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  • The anterior circulation of the brain supplies the retinas and the cerebral hemispheres through the internal carotid artery and its branches: the ophthalmic and the anterior and middle cerebral arteries. Temporary monocular blindness, termed “amaurosisfugax,” is one classic manifestation caused by occlusion of the ophthalmic branch of the internal carotid artery, causing retinal ischemia[21]; patients may complain of “the shade being drawn down” or vision blurred by a “fog” or “mist.” Monoparesis and numbness of the leg are consistent with ischemia to the anterior cerebral artery. Middle cerebral artery ischemia classically causes hemiparesis (most prominent in the face and arm), aphasia (expressive or receptive), or homonymous hemianopsia (from ischemia of the anterior visual pathways between the midbrain and optic chiasm). Occasionally, language difficulties and cognitive or behavioral changes may be present as well.Vertebrobasilar artery ischemia is an entirely different symptom complex, caused by ischemia of the posterior circulation supplying the brain stem, cerebellum, and occipital lobes through the posterior cerebral artery, the basilar and vertebral arteries, and their branches. Vertigo, ataxia, nausea, and vomiting are the most common symptoms. Dysarthria, dysphagia, and diplopia caused by disconjugate gaze, hemiparesis, and hemisensory loss may also occur in posterior circulation ischemia. Because so many long tracts and cranial nerve nuclei are so closely positioned in the brain stem, it is distinctly unusual for any of these symptoms to occur in isolation.Ischemia of the deep circulation of the brain results in “lacunes” or subcortical events. Patients will often present with pure motor or sensory deficits. The classic motor loss is unilateral, equal-intensity weakness in the face, arm, and leg; other presentations include ataxic hemiparesis and dysarthria–clumsy hand syndrome.[22] These patients usually lack “cortical” findings such as aphasia, problems with spatial relationships, and neglect.
  • The anterior circulation consists of the internalcarotid arteries, the middle cerebral arteries, the anterior cerebraarteries, and their tributaries. It receives 80% of the cerebralblood flow and accounts for 80% of transient ischemic attacksThe presence of sensory or motor symptoms withaphasia or neglect suggests cortical involvement and strokes.Limb-shaking transient ischemic attack is an unusual form ofanterior circulation transient ischemic attack and is a harbinger ofcarotid occlusive disease and lacunar strokes.29 It is thought to beprecipitated by anterior cerebral artery ischemia. The presentationusually is a brief, involuntary, coarse, irregular, wavering movementor tremor involving arm-hand alone, or arm-hand and leg together,and can mimic focal seizures.Amaurosisfugaxcan manifest in a variety of ways aside from the classic“curtainlike” visual loss. These alternate manifestations includeclouding, graying, or darkening of vision. A horizontal visualfield defect suggests segmental embolization to the superiorbranch of the retinal artery (with an inferior defect) or theinferior branch (with a superior defect). With critical internalcarotid artery stenosis or occlusion, the patient may report lossof vision in the ipsilateral eye after exposure to bright light (eg,looking outside on a sunny day). This phenomenon is known asزlight-induced amaurosis
  • The posterior circulation receives 20% of the cerebral bloodflow, and 20% of transient ischemic attack or strokes occur inthese vertebrobasilar territories. Cranial nerve findings, ataxia, headache, andcrossed findings (ie, face involvement on one side, with arm andleg involvement on the opposite side) suggest vertebrobasilardisease.thesevertebrobasilar territories.25-27
  • A thorough history of the event and previous episodes may suggest other diagnoses, such as multiple sclerosis, complicated migraine, Meniere's disease, and syncope. See Figure 4 for the common differential diagnostic competitors. Multiple sclerosis is characterized by different neurologic manifestations at different times, and the symptoms last longer than the typical transient ischemic attack. Although difficult to distinguish from transient ischemic attack, complicated migraines will occasionally have a preceding aura or scintillating scotomas associated with the neurologic deficit. [19] It is generally accepted that isolated vertigo is rarely a manifestation of transient ischemic attack [19]; however, this premise may not be reliable among the elderly, given one small study of 24 elderly patients with isolated vertigo: 6 patients (25%) were discovered to have caudal cerebellar infarcts. [20] If vertigo is associated with tinnitus and hearing loss, consider Meniere's disease. Acoustic schwannomas can also present with tinnitus and hearing loss; however, when dizziness exists, it is generally much milder and much more chronic.
