Medicine Seminar

12th July, 2024

Topic – Cerebrovascular Accident
Presenters:
Madhurima Paul (52)
Bhabna De (53)
Padmanava Nath (54)
Nirupam Das (55). Moderator
Md. Monsoor Alom Laskar (56). Dr. Asif Mohammed
Adil Ahnaf Choudhury (57)
Rudraksh Daftari (58)
Saiyed Kawes Khan (59)
Priya Paul (60)
Contents :

 Introduction
 Defintion
 Types of stroke
 Pathophysiology
 Risk factors
 Clincal features
 Investigations
 Management
Introduction :
 Carotid arteries run along the front of the neck and reaches the base of
the neck, where it joins the vertebral arteries to form the CIRCLE OF WILLIS.
I) Anterior Communicating Artery :
It supplies the medial surface of the brain.
Stroke occuring in this area can lead to leg weakness, difficulty in thinking
and making decisions.
II) Middle Cerebral Artery :
It supplies the superolateral surface of the brain.
Stroke in this area can lead to paralysis on one side, change in
sensation, blindness on either side, language problems.
III) Posterior Cerebral Artery :
It supplies the brain stem.
May lead to visual difficulty if stroke occurs in this area.
 STROKE is defined as
~sudden onset of cerebral dysfunction
~persists for 24 hours or longer
~no apparent cause other than of vascular origin.
Types of stroke
Pathophysiology of ischemic stroke
 1. Thrombotic stroke
. Most common pathology leading to thrombotic occlusion of the
cerebral vessels
Lacunar stroke
~ due to occlusion of the small perforating arteries in patients with genetic
small vessel disease leading to lacunar infarcts.
2. Embolic stroke
Cardioembolic stroke
~ Embolus from heart gets lodged in the brain vessels.
~ MCA is most commonly affected.
 As a result of cerebral artery occlusion, the oxygen, glucose and other
. other nutrients fail to reach the brain leading to decline in neuronal
function.
 If not managed immediately the cerebral tissues begin to die if collateral
vessels are not established or the thrombus is not lysed.
 The process of cell death leads to edema of the brain tissue, which can be
life threatening of there is asociated increase in ICT.
Pathophysiology of hemorrhagic stroke

 Commonest cause of intracerebral hemorrhage is rupture of small vessels.

 Hypertension, diabetes, amyloid deposits or genetic factors can damage
small vessels.
 This leads to direct pressure of the hematoma which can continue to grow
after presentation, mass effects from surrounding edema and
inflammation due to degrading blood products.
Transient Ischemic Attacks (TIAs)

 Aka mini stroke

 It is a transient episode of cerebral dysfunction caused by focal brain,
spinal cord or retinal ischaemia without evidence of acute infarction.
 Symptoms resolve within 24 hours.
 Predictor of other vascular diseases such as MI.
Risk Factors

 Non-modifiable
~ Age
~ Sex(Male > Female)
~Previous vascular evensts like myocardial infarction, stroke, peripheral
vascular disease
~Genetic factors like sickle cell disease
 Modifiable
. ~Bloodpressure ~Oestrogen containing drugs
~Cigarette smoking ~Polycythemia
~High HDL cholesterol ~Drugs like cocaine
~Diabetes mellitus ~Heart disease like congestive cardiac
~Chronic Kidney Disease failure
~Excessive alcohol intake
 Additional risk factors ( common in younger patients )
. ~ protein c and s deficiencies
~ antithrombin III deficiency
~ antiphospholipid syndrome
~ sickle cell anemia
~ hyperhomocysteinemia
~ thrombotic thrombocytopenic purpura
~ arterial dissection
~ infections
~ systemic malignancy
Presenting symptoms

 Weakness of
~face (upper motor neuron pattern)
~legs only (anterior cerebral artery involvement)
~quadriparesis (brain stem involvement)1
 Speech disturbance
~cortical stroke can cause dysphasia with difficulty in understanding
speech
~difficulties in producing grammatically correct speech
~slurred speech or dysarthria (stroke in the cortex, white matter, cerebellum
or brainstem).
 Visual deficit
. ~occlusion of the ophthalmic artery by thrombus leads to sudden blindness
in one eye.
~amaurosis fugax or tranisent monocular blindness.
 Visuo-spatial dysfunction
~due to damage to the non dominant cortex
 Ataxia
~due to damage to the cerebellum
~may be associated with diplopia and vertigo due to brainstem
involvement
 Headache
~ cardinal symptom of SAH
 Seizure
 Coma
Investigations

