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Stroke guidelines, 2015

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Proper stroke managment in the scope of AHA/ASA guidelines published in 2013-2015-2016

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Stroke guidelines, 2015

  1. 1. Cerebrovascular Accident (Stroke) Let’s guideline our minds!! Usama Ragab Yousif (Msc.) Internal Medicine Department
  2. 2. Agenda • To be able to differentiate between stroke and other conditions • To discuss the latest stroke treatment strategies (either interventional or non interventional) • To emphasize the role of early evaluation and management of stroke patients
  3. 3. Disease makes men more physical, it leaves them nothing but body. Thomas Mann
  4. 4. Epidemiology • Globally, about 17 million strokes occur every year and stroke is the second leading cause of death after coronary heart disease, and the third most common cause of disability. 1- Krishnamurthi RV: Lancet Glob Health. 2013;1(5):e259. Figure: http://www.who.int/mediacentre/factsheets/fs310/en/
  5. 5. Epidemiology • Globally, the incidence of stroke due to ischemia is 68 %, while the incidence of hemorrhagic stroke (intracerebral hemorrhage and subarachnoid hemorrhage combined) is 32 %. • Men have a higher incidence of stroke than women at younger but not older ages, with the incidence reversed and higher for women by age 75 years and older. Mikulik R: J Intern Med 2015; 278: 145–165. Lozano R, et al: Lancet. 2012 Dec;380(9859):2095-128.
  6. 6. Pathophysiology of Ischemic stroke Normal cerebral blood flow (CBF): > 50 mL/100gm/min of brain tissues.1 18-50 mL/100gm/min of brain = oligemia. Less than 18 mL/100gm/min of brain = neurological deficit due to electrical failure (transiant; TIA or permanent; infarction)  < 8 mL = core infarction. 8-18 mL/100gm/min of brain = Penumbra 1- Cipolla MJ. The Cerebral Circulation. San Rafael (CA): Morgan & Claypool Life Sciences; 2009. Figure: P, Langhorne. "Stroke Disease." Davidson’s Principles and Practice of Medicine. 22nd ed. N.p.: Elsevier, 2014. 1231-248. Print.
  7. 7. Penumbra is zone of reversible ischemia around core of irreversible infarction—salvageable in first few hours after ischemic stroke onset Penumbra damaged by: • Hypoperfusion • Hyperglycemia • Fever • Seizure http://www.strokecenter.org/professionals/brain- anatomy/cellular-injury-during-ischemia/the-ischemic- penumbra/ (HON code certified)
  8. 8. Sir Winston Churchill Prime Minister of the United Kingdom from 1940 to 1945 and again from 1951 to 1955 Famous People Who Died of Stroke http://www.ranker.com/list/famous-people-who-died-of-stroke/reference
  9. 9. Risk factors for stroke POTENTIALLY Modifiable risk factorsFixed risk factors Blood pressure Cigarette smoking Hyperlipidaemia Heart disease Atrial fibrillation Congestive cardiac failure Infective endocarditis Diabetes mellitus Excessive alcohol intake Oestrogen-containing drugs Polycythaemia Age Gender (male > female except at extremes of age) Race (Afro-Caribbean > Asian > European) Previous vascular event  Myocardial infarction  Stroke Peripheral vascular disease Heredity High fibrinogen P, Langhorne. "Stroke Disease." Davidson’s Principles and Practice of Medicine. 22nd ed. N.p.: Elsevier, 2014. 1231-248. Print.
  10. 10. Risk factors for stroke (cont.) TIA is a risk factor for future stroke SC Johnston et al: Validation and refinement of score to predict very early stroke risk after transient ischaemic attack. Lancet 369:283, 2007.
  11. 11. CommentABCD2 Hospital observation may be unnecessary 0-3 Hospital observation justified 4-5 Hospital observation worthwhile 6-7
  12. 12. National Stroke Foundation, 2010 The NSF in 2010 discuss this point in their guideline: Those identified as high risk (e.g. ABCD2 score >3 and/or those with any one of the following AF, carotid territory symptoms or crescendo TIA, should be admitted to a stroke unit (or where available referred to a specialist TIA clinic if the person can be assessed within 24 hours) to facilitate rapid specialist assessment and management (A). Urgent brain imaging (preferably MRI with DWI), ‘urgent’ being immediately where available, but within 24 hours). Carotid imaging should also be undertaken urgently in patients with anterior circulation symptoms who are candidates for carotid re-vascularisation (B). Those identified as low risk (e.g. aBCD2 score <4 and without AF or carotid territory symptoms or crescendo TIA should commence initial therapy (e.g. aspirin) and then be managed in the community by a general practitioner or private specialist or, where possible, be referred to a specialist TIA clinic and seen within seven days (GPP). National Stroke Foundation – Australia (2010)
  13. 13. Joseph Stalin The leader of the Soviet Union from the mid-1920s until his death in 1953 Famous People Who Died of Stroke http://www.ranker.com/list/famous-people-who-died-of-stroke/reference
  14. 14. In brief stroke is either:
  15. 15. Review of Anatomy • Blood reaches the brain through 2 systems: 1. The carotid system (Anterior Circulation) 2. The vertebral system (Posterior Circulation)
  16. 16. Presentation • Sudden onset • Focal neurological deficit • Progresses over minutes to hours • Depends on location • Symptoms include:  SUDDEN numbness or weakness of face, arm or leg  SUDDEN confusion, trouble speaking or understanding.  SUDDEN trouble with vison.  SUDDEN trouble walking, dizziness, loss of balance or coordination.  SUDDEN severe headache.
  17. 17. Presentation (cont.)
  18. 18. Presentation (cont.) P, Langhorne. "Stroke Disease." Davidson’s Principles and Practice of Medicine. 22nd ed. N.p.: Elsevier, 2014. 1231-248. Print.
  19. 19. Time is BRAIN • The longer the time period that the person remains unresponsive, the less likely it is that the person will recover. • It has calculated that in a typical large-vessel acute ischaemic stroke, about 1.9 million neurons die every minute during which stroke is untreated, 14 billion synapses, and 12 km (7.5 miles) of myelinated fibers are destroyed.1 • The first few days after onset is critical. 1- Saver, J. L. (2006). Time is brain—quantified. Stroke, 37(1), 263-266.
  20. 20. Stroke. 2013;44:870-947.
  21. 21. Definition of Classes and Levels of Evidence Used in AHA/ASA Recommendations Conditions for which there is evidence for and/or general agreement that the procedure or treatment is useful and effective. Class I Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment. The weight of evidence or opinion is in favor of the procedure or treatment. Usefulness/efficacy is less well established by evidence or opinion. Class II Class IIa Class IIb Conditions for which there is evidence and/or general agreement that the procedure or treatment is not useful/effective and in some cases may be harmful. Class III Stroke. 2013;44:870-947.
  22. 22. Definition of Classes and Levels of Evidence Used in AHA/ASA Recommendations Therapeutic recommendations Data derived from multiple randomized clinical trials or meta-analyses Level of Evidence A Data derived from a single randomized trial or nonrandomized studies Level of Evidence B Consensus opinion of experts, case studies, or standard of care Level of Evidence C Diagnostic recommendations Data derived from multiple prospective cohort studies using a reference standard applied by a masked evaluator Level of Evidence A Data derived from a single grade A study or 1 or more case control studies, or studies using a reference standard applied by an unmasked evaluator Level of Evidence B Consensus opinion of expertsLevel of Evidence C Stroke. 2013;44:870-947.
  23. 23. Prehospital Evaluation and Management of Potential Stroke Patients Prehospital care providers should use prehospital stroke assessment tools, such as the Los Angeles Prehospital Stroke Screen or Cincinnati Prehospital Stroke Scale (Class I; Level of Evidence B). Cincinnati Stroke Scale (Smile, Wave, Talk) Interpretation: if any of these 3 signs is abnormal, the probability of a stroke is 72%
  24. 24. Assessment You can use the easily memorized FAST assessment
  25. 25. • Patients should be transported rapidly to the closest available certified primary stroke centers (PSC) or comprehensive stroke centers (CSC) or, if no such centers exist, the most appropriate institution that provides emergency stroke care as described in the statement (Class I; Level of Evidence A). • For patients with suspected stroke, EMS should bypass hospitals that do not have resources to treat stroke and go to the closest facility most capable of treating acute stroke (Class I; Level of Evidence B). • Delaying intravenous rtPA therapy until after transport in otherwise eligible patients decreases the chance for a good outcome.
  26. 26. Not RecommendedRecommended Do not initiate interventions for hypertension unless directed by medical commands Assess and manage ABCs Initiate cardiac monitoring Provide supplemental oxygen to maintain O2 saturation >94% Do not administer excessive IV fluids Establish IV access per local protocol Do not administer dextrose- containing fluids in nonhypoglycemic patients Determine blood glucose and treat accordingly Do not administer medications by mouth (maintain NPO) Determine time of symptom onset or last known normal, and obtain family contact information, preferably a cell phone Triage and rapidly transport patient to nearest most appropriate stroke hospital Do not delay transport for prehospital interventions Notify hospital of pending stroke patient arrival During transfer:
  27. 27. Emergency Triage and Initial Evaluation Bock BF. Proceedings of a National Symposium on Rapid Identification and Treatment of Acute Stroke: Response System for Patients Presenting With Acute Stroke. http://www.ninds.nih.gov/ TimeAction ≤10 minutesDoor to physician ≤15 minutesDoor to stroke team ≤25 minutesDoor to CT initiation ≤45 minutesDoor to CT interpretation ≤60 minutesDoor to drug (≥80% compliance) ≤3 hoursDoor to stroke unit admission An organized protocol for the emergency evaluation of patients with suspected stroke is recommended (Class I; Level of Evidence B). The goal is to complete an evaluation and to begin fibrinolytic treatment within 60 minutes of the patient’s arrival in an ED. Designation of an acute stroke team that includes physicians, nurses, and laboratory/radiology personnel is encouraged. !!!!!!!
  28. 28. Assessment (cont.) The use of a stroke rating scale, preferably the NIH Stroke Scale (NIHSS), is recommended (Class I; Level of Evidence B).
