Introduction Mortality after stroke still high –3 nd 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 swelling brain 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 3 rd day CT scans displacement of 4 th 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 –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