Cerbrovascular Accident (CVA) “Stroke”.pdf

Cerbrovascular Accident (CVA) “Stroke”.pdf

• 1.
  Cerbrovascular Accident (CVA) “Stroke”
• 2.
  STROKE • It is3rd common cause of death after cancer & IHD in developed countries • The annual incidence of stroke above the age of 45 years in UK is about 350/100 000 • CVA: is a clinical syndrome characterized by acute onset neurological deficit resulting from disturbance in cerebral circulation • Circle of Willis 1. ACA 2. ACoA 3. PCA 4. PCoA 5. MCA Stroke In Young • The CVA occurs under the age of 40 years, you have to think about other causes and intensive investigation needed to know • The causes: 1. Accelerated atherosclerosis (HTN, DM) 2. Embolic (From Cardiac Origin or Carotid Dissection) 3. Vasculitis (SLE, APL syndrome) 4. Others, like thrombophilia, congenital malformation, AVM 5. Idiopathic · 5 & I
• 3.
  Classification Of StrokeSyndrome (Pathological & Clinical) • Pathological Classification 1. Ischemic (80-85%) Can Be: — Large Vassals: 80% of cases (thrombosis & embolic) which affect medium and large size aa (arteries?) — Small Vassals: 20% of ischemic stroke called lacunar stroke which is due to lipohyalinotic degeneration of small penetrating aa seen mainly in HTN 2. Hemorrhagic(15-20%) which is either — Hypertensive (bleed due to high BP) # seen at common sites (basal ganglia, thalamus, cerebellum and pons, Less commonly Sub cortical or lobar) — Non Hypertensive bleed (SAH, bleeding tendency, drug therapy, traumatic and amyloid angiopathy) • Clinical Classification In term of duration and residual deficit 1. Transient Ischemic Attack (Minutes but less than 24 hour) — It is a major risk factor for disabling stroke, about 13 folds increase as a risk of having stroke in next year 2. Reversible Ischemic ND(RIND) (3-5 days) 3. Completed Stroke (within 6 hour become completed) 4. Stroke in evolution “progressing stroke” (evolution more than 6 hrs) Q/ How you can differentiate between Hemorrhagic & Ischemic stroke? (clinically) A/ Signs & Symptoms 1. Headache 2. Consciousness 3. Meningeal Sign 4. BP 5. Hx IS HS Mild Severe Intact Loss (impaired) Absent Present Normal or Mild Elevated Very High BP Atherosclerosis (HT, DM) Trauma DM Drugs TSA Coagulopathy Hyperlipidemia HTN
• 4.
  Etiology of AcuteIschemic Stroke A. Vascular Causes 1. Atherosclerosis • Common cause of ischemic stroke affecting extracranial arteries in the neck and at the base of brain • The pathogenesis involving — Injury endothelium accumulation off cholesterol (LDLP) — Fatty streaks — Fibrous plague (lipid laden foam cell)+ platelets — Atheromatous lesion which carry risk of thrombus formation especially if ulcerated 2. Fibromuscular dysplasia • Traumatic or congenital segmental non-atherogenic thinning of tunica media with fragmentation of elastica lamina alternating with ring of muscle hyperplasia within media, Female > male, ECBV>ICBV, ICA>VA and usually bilateral 3. Inflammatory disorder: • Giant cell arteritis • PA nodosa • syphilis arteritis infec. or endocarditis 4. Carotid or vertebral artery dissection 5. Lacunar stroke 6. Drug abuse • Cocaine and amphetamine mainly causing bleeding (may be within hours of intake from vasospasm rupture or vasculitis), stroke or SAH are less common • Heroin is causing embolic stroke from endocarditis 7. Moya-moya disease (progressive multiple IC arterial occlusion) • There is bilateral narrowing of Internal Carotid Artery as: — Primary cause (idiopathic or genetic) — Secondary Cause (sickle cell A or basal meningitis) • Diagnosis: — Angiographic (pattern of collateral circulation look like smoke) SLE & APL syndrome Granulomatous angiitis AIDS-direct or by opportunistic 6 #
• 5.
