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Spontaneous Intracerebral ICH Is Common
Hemorrhage Incidence Predicted to Increase
100%
Increase
Raul G Nogueira, MD ICH Proportion of Strokes 100,000
(US)
No. of Persons
Vascular and Critical Care Neurology 75,000
Interventional Neuroradiology and ICH SAH
Endovascular Neurosurgery 9% 3% 50,000
Massachusetts General Hospital
Harvard Medical School 25,000
Boston, MA
0
700,000 Total Strokes Annually 2000 2050
Year
Qureshi AI, et al. N Engl J Med. 2001;344:1450-1460; Thom T, et al. Circulation.
2006;113:e85-e151.
High-Risk Populations Traditionally High Mortality and
● Hypertensive patients (especially poorly controlled) Limited Recovery
● Anticoagulant users
• Mortality
● Patients with multiple comorbid risk factors 100%
– 6-month, 30%-50%
● Age >55 years – 1-year, 50%
90%
80%
● Patients with cerebral microangiopathy (eg, cerebral
Proportion of patients (%)
amyloid angiopathy) • Only 20% of ICH patients 70%
● Patients with dementia are independent at 6 60%
50%
● Certain ethnic populations months vs 60% of
– African Americans ischemic stroke patients 40%
– Hispanics 30%
– Asians (especially Japanese) • Medical costs 20%
10%
● Alcohol abusers – US$125,000 lifetime cost per
person (1990) 0%
● Smokers ICH Ischemic
– Direct and indirect costs (lost
● Patients with renal or liver failure productivity + caregiver burden) Dead Dependent Independent
Hart RG, et al. Stroke. 1995;26:1471-1477; Steiner T, et al. Stroke. 2006;37:256-262;
Mayer SA, Rincon F. Lancet Neurol. 2005;4:662-672; Qureshi AI, et al. N Engl J Med. Manno EM, et al. Mayo Clin Proc. 2005;80:420-433; Mayer SA, Rincon F. Lancet Neurol.
2001;344:1450-1460; Labovitz DL, et al. Neurology. 2005;65:518-522; Kissela B, et al. 2005;4:662-672; Qureshi AI, et al. N Engl J Med. 2001;344:1450-1460; Taylor TN, et al.
Stroke. 2004;35:426-431; Koennecke HC. Neurology. 2006;66:165-171. Stroke. 1996;27:1459-1466; Reed SD, et al. Neurology. 2001;57:305-314.
Predictors of Outcome Sites of Spontaneous ICH
Thalamic
Hemorrhage
(20%)
● Hematoma volume Lobar
Subcortical
● GCS Hemorrhage
(25%)
● Intraventricular
hemorrhage Pontine
Hemorrhage
● Age Putaminal (7%)
Hemorrhage
● ICH location (deep) (35%)
● Increased cerebral edema
(midline shift, herniation) Cerebellar
Hemorrhage
(8%)
Manno EM, et al. Mayo Clin Proc. 2005;80:420-433; Garibi J, et al. Mayer SA, Rincon F. Lancet Neurol. 2005;4:662-672;
Br J Neurosurg. 2002;16:355-361. Qureshi AI, et al. N Engl J Med. 2001;344:1450-1460.
1
Recurrence Risk Distinguishes Lobar Mechanisms of Injury
from Deep ICH
Early hematoma growth
– Hematoma
enlargement
– Increase in ICP,
tissue disruption
and shear forces
Edema and toxic effects
of blood products
– Osmotically active
serum products
– Thrombin
Inflammatory response
Viswanathan Neurology 2006;66:206 Qureshi AI, et al. N Engl J Med. 2001;344:1450-1460.
Hematoma Expansion Hematoma Expansion
Contrast extravasation is independently
associated with hematoma expansion and
worse outcomes!
Patient with spot sign, demonstrating extravasation and hematoma expansion
• 72% have some hematoma expansion over the first 24 hours
• 38% have significant (>33%) expansion over 24 hours
• In 26% of these cases, the enlargement is within 1 hour
Wada, R. et al. Stroke 2007;38:1257-1262
Davis SM, et al. Neurology. 2006;66:1175-1181;
Brott T, et al. Stroke. 1997;28:1-5.
