Acute Stroke andManagement

ACUTE STROKE AND MANAGEMENT

OUTLINE OF THE TOPIC

SUMMARY

1.       Stroke is one of the leading causes of death

2.       Stroke is to be recognized in the right time for  effective treatment

3.       Acute ischemic stroke must be evaluated for IV tPA: patients not fit for it, receive Aspirin

4.       Adequate hydration and oxygenation is to be ensured

5.       Hyperglycemia, and fever are treated aggressively

6.       Treatment of blood pressure is individualized

7.       Ischemic stroke is treated with planned thrombolysis as per published guidelines

8.       Stroke etiology should be evaluated and results guide secondary stroke prevention

DEFINITION

Definition: Sudden loss of brain function caused by blockage or rupture of a blood vessel to the brain,

-with symptoms lasting for more than 24hrs

or imaging study showing acute clinically relevant  brain lesion.

Stroke is one of the three commonest causes of death in most civilized societies.

TYPES OF STOKE

1.      Ischemic Stroke          incidence 85%

2.      Hemorrhagic Stroke      incidence15%

Chart 1.Types of stroke

A.     ISCHEMIC STROKE

Entails two main mechanisms

a.      Athero thrombotic:

Plaque rupture and thrombus formation which blocks cerebral vessels

Can be large vessel thrombus or small vessel thrombus.

 Large vessel- extra cranial or intracranial large vessels.

Small vessel- perforating branches or peripheral branches

b.       Embolic:

Embolism arises from heart, or

from plaques in

 big vessels like aorta, carotid.

Embolic stroke is abrupt in onset

Sources of emboli:                                           

Usually cardiac:                                              

Left atrium in atrial fibrillation;

 Left ventricle in myocardial infarction                          

                              Other sources:-

                              Bifurcation of carotids, vertebral arteries,

                              Arch of aorta

                              Paradoxical emboli in patent foramen ovale

                           

                                       B.  HEMORRHAGIC STROKE

Accounts for 15% of strokes

Two main Types of hemorrhagic stroke:

·         Intra cerebral hemorrhage

·         Subarachnoid hemorrhage

Intra cerebral hemorrhage

    Common Sites of  deep intracerebral hemorrhage:

   Thalamus, putamen, cerebellum, brainstem

 

Subarachnoid hemorrhage

Bleeding into space between pia and arachnoid mater

Sub arachnoid hemorrhage is considered a stroke only if spontaneous;

not if due to accident or fall.

Often ushered in with severe headache plus warning signs

Commonest cause: Rupture of aneurysm of cerebral artery in

Circle of Willis; Typical site of aneurysm is bifurcation of arteries (weak point); aneurysm of diameter >7mm rupture.

Other causes;

A-V malformation in and around the brain

Chronic severe hypertension

 

  C. SPECIAL TYPES OF STROKES

A.      Transient ischemic attacks: (TIA)   synonym- mini stroke

·         Defined as brief episodic neurological deficit caused by focal brain or retinal ischemia with clinical symptoms typically lasting   less than 1hr without evidence of infarction

·         Generally lasts for 15 min to 1hr;

Patient usually recovers within 24 hrs leaving no residual deficit –

Ischemia is transient and symptoms disappear completely

·         TIA cannot be differentiated from acute stoke at the onset hence prompt evaluation is a must here also.

(If the neurological symptoms continue for >24hrs –it is defined as stroke.)

·         TIA is a warning sign for future acute stroke-greatest stroke risk in first week and 10% risk within 90 days

Chart 2.Special types of stroke

Symptoms of TIA:

·         Carotid territory TIA; - 

        Sudden mono ocular blindness

                                             Hemianesthesia, hemiperesis

                                             Transient aphasia (if dominant lobe affected)

·         Vertibrobasilar territory:

          Unconsciousness (reticular formation) Drop –attacks

                                              ‘Bilateral’ limb motor /sensory dysfunction

                                                           Diplopia, Dysarthria, vertigo, tinnitus, ataxia-

                                                     (Not as single symptom but in combination)

                                            (Dysarthria and ataxia are due to cerebellar lesion)

                                            Cortical blindness /homonymous hemianopia

Amaurosis Fugax; a special type of TIA-sudden loss of vision; resolves spontaneously: embolus from carotid occludes ophthalmic artery transiently.

 Causes, pathogenesis and types  of  TIA

Embolic TIA: arising from plaques in big vessels –aortic arch, carotids or from the heart- usually from bifurcation of common carotid.

Low flow TIA: On account of reduced perfusion pressure

e.g. sudden hypotension, cardiac arrest/cervical spondylosis on suddenly turning the neck

Lacunar TIA: due to lypohyalinosis of penetrating branches.

Natural history of TIA:

10% develop infarction in the following year

Another 10% in the next year

Greatest incidence in 3-6mths after initial TIA

A TIA should lead to immediate medical evaluation to determine its cause and

a treatment plan to prevent a stroke from occurring soon after.