  29. 29. ScoreStroke Severity 0No Stroke Symptoms 1-4Minor Stroke 5-15Moderate Stroke 16-20Moderate to Severe Stroke 21-42Severe Stroke NIH Stroke Scale (cont.)  The NIHSS has been found to be an excellent predictor of patient outcomes.  A baseline NIHSS score greater than 16 indicates a strong probability of patient death, while a baseline NIHSS score less than 6 indicates a strong probability of a good recovery.  On average, an increase of 1 point in a patient’s NIHSS score decreases the likelihood of an excellent outcome by 17%.  However, correlation between functional recovery and NIHSS scores was weaker when the stroke was isolated to the cortex. Neurology 53 (1): 126–131.
  30. 30. Assessment (cont.) Teasdale G, Jennett B. (1974). "Assessment of coma and impaired consciousness. A practical scale.". Lancet 13 (2): 81–4. Glasgow Coma Scale: The Glasgow Coma Scale or GCS is a neurological scale that aims to give a reliable, objective way of recording the conscious state of a person for initial as well as subsequent assessment. A patient is assessed against the criteria of the scale, and the resulting points give a patient score between 3 (indicating deep unconsciousness) and either 14 (original scale) or 15 (the more widely used modified or revised scale).
  31. 31. A limited number of hematologic, coagulation, and biochemistry tests are recommended during the initial emergency evaluation, and only the assessment of blood glucose must precede the initiation of intravenous rtPA (Class I; Level of Evidence B). I should be aware of stroke mimics!!!!! Assessment (cont.) ‘Functional’ stroke mimics‘Structural’ stroke mimics Todd’s paresis (after epileptic seizure) Hypoglycaemia Migrainous aura (with or without headache) Focal seizures Ménière’s disease or other vestibular disorder Conversion disorder Encephalitis CO2 narcosis Primary cerebral tumours Metastatic cerebral tumours Subdural haematoma Cerebral abscess Peripheral nerve lesions (vascular or compressive) Demyelination P, Langhorne. "Stroke Disease." Davidson’s Principles and Practice of Medicine. 22nd ed. N.p.: Elsevier, 2014. 1231-248. Print.
  32. 32. Immediate Diagnostic Studies: Evaluation of a Patient With Suspected Acute Ischemic Stroke Stroke. 2013;44:870-947. *Fibrinolytic therapy should not be delayed while awaiting the results unless: (1) there is clinical suspicion of a bleeding abnormality or thrombocytopenia. (2) the patient has received heparin or warfarin. (3) the patient has received other anticoagulants (direct thrombin inhibitors or direct factor Xa inhibitors).
  33. 33. Immediate Diagnostic Studies: Evaluation of a Patient With Suspected Acute Ischemic Stroke Stroke. 2013;44:870-947.
  34. 34.  Baseline electrocardiogram assessment is recommended in patients presenting with acute ischemic stroke but should not delay initiation of intravenous rtPA (Class I; Level of Evidence B).  Baseline troponin assessment is recommended in patients presenting with acute ischemic stroke but should not delay initiation of intravenous rtPA (Class I; Level of Evidence C).  The usefulness of chest radiographs in the hyperacute stroke setting in the absence of evidence of acute pulmonary, cardiac, or pulmonary vascular disease is unclear. If obtained, they should not unnecessarily delay administration of fibrinolysis (Class IIb; Level of Evidence B). Assessment (cont.)
  35. 35. Assessment (cont.) Recommendations for Patients With Acute Cerebral Ischemic Symptoms That Have Not Yet Resolved  Emergency imaging of the brain is recommended before initiating any specific therapy to treat acute ischemic stroke (Class I; Level of Evidence A). In most instances, NECT will provide the necessary information to make decisions about emergency management.  Either NECT or MRI is recommended before intravenous rtPA administration to exclude ICH (absolute contraindication) and to determine whether CT hypodensity or MRI hyperintensity of ischemia is present (Class I; Level of Evidence A).  Intravenous fibrinolytic therapy is recommended in the setting of early ischemic changes (other than frank hypodensity) on CT(Class I; Level of Evidence A). Frank hypodensity on NECT may increase the risk of hemorrhage with fibrinolysis. If frank hypodensity involves more than one third of the MCA territory, intravenous rtPA treatment should be withheld (Class III; Level of Evidence A).
  36. 36. Assessment (cont.) Recommendations for Patients With Acute Cerebral Ischemic Symptoms That Have Not Yet Resolved (cont.) NECT should be obtained within 25 minutes of the patient’s arrival in the ED. NECT definitively excludes parenchymal hemorrhage and can assess other exclusion criteria for intravenous rtPA, such as widespread hypoattenuation. CommentsIts use in acute ischemic stroke However, the ability of observers to detect these early infarct signs on NECT is quite variable and occurs in ≤67% of cases imaged within 3 hours. A sign of cerebral ischemia within the first few hours after symptom onset on NECT is loss of gray-white differentiation. This sign has approx. 100% sensitivity, however only 30% specificity. Increased density within the occluded artery, such as the hyperdense middle cerebral artery (MCA) sign, indicative of large-vessel occlusion. The sensitivity is low (38%) but the specificity is 100%. Hyperdense MCA “dot” sign.
  37. 37. Assessment (cont.) Infarction appears as hypodense (more dark) area on CT
  38. 38. Assessment (cont.) Which become denser with time Case courtesy of Dr David Cuete, Radiopaedia.org, rID: 35732
  39. 39. Assessment (cont.)
  40. 40. Assessment (cont.) Loss of grey-white differentiation Case courtesy of Dr David Cuete, Radiopaedia.org, rID: 35427
  41. 41. Assessment (cont.) Hyperdense MCA sign Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org, rID: 5105 Case courtesy of Dr Jeremy Jones, Radiopaedia.org, rID: 13190 Case courtesy of Dr Mohammed Alghamdi, Radiopaedia.org, rID: 17138
  42. 42. Assessment (cont.) MCA dot sign Case courtesy of Dr Bruno Di Muzio, Radiopaedia.org, rID: 25414
  43. 43. Assessment (cont.) So,…… Case courtesy of Dr Bruno Di Muzio, Radiopaedia.org, rID: 25414
  44. 44. What about MRI…. For diagnosing ischemic stroke in the emergency setting: CT scans (without contrast enhancements): sensitivity= 16%specificity= 96% MRI scan: sensitivity= 83%specificity= 98% MRI reliably documents the extent and location of infarction in all areas of the brain, including the posterior fossa and cortical surface. MRI scanners with magnets of higher field strength produce more reliable and precise images. Diffusion-weighted imaging is more sensitive for early brain infarction than standard MR sequences or CT, as is fluid-ttenuated inversion recovery (FLAIR) imaging.
  45. 45. What about MRI…. Case courtesy of Dr G Balachandran, Radiopaedia.org, rID: 10704 Subtle hypointensity seen in right MCA territory on T1, with increased signal on T2 and FLAIR. DWI b=1000 shows the brightest signal in right MCA territory confirming the cytotoxic odema due to hyperacute infarct.
  46. 46. What about MRI…. Case courtesy of Dr G Balachandran, Radiopaedia.org, rID: 10704 Subtle hypointensity seen in right MCA territory on T1, with increased signal on T2 and FLAIR. DWI b=1000 shows the brightest signal in right MCA territory confirming the cytotoxic odema due to hyperacute infarct.
  47. 47. What about MRI…. Case courtesy of Dr G Balachandran, Radiopaedia.org, rID: 10704 Subtle hypointensity seen in right MCA territory on T1, with increased signal on T2 and FLAIR. DWI b=1000 shows the brightest signal in right MCA territory confirming the cytotoxic odema due to hyperacute infarct.
  48. 48. What about MRI…. Case courtesy of Dr G Balachandran, Radiopaedia.org, rID: 10704 Subtle hypointensity seen in right MCA territory on T1, with increased signal on T2 and FLAIR. DWI b=1000 shows the brightest signal in right MCA territory confirming the cytotoxic odema due to hyperacute infarct.
  49. 49. Assessment (cont.) Recommendations for Patients With Acute Cerebral Ischemic Symptoms That Have Not Yet Resolved (cont.)  CT perfusion and MRI perfusion and diffusion imaging, including measures of infarct core and penumbra, may be considered for the selection of patients for acute reperfusion therapy beyond the time windows for intravenous fibrinolysis. These techniques provide additional information that may improve diagnosis, mechanism, and severity of ischemic stroke and allow more informed clinical decision making (Class IIb; Level of Evidence B).
  50. 50. Assessment (cont.) Recommendations for Patients With Acute Cerebral Ischemic Symptoms That Have Not Yet Resolved (cont.) Using IV administration of gadolinium contrast, MR perfusion studies can be performed. Brain regions showing poor perfusion but no abnormality on diffusion provide, compared to CT, an equivalent measure of the ischemic penumbra. ƒDWI is thought to show the area currently infarcting.ƒBut is there an “area at risk” where blood flow is reduced but cells haven’t died yet? ƒImaging this region (the penumbra) = goal of MR perfusion imaging.
  51. 51. Assessment(cont.) A. Computed tomography (CT) perfusion mean-transit time map showing delayed perfusion of the left MCA distribution (blue). B. Predicted region of infarct (red) and penumbra (green) based on CT perfusion data. C. Conventional angiogram showing occlusion of the left internal carotid–MCA bifurcation (b4 & after successful thrombectomy). D. The clot rmoved by thrombectomy device. E. CT scan of the brain 2 days later; note infarction in the region predicted in B but preservation of the penumbral region by successful revascularization.
