General measures of acute stroke management

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General measures of acute stroke management. Apostolos Ι. Hatzitolios Associate Professor of Internal Medicine 1 st Propedeutic Department of Internal Medicine Department of Vascular Diseases and Hypertension Aristotle University of Thessaloniki, AHEPA Hospital - PowerPoint PPT Presentation

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  • General measures of acute stroke management

    Apostolos . HatzitoliosAssociate Professor of Internal Medicine1st Propedeutic Department of Internal MedicineDepartment of Vascular Diseases and HypertensionAristotle University of Thessaloniki, AHEPA HospitalThessaloniki, Central Macedonia, HELLAS

  • Emerging therapies for acute strokeMain 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.

  • 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 careFluid and electrolyte balanceBlood pressure control Glucose metabolismBody temperatureDysphagia and nutritionGeneral measures of acute stroke management

  • 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 cortexCardiac 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 epilepticusRespiratory care

  • 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

    Cardiac / respiratory care & Electrolyte / fluid homeostasis

  • 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

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

    406080100120140160180200220 transfer 2 hours later1st day2nd dayMean BP mm Hg 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

  • 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

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

    Blood pressure control & Management of hypotension

  • Narrow pathophysiological relationship between Hyperglycemia and Neuronal damage HyperglycemiaBrain ishemiaAnaerobic metabolism - glycolysisLactic production / lactic acidocis ( +) Free radicalsEndonucleasesGlutamicIntracellular Ca+2Mitochondrial damageintracellular oedemaIrreversible neuron cell damage

  • 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 recommendedManagement of hyperglycemia & hypoglycemia

  • 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

  • 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 its management, the favorable action of antioxidants like vitamin E, for the treatment of is controversial

    Prevention of acute stroke complications

  • Prevention of stroke reccurenceSurgical or electrophysiological intervention& anticoagulation in patients with high embolic risk :

    Atrial fibrillationValvular diseaseDilated cardiomyopathyPatent 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 60%,

    Intervention is also discussed, since risk for stroke is also significant (annual 2%, expected reduction 1% )at centers with low perioperative mortality rate (

  • High co-existence percentage of CHD, CeVD & PADTotal risk management with common preventive measuresCoronary Heart diseasePeripheral arterydiseaseCerebrovascular disease15%33%14%12%5%13%8%Stroke = Clinical manifestation of Global Vascular DiseaseAtherothrombotic manifestation from a vascular area should alarm for the existence of vascular disease also in another area

  • Total Risk: Secondary Prevention ofCardio- Cerebro-Vascular & Renal DiseaseLifestyle Changes

    Hypertension (< 130/80 mmHg)

    Dyslipidemia (LDL< 100 mg/dl)

    Diabetes ( HbA1c < 7%)

    Antiplatelets/anticoagulantsAtherosclerosis 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