Brain Attack By Dr. Rabee Alansi Sanaa Yemen

date Review On :

1: gement of Acut Ischemic St 1

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No Weak Links

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Development: Detection: Dispatch: Delivery: Door: Data: Decision: Drug: Disposition:

Protocol and pathway development Early recognition Early EMS activation Transport & management ED triage ED evaluation & management Neurology input, therapy selection Thrombolytic & future agents Admission or transfer 4

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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

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Stroke Time of Onset Determines Treatment Strategy Hyperacute < 3 hours IV tissue plasminogen activator (Activase)

Subacute > 8 hours Augment perfusion, manage systemic complications

Acute 3 – 8 hours catheter interventions/ cerebral revascularization techniques

Secondary Stroke Prevention

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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

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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 strokerelated 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 10 48 hours of onset in patients with acute ischemic stroke, have not been 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. 12

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) 13

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 14

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

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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. 16

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 17

C , General measures Therapeutic Goals “6 norms”: normoglycemia, normovolemia, normothermia, normoxemia, normocapnia, and normotension.

Prevent Complications Aspiration Venous Thromboembolism UTI Contractures 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 German HTN League EUSI UK AHA

Diast.

200 220

100

n.a. 220

n.a. 120

Goal

Year

Max. 20% 2001

120 180/100-105 2000 n.a.*

2000 2004

*only if complications occur within 7 days 20

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Blood Pr es sure in Acute S troke When i s it appropri ate to initi al ?anti hypertensi ve ther apy

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American Stroke Association and the European Stroke Initiative BP less than 220/120 mms of Hg: 2006

Observe (level V): treat when end organ involvement is noted e.g. aortic dissection, acute MI and pulmonary edema.

C. Diastolic BP more than 140 mms of HG: IV Nitroprusside 0.5 mcg/kg/min infusion under constant monitoring: Aim only 10% to 15% reduction.

B BP more than 220/120-140 mms of 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 22 15% reduction of BP.

.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 ganglionblocking 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 30

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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