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Stroke

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Stroke

  1. 1. DEFINITIONS
  2. 2. A stroke * Acute neurologic injury that occurs as a result of ischemic cerebral infarction (80%) or brain hemorrhage (20% ). Transient ischemic attack (TIA) *modern tissue-based definitions is defined as a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.(ischemic stroke is defined as an infarction of CNS tissue). *classic time-based definitions of TIA sudden onset of a focal neurologic symptom and/or sign lasting less than 24 hours, presumably brought on by a transient decrease in blood supply, which rendered the brain ischemic in the area producing the symptom. *Stroke, also known as cerebrovascular accident (CVA), cerebrovascular insult (CVI), or brain attack
  3. 3. Progressive Stroke *A stroke in which the focal neurological deficits worsen with time *Also called stroke in evolution. Completed Stroke *A stroke in which the focal neurological deficits persist and do not worsen with time.
  4. 4. CLASSIFICATION
  5. 5. STROKE (CVA or CVI or BRAIN ATTACK) ISCHEMIC (80%) THROMBOTIC large V & small V (lacunars) EMBOLIC HYPOPERFUSION HEMORRHAGIC (20% ) INTRA- AXIAL.H (blood inside the brain) INTRAPARENCHYMAL INTRAVENTRICULAR EXTRA- AXIAL.H (bl outside the brain, but still inside the cranium) EPIDURAL SUBDURAL SUBARACHNOID
  6. 6. Differentiation between stroke subtypes
  7. 7. Stroke type Clinical course Risk factors Other clues ICH Gradual progression during minutes or hours HTN, trauma, bleeding diatheses, illicit drugs (e g, amphetamines, cocaine), vascular malformations. More common in blacks and Asians than in whites. precipitated by sex or other physical activity. Patient may have reduced alertness. SAH Abrupt onset of sudden, severe headache. Focal Brain dysfunction less common than with othertypes Smoking, HTN, genetic susceptibility (eg, polycystic kidney disease, family history of SAH) and sympathomimetic drugs (eg, cocaine) precipitated by sex or other physical activity. Patient may have reduced alertness.
  8. 8. Stroke type Clinical course Risk factors Other clues Thrombotic Stroke Stuttering progression with periods of improvement. Lacunes develop over hours or at most a few days. Large artery ischemia may evolve over longer periods. Atherosclerotic risk factors (age, smoking, DM, etc.). Men affected more than women. May have history of TIA. May have neck bruit. Embolic Stroke Sudden onset with deficit maximal at onset. Clinical findings may improve quickly. Atherosclerotic risk factors as above. Men more women. History of heart disease (valvular, AF, endocarditis). ppt by getting up at night to urinate, or sudden coughing or sneezing.
  9. 9. Clinical diagnosis of stroke subtypes RISK FACTORS ACTIVITY AT THE ONSET OR JUST BEFORE THE STROKE ASSOCIATED SYMPTOMS General physical examination Neurologic examination SILENT BRAIN INFARCTS UMNL&LMNL Cortical or subcortical stroke
  10. 10. UNMODIFIABLE Prior stroke Male sex Older age Family history of stroke MODIFIABLE FACTORS Hypertension Cigarette smoking Dyslipidemia Diabetes Abdominal obesity Alcoholism Lack of physical activity High-risk diet (eg, high in saturated fats, and calories) Psychosocial stress (eg, depression) Heart disorders (MI,AF,IE) Hypercoagulability (thrombotic stroke only) Vasculitis Intracranial aneurysms (subarachnoid hemorrhage only) Use of certain drugs (eg, cocaine, amphetamines) RISK FACTORS
  11. 11. DIFFERENTIAL DIAGNOSIS  SPACE OCCUPYING LESION(TUMOR)  SEIZURE  MIGRAINE  SUBDURAL HAEMATOMA  METABOLIC DISTURBANCE LIKE HYPOGLYCAEMIA
  12. 12. Hypoglycemia  That transient hypoglycemia may produce a stroke like picture with hemiplegia and aphasia has been known for years.  The wide use of bedside rapid laboratory testing for glucose now makes this easily detectable and treatable. The hemiplegia may resolve immediately with the administration of intravenous glucose but resolution over a hours is also reported
  13. 13. Space Occupying Lesions  Subacute or chronic duration of symptoms, however some patients may present with acutely probably due to bleeding into a tumour  Associated with deep seated bursting headache, projectile vomiting due raised ICT
  14. 14. SEIZURES AND POST ICTAL STATES  Traditional thought is that these postictal symptoms are manifestations of seizure- induced alterations in neuronal function that are reversible; structural neuronal alterations are not present. The postictal weakness or Todd’s paralysis usually follows partial motor seizures but may follow generalized seizures as well. Duration is usually brief but may last 48 hours
  15. 15. MIGRAINE  Migraine may actually precipitate a stroke, but there is also a variant of migraine, hemiplegic migraine, where unilateral hemiparesis outlasts the headache. This is difficult if not impossible to diagnose correctly at first presentation when it must be regarded as a diagnosis of exclusion; only with recurrent, stereotypic attacks can this be suspected. Cases with alternating hemiplegia have been reported. At times this disorder has been shown to be familial.
