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STROKE, SUBARACHNOID
HEMORRHAGE AND HYPOTHERMIA
FOR CARDIAC ARREST
-Andy Rekito
Dallas Presbyterian Hospital
Internal Medicine Resident Lecture
August 27, 2009
Samir Shah, MD
Neurology Consultants of Dallas
Quick Stroke Facts - 2009
FACT: About 795,000 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 17 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 $68.9 billion in 2009 for
stroke related medical costs and disability.
American Heart Association. Heart Disease and Stroke Statistics — 2009
Update. Dallas, Tex.: American Heart Association; 2009.
FACT: Prevalence of stroke in the US is 6.5 million people
(2005). Stroke is a leading cause of serious disability.
Prevalence of Stroke by Age and Sex
NHANES: 1999-2002
Percent of Population
14
12.0 11.5
12
10
8
6.6 6.3
6
4
2
0.4
0.3
1.1 0.8
`
0
20-34
35-44
2.1
1.2
3.1 3.0
45-54
55-64
Ages
Men
Source: CDC/NCHS and NHLBI.
Women
65-74
75+
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.
TIA
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.
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In short, the 24-hour definition of TIA is outdated, confusing,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…
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).
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 first focus on ischemic stroke…
Consult for a 68 year-old man
that has new right-sided
weakness and is “talking
funny.” It started a few hours
ago.
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
MetabolicHypoglycemia/Hyperglycemia
Cerebral venous thrombosis
Psychogenic
Deficit from previous stroke made
worse by general medical condition
Quickly Narrow the Differential
With Imaging
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).
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
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.
Other Acute Studies
Urine pregnancy test
Urine toxicology
Hypercoagulable screen
CXR
Type and Screen
What are the risk
factors for ischemic
stroke?
Risks that can be controlled or
treated
Risk Factors for
Ischemic Stroke
Risks that cannot change
Age
Prior stroke or MI
Gender
Heredity/Ethnicity
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
Estimated 10-Year Rate (%)
Estimated 10-Year Stroke Risk in 55Year-Old Adults According to Levels of
Various Risk Factors - Framingham
Heart Study
27.0
30
22.4
25
19.1
20
14.8
15
8.4
10
5
2.6
4.0
1.1
5.4
2.0
6.3
3.5
0
A
B
C
Men
Systolic BP
Diabetes
Cigarettes
Prior Atrial Fib.
Prior CVD
A
95-105
No
No
No
No
B
130-148
No
No
No
No
D
F
Wom en
C
130-148
Yes
No
No
No
Source: Stroke 1991;22:312-318.
E
D
130-148
Yes
Yes
No
No
E
130-148
Yes
Yes
Yes
No
F
130-148
Yes
Yes
Yes
Yes
Estimates of Vascular Event Rates for Persons With
Various Features of Atherothrombotic Cerebrovascular
Disease
Cerebrovascular Features
General elderly male population
Annual Probability(%)
Stroke Vascular Death
Major stroke
0.6
1.3
2.2
3.7
6.1
9.0
------3.4
3.5
2.3
3.2
3.5
Symptomatic carotid stenosis >70%
15
2.0
Asymptomatic carotid disease
Transient monocular blindness
Transient ischemic attack
Minor stroke
Stroke. 1997;28:1507-1517.
Risk Factors for
Intracerebral and
Subarachnoid
Hemorrhage
++ indicates strong evidence; +,
moderate positive evidence; ?,
equivocal evidence; –, moderate
inverse evidence; and 0, no relation.
ICH SAH
Age
Women
++
-
Race/ethnicity
Hypertension
Cigarette smoking
+ +
++ +
? ++
Heavy use of alcohol
Anticoagulation
Amyloid angiopathy
++
++
++
?
?
0
Hypocholesterolemia
Oral Contraceptives
?
0
0
?
Stroke. 1997;28:1507-1517.
+
+
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)
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
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.
www.ferne.org
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.
