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1. Dallas Presbyterian Hospital
Internal Medicine Resident Lecture
August 28, 2008
Samir Shah, MD
Neurology Consultants of Dallas
STROKE, SUBARACHNOID
HEMORRHAGE AND HYPOTHERMIA
FOR CARDIAC ARREST
-Andy Rekito

2. Quick Stroke Facts - 2008
FACT: About 780,000 Americans suffer a new or recurrent
stroke each year. That means, on average, a stroke occurs every
40 seconds.
FACT: Stroke kills nearly 150,000 people each year. That’s
about 1 of every 16 deaths. It remains the #3 cause of death
behind heart disease and cancer. An American dies of a stroke
every 3 minutes.
FACT: Americans will pay about $63 billion in 2007 for stroke
related medical costs and disability.
American Heart Association. Heart Disease and Stroke Statistics — 2008
Update. Dallas, Tex.: American Heart Association; 2008.

3. Prevalence of Stroke by Age and Sex
NHANES: 1999-2002
Source: CDC/NCHS and NHLBI.
1.1
3.1
6.6
11.5
0.4
1.2
12.0
0.3 0.8
2.1
3.0
6.3
0
2
4
6
8
10
12
14
20-34 35-44 45-54 55-64 65-74 75+
Ages
Percent
of
Population
Men Women
`
FACT: Prevalence of stroke in the US is 5.7 million people
(2004). 15-30% of stroke victims are permanently disabled.

4. Definitions – So We’re All on the
Same Page
An established and universally accepted definition for stroke by the
World Health Organization is "acute neurologic dysfunction of
vascular origin . . . with symptoms and signs corresponding to the
involvement of focal areas of the brain."
Stroke. 1989 Oct;20(10):1407-31.

5. BEFORE
Stroke has also been described as the rapid onset of neurological
deficits that persist for at least 24 hours and are caused either by
intracerebral or subarachnoid hemorrhage or by partial or complete
blockage of a blood vessel supplying or draining a part of the brain,
leading to the infarction of brain tissue. A stroke is distinguished
from a transient ischemic attack (TIA) by the fact that neurological
deficits in TIAs clear spontaneously within 24 hours.

6. NOW
Clinical, experimental, and imaging data have shown that the
24-hour criterion is inaccurate in suggesting an absence of brain
injury and often results in uncertainty — on the part of patients
and practitioners alike — about what to do when a TIA occurs.
In short, the 24-hour definition of TIA is outdated, confusing,
and potentially misleading…

7. NEW DEFINITION
a TIA is a brief episode
of neurologic
dysfunction caused by
focal brain or retinal
ischemia, with clinical
symptoms typically
lasting less than one
hour, and without
evidence of acute
infarction.The
corollary is that
persistent clinical signs
or characteristic imaging
abnormalities define
infarction — that is,
stroke (N Engl J Med
2002;347:1713-1716).

8. THEREFORE
The development of symptoms of acute brain ischemia
constitutes a medical emergency and transient symptoms do not
exclude the possibility of associated brain infarction.
TIME=BRAIN
Now, let’s talk about how we evaluate and manage stroke.
We will focus on ischemic stroke…

9. Consult for a 68 year-old man
that has new right-sided
weakness and is “talking
funny.” It started a few hours
ago.

10. What Else Could It Be?
Stroke Mimics
Abcess
Subdural and Epidural Hematomas
Tumors
Giant aneurysms
Vascular malformations (AVMs)
Hypertensive Encephalopathy
Encephalitis/cerebritis
Seizure/Todd’s paralysis
Migraine
Metabolic-
Hypoglycemia/Hyperglycemia
Cerebral venous thrombosis
Psychogenic
Deficit from previous stroke made
worse by general medical condition

11. When presented with acute onset neurological
dysfunction, stroke should always be on your
differential and one of the first goals in the
evaluation is differentiating hemorrhagic stroke
from ischemic stroke
All patients, with few exceptions should undergo
STAT cranial imaging. In other words, GET A
NON-CONTRAST HEAD CT (MRI if available
STAT).
Quickly Narrow the Differential
With Imaging

12. What Else to Ask for Over the
Phone?
ALL stroke patients should get immediate
CBC with platelets
Bedside glucose
PTT, PT (INR)
Chem 7 (Chem 10)
EKG, continuous cardiac monitoring
IV access, 0.9% NS (no glucose)
NPO
?Troponin

13. What’s the Cardiac Workup for?
Not infrequently, patients with acute cerebral ischemia have
concomitant acute myocardial ischemia
In addition cardiac evaluation helps determine etiology of the
cerebral event
Several small studies have shown that patients with TIA and
stroke have a high prevalence of asymptomatic CHD. These
studies suggest that 20% to 40% of stroke patients may have
abnormal tests for silent cardiac ischemia.
2% to 5% of patients with acute ischemic stroke have fatal
cardiac-related events in the short term after stroke.
Circulation. 2003;108:1278.

