SPONTANEOUS INTRACEREBRAL
HEMORRHAGE
� Intracerebral hemorrhage is an acute and
spontaneous extravasation of blood into the
brain parenchyma that may extend into the
ventricles and subarachnoid space.ventricles and subarachnoid space.
� It is common:� 12-15 cases per 100 000 people per year
� 10% ~ 15% of all cases of stroke� 10% ~ 15% of all cases of stroke
� 6 month mortality is 30-50%
Primary (78% ~ Chronic Amyloid(78% ~ 88%)
Chronic hypertension
Amyloidangiopathy
SecondaryVascular
abnormalities (AVM,
aneurysm)
Tumor Coagulopathy
� Coagulation disorders
Anticoagulation /Thrombolytic therapyHemorrhagic transformation of cerebral infarct
LeukemiaThrombocytopeniaThrombocytopenia
� Delayed post-traumatic
� Post-operativeCarotid endarterectomyCraniotomy for evacuation SDHCraniotomy for excision AVM
� MalignantGlioblastoma multiformeLymphomaMetastasis (melanoma, choriocarcinoma,
renal cell carcinoma , bronchogenic carcinoma)renal cell carcinoma , bronchogenic carcinoma)
� BenignMeningiomaPituitary adenomaHemangioblastomaAcoustic neuromaCerebellar astrocytoma
30
74 2
ICH in young
Rp. AVM 30 %30
24
15
10Undet. 24%
HTN 15%
Aneurym 10%
Drug Abuse 7%
Tumor 4%
Moyamoya 2%
Non-modifiable
Male sex
Modifiable
HypertensionMale sex
Age
Asian and African Americans
• Japanese
Hypertension
Heavy alcohol consumption
Hypercholesterolemia
� Accounts for 60-70% of ICH
� Theory:
� Chronic hypertension causes
degeneration, fragmentation and fibrinoid degeneration, fragmentation and fibrinoid
necrosis of small perforating arteries
� Predisposes to rupture
CHARCOT-BOUCHARD ANEURYSMS
� Discrete arteriolar
microaneurysms
� Most common in the distal
BADJATIA AND ROSAND, INTRACEREBRALHEMORRHAGE. THE NEUROLOGIST, VOL. 11, NO. 6: NOVEMBER 2005
� Most common in the distal
portions of medium and
small arterioles
� Deposition of amyloid β peptide in small and medium sized blood vessels
� Results in fibrinoid necrosis
and microaneurysm formation
� Prevalence increases with age from ~ 9% in age 60-69 to 58% in age >90
�Lobar haemorrhages
�Chances of rebleed : 21% in 2 yrs
� Primary-immediate effects� Hemorrhage growth� Increased ICP
� Secondary effects� Edema
IschemiaEdema
� Ischemia
� Progression of hematoma
� Brott et al:▪ 103 pts � 26% within 1 hours, 38% within 20 hours
� Acute hypertension, local coagulation deficit may be associated
Brott, Stroke 1997;28:1-5
� Early Presentation
� Irregular shape
� Liver disease� Liver disease
� Hypertension
� Hyperglycemia
� Alcohol use
� Hypofibrinogenima
Priorities for Clinical Research in ICH:NINDS ICH Workshop; Stroke March 2005
� Volume more than60 cm3� Deep-93%� Lobar-71%
� Volumes 30-60 cm 3� Deep-60%� Deep-60%� Lobar-60%� Cerebellar-75%
� Volumes less than 30 cm3� Deep-23%� Lobar-7%� Cerebellar-57%
Broderick: Volume of ICH; Stroke Vol 24, No 7
� Classic clinical presentation: Onset of sudden focal neurological deficit which progresses over minutes to hours
� 50% present with headache /vomiting
� LOC , Seizures
� May have onset after exertion or intense emotional activity
� More often during routine activity
� May occur during trauma
� 25% pts � deterioration in the level of consciousness within the first 24 hrs
� Expansion of the hematoma : first 3 hrs� Expansion of the hematoma : first 3 hrs
� Worsening cerebral edema : 24 ~ 48 hrs
� Late progression of edema: 2 ~ 3 weeks
� Mortality rate : 23% ~ 58% in 6 months
(1)GCS score on admission
(2)Hematoma volume & its progression
(3)Presence of IVH(3)Presence of IVH
(4) Use of anticoagulants
(5) Location of bleed
� Broderick et al: mortality rate at 1 month
� GCS < 9 , volume > 60 ml � 90%
� GCS ≥ 9 , volume < 30 ml � 17%
Hemphill et al. Stroke 2001, 32:891-97
CT
� Superior to MRI in acutely
ill / stuporous pt.
