Transcript Intracranial Hemorrhage & Emergency Management of

Intracranial Hemorrhage &
Emergency Management of
Increased ICP
Emergency Neurology Lecture Series
Amy Yu
August 5th 2009
ICH by numbers
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Result of a rupture of blood vessel in the brain
Accounts for 10-15% of all cerebrovascular
accidents
2 million strokes every year worldwide
Rise of admissions in the past 10 years by 18%
Prognosis is poor: estimated mortality
30% at 7 days
 60% at 1 year
 82% at 10 years
 >90% at 16 years
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Outline
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Intracranial hemorrhage
 Mechanism
and pathophysiology
 Clinical features
 Management principles
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Intracranial hypertension
 Monitoring
 Management
principles
Mechanisms of ICH
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Hypertension
Vascular malformations
Intracranial tumors
Bleeding diathesis, anticoagulation, fibrinolysis
Cerebral amyloid angiopathy
Granulomatous angiitis & vasculitides
Sympathomimetic agents (amphetamine, cocaine)
Hemorrhagic infarction
Trauma
Clinical features
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Features of intracranial hypertension
Headache, vomiting, decreased LOC
 Correlated with hematoma size and prognosis
 Progressive over time
 Seizures in lobar ICH
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Focal neurological deficits depending on the
location of ICH
POP QUIZ
When are patients most likely to
suffer from primary ICH?
a)
b)
c)
d)
Midnight (excessive partying…)
8 AM (don’t want to go to work)
Noon (excessive hunger)
5 PM (too much excitement from
ending work)
POP QUIZ
When are patients most likely to
suffer from primary ICH?
a)
b)
c)
d)
Midnight (excessive partying…)
8 AM (don’t want to go to work)
Noon (excessive hunger)
5 PM (too much excitement from
ending work)
Hypertension and ICH
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Most important risk factor (>70% of 1ry ICH)
Bifurcation of small penetrating arteries (50–700
μm diameter)
Atherosclerosis
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Lipid deposition, layering of platelet and fibrin
aggregates, breakage of elastic lamina, atrophy and
fragmentation of smooth muscle, dissections, and
granular or vesicular cellular degeneration
Charcot and Bouchard aneurysm
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Fibrinoid necrosis of the subendothelium  focal
dilatations  rupture of microaneurysm
N Engl J Med 2001;344(19):1450–1460
Lobar hemorrhage 25%
• Penetrating cortical
branches of ACA,
MCA, & PCA
• Peripheral location 
lower frequency of
coma
• Lower mortality
• Better functional
outcome
N Engl J Med 2001;344(19):1450–1460
Basal ganglia 35-40%
• Ascending
lenticulostriate
branches of MCA
• Wide spectrum of
severity extending to
coma and
decerebrate rigidity
• Ventricular extension
carries very poor
prognosis
N Engl J Med 2001;344(19):1450–1460
Thalamus 10-15%
• Ascending
thalamogeniculate
branches of PCA
• Abrupt
hydrocephalus from
aqueductal
obstruction from
intraventricular clot
• Responds to
ventriculostomy
N Engl J Med 2001;344(19):1450–1460
Pons 5%
• Paramedian branches
of the basilar artery
• Bilateral carries very
poor prognosis
(coma, quadriplegia,
decerebrate
posturing, horizontal
ophthalmoplegia,
pinpoint reactive
pupils)
N Engl J Med 2001;344(19):1450–1460
Cerebellum 5-10%
• Penetrating branches
of the PICA, AICA,
SCA
• Abrupt onset vertigo,
h/a, n/v, inability to
walk in absence of
weakness
• Ipsilateral ataxia,
horizontal gaze palsy,
peripheral facial palsy
• Unpredictable
deterioration to coma
N Engl J Med 2001;344(19):1450–1460
Vascular malformations
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Aneurysms, AVM, cavernous angiomas
Younger, female patients, familial history
Imaging may show concurrent SAH
Dx by MRI and cerebral angiography
 Usually supratentorial, lobar ICH
 Cavernous angioma: on MRI (T2) central
nidus of irregular bright signal mixed with
mottled hypointensity, surrounded by
peripheral hypointense ring
Vascular malformations
Intracranial tumour
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Accounts for 10% of cases
GBM or metastases (melanoma, bronchogenic
carcinoma, renal cell carcinoma)
Suggestive features:
Papilledema
 Atypical location (e.g. corpus callosum)
 Disproportionate amount of surrounding edema
 Multiple sites simultaneously
 Non-contrast CT: ring of high-density hemorrhage
with low-density center
 Contrast CT/MRI: presence of enhancing nodules
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POP QUIZ
Which of the following is TRUE?
