1. Neurological complications of acute ischemic stroke
Neurology
R5 林念穎
2012/03/22

3. 原由 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?
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?

4. 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

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 earlier
Within 48~72 hours of stroke onset

6. (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

7. Brain edema
Vol 10 April 2011

8. (1) Brain Edema Brainstem compression is major cause of mortality!!!!
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!!!!

9. Herniation:
Pressure against reticular formation in midbrain consciousness deterioration
- Compression of CN3 pupil dilatation

10. 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%

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 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

13. Cerebellar Edema
Induce brainstem compression & obstructive hydrocephalus
Gaze palsy
Decline in consciousness level
Sudden apnea, cardiac arrhythmias
Hiccups 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 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)

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 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

18. (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

19. Haemorrhagic transformation
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
Vol 10 April 2011

20. (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

21. (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)

22. (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

23. (3) Seizure Early seizures: within 1~2 weeks Delayed: > 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

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

25. (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

26. (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)

27. (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)

28. (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)

29. (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)

30. (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

31. 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!"

32. 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

33. 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

34. 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

35. 下課囉~