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Page 1: General measures of acute stroke management

General measures of acute stroke management

Apostolos Ι. Hatzitolios

Associate Professor of Internal Medicine

1st Propedeutic Department of Internal Medicine

Department of Vascular Diseases and Hypertension

Aristotle University of Thessaloniki, AHEPA Hospital

Thessaloniki, Central Macedonia, HELLAS

Page 2: General measures of acute stroke management

Emerging therapies for acute stroke

• Main target is the early intervention and preservation of penumbra within a short therapeutic interval before necrosis of ischemic area occurs. New drugs are tested on this direction.

• The development of specific therapeutic procedures is an important research priority.

• Advances in this field aim mainly to enlarge the capability of thrombolysis use, despite limitations (since recovery may be achieved with a narrow time window of ~ 3-4.5 h).

• Investigation interest is focusing on the:

– use of neuroprotective agents leading to expansion of the “therapeutic window” (over 3 h),

– immediate MRI with advanced sequences to refine the patient selection and reveal the exact size of infarct,

– use of next-generation thgrombolytics (plasminogen activators and glycoprotein IIb/ IIIa inhibitors),

– use of agents to avoid hemorrhagic transformation of large infarcts, – endovascular approaches to thrombolysis and thrombectomy, and – adjuvant use of ultrasound.

• There is still also no proven therapy for intracerebral hemorrhage, although early results with recombinant activated factor VII look very promising.

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Treatment strategies aiming mainly at stabilizing the critically ill patient in

order to control systemic problems that may impair stroke recovery,

become of the greatest clinical importance

• Cardiac/respiratory care• Fluid and electrolyte balance• Blood pressure control • Glucose metabolism• Body temperature• Dysphagia and nutrition

General measures of acute stroke management

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• Cardiac complications more frequent in ICH and SAH than in ischemic stroke

• 15-40% of stroke patients may experience

- AMI

- Congestive heart failure

- Arrhythmias, particularly AF

- Sudden death

• There is a more significant correlation between cardiac complications and infarcts of the insular cortex

Cardiac care

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• Adequate oxygenation is important to preserve the penumbra.

• Most common causes of hypoxia in stroke: - Preexisting pulmonary diseases - Airway obstruction due to cranial nerves paresis causing oropharyngeal muscular hypotonia or vomiting leading to aspiration (brainstem stroke, reduced vigilance)

- Hypoventilation due to: Large hemispheric infarct or Brainstem infarct or hemorrhage Heart failure Pulmonary embolism Status epilepticus

Respiratory care

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1. Continuous cardiac monitoring in the first 48 hours 2. Oxygenation monitoring and Oxygen administration in case of hypoxemia

3. Monitoring and correction of electrolyte and fluid disturbance

4. Hypotonic solutions are contraindicated due to the risk of brain oedema, caused by the reduced plasma osmolality

Cardiac / respiratory care & Electrolyte / fluid homeostasis

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• In hypertension, cerebral vessels adjust to elevated BP by wall thickening, increased resistance and shift of blood flow autoregulation at higher BP level.

The problem is greater in older patients because of increased vascular resistance and decreased cerebral blood flow

So, great and abrupt BP decrease results in blood flow disturbance, cerebral ischemia and cognitive function deterioration

Management of Hypertension in stroke patients

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Because of cerebral autoregulation abolishment in ischemic

stroke area, blood flow is directly depended on systemic BP

40

60

80

100

120

140

160

180

200

220

transfer 2 hours later 1st day 2nd day

Mea

n B

P m

m H

gm

m H

g

• Therefore, BP increases in acute stroke as response to stress due to increased levels of catecholamines and cortisol, in order to maintain blood flow in the critical ischemic penumbra, while

• BP decreases automatically the next days

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• Target should be the progressively decrease of BP, < 15% /day, without orthostatic phenomena and hypotension, so that gradually more BP decrease becomes tolerable.

1. Routine BP lowering is not recommended, except for extremely elevated values which are lower for hemorrhagic strokes (>200-220 SBP or 120 DBP for ischemic, >180/105 for hemorrhagic stroke)

2. Immediate antihypertensive therapy for more moderate hypertension is recommended in heart failure, aortic dissection, acute MI or acute renal failure co-existence and in case of thrombolysis (avoid SBP above 180mmHg), but should also be applied cautiously.