a) Elevated BP in acute ICH is an indication
of chronic hypertension
b) Hematoma is surrounded by an ischemic
penumbra & BP should be  with caution
c) Hyperglycemia is associated with
hematoma expansion
d) Nitroprusside is the agent of choice for
BP control in acute ICH
POP QUIZ
Which of the following is TRUE?
a) Elevated BP in acute ICH is an indication
of chronic hypertension
b) Hematoma is surrounded by an ischemic
penumbra & BP should be  with caution
c) Hyperglycemia is associated with
hematoma expansion
d) Nitroprusside is the agent of choice for
BP control in acute ICH
Management principles
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A-B-C: Airway support
Decreased level of consciousness
 Bulbar muscle dysfunction
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Blood pressure control
Acute hemostatic treatment
Anticoagulation reversal
Intracranial pressure control
Monitoring
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Neurological and cardiovascular deterioration
greatest in the 24hours following symptom onset
Blood pressure & ICH
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BP is elevated on admission even in patients
who have no history of hypertension
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MAP > 120mmHg in over 2/3 of patients
Precipitant of the hemorrhage?
Reflection of chronic hypertension?
Attempt to maintain CPP?
Sympathetic activation 2ry to pain & anxiety?
Tends to return to baseline 7-10 days post ICH
Acute management of BP
Cerebral autoregulatory curve
CPP = MAP – ICP
Acute management of BP
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PROs
 BP associated with
poor outcome
 risk of hematoma
enlargement
 edema formation
Systemic damage (e.g.
ongoing cardiac
ischemia)
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CONs
Chronic HTN shifts
cerebral autoregulatory
curve to the right
 ICP may require  BP
to maintain CPP
Previously thought to
induce ischemic damage
to the at risk penumbra
Edema & ischemic penumbra?
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Up to 75% increase in volume in the first 24 hours
Peaks around 5 to 6 days and lasts up to 14 days
Early large edema relative to hematoma is a predictor of
poor outcome
Hibernation phase
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Mitochondrial dysfunction causing hypometabolism
Regional hypoperfusion 2ry hypometabolism
Usually not severe enough to cause ischemia
Global cerebral ischemia
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Very elevated ICP and low cerebral perfusion pressure
Acute management of BP
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Baseline blood pressure
Age
Presumed cause of hemorrhage (ruptured aneurysm or AVM?)
Elevated intracranial pressure
How fast should BP be lowered?
 Rapidly lowering MAP by  15% does not lower CBF
 Reductions of 20% can affect CBF
 Current guidelines suggest a reduction of ≤ 20% in the first
24 hrs
Which agents should be used?
 Short and rapidly acting IV antihypertensive
 Labetalol, hydralazine, esmolol, nicardipine, enalapril
 Sodium nitroprusside and nitroglycerin should be used with
caution d/t vasodilation and potential effect on ICP
Acute management of BP
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ASA Guidelines 2007 (Class IIb, Level C)
sBP>200 mmHg or MAP>150 mmHg
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sBP>180 mmHg or MAP>130 mmHg WITH elevated
ICP
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Aggressive BP control with IV infusion and BP monitoring
q5minutes
Consider monitoring ICP
Intermittent bolus or continuous infusion to aim for CPP > 6080 mmHg
sBP>180 mmHg or MAP>130 mm Hg WITHOUT
elevated ICP
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Consider modest BP reduction of blood pressure with
intermittent bolus or continuous infusion
Aim for MAP of 110 mmHg or BP of 160/90 mmHg
Hematoma expansion
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Hematoma enlargement
 >70% have hematoma enlargement w/in 3 hrs of
symptom onset; 1/3 clinically significant
 Most occur within 3 hrs, can be up to 12 hrs
 Independent predictor of worse outcome & 
mortality
Hematoma expansion
Journal of the
Neurological
Sciences 261
(2007) 99–107
Recombinant Factor VIIa
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Factor VIIa has locally action at sites of tissue injury
and vascular-wall disruption by binding tissue factor &
generating thrombin and activating platelets
Recombinant FVIIa directly activates fX on the surface
of activated plts resulting in acceleration of coagulation
Factor Seven for Acute Hemorrhagic Stroke (FAST)
trial, N Engl J Med 2008;358:2127-37
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841 patients, within 4 hours of onset of stroke
Placebo vs. 20 μg/kg vs. 80 μg/kg of rFVIIa
1ry end point: 90-day functional outcome or death
Recombinant Factor VIIa
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Significant reduction in growth of hematoma
volume in the 80 μg/kg group
No significant difference in functional outcome
and mortality
Venous thromboembolic events were similar in