14. Other Acute Studies
Urine pregnancy test
Urine toxicology
Hypercoagulable screen
CXR
Type and Screen

15. What are the risk
factors for ischemic
stroke?

16. Risk Factors for
Ischemic Stroke
Risks that can be controlled or
treated
High Blood Pressure
Smoking
Diabetes Mellitus
Prior TIA
Atrial Fibrillation
Other Heart Disease
Carotid Artery Disease or
atherosclerosis in another arterial bed
Certain blood disorders
Sickle Cell Disease
Hypercholesteremia
Physical Inactivity, Obesity
Excessive alcohol
Illicit drugs
HRT
Risks that cannot change
Age
Prior stroke or MI
Gender
Heredity/Ethnicity

17. 2.6
4.0
5.4
8.4
1.1 2.0
19.1
22.4
14.8
27.0
6.3
3.5
0
5
10
15
20
25
30
A B C D E F
Estimated
10-Year
Rate
(%)
Men Women
Estimated 10-Year Stroke Risk in 55-
Year-Old Adults According to Levels of
Various Risk Factors - Framingham
Heart Study
A B C D E F
Systolic BP 95-105 130-148 130-148 130-148 130-148 130-148
Diabetes No No Yes Yes Yes Yes
Cigarettes No No No Yes Yes Yes
Prior Atrial Fib. No No No No Yes Yes
Prior CVD No No No No No Yes
Source: Stroke 1991;22:312-318.

18. General elderly male population 0.6 -------
Asymptomatic carotid disease 1.3 3.4
Transient monocular blindness 2.2 3.5
Transient ischemic attack 3.7 2.3
Minor stroke 6.1 3.2
Major stroke 9.0 3.5
Symptomatic carotid stenosis >70% 15 2.0
Annual Probability(%)
Stroke Vascular Death
Cerebrovascular Features
Estimates of Vascular Event Rates for Persons With
Various Features of Atherothrombotic Cerebrovascular
Disease
Stroke. 1997;28:1507-1517.

19. Risk Factors for
Intracerebral and
Subarachnoid
Hemorrhage
++ indicates strong evidence; +,
moderate positive evidence; ?,
equivocal evidence; –, moderate
inverse evidence; and 0, no relation.
Age ++ +
Women - +
Race/ethnicity + +
Hypertension ++ +
Cigarette smoking ? ++
Heavy use of alcohol ++ ?
Anticoagulation ++ ?
Amyloid angiopathy ++ 0
Hypocholesterolemia ? 0
Oral Contraceptives 0 ?
ICH SAH
Stroke. 1997;28:1507-1517.

20. What Else Will You Ask?
Exact time of onset or last time the patient was last seen at
baseline
History of seizures? Any seizure activity prior to onset of
symptoms
Migraine headaches
Trauma or neck injury in the preceding days
Recent illnesses
Vomiting, change in level of consciousness
Allergies
Medications
Associated symptoms (?chest pain)

21. What to Do on Exam?
ABCs first
Vital Signs: especially notice BP and don’t
forget weight
Cardiac, vascular, extremity examination
Directed and focused exam based on history -
NIHSS

22. NIH Stroke Scale – focuses on 5 major areas
 Level of consciousness
 Visual function
 Motor function
 Sensation and neglect
 Cerebellar function
NIHSS is easily performed, reliable and valid. It is
strongly associated with outcome with and without
thrombolytics, and can predict those patients likely
to develop hemorrhagic complications from
thrombolytic use.

23. www.ferne.org

24. Goal of History and Physical Is
to Localize Lesion and Its
Vascular Supply
Knowing the location of the lesion and its vascular
supply allow you to begin to speculate on the
underlying pathophysiology as different stroke
mechanisms characteristically affect certain cerebral
vessels.

25. Blood Supply of the Brain
Anterior Circulation: Two ICAs which divide into ACA
and MCA. Each ICA supplies roughly two fifths of the
brain by volume.
Posterior Circulation: Two Vertebrals which join to form
the Basilar which then forms PCAs. The posterior
circulation supplies roughly one fifth of the brain.

