date Review On :

1:
gement of Acut Ischemic St
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 No Weak Links

• Development: Protocol and pathway development

• Detection: Early recognition
• Dispatch: Early EMS activation
• Delivery: Transport & management
• Door: ED triage
• Data: ED evaluation & management
• Decision: Neurology input, therapy selection
• Drug: Thrombolytic & future agents
• Disposition: Admission or transfer
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 Management of Acute
Ischemic
Stroke
1. Immediate emergent stroke protocol

2. Measures to restore or improve

perfusion:

3. General supportive measures

4. Treatment of acute neurological

complications of stroke 5
 Stroke Time of Onset
Determines Treatment Strategy

Hyperacute < 3 hours

IV tissue plasminogen
activator (Activase)
Acute 3 – 8 hours
catheter interventions/
cerebral
Subacute > 8 hours revascularization
Augment perfusion, techniques
manage systemic
complications

Secondary Stroke Prevention 6

 A, IMMEDIATE EMERGENT
STROKE PROTOCOL
(e) Intravenous (IV) access should be obtained and 0.9% normal
saline is started at 50 ml/hour with saline .,

(e) The investigations to be done include

12 lead ECG ( to exclude ischemia or arrhythmia),
Blood sugar (to exclude hypo or hypoglycemia as the cause),
complete hemogram,
electrolytes, metabolic parameters and
coagulation profile.
(f) assessment of stroke through
history for risk factors, to establish the time of stroke,
physical and cardiovascular examination
neurological examination should be done to assess severit and
its quantification as per by NIHS scale8.
Lastly CT scan to exclude hemorrhage and to detect early cerebral
edema. 7
The criteria for
admission to the
intensive care unit

8
 B ,MEASURES TO
IMPROVE
OR RESTORE PERFUSION
The measures available are

(1) IV thrombolysis by rTPA and other thrombolytic agents,

(2) Intra arterial thrombolysis,

(3) Antithrombotic therapy,

(4) Surgical treatment and

(5) Volume expansion, vasodilators, induced hypertension,

9
 1. Do antithrombotic agents reduce stroke mortality and stroke-
related morbidity?
Aspirin (160 mg or 325 mg daily) results in a small but statistically
significant reduction in death and disability when given within 48 hours
after ischemic stroke, as indicated by a combined analysis of available
studies.12
Abciximab, unfractionated heparin, LMW heparins, and heparinoids have
not been shown to reduce mortality or stroke related morbidity when used
within 48 hours of onset in patients with acute ischemic stroke.

2. Do antithrombotic agents reduce early stroke recurrence?

Aspirin reduces the risk of early recurrent ischemic stroke when given
within 48 hours of stroke onset but increases the risk of hemorrhagic stroke
(absolute risk reduction 0.7%; number needed to treat 143). Overall, for
aspirin there is a slight but statistically significant benefit in reducing
recurrent stroke. Conversely,
unfractionated heparin and LMW heparin/heparinoids, when used within
48 hours of onset in patients with acute ischemic stroke, have not been 10
shown to reduce the rate of stroke recurrence.
 Do antithrombotic agents vary in efficacy by .3
?stroke subtype
The slight, beneficial effect of aspirin
in acute ischemic stroke appears not to be influenced by stroke subtype.
There is no convincing evidence that anticoagulants are effective for any
particular stroke subtype.
The finding that danaparoid was of possible benefit in patients with a
large artery stroke was based on a prespecified secondary analysis
unadjusted for multiple comparisons; therefore, the observation awaits
prospective validation
before it can be given any weight.

4. Do antithrombotic agents reduce systemic thrombotic complications such

as deep vein thrombosis and pulmonary emboli?

The frequency of DVT in acute stroke is reduced by anticoagulants but not by

antiplatelet agents.
It is unclear whether frequency of PE is also decreased because too few PE occurred in
the cohorts studied to exclude the possibility of a Type II error. 11
 5. What are the risks of hemorrhage associated with antithrombotic agents?

There is an increase in both systemic and CNS

hemorrhage in patients treated with aspirin,
subcutaneous unfractionated heparin, or LMW
heparin/heparinoids.

