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STROKE

STROKE. Adi Putra Siswoyo Anis Sopiyati Annis Kurnia R Astrid Ayu Alaika Bangun Mulyadi Danang Tri S Dewi Ayu Diyan Dwi Astuti Dwi Ermawati Fajar Nur R. DEFINITION .

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STROKE

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  1. STROKE

  2. Adi Putra Siswoyo AnisSopiyati AnnisKurnia R Astrid AyuAlaika BangunMulyadi Danang Tri S DewiAyu DiyanDwiAstuti DwiErmawati FajarNur R

  3. DEFINITION • Stroke is a disease of the brain functional disorder of acute focal or global symptoms and signs the appropriate part of the brain affected, previously without warning, and can recover completely, cured with a disability or death, resulting from interruption of blood flow to the brain due to bleeding or non bleeding (Junaidi Iskandar, 2002). • Stroke is a clinical syndrome that initial sudden onset, rapid progression, a focal neurological deficit or global and lasting 24 hours or more or the direct cause of death, and solely caused by the interference of non traumatic brain blood circulation (Capita Selekta Medicine, 2000).

  4. ETIOLOGY • Trombosist • Cerebral Embolism • Ischemia • Cerebral Hemorragic

  5. PATHOPHYSIOLOGY • Partial or complete occlusion of a cerebral blood vessel resulting from cerebral thrombosis (due to arteriosclerosis) or embolism. • Ischemia related to decreased blood flow to an area of the brain secondary to systemic disease, such as cardiac or metabolic disease. • Hemorrhage occurring outside the dura (extradural), beneath the durameter (subdural ), in the subarachnoid space (subarachnoid), or within the brain substance (intracerebral). • Risk factor include hypertension,TIAs, heart disease, elevated cholesterol, diabetes mellitus, obesity, carotid stenosis, polycythemia, cigarette smoking.

  6. PATHWAY

  7. CLINICAL MANIFESTATION • Tingling or impaired sensibility and weakness of the limbs, including the face. • Difficulty speaking or understanding speech, and suddenly became confused • Impaired vision in one or both eyes • Difficulty walking, staggering or loss of balance • Severe headache with no apparent cause accompanied by nausea and vomiting • Sudden change of behavior / mental status • Dysarthria

  8. CLASSIFICATION • Stroke Non Haemorragic Stroke is caused by the following factors: a. Stacking of fat in the blood vessels that lead from blood clots. b. Foreign bodies in the blood vessels of heart c. The existence of holes in blood vessels leak blood causing blood flow to the brain is reduced.

  9. CLASSIFICATION • Stroke Haemorragic Stroke is caused by a blood vessel in the brain leaks or ruptures, blood fills the brain cells. a. High blood pressure can cause blood vessel rupture b. Consolidation of the blood vessels that cause blood vessel rupture c. Tumor blood vessels

  10. Differences Between Stroke Haemorragic and Stroke Non Haemorragic

  11. RISK FACTORS • Risk Factors that can be controlled - Hypertension - Diabetes mellitus - Smoking - Heart disease - Overweight / obesity - Hypercholesterolaemiaand hyperuricaemia - Carotid artery abnormalities - Hypercoagulation(simple blood clot) - Excessive alcohol consumption - Drug abuse - Respiratory disorders during sleep (sleep apnea) - Never get transient ischemic attack (TIA) before.

  12. RISK FACTORS • Risk Factors that can’t be controlled • Age • Sex • Racial / Ethnic Groups • Abnormalities congenital / hereditary • History of stroke / TIA previous

  13. COMPLICATION • Depression • Frozen Blood • Pneumonia • Decubitus

  14. RADIOLOGICAL EXAMINATION • CT-Scan • Angigrafi • EEG • MRI • Brainplan • Ultrasonography dopler • SkuliRontgenogram • Substraction Digital Angiography • Eshoencephalography • B. mode Ultrasound

  15. RADIOLOGICAL EXAMINATION • CT-Scan • Angigrafi • EEG • MRI • Brainplan • Ultrasonography dopler • SkuliRontgenogram • Substraction Digital Angiography • Eshoencephalography • B. mode Ultrasound

  16. CASE A 38-year-old man had a sudden onset of right-sided weakness and fell to the ground. On examination in the emergency department, blood pressure was 160/90 mm Hg, and he was alert with dysarthria and reduced speech output. He followed simple, but not two-step, commands. He had a forced left gaze and right visual field cut. Strength in the right arm and leg was antigravity only, and sensation was diminished on that side. Head CT showed a hyperdenseleft MCA sign. He received IV t-PA 150 minutes after symptom onset and was admitted to the ICU for monitoring. The examination remained unchanged over the subsequent 16 hours, but at that point blood pressure climbed to 190/100 mm Hg and he began to complain of headache, had episodes of emesis, and became progressively less alert. The right side became flaccid. Head CT showed a persistent hyperdense left MCA sign as well as hypodensity in the entire left MCA territory with 8 mm of midline shift, subfalcineherniation, and compression of the suprasellar cistern.

  17. CRITICAL MANAGEMENT

  18. Oxygenation teraphy Sample Intubation Procedure for Patients With acute Ischemic Stroke at Risk for Elevated Intracranial Pressure • Preoxygenation : 100% oxygen for approximately 5 minutes Induction : Etomidate0.1 mg/kg to, 0.5 mg/kg or thiopental, 1 mg/kg to 5 mg/kg • Intubation : Application of cricoidpressure (Sellickmaneuver) Laryngoscopywith intubation • Confirmation of Placement : With Auscultation, End-Tidal Carbon Dioxide, and Chest X-ray • Postintubation : Full ventilatorysupport (assist control or intermittent mandatory ventilation) Hyperventilation (increase ventilation to lower arterial P COto 25 mm Hg to 30 mm Hg) if acute neurologic deterioration or suspicion of increased. intracranial pressure is present . Sedation with short-acting agents such as fentanyl, midazolam, or propofol, as needed

  19. 2. Hyperosmolar Therapy Osmotic agents such as mannitoland hypertonic saline lower elevated ICP and can reverse transtentorialherniation, effects that appear to be achieved primarily via extraction of water from the intracellular and interstitial spaces,resultingin temporary brain shrinkage. Mannitolis typically administered as a bolus at a dose of 0.5 g/kg to 1.0 g/kg every 4 to 6 hours Monitoring the clearance of mannitol between administrations is most effectively achieved with the osmolal gap (the difference between osmolalityand osmolarity, calculated using the formula [2 sodium] + [blood urea nitrogen/3] + [glucose/18]) rather than simple osmolalitysince only the former correlates well with mannitollevels (Garcia-Morales et al,2004) Clearanceof mannitolbetween doses should be monitored with the osmolalgap, and urine output should be replaced with isotonic fluids to reduce risk of rebound intracranialhypertensionand renal failure.

  20. NCP

  21. Thank You

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