26. Source: Loyola University Neurovascular Tutorial

30. Four Divisions of the Vertebral Artery

34. Stroke Mechanisms
Can simplify stroke mechanisms or etiologies into 5 categories
ISCHEMIA
1. Thrombosis (60%)
2. Embolism (20%)
3. Decreased Systemic Perfusion
HEMORRHAGE
4. Intracerebral Hemorrhage (12%)
5. Subarachnoid Hemorrhage (8%)

35. Common Stroke Mechanisms
The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy
STROKE
Ischemic Stroke
Primary Hemorrhage
Intraparenchymal
Subarachnoid
Atherosclerotic
Cerebrovascular
Disease
(“Large Artery”)
Hypoperfusion Arteriogenic
Emboli
Penetrating
Artery Disease
(“Lacunes”)
Cardiogenic
Embolism
Cryptogenic
Stroke
Other,
Unusual
Causes
Prothrombotic States
Dissections
Arteritis
Migraine/vasospasm
Drug Abuse
Many More
Atrial Fibrillation
Valve Disease
Ventricular Thrombi
Many Others
15%
85%
20% 25% 20% 30% 5%

36. You are done thinking of stroke
mechanisms and you are almost at the ER
when you get paged by the doctor that
the patient has a blood pressure that is
“sky high” at 182/102 and that he is
going to give him some oral clonidine to
take care of it.
What should you tell her?

37. Cerebral Autoregulation:
It may not be working
DO NOT TREAT BP IN ACUTE ISCHEMIC
STROKE UNLESS BP>200-220/100-120

38. The patient’s daughter is at the bedside. She tells you that her dad
had some right sided weakness yesterday that resolved in 25
minutes and that’s why she brought him in. She says his new
symptoms on the right started in the hospital just 45 minutes ago.
She says he has some kind of heart problem but hasn’t been taking
any of his medications. She’s not sure what he was taking and is
worried about his talking.
The Patient Encounter

39. You examine the patient and with your excellent neurological
skills quickly realize that his “talking funny” is actually an
expressive aphasia and that he has a right facial droop, a left
gaze preference, 2/5 right arm weakness and 4/5 right leg
weakness.
All the labs you wanted are unrevealing, and the EKG shows
evidence of LVH, but otherwise ok. The nurse tells you that
the monitor went off a little while ago for a rapid, irregular
heart rate.
You are astute enough to realize that this guy is in the usual 3
hour window for acute stroke therapy and decide to go look at
the CT scan.

40. Now what?

41. Hyperdense MCA Sign

42. Insular Ribbon Sign
Loss of Gray-White
Junction

43. The New England
Journal of Medicine
©Copyright, 1995, by the Massachusetts Medical Society
Volume 333 DECEMBER 14, 1995 Number 24
TISSUE PLASMINOGEN ACTIVATOR FOR ACUTE ISCHEMIC STROKE
THE NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE rt-PA STROKE STUDY GROUP*
IV t-PA FDA approved for use in acute ischemic stroke < 3
hours from onset in 1996. As compared with patients given
placebo, patients treated with t-PA were at least 30 percent
more likely to have minimal or no disability at three months
on the assessment scales.

44. The Use of IV t-PA
Eligibility
Age 18 or older
Clinical diagnosis of ischemic stroke causing a measurable neurological
deficit
Time of symptom onset well established to be less than 180 minutes
before treatment would begin

45. Contraindications
Evidence of intracranial hemorrhage on pretreatment CT
Clinical presentation suggestive of SAH, even with normal CT
Active internal bleeding
Known bleeding diathesis, including but not limited to:
Platelet count < 100,000/mm3
Patient has received heparin within 48 hours and has an elevated aTT
(greater than upper limit of normal for laboratory)
Current use of oral anticoagulants or recent use with an elevated
prothrombin time > 15 seconds
Within 3 months any intracranial surgery, serious head trauma, or previous
stroke
On repeated measurements, systolic blood pressure greater than 185 mmHg
or diastolic blood pressure greater than 110 mmHg at the time treatment is to
begin, and the patient requires aggressive treatment to reduce blood pressure to
within these limits
History of intracranial hemorrhage
Known AVM or aneurysm

46. Warnings
Only minor or rapidly improving stroke symptoms
History of GI or Urinary tract hemorrhage within 21 days
Recent arterial puncture at a noncompressible site
Recent lumbar puncture
Abnormal blood glucose (<50 or >400 mg/dL)
Post myocardial infarction pericarditis
Patient was observed to have a seizure at the same time the
onset of stroke symptoms were observed

