stroke Department of Neurology, UK 2. LF Aleš Tomek December 2010
Dec 31, 2015
stroke
Department of Neurology, UK 2. LFAleš TomekDecember 2010
Evidence based therapy of stroke
ČNS ČLS JEP – Czech guidelineswww.cmp.cz
ESO Guidelines ischemic 2009, ICH 2006 www.eso-stroke.org
AHA-ASA Guidelines ischemic 2009, SAH 2009, ICH 2010
www.americanheart.org
Reading
Tomek et al. Neurointenzivní péče 2012
Školoudík et al. Neurosonologie 2003Uchino et al. Acute stroke care 2011Mohr, Choi, Grotta et al. Stroke 2008Caplan’s Stroke, 4th ed. 2009
Stroke typesSTROKE
Ischemic
TIA
RIND
Completed stroke
ICH
SAH
Venous thrombosis
3rd most frequent cause of death
11 640 200711 685 200812 192 200911 567 2010
32 deaths per day
(Deaths – total in 2010 - 106 844 persons)
Epidemiology in Czech Rep.
www.uzis.cz 9/2012
Hlavní příznaky - FAST (Face Arm Speech Test) 1x
Clinical signs – minor (2x)
Acute• Coma• Hemihypesthesia• Dysarthria• Hemianopia• Diplopia• Headache• Meningeal signs• Vertigo with nausea
Clinical examination and signs
FAST FaceArmSpeechTest
Internal Esp. cardio-
pulmonaryNeurological Consciousness Speech, mnestic
and cognitive, neglect
Cranial nerves Motoric and
sensory
Stroke scales
COMA GLASGOW COMA FOUR SCORE
ACUTE ISCHEMIC NIHSS
ICH ICH SCORE
SAH HUNT HESS WFNS (WORLD FEDERATION OF NEUROSURGEONS)