3. Generally, recommended target BP in patients - with prior hypertension: 180/100-105mmHg - without prior hypertension: 160-180/100mmHg

4. Hypotension should be also avoided and treated (SBP < 120 mmHg)

since hypovolemia could cause neurological deterioration

Blood pressure control & Management of hypotension

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Narrow pathophysiological relationship between Hyperglycemia and Neuronal damage

HyperglycemiaBrain ishemia

Anaerobic metabolism - glycolysis

Lactic production / lactic acidocis ( Η+)

Free radicals

Endonucleases Glutamic

Intracellular Ca+2

Mitochondrial damage

intracellular oedema

Irreversible neuron cell damage

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• Hyperglycemia, but also hypoglycemia should be treated because they might worsen the ischemic damage and attenuate neuron metabolism and restoration respectively

1. Monitoring of serum glucose levels and treatment with insulin titration is recommended

2. Restoration to normal has to be gradual, especially in diabetics, in order to avoid intracellular neuron oedema

3. Immediate correction of hypoglycemia (i.v. dextrose) is also recommended

Management of hyperglycemia & hypoglycemia

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• Experimentally fever increases infarct size

• Body temperature increases in up to 50% of patients consequent to a severe brain infarct as an acute phase response

• • High body temperature may favor stroke progression and long term bad

outcome

• Treatment of body temperature >37.5C and search of possible infection (site and etiology) is recommended

Dysphagia is present in up to 50% of patients

Predictor of poor prognosis enhancing the risk for aspiration and pneumonia, dehydration and malnutrition

Early commencement of nasogastric feeding, within 48 hours, is recommended in stroke patients with impaired swallowing while PEG (Percutaneous endoscopic gastrostomy) feeding after the first 2 weeks

TemperatureDysphagia & Feeding

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• Most frequent complications of acute stroke are - Bladder dysfunction and urinary tract infections - Bronchopneumonia - Decubital ulcers - Seizures - Deep vein thrombosis and pulmonary embolism

Low molecular weight heparin (or low dose subcutaneous heparin) should be considered for patients at high risk of DVT or PE. Anticoagulant therapy may add a further benefit during stroke in-evolution by preventing clot expansion.

Incidence of venous thromboembolism may be also reduced through early re-hydration and mobilization, as well as compression stockings

Regarding oxidative stress and it’s management, the favorable action of antioxidants like vitamin E, for the treatment of is controversial

Prevention of acute stroke complications

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Prevention of stroke reccurence

Surgical or

electrophysiological intervention

& anticoagulation

in patients with high embolic risk :

• Atrial fibrillation• Valvular disease• Dilated cardiomyopathy• Patent foramen ovale

• Checking for stenosis in the carotids (common/internal) with Triplex Echo and CTA or MRA

• Symptomatic carotid stenosis

– > 70%:requires endarterectomy (at centers with perioperative mortality <6%)

– 50-70%: (benefit of intervention is statistically significant) endarterectomy is also considered

• Asymptomatic stenosis > 60%,

– Intervention is also discussed, since risk for stroke is also significant (annual 2%, expected reduction 1% )

– at centers with low perioperative mortality rate ( <3%)

• Angioplasty ± stenting indicated only in patients with symptomatic stenosis and high perioperative endarterectomy risk.

Heart disease Carotid disease

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High co-existence percentage of CHD, CeVD & PADTotal risk management with common preventive measures

Coronary Heart disease

Peripheral arterydisease

Cerebrovascular disease 15% 33%

14%

12%

5%

13%

8%

Stroke = Clinical manifestation of Global Vascular Disease

Atherothrombotic manifestation from a vascular area should alarm for the existence of

vascular disease also in another area

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Total Risk: Secondary Prevention ofCardio- Cerebro-Vascular & Renal Disease

• Lifestyle Changes

• Hypertension (< 130/80 mmHg)

• Dyslipidemia (LDL< 100 mg/dl)

• Diabetes ( HbA1c < 7%)

• Antiplatelets/anticoagulants

Atherosclerosis progression as well as oxidative stress induction should be inhibited by use of agents exerting endothelium protection, inflammation decrease, stabilization of atherosclerotic plaque and - in case of stroke - possible neuroprotection from ischemia (RAS inhibitors, statins, vitamin E?)

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International guidelines for stroke management& Secondary prevention after stroke/TIA

• European Stroke Organization - ESO

(formerly known as EUSI - European Stroke Initiative)

Recommendations for stroke management

Cerebrovasc Dis 2003;16(4):311-37

(update 200 12th EUSI Stroke Summer School, Lausanne 2008)

• American Stroke Association

Guidelines for the prevention of stroke in patients with ischemic stroke or transient ischemic attack

Stroke 2006;37:577-617

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Thank you for your attention!