  52. 52. Assessment(cont.) A. MRI diffusion-weighted image (DWI) of an 82-year-old woman 2.5 h after onset of right-sided weakness and aphasia reveals restricted diffusion within the left basal ganglia and internal capsule (colored regions). B. Perfusion defect within the left hemisphere (colored signal) imaged (gadolinium contrast). The discrepancy between the region of poor perfusion shown in B and the diffusion deficit shown in A is called diffusion-perfusion mismatch and provides an estimate of the ischemic penumbra. C. Fluid-attenuated inversion recovery image obtained 3 days later showing a region of infarction (coded as white) that corresponds to the initial DWI image in A, but not the entire area at risk shown in B, suggesting that successful embolectomy
  53. 53. Assessment (cont.) Recommendations for Patients With Cerebral Ischemic Symptoms That Have Resolved  Noninvasive imaging of the cervical vessels should be performed routinely as part of the evaluation of patients with suspected TIAs (Class I; Level of Evidence A).  Noninvasive imaging by means of CTA or MRA of the intracranial vasculature is recommended to exclude the presence of proximal intracranial stenosis and/or occlusion (Class I; Level of Evidence A).  Patients with transient ischemic neurological symptoms should undergo neuroimaging evaluation within 24 hours of symptom onset or as soon as possible in patients with delayed presentations. MRI, including DWI, is the preferred brain diagnostic imaging modality. If MRI is not available, head CT should be performed (Class I; Level of Evidence B).
  54. 54. Assessment (cont.) Cerebral Angiography  Conventional x-ray cerebral angiography is the gold standard for identifying and quantifying atherosclerotic stenoses of the cerebral arteries and for identifying and characterizing other pathologies, including aneurysms, vasospasm, intraluminal thrombi, fibromuscular dysplasia, arteriovenous fistulae, vasculitis, and collateral channels of blood flow.  Conventional angiography carries risks of arterial damage, groin hemorrhage, embolic stroke, and renal failure from contrast nephropathy, so it should be reserved for situations where less invasive means are inadequate.
  55. 55. Cerebral Angiography
  56. 56. Assessment (cont.) Carotid Doppler US: Stenosis more than 70% should raise our mind to possible intervention
  57. 57. Repeating Neuroimaging A repeat brain Ct or MRI and acute medical review should be considered urgently when a patient’s condition deteriorates. (GPP) National Stroke Foundation – Australia (2010)
  58. 58. Treatment
  59. 59. General Supportive Care and Treatment of Acute Complications The era of interventional therapy NINDS* and ASA** Recommended Stroke Evaluation Time Benchmarks for Potential Thrombolysis Candidate *National Institute of Neurological Disorders and Stroke **American Stroke Association Time Interval Time Target Door to doctor 10 min Access to neurologic expertise 15 min Door to CT scan completion 25 min Door to CT scan interpretation 45 min Door to treatment 60 min Admission to stroke unit or ICU 3 h
  60. 60. Treatment (cont.) Factors Recommendation Airway &Breathing Airway support and ventilatory assistance are recommended for the treatment of patients with acute stroke who have decreased consciousness or who have bulbar dysfunction that causes compromise of the airway (Class I; Level of Evidence C). Supplemental oxygen should be provided to maintain oxygen saturation >94% (Class I; Level of Evidence C). Supplemental oxygen is not recommended in nonhypoxic patients with acute ischemic stroke (Class III; Level of Evidence B). Blood Glucose Hypoglycemia (blood glucose <60 mg/dL) should be treated in patients with acute ischemic stroke (Class I; Level of Evidence C). The goal is to achieve levels of 140-180 mg/dL (Class IIa; Level of Evidence C). Nutrition A formal screening procedure for dysphagia should be performed in all patients before the initiation of oral intake to reduce the risk of pneumonia (Class I; Level of Evidence B). Insert a nasogastric tube if the patient fails the swallow test. Consider PEG only if prolonged enteral feeding is required (Class I; Level of Evidence B). Stroke. 2013;44:870-947.
  61. 61. Infection and fever Sources of hyperthermia (temperature >38°C) should be identified and treated, and antipyretic medications should be administered to lower temperature (Class I; Level of Evidence C). Routine use of prophylactic antibiotics has not been shown to be beneficial (Class III; Level of Evidence B). Patients with suspected pneumonia or urinary tract infections should be treated with appropriate antibiotics (Class I; Level of Evidence A). Hypovolemia Hypovolemia should be corrected with intravenous normal saline, and cardiac arrhythmias that might be reducing cardiac output should be corrected (Class I; Level of Evidence C). Seizures Clinical seizures should be treated with antiseizure drugs (Class I; Level of Evidence B). Prophylactic antiseizure medication is not recommended (Class III; Level of Evidence C). Prolonged recumbency Subcutaneous administration of anticoagulants is recommended for treatment of immobilized patients with ischemic infarction to prevent deep vein thrombosis (Class I; Level of Evidence A). The use of aspirin is reasonable for treatment of patients who cannot receive anticoagulants for prophylaxis of deep vein thrombosis (Class IIa; Level of Evidence A). Treatment (cont.)
  62. 62. Hypertension in acute stroke a management dilemma Ischemic stroke The treatment of arterial hypertension immediately after stroke is problematic. Observational studies have found that a rapid and steep reduction in BP during the first 24 h after stroke onset might be harmful.1-2 Two important pathophysiologic processes should be considered during management of acute stroke. These are: 1. Impaired cerebral autoregulation. 2. Increased intracranial pressure (ICP). In patients with ischemic stroke, perfusion pressure distal to the obstructed vessel is low, and the distal vessels are dilated. Thus, elevated BP is necessary to maintain brain perfusion in borderline ischemic areas3 . Lowering of BP in patients with acute ischemic stroke has been associated with clinical deterioration. 1- Stroke 2004; 35:520–527. 2- Neurology 2003; 61:1047–1051. 3- Stroke 2009; 40:2251–2256.
  63. 63. Hypertension in acute stroke a management dilemma (cont.) Kaplan, NM. Management of hypertensive emergencies. Lancet 1994; 344:1335.
  64. 64. Hypertension in acute stroke a management dilemma (cont.) The guidelines: In patients with markedly elevated blood pressure who do not receive fibrinolysis, a reasonable goal is to lower blood pressure by 15% during the first 24 hours after onset of stroke. The level of blood pressure that would mandate such treatment is not known, but consensus exists that medications should be withheld unless the systolic blood pressure is >220 mm Hg or the diastolic blood pressure is >120 mmHg. (Class I; Level of Evidence C) If BP is not maintained at or below 185/110 mmHg, do not consider administering recombinant tissue plasminogen activator (rtPA). During and after thrombolytic therapy, BP should be maintained below 180/105 mmHg for at least 24 h (Class I; Level of Evidence B) Circulation 2010; 122 (Suppl 3): S818–S828. Stroke. 2013;44:870-947.
  65. 65. Hypertension in acute stroke a management dilemma (cont.) The guidelines: Evidence from one clinical trial indicates that initiation of antihypertensive therapy within 24 hours of stroke is relatively safe. Restarting antihypertensive medications is reasonable after the first 24 hours for patients who have preexisting hypertension and are neurologically stable unless a specific contraindication to restarting treatment is known (Class IIa; Level of Evidence B). No data are available to guide selection of medications for the lowering of blood pressure in the setting of acute ischemic stroke. (Class IIa; Level of Evidence C). Stroke. 2013;44:870-947.
  66. 66. Hypertension in acute stroke a management dilemma (cont.) The guidelines: Many patients have spontaneous declines in blood pressure during the first 24 hours after onset of stroke. Until more definitive data are available, the benefit of treating arterial hypertension in the setting of acute ischemic stroke is not well established (Class IIb; Level of Evidence C). Patients who have malignant hypertension or other medical indications for aggressive treatment of blood pressure should be treated accordingly. Pre-existing antihypertensive therapy can be continued (orally or via nasogastric tube) provided there is no symptomatic hypotension or other reason to withhold treatment is considered a good practice point (GPP) according to National Stroke Foundation, 2010. Stroke. 2013;44:870-947.
  67. 67. American Heart Association/American Stroke Association. Stroke. 2013;44:870–947. Inclusion criteria: Diagnosis of ischemic stroke causing measurable neurological deficit Onset of symptoms <3 hours before beginning treatment Aged ≥18 years Exclusion criteria: χSignificant head trauma or prior stroke in previous 3 months χSymptoms suggest subarachnoid hemorrhage χArterial puncture at noncompressible site in previous 7 days χHistory of previous intracranial hemorrhage χIntracranial neoplasm, arteriovenous malformation, or aneurysm χRecent intracranial or intraspinal surgery χElevated blood pressure (systolic >185 mm Hg or diastolic >110 mm Hg) χActive internal bleeding The American Heart Association/American Stroke Association (AHA/ASA) inclusion guidelines for the administration of rt-PA in under 3 hours are as follows: Thrombolytic therapy
  68. 68. American Heart Association/American Stroke Association. Stroke. 2013;44:870–947. Exclusion criteria (cont.): χAcute bleeding diathesis χPlatelet count <100 000/mm³ χHeparin received within 48 hours, resulting in abnormally elevated aPTT greater than the upper limit of normal χCurrent use of anticoagulant with INR >1.7 or PT >15 seconds χCurrent use of direct thrombin inhibitors or direct factor Xa inhibitors with elevated sensitive laboratory tests (such as aPTT, INR, platelet count, and ECT; TT; or appropriate factor Xa activity assays) χBlood glucose concentration <50 mg/dL (2.7 mmol/L) χCT demonstrates multilobar infarction (hypodensity >1/3 cerebral hemisphere)
  69. 69. Treatment Recommendations rTPA In selected patients presenting within 3 hours: IV rt-Pa (0.9mg/kg, maximum 90mg ) with 10% given as a bolus followed by an infusion over one hour (Class I; Level of Evidence A). Patients eligible for intravenous r-tPA should receive intravenous r-tPA even if endovascular treatments are being considered (Class I; Level of Evidence A). In patients eligible for intravenous rtPA, benefit of therapy is time dependent, and treatment should be initiated as quickly as possible. The door-to-needle time (time of bolus administration) should be within 60 minutes from hospital arrival (Class I; Level of Evidence A). Intravenous rtPA (0.9 mg/kg, maximum dose 90 mg) is recommended for administration to eligible patients who can be treated in the time period of 3 to 4.5 hours after stroke onset (Class I; Level of Evidence B). Treatment (cont.)
  70. 70. Treatment Recommendations rTPA Intravenous rtPA is reasonable in patients whose blood pressure can be lowered safely (to below 185/110 mm Hg) with antihypertensive agents, with the physician assessing the stability of the blood pressure before starting intravenous rtPA (Class I; Level of Evidence B). In patients undergoing fibrinolytic therapy, physicians should be aware of and prepared to emergently treat potential side effects, including bleeding complications and angioedema that may cause partial airway obstruction (Class I; Level of Evidence B). Intravenous rtPA is reasonable in patients with a seizure at the time of onset of stroke if evidence suggests that residual impairments are secondary to stroke and not a postictal phenomenon (Class IIa; Level of Evidence C). Treatment (cont.)