  • Syncope is defined in the American College of Emergency Physicians’ clinical policy as “a symptom complex that is composed of a brief loss of consciousness [LOC] associated with an inability to maintain postural tone that spontaneously and completely resolves without medical intervention.Transient ischemic attacks are different in that they represent focal cerebral or retinal hypoperfusion. In general, syncope is brief loss of consciousness without focal neurologic signs or symptoms, whereas transient ischemic attacks are brief focal neurologic signs and symptomswithout loss of consciousness.in a study of 242 geriatric patients referred for evaluation of syncope, only 5 (2%) were found to have had a transient ischemic attackIt is even more unlikely that dizziness alone, without other signs or symptoms attributable to the brainstem or posterior circulation (diplopia, dysarthria, or ataxia), would represent a transient ischemic attackIn a study by Kerber et al38 of 1,666 patients presenting to EDs with dizziness, vertigo or imbalance, only 3% had a stroke or transient ischemic attack,and most of these patients had other associated neurologic symptoms. When dizziness symptoms were the only presenting symptom, only 9 of 1,297 (0.7%) patients had a stroke or transient ischemic attack. Therefore, it is important to complete an appropriate neurologic examination on all patients with dizziness, including an evaluation of gait for signs of ataxia. Cerebellar strokes or transient ischemic attacks can present asdizziness but will be associated with ataxiaDrop attack” is an older term for episodes of sudden fallingwithout warning. It can be associated with a brief loss ofconsciousness. Typically, the patient is elderly and experiences aforward fall, with bruising of the knees and nose. The cause isnot well defined.41 About one quarter of such cases areassociated with either a cerebrovascular or a cardiac cause
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    1. 1. Thrombolysing stroke in ED<br />Dr. Ahmed AL Jabri<br /> EM, OMSB<br />R2<br />
    2. 2. Outlines <br />Facts <br />Pathophysiology of ischemic stroke . <br />Clinical features . <br />DDx ( worth to be mentioned ) <br />Ix <br />ESTABLISHING Dx of ACUTE Ischemic stroke ? <br />Safety and efficacy of IV tPA<br />WHOM TO THROMBOLYSE ? ( I and C/I ) <br />TIME FRAME . <br />???? Local stroke team . <br />
    3. 3. Facts <br />80 % of strokes are Ischemic . <br />20 % only of ischemic stroke will arrive to hospital within 3 hrs . <br />2-5% will be thrombolysed<br /> 10-15% of suspected stroke are TIAs . <br />
    4. 4. Review and Meta-Analysis , Arch Intern Med 2007: Early Risk of Stroke After Transient Ischemic Attack<br /> Meta-analysis examined 11 observational studies that estimated the risk of stroke after a transient ischemic attack<br />Early risk of stroke was 9.9% (95% CI 4.9%–14.9%), 13.4% (95% CI 9.8%–17.1%), and 17.3% (9.3%–25.3%) for 2, 30, and 90 days post-TIA, respectively.<br />Facts <br />
    5. 5. Pathophysiology<br />The normal CBF is 40 to 60 mL/100 g of brain/min<br />When CBF decreases to less than 15 to 18 mL/100 g of brain/min, several physiologic changes occur. The brain loses electrical activity and becomes electrically “silent,” although neuronal membrane integrity and function remain intact.<br />Clinically the areas of the brain maintaining electrical silence manifest a neurologic deficit, even though the brain cells are viable.<br />When CBF is less than 10 mL/100 g of brain/min, membrane failure occurs with a subsequent increase in the extracellular potassium and intracellular calcium and eventual cell death.<br />
    6. 6. Pathophysiology<br />ischemic penumbrais the area of the brain surrounding the primary injury, which is preserved by a tenuous supply of blood from collateral vessels.<br />As defined by CBF, the ischemic penumbra constitutes brain tissue with blood flow of 10 to 18 mL/100 g of brain/min <br />
    7. 7. Pathophysiology<br />2 Million Neurones lost every minute<br />
    8. 8. Clinical features<br />Presenting symptoms : be aware <br />
    9. 9.
    10. 10. Clinical syndromes<br />
    11. 11.
    12. 12.
    13. 13.
    15. 15.
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    18. 18.
    19. 19.
    20. 20.
