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 1/3rd 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. ------------------
Common causes of Ascites