  71. 71. Treatment Recommendations rTPA The usefulness of intravenous administration of tenecteplase, reteplase, desmoteplase, urokinase, or other fibrinolytic agents and the intravenous administration of ancrod or other defibrinogenating agents is not well established, and they should only be used in the setting of a clinical trial (Class IIb; Level of Evidence B). The intravenous administration of streptokinase for treatment of stroke is not recommended (Class III; Level of Evidence A). The use of intravenous rtPA in patients taking direct thrombin inhibitors or direct factor Xa inhibitors may be harmful and is not recommended unless sensitive laboratory tests such as aPTT, INR, platelet count, and TT, or appropriate direct factor Xa activity assays are normal, or the patient has not received a dose of these agents for >2 days (assuming normal renal metabolizing function). Similar consideration should be given to patients being considered for intra-arterial rtPA (Class III; Level of Evidence C). Treatment (cont.)
  72. 72. American Heart Association/American Stroke Association. Stroke. 2013;44:870–947. The effectiveness of intravenous treatment with rtPA is not well established (Class IIb; Level of Evidence C) and requires further study for patients who can be treated in the time period of 3 to 4.5 hours after stroke but have 1 or more of the following exclusion criteria: (1) patients >80 years old, (2) those taking oral anticoagulants, even with INR ≤1.7, (3) those with a baseline NIHSS score >25, or (4) those with a history of both stroke and diabetes mellitus.
  73. 73. Stroke. 2016;47:581-641.
  74. 74. J Stroke Cerebrovasc Dis. 2014;23:2130–2138. Survey of US stroke clinicians on their willingness to treat with recombinant tissue-type plasminogen activator (rtPA) in the setting of each individual rtPA exclusion criteria.
  75. 75. Stroke. 2016;47:581-641.
  76. 76. Stroke. 2016;47:581-641.
  77. 77. Stroke. 2016;47:581-641.
  78. 78. Treatment Recommendations Neuroprotective Agents The utility of induced hypothermia for the treatment of patients with ischemic stroke is not well established, and further trials are recommended (Class IIb; Level of Evidence B). At present, no pharmacological agents with putative neuroprotective actions have demonstrated efficacy in improving outcomes after ischemic stroke, and therefore, other neuroprotective agents are not recommended (Class III; Level of Evidence A) = NSF, 2010 guidelines Routine use of nutritional supplements has not been shown to be beneficial (Class III; Level of Evidence B). Anticoagulant s Guidelines: Guidelines issued in 2013 by the American Heart Association/American Stroke Association state that urgent anticoagulation is not recommended for the treatment of patients with acute ischemic stroke. Similarly, 2012 guidelines from the American College of Chest Physicians (ACCP) recommend early aspirin therapy over therapeutic parenteral anticoagulation for patients with acute ischemic stroke or transient ischemic attack (TIA). Treatment (cont.) Stroke. 2013;44:870-947. Chest 2012; 141:e601S National Stroke Foundation – Australia (2010)
  79. 79. Treatment Recommendations Anticoagulant s Guidelines: As well NSF, guideline in 2010 have discussed this point and clearly stated that: the routine use of early anticoagulation in unselected patients following ischaemic stroke/TIA is not recommended (A). Treatment (cont.) National Stroke Foundation – Australia (2010)
  80. 80. Anti Coagulation following Acute non hemorrhagic Stroke  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 (see later).  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. Thus, 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 (however this still a matter of debate), while withholding anticoagulation for two weeks is generally recommended for those with 1large infarctions, 2symptomatic hemorrhagic transformation, or 3poorly controlled hypertension.
  81. 81. Atrial fibrillation and cardioembolic stroke A subject of intense debate is the role of immediate anticoagulation with heparin in stroke patients with atrial fibrillation (AF). A 2007 meta-analysis examined seven trials involving 4624 patients and compared heparin or low molecular weight heparins started within 48 hours for acute cardioembolic stroke with other treatments (aspirin or placebo). The following observations were reported: ●Anticoagulants were associated with a statistically non significant reduction in recurrent ischemic stroke within 7 to 14 days (3.0 vs. 4.9 %, odds ratio [OR] 0.68, 95% CI 0.44-1.06) ●Anticoagulants were associated with a statistically significant increase in symptomatic intracranial hemorrhage (2.5 vs. 0.7 %, OR 2.89, 95% CI 1.19-7.01) ●Anticoagulants and other treatments had a similar rate of death or disability at final follow-up (≈ 74%) Thus, the results do not support early anticoagulant treatment of acute cardioembolic stroke Paciaroni M, et al. Stroke 38.2 (2007): 423-430.
  82. 82. A systematic review updated in 2015 examined the effect of anticoagulant therapy vs. control in the early treatment of patients with acute ischemic stroke. This review included 24 trials involving 23,748 subjects. The anticoagulants tested were standard unfractionated heparin, low molecular weight heparins, heparinoids, oral anticoagulants, and thrombin inhibitors. The following were the major findings: ●Based upon 11 trials (22,776 patients), anticoagulant therapy did not reduce the odds of death from all causes (odds ratio 1.05, 95% CI 0.98-1.12). ●Based upon eight trials (22,125 patients), anticoagulants did not reduce the odds of being dead or dependent at the end of follow-up (odds ratio 0.99, 95% CI 0.93- 1.04). ●Although full anticoagulant therapy was associated with about 9 fewer recurrent ischemic strokes per 1000 patients treated, it was also associated with a 9 per 1000 increase in symptomatic intracranial hemorrhages. Sandercock PA, Counsell C, Kane EJ. Anticoagulants for acute ischaemic stroke. Cochrane Database Syst Rev 2015; 3:CD000024. Anti Coagulation following Acute non hemorrhagic Stroke (con.)
  83. 83. Progressing stroke (Stroke in evolution) • Heparin was once widely used to treat patients who continued to have neurologic deterioration in the first hours or days after ischemic stroke. • However the guidelines stated that: Urgent anticoagulation, with the goal of preventing early recurrent stroke, halting neurological worsening, or improving outcomes after acute ischemic stroke, is not recommended for treatment of patients with acute ischemic stroke (Class III; Level of Evidence A). Also recommended by International stroke foundation, 2010 (A). • Urgent anticoagulation for the management of noncerebrovascular conditions is not recommended for patients with moderate-to-severe strokes because of an increased risk of serious intracranial hemorrhagic complications (Class III; Level of Evidence A). Stroke. 2013;44:870-947. National Stroke Foundation – Australia (2010)
  84. 84. Anti Platelets following Acute Stroke Recommendations NICE, 2008 All people presenting with acute stroke who have had a diagnosis of primary intracerebral haemorrhage excluded by brain imaging should, as soon as possible but certainly within 24 hours, be given (and continued for 2 weeks after onset of stroke): aspirin 300 mg orally if they are not dysphagic or aspirin 300 mg rectally or by enteral tube if they are dysphagic. People with disabling ischaemic stroke who are in atrial fibrillation should be treated with aspirin 300 mg for the first 2 weeks before considering anticoagulation treatment. National Stroke Foundation Guidelines, 2010  Aspirin orally or via a nasogastric tube or suppository (for those with dysphagia) should be given as soon as possible after the onset of stroke symptoms (i.e. within 48 hours) if Ct/MRI scans exclude haemorrhage. the first dose should be at least 150 to 300 mg. Dosage thereafter can be reduced (e.g. 100 mg daily).(A) National Institute for Health and Clinical Excellence (NICE) (2008): Stroke: Diagnosis and initial management of acute stroke and transient ischaemic attack (TIA) National Stroke Foundation – Australia (2010)
  85. 85. Anti Platelets following Acute Stroke Recommendations ACCP, 2012  In patients with acute ischemic stroke or transient ischemic attack (TIA), we recommend early (within 48 h) aspirin therapy at a dose of 160 to 325 mg over no aspirin therapy (Grade 1A).  In patients with acute ischemic stroke or TIA, we recommend early (within 48 h) aspirin therapy with an initial dose of 160 to 325 mg over therapeutic parenteral anticoagulation (Grade 1A).  In patients with a history of ischemic stroke or TIA and atrial fibrillation, including paroxysmal AF, who are unsuitable for or choose not to take an oral anticoagulant (for reasons other than concerns about major bleeding), we recommend combination therapy with aspirin and clopidogrel over aspirin (Grade 1B). Chest . 2012;141(2_suppl):e601S-e636S.
  86. 86. Anti Platelets following Acute Stroke Recommendations ASA/AHA, 2013  Oral administration of aspirin (initial dose is 325 mg) within 24 to 48 hours after stroke onset is recommended for treatment of most patients (Class I; Level of Evidence A).  The usefulness of clopidogrel for the treatment of acute ischemic stroke is not well established (Class IIb; Level of Evidence C).  The use of aspirin is reasonable for treatment of patients who cannot receive anticoagulants for prophylaxis of deep vein thrombosis (Class IIa; Level of Evidence A). The efficacy of intravenous tirofiban and eptifibatide is not well established, and these agents should be used only in the setting of clinical trials (Class Iib; Level of Evidence C). Aspirin is not recommended as a substitute for other acute interventions for treatment of stroke, including intravenous rtPA (Class III; Level of Evidence B). The administration of other intravenous antiplatelet agents that inhibit the glycoprotein IIb/IIIa receptor is not recommended (Class III; Level of Evidence B). Stroke. 2013;44:870-947.
  87. 87. The evidence…. Chinese Acute Stroke Trial (CAST)2International Stroke Trial (IST)1 21,100 patients19.435 patients with suspected acute ischemic stroke Patients allocated to aspirin (300 mg) within 48 hours of symptom onset 60 mg of aspirin daily or placebo, also within 48 hours of the onset of acute ischemic stroke Aspirin-allocated patients experienced a 14 percent reduction in total mortality at four weeks (3.3 versus 3.9 percent). significant reductions in the 14-day recurrence of ischemic stroke (2.8 versus 3.9 percent) and in the combined outcome of nonfatal stroke or death (11.3 versus 12.4 percent). IST and CAST trials3 The combined data demonstrated a reduction in mortality of 13 per 1000 patients after several weeks to six months of follow-up 1- Lancet 1997; 349:1569. 2- Lancet 1997; 349:1641. 3- Stroke 2000; 31:1240.