A simple ABCD score to identify TIA patients who are at high and early risk of going in for stroke is available

Diagnostic point about TIA;

All symptoms start together and reach maximal intensity within seconds.

Non specific dizziness on its own is not diagnostic of TIA of posterior circulation.

Differential diagnosis of TIA:

In migraine and partial seizures symptoms build up more gradually.

In migraine typical h/o headache and aura is present

In partial seizures there are positive symptoms like tonic clonic seizures.

Also symptoms spread from one point to the rest of the limb and then to the other side but in TIA all occur at once.

In hypoglycemia, impairment or loss of consciousness may occur. But this is very uncommon in TIA.

.

Treatment of TIA: Aspirin. If AF is present -Anticoagulants .

 .B.  Lacunar infarct: Lacunar strokes

 Another special type of ischemic stroke; Sub type of thrombotic strokes

Very small ischemic infarcts measuring ½ -1cm in diameter.

Cause –local small vessel disease –occlusion of local small penetrating branches of major intra cranial arteries.

Resolution: the infarct which consists of neurons and glial tissue degenerate; eventually are absorbed by activated microglial cells. Finally a cystic cavity or glial scar remains.

Found in poorly controlled hypertensive.

Occlusions are caused by–lypohyalinisation, fibrin deposition, micro atheroma or embolism.

Final outcome: They are multiple and eventually lead to-Dementia and pseudo bulbar palsy.

Note: TIA does not cause permanent damage but lacunar infarct causes permanent damage but only in very small part of the brain.

Recognized Lacunar syndromes

·         Pure motor hemiplegia 60%   ; - Lesion in internal capsule

·         Pure sensory stroke  10%        :- lesion in thalamus

·         Dysarthric clumsy hand syndrome: lesion in base of the pons or genu of-Internal capsule. Features   : Dysarthria ,clumsiness of hand, facial weakness (contralateral)

·         Ataxic hemiparesis:  hemiperesis (or leg weakness) with ipsilateral ataxia  (pons oand  internal capsule)

Lacunar TIA -heralds lacunar infarct.

C.       Silent ischemic infarcts

Cause no symptoms

Occur in elderly especially those with hypertension and smoking risk

Lead to dementia

Indicate increased risk for future stroke

Large artery strokes

·         Large arteries that can be blocked include:

o   Internal carotid artery, Middle cerebral artery (Left/right)

Features: Contralateral hemiparesis, hemi sensory loss.

(Dysphasia if lesion on left hemisphere)

Signs of cortical dysfunction- aphasia, apraxia, agnosia, visual field defects

·         Vertebral artery(Right or left),Basilar artery

Symptoms: weakness/numbness on either side or both sides, nausea, vomiting, vertigo, ataxia,Diplopia&cranial nerve palsies(brain stem and cerebellar dysfunction

·         Aortic arch atherosclerosis; Thrombus from this can break off and block any of the above large vessels

·         Small  artery strokes :   Synonym: Lacunar infarcts

Small arteries penetrate deep into the brain; block causes any of the symptoms of ischemic stroke. Amount of brain damage is small.

Many lay persons are unable to recognize stroke symptoms though they are aware of its danger

 

 

SIGNS AND SYMPTOMS OF STROKE

Onset:  Almost always acute

In Severe cases: Sudden impaired consciousness;

 ‘Sudden severe headache’ may accompany. (Commoner in hemorrhagic than in ischemic type)

 In less severe cases:

Focal neurological deficit like

Hemiparesis

Hemi sensory loss

Mono ocular or binocular loss of vision

Defect in visual field

Diplopia

Dysarthria

dizziness

Ataxia

Vertigo

Aphasia and

Memory loss, confusion, behavioral changes

Sudden loss of bladder or bowel function

Above symptoms can occur in mild, moderate or severe degree and in any combination.

Lay people’s awareness about these symptoms is essential for reaching hospital early.

Symptoms and signs of Anterior circulation Strokes

 

Distinctive

 (of cortical dysfunction)

Aphasia

Apraxia

             Agnosia

Less specific

Unilateral numbness or weakness

Visual field defect

Dysarthria

Headache

Symptoms and signs of posterior circulation stroke

BRAINSTEM

·         Ipsilateral cranial nerve palsy with contralateral motor or sensory deficit

·         Bilateral motor /sensory deficit

·         Disordered conjugate gaze

CEREBELLUM

·         Cerebellar dysfunction without ipsilateral long tract deficit

OCCIPITAL CORTEX

·         Isolated homonymous visual field defect with macular sparing

ATAXIA

Can be from lesions of

·         Cerebellum,

·         Pons, Medulla

·         Cervical cord

VERTIGO

Hallmark symptom of VBI(Vertibro basilar artery insufficiency)

(Can result from damage to-labyrinth,vestibular nerve,central vestibular  structures   in brainstem)

DIAGNOSIS OF STROKE

Consists of:

1.Medical history,

2.General Examination including vital signs

3.Neurological examination to evaluate Anatomical and etiological diagnosis

(Refer ‘Clinical Examination in Hemiplegia ‘and

‘Diagnosis and management of hemiplegia ‘ by the same author)