� IVH
MRI
� Superior in detecting
underlying structural
lesions ( AVM etc. )� IVH
� CECT –
AVM/Aneurysm/Tumor
� CT Angio
lesions ( AVM etc. )
� Gradient Echo MRI -as
accurate as CT for
identification of acute
hemorrhage & more
accurate for identification
of Chronic hemorrhage
� SAH
� Abnormal calcification
� Obvious vascular malformation� Obvious vascular malformation
� Blood in unusual location, such as sylvian fissure
� No obvious cause of bleeding such as isolated IVH
Zhu XL, Chan MS, Poon WS. Spontaneous intracranial haemorrhage:which patients need diagnostic cerebral angiography? A prospectivestudy of 206 cases and review of the literature. Stroke. 1997;28:1406–1409.
� Potential treatments of ICH � Stopping or slowing the initial bleeding;
� Removing blood from the parenchyma or ventricles;
� Management of complications of blood in the brain, including increased ICP and decreased CPP
� Good clinical practice: � Management of airways, oxygenation, circulation, glucose
level, fever, nutrition, and DVT prevention.
� Lack of definitive randomized trials of either medical or surgical therapies for ICH, great variability in care
� McKissock et al Primary Intracerebral haematoma: a controlled trial of surgical and conservative treatment in 180 unselected cases Lancet 1961; ii: 221-6
� Auer LM et al Endoscopic surgery versus medical treatment for spontaneous intracerebral haematoma. A randomized study J Neurosurg 1989; 70: 530-5
� Batjer Hhet al Failure of surgery to improve outcome in hypertensive putaminalhaemorrhage. A prospective randomised trial. Arch Neurol 1990; 47: 1103-6
� Juvela S et al The treatment of spontaneous intracerebral haemorrhage. A prospective randomised trial of surgical and conservative treatment. J Neurosurg1989; 70: 755-8
� Chen X et al A prospective randomised trial of surgical and conservative treatment of hypertensive intracerebral haemorrhage. Acta Acad Shanghai Med. 1992; 19: 237-40
� Morgenstern LB et al Surgical treatment for intracerebral hemorrhage(STICH). A single-center, randomised clinical trial. Neurology 1998; 51: 1359-63
� Zuccarello M et al Early surgical treatment for intracerebral hemorrage. A randomized feasibility study. Stroke 1999; 30(9):1833-9
� Cheng X-C et al. The randomised multicentric prospective controlled trial in the standard treatment of hypertensive intracerebral hematomas: the comparison of surgical therapeutic outcomes with conservative therapy. Chin JClin Neurosci 2001; 9: 365-8
� Hosseini H et al Stereotactic aspiration of deep intracerebral haematomas under computed � Hosseini H et al Stereotactic aspiration of deep intracerebral haematomas under computed tomographic control, a multicentric prospective randomised trial.
Cerebrovasc Dis 2003;16S4:57.
� Hattori N et al Impact of Stereotactic evacuation on activities of daily living during thechronic period following spontaneous Putaminal hemorrhage: a randomized study. J Neurosurg
2004; 101: 417-20
� Teernstra et al Stereotactic treatment of intracerebral hematoma by means of a plasminogenactivator: a multicenter randomized controlled trial (SICHPA). Stroke 2003; 34: 968-74
� Mendelow AD et al Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): a randomised trial. Lancet 2005;
365:387 - 397.
Comparison of surgery plus medical vs medical treatment for outcome: death or dependence at end of follow-up Prasad K, Shrivastava A. Surgery for primary supratentorial intracerebral haemorrhage (Cochrane
Review) In: The Cochrane Library Issue 4, 2000. Surgery was associated with statistically significant
reduction in the odds of being dead or dependent at final follow up.
