Management Stroke Very Old

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Management stroke in very oldpatients

Prof.Dr.dr. Rusdi Lamsudin SpS(K), M.Med.Sc

Rumah Sakit Islam Surakarta

Bagian Ilmu Penyakit Saraf FKUGM/FKUII


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Prof.Dr.dr. H. Rusdi Lamsudin, M.Med.Sc

Spesialis Saraf Konsultan

Lulus Pendidikan Dokter, UGM, 1971

Spesialis Saraf, Unair-UGM, 1978

Master of Medical Sciences, New Castle Univ, Australia, 1986

Ketua Pengurus RS PKU Muhammadiyah Yogyakarta, 1993-1999

Anggota Majelis Dikti Muhammadiyah, 1993-1999

Pembantu Dekan I, FK UMY, Yogyakarta, 1993-1999

PhD, UGM, 1996

Short-course, Unit Stroke & Neuro-Intensive, Insburck,

Austria,1997 Kepala Unit Stroke RS Sardjito, 2001-2005

Kepala Bagian Ilmu Penyakit Saraf FK-UGM, 2001-2005

Dekan Fakultas Kedokteran, UII, Yogyakarta, 2001-2006, 2006-2010

Kepala Unit Stroke RS YARSIS Surakarta


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Outlines

Background

Risk Factors Stroke in very old

patients Emergency management

General Management

Conclusion


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BACKGROUND


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Background

Stroke is a leading of death and disability inworldwide (including Indonesia)

The economic consequence of stroke aresubstantial

The estimated direct & indirect cost of stroke in

2009 is $68,9 billion

Circulation 2009: 119; e21-e183


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Background

Approx 16 million first-ever stroke occurworldwide annually, with a death toll of 5.7million people per year

Second most common single cause ofdeath after ischemic heart disease

The largest cause of adult disability


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Background

A report indicated that 75-89% of strokesoccur in individuals age >65 years

> 50% occur in people who are age >70 years

25% occur in individual who are aged >85years

Nat . Rev. Neurol 6; 256-265 (2010)


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Background

A report estimates that global occurenceof first-ever strokes will increase to 18millions by 2025 and 23 millions by 2030

Older people or elderly: 65-79 years

Very old =>80 years

Nat . Rev. Neurol 6; 256-265 (2010)


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RISK FACTORS


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Risk factors for firstever strokein elderly

Sex Stroke is common in elderly (individuals age 65-79

years) men (level 1A evidence) although womencomprise the largest proportion of very old (>80

years) patients with stroke (level 1A evidence)

Atrial Fibrillation

The risk of stroke from atrial fibrillation rises with

advencinf age, even the people age >80 years (level1B evidence)

Nat . Rev. Neurol 6; 256-265 (2010)


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Other CVD, such as Ischemic heart

disease and heart failure CVD remains a risk factor for stroke in the

elderly, even in very old individual (level 2Aevidence)

Nat . Rev. Neurol 6; 256-265 (2010)


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Carotid stenosis

Carotid stenosis is a risk factor for stroke inthe elderly, even in octogenarians (level 1A

evidence)

High blood pressure

Hypertension is an important risk factor for stroke inpatient 80 years (level 2A evidence)


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High blood cholesterol

High blood cholesterol remain a rsik factor forstroke in the elderly, but not in the very old

(level 2A evidence)

Metabolic syndrome

Metabolic syndrome is a strong independentrisk factor for acute nonembolic ischemicstroke in older people (level 3B evidence)


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EMERGENCY MANAGEMENT


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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 ofspecific therapeutic procedures is an important research priority.

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

Investigation interest is focusingon the:

use ofneuroprotective agentsleading to expansion of the therapeutic window(over 3 h),

immediate MRI with advanced sequences to refine the patient selection andreveal the exact size of infarct,

use ofnext-generation thgrombolytics (plasminogen activators and glycoproteinIIb/ 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 forintracerebral hemorrhage, although earlyresults with recombinant activated factor VII look very promising.


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85% of strokes are ischaemic, and related toblockage of an artery by a blood clot, so potential

treatments to improve the circulation might be:

Thrombolytic (clot-dissolving): egStreptokinase, TPA. Breaks up clot by

splitting fibrin Anticoagulant (Clot preventing): prevents

formation of fibrin, prevents spreading of clot& formation of new clot

Antiplatelet (clot preventing): preventsplatelets sticking together prevents spreadingof clot & formation of new clot.


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GENERAL MANAGEMENT


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Treatment strategies aiming mainly at stabilizing the critically ill patient inorder 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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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 causingoropharyngeal muscular hypotoniaorvomiting leading to aspiration(brainstem stroke, reduced vigilance)

- Hypoventilation due to:

Large hemispheric infarct or Brainstem infarct or hemorrhageHeart failurePulmonary embolismStatus 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 andshift of blood flow autoregulationat higher BP level.

The problem is greater in older patients because ofincreasedvascularresistance 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

B f b l t l ti b li h t i i h i


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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

120140

160

180

200

220

transfer 2 hours later 1st day 2nd day

MeanBPm

mHg

Therefore, BP increases in acute stroke as response to stress due to increasedlevels of catecholamines and cortisol, in order to maintain blood flow in the criticalischemic penumbra, while

BP decreases automatically the next days


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Target should be the progressively decrease of BP, < 15% /day, withoutorthostatic phenomena and hypotension, so that gradually more BPdecrease becomes tolerable.

1. Routine BP lowering is not recommended, except for extremely elevatedvalues 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 isrecommended in heart failure, aortic dissection, acute MI or acute renalfailure co-existence and in case of thrombolysis (avoid SBP above180mmHg), but should also be applied cautiously.

3. Generally, recommendedtarget 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 damageHyperglycemiaBrain ishemia

Anaerobic metabolism - glycolysis

Lacticproduction / lactic acidocis ( +

)

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 becausethey might worsen the ischemic damage and attenuate neuronmetabolism and restoration respectively

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

2. Restoration to normal has to be gradual, especially in diabetics, in order toavoid 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 asevere 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 andpneumonia, dehydration and malnutrition

Early commencement of nasogastric feeding, within 48 hours, isrecommended 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 beconsidered forpatients at high risk of DVT or PE.Anticoagulant therapy may add afurther 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 its management, the favorable action ofantioxidants 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 orMRA

Symptomatic carotid stenosis

> 70%:requires endarterectomy (at centers withperioperative mortality 60%,

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

at centers with low perioperative mortality rate (


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

Coronary Heartdisease

Peripheral arterydisease

Cerebrovascular

disease

15% 33%

14%

12%

5%

13%

8%

Stroke = Clinicalmanifestation of Global Vascular Disease

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

vascular disease also in another area

S f


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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 inductionshould be inhibited by use of agents exerting endothelium protection,inflammation decrease, stabilization of atherosclerotic plaque and - incase 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 2008 2th EUSI Stroke Summer School, Lausanne 2008)

American Stroke Association

Guidelines for the prevention of strokein patients with ischemic stroke or transientischemic attack

Stroke 2006;37:577-617


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Thank you for yourattention!

Management Stroke Very Old

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