  88. 88. Stroke 2000; 31:1240.
  89. 89. What about Dual antiplatelet agents Circulation 2013; 128:1656.  A 2013 meta-analysis of early dual antiplatelet therapy versus monotherapy for patients with noncardioembolic acute ischemic stroke or TIA identified 14 trials with over 9000 adults.  Dual antiplatelet therapy significantly reduced risk of stroke recurrence (risk ratio, 0.69; 95% confidence interval, 0.60-0.80; P<0.001) and the composite outcome of stroke, TIA, acute coronary syndrome, and all death (risk ratio, 0.71; 95% confidence interval, 0.63-0.81; P<0.001) when compared with monotherapy, and non significantly increased risk of major bleeding (risk ratio, 1.35; 95% confidence interval, 0.70-2.59, P=0.37).
  90. 90. What about Dual antiplatelet agents  In another study published in 2016, analysis of a prospective multicenter stroke registry database from 14 hospitals in South Korea.  Study subjects were divided into 3 groups according to the subsequent antiplatelet therapy strategy pursued; maintaining aspirin monotherapy (MA group), switching aspirin to nonaspirin antiplatelet agents (SA group), and adding another antiplatelet agent to aspirin (AA group). The primary study end point was the composite of stroke (ischemic and hemorrhagic), myocardial infarction, and vascular death up to 1 year after stroke onset. Stroke. 2016;47:128-134.
  91. 91. What about Dual antiplatelet agents Stroke. 2016;47:128-134. Switching to or adding alternative antiplatelet agents could be associated with reduction in future vascular events than maintaining aspirin monotherapy
  92. 92. Treatment of Acute Neurological Complications Patients with major infarctions are at high risk for complicating brain edema and increased ICP. Measures to lessen the risk of edema and close monitoring of the patient for signs of neurological worsening during the first days after stroke are recommended (Class I; Level of Evidence A). Decompressive surgical evacuation of a space-occupying cerebellar infarction is effective in preventing and treating herniation and brain stem compression (Class I; Level of Evidence B). Decompressive surgery for malignant edema of the cerebral hemisphere is effective and potentially lifesaving (Class I; Level of Evidence B).
  93. 93. Treatment (cont.) Stroke. 2015;46:3020–3035.
  94. 94. Treatment (cont.) Endovascular Treatment Stroke. 2015;46:3020–3035. 1- Endovascular Treatment Patients should receive endovascular therapy with a stent retriever if they meet all the following criteria (Class I; Level of Evidence A): a. Prestroke mRS score 0 to 1 b. Acute ischemic stroke receiving intravenous r-tPA within 4.5 hours of onset according to guidelines from professional medical societies c. Causative occlusion of the ICA or proximal MCA (M1), d. Age ≥18 years, e. NIHSS score of ≥6, f. ASPECTS of ≥6, and g. Treatment can be initiated (groin puncture) within 6 hours of symptom onset.
  95. 95. Score Description 0 No symptoms at all 1 No significant disability despite symptoms; able to carry out all usual duties and activities 2 Slight disability; unable to carry out all previous activities, but able to look after own affairs without assistance 3 Moderate disability; requiring some help, but able to walk without assistance 4 Moderately severe disability; unable to walk without assistance and unable to attend to own bodily needs without assistance 5 Severe disability; bedridden, incontinent, and requiring constant nursing care and attention 6 Dead Modified Rankin scale: a commonly used scale for measuring the degree of disability or dependence in the daily activities of people who have suffered a stroke or other causes of neurological disability. Van Swieten JC, Koudstaa PJ, Visser MC, et al. Interobserver agreement for the assessment of handicap in stroke patients. Stroke 1988; 19:604. Modified Rankin scale
  96. 96. Areas caudate M1: "anterior MCA cortex," corresponding to frontal operculum putamen M2: "MCA cortex lateral to insular ribbon" corresponding to anterior temporal lobe internal capsule M3: "posterior MCA cortex" corresponding to posterior temporal lobe insular cortex M4: "anterior MCA territory immediately superior to M1” M5: "lateral MCA territory immediately superior to M2” M6: "posterior MCA territory immediately superior to M3” The Alberta stroke programe early CT score (ASPECTS) Lancet. 2000;355 (9216): 1670-4. Am J Neuroradiol. 2001;22 (8): 1534-42. ASPECTS It is a 10-point quantitative topographic CT scan score used in patients with middle cerebral artery (MCA) stroke. Segmental assessment of the MCA vascular territory is made and 1 point is deducted from the initial score of 10 for every region involved:
  97. 97. Case courtesy of Dr Subash Thapa, Radiopaedia.org, rID: 40018 ASPECTS (cont.)
  98. 98. Treatment (cont.) Stroke. 2015;46:3020–3035. 1- Endovascular Treatment (cont.) As with intravenous r-tPA, reduced time from symptom onset to reperfusion with endovascular therapies is highly associated with better clinical outcomes (Class I; Level of Evidence B). When treatment is initiated beyond 6 hours from symptom onset, the effectiveness of endovascular therapy is uncertain for patients with acute ischemic stroke who have causative occlusion of the ICA or proximal MCA (M1) (Class IIb; Level of Evidence C). Additional randomized trial data are needed. In carefully selected patients with anterior circulation occlusion who have contraindications to intravenous r-tPA, endovascular therapy with stent retrievers completed within 6 hours of stroke onset is reasonable (Class IIa; Level of Evidence C).
  99. 99. Treatment (cont.) Stroke. 2015;46:3020–3035. 1- Endovascular Treatment (cont.) Although its benefits are uncertain, the use of endovascular therapy with stent retrievers may be reasonable for patients with acute ischemic stroke in whom treatment can be initiated (groin puncture) within 6 hours of symptom onset and who have prestroke mRS score >1, ASPECTS <6, or NIHSS score <6 and causative occlusion of the ICA or proximal MCA (M1) (Class IIb; Level of Evidence B). Additional randomized trial data are needed. Use of stent retrievers is indicated in preference to the MERCI device. (Class I; Level of Evidence A).
  100. 100. Treatment (cont.) The idea….. The corkscrew Embolectomy
  101. 101. Treatment (cont.) Removal of the clot may be attempted in those where it occurs within a large blood vessel and may be an option for those who either are not eligible for or do not improve with intravenous thrombolytics. The Merci Retrieval System
  102. 102. Treatment (cont.) Allowing what is called giving the brain a drink!! Stent Retrievers: Solitaire® or Trevo ® systems
  103. 103. Treatment (cont.) Remember; Time = Brain
  104. 104. Treatment (cont.) Remember; Time = Brain
  105. 105. Treatment (cont.) Remember; Time = Brain
  106. 106. Treatment (cont.) Endovascular Treatment Stroke. 2015;46:3020–3035. 2- Imaging prior endovascular treatment The benefits of additional imaging beyond CT and CTA or MRI and MRA such as CT perfusion or diffusion- and perfusion-weighted imaging for selecting patients for endovascular therapy are unknown (Class IIb; Level of Evidence C).
  107. 107. Stroke. 2015;46:2032-2060.
  108. 108. Emergency Diagnosis and Assessment 1. A baseline severity score should be performed as part of the initial evaluation of patients with ICH (Class I; Level of Evidence B). 2. Rapid neuroimaging with CT or MRI is recommended to distinguish ischemic stroke from ICH (Class I; Level of Evidence A). 3. CTA and contrast-enhanced CT may be considered to help identify patients at risk for hematoma expansion (Class IIb; Level of Evidence B), and CTA, CT venography, contrast-enhanced CT, contrastenhanced MRI, magnetic resonance angiography and magnetic resonance venography, can be useful to evaluate for underlying structural lesions including vascular malformations and tumors when there is clinical or radiological suspicion (Class IIa; Level of Evidence B).
  109. 109. • Maximum score described is 5 in which % of mortality at 30 days is nearly 100%. • Although an ICH Score of 6 is possible with the scale, this is rarely observed and is considered highly likely to be fatal. ICH Score JC Hemphill et al: Stroke 32:891, 2001; JC Hemphill et al: Neurology 73:1088,2009.
  110. 110. Neuroimaging  CT is very sensitive for identifying acute hemorrhage and is considered the “gold standard”;  Gradient echo and T2* susceptibility-weighted MRI are as sensitive as CT for detection of acute hemorrhage and are more sensitive for identification of prior hemorrhage.  CT angiography (CTA) and contrast-enhanced CT may identify patients at high risk of ICH expansion based on the presence of contrast within the hematoma, often termed a spot sign. A larger number of contrast spots suggests even higher risk of expansion.  MRI, magnetic resonance angiography, magnetic resonance venography, and CTA or CT venography can identify specific causes of hemorrhage, including arteriovenous malformations, tumors, moyamoya, and cerebral vein thrombosis. Cerebrovasc Dis. 2013;35:582–589.
  111. 111. CT scans (without contrast enhancements): sensitivity= 89%specificity= 100% MRI scan: sensitivity= 83%specificity= 98% CT imaging is also sensitive for detecting SAH (although by itself does not rule it out), and CTA can readily identify intracranial aneurysms. On CT brain, hemorrhage appears as hyperdense region, i.e. more white Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org, rID: 10598
  112. 112. Investigations (cont.)
  113. 113. The CT angiographic (CTA) spot sign is defined as unifocal or multifocal contrast enhancement within an acute primary intracerebral haemorrhage (ICH) visible on CTA source images and discontinuous from adjacent normal or abnormal blood vessels . It should not be present on pre-contrast images. It corresponds to a site of active, dynamic haemorrhage and is an independent predictor of ICH growth and poor outcome The CT angiographic (CTA) spot sign Lancet Neurol. 2012;11 (4): 307-14.
  114. 114. Localization CerebellarPontineBasal ganglia 10%10%80%
  115. 115. Remember
  116. 116. Remember
  117. 117. Investigations (cont.)
