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Intracerebral Hemorrhage
McGill Lecture Series Montreal, QC September 19, 2012 J. Teitlelbaum, MD, FRCP(C) University of McGill
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Case History G.S. 68 year old R HBP, DB2, CAD 5PM, sudden R paresis
Aphasia Ø headache, N or V
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G.S. Exam on arrival BP 190/100 P 75/min
Alert, aware, mixed moderate aphasia CN: PERL, RHHA, R UMN VII, R ↓↓ sensation 2/5 strength R UE & LE ↓↓ sensation R hemi-body
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CT 5:30PM
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G.S. Sudden Deteriororation
Exam at 7PM GCS 10, very somnolent, not obeying commands, groans & opens eyes to voice. Pupils 4mm L 3mm R reactive Poor airway protection Power 0/5 R UE & LE
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CT at 7:05 PM
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G.S. Now what ?? ICH Epidemiology & Etiology:
primary vs secondary Factors that affect prognosis Management Evidence-based Eminence based Experimental & anecdotal
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The Guidelines Broderick J, Connolly S, Feldmann E, et al. Guidelines for the management of spontaneous intracerebral hemorrhage in adults: Circulation. 2007;116:e391–413.
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ICH Incidence in 2003
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Intracerebral Hemorrhage
15% of stroke in the West, 30% in the East 6 month prognosis dismal 40% dead (33% within 1 month) 40% disabled and dependent 20% independent
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Classification of ICH PRIMARY (78-88%) SECONDARY
Hypertensive angiopathy (fibrohyalinosis) Amyloid angiopathy Anticoagulant Associated SECONDARY AVM Aneurysm Cavernoma Neoplasm Coagulopathy Alcoholic liver disease Hemophilia Hemorrhagic infarct Toxic-cocaine
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Dismal Prognosis
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Factors Affecting Prognosis
GCS on presentation Age Hemorrhage location Intraventricular hemorrhage ? Blood pressure Hemorrhage size
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Secondary Damage Hematoma expansion ≥ 80 ml fatal Cerebral edema
Secondary injury
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ICH Score Component ICH score points GCS 3 - 4 2 (34/35 died) 5 - 12
0 (5/60 died) ICH volume ≥ 30 ml 1 ≤ 30 ml IVH yes no Infratentorial Age > 80
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Mortality and ICH Score
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The relationship between ICH volume and patient outcome
DEAD FULL RECOVERY
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Size is the most important predictor for patient outcome
A patient with a haemorrhage the size of a ping pong ball is likely to have a better outcome than a patient with a haemorrhage the size of golf ball: mortality on ’ping pong’ size: app. 40% mortality on ’golf ball’ size: app. 70% 38 ml 43 ml
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Which are Modifiable ? GCS on presentation Age Hemorrhage location
Intraventricular hemorrhage ? Blood pressure Hemorrhage volume
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Early growth occurs in all locations
Brott (1997) N=103 Kazui (1994) N=186 Fujii (1996) N=359 Initial CT time 0-3 hrs 0-24 hrs Putamen 34% 16% 19% Thalamus 50% 21% 10% Lobar 32% 29% 6% Cerebellar 0% 25% 12% Pons 40% 28% Other 43% 13% TOTAL 38% 22% 14%
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Hematoma Evolution 3 h 3 h 2 h 6 h 24 h 24 h
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Predicting ICH expansion
Time since onset Spot sign Blood pressure Shape of the hematoma
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CTA Source Images: Additional Data
Spot Sign shape: spot-like, serpiginous, or linear location: within the margin of a parenchymal hematoma without connection to an outside vessel size: >1.5 mm diameter in at least one dimension density: at least double the density (HU) of the hematoma number: single or multiple not caused by hyperdensity in same location on NCCT
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The Spot Sign: Growth Despite Treatment
2 hours 3 hours (CT Angiogram) 24 hours rFVIIa
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Predictive Value of Spot Sign: Time Dependent?