6. Do antithrombotic agents alter acute cardiovascular complications?

The available data suggest that the incidence of acute

cardiovascular complications is low, and none of the available
studies had sufficientpower to detect a modest treatment effect
on these endpoints.
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Recommendations of SCASA about use of aspirin

(a) Aspirin should be given within 24 to 48 hour of stroke

onset. In most patients (Grade A),

(b) Use of aspirin as an adjunct therapy to rTPA therapy

is not indicated (Grade A),

(c) Aspirin should be used as substitute for other

interventions e.g. rTPA therapy (Grade A),

(d) at present no recommendations can be made about

other antiplatelet agents (Grade C)
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 Recommendations of SCASA about
Heparin

(a) As parentrally administered anticoagulants increase the risk of

serious bleeding complication and do not reduce the risk of early
recurrent stroke, including the patients with cardioembolic
stroke , anticoagulation in acute stroke with an aim to improve
outcome and for prevention of early stroke is not indicated.

(b) Urgent anticoagulation is not indicated in moderate to serious

stroke because of high risk of intracranial bleeding complications
(Grade A),

(c) Anticoagulant therapy within 24 hours of treatment with IV

rTPA is not recommended
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Recommendations of SCASA about Heparin
(c) Parentral anticoagulation should not be given unless
possibility of ICH is excluded by neuroimaging and those
receiving it should have strict dose control to keep the level of
anticoagulation within the desired range,

(d) As one trial showed that anticoagulants might improve out

come in one subgroup i.e. stroke due to large artery
thrombosis More studies are required if any subgroup or
patients at high risk of recurrent embolism may benefit from
urgent anticoagulation,

(e). Additional studies are needed to define the role of

adjunctive anticoagulation in addition to mechanical or
pharmacological role in acute stroke 15
Recommendations of SCASA are :

(a) IA thrombolysis is an option in selected patients with large

stroke and requires an experienced endovascular interventional
radiologist and immediate access to angiography,
(b) The tested drug r-proUK is not available for clinical use,
(c) The extrapolation of the result to and use of IA rTPA is
based on consensus as supported by case series data which
suggest beneficial effects of IA rTPA in basilar artery occlusion
of longer duration,
(d) The availability of IA rTPA therapy should not preclude IV
rTPA therapy and It is not approved by FDA.

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 Surgical Intervention

Though, some surgeons have reported encouraging results from

endarterectomy with a low complications and intracranial extracranial
(IC-EC) bypass surgery in patients with acute stroke and with
anticoagulation followed by delayed operation.
These procedures are associated with high morbidityand a high risk of
intracranial hemorrhagic complications and have failed to improve
outcome .
Endovascular treatment i.e. balloon angioplasty of thrombus, mechanical
removal of clot from MCA, stenting of underlying atherosclerotic stenotic
lesion, suctions thrombectomy, laser assisted thrombolysis of embolus and
power assisted Doppler thrombolysis have been reported .
Intravenous use of glycoprotein IIb/IIIa inhibitor has been used to enhance
the clot lysis. Because of lack of evidence for safety and efficacy of these
procedures, they are not recommended

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 C , General measures

Therapeutic Prevent
Goals Complications

“6 norms”:
normoglycemia, Aspiration
normovolemia, Venous
normothermia, Thromboembolism
normoxemia, UTI
normocapnia, and Contractures
normotension. Recurrent events 18
 Air way management

In patients with infarctions in the brainstem due to occlusive

disease in the posterior circulation, oropharyngeal dysfunction—
pharyngeal weakness and the inability to move the tongue—may
cause airway obstruction.

The decision to intubate patients with ischemic stroke depends

primarily on the failure of oxygenation despite supplemental oxygen
to control tachypnea, respiratory compromise due to
fatigue,
the inability to clear secretions,
or the occurrence of a prolonged seizure requiring medication
that causes marked sedation.

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 G uid eli nes fo rinit ial
antih ypertensive t re atm ent at a cute
is chemic s tr oke

Syst Diast. Goal Year

German HTN League 200 100 Max. 20% 2001

EUSI 220 120 180/100-105 2000
UK n.a. n.a. n.a.* 2000
AHA 220 120 2004
*only if complications occur within 7 days

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21
 Blood Pr es sure in Acute S troke
When i s it appropri ate to initi al
?anti hypertensi ve ther apy
American Stroke Association
and
the European Stroke Initiative
• BP less than 220/120
2006mms of Hg:
B BP more than 220/120-140 mms
Observe (level V): of Hg
treat when end organ involvement is
noted e.g. aortic dissection, Labtalol 10-20 mg IV over one
acute MI and pulmonary edema. minute: repeat or double the dose
every 10 minutes (maximum
300mg) or
C. Diastolic BP more than 140 mms Nicardipine 5 mg/hr Iv infusion
of HG:
and titration to desired levels by
IV Nitroprusside 0.5 mcg/kg/min
Increasing 2.5 mg every 5 minutes
infusion under constant monitoring:
(maximum 15 mg/hr). Aim for10 to
Aim only 10% to 15% reduction.
15% reduction of BP. 22
 .Hypotension

Normovolemia is imperative, and fluid management with use of 0.9% saline

administered initially at 100 mL/h often is needed.