    21. 21. Structural brain lesion from tumor, hemorrhage, arteriovenous malformation<br />or aneurysm<br />Infection (focal abscess, septic emboli)<br />Todd’s paralysis (neurologic deficit postseizure)<br />Epilepsy<br />Complicated migraine<br />Multiple sclerosis flare<br />Hypoglycemia<br />Carotid dissection . <br />Differential diagnosis of ischemic stroke<br />
    22. 22. Syncope from any cause (especially arrhythmia)<br />Labyrinthine disorders<br />Benign positional vertigo (duration of vertigo <1 min), <br />Meniere’s disease<br />Hyperventilation/panic attack<br />Drop attack<br /> vestibular neuronitis.<br />Ménière's disease <br />DDx<br />
    23. 23. Investigations <br />Should be individulaized<br />ALL P.Ts Must have emergently : <br />REFLOW <br />ECG <br />NCCT BRAIN <br />
    24. 24. Investigations<br />CBC ( PLT COUNT ) , <br />U&E1 <br />COAGULATION <br />? ECHO<br />? CAROTID DUPLEX<br />? MRI ( detect early strokes ?? Practicality ) <br />
    25. 25. NCCT BRAIN<br />quickly differentiate an ischemic stroke from ICH and other mass lesions<br />can identify almost all parenchymal bleeds greater than 1 cm and 95% of all subarachnoid hemorrhages<br />ultra-early changes in ischemia includes : <br />hyperdense artery sign (acute thrombus in a vessel),<br />sulcal effacement, <br />loss of the insular ribbon,<br /> loss of gray-white interface, <br />mass effect, <br />and acute hypodensity<br />
    26. 26. Hyperacute Stroke: Modern Approach<br />Aim: Revascularization of penumbra  <br /> Break down Clot!<br />Methods: IV, IA, Mechanical Thrombolysis<br />Most practical, with proven efficacy: IV thrombolysis with Alteplase<br />
    27. 27. Time is Brain<br />
    28. 28. Time is Brain : NINDS Recommended Stroke Evaluation Targets for Potential Thrombolytic Candidates<br />
    29. 29. i.V ALTEPLASE : what is known and updates<br />
    30. 30. Stroke Thrombolysis: Evidence for tPA < 3 Hours<br />
    31. 31.
    32. 32.
    33. 33.
    34. 34.
    35. 35.
    36. 36. Benefits<br />11-13% absolute & 30-50% reletive increase in favourable outcome at 3 months-By BI,MRS,GOS,NIHSS<br />NNT: For every 100 patients treated with rtPA 14 avoided death or dependence<br />Recanalization of arteries: 35%<br />
    37. 37. Stroke Thrombolysis: Durable Benefit?<br />6 i.v. rtPA trials: Pooled Analysis – Benefits similar to NINDS study<br />Dependant on adherence to Protocol.<br />Complication rates also similar.<br />
    38. 38. Stroke Thrombolysis: Durable Benefit?<br />Thrombolytic therapy must be given by an experienced stroke physician after the imaging of the brain is assessed by physicians experienced in reading this imaging study2<br />1: Hacke W et al.: Lancet (2004) 363:768-74<br />2: Wahlgren N et al.: Lancet (2007) 369:275-82<br />
    39. 39. Stroke Thrombolysis: Evidence for tPA at 3 – 4.5 hrs<br />
    40. 40. Stroke Thrombolysis at 3-4.5 Hrs: Evidence<br />ECASS-III Study<br />A multicenter, randomized, placebo-controlled trial<br />N= 821<br />Randomized: IV tPA v/s placebo<br />
    41. 41. Stroke Thrombolysis at 3-4.5 Hrs Exclusion Criteria<br />Age >80 years<br />On oral anticoagulants regardless of INR<br />NIHSS of >25 (Severe stroke)<br />History of both stroke and diabetes. <br />(Diabetes – arbitrary exclusion)<br />
    42. 42. ECASS III – Results<br />
    43. 43. ECASS 3 Results<br />tPA Placebo p<br />Favourable outcome : 52.4% 45.2% 0.04<br /> Any ICH 27.0% 17.6% 0.001<br />Symptomatic ICH* 7.9% 3.5 %; 0.006 <br />Mortality similar 7.7% 8.4% 0.68<br />Other serious adverse events: Similar.<br />
    44. 44. ECASS 3: Outcome on Modified Rankin Score 0=No Sx; 6=Dead<br />
    45. 45. Extended time window for Stroke Thrombolysis: International Guidelines<br />AHA, European Stroke Intiative, UK-NICE recommended<br />Eligible patients who can be treated 3 to 4.5 hours after onset of stroke symptoms should receive tPA. <br />AHA: Class I recommendation, level B.<br />EUSI: Class I, Level A<br />
    46. 46.