  8. Migraine 9. Venoussinus thrombosis B. Cardiac Causes 1. Mural thrombosis; as complication of MI or cardiomyopathy 2. Rheumatic heart dis. as MS 3. Arrhythmias: AF, sick sinus, pan-cerebral hypo-perfusion 4. Endocarditis: infective (bacterial or fungal) during active stage or few months after antibiotic cure 5. Nonbacterial (marantic): in setup of systemic malignancy 6. MVP (Mitral valve prolapse Mitral) 7. Paradoxical emboli: ASD & PFO 8. Atrial myxoma 9. Prosthetic valve : artificial one C. Hematological Causes 1. Thrombocytosis 2. Polycythemia 3. Sickle C .A. 4. Leukocytosis 5. Hyper coaguable state like APL syndrome ,LA. 6. Protein S or C factor V Leiden & antithrombin III deficiency 7. Homocystinuria Pathophysiology A. Ischemic stroke • When there is occlusion of Brain vassal the brain tissue supplied by that BV got ischemia. the effect depending on severity of ischemia, duration, and potency and patency of collateral circulation As a result, the patient may develop one of the following: 1. No Symptom 2. TIA (The flow is return before cellular death) Endocarditis Valve - Af ASD A. Myxo. RHD (MS) PV MVP 5 S
• 6.
  3. Stroke (Theflow is not returned in which there will be area of dead tissue)(<50ml/100gm BT) which is surrounded by an area of ischemia (viable but not functioning) called ischemic penumbra • Our aim in approaching any case of stroke is to save or to make IP area viable and functioning by keeping balanced homeostasis: 1. Bp 2. B.sugar 3. Good oxygenation • Histopathology (Cascade of cellular changes in ischemia) 1. There is ATPase pump failure 2. Influx (flow) of sodium and water 3. Cytotoxic edema 4. Release of excitatory amino acid mainly glutamate 5. Further Ca+2 influx —> more damage • The process fatherly worsened by anaerobic production of lactic A and fall in tissue PH, restoration of Blood Flow may cause hemorrhage in ischemic area (hemorrhagic transformation) especially in embolic stroke. So be careful in using AC in acute periode B. Hemorrhagic Stroke (Intracerebral bleeding) • The damage here depending upon bleeding severity, as the neurons structurally disrupted and WM fibers are splits apart (pushed). the big hematoma can cause sever increase in ICP and conning. Risk Factors for Ischemic Stroke (How to prevent stroke?) A. Unmodifiable • Age • Race • Gender B. Modifiable • Life Style Modification (Weight Loss & Exercise) • Early Dx & Rx (Hypertension, Hyperlipedemia, Hyperglycemia) • Avoid & Stop (Smoking, Contraceptive Pill & Alcohol Intake) • Previous Stroke • Genetic Male 70 yrs, PMH 2 stroke & +ve FH of Stroke
• 7.
  Clinical Approach (CasePresentation) A. History: A 56 years old man diabetic and HT; presents to EU with sudden onset right sided weakness and aphasia of one hour duration. No loss consciousness, mild headache. He is controlling sphincter B. Exam: • General: un remarkable apart of irregular pulse, BP= 160/100 • Medical: abnormal heart sound • Neurological: aphasic but conscious Cranial R. facial upper motor palsy No meningeal signs • Motor: Right sever hemi paresis grade 2 in UL and grade 3 in LL • Sensation: intact I. Ask? Is it stroke? Sudden Onset Neurological Deficit? # Sudden onset Rt sided weakness & aphasia of one hour duration II. Is it Ischemic or hemorrhage (pathological)? # No loss consciousness, mild headache, 56 yrs DM & HTN III. If Ischemia 1. Anterior or Posterior Circulation? “Not Absolute” • Anterior Ischemia — Weakness or and Cortical Symptoms (Seizure, Sensory Loss & Aphasia) • Posterior ischemia — Drop Attack, Crossed Hemi-Paresis, Dysarthria, Vertigo, Ataxia, Diplopia, Dysphagia, CN palsy & Altered conscious 2. Which Clinical Type? • TIA • RIND • Complete Stroke • Stroke in Evolution L may be most like
• 8.
