The document provides guidelines for diagnosing and managing different types and severities of acute brain attacks or strokes. It discusses classifying strokes as TIA, mild, moderate or severe based on symptoms. For TIA and mild strokes, the guidelines recommend emergent diagnostic tests like CT scan and treating conditions like high blood pressure. For moderate strokes, the priorities are supportive care, monitoring vitals, diagnostics like blood tests and CT scan. The guidelines provide recommendations for diagnosing the type of stroke and identifying underlying causes through further diagnostic testing.

1. ACUTE BRAIN ATTACK - 911 RUBEN T. DELA CRUZ MD, FPNA ACUTE STROKE UNIT- MANILA ADVENTIST MEDICAL CENTER

2. OBJECTIVES STROKE IMPACT KNOW THE CLASSIFICATION OF STROKES HOW TO DIAGNOSE STROKES GUIDELINES FOR ACUTE STROKE TREATMENT

3. STROKE IMPACT STROKE IS BRAIN ATTACK ! Sudden onset of focal neurological deficit lasting more than 24 hours due to an underlying vascular pathology. No. 2 Killer worldwide No. 1 Killer in Asia- Western Pacific, China, and Japan 20 million people every year with 5 million deaths Locally: 500 strokes per 100,000 population

4. CLINICAL STROKE CLASSIFICATION TIA AND MILD STROKE MODERATE STROKE SEVERE STROKE

5. TIA and MILD STROKE Transient Ischemic Attack- deficits resolved within 24 hours including transient blindness in one eye OR ALERT Patient with any of the ff: a. mild pure motor weakness of one side of the body. b. pure sensory deficit c. slurred speech but intelligible d. vertigo with incoordination e. visual field defects alone f. combination of a and b

6. MODERATE STROKE Awake patient with significant motor and/or sensory and/or language and/or visual deficit OR Disoriented , drowsy, or stuporous patient but with purposeful response to painful stimuli

7. SEVERE STROKE Comatose patient with nonpurposeful response, decorticate, OR Decerebrate posturing to painful stimuli or comatose patient with no response to painful stimuli

8. DIAGNOSING STROKE Clinical – (80%) 2. Neuroimaging – (20%) * Establish the time of onset of symptoms * Cranial CT scan is the initial imaging study of choice Sudden, focal, Loss of function History, Physical & Neurological Exam

9. ROLE of DIAGNOSTIC EXAM Confirm & establish the clinical diagnosis Rule out stroke “mimickers” Determine pathologic type Infarct, ICH, SAH Determine etiology & stroke mechanism Screen for medical & neurologic complications of stroke

10. COMMON STROKE “MIMICKERS” Seizures Systemic infection Brain tumor Toxic-metabolic enceph Positional vertigo Syncope Trauma Subdural hematoma Herpes enceph Transient global amnesia Dementia Demyelinating dse Cervical spine fracture Myasthenia gravis Parkinson’s dse Hypertensive enceph Conversion disorder Bell’s palsy

11. DIFFERENTIAL DIAGNOSIS OF STROKE Pure hemifacial weakness (e.g. Bell’s palsy) Fever prior to onset of symptoms Trauma Recurrent seizures Weakness with atrophy Recurrent headaches If any of the ff conditions is present, STROKE is probably UNLIKELY …. SSP Guidelines for the Prevention & Management of Brain Attack, 2003

12. With the advent of numerous diagnostic modalities, appropriate sequential diagnostic examinations are most important to confirm the clinical diagnosis of stroke. First-line (emergent) diagnostic exam Second-line diagnostic investigations

13. CBC, PT/ PTT, Blood sugar Plain Cranial CT EMERGENT DIAGNOSTIC EXAM SSP Guidelines for the Prevention & Management of Brain Attack, 2003 Electrocardiogram

14. SECOND-LINE DIAGNOSTIC STUDIES (To Identify Etiology and Stroke Mechanism) Neurovascular Studies Carotid Duplex Transcranial Doppler studies(TCD) Catheter Angiography CT Angiography Magnetic Resonance Angiography (MRA) Cardiac investigation Echocardiography 24 hour Holter

