Intracranial Intracranial Hemorrhage & Hemorrhage &

Emergency Emergency Management of Management of Increased ICPIncreased ICPEmergency Neurology Lecture Emergency Neurology Lecture

SeriesSeries

Amy YuAmy Yu

August 5August 5thth 2009 2009

ICH by numbersICH by numbers Result of a rupture of blood vessel in the Result of a rupture of blood vessel in the

brainbrain Accounts for Accounts for 10-15%10-15% of all of all

cerebrovascular accidentscerebrovascular accidents 2 million2 million strokes every year worldwide strokes every year worldwide Rise of admissions in the past 10 years Rise of admissions in the past 10 years

by by 18%18% Prognosis is poor: estimated mortalityPrognosis is poor: estimated mortality

30% at 7 days30% at 7 days 60% at 1 year60% at 1 year 82% at 10 years82% at 10 years >90% at 16 years>90% at 16 years

OutlineOutline Intracranial hemorrhageIntracranial hemorrhage

Mechanism and pathophysiologyMechanism and pathophysiology Clinical featuresClinical features Management principlesManagement principles

Intracranial hypertensionIntracranial hypertension MonitoringMonitoring Management principlesManagement principles

Mechanisms of ICHMechanisms of ICH HypertensionHypertension Vascular malformationsVascular malformations Intracranial tumorsIntracranial tumors Bleeding diathesis, anticoagulation, Bleeding diathesis, anticoagulation,

fibrinolysisfibrinolysis Cerebral amyloid angiopathyCerebral amyloid angiopathy Granulomatous angiitis & vasculitidesGranulomatous angiitis & vasculitides Sympathomimetic agents (amphetamine, Sympathomimetic agents (amphetamine,

cocaine)cocaine) Hemorrhagic infarctionHemorrhagic infarction TraumaTrauma

Clinical featuresClinical features

Features of intracranial Features of intracranial hypertensionhypertension Headache, vomiting, decreased LOCHeadache, vomiting, decreased LOC Correlated with hematoma size and Correlated with hematoma size and

prognosisprognosis Progressive over timeProgressive over time Seizures in lobar ICHSeizures in lobar ICH

Focal neurological deficits Focal neurological deficits depending on the location of ICHdepending on the location of ICH

POP QUIZWhen are patients most likely tosuffer 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 QUIZWhen are patients most likely tosuffer 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 ICHHypertension and ICH Most important risk factor (>70% of 1ry Most important risk factor (>70% of 1ry

ICH)ICH) Bifurcation of small penetrating arteries Bifurcation of small penetrating arteries

(50–700 μm diameter)(50–700 μm diameter) AtherosclerosisAtherosclerosis

Lipid deposition, layering of platelet and fibrin Lipid deposition, layering of platelet and fibrin aggregates, breakage of elastic lamina, aggregates, breakage of elastic lamina, atrophy and fragmentation of smooth muscle, atrophy and fragmentation of smooth muscle, dissections, and granular or vesicular cellular dissections, and granular or vesicular cellular degenerationdegeneration

Charcot and Bouchard aneurysmCharcot and Bouchard aneurysm Fibrinoid necrosis of the subendothelium Fibrinoid necrosis of the subendothelium

focal dilatations focal dilatations rupture of microaneurysm rupture of microaneurysm

N Engl J Med 2001;344(19):1450–1460

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

Vascular malformationsVascular malformations Aneurysms, AVM, cavernous angiomasAneurysms, AVM, cavernous angiomas Younger, female patients, familial historyYounger, female patients, familial history Imaging may show concurrent SAHImaging may show concurrent SAH Dx by MRI and cerebral angiographyDx by MRI and cerebral angiography

Usually supratentorial, lobar ICHUsually supratentorial, lobar ICH Cavernous angioma: on MRI (T2) Cavernous angioma: on MRI (T2)

central nidus of irregular bright signal central nidus of irregular bright signal mixed with mottled hypointensity, mixed with mottled hypointensity, surrounded by peripheral hypointense surrounded by peripheral hypointense ringring

Vascular malformationsVascular malformations

Intracranial tumourIntracranial tumour Accounts for 10% of casesAccounts for 10% of cases GBM or metastases (melanoma, GBM or metastases (melanoma,

bronchogenic carcinoma, renal cell bronchogenic carcinoma, renal cell carcinoma)carcinoma)