  3. Thrombotic orEmbolic? • If onset is stepwise over minutes or hours, preceded by TIA is go with thrombosis • If it is sudden with max. deficit at the onset, not preceded by TIA, presence of cardiac lesion and hemorrhagic transformation in CT scan are consistent with embolic 4. Large or small VD (lacunar)? # Seizure: seen in 10-25%, more with embolic, cortical lesion & permanent ND (up to 50%) # Headache: seen more with bleeding and in 15-25% of Ischemic stroke Clinico-Anatomic correlation to decide which Vassal is involved A. Anterior Circulation 1. ACA (Uncommon) • Motor Contralateral Hemiparesis Affecting L. Limb> U. Limb • Sensory defect Affecting Lower Limb > Upper Limb • Sphincter (often affected “Urinary & Bowel Incontinence) 2. MCA (Typically do not directly affect sphincter control) I. Main Stem: • Contralateral Hemiplegia (dense) • Global Aphasia if dominant (Lt. MCA?) Hemisphere is affected II. Deep lenticulostriate Atery: • Contralateral dense sensory-motor H. +/- capsular aphasia and transcortical aphasia (repetition intact) if D. H is affected III. Superior Division: • contralateral weakness affecting face, arm (UL) & hand sparing leg, no VF defect, motor or expressive aphasia if dominant H. affected IV. Inferior division: • Weakness less prominent • VF defect contralateral, sensory dysfunction include marked cortical sensory dysfunction (look at 2nd lecture) ~ -
• 9.
  • VF defectcontralateral, sensory dysfunction include marked cortical sensory dysfunction (look at 2nd lecture) • spatial thought disorder in non D hemisphere, lack of awareness that deficit is exist (anisoagnosia), neglect or and failure to recognize contralateral limb • In D. Hemisphere affection sensory aphasia & Gersmann syndrome (agraphia, acalculia, left right disorient & finger agnosia) • Non-D H affection dressing apraxia, constructional apraxia and some times acute confusional like state 3. ICA occlusion (20% of cases) I. May be asymptomatic II. Symptomatic: • Ophthalmic a: range from Amurosis fugax (TIA) to permanent V. loss due to affection of retinal a. and Ciliary a. (AION) • Features of MCA & ACA occlusion # Trans-cortical: motor or sensory or global sub-cortical aphasias (left thalamic and putamen lesion) B. Posterior Circulation 1. PCA: depending on site of occlusion • Distal part —> cortical dysfunction —> contra lateral H. H more dense superiorly • More proximal (affect sub thalamus, thalamus, midbrain & CN) • Lead to vertical gaze palsy, third nerve palsy, inter N. ophthalmoplegia and vertical skew deviation of eye • Distal part features = cortical dysfunction as: • Dominant H: anomic aphasia, alexia without agraphia, and V. agnosia ==inability to identify object in seen in L side of V. field caused by lesion affecting corpus collasum which connect the R. Visual cortex from language area in dominant H • bilateral: Balint’s syndrome (bilateral parietal occipital lesion) leading to failure of sending impulse to frontal area
• 10.
  • Balint's syndrome?due to bilateral parietal-occipital infarction ,the pt. not moving the eyes voluntarily but reflexly (reflex EM) (psychic paralysis of gaze) • The patient appear to have ataxia in reaching an object (optic ataxia) • He or she is looking to detailed aspect of picture without looking for it’s meaning of picture (asimultagnosia) with memory disturbance+ inability to recognize familiar faces (prospagoagnosia + variety of exotic V. and behavioral changes • Anton’s syndrome? bilateral O. infarction, cortical blindness with denial Basilar artery (Either thrombosis or embolic) • Variety of clinical syndrome, some are incompatible with life, can produce bilateral N. involvement with coma or disturbance of consc., Occlusion of both vertebral arteries or one alone congenital vertebral artery can produce same clinical features • stenosis or occlusion of subclavian artery before it has given rise to vertebral arteries, Lead to subclavian steal syndrome? As the blood passes from vertebral arteries into distal subclavian a. with physical exercise of ipsilateral limb • Is it predictive of stroke in vertebrobasilar (VB) distribution? (Patient usually asymptomatic) Basilar Thrombotic Occlusion • it affect proximal portion which supply the pons(tegmentum) produces feature of posterior circulation ischemia like: — unilateral or bilateral 6th nerve palsy & ataxia — horizontal gaze palsy — pupil is constricted ? — vertical N. and ocular bobbing Some time the infarction affecting Basis Pontis with sparing of tegmentum, end result is locked in syndrome (pt. is cons., tetraplegia, only moves eye vertically to command& EEG is normal to differentiate it from:
• 11.
