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Intracranial Hemorrhage & Emergency Management of Increased ICP Emergency Neurology Lecture Series...
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Transcript of Intracranial Hemorrhage & Emergency Management of Increased ICP Emergency Neurology Lecture Series...
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