Goldstein JN Neurology. 2007 Mar 20;68(12):889-94.
9 10
Common Etiologies of ICH Common Etiologies of ICH
Primary Hypertension Cerebral Amyloid Angiopathy
Features and Characteristics Features and Characteristics
Location
Typical sites – Lobar hemorrhage
– Putamen – 50% – Multiple, bilateral
– Thalamus – 15% – Parieto-occipital location
– Lobar – 15% Associated with dementia/AD
– Cerebellum – 10%
Elderly patients (>70 years)
– Pons – 10%
Typically less severe than
Typically more severe than HTN-related ICH
cerebral amyloid angiopathy-
related ICH Risk of recurrence
5%-15% annually
Risk of recurrence ~2%
annually (if BP controlled) Microbleeds on
gradient-echo MRI
Woo D, et al. Stroke. 2002:33:1190-1195; Labovitz DL, et al. Neurology. Labovitz DL, et al. Neurology. 2005;65:518-522; Mayer SA, Rincon F. Lancet Neurol.
2005;65:518-522; Mayer SA, Rincon F. Lancet Neurol. 2005;4:662-672; 2005;4:662-672; Yen CP, et al. Acta Neurochir. 2005;147:393-399; Woo D, et al. Stroke.
Qureshi AI, et al. N Engl J Med. 2001;344:1450-1460. 2002;33:1190-1195.
2
Common Etiologies of ICH Common Etiologies of ICH
Acquired Coagulopathy – Anticoagulation Acquired Coagulopathy – Thrombolytic Therapy
tPA increases risk of ICH
Warfarin and Hematoma (6% absolute risk in NINDS trial)
Expansion 18.5% of bleeds at sites distant
from stroke
Hematoma Expanders
1.00
No Warfarin (n=9)
Proportion of Risk factors
0.75
Warfarin indicated in DVT, PE, AF – Age >70 years
0.50 P<.001
Incidence of anticoagulant-associated
ICH rose from 5% to 18% of cases of 0.25
– Serum glucose >300 mg/dL
spontaneous ICH in 1990s Warfarin (n=7)
– NIHSS >20
INR 2.5-4.5 increases risk of ICH 10X 0.00
0 12 24 36 48 60 – Early ischemic changes
Associated with longer duration of ICH Time (h) detected on CT
expansion
Doubles ICH mortality! – Not time to treatment!
Hart RG, et al. Stroke. 1995;26:1471-1477; Steiner T, et al. Stroke. 2006;37:256-262;
reproduced with permission from Flibotte JJ, et al. Neurology. 2004;63:1059-1064;
Rosand J, et al. Arch Intern Med. 2004;164:880-884; Flaherty ML, et al. Stroke.
NINDS t-PA Stroke Study Group. Stroke. 1997;28:2109-2018.
2006;37:623.