Suggestive features:Suggestive features: PapilledemaPapilledema Atypical location (e.g. corpus callosum)Atypical location (e.g. corpus callosum) Disproportionate amount of surrounding edemaDisproportionate amount of surrounding edema Multiple sites simultaneouslyMultiple sites simultaneously Non-contrast CT: ring of high-density Non-contrast CT: ring of high-density

hemorrhage with low-density centerhemorrhage with low-density center Contrast CT/MRI: presence of enhancing Contrast CT/MRI: presence of enhancing

nodulesnodules

POP QUIZWhich of the following is TRUE?a) Elevated BP in acute ICH is an

indication of chronic hypertensionb) 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 QUIZWhich of the following is TRUE?a) Elevated BP in acute ICH is an

indication of chronic hypertensionb) 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 principlesManagement principles A-B-C: Airway supportA-B-C: Airway support

Decreased level of consciousnessDecreased level of consciousness Bulbar muscle dysfunctionBulbar muscle dysfunction

Blood pressure controlBlood pressure control Acute hemostatic treatmentAcute hemostatic treatment Anticoagulation reversalAnticoagulation reversal Intracranial pressure controlIntracranial pressure control MonitoringMonitoring

Neurological and cardiovascular Neurological and cardiovascular deterioration greatest in the 24hours deterioration greatest in the 24hours following symptom onsetfollowing symptom onset

Blood pressure & ICHBlood pressure & ICH

BP is elevated on admission even in patients BP is elevated on admission even in patients who have no history of hypertensionwho have no history of hypertension MAP > 120mmHg in over 2/3 of patientsMAP > 120mmHg in over 2/3 of patients

Precipitant of the hemorrhage?Precipitant of the hemorrhage? Reflection of chronic hypertension?Reflection of chronic hypertension? Attempt to maintain CPP?Attempt to maintain CPP? Sympathetic activation 2ry to pain & Sympathetic activation 2ry to pain &

anxiety?anxiety? Tends to return to baseline 7-10 days post Tends to return to baseline 7-10 days post

ICHICH

Acute management of BPAcute management of BP

Cerebral autoregulatory curveCerebral autoregulatory curve

CPP = MAP – ICPCPP = MAP – ICP

Acute management of BPAcute management of BP

PROsPROs BP associated BP associated

with poor outcomewith poor outcome risk of hematoma risk of hematoma

enlargementenlargement edema formationedema formation Systemic damage Systemic damage

(e.g. ongoing (e.g. ongoing cardiac ischemia)cardiac ischemia)

CONsCONs Chronic HTN shifts Chronic HTN shifts

cerebral cerebral autoregulatory curve autoregulatory curve to the rightto the right

ICP may require ICP may require BP to maintain CPPBP to maintain CPP

Previously thought to Previously thought to induce ischemic induce ischemic damage to the at risk damage to the at risk penumbrapenumbra

Edema & ischemic Edema & ischemic penumbra?penumbra?

Up to 75% increase in volume in the first 24 Up to 75% increase in volume in the first 24 hourshours

Peaks around 5 to 6 days and lasts up to 14 Peaks around 5 to 6 days and lasts up to 14 daysdays

Early large edema relative to hematoma is a Early large edema relative to hematoma is a predictor of poor outcomepredictor of poor outcome

Hibernation phaseHibernation phase Mitochondrial dysfunction causing hypometabolismMitochondrial dysfunction causing hypometabolism Regional hypoperfusion 2ry hypometabolismRegional hypoperfusion 2ry hypometabolism Usually not severe enough to cause ischemiaUsually not severe enough to cause ischemia

Global cerebral ischemiaGlobal cerebral ischemia Very elevated ICP and low cerebral perfusion Very elevated ICP and low cerebral perfusion

pressurepressure

Acute management of BPAcute 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 BPAcute management of BP ASA Guidelines 2007 (Class IIb, Level C)ASA Guidelines 2007 (Class IIb, Level C) sBP>200 mmHg or MAP>150 mmHgsBP>200 mmHg or MAP>150 mmHg

Aggressive BP control with IV infusion and BP Aggressive BP control with IV infusion and BP monitoring q5minutesmonitoring q5minutes

sBP>180 mmHg or MAP>130 mmHg sBP>180 mmHg or MAP>130 mmHg WITHWITH elevated ICPelevated ICP Consider monitoring ICPConsider monitoring ICP Intermittent bolus or continuous infusion to aim Intermittent bolus or continuous infusion to aim

for CPP > 60-80 mmHgfor CPP > 60-80 mmHg sBP>180 mmHg or MAP>130 mm Hg sBP>180 mmHg or MAP>130 mm Hg

