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::ement of Acutement of AcutIschemicSSate Review On :ate Review On :
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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
No Weak Links
4
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Management of AcuteIschemic
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
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Stroke Time of Onset
Determines Treatment Strategy
Hyperacute < 3 hours
IV tissue plasminogen
activator (Activase)
Acute 3 8 hourscatheter interventions/
cerebral
revascularization
techniquesSubacute > 8 hours
Augment perfusion,
manage systemic
complications
Secondary Stroke Prevention
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(f) assessment of stroke through
historyfor 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.
(e)Intravenous (IV) access should be obtained and 0.9% normalsaline 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, metabolicparameters and
coagulation profile.
A, IMMEDIATE EMERGENTSTROKE PROTOCOL
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The criteria foradmission to the
intensive care unit
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B ,MEASURES TOIMPROVE
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,
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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.
The slight, beneficial effect of aspirinin 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.
Do antithrombotic agents vary in efficacy by .3
?stroke subtype
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The available data suggest that the incidence of acutecardiovascular complications is low, and none of the available
studies had sufficientpower to detect a modest treatment effect
on these endpoints.
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?
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(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 therapyis 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)
Recommendations of SCASA about use of aspirin
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(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 improveoutcome 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
Recommendations of SCASA about
Heparin
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(c) Parentral anticoagulation should not be given unlesspossibility 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
Recommendations of SCASA about Heparin
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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 ofintracranial 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
Goals
6norms:
normoglycemia,
normovolemia,normothermia,
normoxemia,
normocapnia, and
normotension.
Prevent
Complications
Aspiration
Venous
Thromboembolism
UTI
Contractures
Recurrent events
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Air way management
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.
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 tonguemay
cause airway obstruction.
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G uid e li nes fo r in it i a lan tih y pe r tens i v e t re a tm ent a t a cu te
is c h e m ic s tr o k e
*only if complications occur within 7 days
Syst Diast. Goal Year
German HTN League
EUSI
UK
AHA
200
220
220
100
120
120
Max. 20%
180/100-105
n.a. n.a. n.a.*
2004
2000
2000
2001
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BP less than 220/120mms of Hg:
Observe (level V):treat when end organ involvement is
noted e.g. aortic dissection,
acute MI and pulmonary edema.
B lood Pr es sure in A cute S trokeW hen i s it appropri ate to initi al
?anti hypertensi ve ther apy
C. Diastolic BP more than 140mmsofHG:
IV Nitroprusside 0.5 mcg/kg/min
infusion under constant monitoring:
Aim only 10% to 15% reduction.
B BP more than 220/120-140mmsof Hg
Labtalol 10-20 mg IV over one
minute: repeat or double the dose
every 10 minutes (maximum
300mg) or
Nicardipine 5 mg/hr Iv infusion
and titration to desired levels by
Increasing 2.5 mg every 5 minutes
(maximum 15 mg/hr). Aim for10 to
15% reduction of BP.
American Stroke Associationandthe European Stroke Initiative2006
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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 afterbloodpressure is reduced, the blood pressure can be supported with intravenous
dopamine, 10 to 14 g/kg, titrating to a mean arterial blood pressure of 110 to130 mm Hg.
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Management of Temperature Control
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.
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.
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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 maintainintravascular volume and Cerebral Perfusion Pressure
Fluidbalance 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.
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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 orunwilling to use pneumatic compression devices.
.
D
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D , Treatment of Acute Neurological:Complications
Raised intracranial Pressure (ICP) & CerebralEdema
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 aslong 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 surgery
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Raised intracranial Pressure (ICP) &
Cerebral EdemaOsmotherapy. 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 osmoticgradient,
furosemide (10 mg Q 28 h)
may be administered simultaneously with osmotherapy. Serum
osmolality should be measured twice daily in patients receivingosmotherapy 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
not shown benefit
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Raised intracranial Pressure (ICP) &
Cerebral Edema
HyperventilationHypocarbia causes cerebral vasoconstriction. Reduction of cerebral
blood flow is almost immediate, Reduction of pCO2 to 3530 mm Hg,
best achieved by raising ventilation rate at constant tidal volume
(1214 mL/kg), lowers ICP 25% to 30% in most patients (Failure of
elevated ICP to respond to hyperventilation indicates a poorprognosis.
Muscle relaxantsNeuromuscular paralysis in combination with adequate sedation can
reduce elevated ICP by preventing increases in intrathoracic andvenous 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 .
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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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