DIFFERENTIALDIAGNOSIS FOR STROKE

STROKE MIMICKERS   (Disorders that mimic stroke)

1.       Seizures

2.       Tumors especially metastatic

3.       Systemic infections

4.       Toxic metabolic  disturbances

5.       Migranous aura

6.       Hypoglycemia

7.       Multiple sclerosis

8.       Intracranial hematoma(subdural,intradural)

9.       Infective  encephalitis

10.   Hyponatremia

Commonest are Seizure, Migraine and Brain tumor

Table1.DIFFERENTIAL DIAGNOSIS FOR STROKE

CLINICAL CONDITION	SIMILARITIES	DIFFERENTIATING FEATURES
SEIZURES	Todd paralysis in immediate postictal period (without immediate resolve may  persists  for a day or fits  may  have  been unobserved by attendants or out of patient’s recall	H/o established seizure, h/o paralysis developing  from one point to other parts gradually not all at once.
CEREBRAL NEOPLASMS Primary or secondary	1. hemorrhage within tumor can cause acute stroke like deterioration 2.Tumor  associated seizure activity may simulate stroke	Often focal deficit is gradual in onset
MIGRAINOUS  AURA	if aura  prolonged, can simulate stroke ;rarely ischemic stroke can complicate migraine	Typical  h/o prior similar symptoms Associatedheadache,nausea,vomiting,photophobia
HYPOGLY CEMIA	Can cause acute focal signs of stroke	But resolve rapidly with treatment (  So think of and exclude hypoglycemia in all cases of  apparent stoke  in diabetics under treatment)
HYPERTENSIVE ENCEPHALOPATHY	Can mimic stroke	Associated with h/o hypertension
MULTIPLE SCLEROSIS	May develop signs like acute stroke	Careful history and selective diagnostic tests
INTRA CRANIAL HEMATOMA (sub dural/epidural)	Can manifest like stroke In chronic sub- dural hematoma	often h/o headache and h/o fluctuating level of consciousness in subdural hematoma h/o trauma may be missing or patient if elderly and is  on warfarin
INFECTIVE ENCEPHALITIS	Can mimic acute stroke	Fever, fits, altered sensorium  and abnormal CSF findings help in differentiation.

COMPLICATIONS OF STROKE

1.       Most deadly complication:

Raised ICP -can be direct effect of cerebral edema or hematoma

Cytotoxic edema after ischemic stroke-manifests in 1-4 days

Signs of increased ICP are- altered sensorium, unequal pupils, VI ^th nerve palsy, papilledema

Tmt: fluid restriction,elevation of head end of bed,infuse osmotic diuretics,hyperventilation

2.       Stroke progression in25%

3.       Functional Disability with complete or partial dependence

4.    Recurrence

        5.    Seizures

Common in  

Intracerebral hemorrhage 

Subarachnoid hemorrhage

Large lesion involving cerebral cortex

Stroke induced seizures are usually controlled with a single anticonvulsant

        6. Vascular cognitive impairment or frank dementia

As per recent studies Choline esterase inhibitors may help in this condition

       7. Post stroke depression in 60% 

       8. Medical complications:

 Cardiac arrhythmias, myocardial infarction, pulmonary embolism, pneumonia, urinary infection, gastrointestinal bleeding.

INVESTIGATIONS FOR STROKE

 Urgent Imaging studies to distinguish ischemic from hemorrhagic stroke

IMAGING OPTIONS AVAILABLE

·         CT scan of the brain

·         MR I of the brain

Currently controversy exists as to which is better.

Both CT and MRI can accurately distinguish between ischemia and hemorrhage

CT -Advantages:   Available in most centers; available 24hrs

                             CT is gold standard for detecting Hemorrhage fast

In 60% infarct is detected in 3-6 hrs; all in 24 hrs.

Low cost

Primary advantage-ability to detect acute hemorrhage

 Can exclude other focal causes

CT Disadvantages:  less sensitive than MRI; Detection of early signs of ischemia is not good:

in 40% stroke may not show up to 3-6hrs; sometimes up to 48hrs.

So a repeat CT scan may be required

Small strokes may not show at all.

MRI: Advantage: It is more sensitive; can diagnose infarct missed in CT and small vessel infarcts

    Disadvantage: More time consuming:  scanning time-15 minutes or little more

Not available in all hospitals, all 24 hrs

 Patient’s preparation takes some more time

 All Patients may not be cooperative-(may not hold still during procedure)

 MRI is contraindicated in certain cases.

(if patient is unstable/If with pacemakers or implanted metal devices)

Upto 2-4 hrs MRI also may be negative for infarct signs

Currently plain CT without contrast is used as ideal first line test in many centers

NOTE: If CT already shows a stroke or cerebral edema it indicates a large stroke has occurred-which has increased risk of hemorrhage; in this situation tPA can precipitate the hemorrhage

More high quality images are available for better guidance in diagnosis and Treatment

CT/MR perfusion technique:

 Help to image two factors 1.core area of infarct 2.The ischemic penumbra

Core area -area of irreversible damage inside infarct

Penumbra is the surrounding area which could be salvaged if blood flow is restored rapidly.

