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Vivien Puspitasari, dr, SpS

Faculty of Medicine
Pelita Harapan University

 Anatomy

& Brain circulation
 Stroke definition
 Types of stroke
 Pathophysiology
 Sign and symptom
 Diagnosis
 Treatment

which is thought to be due to either spontaneous haemorrhage into or over the brain substance (primary intracerebral haemorrhage or subarachnoid haemorrhage respectivelyhaemorrhagic stroke) or inadequate blood supply to a part of the brain as a result of flow. thrombosis or embolism associated with diseases of the blood vessel. heart or blood (ischemic stroke/cerebral infarction) .Stroke is clinical syndrome characterised by an acute loss of focal brain function lasting more than 24 hours or leading to death.

. heart or blood.Transient Ischemic Attack clinical syndrome characterised by the acute loss of focal brain or monocular function lasting less than 24 haours. thrombosis or embolism associated with diseases of the blood veseels. due to inadequate blood supply to a part of the brain or eyes as a result of low blood flow.

AVM .mortality 40%  50% . middle cerebral) ▪ Small vessel 20% (lacunar stroke)  30% Embolic (heart disease/ atherosclerosis)  Cardioembolic  Artery-to-artery  Hemorrhage: Incidence 20% . aneurysm. Infarction: Incidence 80% .Thrombotic – atherosclerosis ▪ Large-vessel 30% (carotid.mortality 60%  Intracerebral or subarachnoid  hypertension.

Carotid system = anterior b. completed stroke Based on vascular system a. TIA. POCI . Vertebrobasilar = posterior Bamford Classification TACI.Based on stadium / course a. PACI. LACI. RIND b. stroke in evolution c.

family history.carotis bifurcation  Risk factors: Hypertension.Atheroma  important factor in embolic & thrombotic stroke  Commonly rises at the junctions of arteries ex. Diabetes.Cholesterol. excess alcohol intake Cardioemboli  AF . smoking.

140 mm Hg . CBF = CPP/CVR  To maintaine CBF 50 ml/100mg/menit needs CPP 40 .AUTOREGULATION  Normally : CPP 70 – 100 mmHg (CPP=MAP – ICP) .

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saveable Around penumbra—hyperemia & edema.Neuron degeneration.   ISCHEMIC CORE  the lowest CBF . Dilatated blood vessel —high CBF—hyper perfusion . blood vessel dilatated . low Po2— nekrosis PENUMBRA  around ischemic core –higher CBF —loss cell function . High lactic acid .

lobar white matter (20%). pons (10%).Usually due to hypertension or ruptered aneurysm/ AVM. cerebellum (10%)  . bleeding disorders  Hypertension  Lipohyalinosis & microaneurysm (Charcot-Bouchard aneurysm) of small penetrating arteries within the brain  Ganglia basal (50%).

ANEURYSM HYPERTENSION .

a. anterior. komunikans anterior. serebri media.    Ruptured saccular aneurysm a. a. neck stiffness Complication : hydrocephalus . komunikans posterior Symptom: sudden severe headache = like being hit by a baseball bat = thunder clap.

 History taking  Physical & neurologic examination  Supportive examination  Treatment .

intracranial . infarct : . brain stem -Vascular system : Carotid Vertebrobasilar Etiopathology Ischemi.trombosis .Subarachnoid (SAH) Stadium •Stroke in evolution •Completed stroke •TIA : < 24 hours •RIND : < 2 weeks .emboli Hemorrhagic : .Stroke Stroke like No Yes Location -Brain : hemiphere .

cortical blindness  Ataksia  Vertigo  Tetraparesis  Dysphagia . extremities pareses (contralateral lesion)  Deficit of sensibilities  Afasia  Dysartria Vertebrobasilar system  Visual disturbance : diplopia.Carotis system symptom  Facial.

Trauma .Recurrent headaches (migrain) .Pure hemifacial weakness including forehead (Bell’s palsy) .Weakness with atrophy .Recurrent seizures .Fever prior to onset of symptoms .Gradual progressive course and insidious onset .The presence of any of the following should alert the physician to consider conditions other than stroke: .

1xdiastolic)-(3xateroma)-12  Score >1 haemorrhage  Score <1 infarct Consciousness: CM=0 . yes=1 Ateroma – diabetic history none=0 .3% and 93. .claudicatio Sensitivity : 89. Siriraj score SIRIRAJ STROKE SCORE (2.angina one/more=1 .3%.  Score system: Gajah Mada score.5xconcious)+(2x vomiting)+ (2xheadache) + (0. semi coma/coma=2 Vomiting & headache within 2 h : no=0. drowsy/stupor=1.2% Specificity : 90.