16. Hematologic Studies Hypercoagulable states – Protein C, S, Fibrinogen Antithrombin III APAS - ANA, Anticardiolipin Ab, Lupus anticoagulant Homocysteine Drug Levels – e.g. Metamphetamine Genetic – Familial homocystinuria, MELAS, CADASIL SECOND-LINE DIAGNOSTIC STUDIES (To Identify Etiology and Stroke Mechanism) Biopsy – e.g Vasculitis, Temporal arteritis

17. Plain Cranial CT is recommended Neuroimaging in Acute Stroke Hyperacute 3 hours 12 hours 48 hours First-line modality imaging in suspected stroke cases Widely available, relatively inexpensive, non - invasive & quick Accurately differentiates hemorrhagic and ischemic strokes Should be performed & interpreted ASAP

18. RATIONALE FOR NEUROIMAGING Identify the lesion (is it a stroke?) Determine the type of stroke (ischemic or hemorrhage?) Localize the stroke (where is it?) Quantify the lesion (how large is it?) Determine the age of the lesion

19. BASIC CONCEPTS Cranial computed (x-ray) tomography scan Air, Fluid (e.g. CSF, infarction) = hypodense Bone, calcification, blood = hyperdense

20. CT FINDINGS in HYPERACUTE INFARCTION (0 - 6 hrs) Almost 60% of CT scans done in the first few hours of ischemic stroke: NORMAL However, the following signs may be seen: Hyperdense artery (“dense MCA sign”) Obscuration of lentiform nuclei Loss of grey-white interphase along lateral insula (“insular ribbon sign”) Effacement of sulci

21. Early signs of infarction on Cranial CT Dense Artery sign Insular Ribbon sign (loss of insular stripe) Obscuration of lentiform nuclei Effacement of sulci

22. CRANIAL CT in ACUTE ISCHEMIC STROKE Infarction: focal hypodense area in cortical, subcortical, or deep gray or white matter, following a vascular territory, or watershed distribution

23. CT FINDINGS in SUBACUTE / CHRONIC INFARCTION Wedge-shaped large cortical infarct Round / ovoid small subcortical infarcts

24. Subacute R-ICA infarct Subacute L-MCA infarct CT FINDINGS in SUBACUTE / CHRONIC INFARCTION

25. Hyperdense lesion in left lentiform nucleus with hypodense rim (vasogenic edema) CT FINDINGS in INTRACEREBRAL HEMORRHAGE

26. Common Sites of Hypertensive ICH

27. Common Sites of Hypertensive ICH

28. Cranial CT of Hemorrhagic Stroke Stroke Society of the Philippines recommendations for computation of hematoma volume Planimetric Method or Pixel Method Modified Kothari method (ABC/2)

29. A - greatest hemorrhage diameter B - diameter 90 degrees to A C - no of CT slices with hemorrhage x by the slice thickness * Measurement of Hematoma Volume Modified Kothari Method A x B x C / 2 Select the CT slice with the largest area of hemorrhage A B Hemorrhage > 75% of the largest area = 1 slice Hemorrhage > 25 – 75% of the largest area = 0.5 slice Hemorrhage < 25% of the largest area - 0

30. Interpretation of Hematoma Volume for Supratentorial Hemorrhages < 30cc small medical 30 – 50cc moderate > 50cc large surgical * Factor in age, neurologic status, concomitant medical conditions

31. CT SCAN FINDINGS in SUBARACHNOID HEMORRHAGE

32. Advantages of Cranial MRI DIAGNOSING STROKE: Other Neuroimaging Techniques More sensitive in detecting small lesions / lacunar infarcts early infarction brainstem / post fossa lesions Can detect lesions as early as 6 hours from onset of stroke (as early as 90 mins. for Diffusion MRI)

33. Early signs of infarction on MRI Slow flow (absence of normal flow void) in involved artery Parenchymal signal changes (hypointense on T1) T1 DWI: acute infarct appears bright Parenchymal signal changes (hyperintense on T2) T2