Other Etiologies of ICH
Other Etiologies of ICH
Hemorrhagic ICH
Drug-related conversion of
ischemic stroke
Cocaine Neoplasms
Melanoma
Amphetamines
Renal Cell Ca
Head trauma
Other illicit drugs Thyroid Ca
(eg, talwin-pyribenzamine, phencyclidine) ChorioCa
Lung Ca
MAO inhibitors
Pial Arteriovenous Malformations
Other Etiologies of ICH 61 y/o man p/w acute onset of speech difficulties and right HH in
the setting of a left tempo-occipital ICH
Vascular lesions
Cerebral aneurysm
Arteriovenous malformations
Dural A-V fistulas
Cavernous malformation
Venous angioma/capillary telangectasia
3
Dural Arteriovenous Fistula
Other Etiologies of ICH
59 y/o female p/w severe left-sided
h/a f/by expressive aphasia in the
Other Etiologies
setting of a L frontotemporoparietal Vasculitis
ICH
Other vasculopathies (post partum,
DAVF with Cortical Venous Reflux pheocromocytoma, etc)
Mycotic aneurysm
Moya-moya
Intracranial dissection
Dural venous sinus thrombosis
45 YEAR OLD MAN PRESENTS WITH HEADACHES AND CONFUSION 45 YEAR OLD MAN PRESENTS WITH HEADACHES AND CONFUSION
BASELINE ANGIOGRAM
ANGIOGRAM POST REMOVAL OF PHEOCROMOCYTOMA
Screening for ICH ICH Management in ED
Clinical Symptoms Assessment and Stabilization
The likelihood of ICH doubles* when one of the Activate Stroke Team Prior to Arrival
following is present:
Immediate General Assessment/Stabilization
● Impaired level of consciousness
• Assess ABCs/vital signs, monitor BP closely
● Vomiting • O2 (if hypoxic)
● Severe headache • IV access and labs (coagulation, platelets, CBC, electrolytes)
● Warfarin therapy • Check glucose and treat (if indicated)
● SBP >220 mm Hg • Quick history
• Neurologic screening assessment (GCS, NIHSS)
● Hyperglycemia (glucose >170 mg/dL)
• Emergent CT scan of brain (ASAP)
in nondiabetic patients
• 12-lead ECG
*Likelihood ratio 2.4; 95% CI, 1.8-3.2.
Goldstein LB, Simel DL. JAMA. 2005;293:2391-2402. AHA Adult Stroke Guidelines. Circulation. 2005;112(suppl 24):IV-111-IV-120.
4
Diagnosis of ICH Diagnostic Imaging
AHA Guidelines (2007) “Blood in the Brain” – What Type of Hemorrhage?
• Vomiting, early change LOC, and ↑ BP suggest ICH
• CT or MRI are both first choice for initial evaluation
• MRI and MRA in selected patients
– Suspected cavernous malformation in normotensive
surgical candidates with lobar hemorrhage
• Consider angiography (CTA or angiogram)
– All surgical candidates without clear cause
– Particularly young, clinically stable patients Intracerebral Intraventricular Subarachnoid
– Timing depends on factors including clinical state hemorrhage (ICH) hemorrhage (IVH) hemorrhage (SAH)
Broderick JP, et al. Stroke. 1999;30:905-915.
Broderick JP, et al. Stroke 2007;38;2001-2023. Images courtesy of i TEAM Scientific Committee.
ICH Mortality Rate Is Reduced
General Management of ICH
With Admission to an NICU
Goals Provide general supportive care in the 1.0
ED and ICU/NICU to manage the primary brain injury Non-NICU admission is associated
and limit the secondary brain injury with increased in-hospital mortality
Cumulative Survival
.9
(OR, 3.4; 95% CI, 1.65-7.6)
• Continue to support ABCs
.8
• Monitoring (BP, fever, ICP, labs)
Neuro
• Intubation General
• BP management .7
• Seizure management
• Reverse anticoagulation immediately .6
0 5 10 15 20 25 30 35 40 45 50
Day
Diringer MN, Edwards DF. Crit Care Med. 2001;29:635-640.
Should BP Be Lowered in ICH? Should BP Be Lowered in ICH?
• Current data are inconclusive as to whether BP lowering is useful and about
defining a target
• Potential benefits
– Limit hematoma growth
– Decrease perihematoma edema
• Isolated SBP ≤210 mmHg not clearly related to hemorrhagic expansion or to
neurological worsening
• Baseline BP not associated with ICH growth in the largest prospective study of ICH
growth
• Potential downside
– Create or exacerbate perihematoma ischemia
• No significant change was observed in either global CBF or periclot CBF as measured
by PET after 15% MAP reduction
• Even if BP lowering isn’t harmful, does it help?
– Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH) Study
– INTERACT study (Intensive Blood Pressure Reduction in Acute Cerebral
Hemorrhage)
• Different approaches based on ICH etiology (AVM, aneurysm, CAA)? Broderick JP, et al. Stroke. 1999;30:905-915; Broderick JP, et al. Stroke
2007;38;2001-2023 Manno EM, et al. Mayo Clin Proc. 2005;80:420-433; Mayer
SA, Rincon F. Lancet Neurol. 2005;4:662-672; Qureshi AI, et al. N Engl J Med.