CT scan is 100% sensitive in documenting intracranial hemorrhage (ICH) and 96% sensitive in documenting subarachnoid hemorrhage (SAH). Obscuration of the lentiform nucleus 3.   Plain CT scan of the head is the initial neuroimaging study of choice in acute stroke. The main objective is to exclude hemorrhagic stroke and stroke mimickers. Effacement of the sulci . Dense MCA sign 2. 60% have “early” infarct signs when viewed very closely: 1. However. Loss of the gray-white interphase along the lateral insula (Insular ribbon sign) 4. Cerebral infarcts are often not documented within 3 hours from stroke onset.

Obscuration of lentiform nucleus Dense MCA sign Insular ribbon sign .

MRI is not recommended as routine evaluation of patients with acute ischemic stroke. time-consuming and less readily available. . It is more expensive. MRI has the technical advantage of documenting small lesions or those located in the brainstem or posterior fossa  MRI can detect early infarction as early as 90 minutes using Diffusion Weighted Imaging (DWI)  Despite the superior diagnostic yield of MRI over CT.

MRI DIFFUSION .

ventricular extension and hydrocephalus. a repeat plain CT scan after 24 hours is recommended especially in cases showing clinical deterioration to document hematoma enlargement and/or development of hydrocephalus.   CT can accurately document the exact location of the hemorrhage and the presence of mass effect. In hypertensive ICH. Computation of Hematoma Volume (Kothari method) Hematoma volume (in cc) = ( A x B x C ) : 2 A= Largest diameter of hematoma (in cm) B= Diameter perpendicular to A (in cm) C= Number of slices on CT scan with hemorrhage X slice thickness (in cm) .

RADIOIAMAGING: CT SCAN Ischemic stroke Hemorrhagic stroke .

MULTISLICES CT SCAN : CT Angiography .

pupils Perform stroke scales (NIHSS. diabetes. when needed use easily titratable IV or oral antihypertensive medication. RR. temperature. BP. If IVF is needed. liver disease.          Ascertain clinical diagnosis of stroke (history and physical exam are very important) Exclude common stroke mimickers Basic emergent supportive care (ABCs of resuscitation) Neuro-vital signs. Identify comorbidities (cardiac disease. GCS) Monitor and manage BP. gastric ulcer.9% NaCl . etc. use 0.) Recognize and treat early signs and symptoms of increased ICP Ensure appropriate hydration. MAP. treat if SBP>220 or DBP>120 or MAP>130 Precaution: Avoid precipitous drop in BP (not >20% of baseline MAP) Do not use rapid-acting sublingual agents.

 Allow “permissive hypertension” during the first week to ensure adequate CPP but ascertain cardiac and renal protection a. Treat if SBP>220 or DBP>120 or MAP>130 b. unless in the presence of:  Acute MI  Congestive heart failure  Aortic dissection  Acute pulmonary edema  Acute renal failure  Hypertensive encephalopath y . Defer emergency BP therapy if MAP is within 110-130 or SBP=185-220 mmHg or DBP=105-120 mmHg.

Thrombolytic therapy    If within 3 hours of stroke onset. the rest as infusion over 60 minutes. . If within 6 hours of stroke onset and in specialized centers. consider IV recombinant tissue plasminogen activator (rtPA) -----at least 30% more likely to have minimal or no disability at 3 months. Dose of rtPA is 0. 10% of total dose is given as IV bolus.9 mg/kg (maximum 90 mg). consider intra-arterial (IA) thrombolysis Streptokinase has no role in acute thrombolysis for ischemic stroke .

Antithrombotic therapy  Stroke non-cardioembolic : Aspirin 160-325 mg/day start as early as possible and continue for 14 days Anticoagulation  Stroke cardioembolic If source of embolism can be demonstrated. consider early anticoagulation with IV heparin or low molecular-weight heparin (LMWH) or Aspirin 160-325 mg/day (if anticoagulation is not possible or contraindicated) .

hypoxemia. hyperglycemia or hypoglycemia and hyperthermia (fever) during acute stroke in an effort to "salvage“ the ischemic penumbra .Neuroprotection Neuroprotective Interventions: The 5 “H” Principle  Avoid hypotension.

inflammatory cytokines.Neuroprotectans  Protect against excitotoxins and prolong neuronal survival  Block the release of glutamate. free radicals. and the accumulation of intracellular calcium cations. CITICHOLINE / CDP–choline helps increase phosphatidylcholine synthesis and inhibition of phospholipase A2 within the injured brain during ischemia .