  16. 16. ACTIVITY AT THE ONSET OR JUST BEFORE THE STROKE HEMORRHAGIC STROKE Physical activity Sex Trauma ISCHEMIC STROKE Morning hours Sudden coughing and sneezing Getting up during the night to urinate
  17. 17. ASSOCIATED SYMPTOMS
  18. 18. HEADACHE *Severe headache at the onset of neurologic symptoms favors SAH. *Headache after symptom onset that is accompanied by gradually increasing neurologic signs, decreased consciousness, and vomiting is most often indicative of ICH. *Headaches in the prodromal period before thrombotic strokes. *A prior history of intermittent severe headaches that are instantaneous in onset, persist for days, and prevent daily activities often reflects the presence of an aneurysm.
  19. 19. VOMITING *Vomiting is common in patients with ICH, SAH, and posterior circulation large artery ischemia. FEVER & INFECTIONS *Fever raises the suspicion of endocarditis and resulting embolic stroke. *Infections activate acute phase blood reactants, predisposing to thrombosis. SEIZURES *Seizures in the acute phase of stroke are more common in hemorrhagic than ischemic stroke.
  20. 20. ALTERD MENTAL STATUS *Hemorrhagic strokes. *Thrombotic and embolic strokes that are large or involve the posterior circulation large arteries. *Ischemia involving the tegmentum of the pons. *Large hemispheric infarcts are typically followed by edema that can progress to coma. Focal Signs *Focal neurologic signs are suggestive of ICH, while the absence of focal signs suggests SAH.
  21. 21. GENERAL PHYSICAL EXAMINATION
  22. 22. General physical examination *Absent pulses (inferior extremity, radial, or carotid) favors a diagnosis of atherosclerosis with thrombosis. *Sudden onset of a cold, blue limb favors embolism. *Occlusion of the common carotid artery in the neck can be diagnosed by the absence of a carotid pulse. *The presence of a neck bruit suggests the presence of, occlusive extracranial disease. *Cardiac findings, especially A F, murmurs and cardiac enlargement, favor cardiac-origin embolism. *Subhyaloid hemorrhages in the eye suggest a suddenly developing brain or SAH.
  23. 23. NEUROLOGIC EXAMINATION
  24. 24. NEUROLOGIC EXAMINATION *Weakness of the face, arm, and leg on one side of the body unaccompanied by sensory, visual, or cognitive abnormalities (pure motor stroke) favors the presence of a thrombotic stroke involving penetrating arteries or a small ICH. *Large focal neurologic deficits that begin abruptly or progress quickly are characteristic of embolism or ICH. *Abnormalities of language suggest anterior circulation disease, as does the presence of motor and sensory signs on the same side of the body . *Vertigo, staggering, diplopia, deafness, crossed symptoms (one side of the face and other side of the body), bilateral motor and/or sensory signs, and hemianopsia suggest involvement of the posterior circulation. * The sudden onset of impaired consciousness in the absence of focal neurologic signs is characteristic of SAH.
  25. 25. SILENT BRAIN INFARCTS *Silent brain infarcts are infarcts identified only by neuroimaging. *There is no accompanying clinical history of stroke or TIA. *This relationship is somewhat clouded because a more detailed history may elicit symptoms to suggest that a lesion is not truly silent. *In addition, these lesions seem to be associated with cognitive deficits. *More appropriate to refer to these clinically unrecognized lesions as covert brain infarcts. *Patients with TIA and minor stroke appear to have a high risk of covert infarcts as well as clinically symptomatic infarcts.