OUTCOME MODIFIED RANKIN SCALE
Prehospital care
ABCCorrect diagnosis or suspicion of
stroke (FAST)Do not lower blood pressure
(220/120) Immediate transportation to stroke
center
Situace u nás 2013
Tvorba sítě iktových center (Věstník 2 a 8/2010 MZd ČR), start 1.1.2011
KCC (komplexní cerebrovaskulární centrum) 10 center
IC (iktové centrum) 1. vlna - 23 center 2. vlna – 12 center
Soláň 13. - 14. 1. 2012
Ústecký kraj
I. MNUL
II. Chomutov
II. Děčín
II. Teplice Liberecký kraj
I. KN Liberec
II. Česká Lípa
Jihočeský kraj
I. Nemocnice Č. Budějovice
II. Nemocnice Písek
Královéhradecký kraj
I. FN Hradec Králové
II. Obl.nem.Trutnov
Jihomoravský kraj
I. FNUSA + FN Brno
II. Břeclav
II. Vyškov
Moravskoslezský kraj
I. FN Ostrava II. MN Ostrava
II. Vítkovická nemocnice
II. Krnov
II. Třinec
II. Karviná
Olomoucký kraj
I. FN Olomouc
Kraj Praha
I. Nemocnice Na Homolce
I. ÚVN
II. FN Motol II. VFN
II. FNKV + FTNsP
Plzeňský kraj
I. FN Plzeň
Karlovarský kraj
II. Nem. Sokolov
Zlínský kraj
II. Krajská nem.
T. Bati ZlínKraj Vysočina
II. Nemocnice Jihlava
Středočeský kraj
II. Kolín
II. Kladno
Pardubický kraj
II. Pardubice
II. Litomyšl
Komplexní cerebrovaskulár
ní a iktová centra
Soláň 13. - 14. 1. 2012
Ústecký kraj
Ústí n. Labem
Chomutov
Děčín
Teplice
Nem. Litoměřice
Liberecký kraj
KN Liberec
Česká Lípa
Jihočeský kraj
I. Nemocnice Č. Budějovice
II. Nemocnice Písek
Královéhradecký kraj
FN Hradec Králové
Obl.nem.Trutnov
Obl. Nem. Náchod
Jihomoravský kraj
FNUSA + FN Brno
Břeclav
Znojmo
Vyškov
Moravskoslezský kraj
FN Ostrava MN Ostrava
Vítkovická nemocnice
Krnov
Třinec
Karviná
Olomoucký kraj
IFN Olomouc
Prostějov
Hl. m. Praha
Nemocnice Na Homolce
ÚVN
FN Motol VFN
FNKV + FTNsP
Plzeňský kraj
I. FN Plzeň
Karlovarský kraj
Nem. Sokolov
Nem. Karlovy Vary
Zlínský kraj
Zlín (T. Bati)
Uh. Hradiště
Kraj Vysočina
JihlavaNové Město na Moravě
Středočeský kraj
Kolín
Kladno
Mladá Boleslav
Příbram
Pardubický kraj
Pardubice
Litomyšl
Komplexní cerebrovaskulár
ní a iktová centra
TIA x ischemic stroke
TIA x RIND x completed stroke 35% of TIA’s have DWI MR lesions Same mortality and morbidity as
minor stroke AHA-ASA 2009 new definition of TIA:= tissue definition
No signs of acute MR or CT lesion
Stroke imaging - CT
• Gold standard• ischemic / hemorhagic + availability, speed, senzitivity for
hemorhagy,... - negative first 3-6 hours, poor for
brainstem
ischemie
hemorhagie
Early CT diagnostics of stroke
Native CT – markers of early ischaemia:
Early hypodenzityLower difference between gray x white matter Lost gyrification (SA space)Dense artery sign (MCA)
MR diagnostics of stroke
More senzitive for smaller strokes and for brainstem
Early vs. Old ischemic stroke (DWI)Availability and duration of exam
ischemie
ischemie
akutní ischemie
Penumbra concept
Penumbra
Benign oligemia
Ischemic core
CBF < 10 ml/100g/min (< 20%)Cytotoxic oedema + neuronal cell deathCBV, CMRO2 decreased to zeroOEF 100%CBF 10-18 ml/100g/min
Cell death without reperfusionLoss of function of neuronsOEF 100% can not stop decline CMRO2
Normal tissue CBF 20-50 ml/100g/minSurvives without reperfusionElevated oxygen extraction fraction (OEF) Normal cerebral metabolic rate of oxygen (CMRO2)
CBF 50-60 ml/100g/minFunctional for CPP 60-130 mmH, changes CBV Warach S. Stroke 2001;32:2460-2461.
DWI PWI mismatch
24 hours later….
CT Perfusion
CT angiography
Ultrasound (TCD and carotid)
MR angiography
DSA – digital subtraction angiography
Strategy of ischemic stroke therapy
RecanalizationNeuroprotectionTherapy of complications (oedema,
epilepsy, infection…)Secondary prevention of recurrent
strokeRestoration of function
(physiotherapy, occupational therapy
The only causal therapy - recanalization
Katzan et al, Arch Neurol 2004Thomas et al, N Engl J Med 2006
Intravenous
thrombolysis
Intraarterial
thrombolysis
Mechanical recanalization
Sonothrombotripsy2 - 30% patients with stroke
IVT
“Time is brain”
NNT 2
NNT 7 (3,1)
NNT 14
Saver JL. Stroke 2006;37(1):263-6.Hacke W et al. NEJMN 2008;359:1317 29.
Every 1 minute: • 1 900 000 neurons• 14 000 000 000 synapsis• 12 km of myelinated fibers
90 minutes
180 minutes
270 minutes
rtPA (Actilyse)
r-TPA (Actilyse) 0,9mg/kg, max. 90 mg t½= 3-8min
IVT limitations
CT or MR without blood
Max. 4,5 hours after beginning
Min. 30 min of duration
Serious disability NIHSS 4 – 25 (relative)
Age 18-80 (relative)
Rescue therapy after IVT
Assessment of efficiency Examination in 60. minute Recanalized only in 40-50% cases, early
reocclusion, recanalisation does not mean clinical effect
Our goal: What happened during IVT? TCCS or NIHSS (40% points down) Ultimate DSA (after 30/60 minutes)
RESCUE = mechanical
Intraarterial thrombolysis – IATCombined IVT + IAT
Sonothrombotripsy
Mechanical recanalization MERCI
Experimental methods
PTA balloon angioplasty and stenting +/- IAT laser microcavitation: LaTIS, EPAR Ultrasound cavitatione: Ekos, ACS Thrombus aspiration: AngioJet, Oasis, Neurojet
Solitaire FR
Solitaire FR
Solitaire FR
Stroke diagnosisIschemic
85%Before 4,5 hours
IVT
4,5 – 8 h w. penumbra
4,5-6 IA
4,5-8 IA, mech,
TT
After 4,5 hrs. Wo. penumbra
ICH 12-15%SAK 1%Correction of hemostasis and oedema
Timetable of stroke th.