WITHOUTWITHOUT elevated ICP elevated ICP Consider modest BP reduction of blood pressure Consider modest BP reduction of blood pressure

with intermittent bolus or continuous infusion with intermittent bolus or continuous infusion Aim for MAP of 110 mmHg or BP of 160/90 Aim for MAP of 110 mmHg or BP of 160/90

mmHgmmHg

Hematoma expansionHematoma expansion Hematoma enlargementHematoma enlargement

>70% have hematoma enlargement >70% have hematoma enlargement w/in 3 hrs of symptom onset; 1/3 w/in 3 hrs of symptom onset; 1/3 clinically significantclinically significant

Most occur within 3 hrs, can be up to Most occur within 3 hrs, can be up to 12 hrs12 hrs

Independent predictor of worse Independent predictor of worse outcome & outcome & mortality mortality

Hematoma expansionHematoma expansion

Journal of the Neurological Sciences 261 (2007) 99–107

Recombinant Factor VIIaRecombinant 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 VIIaRecombinant 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 sizeABC of hematoma size Broderick, JP et al. Stroke 1993;24:987-993

1.26 million subjects from Greater Cincinnati

ABC of hematoma sizeABC of hematoma size Bedside Bedside ABC/2 methodABC/2 method for hemorrhage volume in for hemorrhage volume in

cmcm33

1. Identify the CT slice with the largest area of hemorrhage1. Identify the CT slice with the largest area of hemorrhage2. Measure the largest diameter of the hemorrhage on this 2. Measure the largest diameter of the hemorrhage on this

slice (A)slice (A)3. Measure the largest diameter 90° to (A) on the same slice 3. Measure the largest diameter 90° to (A) on the same slice

(B)(B)4. Approximate number of 10-mm slices on which the ICH 4. Approximate number of 10-mm slices on which the ICH

was seen was calculated (C)was seen was calculated (C) If area > 75% compared to where the hemorrhage was If area > 75% compared to where the hemorrhage was

largest, the slice was considered 1 hemorrhage slicelargest, the slice was considered 1 hemorrhage slice If area 25% to 75%, the slice was considered 1/2 a sliceIf area 25% to 75%, the slice was considered 1/2 a slice If area < 25%, the slice was not considered a sliceIf area < 25%, the slice was not considered a slice

A, B, and C were then multiplied and the product A, B, and C were then multiplied and the product divided by 2divided by 2

CT-A “Spot Sign”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”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 Anticoagulation associated ICHassociated ICH

Warfarin is a Vit K antagonistWarfarin is a Vit K antagonist Inhibits biosynthesis of factors II, VII, IX, XInhibits biosynthesis of factors II, VII, IX, X Maximum effect is 48 hrs after administrationMaximum effect is 48 hrs after administration

Incidence of ICH is 0.3-0.6% per year in Incidence of ICH is 0.3-0.6% per year in patients on chronic warfarin patients on chronic warfarin anticoagulationanticoagulation

Risk factorsRisk factors Age, chronic hypertension, CAA, leukoaraiosisAge, chronic hypertension, CAA, leukoaraiosis Elevation of INR (doubled risk for 0.5 Elevation of INR (doubled risk for 0.5 above above

4.5!)4.5!) INR correlated with hematoma expansion INR correlated with hematoma expansion

and prognosisand prognosis

Anticoagulation Anticoagulation associated ICHassociated ICH

Goal of treatment: fully reverse INR to normal Goal of treatment: fully reverse INR to normal rangerange

High dose High dose Vitamin KVitamin K 10-20 mg IV slow infusion 10-20 mg IV slow infusion Effect takes 12-24hrsEffect takes 12-24hrs Helps achieving sustained reversal of INRHelps achieving sustained reversal of INR

Fresh frozen plasmaFresh frozen plasma 15cc/kg 15cc/kg 4U 4U Volume overload, insufficient factor IXVolume overload, insufficient factor IX ABO compatibility, thawing, infusion time (30hrs)ABO compatibility, thawing, infusion time (30hrs)

Prothrombin Complex ConcentratesProthrombin Complex Concentrates (PCC, (PCC, Octaplex)Octaplex) Combination of II, VII, IX, X, variable protein C and SCombination of II, VII, IX, X, variable protein C and S Dosage dependant on initial INRDosage dependant on initial INR Smaller volume, correct INR as fast as 30 minSmaller volume, correct INR as fast as 30 min