34. R medullary Infarction T1 T2 MAGNETIC RESONANCE IMAGING in BRAINSTEM INFARCTION R Pontine Infarction

35. Limitations of Cranial MRI DIAGNOSING STROKE: Other Neuroimaging Techniques More expensive & less widely available Longer acquisition time compared to CT (difficult in uncooperative patients) Contraindicated in patients with metallic implants (e.g. pacemaker) Not sensitive in detecting acute hemorrhage

36. MRI is not sensitive in detecting ACUTE HEMORRHAGE Cranial MRI Cranial CT scan Pontine Hemorrhage

37. NEUROVASCULAR EVALUATION Ultrasound Techniques Catheter Angiography CT Angiography MR Angiography

38. RATIONALE for NEUROVASCULAR EVALUATION Identifying occlusive arterial disease (Is there blockage ?) Localizing the occlusion (Where ?, carotid ?, intracranial ?) Quantifying the degree of stenosis (How severe ?) Determining the pathology (Athero ?, dissection ?, others ?) Identifying other vascular lesions

39. Recommendations for Neurovascular Imaging in Patients with Stroke A non-invasive screening technique is indicated as an initial diagnostic test Conventional radiographic angiography may be indicated based on findings of non-invasive screening procedures (i.e. severe stenosis, occlusion) Cerebral arteriography may also be required when a diagnosis of vasculitis, dissection, vascular malformation needs confirmation or exclusion

40. Transcranial Doppler (TCD) Carotid/vertebral Duplex VASCULAR ULTRASOUND “ NEUROSONOLOGY ”

41. CAROTID DUPLEX Established technique to identify extracranial carotid / vertebral artery disease Advantages: non-invasive, bedside availability, low cost Disadvantages: operator dependent, unable to differentiate occlusion from near occlusion

42. TRANSCRANIAL DOPPLER Established technique to evaluate basal intracranial arteries Established utility in stroke (e.g. stenosis, vasospasm,  ICP, vasomotor reactivity) Advantages: non-invasive, bedside availability, low cost, allows serial monitoring, detects micro emboli Disadvantages: operator dependent, poor temporal window, circle of Willis variation

43. Stenosis / occlusion Emboli detection Collateralization Vasospasm Increased ICP / Brain death Cerebral Autoregulation TCD APPLICATION in STROKE

44. MAGNETIC RESONANCE ANGIOGRAPHY CT ANGIOGRAPHY Other Non-Invasive Neurovascular Imaging Procedures

45. Severe Carotid Stenosis CATHETER ANGIOGRAPHY Vertebral Artery Stenosis MCA Stenosis “ Gold standard”

46. AV Malformation CATHETER ANGIOGRAPHY Venous angioma Aneurysm Cost, availability, invasive procedure Risks (vascular damage, stroke, ionizing radiation, reaction to contrast) Exclusion: poor renal function, absent femoral pulses, coagulopathy

47. CARDIAC EVALUATION Holter Monitoring 2 D Echocardiography

48. Recommendations for Echocardiography in Patients with Stroke … Clinical evidence of heart disease Less than or equal 45 years of age Older patients, without evidence of extra or intracranial occlusive disease or other obvious cause Abrupt occlusion of major peripheral or visceral artery Suspect embolic disease (non-lacunar syndrome, multiple arterial territory involvement) Clinical therapeutic decision will depend on results of echocardiography

49. LV thrombus LV dyskinesia Mitral stenosis Mitral annular calcification Mitral valve prolapse Atrial thrombus Atrial appendage thrombus Atrial septal aneurysm Patent foramen ovale Aortic arch athero / dissection Transthoracic vs Transesophageal Echocardiography TTE Preferred TEE Preferred

50. Proper use of diagnostic examinations in stroke requires an understanding of: Underlying disease process Principles of test involved Advantages & limitations of each procedure How each investigation influences patient management

51. SUMMARY Rule out stroke mimickers History, PE & NE should be done immediately on patients with stroke Do emergent diagnostic tests to determine patient’s eligibility for rTPA

52. SUMMARY CT scan remains to be the most important brain imaging test. Cranial MRI is not recommended for routine evaluation of acute stroke patients Differentiation of ischemic & hemorrhagic stroke is important because of marked difference in the management Second line diagnostic tests need not be done in the ER setting and should not delay treatment