 

 

.CT ANGIOGRAM: or MR angiogram

 Once infarction is diagnosed next to know is the vessel involved-through CT-Angiogram

This test quickly identifies large vessel occlusion and carotid stenosis;

 Thus makes urgent surgery or endovascular intervention possible.

 It is also useful in identifying the vascular territory / exact vessel involved –to facilitate intra arterial infusion of tPA

In addition can diagnose intracerebral hemorrhage.

Doppler Ultrasound of the Neck; used to check carotid plaques

Other names; carotid ultrasound/carotid duplex ultrasound

Trans cranial Doppler: Detects atherosclerotic narrowing of intracranial blood vessels

SPECTand PET (Sigle Photon Emission Computed Tomography and Positron Emission Tomography)

Using radioactive material damaged area in the brain is delineated

General Investigations

Blood :  sugar, lipids, Urea, creatinine

Coagulation time

Test for thrombophilia; proteinC, proteinS, antithrombin

Anticardiolipin antibodies

Platelet count

Test for polycythemia

Test for vasculitis:  ESR, RP, and ANCA

12lead ECG, serum Cardiac enzymes

Test for Cardiac Embolism:  ECG, HOLTER MONITORING, ECHO CARDIOGRAM, TEE/TTE

TREAMENT FOR ACUTE ISCHEMIC STROKE

Time factor in stroke therapy:

1.       Time is the most crucial factor, “TIME IS BRAIN”

2.       Prompt treatment can reverse the effects of stoke by reestablishing the blood flow.

3.        Hence history taking and evaluation must be rapid

4.       Determine the exact time of onset of the stroke

        Estimate the time period that has elapsed after onset of symptoms  

       (When was patient completely normal last of all?)

Evaluation of patient must be concluded within 60 minutes of arrival in causality.

5.       Stroke is best treated in stroke unit -A unit for organized stroke care with emergency stroke management team-outcome better,mortality is lessand hospital stay is shortened.

6.       After ruling out cerebral hemorrhage, accepted best treatment is  the administration of thrombolytic-  tPA –Tissue plasminogen activator

7.       Window period-window of opportunity to rescue the penumbra

Window period and tPA

 If patient’s criteria for selection is met with

1.      Within 0 to 3 hours of onset of symptoms- “intravenous “ thrombolytic –through vein of arm is indicated.

(The most important point in history thus is time of onset of symptoms.)

2.      Between 3 to 6 hours  of onset of symptoms –“ Intra arterial” thrombolytic - administered

i.e. intra arterial tPA is   directly infused right at the site of thrombosed blood vessel via a thin flexible catheter inserted in femoral artery

But only interventional radiologist/neurosurgeon can perform this

                3.{For posterior circulation Stroke window time may be extended up to 18 hrs    

                 (AmericanStroke association)

              4. 0-8hrs- is window for Mechanical embolectomy

                                  

MODALITIES OF ENDOVASCULAR TREATMENT OF ACUTE ISCHEMIC STROKE

                   I.            Systemic thrombolysis

                II.            Local intra arterial thrombolysis

             III.            Mechanical or non pharmacological methods of revascularization

I.       SYSTEMIC THROMBOLYSIS

1. Drug of choice t-pa

2. Route-Intravenous t-PA

3. PROTOCOL GUIDELINES

3a.Patient selection and Eligibility criteria

·         Age above 18 or older

·         Clinical diagnosis of ischemic stroke causing measurable neurological deficit

·         Time of onset of symptoms less than 3hours

3b. Contra indications for t-pa

1.      Evidence of intracranial hemorrhage on pretreatment CT

2.      Clinical features suggestive of subarachnoid hemorrhage even with normal CT

3.      Active internal bleeding

4.  Known bleeding diathesis including

5.  Platelet count<100000/ml

6.  If patient has received heparin within 48 hours and has an elevated APTT

7.  Current use of oral anticoagulants (e.g.warfarin) or recent use with an

    elevated -Prothrombin time>15 sec

8. Within previous 3 months any Intracranial surgery, serious head trauma or any serious stroke

         9. On repeated measurement systolic pressure greater than 185mmof Hg or

         diastolic pressure greater than100mmofHg at the time treatment is to begin.  

         patient requires aggressive treatment to reduce BP within these limits

10    .H/O intracranial hemorrhage and  known arteriovenous malformation or aneurysm

WARNINGS AGAINST USE OF t-PA

Only minor or rapidly improving stroke symptoms

 If patient has had major surgery or trauma excluding head trauma in the previous 14 days

Recent arterial puncture at a non compressible site.

Recent lumbar puncture.

Abnormal blood glucose <50mg or >.400 mg/dl

Post myocardial infarction pericarditis

Patient was observed to have seizures at the same time the onset of stroke symptoms were observed

3C.Dose of t-PA

            0.9mg/kg (maximum of 90mg) of t-PA,

             infused over 60minutes ,

             with 10% of total dose administered as initial Intravenous bolus over 1minute.