Anticoagulation Anticoagulation associated ICHassociated ICH

ICH associated with IV heparinICH 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 AAICH – restarting anticoagulationanticoagulation

1% recurrent ICH in initial 3 mths post ICH Risk estimated to double with anticoagulation

Stroke. 2007;38:2001-2023

MiscellaneousMiscellaneous 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:Part II:Management of Management of

Increased Intracranial Increased Intracranial PressurePressure

Basic concepts of ICPBasic concepts of ICP

Monro-Kellie Monro-Kellie doctrinedoctrine Blood + CSF + Blood + CSF +

Brain = constantBrain = constant CPP = MAP – ICPCPP = MAP – ICP CBF = CPP / CVRCBF = CPP / CVR Intracranial Intracranial

elastance =elastance = ICP / ICP / volume volume

AAN Continuum Feb 2006

POP QUIZ37♂ MVA, consciousat the scene, became obtunded in the ER.He was intubated andunderwent CT of thehead.

POP QUIZShould this candidate have invasiveintracranial pressure monitoring?

a) Yesb) Noc) It depends

POP QUIZShould this candidate have invasiveintracranial pressure monitoring?

a) Yesb) Noc) It depends

Indications for ICP Indications for ICP monitoringmonitoring

ABSOLUTE 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 Impossible serial

neurological examination due to: Intubation, deep

sedation or paralysis Immediate non-

neurosurgical procedure

Large cerebral infarction with high risk of cerebral edema

SAH with hydrocephalus CNS tumor CNS infection

Rationale for ICP Rationale for ICP monitoringmonitoring

Development of pressure gradient Development of pressure gradient and brain herniationand brain herniation

Help guide blood pressure Help guide blood pressure managementmanagement

Goals of treatmentGoals of treatment ICP should be maintained < 20 mmHgICP should be maintained < 20 mmHg CPP should be maintained between 60-CPP should be maintained between 60-

70 mmHg70 mmHg

POP QUIZWhat is the most appropriate next step inmanagement in the ER pending neurosurgical evaluation?a) Immediate insertion of an external

ventricular drainb) Hyperventilationc) Mannitol followed by hypertonic salined) Head elevation

POP QUIZWhat is the most appropriate next step inmanagement in the ER pending neurosurgical evaluation?a) Immediate insertion of an external

ventricular drainb) Hyperventilationc) Mannitol followed by hypertonic salined) Head elevation

Approach to ICP Approach to ICP managementmanagement

CSF volumeCSF volume Mannitol or

hypertonic solution

External CSF drainage

Ventricular catheter

Ventriculo -peritoneal or atrial shunt

Lumbar drain Serial lumbar

punctures

Brain Brain volumevolume

Mannitol or hypertonic saline

Decompressive craniectomy

Resection of tumor or other mass lesion

Blood Blood volumevolume

Mannitol or Mannitol or hypertonic hypertonic salinesaline

HyperventilatHyperventilationion

HypothermiaHypothermia Head Head

elevation, elevation, neutral neck neutral neck positionposition

Deep Deep propofol or propofol or barbiturate barbiturate sedation ± sedation ± paralysisparalysis

Seizure Control

HyperventilationHyperventilation

Useful in initial resuscitation: Useful in initial resuscitation: effectively and rapidly reduce ICP in effectively and rapidly reduce ICP in acute rises until definitive therapyacute rises until definitive therapy

Generalized vasoconstriction: Generalized vasoconstriction: cerebral blood volume, cerebral blood volume, ICP ICP

Chronic hyperventilation should be Chronic hyperventilation should be avoided because avoided because CBF puts the brain CBF puts the brain at risk of ischemiaat risk of ischemia Safety of duration is uncertainSafety of duration is uncertain

Resection of mass lesionResection of mass lesion

Subdural or epidural hemorrhageSubdural or epidural hemorrhage Hematoma evacuationHematoma evacuation

TumoursTumours Surgical resectionSurgical resection

CSF drainageCSF drainage

Communicating hydrocephalus (e.g. Communicating hydrocephalus (e.g. SAH, IVH)SAH, IVH) Temporary external ventricular drainTemporary external ventricular drain Long term VP or VA shuntLong term VP or VA shunt

Obstructive hydrocephalus (e.g. Obstructive hydrocephalus (e.g. tumours)tumours) Temporary external ventricular drain Temporary external ventricular drain

until definitive tumour resectionuntil definitive tumour resection

Head elevationHead elevation

Head of bed at 20Head of bed at 20 to 30 to 30 is optimizes is optimizes cerebral venous returncerebral venous return