  26. 26. UPPER AND LOWER MOTOR NEURON LESION (UMNL&LMNL )
  27. 27. UMNL LMNL Paralysis Spastic- clasp knife-affect movement-hypertonic Flaccid- affect muscles-hypotonic weakness Without Atrophy ( only Disuse) With Atrophy D T R Hyperreflexia often with clonus Hyporeflexia or absent Babinski Sign extensor planter Superficial Reflex Absent( abd reflex abscent) Present Fasciculation &Fibrillation Present Absent
  28. 28. Spasticity *Spasticity is a state of sustained increase in muscle tension in response to muscle lengthening, in particular, with passive movements. *Increased resistance to passive movement in antigravity muscle (flexor in arm, extensor in leg). *Clasp Knife Phenomenon. *Sign of Upper Motor Neuron Syndrome, especially IC lesion. Rigidity *Increased muscle tone, no increased DTR. *Cogwheel Phenomenon *Symptom of basal ganglia .
  29. 29. PSEUDOBULBAR PALSY BULBAR PALSY LESION upper motor neuron lesion of cranial nerves IX, X and XII. lower motor neuron lesion of cranial nerves IX, X and XII. BULBAR SYMPTOMS Dysphagia-Nasal regurgitation- dysarthria. hoarseness of voice QUADRIPLEGIA Present(Spastic) Absent TONGUE (WASTED &FASCICULATIONS) Absent Present PALATAL AND PHARYNGEAL REFLEXES Exaggerated Absent JAW REFLEX Exaggerated(if the lesion is above the pons). Absent EMOTIONAL&MOOD CHANGES may be present Absent
  30. 30. Causes Bulbar palsy Pseudobulbar palsy Motor neurone disease cause is bilateral CVAs affecting the IC( commonest). Brainstem CVA Multiple sclerosis Guillain-Barre syndrome Motor neurone disease Poliomyelitis High brainstem tumours Subacute menignitis (carcinoma, lymphoma) Head injury Neurosyphilis Syringobulbia
  31. 31. Differentiating features between ant and post. circulation stroke Clinical features Post.circ Ant. circ Vertigo Present Absent Unsteadiness Present Absent Crossed hemiplegia Present Absent Bilateral deficits Present Absent Cerebellar signs Present Absent Ocular Present Absent Dissociated sensory loss Present Absent Horners syndrome Present Absent
  32. 32. CORTICAL OR SUBCORTICAL STROKE Patient with any of the following signs may have a cortical stroke, not subcortical stroke: *gaze preference or gaze deviation *expressive or receptive aphasia *visual field deficits *visual or spatial neglect
  33. 33. LABORATORY STUDIES
  34. 34. All patients *Noncontrast brain CT or brain MRI. *Serum glucose. *Oxygen saturation. *ECG *Serum electrolytes, urea nitrogen, creatinine. *CBC *Cardiac enzymes and troponin. *Coagulation profile. SELECTED PATIENTS *ABG if hypoxia is suspected. *EEG if seizures are suspected. *Chest radiograph if lung disease is suspected. *Pregnancy test in women of child-bearing potential. *Liver function tests *Toxicology screen *Blood alcohol level BIOMARKER (Serum D-dimer ) *Useful in separating stroke subtypes. *highest in those with cardioembolic strokes and cerebral venous thrombosis *lowest in those with brain ischemia due to penetrating artery disease. *In patients with large artery thromboembolism, D-dimer levels are lower than in patients with cardiogenic embolism but higher than in those with penetrating artery disease.
  35. 35. ACUTE STROKE MANAGEMENT
  36. 36. MAIN GOALS *Ensure medical stability. *Quickly reverse conditions that are contributing to the pt's problem. *Determine if pt with acute ischemic stroke are candidates for thrombolytic therapy. Evaluation and management *Vital signs and ABC stabilization. *Obtaining a rapid but accurate history and ex to help distinguish between ischemic and hemorrhage stroke, and DD of acute stroke. *Obtaining emergent brain CT or MRI and other important lab, cardiac monitoring during the first 24 hours after the onset of ischemic stroke .
  37. 37. *Assessing swallowing and preventing aspiration . Position of the pt *for patients in the acute phase of stroke who are at risk for elevated intracranial pressure, aspiration, cardiopulmonary decompensation, or oxygen desaturation, we recommend keeping the head in neutral alignment with the body and elevating the head of the bed to 30 degrees; *for patients in the acute phase of stroke who are not at risk for elevated intracranial pressure, aspiration, or worsening cardiopulmonary status, we suggest keeping the head of bed flat (0 to 15 degree head-of-bed position) Fever *Evaluating and treating the source of fever; for patients with acute stroke, we suggest maintaining normothermia for at least the first several days after an acute stroke .