2001;344:1450-1460.
5
Seizures and ICH
Management of Seizures
• Seizures are more frequent • Poorer outcomes
in ICH than in ischemic AHA guidelines recommend administering
stroke – Neuronal injury and
destabilization of anticonvulsants for seizure at onset of ICH
• Seizure risk is 8% after ICH critically ill patient
• Most seizures at onset or – Nonconvulsive seizures Consider anticonvulsants for ≤1 month in
≤24 h of ICH may contribute to coma
selected patients with lobar hemorrhage
• More commonly associated – Seizures associated
with lobar than deep ICH with deterioration of
NIHSS and increase in
midline shift
Vespa PM, et al. Neurology. 2003;60:1441-1446; Mayer SA, Rincon F. Lancet Neurol.
2005;4:662-672; Passero S, et al. Epilepsia. 2002;43:1175-1180; Qureshi AI, et al. Broderick JP, et al. Stroke. 1999;30:905-915; Qureshi AI, et al. Stroke.
N Engl J Med. 2001;344:1450-1460; Broderick JP, et al. Stroke. 1999;30:905-915. 2001;33:1916-1919; Passero S, et al. Epilepsia. 2002:43:1175-1180.
ICH Expansion ED Management:
Preventing Hematoma Expansion
• Warfarin reversal
• Hemostatic therapy (clinical trial)
• Blood pressure control (clinical trial)
First CT (50 minutes) Second CT (160 minutes)
Reversing Warfarin Effect: ED Management:
Time Counts! Should All Patients Be Reversed?
• 69 consecutive patients with warfarin-related ICH
• All patients had repeated INR measures and were
treated aggressively for ICH in the MGH ED Because of the high mortality of
OAT-ICH and high risk of
INR reversed at 24 hours
hematoma expansion, ALL OAT-
Characteristic No (N=12) Yes (N=57) p value ICH patients should receive rapid
Door to CT (min) and complete reversal of
(Median (25-75%)) 65 (30-90) 40 (25-85) 0.5
CT to FFP (min) 210 (100-375) 90 (60-205) 0.02
anticoagulant effect in the
FFP dose (units) 2 (1-5) 4 (2-6) 0.1 Emergency Department.
CT to Vitamin K (min) 245 (37-361) 87 (25-210) 0.2
6
Reversing Warfarin Effect in the
Reversing Anticoagulation
Emergency Department
ICH in any patient on warfarin (with INR ≥1.5)
Current MGH Guidelines for ICH patients should be considered life-threatening
• Vitamin K 10 mg IV over 10 minutes STAT
Goal Normalize INR to <1.4 ASAP
• FFP 10 ml/kg over 90 minutes (Prothrombin Concentrate may
be substituted for FFP.) • Time until initiation of warfarin reversal is the
strongest predictor of 24-h coagulation reversal
• Team must designate a single physician to take personal
responsibility for ensuring that these therapies are administered
as fast as possible. • Reversal may not occur in 1 of 6 patients
• As soon as FFP ordered, “runner” dispatched to blood bank to
collect FFP.
www.stopstroke.org
Goldstein JN, et al. Stroke. 2006;37:151-155.
Hanley. J Clin Path 2004;57:1132-39
Reversing Anticoagulation (cont.) Reversing Anticoagulation (cont.)
• Discontinue warfarin • ASA-related coagulopathy
• Agents used for reversal – Platelet transfusion
– Fresh frozen plasma (FFP)
– Vitamin K • No antidote for clopidogrel-related coagulopathy
– Prothrombin complex concentrates (PCC)
– Recombinant factor VIIa • Thrombolytic therapy-related coagulopathy
– Stop thrombolytic agent
• Issues to consider – 6-8 units of cryoprecipitate containing factor VIII
– Normalization with FFP may take hours to days
– FFP carries viral risk – 6-8 units of platelets
– PCC factor concentrations vary by batch/manufacturer • Heparin- and enoxaparin-induced anticoagulation
– PCC and rFVIIa have smaller volumes and more rapid
administration than FFP – Protamine sulfate
– Vitamin K is commonly used with the other 3 approaches
Ansell J, et al. Chest. 2001;119(suppl 1):22S-38S; Hanley JP. J Clin Pathol. 2004;57:1132-
1139; Baker RI, et al. Med J Aust. 2004;181:492-497; Mayer SA, Rincon F. Lancet Neurol.