47. Other relative contraindications (not NINDS)
Bacterial endocarditis or CNS lesion likely to hemorrhage after t-PA
Significant trauma within 3 months
CPR with chest compressions within past 10 days
Major surgery within past 14 days, minor surgery within past 10 days
Pregnant (up to 10 days postpartum) or nursing woman
Life expectancy < 1 year from other causes
Peritoneal dialysis or hemodialysis

48. What to Tell the Family
After you determine your patient’s eligibility based on
NINDS criteria, you go and talk with the daughter
about the risks and benefits
What are the risks?
Bleeding and its complications (6% vs <1%) and
allergic reaction (1 to 2%)
She asks what is the benefit?
Patient’s treated with t-PA were at least 30% more
likely to have minimal or no disability at three months
despite increased risk of hemorrhage. ARR=16%,
NNT=6 (Similar to CEA for symptomatic carotid
stenosis)

49. Copyright ©1999 American Heart Association
Grotta, J. C. Stroke 1999;30:1722-1728
Distribution of outcomes on NIH Stroke Scale (NIHSS) (top), Barthel index (middle), and
Rankin scale (bottom) in parts 1 and 2 combined of the NINDS rtPA Stroke Study

50. You write to administer t-PA at 0.9mg/kg (max 90mg) infused
over 60 minutes with 10% of the dose administered as a bolus
over 1 minute. You ensure that BPs have been consistently less
than 185/110 prior to administration. You also make sure that no
other antithrombotics or anticoagulants will be given in the next
24 hours and write for a Head CT in 24 hours. You also write
orders for ICU admission as you know the patient will need close
BP monitoring over the next 24 hours per NINDS protocol to
maintain BP<180/105.

51. Let’s Get Serious
Only a small fraction of ischemic strokes (likely 1-3%) are treated
with IV t-PA, mostly because patients arrive to medical attention
after the 3 hour time window. At places without 24 hour
neurointerventional capability, what do we do for a stroke acutely
when the patient is not eligible for IV t-PA?

52. This CT has a clear
hypodensity. This patient
is not eligible for IV-tPA
given days duration of
symptoms. In patients
that do not receive
thrombolysis: In the
acute period, all
ischemic stroke patients
should receive 160-
325mg of ASA within
48hours of onset. (some
may advocate acute
anticoagulation for certain
stroke subtypes).
Antithrombotic and Thrombolytic Therapy for Ischemic Stroke: The
Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy

53. Copyright ©2000 American Heart Association
Chen, Z. et al. Stroke 2000;31:1240-1249
Absolute effects in CAST and IST of early use of aspirin in 40 000 randomized patients
with suspected acute ischemic stroke
For every 1000 acute strokes treated with ASA, 7 fewer
early recurrent ischemic strokes were observed and 13 fewer
patients will be dead or dependent at 6 months at the
expense of two or more ICHs.

54. All stroke patients should be admitted to the hospital for
observation, diagnostic evaluation, and determination of
treatment for secondary stroke prevention. All patients should
be admitted to a stroke unit or when not available to a cardiac
monitored bed with staffing to perform frequent neurological
checks.
As already discussed, thrombolysis patients need ICU care.
Admit the Patient

55. Where would you admit this patient?

56. How about this patient?

57. Let’s say the patient’s
symptoms resolved by the
time you got there and he now
feels fine and wants to go
home

58. TIAs carry a substantial short term risk of stroke,
hospitalization for cardiovascular events, and death. Of
1,707 TIA patients evaluated in an emergency
department of a large health care plan, 180 patients or
10 percent developed stroke within 90 days. 91 patients
or 5 percent did so within 2 days. Predictors of stroke:
more than 60 years of age, DM, focal symptoms of
weakness or speech impairment, and TIA lasting longer
than 10 minutes (JAMA 2000;284:2901-6).
PATIENT IS AT HIGH RISK AND NEEDS TO BE ADMITTED

59. Evaluation During Admission
1. Labs: LFTs, fasting lipid profile and glucose, QID bedside glucose
and SSI. Consider Hypercoagulable workup, ESR, ANA, hsCRP,
HbA1c, homocysteine, LP
2. Imaging: All patients should have MRI imaging of brain and vascular
imaging of head and neck. Consider TCD, PET, SPECT or other
study based on clinical findings
3. Echocardiogram: all patient should have echo – TTE when h/o of
CAD or abnormal EKG or lacunar event. All others TEE (more
sensitive and cost effective in evaluation of stroke. Ann Intern Med.
1997 Nov 1;127(9):775-87.)
4. Rehabilitation evaluation
5. Bedside or formal swallow evaluation
6. Medications: Home medications except BP meds. Restart or add
after patient stable for >48hrs. Again, in general do not treat BP unless
>220/120 in the acute phase
7. DVT and GI prophylaxis if indicated

