[Int. med] cerebrovascular accident from SIMS Lahore

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Dr. Tahir Bashir Assistant Professor Medical unit-4

Transcript of [Int. med] cerebrovascular accident from SIMS Lahore

Dr. Tahir BashirAssistant Professor

Medical unit-4

Stroke is an acute CNS injury that results in neurologic signs and symptoms caused by a reduction or absence of perfusion to a territory of the brain. The disruption in flow is from either an occlusion (ischemic) or rupture (hemorrhagic) of the blood vessel.

Cerebrovascular Accident Ischemic Stroke

Thrombotic Embolic Lacunar infarct TIA

Hemorrhagic Stroke ICH SAH

Occlusion of large cerebral vessel

Older population Sleeping/resting Rapid event, but slow

progression (usually reach max deficit in 3 days)

Embolus becomes lodged in vessel and causes occlusion

Bifurcations are most common site

Sudden onset with immediate deficits

Minor deficits Paralysis and sensory

loss Lacune Small, deep penetrating

arteries High incidence:

Chronic hypertension Elderly DIC

Warning sign for stroke Brief localized

ischemia Common

manifestations: Contralateral

numbness/weakness of hand, forearm, corner of mouth

Aphasia Visual disturbances-

blurring

Deficits last less than 24 hours (usually less than 1 or 2 hrs)

Can occur due to: Inflammatory

artery disorders Sickle cell anemia Atherosclerotic

changes

Intracerebral hemorrhage Intracranial hemorrhage Parenchymal hemorrhage Intraparenchymal hematoma Contusion Subarachnoid hemorrhage

Rupture of vessel Sudden Active Fatal HTN Trauma Varied

manifestations

Intracerebral Hemorrhage

Subarachnoid Hemorrhage

Changes in vasculature Tear or rupture Hemorrhage Decreased perfusion Clotting Edema Increased intracranial pressure Cortical irritation

Hearing/association & Smell & taste Short term Memory

Voluntary Motor

Sensations Pain & Touch Taste

Balance, Coordination of each muscle group

Arms

Head

LegsMom: Bowel/bladder Reasoning/judgment Long term memory

Vision & visual memory

CN 5,6,7,8 P,R, B/P CN 9,10,11,12

Tracks cross over Coordinate movement, HR,B/P

Right Side

NON-MODIFIABLE MODIFIABLE

Age 2/3 over 65

Gender M=F Female>fatality

Race AA > hispanics, NA Asians > hem

Heredity Family history Previous TIA/CVA

Hypertension Diabetes mellitus Heart disease A-fib Asymptomatic carotid stenosis Hyperlipidemia Obesity Oral contraceptive use Heavy alcohol use Physical inactivity Sickle cell disease Smoking Procedure precautions

EMBOLISMPROTHROMBOTIC STATES

Atrial fib Sinoatrial D/O Recent MI Endocarditis Cardiac tumors Valvular D/O Patent foramen ovale Carotid/basilar artery

stenosis Atherosclerotic lesions Vasculitis

Hemostatic regulatory protein abnormalities

Antiphospholipid antibodies

Chronic HTN** Cerebral Amyloid Angiopathy* Anticoagulation* AVM Ruptured aneurysm (usually subarachnoid) Tumor Sympathomimetics Infection Trauma Transformation of ischemic stroke Physical exertion, Pregnancy Post-operative

Localized dilation of arterial lumen Degenerative vascular disease Bifurcations of circle of Willis

85% anterior 15% posterior

SAH Mortality 70% Nuchal rigidity Fever Photophobia Lethargy Nausea Vomiting

Complications HCP Vasospasm

Triple H Therapy HTN Hemodilution Hypervolemia

Surgical treatment Clip Coil INR

AVM Tangled mass of arteries and veins Seizure or ICH

Sudden onset Focal neurological deficit Progresses over minutes to hours Depends on location

SUDDEN numbness or weakness of face, arm or leg

SUDDEN confusion, trouble speaking or understanding.

SUDDEN trouble with vison.

SUDDEN trouble walking, dizziness, loss of balance or coordination.

SUDDEN severe headache.

Vertebral Artery Pain in face, nose, or eye Numbness and weakness of face (involved

side) Gait disturbances Dysphagia Dysarthria (motor speech)

Internal carotid artery Contralateral paralysis (arm, leg, face) Contralateral sensory deficits Aphasia (dominant hemisphere involvement) Apraxia (motor task), Agnosia (obj. recognition), Unilateral neglect (non-dominant hemisphere

involvement) Homonymous hemianopia

Neurological Hyperthermia Neglect syndrome Seizures Agnosias (familiar

obj)

Communication deficits Aphasia (expressive,

receptive, global) Agraphia

Visual deficits Homonymous

hemianopia Diplopia Decreased acuity Decreased blink reflex

Neurological (cont.) Cognitive changes

Memory loss Short attention

span Poor judgment Disorientation Poor problem-

solving ability

Behavioral changes Emotional

lability Loss of

inhibitions Fear Hostility

Musculoskeletal Hemiplegia or

hemiparesis Contractures Bony ankylosis Disuse atrophy Dysarthria - word

formation Dysphagia – swallow Apraxia – complex

movements Flaccidity/spasticity

GU Incontinence Frequency Urgency Urinary retention Renal calculi

Integument Pressure ulcers

Respiratory Respiratory center damage Airway obstruction Decreased cough ability

GI Dysphagia Constipation Stool impaction

Neurological assessment Call “Stroke Alert” Code Ensure patient airway Vital signs IV access Maintain BP within parameters Position head midline CT Brain Anticipate thrombolytic therapy for

ischemic stroke

Tests for the Emergent Evaluation of the Patient with Acute Ischemic Stroke

CT head (-) Electrocardiogram Chest x-ray Hematologic studies (complete blood count,

platelet count, prothrombin time, partial thromboplastin time)

Serum electrolytes Blood glucose Renal and hepatic chemical analyses

ISCHEMIC STROKE HEMORRHAGIC STOKE

BP Factor VII, Vit K,

FFP ICP

Sedation Hyperventilation Paralytics

Fluid management Seizure prophylaxis Sedation Body temperature DVT prophylaxis

ISCHEMIC HEMORRHAGIC

Medical management

TpA Endovascular

Carotid endarectomy Merci clot removal

Medical management

Decompression Craniotomy Craniectomy

REHABILITATION

Anti-coagulants – A fib & TIA Antithrombotics Calcium channel blockers – Nimotop (nimodipine) Diuretics – Mannitol, Lasix (Furosemide) Anticonvulsants – Dilantin (phenytoin) or Cerebyx

(Fosphenytoin Sodium Injection) Thrombolytics - tPA (recombinant tissue

plasminogen activator)