Brain Attack By dr. RABEE ALANSI SANAA YEMEN

8/14/2019 Brain Attack By dr. RABEE ALANSI SANAA YEMEN

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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

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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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Brain Attack By dr. RABEE ALANSI SANAA YEMEN