  1. Persistent vegetativestate (due diffuse cortical damage due any cause like diffuse cortical anoxia or ischemia) = Hemiplegia or quadriplegia usually present with disturbed cons. May be coma 2. Pontine bleed in which the patient is comatose ,hyperthermic with pinpoint pupil but reacting to light ,diagnosis by CT scan Basilar A. Embolism • Affecting distal seg. rarely proximal seg, The origin of emboli either Basilar A or Vertebral A. ascend up to be arrested at bifurcation of 2 PCA. leading to: — Immediate loss of cons. (thalami and RAS) — unilateral or bilateral 3rd nerve palsy (midbrain) & ataxia — hemiplegia or quadriplegia (cerebral p.) — features of one or both occipital lobe dysfunction? As emboli may dislodge and ascend up to occlude one or both PCA • posterior inferior cerebellar a.= PICA syndrome (Wallenberg’s) due to atheromatous lesion thrombosis, less likely embolic of pica or VA. ipsilaterally :ataxia, diplopia vertigo and nystagmus, Horner’s syndrome, deafness, facial sensory loss, dysphagia ,and hoarseness of voice, loss of taste. • controlateral there is sensory loss in UL &LL. (crossed sensory loss) • Balint’s Syndrome ? Bilateral cortical occipital infarction • Anton’s syndrome ?bilateral O . infarction ------cortical blindness with denial. • Alexia without agraphia and Visual agnosia ( PCA affection) • lacunar infarction?20%?cause? CF?
• 12.
  Approach 1. History 2. PhysicalExamination • General examination: — looking for the signs which are suggestive of underlying systemic disorder especially treatable one ex; polycythemia, xanthelasma — Eye (Arcus Senilis, Retina for HTN, DM retinopathy and emboli) — Facial weakness — Motor and sensory system looking for Hemi-paresis and sensory defect including cortical one. Even if the pt. comatose? • Vital Signs — BP (HTN is well risk factor for stroke) — HR # Compares of BP and pulse on 2 sides? — SpO2 — Temp. — RR • Palpation of temporal A? • Examination of the neck & Chest — Thyroid (AF) — Cardiovascular Examination • Neurological examination (May be Normal as in TIA) — GCS — Look for (Cognitive, Cranial, Meningeal Signs, UL&LL Exam. # Cognitive function assessment: is of significant in ACA disease specially in cortical lesion, speech is affected also. — Babinski Sign • Ophthalmoscope examination; retina may provide a hint to an embolic phenomenon in RA; Optic disc for PD or DM & HT changes. • v. field defect • ocular palsies, nystagmus, and INO (in posterior circulation) • cerebellar signs sh
• 13.
  Management of acutestroke in Emergency Unit: • Ensure ABCDE (vital signs, oxygen saturation, urine output) • Keep the patients in 30 degree position unless the patient had feature of impending herniation • Control fit if present with 10 mg diazepam over 5 min infusion + phenytoin, can be repeated if fit persistent with monitoring RR, PR • IV line (draw blood for blood sugar, urea and Creatinine, HB) • ECG for any cardiac problem specially ischemia • Control high blood pressure (only if MAP> 120 mm Hg) and sugar before sending patient to CT scan.??? • If thrombolytic therapy is available or decided (send for all blood profile) • Stroke is a medical emergency, needs urgent thrombolysis within 4.5 hrs. from onset, +/- mechanical Thrombectomy within 6 hours • No manitol or dexamethasone should be given in 1st 3 days • Subsequent treatment: depending on type of stroke-physician decision • General measures: Care to skin, swallowing and bladder from the beginning please • Non specific Management include Treatment of risk factors, secondary preventive measures with antiplatelet or anticoagulation and lipid lowering agents, Skin and bladder care, prophylaxis of DVT and pulmonary embolism and aspiration pneumonia F
• 14.
  Thrombolytic therapy-1 st1-3 hour (within 4.5 hours of N deficit) Patient presented within 3 hours of ischemic stroke should be evaluated for iv recombinant tissue plasminogen activators(rt-PA): • Clinical Evaluations: NO treatment if 1. Stroke or head trauma in last 90 d 2. Surgery <14 d or hemorrhage <12 d 3. Rapidly improvement (TIA) 4. BP > 185/110 (should be below 175/100 ) 5. Seizure at onset 6. Hx. cerebral bleeding 7. AC within 48 hr • Lab. evaluations: NO treatment if 1. Sever anemia 2. Platelet count < 100000/cu.mm 3. PT >15 sec 4. Glucose <50 or >400 mg/dl • Radiological evaluation: NO treatment if 1. CT-scan is positive for blood or non-stroke disease • Strategies for it’s use: you have to explain to the patient or family that there is 6% risk of symptomatic IC bleeding and 50% chance of little or no disability compared to 38% chance without rt-PA Mechanical Thrombectomy (after failure Ineligible for thrombolytic T.) • If Can not give IV rt-PA, who have significant stroke deficits (NIH Stroke Scale score of 8 or greater), endovascular therapy should be considered if treatment can be initiated within 6 hours • Mechanical embolectomy devices, including the Penumbra Aspiration System, the Solitaire Stent Retriever, and the TREVO2 Stent Retriever, report revascularization rates exceeding%80. MT Beyond 6 hours from onset who will benefit from acute reperfusion therapies remains to determined Score Stroke severity 0 No stroke symptoms 1–4 Minor stroke 5–15 Moderate stroke 16–20 Moderate to severe stroke 21–42 Severe stroke
• 15.