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.
Source: Loyola University Neurovascular Tutorial
Four Divisions of the Vertebral Artery
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%)
Common Stroke Mechanisms
The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy
STROKE
85%
15%
Primary Hemorrhage
Intraparenchymal
Subarachnoid
Ischemic Stroke
20%
Atherosclerotic
Cerebrovascular
Disease
(“Large Artery”)
25%
Penetrating
Artery Disease
(“Lacunes”)
20%
Cardiogenic
Embolism
Atrial Fibrillation
Valve Disease
Ventricular Thrombi
Hypoperfusion
Arteriogenic
Emboli
Many Others
30%
Cryptogenic
Stroke
5%
Other,
Unusual
Causes
Prothrombotic States
Dissections
Arteritis
Migraine/vasospasm
Drug Abuse
Many More
You are done thinking of stroke
mechanisms and you are almost at the ER
when you get paged 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?
Cerebral Autoregulation:
It may not be working
DO NOT TREAT BP IN ACUTE ISCHEMIC
STROKE UNLESS BP>200-220/100-120
The Patient Encounter
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.
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.
Now what?
Hyperdense MCA Sign
Insular Ribbon Sign
Loss of Gray-White
Junction
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.
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 (most now say less than 270 minutes)
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 (INR>1.7)
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
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
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
Additional exclusion criteria for extended time window
Age >80
NIHSS >25
Any oral anticoagulant use
History of both previous stroke and diabetes
del Zoppo GJ, Saver JL, Jauch EC, Adams HP Jr; on behalf of the American Heart Association Stroke Council.
Expansion of the time window for treatment of acute ischemic stroke with intravenous tissue plasminogen
activator: a science advisory from the American Heart Association/American Stroke Association. Stroke.
2009;40:2945-8.
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) (14 for extended time window)
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
Grotta, J. C. Stroke 1999;30:1722-1728
Copyright ©1999 American Heart Association
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.
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?
Antithrombotic and Thrombolytic Therapy for Ischemic Stroke: The
Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy
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 160325mg of ASA within
48hours of onset. (some
may advocate acute
anticoagulation for certain
stroke subtypes).
Absolute effects in CAST and IST of early use of aspirin in 40 000 randomized patients
with suspected acute ischemic stroke
Chen, Z. et al. Stroke 2000;31:1240-1249
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.
Copyright ©2000 American Heart Association
Admit the Patient
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.
Where would you admit this patient?
How about this patient?
Let’s say the patient’s
symptoms resolved by the
time you got there and he now
feels fine and wants to go
home
PATIENT IS AT HIGH RISK AND NEEDS TO BE ADMITTED
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).
Evaluation During Admission
1.
2.
3.
4.
5.
6.
7.
Labs: LFTs, fasting lipid profile and glucose, QID bedside glucose
and SSI. Consider Hypercoagulable workup, ESR, ANA, hsCRP,
HbA1c, homocysteine, LP
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
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.)
Rehabilitation evaluation
Bedside or formal swallow evaluation
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
DVT and GI prophylaxis if indicated
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
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
Acute Intraparenchymal Hematoma Imaged With Computed Tomography and With Magnetic
Resonance Imaging
Kidwell, C. S. et al. JAMA 2004;292:1823-1830.
Copyright restrictions may apply.
The Ischemic Penumbra
Approximated by PWI-DWI MRI Mismatch and used to help
guide interventional acute stroke therapies…
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.
Traditionally High Mortality and
Limited Recovery
• Mortality
100%
– 6-month, 30%-50%
– 1-year, 50%
• Medical costs
– US$125,000 lifetime cost per
person (1990)
– Direct and indirect costs (lost
productivity + caregiver burden)
Proportion of patients (%)
• Only 20% of ICH patients
are independent at 6
months vs 60% of
ischemic stroke patients
90%
80%
70%
60%
50%
40%
30%
20%
10%
0%
ICH
Dead
Ischemic
Dependent
Manno EM, et al. Mayo Clin Proc. 2005;80:420-433; Mayer SA, Rincon F. Lancet Neurol.