3 hours hours hours Spot Sign
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Early Growth: Conventional angiography
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Prognosis and Acute Blood Pressure
↑ Early Neurological Deterioration ↓ Functional Outcome (90 days) 1 month mortality (%) 1 month mortality (%) MAP (mm Hg) Fogelhom et al, Stroke, 28: , 1997 Okumura et al, J. Hypertension, 23: , 2005
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Blood Pressure and Hematoma Evolution
Target max SBP No Enlargement Hematoma Enlargement 140 mmHg 16 2 9% p=0.025 150 mmHg 14 1 160 mmHg 22 8 30% 170 mmHg 5 Ohwaki et al, Stroke, 35: , 2004 28
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ICH Management
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Treatment Modalities General supportive care Treatment of ICHT
Hematoma resection Management of intra-ventricular hemorrhage Seizure prophylaxis Prevention of hematoma growth BP management
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Basic Algorithm ABC’s Do no harm Pain management & sedation
Hyperventilation pCO mm Hg Osmotic therapy Ventricular drainage
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General Supportive Care
HOB 30° SO2 ≥ 95% Glucose control ≤ 6.0 mmol T° control ≤ 37.5° C Pain control, sedation
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Hyperventilation Regional blood flow Oxygen extraction
But: CMRO2 stable ad pCO2 = 10 mm Hg At the levels used in TBI, hyperV does not result in ischemia Pressure autoregulation dysfunction is improved
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Hyperventilation Present recommendation: Avoid during 1st 24H post TBI
pCO2 30 – 35 mm Hg If no response: 25 – 30 mm Hg
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Hyperventilation My recommendation:
Use for acute ICHT, temporizing measure pCO2 30 – 35 mm Hg – 30 mm Hg Has no associated ischemia ad pCO2 10 Beware of hypoperfused areas that are more fragile
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Osmotic Agents Mechanisms of Action
Mannitol BW in intact > affected brain volume vasoconsriction viscosity CBF vasoconstriction size of CVA, apoptosis HS BW in intact = affected brain Possible in size of CVA
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Osmotic Agents Clinical Use
Routinely recommended in edema of trauma and stroke Lack of evidence of beneficial outcome Little evidence of efficacy in stroke or ICH (especially Na)
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Osmotic Agents Clinical Use
Intermittent boluses allowing clearing of solute from blood. Avoid continuous infusions Smallest doses at the largest possible intervals, with prn according to ICP
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Osmotic Agents Clinical Use
ICH with ICHT: MN first HS if refractory, Cr, OG Refractory to one agent: use the other 250cc MN, then 100cc alternating MN/HS
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Treatment of ICHT No Δ in outcome Intubation Hyperventilation
Sedation Steroids: NO role Osmotic agents Mannitol Hypertonic saline No Δ in outcome
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Hematoma Resection STICH trial MISTIE:
ICH within a centimeter of the cortical surface showed a benefit for early surgery mortality, no other effect on morbidity MISTIE: Intra-lesion rtpa with subsequent aspiration
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Intra-ventricular Hemorrhage
EVD Intra- ventricular rtpa (CLEAR)
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Intra-ventricular rTPA
Hanley DF: pilot, prospective, randomized, double-blind, controlled trial Speeds clearance of aneurysmal intraventricular hemorrhage Normalizes intracranial pressure Reduces ventricular catheter obstruction
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Early Hematoma Growth 2.0 hours after onset 6.5 hours after onset
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Prevent ICH Growth By BP By rFVIIa
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Percent Change in ICH Volume at 24 Hours
Boxes depict 98.3% confidence intervals 29% 16% 14% 11% 45% RR 52% RR 62% RR
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Modified Rankin Scale at Day 90
160 µg/kg 80 µg/kg mRS 0-1 mRS 2-3 mRS 4-5 40 µg/kg mRS 6 Placebo 100% 80% 60% 40% 20% 0%
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Hematoma Evolution and rFVIIa
Onset-CT interval (h) Prospective Retrospective Brott Fujii Kazui Takizawa 0-3 38% 18% 36% 17% 3-6 N/A 8% 16% 6% 6-24 2% 10% 0% 3.3ml 4.5ml 5.8ml rFVIIa within 4 hours: Dose dependent attenuation of hematoma expansion no effect on mRS at 90 days Mayer et al. NEJM 2005; 352:
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CTA Based rFVIIa Selection Trials
The SpoT sign fOr Predicting and treating ICH growTh study: STOP-IT SPOTRIAS/NINDS PI: M. Flaherty ‘SPOT sign’ seLection of Intracerebral hemorrhage to Guide Hemostatic Therapy: SPOTLIGHT CSN/ CIHR PI: D. Gladstone Acute ICH < 6 hours CTA Spot Sign Positive Spot Sign Negative rFVIIa Placebo NCCT at 24 hours
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Seizure Prophylaxis Are seizures frequent post ICH ?
Do they change outcome ? Does prophylaxis frequency ? Does a in Sz affect outcome ? Is therapy associated with adverse events ?
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Are seizures frequent post ICH ?
↑early Sz and late epilepsy ( ) 1/3 pts: 50% electrographic (Neurology 2007)
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Do they change outcome ? Associated with expanding hemorrhages
ICU stay Greater treatment cost edema, midline shift, re-bleeding, decreased functional recovery likelihood of poor long-term outcomes
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Does prophylaxis Sz frequency ?
Redding et al 2011: No (DPH) Taylor 2011 Neurocrit Care: Yes (Keppra) 21% vs 16%
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Does a in Sz Improve Outcome
Taylor 2011 Neurocrit Care: Yes (Keppra) Improved cognitive outcome vs DPH No untreated group CHANT study 2009: No (DPH mainly)
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So… There is an ↑in Sz post ICH (lobar)
There is a likely effect on outcome Rx do ↓ Sz incidence This MAY improve outcome (Keppra IV)
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ICH BP Management Does BP affect outcome ?