  118. 118. Investigations (cont.) Modified Fisher scale on CT brain (predict risk of vasospasm): Risk of vasospasmIVHSAH 24%-No or minimalGrade I 33%+MinimalGrade II 33%-Diffuse focal or thickGrade III 40%+Diffuse focal or thickGrade IV Frontera, Jennifer A., et al. "Prediction of Symptomatic Vasospasmafter Subarachnoid Hemorrhage: the Modified Fisher Scale." Neurosurgery 59.1 (2006): 21-27.
  119. 119. Fisher, CM, Kistler, JP, Davis, JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by CT scanning. Neurosurgery 1980; 6:1. Frontera, Jennifer A., et al. "Prediction of Symptomatic Vasospasmafter Subarachnoid Hemorrhage: the Modified Fisher Scale." Neurosurgery 59.1 (2006): 21-27.
  120. 120. Ageing blood on MRI The imaging characteristics of blood on MRI are variable and change with the age of the blood. In general, five stages of haematoma evolution are recognised: isointense on T1 isointense to hyperintense on T2 1- Hyperacute T2 signal intensity drops (T2 shortening) T1 remains intermediate-to-long 2- Acute (1-2 days) T1 signal gradually increases (T1 shortening) to become hyperintense 3- Early subacute (2-7days) increase in T2 signal4- Late subacute (7-14days) low on both T1 and T25- Chronic (>14-28 days)
  121. 121. Exapmple to Subacute ICH in MRI
  122. 122. Hemostasis and Coagulopathy, Antiplatelet Agents, and DVT Prophylaxis 1. Patients with a severe coagulation factor deficiency or severe thrombocytopenia should receive appropriate factor replacement therapy or platelets, respectively (Class I; Level of Evidence C). 2. Patients with ICH whose INR is elevated because of VKA should have their VKA withheld, receive therapy to replace vitamin K–dependent factors and correct the INR, and receive intravenous vitamin K (Class I; Level of Evidence C). PCCs may have fewer complications and correct the INR more rapidly than FFP and might be considered over FFP (Class IIb; Level of Evidence B). rFVIIa does not replace all clotting factors, and although the INR may be lowered, clotting may not be restored in vivo; therefore, rFVIIa is not recommended for VKA reversal in ICH (Class III; Level of Evidence C).
  123. 123. Hemostasis and Coagulopathy, Antiplatelet Agents, and DVT Prophylaxis 3. For patients with ICH who are taking dabigatran, rivaroxaban, or apixaban, treatment with FEIBA, other PCCs, or rFVIIa might be considered on an individual basis. Activated charcoal might be used if the most recent dose of dabigatran, apixaban, or rivaroxaban was taken <2 hours earlier. Hemodialysis might be considered for dabigatran (Class IIb; Level of Evidence C). 4. Protamine sulfate may be considered to reverse heparin in patients with acute ICH (Class IIb; Level of Evidence C). 5. The usefulness of platelet transfusions in ICH patients with a history of antiplatelet use is uncertain (Class IIb; Level of Evidence C). 6. Although rFVIIa can limit the extent of hematoma expansion in noncoagulopathic ICH patients, there is an increase in thromboembolic risk with rFVIIa and no clear clinical benefit in unselected patients. Thus, rFVIIa is not recommended (Class III; Level of Evidence A). It was also not recommended by ESO, 2010 Stroke. 2015; 46: 3020-3035 International journal of stroke 9.7 (2014): 840-855.
  124. 124. Hemostasis and Coagulopathy, Antiplatelet Agents, and DVT Prophylaxis 7. Patients with ICH should have intermittent pneumatic compression for prevention of venous thromboembolism beginning the day of hospital admission (Class I; Level of Evidence A). Graduated compression stockings are not beneficial to reduce DVT or improve outcome (Class III; Level of Evidence A). 8. After documentation of cessation of bleeding, low dose subcutaneous low- molecular-weight heparin or unfractionated heparin may be considered for prevention of venous thromboembolism in patients with lack of mobility after 1 to 4 days from onset (Class IIb; Level of Evidence B). 9. Systemic anticoagulation or IVC filter placement is probably indicated in ICH patients with symptomatic DVT or PE (Class IIa; Level of Evidence C). The decision between these 2 options should take into account several factors, including time from hemorrhage onset, hematoma stability, cause of hemorrhage, and overall patient condition (Class IIa; Level of Evidence C).
  125. 125. Hemostasis and Coagulopathy, Antiplatelet Agents, and DVT Prophylaxis
  126. 126. Hypertension in acute stroke a management dilemma Hemorrhagic stroke The conflict1 : (1) Severe elevations in BP may worsen ICH. (2) Enlargement of the hematoma is associated with neurologic deterioration and worse outcomes. These observations indicate that significant improvements in patient outcome from ICH can be achieved by minimizing hematoma enlargement. 1- Stroke 2007; 38:1072–1075.
  127. 127. Hypertension in acute stroke a management dilemma (cont.) The guidelines: For ICH patients presenting with SBP between 150 and 220 mm Hg and without contraindication to acute BP treatment, acute lowering of SBP to 140 mm Hg is safe (Class I; Level of Evidence A) and can be effective for improving functional outcome (Class IIa; Level of Evidence B). For ICH patients presenting with SBP >220 mmHg, it may be reasonable to consider aggressive reduction of BP with a continuous intravenous infusion and frequent BP monitoring (Class IIb; Level of Evidence C). This is also supported by European Stroke Organisation (ESO) guidelines in 2014 who recommends In acute ICH within 6 h of onset, intensive blood pressure reduction (systolic target <140 mmHg in <1 h) is safe and may be superior to a systolic target <180 mmHg. No specific agent can be recommended. Stroke. 2015; 46: 3020-3035 International journal of stroke 9.7 (2014): 840-855.
  128. 128. Hypertension in acute stroke a management dilemma (cont.) Studies have been carried out in that respect: (1) In a randomized controlled trial [INTensive Blood Pressure Reduction in Acute Cerebral Hemorrhage trial (INTERACT1)]1 on 404 patients with acute spontaneous ICH, intensive BP lowering treatment (target SBP 140 mmHg), compared with traditional management (target SBP 180 mmHg), was associated with a reduction in hematoma growth at 24 h (14 vs. 26%). The study showed that SBP greater than 140–150 mmHg within 12 h of ICH is associated with more than double the risk of subsequent death or dependency. Most recently, the main phase [(INTERACT2)]2 trial has shown no increase in death or serious adverse events from early intensive BP lowering in eligible patients with elevated SBP.1 (2) The Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH) trial further confirmed these findings.3 1- Stroke. 2012;43:2236–2238. 2- N Engl J Med. 2013;368:2355–2365. 3- Neurocrit Care 2007; 6:56–66.
  129. 129. Louis Pasteur French chemist and microbiologist Famous People Who Died of Stroke http://www.ranker.com/list/famous-people-who-died-of-stroke/reference
  130. 130. Treatment (cont.) Factors Recommendation General Monitoring and Nursing Initial monitoring and management of ICH patients should take place in an intensive care unit or dedicated stroke unit with physician and nursing neuroscience acute care expertise (Class I; Level of Evidence B). Airway &Breathing Supplemental oxygen should be provided to maintain oxygen saturation >94% (Class I; Level of Evidence C). Supplemental oxygen is not recommended in nonhypoxic patients with acute ischemic stroke (Class III; Level of Evidence B). Mobilization Early mobilization of less severely affected patients and measures to prevent subacute complications of stroke are recommended (Class I; Level of Evidence C). Nutrition A formal screening procedure for dysphagia should be performed in all patients before the initiation of oral intake to reduce the risk of pneumonia (Class I; Level of Evidence B). Insert a nasogastric tube if the patient fails the swallow test. Consider PEG only if prolonged enteral feeding is required (Class I; Level of Evidence B). Stroke. 2015; 46: 3020-3035
  131. 131. Infection and fever Treatment of fever after ICH may be reasonable (Class IIb; Level of Evidence C). Sources of hyperthermia (temperature >38°C) should be identified and treated, and antipyretic medications should be administered to lower temperature in hyperthermic patients with stroke (Class I; Level of Evidence C). Routine use of prophylactic antibiotics has not been shown to be beneficial (Class III; Level of Evidence B). Patients with suspected pneumonia or urinary tract infections should be treated with appropriate antibiotics (Class I; Level of Evidence A). Seizures Clinical as well as EEG documented seizures should be treated with antiseizure drugs (Class I; Level of Evidence A). Prophylactic antiseizure medication is not recommended (Class III; Level of Evidence B). Blood Glucose Glucose should be monitored. Both hyperglycemia and hypoglycemia should be avoided (Class I; Level of Evidence C). Treatment (cont.)
  132. 132. Prolonged recumbency As regard ICH, After documentation of cessation of bleeding, lowdose subcutaneous low-molecular-weight heparin or unfractionated heparin may be considered for prevention of venous thromboembolism in patients with lack of mobility after 1 to 4 days from onset (Class IIb; Level of Evidence B). Patients with ICH should have intermittent pneumatic compression for prevention of venous thromboembolism beginning the day of hospital admission (Class I; Level of Evidence A). Brain dehydratin measures Corticosteroids should not be administered for treatment of elevated ICP in ICH (Class III; Level of Evidence B). In agreement with International stroke foundation guidelines, 2010 (A) Treatment (cont.) National Stroke Foundation – Australia (2010)
  133. 133. Prevention of Recurrent ICH 1. BP should be controlled in all ICH patients (Class I; Level of Evidence A). Measures to control BP should begin immediately after ICH onset (Class I; Level of Evidence A). A long-term goal of BP <130 mmHg systolic and 80 mmHg diastolic is reasonable (Class IIa; Level of Evidence B). 2. Lifestyle modifications, including avoidance of alcohol use greater than 2 drinks per day, tobacco use, and illicit drug use, as well as treatment of obstructive sleep apnea, are probably beneficial (Class IIa; Level of Evidence B). 3. Avoidance of long-term anticoagulation with warfarin as a treatment for nonvalvular atrial fibrillation is probably recommended after warfarin- associated spontaneous lobar ICH because of the relatively high risk of recurrence (Class IIa; Level of Evidence B).