Fluids containing free water should be avoided.

If patients seem pressure dependent with recurrent symptoms afterblood

pressure is reduced, the blood pressure can be supported with intravenous
dopamine, 10 to 14 μg/kg, titrating to a mean arterial blood pressure of 110 to
130 mm Hg.

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 Management of Temperature Control
Mechanisms of injury :
is the release of excitotoxic aminoacids,
enhancement of detrimental inflammatory responses,
Release of free radicals or an increase in thereby
increasing blood flow and ICP.

Aggressive management of temperature seems warranted;

acetaminophen (up to 4 g/d in divided doses),
cooling blankets,
And gastric ice water lavage should be used as necessary.

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 Management of AIS
Fluids: Avoid Hyponatremia
Brain injury patients are prone to sodium dysregulation,
Na goal >140 meq/L Normal Saline 0.9% NaCl to maintain
intravascular volume and Cerebral Perfusion Pressure

Fluid balance is calculated by measuring daily urine production

and adding for insensible water loss (urine output plus 500 mL
for insensible loss plus 300 mL per degree in febrile patients).
Enteral Nutrition:
- concentrated 2kcal/ml
(less free water available for absorption)
- glucose sparing formulas are 1kcal/ml
However, patients with a blood glucose level higher than
(10 mmol)-300 mg/dL should be considered for treatment
with insulin infusion
“tight” 80-110 mg/dl is the goal. 25
 Prevention of DVT and Pulmonary
embolism

use of intermittent pneumatic compression devices on the lower

limbs is probably sufficient to prevent this condition.

Subcutaneous heparin can be considered for those unable or

unwilling to use pneumatic compression devices.

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D, Treatment of Acute Neurological
:Complications
Raised intracranial Pressure (ICP) & Cerebral
Edema

Treatment modalities include

(a) mild fluid restriction
(c) avoidance of hypoosmolar fluids (i.e. 5% dextrose),

(e) Treating exacerbating factors (e.g. hypoxia, hypercarbia, and

hyperthermia),

(g) elevation of head by 15-30 0 to improve venous drainage is safe as

long as CPP is more than 70 mms
(h) management of BP, as discussed earlier, for maintaining an
adequate CPP (and
(f) treatment of raised ICP (No controlled trial to asses the efficacy
ofhyperventilation, osmotic diuretics, CSF drainage and surgery27
 Raised intracranial Pressure (ICP) &
Cerebral Edema
Osmotherapy
. Mannitol 20% (0.25– 0.5 g/kg every 4 h However, it should not be used
prophylactically) is reserved for patients with type B ICP waves,
progressively increasing ICP values, or clinical deterioration
associated with mass effect Due to its rebound phenomenon,
mannitol is recommended for only #5 d. To maintain an osmotic
gradient,

furosemide (10 mg Q 2–8 h)

may be administered simultaneously with osmotherapy. Serum
osmolality should be measured twice daily in patients receiving
osmotherapy and targeted to #310 mOsm/L.

No steroids
Corticosteroids in ICH are generally avoided because multiple
potential side effects must be considered and clinical studies have
28
not shown benefit
 Raised intracranial Pressure (ICP) &
Cerebral Edema
Hyperventilation
Hypocarbia causes cerebral vasoconstriction. Reduction of cerebral
blood flow is almost immediate, Reduction of pCO2 to 35–30 mm Hg,
best achieved by raising ventilation rate at constant tidal volume
(12–14 mL/kg), lowers ICP 25% to 30% in most patients (Failure of
elevated ICP to respond to hyperventilation indicates a poor
prognosis.

Muscle relaxants
Neuromuscular paralysis in combination with adequate sedation can
reduce elevated ICP by preventing increases in intrathoracic and
venous pressure
associated with coughing, straining, suctioning, or “bucking” the
ventilator Nondepolarizing agents, such as vecuronium or
pancuronium, with only minor histamine liberation and ganglion-
blocking effects, are preferred in this situation . 29
Raised intracranial Pressure (ICP) & Cerebral
Edema

Surgical interventions
including CSF drainage may be used to treat raised
ICP secondary to hydrocephalus

Surgical decompression for large cerebellar

infarction causing brainstem compression and
hydrocephalus, is
indicated

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 Treatment of Acute Neurological
Complications:
Seizures

while recurrent seizures develops in 20% to 80%

patients.
Intermittent seizures do not alter the prognosis But
status epilepticus is life threatening

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