Management stroke in very old patients

Prof.Dr.dr. Rusdi Lamsudin SpS(K), M.Med.Sc Rumah Sakit Islam Surakarta Bagian Ilmu Penyakit Saraf FKUGM/FKUII

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, 20062010 Kepala Unit Stroke RS YARSIS Surakarta

Outlines
Background Risk Factors Stroke in very old patients Emergency management General Management Conclusion

BACKGROUND

Background
Stroke is a leading of death and disability in worldwide (including Indonesia) The economic consequence of stroke are substantial The estimated direct & indirect cost of stroke in 2009 is $68,9 billion
Circulation 2009: 119; e21-e183

Background
Approx 16 million first-ever stroke occur worldwide annually, with a death toll of 5.7 million people per year Second most common single cause of death after ischemic heart disease The largest cause of adult disability

Background
A report indicated that 75-89% of strokes occur in individuals age >65 years
> 50% occur in people who are age >70 years 25% occur in individual who are aged >85 years

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

Background
A report estimates that global occurence of first-ever strokes will increase to 18 millions 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)

RISK FACTORS

 Sex Stroke is common in elderly (individuals age 65-79 years) men (level 1A evidence) although women comprise the largest proportion of very old (>80 years) patients with stroke (level 1A evidence)

Risk factors for first ever stroke in elderly

Atrial Fibrillation The risk of stroke from atrial fibrillation rises with advencinf age, even the people age >80 years (level 1B evidence)
Nat . Rev. Neurol 6; 256-265 (2010)

Risk factors for first ever stroke in elderly

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 2A evidence)

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

Risk factors for firstever stroke in elderly

Carotid stenosis
Carotid stenosis is a risk factor for stroke in the elderly, even in octogenarians (level 1A evidence)
High blood pressure
Hypertension is an important risk factor for stroke in patient <80 years but is less important for patients >80 years (level 2A evidence)

Risk factors for firstever stroke in elderly

High blood cholesterol
High blood cholesterol remain a rsik factor for stroke in the elderly, but not in the very old (level 2A evidence)

Metabolic syndrome
Metabolic syndrome is a strong independent risk factor for acute nonembolic ischemic stroke in older people (level 3B evidence)

EMERGENCY 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.

85% of strokes are ischaemic, and related to blockage of an artery by a blood clot, so potential treatments to improve the circulation might be: Thrombolytic (clot-dissolving): eg Streptokinase, 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): prevents platelets sticking together prevents spreading of clot & formation of new clot.

GENERAL MANAGEMENT

General measures of acute stroke management

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

Respiratory care
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

Cardiac / respiratory care & Electrolyte / fluid homeostasis

1. 2. 3. 4. Continuous cardiac monitoring in the first 48 hours Oxygenation monitoring and Oxygen administration in case of hypoxemia Monitoring and correction of electrolyte and fluid disturbance Hypotonic solutions are contraindicated due to the risk of brain oedema, caused by the reduced plasma osmolality

Management of Hypertension in stroke patients

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

Because of cerebral autoregulation abolishment in ischemic stroke area, blood flow is directly depended on systemic BP

220 200 180 160 140 120 100 80 60 40

Mean BP mm Hg

transfer

2 hours later

1st day

2nd day

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

Blood pressure control & Management of hypotension

Target should be the progressively decrease of BP, < 15% /day, without orthostatic phenomena and hypotension, so that gradually more BP decrease becomes tolerable. 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) 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. Generally, recommended target BP in patients - with prior hypertension: 180/100-105mmHg - without prior hypertension: 160-180/100mmHg

1.

2.

3.

4.

Hypotension should be also avoided and treated (SBP < 120 mmHg)
since hypovolemia could cause neurological deterioration

Narrow pathophysiological relationship between Hyperglycemia and Neuronal damage

Brain ishemia Hyperglycemia

Anaerobic metabolism - glycolysis Lactic production / lactic acidocis ( +)

Free radicals
Endonucleases Glutamic

Intracellular Ca+2

Mitochondrial damage intracellular oedema

Irreversible neuron cell damage

Management of hyperglycemia & hypoglycemia

Hyperglycemia, but also hypoglycemia should be treated because they might worsen the ischemic damage and attenuate neuron metabolism and restoration respectively
Monitoring of serum glucose levels and treatment with insulin titration is recommended
Restoration to normal has to be gradual, especially in diabetics, in order to avoid intracellular neuron oedema Immediate correction of hypoglycemia (i.v. dextrose) is also recommended

1.

2.

3.

Temperature Dysphagia & Feeding

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

Prevention of acute stroke complications

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 rehydration and mobilization, as well as compression stockings Regarding oxidative stress and its management, the favorable action of antioxidants like vitamin E, for the treatment of is controversial

Prevention of stroke reccurence

Heart disease
Surgical or electrophysiological intervention & anticoagulation in patients with high embolic risk : Atrial fibrillation Valvular disease Dilated cardiomyopathy Patent foramen ovale

Carotid disease
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.

High co-existence percentage of CHD, CeVD & PAD

Total risk management with common preventive measures

Cerebrovascular disease

15%

13%

33%

Coronary Heart disease

5%
Peripheral artery disease

8% 14%

12%

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

Total Risk: Secondary Prevention of Cardio- 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?)

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 stroke in patients with ischemic stroke or transient ischemic attack
Stroke 2006;37:577-617

Thank you for your attention!