Manno EM, et al. Mayo Clin Proc. 2005;80:420-433; Makris M, et al. Br J Haematol.
2005;4:662-672; Steiner T, et al. Stroke. 2006;37:256-262;Freeman WD, et al. Mayo Clin
2000;80:420-433.
Proc. 2004;79:1495-1500; Huttner HB, et al. Stroke. 2006;37:1465-1470.
Reducing Hematoma Expansion Reducing Hematoma Expansion
Many Potential Hemostatic Agents Early Hemostatic Therapy With Factor VIIa
• Currently approved for use in hemophiliacs; initiates hemostasis
• Aminocaproic acid • DDAVP (Desmopressin) • Well suited for limiting early hematoma growth in ICH
• Prothrombin-complex • Tranexamic acid • Local effects in endothelial disruption and vascular injury
concentrates • Cryoprecipitate • Reduces bleeding in patients without coagulopathy
– Concentrated • Rapidly normalizes INR in anticoagulant-associated ICH
vitamin K–dependent
• Aprotinin (Trasylol)
• Has been studied as a therapy for ICH in:
factors (factors II, VII, – 2 phase IIa dose-escalation studies
IX, X) – Phase IIb global dose-response study
• Recombinant factor VIIa – Phase III
Mayer SA. Stroke. 2003;34:224-229; Micieli G, et al. Neurol Sci. 2005;26(suppl 1):S34-S36;
Conti S, et al. Clin Lab Haematol. 2005;27:283-285; Mayer SA, et al. Stroke. 2005;36:74-79;
Mayer SA, et al. N Engl J Med. 2005;352:777-785; Busani S, et al. Thromb Haemost.
2005;93:381-382; Stroke Trials Registry. Internet Stroke Center. Available at:
http://www.strokecenter.org/trials.
7
rFVIIa Dose-Response Study rFVIIa Phase IIb Dose-Response Study
Change in Hematoma Volume at 24 Hours
3 Hours 60 Min 24 Hours 90 Days
Percent Change in ICH Volume: Baseline → 24 Hours
35
Placebo Clinical outcome 30
n=100 • Mortality
• mRS 29%
25
• Barthel Index
% Increase
rFVIIa • E-GOS 20
40 g/kg • NIHSS P=.07
Efficacy • GCS P=.049 P=.012*
n=100
N=400 Baseline Percent change • Euro-QOL
15
16% P=.015*
randomized CT scan in ICH volume 14% 14%
rFVIIa on 24-hour CT 10
80 g/kg Safety 11%
n=100 Adverse events 5
until discharge
Serious adverse
rFVIIa 0
events until Placebo 40 g/kg 80 g/kg 160 g/kg Combined
160 g/kg day 90 Treatment
n=100 Groups
*ICTR values
Mayer S, et al. N Engl J Med. 2005;352:777-785. Mayer S, et al. N Engl J Med. 2005;352:777-785.
rFVIIa Dose-Response Study rFVIIa Dose-Response Study
Survival at 90 Days Functional Outcome at 90 Days
1.0
Modified Rankin Scale
0.9
160 g/kg
0.8
Proportion Surviving
0.7
80 g/kg
0.6 38% ↓ mortality
0.5 (P=.02)
40 g/kg
0.4
Placebo Placebo
0.3
rFVIIa, 40 /kg
0.2 rFVIIa, 80 /kg
0% 20% 40% 60% 80% 100%
0.1 rFVIIa, 160 /kg
0.0 0-1 no significant disability 4-5 moderate–severe-to-severe disability
0 15 30 45 60 75 90
2-3 slight-to-moderate disability 6 dead
Days
Reproduced with permission from Mayer SA, et al. N Engl J Med. 2005;352:777-785. Adapted with permission from Mayer SA, et al. N Engl J Med. 2005;352:777-785.