           Do not use cardiac dose.

                      

                        4. TREATMENT PROTOCOL                   

                                        

  4. TREATMENT PROTOCOL

4. A. Initial assessment

1. Determine whether time is available to start treatment with tPA before 3hrs

1.      Draw blood for tests while preparations are made to perform non contrast CT scan

2.      Start recording BP

3.      Neurological examination

4.      CT scan without contrast

5.      Determine if CT has evidence of hemorrhage

6.      If patient had severe head or neck pain or is somnolent or stuporous, be sure there is no evidence of subarachnoid hemorrhage

7.      If there s a significant abnormal lucency suggestive of infarction, reconsider the patient-since the stroke might have occurred earlier

4B. Review of required test results

a. Hematocrit

b. Platelets

c. Blood glucose

d. PT or APTT (in patients with recent h/o oral anticoagulants or heparin)

e. Review patient selection criteria

4C. infuse t-pa

·         Give 0.9mg/kg,10% as a bolus intravenously

·         Do not use cardiac dose

·         Do not exceed 90mg maximum dose

·         Do not give aspirin, heparin or warfarin for 24 hrs

·         Monitor the patient carefully, especially the BP; follow the BP algorithm

·         Monitor neurological sign

5. adjunctive therapy

·         No concomitant heparin, warfarin or aspirin in first 24 hrs after symptoms onset.

·         If heparin or any other anticoagulant is indicated, after 24 hrs, consider performing a noncontract-or other sensitive diagnostic imaging method to rule out any intracranial hemorrhage before starting-an anticoagulant.

6. Other general measures in treatment

(In summary give basic life support, maintain electrolytes, treat fever, infection and other comorbid conditions.)

·         Intravenous hydration with normal saline

·         Supplemental oxygen

·         Insulin for hyperglycemia

·         Antipyretics for fever

·         ECG to be performed and patient is to be put on continuous cardiac monitoring

·         No oral intake is permitted until the patient passes a swallow test with sips of water

or if arrives late but within 8hrs or along with tPA

·         Treatment of Raised intracranial tension

o   Osmotic  diuretic mannitol, Loop diuretics, Hyperventilation

·         Key clinical points in treating hypertension

High BP found after ICH or SCH should not be brought down over- enthusiastically. Reasons: 1. it could be transient acute rise consequent to bleed.

2. Damaged brain tissue needs good perfusion pressure to maintain a good blood flow.

Damaged   brain tissue has lost its ability to auto regulate.

( i.e healthy brain tissue  is able to maintain  constant blood flow rate despite varying BP levels. This called auto regulation)

Low BP hence leads to low blood flow in the recently damaged area of brain

Unless SystolicBP>220orDiastolic>120and sustained, with repeated reading do not treat for within first days.

Refer table on antihypertensive treatment   for details

Table2. ANTI HYPERTENSIVE THERAPY FOR ACUTE STROKE

BLOOD PRESSUREb	TREATMENT
IN NON THROMBOLYTIC CANDIDATES
DBP>140mmof Hg	Sodium nitroprusside 0.5µgm/kg/min)Aim for10- 20% reduction in DBP
SBP>220,DBP>120,or MAPc>130mmHg	10-20 mg labetalold IV push over 1-2 min. May  repeat or double labetalol every 20 min to a maximum dose of 150 mg.
SBP<220,DBP>120,orMAP>130mm Hg	Emergency anti hypertensive is deferred in the absence of aortic dissection, acute myocardial infarction, severe congestive heart failure or hypertensive encephalopathy.
IN THROMBOLYTIC CANDIDATES  PRE TREATMENT
SBP>185orDBP>110mmHg	1-2 inches of nitro paste or 1-2 doses of10-20mg labetalold IV push. if BP is not reduced and maintained to<180/110mmHg the patient should not be treated with tPA.
DURING AND AFTER TREATMENT
Monitor BP for 24 hrs after starting  tmt, Look for hypotension	BP is monitored every15 min for 2hrs,then every 30 min for 6hrs and then every 1 hr for 16 hrs
DBP>140mmHg	Sodium nitroprusside(0.5µgm/kg/min) infusion
SBP>230or DBP121to140mmHg	1)10mg labetalold IVP over1-2 minutes. May repeat or double labetalol every 10minto a maximum dose of 150mg or give the initial labetalol bolus and set a labetalol drip at 2-8mg/mintill desired BP reached 2) If BP not controlled by labetalol consider sodium nitroprusside.
SBP 180-230or DBP105- 120mmof Hg On 2 readings 5-10min apart	10mg labetalol IVover1min. may repeat or double labetalol every 10 to 20 min to a maximum dose of 150mgor give initial labetalol bolus and start a labetalol drip at 2-8 mg/min

^bAll initial blood pressures should be verified before treatment by repeating reading in5 min.

^cAs estimated by 1/3^rd  the sum of systolic and double diastolic pressure.