  38. 38. VOLUME DEPLETION AND ELECTROLYTE DISTURBANCES * Intravascular volume depletion is frequent in the setting of acute stroke, particularly in older adult patients, and may worsen cerebral blood flow. *For most patients with acute stroke and volume depletion, isotonic saline without dextrose is the agent of choice for intravascular fluid repletion and maintenance fluid therapy. *Avoid excess free water (eg, as in ½ isotonic saline) because hypotonic fluids may exacerbate cerebral edema in acute stroke and are less useful than isotonic solutions for replacing intravascular volume. *Avoid fluids containing glucose, which may exacerbate hyperglycemia. * Fluid management must be individualized on the basis of cardiovascular status, electrolyte disturbances, and other conditions that may perturb fluid balance,In particular, hyponatremia following SAH may be due to SIADH.
  39. 39. SERUM GLUCOSE *Checking serum glucose. * Low serum glucose (<60 mg/dL or 3.3 mmol/L) should be corrected rapidly. *Normoglycemia is the desired goal. *Treatment with insulin if serum glucose concentrations >180 mg/dL (>10 mmol/L).
  40. 40. Management of blood pressure Acute ischemic stroke *For patients who will receive thrombolytic therapy, antihypertensive treatment is recommended so that systolic blood pressure is ≤185 mmHg and diastolic blood pressure is ≤110 mmHg. *For patients who are not treated with thrombolytic therapy, we suggest treating high blood pressure only if 1- Hypertension is extreme (systolic blood pressure >220 mmHg or diastolic blood pressure >120 mmHg) OR 2- If the patient has another clear indication (active ischemic coronary disease, heart failure, aortic dissection, hypertensive encephalopathy, acute renal failure, or pre-eclampsia/eclampsia) .
  41. 41. *When treatment is indicated, we suggest cautious lowering of blood pressure by approximately 15 percent during the first 24 hours after stroke onset. Hemorrhagic stroke *In both (ICH) and SAH, the approach to blood pressure lowering must account for the potential benefits (eg, reducing further bleeding) and risks (eg,reducing cerebral perfusion). *Recommendations for blood pressure management in acute ICH and SAH are discussed in detail separately.
  42. 42. Thrombolytic therapy (Alteplase) *For eligible patients with acute ischemic stroke, we recommend intravenous alteplase therapy(0.9mg /kg ivi over 60 min), provided that treatment is initiated within three hours of clearly defined symptom onset. Inclusion criteria *Clinical diagnosis of ischemic stroke causing measurable neurologic deficit. *Onset of symptoms <4.5 hours before beginning treatment; if the exact time of stroke onset is not known, it is defined as the last time the patient was known to be normal. *Age ≥18 years. *no contraindication .
  43. 43. Antithrombotic therapy *there are two major classes of antithrombotic drugs that can be used to treat acute ischemic stroke: 1- Antiplatele 2- Anticoagulants ASPIRIN (160 to 325 mg daily) *STARTING within 48 hours of presumed ischemic stroke onset. *Reduce the risk of early recurrent ischemic stroke without a major risk of early hemorrhagic complications and improved long- term outcome. * Although aspirin, clopidogrel, and the combination of aspirin- extended-release dipyridamole are all acceptable options for secondary stroke prevention, aspirin is the only antiplatelet agent that has been established as effective for the very early treatment of acute ischemic stroke.
  44. 44. *Clopidogrel is alternatives for patients intolerant to aspirin, although the effectiveness of these antiplatelets in acute stroke is not established. *The use of dual antiplatelet therapy remains largely unproven, with the exception that short-term treatment with clopidogrel plus aspirin appears to be beneficial for high-risk TIA and minor stroke in Asian populations . *We recommend early dual antiplatelet treatment with clopidogrel plus aspirin for 21 days, followed by clopidogrel monotherapy through at least day 90, for Asian patients with high-risk TIA (ie, ABCD2 score of ≥4) or minor stroke.
  45. 45. *Beyond the acute phase of ischemic stroke and TIA, long-term antiplatelet therapy for secondary stroke prevention should be continued with aspirin, clopidogrel, or the combination of aspirin- extended-release dipyridamole. *Aspirin and other antiplatelet agents may be used in combination with subcutaneous heparin and low molecular weight heparin for D V T prophylaxis. *The available evidence suggests that early anticoagulation with heparin or low molecular weight heparin is associated with a higher mortality and worse outcomes compared with aspirin treatment initiated within 48 hours of ischemic stroke onset .
  46. 46. *Antiplatelet agents should be started as early as possible after the diagnosis of ischemic stroke is confirmed. *Aspirin and other antithrombotic agents should not be given alone or in combination for the first 24 hours following treatment with intravenous alteplase. *While parenteral anticoagulation is not recommended during the first 48 hours after acute ischemic stroke, oral anticoagulation is recommended for secondary stroke prevention in patients with atrial fibrillation and other high risk sources of cardiogenic embolism. *The timing of its initiation for such patients is mainly dependent on the size of the infarct, which is presumed to correlate with the risk of hemorrhagic transformation.