rFVIIa Phase IIb Dose-Response
Study: Conclusions
● Compared with placebo, rFVIIa treatment
– Significantly reduced hematoma growth (P=.01)
– Significantly reduced mortality: 38% decrease (P=.02)
– Significantly improved patient outcome
● Thromboembolic serious adverse events, mainly myocardial and
cerebral infarction, occurred in 7% of rFVIIa patients compared
with 2% of placebo patients (P=.12)
● Thromboembolic serious adverse events that were possibly or
probably related to treatment and that were fatal or disabling
occurred in 2% of rFVIIa-treated patients and in 2% of the
placebo group
Mayer S, et al. N Engl J Med. 2005;352:777-785.
8
Management of Increased ICP Restarting Anticoagulation After ICH
Treatment Options ACC/AHA 2006 Guideline
• Osmotherapy • Positional factors • Discontinue anticoagulants and antiplatelets ≥1-2 weeks
– 3% or 23.4% saline – Raise head of bed 30º
– Mannitol bolus – Keep head at midline • Reverse anticoagulation as soon as possible
0.25-0.5 g/kg q4h – Avoid head and neck positions (vitamin K, FFP)
– Target 310 mOsm/L that compress jugular veins
– Avoid hypo-osmolar fluids
– Maintain euvolemia
– Avoid flat-supine position
– Tracheostomy/ETT ties loose
• If required, resume oral anticoagulation after
3-4 weeks (rigorous monitoring, INR in lower range); if
• Hyperventilation • Sedation, short-term
neuromuscular paralysis anticoagulation is needed sooner after ICH, IV heparin
– Temporary measure as bridge
for definitive intervention • Ventricular drain (with PTT 1.5 to 2.0 times normal) or LMWH may be better
– Prolonged use can cause (especially for hydrocephalus) acute therapy than oral warfarin
cerebral ischemia
• Higher risk of recurrent ICH if anticoagulation resumed in
Broderick JP, et al. Stroke. 1999;30:905-915; Manno EM, et al. Mayo Clin Proc. lobar ICHs, microbleeds, and suspected CAA on MRI
2005;80:420-433; Mayer SA, Rincon F. Lancet Neurol. 2005;4:662-672; Manno EM, et al.
Mayo Clin Proc. 2005;80:420-433; Audibert G, et al. Ann Fr Anesth Reanim. 2005;24:
492-501; Qureshi AI, et al. Neurosurgery. 1999;44:1055-1063; Saltarini M, et al.
Eur J Emerg Med. 2002;9:262-265. Adapted from Sacco RL, et al. Stroke. 2006;37:577-617.
Other Issues in Medical Management
• Steroids – No
• Fever is bad Surgical Intervention in ICH
– Does controlling fever help?
– Important in first 24 hours
• Hyperglycemia
Goal Remove as much blood clot as
– Insulin infusions are en vogue in ischemic stroke
– Little data for ICH either way
possible, as quickly as possible, with the
• Don’t forget DVT prophylaxis least amount of brain trauma
– When can heparin be started?
• Some say never and to use TEDS/SCDs
• Others start SQ heparin or LMWH sometime after 48 hours
• DVT = IVC Filter
• Don’t forget nutrition!
• Start rehab early
– Begin range-of-motion exercises in ICU, even in comatose patients
– Extent of rehab activities will depend on patient’s condition
Hemphill JC, et al. Stroke. 2006;37:724; Mayer SA, et al. Lancet Neurol. 2005;4:662-672;
Qureshi AI, et al. N Engl J Med. 2001;344:1450-1460. Broderick JP, et al. Stroke. 1999;30:905-915.
Surgical Modalities: Surgical Issues
Craniotomy, Stereotactic • Evidence that it works?