^DLabetalol should be avoided in patients with asthma, cardiac failure or severe abnormalities in cardiac conduction.

Labetalol  has Short half life, easily titratable,does not increase ICP

But  nitrates-nitroprusside and nitroglycerine  can raise ICP;often avoided

ACE inhibitors –slow onset ;not first line agent in ICH

Reference;American heart Association 

If during treatment ICH is suspected clinically, stop tPA treatment

POINTS TO CONSIDER

·         Patient’s BP may decline spontaneously in first 24 hrs after stroke

·         BP reduction in acute phase should be avoided if possible.

·         BP should be maintained  high enough to maintain a cerebral perfusion pressure of >60

·         Antihypertensive drugs are withheld unless diastolic BP is >130 and SBP>220

·         When treatment indicated BP should be lowered cautiously.

In hemorrhagic stroke BP Should be maintained below 180/100 -American heart Association

After use of tPA BP -maintained at185/110

7. MECHANICAL OR NON PHARMACOLOGICAL METHODS OF REVASCULARISATION

1.        CAROTID ENDARTERECTOMY or PLACEMENT OF CAROTID STENT

2.        MERCI retriever: Mechanical Embolus Removal in Cerebral Ischemia

A mechanical cork screw shaped device is used at end of the catheter to pull out the clot

Procedure:   approved by FDA;  it an Endovascular procedure;

Limitation:  clot must be visible and accessible, small pieces may lodge further down

 But at least area of damage can be smaller

Only super specialists can perform the procedure

PATIENT AND CARE GIVER’S EDUCATION

Educate patient to recognize   stroke symptoms and to seek medical help promptly.

Post stroke depression must be detected and treated

When applicable secondary stroke prevention methods must be emphasized

STROKE CODE ALGORITHM FOR ISCHEMIC STROKE

  

Mechanical Clot busting:   Indications:  patient if unsuitable for tPA

 

PREVENTION OF STROKE

·         Hypertension is important modifiable risk factor BP is to be maintained ,140/90 to

Reduce the risk of stroke

·         For primary and secondary prevention no difference between drug classes; but

        Losartan may offer benefit beyond BP lowering.

RISK FACTORS FOR STROKE

Modifiable Risk factors:

·         Hypertension

·         Diabetes mellitus

·         High cholesterol level

·         Obesity

·         Sedentary life style

·         Smoking

·         Heavy drinking

·         Low fiber, high fat diet

·         Cardiac Disease

·         Carotid stenosis

·         Atrial fibrillation

·         TIA/prior stroke

·         Sickle cell disease, polycythemia

·         Sleep apnea

Non modifiable risk factors

·         Age above 55

·         Gender; males are more prone

·         Family history

·          Race/ethnicity: African –American race

Prevention

Aim: Prevent not only disability but also long term dementia that can occur (after silent strokes); many strokes can be prevented with the use of modern medicines

TYPES OF PREVENTION

1.       Primary prevention

2.      Secondary prevention-needs  to be aggressive

. STROKE PREVENTION IS A MULTIFACTORIAL APPROACH

                                  Table 3.  MEASURES FOR STROKE PREVENTION

PRIMARY PREVENTION	SECONDARY PREVENTION
Treat hypertension	All primary prevention treatment
Treat  hyperlipedemia	Carotid endarterectomy/stent
Quit smoking	Anticoagulation for cardiac emboli
Exercise	Antiplatelet therapy ;ASA ,CLOPIDOGREL  ASA/extended release Dipyridamole
Detect and treat atrial fibrillation
Aspirin for  myocardial infarction and stroke

·         Treatment of risk factors prevents most strokes

·         Diet, exercise, cessation of smoking, antihypertensive, lipid lowering agents are highly  important in primary prevention

·         in secondary prevention also, same measures are important

·         Anticoagulation warfarin is for atrial fibrillation and related cardiac source of embolism.

·          For related cardio embolic strokes cardiomyopathy, MVPS, MR, aortic disease-  Aspirin.

·         Carotid endarterectomy/stenting for secondary stroke prevention if causing TIA or minor stroke

·         Anti platelet therapy for all but  for warfarin indicated patients;

·          increasing evidence for ASA and Extended Release  dipyridamole  combination ;makes a very effective combination

No evidence for ASA+clopidogrel combination but each   can be used alone; Combination increases bleeding risk. (But used in acute coronary syndrome, coronary stent patients

·         New ASA guidelines for secondary stroke prevention are published

Pharmaco therapeutic strategies for stroke prevention

HYPERTENSION

·         Hypertension -An Important stroke risk factor-increases risk by 5-6 fold

·         Treatment of hypertension is crucial in secondary prevention also

·         Anti hypertensive to be chosen for stroke prevention

o   ACE Inhibitors seem especially effective HOPE STUDY

o   perhaps a diuretic combination is more effective

o   ARB also effective

o   Time  to start treatment for hypertension after stroke

§  ARB (Candesartan) initiated on day1afterstroke has shown long term benefit.ACCESS STUDY

·         In summary ACEI or ARB + diuretic may be advantageous.