    47. 47. Acute Stroke Rx Guidelines IV tPA<br />Recommendations<br /><ul><li>Intravenous rtPA(0.9 mg/kg BW, maximum 90 mg), with 10% of the dose given as a bolus followed by a 60-minute infusion, is recommended within 3 hours of onset of ischaemic stroke (Class I, Level A)
    48. 48. Intravenous rtPAalso benefits acute ischaemic stroke at 3 – 4.5 hours after onset (Class I, Level A).</li></li></ul><li>Acute Stroke Rx GuidelinesIV tPA<br />Recommendations<br /><ul><li>Blood pressure of 185/110 mmHg or higher must be lowered before thrombolysis
    49. 49. May be used in patients with seizures at stroke onset, if the neurological deficit is related to acute cerebral ischaemia .
    50. 50. Intravenous rtPA may also be administered in selected patients over 80 years of age</li></li></ul><li>
    51. 51. Contraindications for alteplase<br />Absolute CI<br /><ul><li>History or evidence of intracranial hemorrhage
    52. 52. Possible subarachnoid hemorrhage
    53. 53. Arteriovenous malformation
    54. 54. Seizure with postictal residual neurologic impairment</li></ul>Systolic BP >185 mm Hg or DBP >110 mm Hg despite repeated measurements and treatment.<br />Platelets <100,000/mm3<br />PT >15 or INR >1.7<br />Active internal bleeding or acute trauma (fracture)<br />
    55. 55. Contraindications for alteplase<br />Relative CI<br />Suspected acute pericarditis<br />Rapidly improving stroke symptoms<br />MI with in 3 mo<br />Glucose level <3.5 mM or > 22 mM/l<br />Head trauma or stroke in the previous 3 months<br />Arterial puncture at a noncompressible site within 1 week<br />
    56. 56. Post –tPA management<br />Close observation in ICU for 24 hr<br />Monitor: BP, Sensorium, Vitals for e/o: Hypertension, ICH, Systemic hemorrhage.<br />Serial BP at 15 min to 1 hr intervals<br />BP goal of <180/115 mm Hg. <br />In case of higher BP: IV Labetalol, Nicardepine<br />
    57. 57. If intracranial hemorrhage present: <br />Obtain fibrinogen results. <br />Prepare for administration of 6 to 8 units of cryoprecipitate containing factor VIII. <br />Prepare for administration of 6 to 8 units of platelets.<br />Consider alerting and consulting a hematologist or neurosurgeon. <br />Consider decision regarding further medical and/or surgical therapy. <br />Consider second CT to assess progression of intracranial hemorrhage. <br />A plan for access to emergent neurosurgical consultation is highly recommended.<br />
    58. 58. Putting it all together<br />
    59. 59. Pre - hospital<br />
    60. 60. Our protocol<br />Age 18-80<br />Clinical diagnosis of a stroke causing a measurable neurological difference<br />Time of symptom onset is known<br />Sufficient time in 3 hour therapeutic window to assess and treat patient<br />No clear contra-indications to thrombolysis<br />
    61. 61. Our protocol<br />Contra-indications<br />Intracranial haemorrhage on CT scan <br />> 3 hours since onset of stroke<br />Improving symptoms<br />Seizure at onset<br />Bleeding disorder<br />Active cancer<br />
    62. 62. Relative contra-indications<br />Age <18 and >80<br />Warfarin Rx with INR >1.6<br />NIHSS <4 or > 25<br />CT showing early ischaemic change<br />
    63. 63. Putting it all together!<br /> spouse nurse<br /> paramedic BP + RBS<br /> arrange clinical venflon<br />CTscan assessment bloods<br />porter DOCTOR-PATIENT relatives<br /> arrange assent/consent<br />bed NIHSScore<br /> weight/dose<br /> BP (again)<br /> read CT scan start drug<br />
    64. 64. Qs, COMMENTS<br />