60. Hospital Initiation of Secondary
Prevention
All patients receive statin with goal LDL<100. Established evidence
in patients with CAD and atherosclerotic ischemic stroke.
Atorvastatin 80mg qd SPARCL
All patients given BP meds with goal <140/90 or <130/80 with DM
or renal disease. Prefer ACEI or ARB and thiazide diuretic
PROGRESS (B-blocker if CAD)
Smoking Cessation
Diet and Exersice Regimen
Stroke Education

61. Antithrombotic / Anticoagulant
Therapy
In patients who have experienced a noncardioembolic stroke or
TIA, we recommend treatment with an anti-platelet agent. Aspirin at
a dose of 50 to 325mg qd; the combination of aspirin, 25mg and
extended-release dipyridamole, 200mg bid; or clopidogrel, 75mg qd,
are all acceptable options for initial therapy
No good evidence on what to do if patient already on therapy
In patients with Afib who have suffered a recent stroke or TIA, we
recommend long-term oral anticoagulation, INR range 2-3
?Best treatment in cryptogenic stroke, PFO, aortic disease, post-MI
?Use of IV Heparin in certain situations—brain goal PTT of 45-65
Antithrombotic and Thrombolytic Therapy for Ischemic Stroke:
The Seventh ACCP Conference on Antithrombotic and Thrombolytic
Therapy

62. Copyright restrictions may apply.
Kidwell, C. S. et al. JAMA 2004;292:1823-1830.
Acute Intraparenchymal Hematoma Imaged With Computed Tomography and With Magnetic
Resonance Imaging

71. The Ischemic Penumbra
Approximated by PWI-DWI MRI Mismatch and used to help
guide interventional acute stroke therapies…

72. IA t-PA within 6 hours of stroke onset in anterior circulation and
24+ hours in posterior circulation
Mechanical Clot removal within 8+ hours of ischemic stroke
(MERCI) Stroke. 2005;36:1432.

75. Subarachnoid Hemorrhage
Causes:
Aneurysm (80% of non-traumatic cases)
Trauma
Vascular Malformations
Tumors
Infection
Venous Thrombosis

76. Subarachnoid Hemorrhage
(Aneurysmal)
Demographics:
Mean age = 55 years
Women 1.6X > Men
Blacks > Whites
Average Case Fatality Rate > 50%

77. Subarachnoid Hemorrhage
(Aneurysmal)
Risk Factors:
Smoking
Hypertension
Cocaine Use
Heavy alcohol use
First degree relatives with SAH

78. Subarachnoid Hemorrhage
Clinical Features:
Sudden severe headache (thunderclap headache)
Nausea
Vomiting
Neck Pain
Photophobia
Loss of consciousness
Retinal hemorrhages (subhyaloid hemorrhage)
Meningismus
Localizing neurological signs

79. Subarachnoid Hemorrhage
Diagnostic Evaluation:
Head CT
Sensitivity > 90% in first 24 hours
Sensitivity drops to 50% at 1 week
Lumbar Puncture
Finding to look for is xanthochromia
(12 hours to develop)

80. Subarachnoid Hemorrhage
Treatment:
Blood Pressure
Low before aneurysm secured
High after aneurysm secured
Treat hyperglycemia and hyperthermia
DVT prophylaxis (Heparin after aneurysm secured)
Nimodipine 60mg PO q 4 hours X 21 days
Secure aneurysm
Neurosurgical Clipping
Endovascular Coiling (favored in ISAT)

81. Subarachnoid Hemorrhage
Complications:
Rebleeding (7%)
Vasospasm (46%) Highest incidence 3-12 days after SAH
Screen with TCD
Treat with Hypervolemia and Induced Hypertension
Angiography
Hydrocephalus (20%)
EVD
Permanent Shunt
Seizures (30%)
Antiepileptics for 1 week to 1 month

82. Unconscious adult patients with spontaneouscirculation
after out-of-hospital cardiac arrest should be cooled to 32°C
to 34°C for 12 to 24 hours when the initial rhythm was
ventricularfibrillation (VF).
HYPOTHERMIA
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrest.
Circulation. 2003;108:118