all three groups
Arterial thromboembolic events were
significantly more frequent in the 80 μg/kg
group
ABC of hematoma size
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Broderick, JP et al. Stroke 1993;24:987-993
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1.26 million subjects from Greater Cincinnati
ABC of hematoma size
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Bedside ABC/2 method for hemorrhage volume in cm3
1. Identify the CT slice with the largest area of hemorrhage
2. Measure the largest diameter of the hemorrhage on this slice (A)
3. Measure the largest diameter 90° to (A) on the same slice (B)
4. Approximate number of 10-mm slices on which the ICH was
seen was calculated (C)
 If area > 75% compared to where the hemorrhage was
largest, the slice was considered 1 hemorrhage slice
 If area 25% to 75%, the slice was considered 1/2 a slice
 If area < 25%, the slice was not considered a slice
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A, B, and C were then multiplied and the product
divided by 2
CT-A “Spot Sign”
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Focal area of
enhancement within the
hematoma on CTA have
been shown to be:
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Independent predictor of
hematoma expansion
Associated with longer
median hospital stay
Independent of time to
presentation
Sensitivity 91%,
specificity 89%, NPV
96%
CT-A “Spot Sign”
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Recent proposal of a “Spot Sign” definition
(Can J Neurol Sci 2009;36:456-461)
Serpiginous and/or spot-like appearance
 Within the margin of the parenchymal hematoma
without connection to an outside vessel
 >1.5mm diameter in maximal axial dimention
 >Double the HU density compared to background
hematoma (>150 HU)
 Multiple or single in number
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Comparison to unenhanced CT for mimickers
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Calcifications (tumour, choroid, infectious, etc)
Anticoagulation associated ICH
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Warfarin is a Vit K antagonist
Inhibits biosynthesis of factors II, VII, IX, X
 Maximum effect is 48 hrs after administration
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Incidence of ICH is 0.3-0.6% per year in
patients on chronic warfarin anticoagulation
Risk factors
Age, chronic hypertension, CAA, leukoaraiosis
 Elevation of INR (doubled risk for 0.5  above 4.5!)
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INR correlated with hematoma expansion and
prognosis
Anticoagulation associated ICH
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Goal of treatment: fully reverse INR to normal range
High dose Vitamin K 10-20 mg IV slow infusion
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Fresh frozen plasma 15cc/kg  4U
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Effect takes 12-24hrs
Helps achieving sustained reversal of INR
Volume overload, insufficient factor IX
ABO compatibility, thawing, infusion time (30hrs)
Prothrombin Complex Concentrates (PCC, Octaplex)
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Combination of II, VII, IX, X, variable protein C and S
Dosage dependant on initial INR
Smaller volume, correct INR as fast as 30 min
Anticoagulation associated ICH
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ICH associated with IV heparin
Rapidly normalize activated partial thromboplastin time
Protamine sulfate 1 mg per 100 U heparin, adjusted for
time since last heparin dose
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30-60 min: 0.5 to 0.75 mg per 100U heparin
60-120 min: 0.375 to 0.5 mg per 100 U heparin
>120min: 0.25 to 0.375 mg per 100 U heparin
Slow IV injection (<5 mg/min, max dose 50 mg)
Beware of systemic hypotension
AAICH – restarting anticoagulation
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1% recurrent ICH in initial 3 mths post ICH
Risk estimated to double with anticoagulation
Stroke.
2007;38:200
1-2023
Miscellaneous
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Venous thromboembolism prophylaxis
Intermittent pneumatic compression
 Heparin SQ prophylaxis (3-4 d if no bleeding)
 IVC filter (proximal venous thrombosis)
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Hyperglycemia
Associated with poor outcome and  mortality
 Marker of outcome or contributor?
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Hyperpyrexia
Associated with poor outcome and neuro deterioration
 Septic workup, treat with antipyretics or cooling devices
 Often central in origin
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Part II:
Management of Increased
Intracranial Pressure
Basic concepts of ICP
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Monro-Kellie doctrine
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Blood + CSF + Brain =
constant
CPP = MAP – ICP
CBF = CPP / CVR
Intracranial elastance =
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 ICP /  volume
AAN Continuum Feb 2006
POP QUIZ
37♂ MVA, conscious
at the scene, became
obtunded in the ER.
He was intubated and
underwent CT of the
head.