  134. 134. Prevention of Recurrent ICH 4. The optimal timing to resume oral anticoagulation after anticoagulant- related ICH is uncertain. Avoidance of oral anticoagulation for at least 4 weeks, in patients without mechanical heart valves, might decrease the risk of ICH recurrence (Class IIb; Level of Evidence B). If indicated, aspirin monotherapy can probably be restarted in the days after ICH, although the optimal timing is uncertain (Class IIa; Level of Evidence B). 5. The usefulness of dabigatran, rivaroxaban, or apixaban in patients with atrial fibrillation and past ICH to decrease the risk of recurrence is uncertain (Class IIb; Level of Evidence C). 6. There are insufficient data to recommend restrictions on the use of statins in ICH patients (Class IIb; Level of Evidence C).
  135. 135. Statins and ICH There are conflicting reports regarding the use of statins in patients with ICH. Stroke Prevention With Aggressive Reduction in Cholesterol Levels (SPARCL) study, the benefit of high-dose atorvastatin in reducing recurrent ischemic stroke was offset in part by an increased risk of ICH. However it was non significant. Also a study in 2012 over 163 patients with ICH 40 was on statin treatment, published in Stroke journal concluded that Statin use in patients with ICH is independently associated with microbleeds However another metanalysis in 2013, studied 31 randomized controlled trials that included 91 588 statin-treated patients found no significant association between statin use and ICH (OR, 1.08; 95% CI, 0.88–1.32; P=0.47). It remains unclear whether statins should be continued or discontinued in ICH patients. Stroke. 2012;43:2677-2681 Neurology. 2008;70(24 Pt 2):2364–2370. Stroke.2012;43:2149–2156.
  136. 136. By the year 2000 the commonest killers such as coronary heart disease, stroke, respiratory, diseases and many cancers will be wiped out. Anonymous Irish Times (24 Apr 1987)
  137. 137. Stroke. 2014;45:3754-3832
  138. 138. 1- Primary Prevention FACTORS RECOMMENDATION Physical activity Physical activity is recommended because it is associated with a reduction in the risk of stroke (Class I; Level of Evidence B). Diet Reduced intake of sodium and increased intake of potassium as indicated in the US Dietary Guidelines for Americans are recommended to lower BP (Class I; Level of Evidence A). A DASH-style diet, which emphasizes fruits, vegetables, and low-fat dairy products and reduced saturated fat, is recommended to lower BP127,218 (Class I; Level of Evidence A). Hypertension Annual screening for high BP and health-promoting lifestyle modification are recommended for patients with prehypertension (SBP of 120 to 139 mmHg or DBP of 80 to 89 mmHg) (Class I; Level of Evidence A). Patients who have hypertension should be treated with antihypertensive drugs to a target BP of <140/90 mm Hg (Class I; Level of Evidence A). Stroke. 2014;45:3754–3832.
  139. 139. 1- Primary Prevention (cont.) FACTORS RECOMMENDATION Dyslipidemia In addition to therapeutic lifestyle changes, treatment with an HMG coenzyme-A reductase inhibitor (statin) medication is recommended for the primary prevention of ischemic stroke in patients estimated to have a high 10-year risk for cardiovascular events as recommended (Class I; Level of Evidence A). Obesity Among overweight (BMI=25 to 29 kg/m2) and obese (BMI >30 kg/m2) individuals, weight reduction is recommended for lowering BP and reducing the risk of stroke (Class I; Level of Evidence A). Diabetes mellitus Control of BP in accordance with guidelines to a target of <140/90 mm Hg is recommended in patients with type 1 or type 2 diabetes mellitus (Class I; Level of Evidence A). Treatment of adults with diabetes mellitus with a statin, especially those with additional risk factors, is recommended to lower the risk of first stroke (Class I; Level of Evidence A). Smoking Cessation of smoking. Stroke. 2014;45:3754–3832.
  140. 140. 1- Primary Prevention (cont.) FACTORS RECOMMENDATION AF For patients with valvular AF at high risk for stroke, defined as a CHA 2DS2-VASc score of ≥2 and acceptably low risk for hemorrhagic complications, long-term oral anticoagulant therapy with warfarin at a target INR of 2.0 to 3.0 is recommended (Class I; Level of Evidence A). For patients with nonvalvular AF, a CHA2DS2-VASc score of ≥2, and acceptably low risk for hemorrhagic complications, oral anticoagulants are recommended (Class I). Options include warfarin (INR, 2.0 to 3.0) (Level of Evidence A), dabigatran (Level of Evidence B), apixaban (Level of Evidence B), and rivaroxaban (Level of Evidence B). Alcohol Reduction or elimination of alcohol consumption in heavy drinkers (Class I; Level of Evidence A). Prophylactic aspirin ! Aspirin is not useful for preventing a first stroke in lowrisk individuals (Class III; Level of Evidence A).  Aspirin is not useful for preventing a first stroke in people with diabetes mellitus in the absence of other highrisk conditions (Class III; Level of Evidence A). Stroke. 2014;45:3754–3832.
  141. 141. Primary Prevention (cont.) CHADS2 and CHA2DS2 VASc
  142. 142. Primary Prevention (cont.) CHADS2 and CHA2DS2 VASc
  143. 143. Primary Prevention (cont.) CHADS2 and CHA2DS2 VASc
  144. 144. Primary Prevention (cont.) HAS BLED score HAS-BLED categorizes those into low (score 0-2) or high (≥3) risk, where the latter can be identified for more regular review and follow-up.
  145. 145. Primary Prevention (cont.) SAMe-TT2R2 Score b= Two of the following: hypertension, diabetes mellitus, coronary artery disease or myocardial infarctions, peripheral artery disease, congestive heart failure, previous stroke, pulmonary disease, or hepatic or renal disease.
  146. 146. Primary Prevention (cont.) SAMe-TT2R2 Score  The SAMe-TT2R2 score is proposed as a means to help with decision making, to identify those newly diagnosed nonanticoagulated AF patients who have a probability of doing well while taking a vitamin K antagonist (VKA) (with SAMe- TT 2R2 score, 0-2) and achieve a time in therapeutic range (TTR) of at least 65% or 70%.  In contrast, a SAMe-TT2R2 score of more than 2 suggests that such patients are unlikely to achieve a good TTR while taking a VKA, and a non-VKA oral anticoagulant should be used upfront, without a “trial of warfarin” period.
  147. 147. Primary Prevention (cont.) Jacobson et al. Journal of Clinical Lipidology (2014) 8, 473–488
  148. 148. SPRINT trial The SPRINT Research Group N Engl J Med 2015; 373:2103-2116 9361 persons was randomly assigned were at least 50 years old with a systolic blood pressure of 130 mm Hg or higher (180 mmHg) and an increased cardiovascular risk, but without diabetes, to a systolic blood- pressure target of less than 120 mm Hg (intensive treatment) or a target of less than 140 mm Hg (standard treatment).
  149. 149. SPRINT trial (cont.) The SPRINT Research Group N Engl J Med 2015; 373:2103-2116 All participants had at least 1 other significant cardiovascular risk factor, including chronic kidney disease; age 75 years or older; a previous cardiovascular event (except stroke); or an elevated cardiovascular risk based on their Framingham risk score.
  150. 150. SPRINT trial (cont.) The SPRINT Research Group N Engl J Med 2015; 373:2103-2116 The primary composite outcome was myocardial infarction, other acute coronary syndromes, stroke, heart failure, or death from cardiovascular causes. (Funded by the National Institutes of Health; ClinicalTrials.gov
  151. 151. The mean baseline blood pressure among all participants was 139.7/78.1 mm Hg. Mean blood pressure values at 1 year into the study were 121.4/68.7 mm Hg in the intensive treatment group and 136.2/76.3 mm Hg in the standard treatment group. 1- ClinicalTrials.gov. Systolic Blood Pressure Intervention Trial (SPRINT). https://clinicaltrials.gov/ct2/show/NCT01206062?term=Systolic+Blood+Pressure+Intervention+Trial&rank=1. Accessed November 9, 2015.
  152. 152. The intervention was stopped early after a median follow-up of 3.26 years in stead of December 2018 which was the Estimated Study Completion Date1 1- ClinicalTrials.gov. Systolic Blood Pressure Intervention Trial (SPRINT). https://clinicaltrials.gov/ct2/show/NCT01206062?term=Systolic+Blood+Pressure+Intervention+Trial&rank=1. Accessed November 9, 2015.
  153. 153. SPRINT trial (cont.)
  154. 154. SPRINT trial (cont.) The SPRINT Research Group N Engl J Med 2015; 373:2103-2116  The lower target group of less than 120 mm Hg systolic blood pressure had a 25% lower relative risk for the primary composite end point of myocardial infarction, acute coronary syndrome, stroke, acute decompensated heart failure, and cardiovascular death vs the group with a target of less than 140 mm Hg.
  155. 155. SPRINT trial (cont.) The SPRINT Research Group N Engl J Med 2015; 373:2103-2116  In addition, the lower-target group had 27% lower risk for all-cause mortality and 43% lower risk for cardiovascular death. However, this group also had higher adverse events such as hypotension, syncope, and acute kidney injury or kidney failure.
  156. 156. SPRINT trial (cont.) The SPRINT Research Group N Engl J Med 2015; 373:2103-2116 Rates of serious adverse events of hypotension, syncope, electrolyte abnormalities, and acute kidney injury or failure, but not of injurious falls, were higher in the intensive-treatment group than in the standard-treatment group.
  157. 157. SPRINT trial (cont.) The SPRINT Research Group N Engl J Med 2015; 373:2103-2116 CONCLUSIONS Among patients at high risk for cardiovascular events but without diabetes, targeting a systolic blood pressure of less than 120 mm Hg, as compared with less than 140 mm Hg, resulted in lower rates of fatal and nonfatal major cardiovascular events and death from any cause, although significantly higher rates of some adverse events were observed in the intensive-treatment group.