Open craniotomy + Gets all the blood • Careful diagnosis
– Invasive, disrupts tissue • Timing of intervention: ultra-early, early, late
• Site of hemorrhage
Endoscopic aspiration + Visualization
– Slow, leaves volume • Technique – craniotomy, stereotactic
• Consistent, good medical management
Stereotactic evacuation + No disruption – Monitoring
– Slow, leaves volume – Preventing re-bleeding
Intra-hematoma thrombolysis? – Managing BP
• Understand pathophysiology
Qureshi AI, et al. N Engl J Med. 2001;344:1450-1460; Broderick JP, et al. Stroke.
1999;30:905-915; Vespa P, et al. Neurocrit Care. 2005;2:274-281; Y Nievas MC, et al. Hankey GJ, et al. Stroke. 1997;28:2126-2132;
Neurol Res. 2005;27:755-761; Nasser JA, et al. Arq Neuropsiquiatr. 2002;60:362-366. Fernandes HM, et al. Stroke. 2001;31:2511-2516.
9
STICH STICH
International Surgical Trial in Intracerebral Hemorrhage International Surgical Trial in Intracerebral Hemorrhage
1033 patients with ICH randomized 1.0
• Randomized
prospective trial
0.9 No overall benefit
0.8
from early surgery
Probability of survival
503 allocated to 530 allocated to
• N=1033 early surgery initial conservative 0.7
vs conservative
7 lost to treatment
0.6
• Early surgery follow-up 1 lost to treatment
follow-up 0.5
(24 h to surgery; 496 analyzed
>96 h from onset) vs
at 2 weeks 529 analyzed
at 2 weeks
0.4 Early surgery Benefit in subgroup
19 lost to Initial conservative
initial conservative follow-up 24 lost to 0.3 with hematoma
follow-up
treatment 477 followed 505 followed
0.2 ≤1 cm from
up at 6 months
• GCS >5 and ICH
9 alive but up at 6 months
8 alive but
0.1
cortical surface
status status
diameter ≥2 cm unknown unknown
0
0 30 60 90 120 150 180 210 240
(absolute benefit,
468 analyzed at 497 analyzed at
6 months: 6 months: Days 8%; 95% CI, 0-15)
• 1º outcome = 6 early follow-up 4 early follow-up Numbers at risk (alive)
death or disability 327 timely follow-up
135 late follow-up
347 timely follow-up
146 late follow-up
Early surgery 477 366 337 321 314 309 304 304 304
Initial
505 380 349 339 329 324 319 316 316
conservative
Reproduced with permission from Mendelow AD, et al; for the STICH Investigators.
Lancet. 2005;365:387-397. Reproduced with permission from Mendelow AD, et al. Lancet. 2005;365:387-397.
Stereotactic Treatment of Deep ICH
BEFORE Reduction in Mass Effect
100
mm (midline) or cc (edema,vol)
90
80
70
60
Initial
50
Final
AFTER 40
30
20
10
0
Edema ICH Volume Midline shift
Vespa et al Neurocritical Care 2005;2:274-81
Surgical Candidates
AHA Guidelines (2007) Treatment of ICH
• Cerebellar hemorrhage >3 cm with neurological deterioration or • Prevention
brain stem compression and/or hydrocephalus should have surgical
– Modify risk factors
removal of the hemorrhage ASAP (Class I, Level of Evidence B).
• Control hypertension
• Lobar clots within 1 cm of the surface, evacuation of supratentorial
ICH by standard craniotomy might be considered (Class IIb, Level of • Limit anticoagulation
Evidence B). • Acute intervention when it occurs
• No clear evidence indicates that ultra-early craniotomy improves – Alter hemostasis
functional outcome or mortality rate. Operative removal within 12 • rFVIIa for acute ICH
hours, particularly by less-invasive methods, has the most • Rapid reversal of coagulopathy in warfarin-
supportive evidence, but the number of subjects treated within this related ICH
window is very small (Class IIb, Level of Evidence B).
– Surgery
• Very early craniotomy may be associated with an increased risk of
recurrent bleeding (Class IIb, Level of Evidence B).
• Alternatives to craniotomy
– Neuroprotection, rehabilitation, etc.
Broderick JP, et al. Stroke 2007;38;2001-2023
10
Thank you for your
attention!
11
