therapy

• Antithrombotics not recommended for use in first 24hrs after thrombolytic treatment

• Management– Asymptomatic: no specific intervention– Symptomatic

•Medical•Surgical

(2) Hemorrhagic Transformation

• Medical: – Stop anti-thrombotic medication– Secondary to thrombolytic therapy

platelet and cryoprecipitate infusion to correct systemic fibrinolytic state created by alteplase (level 2BC)

– Intravenous vitamin K to reverse effects of warfarin (level 1B)

• Surgical:– Supratentorial: lobar clots >30 mL and

within 1 cm of surface (level 2B)– Cerebellar hemorrhage > 3cm (level 1B)

(2) Hemorrhagic Transformation

• Management– Antithrombotic therapy after hemorrhagic

transformation • Depends on risk of subsequent arterial or venous thromboembolism,

risk of recurrent intracerebral hemorrhage and clinical state of patient

• Antiplatelet: – safer choice than warfarin for patients with lower risk

of cerebral infarction (eg non-valvular Af), but with higher risk of rebleeding (eg elderly with lobar ICH, possible amyloid angiopathy)

• Warfarin: – In patients with high risk of thromboembolism (Level

2B)– Can be restarted 7~10 days after onset of

ICH

(3) Seizure• Early seizures: within 1~2 weeks

– Frequency: 2~23%– Cellular biochemical dysfunction electrically

excitable tissue– Recurrence rate 16%

• Delayed: > 2 weeks– Frequency: 3%~67%– Mechanism: gliosis, meningocerebral cicatrices

(scar)– Recurrence rate more than 50%

• Prognosis:– Recurrent seizure in post-stroke seizures increase

disability, vascular cognitive impairment

(3) Seizure

• Risk factors:– Venous sinus thrombosis (more than

arterial stroke)• In one study, 40% CVST had seizure at

presentation, additional 7% within 2 weeks of diagnosis

– Large cortical infarcts, multiple infarcts, embolic stroke, hemodynamic and metabolic disturbances

(3) Seizure

• Management– No clear guideline for when to initiate

anticonvulsant therapy, choice of therapy, or for duration of therapy

– Prophylactic use not recommended– Early seizures short-term AED for 3~6

months– Late seizures require long-term treatment

(4) Recurrent Stroke

• Risk of early stroke recurrence: 10% at 1 week, 2~4% at 1 month, 5% yearly thereafter

• Major risk factors of recurrence: – Old age, – previous stroke, – diabetes, – hypertension, – atrial fibrillation, cardiac diseases, – smoking, – carotid/vertebrobasilar stenosis (large artery

atherosclerosis)

(4) Recurrent Stroke

• Management– Antiplatelet therapy

• First line for non-cardioembolic ischemic stroke or TIA (level 1A)

– Anticoagulation for atrial fibrillation• 68% RRR with warfarin vs 19% with aspirin (level 1A)

– Carotid endarterectomy and endovascular interventions

• Early carotid endarterectomy (first 2 weeks) more beneficial (level 1A)

• Carotid angioplasty reserved for those contraindicated to carotid endarterectomy (level 2B)

(4) Recurrent Stroke

– Treatment of hypertension• Controversial

– Reduction of elevated cholesterol (level 1A)

– Blood sugar control• Hyperglycemia (> 140 mg/dL) insulin therapy in

acute ischemic stroke (level 2C)

(5) Sleep disorders

• Frequent in initial stages after stroke– 10~50% of stroke patients– Hypersomnia (increased sleep need), excessive daytime

sleepiness, insomnia

• Bilateral paramedian thalamus, brainstem, large hemispheric stroke with mass effect

• Associated with depression, anxiety, sleep-disordered breathing, drugs, post-stroke pain, medical complications (UTI, respiratory infections, nocturia), environmental factors (noise, light)

(5) Sleep-disordered Breathing

• Obstructive apnea– Most common form, over 50% of patients– Share same risk factors as stroke: age, obesity, hypertension – Collapse of upper airway– Treat with continuous positive airway pressure

breathing

• Central apnea= Ondine’s curse

• Mixed apnea

• 50~72% of stroke patients

Ondine’s curse

Ondine is a water nymph and falls in love with a handsome knight, Sir Lawrence, and they are married.

One afternoon, she sees Lawrence lying in the arms of another woman.

Ondine curses him, “You swore faithfulness to me with every waking breath. As long as you are awake, you shall have your breath, but should you ever fall asleep, then that breath will be taken from you and you will die!"

Ondine’s curse

• Respiratory control:– Voluntary: supramedullary respiratory

control; cerebral cortex corticospinal tract

– Automatic: 　• Regulates breathing automatically in response to

the changes in oxygen and carbon dioxide in the blood

• Respiratory center in medulla and pons

Ondine’s curse

• Ondine’s curse– impairment of the automatic respiration– no damage to the voluntary respiration

• Lateral medullary infarction in distal vertebral artery occlusion

• Central apnea during sleep

• Progress to fatal respiratory failure need mechanical ventilation

Take home message

• Neurological complications occur early after ischemic stroke lead to death within first few days (high mortality rate)

• Improved detection and management is important

• Neurological complications include:– Brain edema– Hemorrhagic transformation– Post-stroke seizures– Recurrent stroke– Sleep disorder and sleep-disordered breathing– Delirium

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