53. GUIDELINES FOR TIA AND MILD STROKE MANAGEMENT PRIORITIES Ascertain clinical diagnosis of stroke or TIA Exclude common stroke mimickers Monitor and manage blood pressure SBP = 220 or DBP= 120 MAP= 130 Avoid precipitous drop in BP> 20% of baseline MAP No rapid-acting sublingual agents Use oral or easily titratable IV antihypertensive Ensure appropriate hydration. No hypotonic IV fluids

54. GUIDELINES FOR TIA AND MILD STROKE EMERGENT diagnostics Complete Blood count (CBC) Blood sugar (CBG, HGT, or RBS) Electrocardiogram (ECG) PT/PTT (Atrial Fibrillation or possible cardioembolic source) Plain CT Scan Of brain as soon as possible

55. GUIDELINES FOR TIA AND MILD STROKE EARLY SPECIFIC TREATMENT FOR THROMBOTIC OR LACUNAR STROKE (CTSCAN CONFIRMED ) Aspirin 160-325 mg start as early as possible for 14 days Neuroprotection Early rehabilitation within 72 hours

56. GUIDELINES FOR TIA AND MILD STROKE EARLY SPECIFIC TREATMENT FOR CARDIOEMBOLIC (CTSCAN CONFIRMED) Anticoagulation with IV heparin or subcutaneous LMWH Or Aspirin 160-325 mg/day (If anticoagulation not available) Neuroprotection Early rehabilitation within 72 hours If infective endocarditis is suspected, give antibiotics and do not anticoagulate.

57. GUIDELINES FOR TIA AND MILD STROKE EARLY SPECIFIC TREATMENT FOR HEMORRHAGIC If there is suspicion of nonhypertensive cause for ICH (e.g. AVM, aneurysm), REFER to neurosurgeon. Neuroprotection Early rehabilitation with in 72 hrs

58. GUIDELINES FOR TIA AND MILD STROKE EARLY SPECIFIC TREATMENT FOR T.I.A. Aspirin 160-325 mg/ day If crescendo T I A (multiple events within hours, Increasing severity and duration of deficits), consider ANTICOAGULATION with intravenous heparin

59. GUIDELINES FOR TIA AND MILD STROKE CT SCAN NOT AVAILABLE No specific emergent drug treatment recommended Neuroprotection Consult a neurologist or neurosurgeon Early supportive rehabilitation

60. GUIDELINES FOR TIA AND MILD STROKE PLACE OF TREATMENT Admit to Hospital (Stroke Unit) 1. Stroke onset within 48 hours 2. Patients requiring specific active intervention for any of the following: a. BP control, monitoring, and stabilization b. Cardiac stabilization, incl. Atrial fibrillation, CHF, acute MI c. Hydration d. Anticoagulation, if ICH ruled out by CT

61. GUIDELINES FOR TIA AND MILD STROKE PLACE OF TREATMENT Admit to Hospital (Stroke Unit) 3. Rapidly worsening deficits 4. >4 TIA’s in 2 weeks prior to consult 5. 1-4 TIA’s in 2 weeks but high risk (multiple events within hours, increasing severity and duration of deficits

62. GUIDELINES FOR TIA AND MILD STROKE PLACE OF TREATMENT URGENT OUTPATIENT WORK-UP 1. S ingle TIA more than 2 weeks ago 2. 1-4 TIA’s in 2 weeks, but not high risk (no change in severity and duration of deficit, cardiac arrhythmia, carotid bruit) 3. Transient monocular blindness alone 4. Stable mild strokes occurring > 48 hrs not requiring specific active intervention *Advise immediate re-consult if there is worsening of deficit .