Does BP affect the penumbra? Does BP influence ICH growth? Does treatment alter any of these??
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Prognosis and Acute Blood Pressure: ICH
1 month mortality (%) A number of observational studies have examined the association of presentation BP levels with clinical outcomes. Left figure shows survival curves of acute ICH according to BP quartiles. The risks of early death were greater among higher BP groups. Likewise, most studies have shown that higher BP levels are associated with worse outcomes. In contrast, some studies have also identified J-shaped associations (right fig). What is clear is that if there is any adverse effect of low BP it is not apparent until SBP levels reach 140 or less. MAP (mm Hg) Fogelhom et al, Stroke, 28: , 1997 Okumura et al, J. Hypertension, 23: , 2005
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Acute BP Management: Competing Rationales
Impaired Autoregulation IV therapy suggested only for Systolic BP ≥ 180 mmHg (AHA Guidelines)
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Guidelines for Acute BP Management: ICH
Stroke Council, American Heart Association IV therapy suggested only for Systolic BP ≥ 180 mmHg (or MAP > 130 mmHg) 2007: Consider target of 160 mmHg systolic, IF ↑ ICP not suspected Very high BP levels in acute ICH are generally considered to require treatment, but there is a wide range of recommendations for BP management available from national and international guidelines. This marked variation serves to highlight the persisting clinical uncertainty. 59
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Acute ICH BP Treatment Trials
Target Blood Pressure Agent(s) ATACH n=60 ; ; systolic Nicardipine INTERACT n=400 <140 mmHg systolic Multiple ICH ADAPT n=164 <150 mmHg systolic Labetalol± Hydralazine 60
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Blood Pressure and Hematoma Evolution
Target max SBP No Enlargement Hematoma Enlargement 140 mmHg 16 2 9% p=0.025 150 mmHg 14 1 160 mmHg 22 8 30% 170 mmHg 5 Ohwaki et al, Stroke, 35: , 2004 61
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Temporal Profile of BP after ICH
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INTERACT: Efficacy of Antihypertensives
Target achieved: 42% (1h) 66% (6h) Drugs Used: 1. Furosemide 2. Urapidil 63
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INTERACT: Hematoma Expansion
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Rationale for Not Treating Blood Pressure
One fear is that normal cerebral autoregulation of CBF is impaired in patients with acute ICH. Thus, any decrease in BP may result in a concomitant fall in CBF. The autoregulatory curve described above is an oversimplified MODEL, based on animal data primarily and the McHenry study of low bp in medical students (1961); work of Derdeyn and Powers + others show that rCBF decreases and OEF increases approx 18% IN the autoregulatory range as CPP falls; the relationship also differs between individuals. Based on Dirangl and Pulsinelli, JCBFM, 1990 (SHR ICAO/MCAO)
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Autoregulation in ICH Systolic BP (mmHg)
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Peri-hematoma Edema and Injury
Ischemic? Vasogenic? Astrocyte Plasma Extravasation Pc Capillary 67
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Perihematoma Edema is Not Cytotoxic
Butcher et al, Stroke 35: , 2003
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Peri-hematomal Oligemia: CT Perfusion
Maps of CBF (flow) and CBV (volume) generated with CTP in an acute ICH patient. Once again, we see oligemia, but not ischemia.
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Peri-hematoma Oligemia: rCBF
* Penumbral Threshold Perihematoma CBF (32.585.64 ml/100g/min) was significantly lower than contralateral homologous regions (35.195.60 ml/100g/min; p=0.001). This corresponded to a reduction in perihematoma CBV (2.910.58 vs 3.130.55 ml/100g; p=0.006).
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Extreme BP Reduction and CBF
Tie BP (mmHg) Time (minutes)
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Acute ICH - onset within 24 hours
Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial (ICH ADAPT) Protocol Acute ICH - onset within 24 hours SBP ≥ 150 mmHg Randomization (N=74) Target SBP <150 mmHg Target SBP <180 mmHg Labetalol ±Hydralazine Outline of ICH ADAPT trial, which utilizes a physiological endpoint (CBF) to assess the effects of two different BP targets. Primary Endpoint: rCBF measured with CT perfusion 2 hours after randomization Butcher et al, IJS, 2010 72
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So… in BP will prevent hematoma growth if:
Within 1 hour To ≤ 160 mm Hg systolic Labetalol / Hydralazine BP does CBF but no in ischemia Ideal BP: 150 – 160 mm Hg systolic
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ICH Summary Poor prognosis Hematoma expands early (≤4h)
ICH Expansion can be predicted HBP is a likely factor in prognosis Expansion Edema formation other
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ICH Summary Treatment: General Prevention of ICH enlargement:
BP within 1h to ≤ 160 mm Hg syst rFVIIa Seizure prophylaxis: likely useful (Keppra IV) ICHT therapy: no Δ in outcome Sx: little if any benefit
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