POP QUIZ
Should this candidate have invasive
intracranial pressure monitoring?
a) Yes
b) No
c) It depends
POP QUIZ
Should this candidate have invasive
intracranial pressure monitoring?
a) Yes
b) No
c) It depends
Indications for ICP monitoring
ABSOLUTE
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Severe head injury (GCS 
8) AND abnormal CT
Severe head injury (GCS 
8), normal CT, AND at
least 2 of the following:
 Age 40 years or greater
 Motor posturing
 Systolic BP  90 mm
Hg
RELATIVE
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Impossible serial
neurological examination
due to:
 Intubation, deep
sedation or paralysis
 Immediate nonneurosurgical procedure
Large cerebral infarction
with high risk of cerebral
edema
SAH with hydrocephalus
CNS tumor
CNS infection
Rationale for ICP monitoring
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Development of pressure gradient and brain
herniation
Help guide blood pressure management
Goals of treatment
ICP should be maintained < 20 mmHg
 CPP should be maintained between 60-70 mmHg
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POP QUIZ
What is the most appropriate next step in
management in the ER pending
neurosurgical evaluation?
a) Immediate insertion of an external
ventricular drain
b) Hyperventilation
c) Mannitol followed by hypertonic saline
d) Head elevation
POP QUIZ
What is the most appropriate next step in
management in the ER pending
neurosurgical evaluation?
a) Immediate insertion of an external
ventricular drain
b) Hyperventilation
c) Mannitol followed by hypertonic saline
d) Head elevation
Approach to ICP management
CSF volume
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Mannitol or
hypertonic
solution
External CSF
drainage
Ventricular
catheter
Ventriculo peritoneal or
atrial shunt
Lumbar drain
Serial lumbar
punctures
Blood volume
Brain volume
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Mannitol or
hypertonic
saline
Decompressive
craniectomy
Resection of
tumor or other
mass lesion
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Seizure Control
Mannitol or
hypertonic saline
Hyperventilation
Hypothermia
Head elevation,
neutral neck
position
Deep propofol or
barbiturate
sedation ±
paralysis
Hyperventilation
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Useful in initial resuscitation: effectively and
rapidly reduce ICP in acute rises until definitive
therapy
Generalized vasoconstriction:  cerebral blood
volume,  ICP
Chronic hyperventilation should be avoided
because  CBF puts the brain at risk of ischemia
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Safety of duration is uncertain
Resection of mass lesion
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Subdural or epidural hemorrhage
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Hematoma evacuation
Tumours
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Surgical resection
CSF drainage
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Communicating hydrocephalus (e.g. SAH, IVH)
Temporary external ventricular drain
 Long term VP or VA shunt
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Obstructive hydrocephalus (e.g. tumours)
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Temporary external ventricular drain until definitive
tumour resection
Head elevation
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Head of bed at 20 to 30 is optimizes cerebral
venous return
Ensure neutral neck position
Caution in hypovolemic patients to avoid
reduction in MAP and therefore CPP
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CPP = MAP – ICP
Paralysis, Sedation, Hypothermia
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To prevent excess motor activity (posturing, coughing,
straining against ventilator)
To  cerebral metabolic rate and  CBF (must maintain
MAP to improve CPP  caution in HD unstable
patients)
Role of EEG
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Rule out ongoing seizure activity
Titration of sedation with goal of achieving burst suppression
Hypothermia, controversial
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Attenuates deleterious biochemical cascade
 cerebral metabolic rate
 risk pneumonia, wound infection, abnormal lytes/coags
Mannitol and Hypertonic saline (HS)
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Mannitol 20% or 25% solution (0.25 – 1gm/kg IV)
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Follow serum osmolarity (<320 mOsm)
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Intravascular fluid shift from osmotic effect
Decreased blood viscosity and improved flow (? reflex
vasocontriction)
Decreases production of CSF
Avoid systemic dehydration & renal injury
Can consider adding Furosemide
Hypertonic saline, if refractory to mannitol
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BBB is impermeable to Na+ ions  Osmotic gradient
Less severe electrolyte disturbances, less brisk diuresis
Lack of standard guideline (3-7.5% solution at 20-40cc/h)
Slow taper to avoid rebound hyponatremia
Decompressive craniectomy
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Surgical removal of cranial bone flap to relieve
intracranial pressure
Useful in large ischemic CVA with profound
edema
Role in traumatic brain injury still needs to be
established
Conclusions
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ICH has an increasing incidence, but continues
to have a very poor prognosis
Hypertension is a major risk factor
Acute BP reduction of 15-20% is safe
Anticoagulation should be reversed ASAP
Absolute indications for ICP monitoring
Major categories of increased ICP management
Thank you!
References
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Goldstein, JN et al. Contrast extravasation on CT angiography
predicts hematoma expansion in intracerebral hemorrhage,
Neurology 2007;68:889–894
Qureshi AI et al. Intracerebral hemorrhage, Lancet 2009; 373:
1632–44
Wada, R et al. CT Angiography “Spot Sign” Predicts Hematoma
Expansion in Acute Intracerebral Hemorrhage, Stroke
2007;38:1257-1262
Diringer MN. Update on intracerebral hemorrhage, AAN
Continuum, 2009
Kincaid MS and Lam AM, Monitoring and managing ICP, AAN
Continuum, 2006