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Evaluation of stroke


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Evaluation of Stroke

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Evaluation of stroke

  1. 1. Evaluation of Stroke
  2. 2. Stroke • Result from ischemic infarction or bleeding into part of the brain manifest by rapid onset (seconds to mnutes) of CNS focal neurologic deficits
  3. 3. Classification of pathophysiologic processes: A. Intrinsic to the vessel: 1) Atherosclerosis 2) Lipohyalinosis 3) Inflammation 4) Amyloid deposition 5) Arterial dissection 6) Developmental malformation 7) Aneurysmal dilatation 8) Venous thrombosis
  4. 4. Classification of pathophysiologic processes: B. Originate remotely - Embolus from heart/extracrainal circulation C. Inadequate cerebral blood flow – decreased perfusion pressure/ increased blood viscosity The first three cause: TIA/ ischemic stroke D. Rupture of vessel in subarachnoid space or intracerebral tissue - SAH/ ICH
  5. 5. TIA • Transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia WITHOUT acute infarction • Relies on the absence of end organ injury based on imaging or other tests • Temporary occlusion of part of cerebral circulation by emboli • Sx <24hours
  6. 6. Intracerebral hemorrhage • Bleeding from small arteries/arterioles • Bleeding directly into the brain  localized hematoma  hematoma gradually enlarges • Cause: HTN, trauma, bleeding diathesis, amyloid angiopathy, illicit drug use and vascular malformations • less common: bleeding tumors, aneurysmal rupture & vasculitis
  7. 7. SAH • Spontaneous bleeding into subarachnoid space • Aneurysmal rupture (saccular)  blood in subarachnoid space  CSF rapidly increasing ICP • Other causes: vascular malformation, bleeding diathesis, trauma, amyloid angiopathy & illicit drug use • Sx: severe headache, pain lateralised to the side of the aneurysm +/- brief LOC, seizure, N/V, focal neuro deficit, stiffneck, kernig’s sign, retinal or subhyaloid hemorrhages
  8. 8. Subtypes of Brain Ischemia 1) Thrombotic stroke: - Thrombus formation in an artery produces a stroke by reduced bld flow distally (low flow) or embolic fragment that breaks off and travels to a more distant vessel (artery to artery embolism) a) Large vessel disease – atherothrombosis - extra/intracranial arterial system a) Small vessel disease – penetrating arteries arising from the distal vertebral artery, basilar artery, MCA stem & arteries of COW
  9. 9. Subtypes of Brain Ischemia 2) Embolic stroke- particle of debris originating elsewhere that block particular access to the brain regon Causes: a) known sourcem- cardiac b) ? Cardiac/ aortic – based on Echocardiographic findings c) arterial source d) unknown source
  10. 10. Subtypes of Brain Ischemia 3) Systemic Hypoperfusion – reduced perfusion due to cardiac pump failure by cardiac arrest, arrythmia or reduced cardiac output  AMI, Pericardial effusion or bleeding
  11. 11. Initial General Assesment • A, B, C • BP: usually elevated in stroke • Breathing: pt with ICP  decreased respi drive or muscular airway obstruction • Fever: can worsen brain ischemia • Hx & PE: DDX: seizures, syncope, migraine & hypoglycemia
  12. 12. Initial General Assesment • Non-contrast CT brain – widespread acces and speed of acquisition - highly sensitive for the diagnosis of bleeding in acute cases - focal white hyperdense lesionwithin the brain parenchyma
  13. 13. Initial General Assesment • MRI brain: - Can show old hemorrhages since sensitive to hemosiderin - More sensitive than CT inearly detection of infarction • LP: - Needed to make diagnosis for SAH
  14. 14. Initial General Assesment • ? Thrombolytic Therapy – rt-PA - Extracranial & intracranial US, CTA, MRA-show occlusive thromboembolus - Most severe complication: intracranial hemorrhage (6%)
  15. 15. history • Clinical course: - Embolic stroke: occurs suddenly, focal loss of brain function that is usually maximal, rapid recovery - Thrombosis – normal or abnormal or progressing in a stepwise fashion with some periods of improvements - Penetrating artery occlusion- sx develop in hours or a few days
  16. 16. history - Intracerebral hemorrhage: does not improve during the early period, progresses gradually during minutes or few hours - Aneurysmal SAH: develops instantly, focal brain dysfunction is less common
  17. 17. history • Ecology – age, sex and race - Thrombotic and embolic strokes related to atherosclerosis – occur in older patients - Rare in <40yo, unless: DM, HTN, HLD, smoker, strong Family Hx - Cardiac origin embolism – common in young pt with heart disease
  18. 18. history - HTN ICH – common: blacks, in asians • Previous TIA: strongly favors the presence of a local vascular lesion (thrombosis) • Activity at the onset or just before the stroke: a) hemorrhages can be precipitated by physical activities b) trauma before stroke: traumatic dissection/ occlusion of arteries/traumatic brain hemorrhages
  19. 19. history • Associated symptoms: - Fever – endocarditis  embolic stroke - Infections  activate acute phase reactants  predisposing to thrombosis - Headache: fx of hmg stroke, prodromal period before thrombotic strokes - Seizures: seen in lobar ICH or brain embolism - Reduced alertness: indicates hemorrhage and: (+) neurologic signs ICH (-) neurologic signs SAH
  20. 20. PE: • Absent of pulses: atherosclerosis with thrombosis • Unpalpable ICA (neck): occlusion of CCA • Cardiac findings: AF, mumur, cardiac enlargement cardiac origin embolism
  21. 21. Neurologic exam • Weakness of face, arm, leg on one side without sensory/visual/cognitive abnormalities (pure motor stroke)  thrombotic stroke in penetrating arteries / small ICH • Large focal neurlo deficits that begin abruptly/ progresses quicklyembolism / ICH • Language abno, motor and sensory signs same side of body anterior circulation disease
  22. 22. Confirm the diagnosis • Vascular Studies: 1) Anterior circulation – exracranial and intracranial carotid arteries , middle and anterior cerebral artery branches should be the focus - Duplex US of neck & transcranial Doppler of intracranial arteries 2) Posterior circulation – vertebrobasilar system – extracranial & intracranial vertebral arteries, basilar arteries & posterior cerebral arteries should be the focus
  23. 23. Confirm the diagnosis 3) CT angiography or MR angiography of neck and head arteries – done when the screening test do not fully define the lesion and more characterization is warranted and when surgery or interventional treatment by an arterial catheter may be indicated
  24. 24. Confirm the diagnosis • Cardiac Evaluation: 1) ECG & 24 Holter - ? AF as source of emboli 2) Echocardiography- for all patient suspected for embolic stroke a) TEE- examines the atria, atrial region and the aorta - to exclude ascending aortic atheromatous disease, look for patent foramen ovale or atrial septal aneurysm b) TTE-
  25. 25. • Blood tests: 1) FBC 2) PT, INR, APTT 3) Thrombin Time 4) LIPIDS
  26. 26. Blood tests: Hypercoagulable Studies: 1) Protein C, Protein S, antithrombin III 2) Lupus Anticoagulant 3) Anticardiolipin antibodies 4) Activated protein C resistance/ factor Leiden mutation 5) Prothrombin Mutation
  27. 27. Antiphospholipid antibody testing is recommended in: 1. Hx of Lupus or sx compatible with Lupus 2. Fx suggestive of Antiphopholipid Syndrome: a) Miscarriages b) Venous thrombosis c) Migraine headaches 3. Cryptogenic stroke / TIA at young age
  28. 28.