  Specific medical Antiplatelet: • Aspirin:is act through irreversible inhibition of cyclooxygenase enzyme, inhibition of thromboxane A2 (a platelet aggregating and PG vasoconstriction properties) • Ticlopedine: block ADP receptor on P. preventing cascade activation of GP11b/111a complex on P. (clopidogrel have same effect) that lead to binding of fibrinogen to P. .It is given in dose of 25o twice .low incidence reversible neutropnia (BM suppression) should be followed, skin rash and diarrhea • Dipyridamole: P. phosphodiesterase inhibition which inhibit breakdown of cAMP which inhibits P. aggregation • Clopidogrel: 75 mg daily ,proved to be effective in some studies especially if combined with aspirin in patient at high risk of CVS events ,but risk of bleeding is high. It should be stopped few days before surgery • Abciximb: monoclonal antibody to block GP111b/111a receptors complex activation Anticoagulation • Heparin or nadroparin (enoxaparin) and warfarin. INDICATION although AP therapy remains the treatment of choice to prevent recurrent thrombo-embolism in majority of patient with stroke the AC is indicated in cases of stroke in set up of AF, cardiac ischemia, progressing or stroke in evolution (propagated thrombus) • To use AC you need: CT scan to exclude IC bleed or SAH, baseline PT, PTT & platelet count, History of active PU or uncontrolled HT (systolic BP>200) preclude use of AC in stroke, unless the benefit out weight the risks
• 16.
  Neurotropic • Drugs likeNeuroaids, citicholine may be used Surgical treatment in STROKE • SAH (Angio) surgery as early as possible • ICH, Some time evacuation. • Cerebellar H. and Malignant edema, Infarctionectomy Primary Stroke Prevention 1. Identification & reduction of stroke risk factors are crucial to decrease the incidence of stroke, including treatment of DM, HTN, Cardiac disease and Hyperlipedemi Atrial fibrillation & cardiac disease • In setting of valvular heart disease(17 fold risk/year), AC with warfarin to INR reaching 2-3 • In setting of non valvular AF with no other risk factors, ASA 325mg/d is effective • CHA2DS2 score, Risk of stoke in non valvular AF • Patient with prosthetic valve (long term AC is important) • Patient with bacterial endocarditis (AC should be avoided) 2. Stop smoking, contraceptive pill ·
• 17.
  General measure instroke management (Mx. of Complications) 1. Nursing measures • Reducing the risk of complication resulting from immobility such as pneumonia, DVT & UTI • Early physical, occupational and speech therapy • Early assessment of swallowing ability reduce morbidity • Prevention and treatment of hyperthermia • Early observation of post stroke depression 2. Rehabilitation • The main cause of death among stroke patient are related to medical complication (MI, pneumonia, sepsis & P. embolism) • Reh. program should be started from the onset of stroke. Control blood sugar. Keep it below 160 mg/dl 3. Management of cerebral edema • Only in cases of big cerebral ischemia there is edema enough to cause brain shift & herniation, that necessitate intubation & hyperventilation produce transient c. vasoconstriction and may reduce ICP • Manitol infusion acts by reducing the volume of surrounding unaffected brain but it’s effect is also transient. • corticosteroid is of no help in cytotoxic edema. Hypertensive encephalopathy • It is diffuse cerebral effect of sever hypertension that are not caused by ischemia or bleed and it is potentially reversible upon controlling of BP • Patient presented with Headache, visual blurring, confusion and drowsiness. seizure may develop • On exam.: the BP is very high (240/150) with papilledema and retinal bleed on fundoscopic examination. • CT &MRI is often revealed diffuse C. edema with predilection to occipital lobe. • Treatment : is a medical emergency ,you have to reduce BP urgently but smoothly to avoid hypotension by using labetolol , or sodium nitoprusside, or hydralazine • This condition clinically and pathophysiologically is similar to eclampsia.