Intracranial Hemorrhage &

Emergency Management of
Increased ICP
Emergency Neurology Lecture Series
Amy Yu
August 5th 2009
 ICH by numbers
 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
 Outline
 Intracranial hemorrhage
 Mechanism and pathophysiology
 Clinical features

 Management principles

 Intracranial hypertension
 Monitoring

 Management principles
 Mechanisms of ICH
 Hypertension
 Vascular malformations
 Intracranial tumors
 Bleeding diathesis, anticoagulation, fibrinolysis
 Cerebral amyloid angiopathy
 Granulomatous angiitis & vasculitides
 Sympathomimetic agents (amphetamine, cocaine)
 Hemorrhagic infarction
 Trauma
 Clinical features
 Features of intracranial hypertension
 Headache, vomiting, decreased LOC
 Correlated with hematoma size and prognosis

 Progressive over time

 Seizures in lobar ICH

 Focal neurological deficits depending on the

location of ICH
 POP QUIZ
When are patients most likely to
suffer from primary ICH?

a) Midnight (excessive partying…)

b) 8 AM (don’t want to go to work)
c) Noon (excessive hunger)
d) 5 PM (too much excitement from
ending work)
 POP QUIZ
When are patients most likely to
suffer from primary ICH?

a) Midnight (excessive partying…)

b) 8 AM (don’t want to go to work)
c) Noon (excessive hunger)
d) 5 PM (too much excitement from
ending work)
 Hypertension and ICH
 Most important risk factor (>70% of 1ry ICH)
 Bifurcation of small penetrating arteries (50–700
μm diameter)
 Atherosclerosis
 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
 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
 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
 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
 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
 A-B-C: Airway support
 Decreased level of consciousness
 Bulbar muscle dysfunction

 Blood pressure control

 Acute hemostatic treatment
 Anticoagulation reversal
 Intracranial pressure control
 Monitoring
 Neurological and cardiovascular deterioration
greatest in the 24hours following symptom onset
 Blood pressure & ICH
 BP is elevated on admission even in patients
who have no history of hypertension
 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
PROs CONs
  BP associated with  Chronic HTN shifts
poor outcome cerebral autoregulatory
  risk of hematoma curve to the right
enlargement   ICP may require  BP
  edema formation to maintain CPP
 Systemic damage (e.g.  Previously thought to
ongoing cardiac induce ischemic damage
ischemia) to the at risk penumbra
 Edema & ischemic penumbra?
 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
 Mitochondrial dysfunction causing hypometabolism
 Regional hypoperfusion 2ry hypometabolism
 Usually not severe enough to cause ischemia
 Global cerebral ischemia
 Very elevated ICP and low cerebral perfusion pressure
 Acute management of BP
 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
 ASA Guidelines 2007 (Class IIb, Level C)
 sBP>200 mmHg or MAP>150 mmHg
 Aggressive BP control with IV infusion and BP monitoring
q5minutes
 sBP>180 mmHg or MAP>130 mmHg WITH elevated
ICP
 Consider monitoring ICP
 Intermittent bolus or continuous infusion to aim for CPP > 60-
80 mmHg
 sBP>180 mmHg or MAP>130 mm Hg WITHOUT
elevated ICP
 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
 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
 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
 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
 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
 Broderick, JP et al. Stroke 1993;24:987-993
 1.26 million subjects from Greater Cincinnati
 ABC of hematoma size
 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

 A, B, and C were then multiplied and the product

divided by 2
 CT-A “Spot Sign”
 Focal area of
enhancement within the
hematoma on CTA have
been shown to be:
 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”
 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

 Comparison to unenhanced CT for mimickers

 Calcifications (tumour, choroid, infectious, etc)
 Anticoagulation associated ICH
 Warfarin is a Vit K antagonist
 Inhibits biosynthesis of factors II, VII, IX, X
 Maximum effect is 48 hrs after administration

 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!)

 INR correlated with hematoma expansion and

prognosis
 Anticoagulation associated ICH
 Goal of treatment: fully reverse INR to normal range
 High dose Vitamin K 10-20 mg IV slow infusion
 Effect takes 12-24hrs
 Helps achieving sustained reversal of INR
 Fresh frozen plasma 15cc/kg  4U
 Volume overload, insufficient factor IX
 ABO compatibility, thawing, infusion time (30hrs)
 Prothrombin Complex Concentrates (PCC, Octaplex)
 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
 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
 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
 1% recurrent ICH in initial 3 mths post ICH
 Risk estimated to double with anticoagulation

Stroke.
2007;38:200
1-2023
 Miscellaneous
 Venous thromboembolism prophylaxis
 Intermittent pneumatic compression
 Heparin SQ prophylaxis (3-4 d if no bleeding)
 IVC filter (proximal venous thrombosis)

 Hyperglycemia
 Associated with poor outcome and  mortality
 Marker of outcome or contributor?

 Hyperpyrexia
 Associated with poor outcome and neuro deterioration
 Septic workup, treat with antipyretics or cooling devices
 Often central in origin
 Part II:
Management of Increased
Intracranial Pressure
 Basic concepts of ICP
 Monro-Kellie doctrine
 Blood + CSF + Brain =
constant
 CPP = MAP – ICP
 CBF = CPP / CVR
 Intracranial elastance =
  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 RELATIVE
 Severe head injury (GCS   Impossible serial
8) AND abnormal CT neurological examination
 Severe head injury (GCS  due to:
8), normal CT, AND at  Intubation, deep
least 2 of the following: sedation or paralysis
 Age 40 years or greater  Immediate non-
 Motor posturing neurosurgical procedure
 Systolic BP  90 mm  Large cerebral infarction
Hg with high risk of cerebral
edema
 SAH with hydrocephalus
 CNS tumor
 CNS infection
 Rationale for ICP monitoring
 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
 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 Brain volume Blood volume
 Mannitol or  Mannitol or  Mannitol or
hypertonic hypertonic hypertonic saline
solution saline
 External CSF  Decompressive  Hyperventilation
drainage craniectomy  Hypothermia
 Ventricular  Resection of  Head elevation,
catheter tumor or other
 Ventriculo - mass lesion neutral neck
peritoneal or position
atrial shunt  Deep propofol or
 Lumbar drain barbiturate
 Serial lumbar sedation ±
punctures Seizure Control
paralysis
 Hyperventilation
 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
 Safety of duration is uncertain
 Resection of mass lesion
 Subdural or epidural hemorrhage
 Hematoma evacuation
 Tumours
 Surgical resection
 CSF drainage
 Communicating hydrocephalus (e.g. SAH, IVH)
 Temporary external ventricular drain
 Long term VP or VA shunt

 Obstructive hydrocephalus (e.g. tumours)

 Temporary external ventricular drain until definitive
tumour resection
 Head elevation
 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
 CPP = MAP – ICP
Paralysis, Sedation, Hypothermia
 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
 Rule out ongoing seizure activity
 Titration of sedation with goal of achieving burst suppression
 Hypothermia, controversial
 Attenuates deleterious biochemical cascade
  cerebral metabolic rate
  risk pneumonia, wound infection, abnormal lytes/coags
Mannitol and Hypertonic saline (HS)
 Mannitol 20% or 25% solution (0.25 – 1gm/kg IV)
 Intravascular fluid shift from osmotic effect
 Decreased blood viscosity and improved flow (? reflex
vasocontriction)
 Decreases production of CSF
 Follow serum osmolarity (<320 mOsm)
 Avoid systemic dehydration & renal injury
 Can consider adding Furosemide
 Hypertonic saline, if refractory to mannitol
 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
 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
 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
 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