4 Introduction Mortality after stroke still high 3nd most common, after ischemic heart disease and all neoplastic diseasesPost-stroke complications account for 23~50% of deathsNeurological and medical complications
5 Introduction (1) brain edema (2) haemorrhagic transformation 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 earlierWithin 48~72 hours of stroke onset
6 (1) Brain EdemaBrain edema: leading cause of death after stroke, in the first weekIonic imbalance due to energy depletionTwo types:Cytotoxic:Occurs early, blood-brain barrier intactHigh signal in diffusion-weighted MRI (DWI), low signal in apparent diffusion coefficient (ADC)Vasogenic:Late; blood-brain barrier compromisedHigh signal in T2-weighted and T2-FLAIRIncreased intracranial pressure, herniation, additional ischemic injuries
8 (1) Brain Edema Brainstem compression is major cause of mortality!!!! Younger patients fatal brain edema, malignant MCA syndromeOverall risk of cerebral edema in anterior circulation ischemic stroke: 10~20%Occurs within first 4 daysBrain edema increased intracranial hypertension (IICP)Headache, vomitingHerniations （腦疝脫）Brainstem compression is major cause of mortality!!!!
9 Herniation:Pressure against reticular formation in midbrain consciousness deterioration- Compression of CN3 pupil dilatation
10 Malignant MCA Infarction MCA territory completely infarctionrapidly developing massive swellingbrain herniation as near as 20 hour after onset1~10% of all supratentorial ischemic strokesOverall 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%
11 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.
12 Cerebellar EdemaCommon in cerebellar infarctions; 17~54% of cerebellarPosterior fossa provides little space for compensation of mass effectUsually peaks on the 3rd dayCT scans displacement of 4th ventricle, obstructive hydrocephalus, obliteration of basal cisterns
13 Cerebellar EdemaInduce brainstem compression & obstructive hydrocephalusGaze palsyDecline in consciousness levelSudden apnea, cardiac arrhythmiasHiccups lesions of lateral medulla, pontomedullary area of brainstem
14 (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).
15 (1) Brain Edema Treatment- medical General: close monitor for neurological worseningOsmotherapy:Glycerol, mannitol, hyperosmolar saline solutions, corticosteroids, barbiturates; unproven (level 3C)May be harmfal in CVSTHypothermia (32~35℃):in small RCT (n=25), in addition to decompressive surgery led to better outcome than surgery alone (level 3C)
16 (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
17 (2) Hemorrhagic Transformation Common; 30~40% of acute ischemic strokeSymptomatic:0.6% in those with supportive careAspirin: small increase in bleeding risk, but non-significant6% of intravenous alteplase7% of intra-arterial fibrinolytics and mechanical embolectomy
18 (2) Hemorrhagic Transformation Risk factors of thrombolysis-related ICHOld 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 imagingHigh baseline systolic blood pressureCongestive heart failureHigh glucose concentrations/diabetes mellitusExpands brain edema, increase ICP higher mortality
19 Haemorrhagic transformation ECASS classification of hemorrhagic transformation:Hemorrhagic infarction (HI)HI-1: small petechiae along margins of infarcted areaHI-2: conflent petechiae within infarcted area; no mass effectParenchymal hemorrhages (PH)PH-1: hematoma less than 30% of infarcted area, with mild mass effectPH-2: hematoma in more than 30% of infarcted area with notable mass effectVol 10 April 2011
20 (2) Hemorrhagic Transformation No intervention to reduce risk of hemorrhagic transformationCareful selection of suitable patients for thrombolytic therapyAntithrombotics not recommended for use in first 24hrs after thrombolytic treatmentManagementAsymptomatic: no specific interventionSymptomaticMedicalSurgical
21 (2) Hemorrhagic Transformation Medical:Stop anti-thrombotic medicationSecondary to thrombolytic therapyplatelet 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)
22 (2) Hemorrhagic Transformation ManagementAntithrombotic therapy after hemorrhagic transformationDepends on risk of subsequent arterial or venous thromboembolism, risk of recurrent intracerebral hemorrhage and clinical state of patientAntiplatelet: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
23 (3) Seizure Early seizures: within 1~2 weeks Delayed: > 2 weeks Frequency: 2~23%Cellular biochemical dysfunction electrically excitable tissueRecurrence rate 16%Delayed: > 2 weeksFrequency: 3%~67%Mechanism: gliosis, meningocerebral cicatrices (scar)Recurrence rate more than 50%Prognosis:Recurrent seizure in post-stroke seizures increase disability, vascular cognitive impairment
24 (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 diagnosisLarge cortical infarcts, multiple infarcts, embolic stroke, hemodynamic and metabolic disturbances
25 (3) SeizureManagementNo clear guideline for when to initiate anticonvulsant therapy, choice of therapy, or for duration of therapyProphylactic use not recommendedEarly seizures short-term AED for 3~6 monthsLate seizures require long-term treatment
26 (4) Recurrent StrokeRisk of early stroke recurrence: 10% at 1 week, 2~4% at 1 month, 5% yearly thereafterMajor risk factors of recurrence:Old age,previous stroke,diabetes,hypertension,atrial fibrillation, cardiac diseases,smoking,carotid/vertebrobasilar stenosis (large artery atherosclerosis)
27 (4) Recurrent Stroke Management Antiplatelet therapyFirst line for non-cardioembolic ischemic stroke or TIA (level 1A)Anticoagulation for atrial fibrillation68% RRR with warfarin vs 19% with aspirin (level 1A)Carotid endarterectomy and endovascular interventionsEarly carotid endarterectomy (first 2 weeks) more beneficial (level 1A)Carotid angioplasty reserved for those contraindicated to carotid endarterectomy (level 2B)
28 (4) Recurrent Stroke Treatment of hypertension ControversialReduction of elevated cholesterol (level 1A)Blood sugar controlHyperglycemia (> 140 mg/dL) insulin therapy in acute ischemic stroke (level 2C)
29 (5) Sleep disorders Frequent in initial stages after stroke 10~50% of stroke patientsHypersomnia (increased sleep need), excessive daytime sleepiness, insomniaBilateral paramedian thalamus, brainstem, large hemispheric stroke with mass effectAssociated with depression, anxiety, sleep-disordered breathing, drugs, post-stroke pain, medical complications (UTI, respiratory infections, nocturia), environmental factors (noise, light)
30 (5) Sleep-disordered Breathing Obstructive apneaMost common form, over 50% of patientsShare same risk factors as stroke: age, obesity, hypertensionCollapse of upper airwayTreat with continuous positive airway pressure breathingCentral apnea= Ondine’s curseMixed apnea50~72% of stroke patients
31 Ondine’s curseOndine 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!"
32 Ondine’s curse Respiratory control: Voluntary: supramedullary respiratory control; cerebral cortex corticospinal tractAutomatic: Regulates breathing automatically in response to the changes in oxygen and carbon dioxide in the bloodRespiratory center in medulla and pons
33 Ondine’s curse Ondine’s curse impairment of the automatic respirationno damage to the voluntary respirationLateral medullary infarction in distal vertebral artery occlusionCentral apnea during sleepProgress to fatal respiratory failure need mechanical ventilation
34 Take home messageNeurological complications occur early after ischemic stroke lead to death within first few days (high mortality rate)Improved detection and management is importantNeurological complications include:Brain edemaHemorrhagic transformationPost-stroke seizuresRecurrent strokeSleep disorder and sleep-disordered breathingDelirium