Ensure neutral neck positionEnsure neutral neck position Caution in hypovolemic patients to Caution in hypovolemic patients to

avoid reduction in MAP and avoid reduction in MAP and therefore CPPtherefore CPP CPP = MAP – ICPCPP = MAP – ICP

Paralysis, Sedation, Paralysis, Sedation, HypothermiaHypothermia

To prevent excess motor activity (posturing, To prevent excess motor activity (posturing, coughing, straining against ventilator)coughing, straining against ventilator)

To To cerebral metabolic rate and cerebral metabolic rate and CBF (must CBF (must maintain MAP to improve CPP maintain MAP to improve CPP caution in caution in HD unstable patients)HD unstable patients)

Role of EEGRole of EEG Rule out ongoing seizure activityRule out ongoing seizure activity Titration of sedation with goal of achieving burst Titration of sedation with goal of achieving burst

suppressionsuppression Hypothermia, controversialHypothermia, controversial

Attenuates deleterious biochemical cascadeAttenuates deleterious biochemical cascade cerebral metabolic ratecerebral metabolic rate risk pneumonia, wound infection, abnormal risk pneumonia, wound infection, abnormal

lytes/coagslytes/coags

Mannitol and Hypertonic Mannitol and Hypertonic saline (HS)saline (HS)

MannitolMannitol 20% or 25% solution (0.25 – 1gm/kg 20% or 25% solution (0.25 – 1gm/kg IV)IV) Intravascular fluid shift from osmotic effectIntravascular fluid shift from osmotic effect Decreased blood viscosity and improved flow (? Decreased blood viscosity and improved flow (?

reflex vasocontriction)reflex vasocontriction) Decreases production of CSFDecreases production of CSF

Follow serum osmolarity (<320 mOsm)Follow serum osmolarity (<320 mOsm) Avoid systemic dehydration & renal injuryAvoid systemic dehydration & renal injury

Can consider adding FurosemideCan consider adding Furosemide Hypertonic salineHypertonic saline, if refractory to mannitol, if refractory to mannitol

BBB is impermeable to NaBBB is impermeable to Na+ + ions ions Osmotic gradient Osmotic gradient Less severe electrolyte disturbances, less brisk Less severe electrolyte disturbances, less brisk

diuresisdiuresis Lack of standard guideline (3-7.5% solution at 20-Lack of standard guideline (3-7.5% solution at 20-

40cc/h)40cc/h) Slow taper to avoid rebound hyponatremiaSlow taper to avoid rebound hyponatremia

Decompressive Decompressive craniectomycraniectomy

Surgical removal of cranial bone flap Surgical removal of cranial bone flap to relieve intracranial pressureto relieve intracranial pressure

Useful in large ischemic CVA with Useful in large ischemic CVA with profound edemaprofound edema

Role in traumatic brain injury still Role in traumatic brain injury still needs to be establishedneeds to be established

ConclusionsConclusions

ICH has an increasing incidence, but ICH has an increasing incidence, but continues to have a very poor prognosiscontinues to have a very poor prognosis

Hypertension is a major risk factorHypertension is a major risk factor Acute BP reduction of 15-20% is safeAcute BP reduction of 15-20% is safe Anticoagulation should be reversed Anticoagulation should be reversed

ASAPASAP Absolute indications for ICP monitoringAbsolute indications for ICP monitoring Major categories of increased ICP Major categories of increased ICP

managementmanagement

Thank you!Thank you!

ReferencesReferences 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 Qureshi AI et al. Intracerebral hemorrhage, Lancet 2009; 373: 1632–442009; 373: 1632–44

Wada, R et al. CT Angiography “Spot Sign” Predicts Wada, R et al. CT Angiography “Spot Sign” Predicts Hematoma Expansion in Acute Intracerebral Hematoma Expansion in Acute Intracerebral Hemorrhage, Stroke 2007;38:1257-1262Hemorrhage, Stroke 2007;38:1257-1262

Diringer MN. Update on intracerebral hemorrhage, Diringer MN. Update on intracerebral hemorrhage, AAN Continuum, 2009AAN Continuum, 2009

Kincaid MS and Lam AM, Monitoring and managing Kincaid MS and Lam AM, Monitoring and managing ICP, AAN Continuum, 2006ICP, AAN Continuum, 2006