 Neuroimaging
~CT has a high sensitivity for acute intracranial hemorrhage.
~brain tissue perfusion can be demonstrated with CT after injection of
contrast media
~MRI takes longer time than CT, but are more sensitive than CT in strokes
affecting brain stem and cerebellum.
 Vascular imaging
~to identify carotid stenosis in patients with recent ischemic stroke or TIA.
~MR or CT angiography can be used
 Cardiac investigation
~20% Ischemic stroke are due to embolism from the heart
~most common cause is atrial fibrillation, others include prosthetic heart
valve, endocarditis, valve abnormalities or recent MI
~transthoracic or transoesophageal echocardiogram can identify
endocarditis, or patent foramen ovale.
 Blood tests
~to identify high FBS, anemia, electrolyte disturbance or any inflammatory
response
~clotting abnormalities
 Blood tests
~to identify high FBS, anemia, electrolyte disturbance or any inflammatory
response
~clotting abnormalities
Management of ischemic stroke
 Intravenous thrombolysis
Intravenous administration of recombinant tpa at the rate of 0.9 mg/kg
(max. 90mg) as 10% of total dose as an iv bolus and the remainder as iv
infusion over 60 mins.
Indications
~onset of symptoms to time of administration<= 3 hrs
~age > 18yrs
~no hemorrhage or infarct on ct scan
Contraindications
~sustained bp > 185/110 mm Hg despite treatment
~platelets < 100,000/micro litres
~hematocrit < 25%
~heparin or warfarin usage within 48 hrs
~prior intracranial hemorrhage / prior stroke within 3 months
~recent major surgery
~pregnancy
~age > 80 yrs
 Endovascular thrombectomy
In patients who are ineligible for or contraindicated for thrombolytics
 Antiplatelet therapy
Aspirin 150mg + Clopidogrel 75 mg daily causes platelet inhibition
 Anticoagulation for acute ischemic stroke
Indications are
~ potential high risk of early cardiogenic re-embolization
~ known hypercoagulable state
~ cerebral venous sinus thrombosis
 Medical support
1. Prevention of common complications in bed ridden patients
. ~ inections ( pneumonia, uti, skin infections) > prophylactic antibiotics
~ deep venous thrombosis with pulmonary embolism
~ others ( catheterisation, ryle’s tube for feeding, management of hygiene )
2. Maintenance of blood pressure
~ first 24-48 hrs post stroke, iv TPA is given if bp < 185/ 110 mm Hg
Drugs used are
First line agents – Labetalol, Nicardipine, Clevidipine
Second line agents – Nitroprusside
3. Fever should be treated with antipyretics
4. Serum glucose should be monitored and kept at <110 mg/dl
5. Decrease intracranial tension
6. Statins
. ~ atorvastatin ( 20-40 mg ), rosuvastatin ( 10-20 mg )
7. Rehabilitation
~ this includes early physical and speech therapy
~ it is directed towards education of patient and family about the
neurological deficits, preventing complications and providing
encouragement and instructions to overcome the deficits
Management of hemorrhagic stroke
 Any coagulopathy should be reversed immediately
~ patients on vit. K antagonists should be administered prothrombin
complex concentrate, followed by fresh frozen plasma and vitamin k
~ when ICH is associated with thrombocytopenia, fresh platelets can be
administered
 Control of blood pressure
~ bp> 185/110 increases the size of hematoma by more bleeding, so
maintain a mean arterial pressure < 130 mm Hg
~ non vasodilating drugs can be used such as Nicardipine, Labetalol or
Esmolol
 Hyperosmolar therapy
. ~ Mannitol ( bolus of 0.25 – 1 g/ kg body weight )
~ Hyeprtonic saline, concentration ranging from 3 – 23.4%
 Treatment of raised intracranial tension
. ~ if the hematoma causes marked midline shift of structures, osmotic
agents coupled with induced hyperventilation can be instilled to
lower ICP.
~ further hyperventilation and osmotic therapy can be tailored to keep
cerebral perfusion above 60 mm Hg.
~ if ICP is still raised, CSF can be drained from the ventricular space and
osmotic therapy continued.
~ persistent or progressive rise in ICP may prompt evacuation of the clot.
Secondary prevention of stroke and
transient Ischemic attack
 Treatment of atherosclerosis
1. Atorvastatin in the dose of 80 mg daily
2. Antiplatelet agents like aspirin, clopidogrel or dipyridamole are used
3. Anticoagulation therapy for embolic stroke
 Treatment for carotid atherosclerosis
~ it can be either high grade or low grade stenosis of carotid artery
~ balloon angioplasty coupled with stenting to open stenotic carotid
arteries and maintains their patency
3. Treatment for intracranial atherosclerosis
Dural sinus thrombosis , by short term anticoagulants regardless of the
presence of ICH
THANK YOU