  47. 47. • For medically stable patients with a small or moderate-sized infarct, warfarin can be initiated soon (after 24 hours) after admission with minimal risk of transformation to hemorrhagic stroke, while withholding anticoagulation for two weeks is generally recommended for those with large infarctions, symptomatic hemorrhagic transformation, or poorly controlled hypertension. *Urgent anticoagulation is not recommended for the treatment of patients with acute ischemic stroke . Statin therapy . *For patients receiving statin therapy prior to stroke onset, we suggest continuing statin treatment.
  48. 48. SAH *The optimal therapy of hypertension in SAH is not clear. *While lowering blood pressure may decrease the risk of rebleeding, this benefit may be offset by an increased risk of infarction. *A decrease in systolic blood pressure to <160 mm Hg in the setting of an unsecured aneurysm is reasonable. *Agents such as labetalol, nicardipine, and enalapril are preferred. *Nimodipine (60 mg po or NGT /4h) improve neurologic outcomes in SAH. * Nimodipineis started within four days of onset and is continued for 21 days.
  49. 49. *Prophylactic antiepileptic drug (AED) therapy is not required in all patients, but may be considered in some with unsecured aneurysms and large concentrations of blood at the cortex. *Seizures should be treated promptly. *Continuation of AED therapy may not be necessary in patients without acute seizures after the aneurysm is secured. *AEDs are usually continued for approximately six months in patients who have experienced an acute seizure (within seven days) following SAH.
  50. 50. ACUTE ICH Patients with acute ICH should be managed in an ICU. 1- General management issues include: *D/C of all anticoagulant and antiplatelet drugs, and immediate reversal of anticoagulant effects with the appropriate agents. *Maintenance of normothermia and evaluation and treatment of fever source. *Normal saline initially should be used for maintenance and replacement fluids. *Treating hyperglycemia (elevated serum glucose >185 mg/dL (>10.3 mmol/L) with insulin; hypoglycemia should be avoided.
  51. 51. *NPO until swallowing function is evaluated to prevent aspiration . 2-Management of of elevated ICP *includes elevating the head of the bed to 30 degrees and use of analgesia and sedation. *Suggested iv agents for sedation are propofol, etomidate, or midazolam. *Suggested agents for analgesia and antitussive effect are morphine or alfentanil. *Invasive monitoring and treatment of ICP should be considered for patients with GCS <8, those with clinical evidence of transtentorial herniation, or those with significant IVH or hydrocephalus.
  52. 52. *More aggressive therapies for reducing elevated ICP include osmotic diuretics (eg, mannitol), ventricular catheter drainage of cerebrospinal fluid, and neuromuscular blockade . 3-Blood pressure *Severe elevations in blood pressure may worsen ICH by representing a continued force for bleeding. *Labetalol, esmolol, hydralazine, nitroprusside, and nitroglycerin are useful iv agents for controlling BP. *For patients with systolic blood pressure (SBP) >200 mmHg or MAP >150 mmHg, we suggest aggressive reduction of B P with continuous intravenous infusion of medication accompanied by blood pressure monitoring every five minutes.
  53. 53. *For patients with SBP >180 mmHg or MAP >130 mmHg and evidence or suspicion of elevated ICP, we suggest monitoring ICP and reducing B P using intermittent or continuous intravenous medication to keep cerebral perfusion pressure in the range of 61 to 80 mmHg . *For patients with SBP >180 mmHg or MAP >130 mmHg and no evidence or suspicion of elevated ICP, we suggest a modest reduction of B P to a target MAP of 110 mmHg or target blood pressure of 160/90 mmHg using intermittent or continuous intravenous medication accompanied by reexamination of the patient every 15 minutes.
  54. 54. 4- antiepileptic treatment *Appropriate iv antiepileptic treatment should be used to quickly control seizures for patients with ICH and clinical seizures. 5-Cerebellar hemorrhages *For patients with cerebellar hemorrhages >3 cm in diameter who are deteriorating or who have brainstem compression and/or hydrocephalus due to ventricular obstruction, we recommend surgical removal of hemorrhage . 6- Treating hypertension is the most important step to reduce the risk of ICH, and probably recurrent ICH. 7-Stopping smoking, heavy alcohol use, and cocaine use are also recommended.
  55. 55. HAEMORRHAGIC LESION
  56. 56. ISCHAEMIC LESION

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