Maintain MAP <130. Maintain adequate nutrition. 9. Manage increased ICP 4. Start anticonvulsants only if with seizures 5. 8. Rehabilitate early once stable. maintain normothermia and normoglycemia. The goals are to prevent complications and careful manage BP.Medical Treatment for all ICH: 1. but not lower than 110 mmHg 3. Prevent and treat infections. Prevent and treat respiratory complications.Practice bedsore precautions. 10. 11. 2. Ensure proper fluid and electrolyte balance. 6.Deep-vein thrombosis and pulmonary embolism prophylaxis . 7.

Non-surgical candidates  Patients with small hemorrhages (<10 mL) or minimal neurological deficits  Patients with GCS<5 except those who have cerebellar hemorrhage and brainstem compression  Patients with hematoma volume > 85 mL .

.Candidates for immediate surgery  Patients with cerebellar hemorrhage >3 cm who are neurologically deteriorating or have brainstem compression and hydrocephalus from ventricular obstruction  Patients with bleed associated with a structural lesion such as an aneurysm. AV malformation or cavernous angioma if there is a chance for good outcome and the vascular lesion is surgically accessible  Clinically deteriorating young patients with moderate or large lobar hemorrhage.  Ventricular drainage for patients with intraventricular hemorrhage with moderate to severe hydrocephalus.

All other patients may benefit from surgery  Patients with basal ganglia or thalamic hemorrhage  Patients with GCS >4  Patients with supratentorial hematoma with volume >30 cc .

vomit . Anisocoria 4. Bradycardia iii. Irregular respiration 3. Headache. Cushing’s triad i. Hypertension ii. Deteriorating level of sensorium 2.Signs and symptoms of increased ICP 1.

1. Strict glucose control between 80-110 mg/dL 5. Control agitation and pain with short-acting medications. 4. 2. May treat with phenytoin with a loading dose of 18-20 mg/kg IV then maintained at 3-5 mg/kg. Hyperglycemia may extend ischemic zone (penumbra) and further cause cerebral edema 6. Control seizures if present. Use stool softeners to prevent straining. No dextrose-containing IVF. Control fever. 3. Avoid hyperthermia. . such as NSAIDS and opioids. Status epilepticus should be managed accordingly.

Otherwise maintain normal pCO2 between 35 and 40.5-0.    Elevate the head at 30 to 45 degrees to assist venous drainage. Aim for serum osmolarity=310 mOsm/L. maintenance dose at 0.75 mg/kg) to decrease intravascular volume and free water.8) Hyperventilate only in impending herniation by adjusting tidal volume and pCO2 between 25 to 30. (Serum osmolarity = 2 (Na) + Glucose/18 + BUN /2. . Lost fluids must be replaced. Give osmotic diuretics: Mannitol 20% loading dose at 1 g/kg. This maneuver is usually effective only for approximately 6 hours. Hypertonic saline is an option and has the advantage of maintaining an effective serum gradient for a prolonged period with lower incidence of rebound intracranial hypertension.

Do CSF drainage in patients with intraventricular hemorrhage (IVH) or hydrocephalus.     Carefully intubate patients with GCS 8 or less. Available locally is thiopental (loading dose=10 mg/kg. maintenance dose titrated at 112 mg/kg/hour continuous infusion) Consider surgical evacuation for mass lesions. Consider decompressive hemicraniectomy in cases of malignant middle cerebral artery infarcts . or those unable to protect the airway. Use barbiturates if all other measures fail.

1989. * and who have mainly brainstem features → scores less severe despite significant deficits .Goldstein et al 1989) NIHSS is a 0– 24 point scale (11 item) Score : * higher than 15 points – major stroke * a score of 4 – 15 points – moderate stroke * less than 4 points – mild stroke NIHSS is performed during the bedside neurological evaluation (twice exam : 24 hours and discharge) Disadvantage of NIHSS scale is * not good for posterior circulation stroke.     NIHSS was developed to quantify neurological deficits status in stroke patients based on a scale originally devised at the university of Cincinnati Stroke Center (Brott et all.

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Grade 0 No symptoms at all Grade 1 No significant disability despite symptoms: able to carry out usual duties and activities  Grade 2 Slight disability: unable to carry out all previous activities but able to look after own affairs without assistance  Grade 3 Moderate disability: requiring some help. and unable to attend to own bodily needs  Grade 5 Severe disability: bedridden. incontinent. but able to walk without assistance  Grade 4 Moderate severe disability: unable to walk without assistance. and requiring constant nursing care and attention  Grade 6 Deceased   .

ticlopidine. dipyridamole. extended-release dipyridamole + aspirin combination.     Control of risk factors Antiplatelets (aspirin. cilostazol) Anticoagulation ----for cardioembolic Carotid ultrasound ---carotid stent TCD (Trancranial dopler) . clopidogrel.

 Long-term strict BP control and monitoring  Consider CT angiography. AV malformation or vasculitis .or 4vessel angiography in suspected cases of aneurysm. MRA.

THANK YOU .