Dr Farzadfard

Stroke types

Infarcts Artery Vein

Hemorrhages ICH IVH SAH

Presentation

• Abrupt Onset• Fit the distribution of a single vascular territory• early decrease in level of consciousness, nausea

and vomiting, headache, and accelerated hypertension are more common with hemorrhages.

• Subarachnoid hemorrhages classically present as a bursting very severe headache (‘‘the worst headache of my life’’), and are often accompanied by stiff neck, decreased consciousness, nausea and vomiting

Signs and symptoms characteristic of the various arterial territories • Middle cerebral – contralateral loss of strength and

sensation in the face, arm, and to a lesser extent leg. Aphasia if domi nant hemisphere, neglect if non-dominant.

• Anterior cerebral – contralateral loss of strength and sensation in the leg and to a lesser extent arm.

• Posterior cerebral – contralateral visual field deficit. Possibly confusion and aphasia if dominant hemisphere.

• Penetrating (lacunar syndrome) – contralateral weakness or sensory loss (usually not both) in face, arm, and leg. No aphasia, neglect, or visual loss. Possibly ataxia, dysarthria.

• Vertebral (or posterior inferior cerebellar) – truncal ataxia, dysarthria, dysphagia, ipsilateral sensory loss on the face, and contralateral sensory loss below the neck.

• Basilar – various combinations of limb ataxia, dysarthria, dysphagia, facial and limb weakness and sensory loss (may be bilateral), pupillary asymmetry, disconjugate gaze, visual field loss, decreased responsiveness

DIAGNOSIS

• History• Exam• presence of comorbidities• Absence of seizures or other stroke

mimics• Imaging

Differential diagnosis

Seizures Migraine Syncope Hypoglycemia Metabolic encephalopathy Drug overdose Central nervous system tumor Herpes simplex encephalitis (HSE) Subdural hematoma

Peripheral compression neuropathy Bell’s palsy (peripheral seventh

nerve palsy) Benign paroxysmal positional vertigo

(BPPV) Conversion disorder

What to do first

O2 via nasal cannula Intubation may be necessary Consider putting the head of the bed

flat Consider normal saline bolus

All patients brain CT (brain MRI could be

considered at qualified centers) electrocardiogram blood glucose serum electrolytes renal function tests complete blood count, including

platelet count PT, INR,PTT

Selected patients hepatic function tests toxicology screen blood alcohol determination pregnancy test oxygen saturation or arterial blood gas tests

(if hypoxia is suspected) chest radiography (if lung disease or aortic

dissection are suspected) lumbar puncture (if subarachnoid hemorrhage

is suspected and CT is negative for blood) electroencephalogram (if seizures are

suspected)

Do not treat hypertension acutely unless:

(1) the patient was treated with TPA (2) the patient has acute hypertensive end

organ damage (congestive heart failure, myocardial infarction, hyperten sive encephalopathy, dissecting aortic aneurysm, etc.)

(3) systolic or diastolic pressures are above 220 or 120 mm Hg

Proven acute medical treatment for ischemic stroke tissue plasminogen activator (rt-PA)

Age 18 or older Clinical diagnosis of ischemic stroke causing a measurable

neurological deficit Onset of stroke symptoms well established to be less than 180

minutes (3 hours) before treatment would begin

aspirin with 48 hours of stroke onset Clopidogrel (Plavix) 375 mg, and then aspirin 81mg and

clopidogrel 75mg once daily for the first few days In patients who :

while already on antiplatelet therapy have a fluctuating neurological course have a heavy burden of atherosclerotic risk factors

or atherosclerotic lesions

Based on the NINDS rt-PA study, the requirements for administering rt-PA include a CT scan of the head, which is negative for

hemorrhage a serum glucose level between 50 and 400

mg/dL INR less than 1.7 platelet count more than 100,000 per cubic mL systolic blood pressure less than 185 mmHg

systolic no recent major procedures, traumas, or stroke

Later head CT (day 2) revealing hypodensity within the left MCA distribution

Acute anticoagulant therapy

patients with a cardioembolic condition at high risk for recurrence (thrombus on valves, or mural thrombus),

documented large-artery (ICA, MCA, or basilar artery ) occlusive clot at risk for distal embolism

arterial dissection venous thrombosis

Treat

HYPERGLYCEMIA HYPERTHERMIA

DVT prophylaxis

Heparin 5000 units SC every 12 hours

Enoxaparin (Lovenox, Clexane) 40 mg SC once daily

Dalteparin (Fragmin) 5000 units SC once daily

Sequential compression devices (non-drug)

Compression (TED) stockings

TIA brief episode of neurologic dysfunction

caused by focal brain or retinal ischemia The causes are the same as for ischemic

stroke the management is similar to that for

acute ischemic stroke Observe the patient for 24 hours Start daily antiplatelets EKG Cardiovascular risk-factor evaluation of

blood pressure, lipids, and fasting glucose

Intracerebral hemorrhage

Spontaneous bleeding into the brain parenchyma or ventricles from a ruptured artery, vein, or other vascular structure

Etiology

Hypertension (most common) Amyloid angiopathy Drugs Vascular malformation Cerebral vein thrombosis Tumor Trauma

Initial assesment of ICH

History and physical exam Glasgow coma scale (GCS) and brainstem

reflexes if comatose, NIHSS score if awake. Measure blood pressure Oxygen saturation Brain CT Check platelet count, INR, and PTT, and urine

drug screen EKG

HEMATOMA ENLARGEMENT blood pressure levels be maintained below a

mean arterial pressure of 130 mm Hg WARFARIN (COUMADIN)-RELATED

INTRACEREBRAL HEMORRHAGE Goal: normal INR using fresh frozen plasma (FFP) 20 mL/kg and

vitamin K Activated factor VII

HEPARIN-RELATED INTRACEREBRAL HEMORRHAGE Stop heparin CT brain immediately INR, PTT, platelets, CBC, fibrinogen, thrombin time, D-dimers Type and cross Give protamine: 25mg initial dose; check stat PTT 10 minutes later

and if increased give 10mg additionally; repeat until PTT normal

Subarachnoid hemorrhage

The worst headache of my life ‘‘Thunder-clap headache Headache is sometimes associated

with focal neurologic symptoms

DIAGNOSIS OF SUBARACHNOID HEMORRHAGE

CT of the head without contrast If head CT is normal, but you have a high clinical

suspicion for SAH, you must do a lumbar puncture, because CT can miss small or subtle SAHs, especially if more than 72 hours has passed since the ictus

DIAGNOSIS OF INTRACRANIAL ANEURYSMS Digital subtraction angiography

(DSA) CT angiography MRA

CAUSES OF SAH OTHER THAN INTRACRANIAL ANEURYSM Perimesencephalic SAH Arteriovenous malformation (AVM) Arterial dissection (vertebral artery

usually) Arteriovenous fistula Pituitary apoplexy Cocaine Trauma Vasculitis

GOALS

Prevention of rebleeding Blood pressure control may be important before

definitive treatment to reduce rebleeding Bed rest in ICU with monitoring

Treatment of the aneurysm itself: clip or coil

Prevention and treatment of complications: hydrocephalus, seizure, vasospasm, hyponatremia, infections, and DVTs.