63. GUIDELINES FOR MODERATE STROKE MANAGEMENT PRIORITIES 1. Basic emergent supportive care (ABC of resuscitation) 2. Monitor and manage blood pressure. Treat if SBP>220; DBP>120; MAP= >130 Precautions: Avoid precipitous drop in BP >20% MAP No Sublingual agents 3. Exclude stroke mimickers 4. Identify co-morbidities (cardiac dis. Gastric ulcer, etc) 5. Recognize and treat early signs of increased ICP

64. GUIDELINES FOR MODERATE STROKE EMERGENT DIAGNOSTICS Complete Blood Count Blood sugar (CBG, HGT, RBS) PT/PTT Serum Na and K+ Electrocardiogram (ECG) Plain CT Scan of brain ASAP

65. GUIDELINES FOR MODERATE STROKE EARLY SPECIFIC TREATMENT (CTSCAN CONFIRMED) Ischemic- Noncardioembolic (Thrombotic/ Lacunar ) - If within 3 hours of stroke onset, consider rtPA treatment and refer to specialist - Aspirin 160-325 mg/day start as early as possible - Neuroprotection - Early supportive rehabilitation

66. GUIDELINES FOR MODERATE STROKE EARLY SPECIFIC TREATMENT (CTSCAN CONFIRMED ) CARDIOEMBOLIC - If within 3 hours of stroke onset consider rtPA ` treatment and refer to specialist - Aspirin 150- 325 mg/day start as early as pos. - Early anticoagulation if source of embolism can be demonstrated - Neuroprotection - Early supportive rehabilitation * If infective endocarditis is suspected, give antibiotics and DO NOT anticoagulate

67. GUIDELINES FOR MODERATE STROKE EARLY SPECIFIC TREATMENT (CTSCAN CONFIRMED ) HEMORRHAGIC - Supportive treatment: 1. Mannitol 20% 0.5 mg/kg BW q 6 h for 2- 5 days 2. Neuroprotection - Neurosurgery consult for hematomas distorting or displacing 4 th ventricle - Within 12-24 h, recommended surgery for hematoma: 1. size 10-30 cc (non-dominant subcortical frontal/temporal) 2. size >30 cc (subcortical, putaminal, cerebellar) - Early supportive rehabilitation

68. GUIDELINES FOR MODERATE STROKE CT SCAN NOT AVAILABLE = USE SCORING SYSTEM Likely Ischemic Likely Hemorrhagic No specific emergent drug Tx. Neuroprotection Refer to Specialist Early Supportive Rehabilitation Refer to Neurologist/ Neurosurgeon further Dx workups and/or subsequent surgery Neuroprotection Early supportive rehabilitation

69. GUIDELINES FOR SEVERE STROKE Management Priorities Basic Emergent supportive care (ABC of Resus.) Neurovital signs: BP; PR, CR, RR, Temp, Pupils. Glasgow Coma scale, Recognize and Treat early signs of increased ICP Monitor and manage blood pressure. Treat if SBP is 220 or DBP of 120 or MAP of 130. Precautions: *Avoid precipitous drop in BP >20% of MAP *Do not use sublingual agents Ascertain clinical Dx; exclude stroke mimickers Identify co-morbidities (cardiac dis. Gastric ulcer, etc)

70. GUIDELINES FOR SEVERE STROKE EMERGENT DIAGNOSTICS: Complete blood count, Blood Sugar, PT/PTT, Serum Na, K Electrocardiogram, Plain CTscan of the brain

71. GUIDELINES FOR SEVERE STROKE EARLY SPECIFIC TREATMENT (CTSCAN CONFIRMED) Non-cardioembolic (Thrombotic/Lacunar) - May give aspirin 160-325mg/day - Neuroprotection - If cerebellar infarct, consult neurosurgeon ASAP - Early supportive rehabilitation Place of Treatment: Hospital, Intensive Care Unit or Acute Stroke Unit

72. GUIDELINES FOR SEVERE STROKE EARLY SPECIFIC TREATMENT (CTSCAN CONFIRMED) HEMORRHAGIC - Supportive Treatment: 1. Mannitol 20% 0.5 mg/kg q 6h for 2-5 days 2. Neuroprotection - Neurosurgery consult if: 1. Patient not herniated, hematoma in putamen, subcortical, cerebellum and goal is to reduce mortality’ 2. Herniated patient but family is willing 3. ICP monitoring contemplated and salvage surgery is considered Place of Tx.: Intensive Care Unit

73. BRING HOME MESSAGE STROKE IS BRAIN ATTACK! STROKE IS AN EMERGENCY! STROKE IS TREATABLE! STROKE IS PREVENTABLE!

74. CIFIC TREATMENT