·         But control of BP is more important than choice of agent.

·         African-Americans require ACEI+DIURETIC or perhaps Calcium channel blockers

·         Detection and aggressive treatment of hypertension prevents primary stroke40-50%:

       Secondary stoke prevention 28%

·         Absolute target level of BP reduction-uncertain; Must be individualized(AHA guideline)

·         If diabetes  and hyperlipedemia associated, more vigorous control of BP  is required

DIABETES

Control to near normoglycemic levels

Vigorous treatment of hypertension and hyperlipedemia indicated

More than 1 agent may be required. First choice are ACEI and ARBs

 CHOLESTEROL AND STROKE

·          Direct correlation between cholesterol and stroke is small

·         But STATINS have shown to have Pleotropic effect: plaque stability, antithrombotic anti platelet, anti inflammatory (CRP) effect.

·         Studies show that Statins prevent stroke as well as recurrent MI

·         HPS SPARCL studies suggest Statin indication after stroke

·         FDA has  approved simvastatin 40mg /pravastatin for secondary stroke prevention

·         Should be managed according to NECP guidelines

SECONDARY STROKE PREVENTION

I.ANTICOAGULANTS 

1. WARFARIN:

Clearly benefits patients with atrial fibrillation in preventing stroke especially those with high risk. (History of CHAD-Congestive heart failure, Hypertension. age >75 Diabetes, Stroke/TIA)

 For Non cardio embolic stroke; warfarin not indicated

For recurrent Stroke: Aspirin only indicated not warfarin

2.ANTI PLATELET AGENTS

Aspirin

Combination of aspirin and extended release dypiridamole studied to be better than Aspirin alone

No evidence for aspirin and clopidogrel combination (increased risk of bleeding)

Table4. SECONDARY STROKE PREVENTIVE THERAPIES
CLASS	AGENTS
Anticoagulant	Warfarin only in atrial fibrillation with high risk –target INR2-3.
Antiplatelet agents	Aspirin 160-300mg /day within 48 hrs
	Aspirin+ Extended release dipyridamole (Aspirin25mg+ dipyridamole 200mg)
	Clopidogrel 75mg daily- For patients allergic to aspirin
Antihypertensives	ACEI
	ARBs
Antihyperlipedemia	Statins

                          Table5.COMPARISION OF ANTIPLATELET AGENTS

	CLOPIDOGREL	ASPIRIN	Aspirin with dipyridamole SR
Efficacy	+++	++	++++
Tolerability	+++	+++	++
Routine blood monitoring	NO	NO	NO
Dosing frequency	od	od	bid
Cost	++++	+	+++

SURGICAL TREATMENT OF ISCHEMIC STROKE

                                        (Also serves as secondary stroke prevention)

IA. CAROTID ENDARTERECTOMY OR STENTING

Indication:

In symptomatic carotid stenosis ≥ 70%

                           In some patient with ≥ 50% symptomatic carotid stenosis

Beneficial in selected patients

IB.  Angioplasty and Stenting

Indication: in those with high risk with unstable heart disease,

Unstable neurological status,

Contralateral occlusion

Procedure: A catheter is inserted via femoral artery into

the intra cerebral artery that is narrowed; tiny balloon at the end of

 the catheter is inflated to flatten the thrombus; a wire mesh stent is placed

to retain the artery open

·         Stenting/angioplasty is also performed for cervical arteries

II.MERCI RETRIEVER: MECHANICAL EMBOLUS REMOVAL IN CEREBRAL ISCHEMIA

·         Indication: patient if unsuitable for tPA/arrive late  but within 8hrs/companion to tPA

·         A mechanical cork screw shaped device is used at end of the catheter to pull out the clot

·         Procedure:

 An endovascular procedure;  approved by FDA;speeds up the process of  clot removal jn ischemic stroke

A mechanical cork screw shaped device is used at end of the catheter to grab and pull out the clot

·         Limitation:  clot must be visible and accessible, small pieces may lodge further down

·         But at least area of damage can be smaller

·         Only super specialists can perform the procedure

INTRA CEREBRAL HEMORRHAGE (ICH)

ICH is bleeding within the brain

Etiology:

Commonest cause   ; chronic hypertension

Less common:

Amyloidal angiopathy of cerebral vessels

Other causes;

Congenital, causes-Cerebral aneurysm, Arterio venous malformation

Traumatic or inflammatory pathology of cerebral vessel

 Tumors

Bleeding disorders, high dose anticoagulants

Others;atherosclerotic aneurysm,mycotic aneurysm,

Note: Ischemic   stroke can get transformed into hemorrhagic stroke. But they are commonly asymptomatic

Clinical presentation

 Characteristic “Severe headache”, nausea, vomiting, seizure

In old people headache may be mild or absent

 Progressive neurologic deficit-Unilateral motor/sensory loss

 Dimness/loss of vision in one eye

Neck stiffness

Impaired level of consciousness,/coma

Sudden onset, progressive

High, uncontrolled BP- systolic blood pressure greater than 220 mm Hg,

Features of high possibility of ICH: anticoagulation, hyperglycemia in a non diabetic