  158. 158. SPRINT trial (cont.) Dr Marc Pfeffer (Harvard Medical School, Boston, MA) CAUTIONS AS REGARD STUDY A lot of effort is required to hit this target, including initial combination therapy and frequent office visits “marathon effort”. Excluding diabetics is "a black hole" in the study and limits its applicability. Only approximately half of adults achieve a blood pressure of 140 mm Hg or less, as consistent with current recommendations. “Physicians "shouldn't expect a 'thank you' from patients when you add another pill to reduce their blood pressure.“1
  159. 159. Alfred Nobel Swedish chemist, engineer, innovator, and armaments manufacturer. He was the inventor of dynamite. Famous People Who Died of Stroke http://www.ranker.com/list/famous-people-who-died-of-stroke/reference
  160. 160. Stroke. 2014;45:2160-2236.
  161. 161. 3- Secondary Prevention The major treatable atherosclerotic risk factors for stroke are the following: ●Hypertension ●Diabetes mellitus ●Smoking ●Dyslipidemia Factors Treatment Recommendations Hypertension Initiation of BP therapy is indicated for previously untreated patients with ischemic stroke or TIA who, after the first several days, have an established BP ≥140 mm Hg systolic or ≥90 mm Hg diastolic (Class I; Level of Evidence B). Resumption of BP therapy is indicated for previously treated patients with known hypertension for both prevention of recurrent stroke and prevention of other vascular events in those who have had an ischemic stroke or TIA and are beyond the first several days (Class I; Level of Evidence A). ASA/AHA. Stroke. 2014; 45: 2160-2236
  162. 162. 3- Secondary Prevention (cont.) Factors Treatment Recommendations Hypertension (cont.) Goals for target BP level or reduction from pretreatment baseline are uncertain and should be individualized, but it is reasonable to achieve a systolic pressure <140 mm Hg and a diastolic pressure <90 mm Hg (Class IIa; Level of Evidence B). For patients with a recent lacunar stroke, it might be reasonable to target a systolic BP of <130 mm Hg (Class IIb; Level of Evidence B). Glucose disorders After a TIA or ischemic stroke, all patients should probably be screened for DM with testing of fasting plasma glucose, HbA1c, or an oral glucose tolerance test. (Class IIa; Level of Evidence C). Use of existing guidelines from the ADA for glycemic control and cardiovascular risk factor management is recommended for patients with an ischemic stroke or TIA who also have DM or pre- DM (Class I; Level of Evidence B).
  163. 163. 3- Secondary Prevention (cont.) Factors Treatment Recommendations Dyslipidemia Statin therapy with intensive lipid-lowering effects is recommended to reduce risk of stroke and cardiovascular events among patients with ischemic stroke or TIA presumed to be of atherosclerotic origin and an LDL-C level ≥100 mg/dL with or without evidence for other ASCVD (Class I; Level of Evidence B). Statin therapy with intensive lipid-lowering effects is recommended to reduce risk of stroke and cardiovascular events among patients with ischemic stroke or TIA presumed to be of atherosclerotic origin, an LDL-C level <100 mg/dL, and no evidence for other clinical ASCVD (Class I; Level of Evidence C). Obesity All patients with TIA or stroke should be screened for obesity with measurement of BMI (Class I; Level of Evidence C). Smoking Healthcare providers should strongly advise every patient with stroke or TIA who has smoked in the past year to quit (Class I; Level of Evidence C). It is reasonable to advise patients after TIA or ischemic stroke to avoid environmental (passive) tobacco smoke (Class IIa; Level of Evidence B).
  164. 164. 3- Secondary Prevention (cont.) Factors Treatment Recommendations Intracranial atherosclero sis For patients with recent stroke or TIA (within 30 days) attributable to severe stenosis (70%–99%) of a major intracranial artery, the addition of clopidogrel 75 mg/d to aspirin for 90 days might be reasonable(Class IIb; Level of Evidence B). For patients with a stroke or TIA attributable to 50% to 99% stenosis of a major intracranial artery, maintenance of systolic BP below 140 mm Hg and high-intensity statin therapy are recommended(Class I; Level of Evidence B). AF For patients who have experienced an acute ischemic stroke or TIA with no other apparent cause, prolonged rhythm monitoring (≈30 days) for AF is reasonable within 6 months of the index event (Class IIa; Level of Evidence C). VKA therapy (Class I; Level of Evidence A), apixaban (Class I; Level of Evidence A), and dabigatran (Class I; Level of Evidence B) are all indicated for the prevention of recurrent stroke in patients with nonvalvular AF, whether paroxysmal or permanent.
  165. 165. 3- Secondary Prevention (cont.) Factors Treatment Recommendations AF (cont.) Rivaroxaban is reasonable for the prevention of recurrent stroke in patients with nonvalvular AF (Class IIa; Level of Evidence B). For patients with ischemic stroke or TIA and AF who are unable to take oral anticoagulants, aspirin alone is recommended (Class I; Level of Evidence A). The addition of clopidogrel to aspirin therapy, compared with aspirin therapy alone, might be reasonable (Class IIb; Level of Evidence B). For most patients with a stroke or TIA in the setting of AF, it is reasonable to initiate oral anticoagulation within 14 days after the onset of neurological symptoms (Class IIa; Level of Evidence B). In the presence of high risk for hemorrhagic conversion (ie, large infarct, hemorrhagic transformation on initial imaging, uncontrolled hypertension, or hemorrhage tendency), it is reasonable to delay initiation of oral anticoagulation beyond 14 days (Class IIa; Level of Evidence B).
  166. 166. 3- Secondary Prevention (cont.) Factors Treatment Recommendations Extracranial astheroscler osis For patients with a TIA or ischemic stroke within the past 6 months and ipsilateral severe (70%–99%) carotid artery stenosis as documented by noninvasive imaging, carotid endartrectomy (CEA) is recommended if the perioperative morbidity and mortality risk is estimated to be <6% (Class I; Level of Evidence A). For patients with recent TIA or ischemic stroke and ipsilateral moderate (50%–69%) carotid stenosis as documented by catheter-based imaging or noninvasive imaging with corroboration (eg, magnetic resonance angiogram or computed tomography angiogram), CEA is recommended depending on patient-specific factors, such as age, sex, and comorbidities (Class I; Level of Evidence B). When the degree of stenosis is <50%, CEA and CAS are not recommended (Class III; Level of Evidence A). Optimal medical therapy, which should include antiplatelet therapy, statin therapy, and risk factor modification, is recommended for all patients with carotid artery stenosis(Class I; Level of Evidence A).
  167. 167. 3- Secondary Prevention (cont.) Factors Treatment Recommendations Antiplatelet For patients with noncardioembolic ischemic stroke or TIA, the use of antiplatelet agents rather than oral anticoagulation is recommended to reduce the risk of recurrent stroke and other cardiovascular events (Class I; Level of Evidence A). Aspirin (50–325 mg/d) monotherapy (Class I; Level of Evidence A) or the combination of aspirin 25 mg and extended-release dipyridamole 200 mg twice daily (Class I; Level of Evidence B) is indicated as initial therapy after TIA or ischemic stroke for prevention of future stroke. Clopidogrel (75 mg) monotherapy is a reasonable option for secondary prevention of stroke in place of aspirin or combination aspirin/dipyridamole (Class IIa; Level of Evidence B). The combination of aspirin and clopidogrel might be considered for initiation within 24 hours of a minor ischemic stroke or TIA and for continuation for 21 days (Class IIb; Level of Evidence B).
  168. 168. 3- Secondary Prevention (cont.) Factors Treatment Recommendations Antiplatelet The combination of aspirin and clopidogrel, when initiated days to years after a minor stroke or TIA and continued for 2 to 3 years, increases the risk of hemorrhage relative to either agent alone and is not recommended for routine long-term secondary prevention after ischemic stroke or TIA (Class III; Level of Evidence A). For patients with noncardioembolic ischemic stroke or TIA, the use of antiplatelet agents rather than oral anticoagulation is recommended to reduce the risk of recurrent stroke and other cardiovascular events (Class I; Level of Evidence A).
  169. 169. 3- Secondary Prevention (cont.) Factors Treatment National Stroke Foundation Guidelines, 2010 Antiplatelet (cont.) Long-term antiplatelet therapy should be prescribed to all people with ischaemic stroke or TIA who are not prescribed anticoagulation therapy (A). Low-dose aspirin and modified release dipyridamole or clopidogrel alone should be prescribed to all people with ischaemic stroke or TIA, taking into consideration patient co-morbidities (A) Aspirin alone can be used, particularly in people who do not tolerate aspirin plus dipyridamole or clopidogrel (A). The combination of aspirin plus clopidogrel is not recommended for the secondary prevention of cerebrovascular disease in people who do not have acute coronary disease or recent coronary stent (A). National Stroke Foundation – Australia (2010)
  170. 170. Treatment (cont.) Known Factors That Cause Stroke Progression • Hypotension • Hyperglycemia • Hyperthermia • Infection • Cerebral hypoperfusion These factors affect penumbra………………
  171. 171. ACS vs. Stroke The success of thrombolytic therapy in coronary occlusive syndromes created high expectations for thrombolytic therapy in acute, ischemic stroke, and these expectations prompted a massive effort to create “stroke centers” in major hospitals, each with a “stroke team” to direct the management of acute stroke. The following is an accounting of what this effort has accomplished: Number of strokes each year in the United States 700,0001 Number of ischemic strokes (88% ) 616,000 Number of stroke patients who receive lytic therapy (2%) 12,320 Number of patients who benefit from lytic therapy (1 in 9) 1,369 % of strokes that benefit from lytic therapy (1369/700,000) 0.2% True Story…. 1- Mozzafarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics—2015 update: a report from the American Heart Association.Circulation. 2015:e29–322.
  172. 172. Overall Bottom Line Remember • “Time is brain” • Stroke awareness: health care team, info for everyone • Common mistakes may lead to fatal consequences • “There is no Stroke Motel”: Patients will receive best care; if length of stay shortened
  173. 173. Don’t forget rehabilitation
  174. 174. Yasser Arafat Palestinian leader Died on 11 November 2004 at the age of 75 of what French doctors called a massive hemorrhagic cerebrovascular accident (hemorrhagic stroke). Famous People Who Died of Stroke http://www.ranker.com/list/famous-people-who-died-of-stroke/reference
  175. 175. Thanks TIME = LIFE

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