2005;4:662-672; Qureshi AI, et al. N Engl J Med. 2001;344:1450-1460; Taylor TN, et al. Stroke.
1996;27:1459-1466; Reed SD, et al. Neurology. 2001;57:305-314.
Independent
Predictors of Outcome
●
Hematoma volume
●
GCS
●
Intraventricular
hemorrhage
●
Age
●
ICH location (deep)
●
Increased cerebral edema
(midline shift, herniation)
Manno EM, et al. Mayo Clin Proc. 2005;80:420-433; Garibi J, et al. Br J
Neurosurg. 2002;16:355-361.
Predictors of Outcome
The ICH Score
Component
ICH score
points
3-4
2
5-12
1
13-15
0
>30
1
<30
0
Intraventricular
hemorrhage
Yes
1
No
0
Infratentorial
origin
Yes
1
No
0
GCS
ICH volume (cc)
Age (y)
>80
1
<80
0
Total ICH score
30-day Mortality
100
80
60
40
20
0
Overall
0
0-6
Reproduced with permission from Hemphill JC III, et al. Stroke. 2001;32:891-987.
1
2
ICH Score
3
4
5
Sites of Spontaneous ICH
Thalamic
Hemorrhage
(20%)
Lobar
Subcortical
Hemorrhage
(25%)
Putaminal
Hemorrhage
(35%)
Pontine
Hemorrhage
(7%)
Cerebellar
Hemorrhage
(8%)
Reproduced with permission from Mayer SA, Rincon F. Lancet
Neurol. 2005;4:662-672; Qureshi AI, et al. N Engl J Med.
2001;344:1450-1460.
General Management of ICH
Goals
Provide general supportive care in the ED and
ICU/NICU to manage the primary brain injury and limit the
secondary brain injury
•
•
•
•
•
•
Continue to support ABCs
Monitoring (BP, fever, ICP, labs)
Intubation
BP management
Seizure management
Reverse anticoagulation immediately
Blood Pressure Management
AHA/ASA Guidelines (2007)
• BP thresholds (limited supportive data)
• Select target BP on basis of
patient factors
– Baseline BP
– Interval since ICH onset
– Cause of hemorrhage
– Age
– Elevated ICP
– SBP ≤180 mm Hg and/or
– MAP <130 mm Hg
• Closely titrate short-acting IV agents
Suggested Guidelines for Elevated BP in ICH
If SBP >200 mm Hg or
MAP >150 mm Hg
• Consider “aggressive”
•
•
BP reduction
Continuous IV
Frequent BP monitoring
If SBP >180 mm Hg or
MAP >130 mm Hg
and ↑ ICP
• Monitor ICP
• Intermittent/continuous
IV (CPP >60-80 mm Hg)
Broderick J, et al. Stroke. 2007;38:2001-2023.
If SBP >180 mm Hg or
MAP >130 mm Hg
and no ↑ ICP
• Consider “modest” BP
•
reduction
Intermittent/continuous
IV
Subarachnoid Hemorrhage
Causes:
Aneurysm (80% of non-traumatic cases)
Trauma
Vascular Malformations
Tumors
Infection
Venous Thrombosis
Subarachnoid Hemorrhage
(Aneurysmal)
Demographics:
Mean age = 55 years
Women 1.6X > Men
Blacks > Whites
Average Case Fatality Rate > 50%
Subarachnoid Hemorrhage
(Aneurysmal)
Risk Factors:
Smoking
Hypertension
Cocaine Use
Heavy alcohol use
First degree relatives with SAH
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
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)
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)
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
HYPOTHERMIA
Unconscious adult patients with spontaneous circulation
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
ventricular fibrillation (VF).
Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrest.
Circulation. 2003;108:118