Neuro imaging

ICH and infarction cannot be distinguished by clinical exam alone

Neuro imaging is mandatory-CT/MRI brain

Treatment

 Best treated in stroke unit

Medical

Surgical

Currently no specific drug or surgery for ICH

Medical treatment

1. Stabilisation of the patient

2. Monitoring of blood pressure simultaneously ensuring adequate intracerebral flow

(Refer details of anti hypertensive therapy given under ischemic stroke)

3. Treatment of raised intracranial pressure

Intravenous mannitol with or without frusemide

4. for patients on warfarin and elevated INR and ICH-options available are: vitamin K

Administration of clotting factors, fresh frozen plasma, Prothrombin complex concentrate (PCC), recombinant factor VIIa

Surgical treatment-in selected cases and if refractory to medical treatment

1.      Evacuation of hematoma - moderate hematoma in awake and conscious patient

(In comatose patient and if hematoma is greater than 6cm diameter or more than 80ml with or without surgery outcome is poor; Awake patient with hematoma of less than 3cm and >20ml usually recover without surgery)

2.      Evacuation of cerebellar hematoma: prevents brainstem compression and death.

3.      For supratentorial ICH neuro surgical opinion is sought

 3. Two primary surgical treatment of cerebral aneurysm

  1. clipping: placing a metal clip across the neck of the aneurysm to prevent blood flow into aneurismal sac.

2. Coiling; tiny platinum coils are filled into aneurysm thus preventing rupture

(Aneurysm is accessed via a femoral catheter, advanced into  concerned cerebralartery)

4.      Arterio venous malformations

Three main modalities of therapy

Endovascular therapy, microsurgery, stereotactic radio surgery with gamma knife

SUB ARACHNOID HEMORRHAGE (SAH)

SAH refers to bleeding into space between pia and arachnoid

Age incidence-25-65

CAUSES OF SAH

Most common cause rupture of intracranial aneurysm, trauma

·         Head trauma –(not considered as stroke)

·         Intra cranial aneurysm cause 80% non traumatic SAH

o    Common Site – berry aneurysm of circle of Willis (MCA bifurcation, ACA,PCA )

o   Also ophthalmic  arteries, vertebral/basilar arteries

·         Benign peri midbrain hemorrhage

·         Less common causes of SAH

o   Arterio venous malformation

o   Extension from ICH

o   AV fistula, meningitis, neoplasm

Risk factors:

Hypertension, Vasculitis, fibro muscular dysplasia/o poly cystic kidney disease

                                      

Clinical presentation

Most  classical symptom: headache,(worst headache of life),abrupt, reaching maximum intensity in seconds(thunder clap headache)

Neck stiffness/signs of meningism

Nausea, vomiting, altered sensorium,

Signs of raised ICT

Intraocular/subhyaloid hemorrhage

Seizures

Sharp increase in BP (adrenaline release) cardiac arrhythmias, cardiac arrest

Neurogenic pulmonary edema

CSF may be bloody

Imaging Studies

Plain CT brain/MRI

CT Angio, MR Angio

Acute hemorrhage appears as high attenuation material (white) that fills the normally black subarachnoid space. Acute hemorrhage is most evident 2-3 days after acute bleed.
 

TREATMENT FOR SUBARACHNOID HEMORRHAGE

1.       Medical

2.      Surgical

1. Medical

Bed rest, normalizing the BP, analgesic to relieve headache plus

Nimodipine for reducing BP and for decrease brain cell loss

Nimodipine also relieves vaso spasm

2. Surgical treatment-May be required

Angiogram performed to identify source of bleeding

Common cause –aneurysm-surgical repair undertaken

Nimodipine  is shown to improve outcome in SAH

Prognosis: death or severe disability in nearly half. Survivors get neurological impairment

COMPLICATIONS

ACUTE

Chemical meningitis

Neurogenic pulmonary edema,

Brain stem herniation

Cardiac arrhythmias, myocardial infarction

Sub acute

Vasospasm cerebral ischemia

Syndrome of inappropriate ADH secretion-Hyponatremia

Chronic

Pneumonia,

Pulmonary embolism

Recurrence of SAH

Venous stroke

Bilateral involvement common

Convulsions – in 50% of cases

Common in post partum females

CSF is hemorrhagic

CT scan shows delta sign

Recurrent stroke

Arterial dissection

Patent foramen ovale

Hyperhomocysteinemia

Hypercoagulable state

Sickle cell disease

Cerebral venous thrombosis

Post stroke rehabilitation

• Post Stroke Rehabilitation;
• Help in recovery after stroke.
• Help patient and family to return home after stroke.
• Driving recommendations after stroke.
• Depression after stroke.
• Help patient and family understand prognosis and recovery after stroke.
• Memory loss after stroke.
• Recommendation of Speech Therapy
• Occupational therapy

    Disclaimer:Please note that treatment part is not uptodate.                                              ------------------