Secondary prevention
Antithrombotic Antiplatelet Anticoagulation (VKA)
ACEI or AT1 blocker, diuretic
Statine
TOAST subtypes
TOAST, Adams et al, Stroke 1993N = incidence for 100 000 persons, Kolominsky-Rabas et al, Stroke 2001
Small vessel disease
25.8/100 000
Large vessel disease
15.3/100 000
Cardiogenic
30.2/100 000
Other known
2,1/100 000
Cryptogenic
39,3/100 000
Cerebral veins (sinuses) thrombosis = CVT
Therapy of CVT
Anticoagulation (3, 6 months, chronic)
Lifestyle changes (smoking, hormonal, drinking)
Depends on etiology of thrombofilic state Inborn (Leiden, homocysteine…) Acquired (hormonal, posttraumatic, post
infection, surgery…etc)
Intracerebral hemorrhage (ICH)
Dynamics of ICH
**Kazui et al. Stroke. 1996;27:1783-1787.
*Brott et al. Stroke. 1997;28:1-5
First 24 hrs– 20*-36%**volume progression(majority first 3 hours)
Treatment options in ICHTherapy
Stabilisation of hemostasis
Blood pressure correction
Surgery – treatment of mass effect and
of source of bleeding
Antioedematous therapy,
decompression
EVD, shunts
DiagnosticsCT
AngiographyMRI + MRA
RHB
Bleedingprogression
24hrs
Brain oedema
3-5.day
Hydrocephalus
14 days
RHB
Hypertension
Goal – 140/90
Hypertonics Aim 120 MAP (160/100), maximum 180/105, no more than
than 20% Normotonisi – aim 110 MAP (150/90),
max.160/95 ABP monitoring , i.v. therapy (Urapidil,
Esmolol, Enalapril, Nitroprusid)
hemostasis
APTT, Quick, trombocytes Trombocytes
treat <75 000, substitution in caso of antiplatelet medication
Warfarine INR <8 FP 2-3 TU INR >8 FP 6 TU Better concentrated prothrombin complex (fa. II, VII,
IX, X) Prothromplex Total TIM4 rFVIIa – best ever- 10 minutes (10-40 μg/kg) Vitamin K - after 6-12 hoours
Heparine protamine sulphate (1mg/100 IU, max. 50mg/10 min)
Surgery
Craniectomy (mass + source)Stereotactic – event. + rtPAExternal ventricular drainage
– event. + rtPA
Surgery yes:
Cerebellar above 10ml (>3-4cm) + GCS =<13
Lobar superficial (temporal lobe) 10-40ml or with later clinical progression
Typical BG initialy 10-30ml with good clinical state and later worsening (first 24-48 hrs)
ICH score 3 and age under 50 years Ultimum refugium in case of cranio-
caudal deterioration
Secondary prevention of ICH
PRIMARY 80% Recurrence/ yearHypertensive microangiopathy 2%Amyloid angiopathy 10,5%AVM 18%Cavernous angioma 4,5%
SECONDARY 20%Tumors
Exclude the source of bleeding (if possible)HypertensionCorrection of bleeding disorders and exclusion of anticoagulantsLifestyle - smoking, alcohol
Subarachnoidal hemorrhage (SAH)
SAH diagnostics
Headache 97%Meningeal syndrome (after 6-24
hrs)Nausea, vomitting, loss of
conscioussness + neurological deficite
Grading by Hunta and Hess HH 1-5 or WFNS
Diagnostic problems with HH1 – CSF exam.
In the first 24 hours DSA – to find and treat source of bleeding
SAH: Coiling x Cliping
Specific complications of SAHRebleeding (7%)- Majority in the first two weeks (4% first
day, after that 1,5% daily for the first 2 weeks)
Hydrocephalus (20%)- Obstruction type acute (EVD),
hyporesorbtive type later (shunting)
Vasospasms (46%)- Max. 5. – 12. day- TCD daily