Prasad, K. et al. Stroke 2009;40:e624-e626
� International surgical trial in ICH (STICH) with 1,033 patients showed no difference in outcome, but some potential benefit in subgroup with lobar ICHsubgroup with lobar ICH
� ISTICH-II will include only lobar ICH with a subset analysis of those treated with rFVIIa
Mendelow AD, et al. for the STICH Investigators. Lancet.
2005;365:387-397.
� 1995 – 2003
� 83 centers in 27 countries� 83 centers in 27 countries
� 1033 pts
� 503 early surgery and 530 initial conservative t/t
� Results
�Favorable outcome at 6 months
122 (26%) with surgery 118 (24%) with
initial conservative t/t (p=0.414)initial conservative t/t (p=0.414)
�Mortality 36% vs. 37%
� Conclusion
No overall benefit from early surgery
compared with initial conservative treatment
Early surgery Initial conservative
t/tGCS 5-8 99 (20%) 106 (20%)GCS 5-8 99 (20%) 106 (20%)
9-12 199 (40%) 211 (40%)13-15 205 (41%) 213 (40%)
SiteLobar 196 (39%) 214 (40%)BG/Thalamic 210 (42%) 224 (42%)Both 94 (19%) 90 (17%)
Early surgery Initial conservative t/t
Volume (ml) 40 (24-63) 37 (23-60)Volume (ml) 40 (24-63) 37 (23-60)
Surgery 465 (94%) 140 (26%)Craniotomy 346 (75%) 119 (85%)Stereotaxy 34 (7 %) 3 (2 %)Endoscopy 31 (7 %) 7 (5 %) Other 54 (11%) 11 (8 %)
� The STICH results do not significantly change current practice.
� Patients with a subcortical or cerebellar hematoma at least 3 cm and impaired consciousness should be operated on.operated on.
� Comatose patients (GCS 8) with ICH in the basal ganglia or thalamus very unlikely benefit from clot removal.
� Minimally invasive methods may be useful if done early after ICH onset, but control of hemostasis may be difficult.
� To establish whether earlier surgical evacuation of lobar ICH will improve outcome compared initial conservative treatment.
� To better define the indications for early surgery.
� This will overcome two of the criticisms of STICH (timing was too late and sometimes location was too deep).
� Inclusion:
� Spontaneous lobar ICH on CT Scan
� Patient randomised within 48 hours of ictus � Patient randomised within 48 hours of ictus
� Surgeon is in equipoise
� Best EYE score of 2 or more & M5/M6
� Volume of haematoma 10 - 100ml
� Exclusion:
� Aneurysm, tumour, trauma, angiographically proven AVM .
� Brain stem / cerebellar haemorrhage.
� Intraventricular haemorrhage , Hydrocephalus .
� Surgery cannot be performed within 12 hours.
� Unreversed clotting or coagulation problems.
� Severe pre-existing physical or mental disability or severe co-morbidity
� Patient randomized within 48 hours of ictus .
� If randomized to early surgery this should be undertaken within 12 hours.
� CT scan at about five days (+/- 2 days) .� CT scan at about five days (+/- 2 days) .
� 600 patients will be recruited 30 months.
� FU will take 6 months with analysis and reporting taking 1 year.
� Outcome will be measured at 6 months via a postal questionnaire incl. the GOS, MRS, EuroQol and Barthel.
� Many techniques� Ultrasonic aspiration
� High pressure fluid irrigation
� Endoscopic aspiration
� Modified nucleotome
� Catheter aspiration withinjection of thrombolytic agent(UK or tPA)
� Potential advantages
� Deep putaminal or thalamic haemorrhages may be accessible
� Less damage to overlying brain
� 77% reduction in ICH volume at 48 hours, with no bleeding- Saline irrigation and aspiration after 1 mgrtPA q8h
Vespa P, et al. Neurocritical Care. 2005;2:274.
Emergency diagnosis and
assessment of ICH and its
causes
Rapid neuroimaging with
CT or MRI is
recommended to
distinguish ischemic
stroke from ICH.
Class I, Level A
Medical treatment for ICH Patients with a severe
coagulation factor
deficiency or severe
thrombocytopenia should
receive appropriate factor
replacement therapy or
platelets, respectively.
Class I, Level C
Hemostasis/antiplatelets/DV
T prophylaxis
Patients with ICH whose INR
is elevated due to OAC should
have their warfarin withheld,
receive therapy to replace
vitamin K–dependent factors
and correct the INR, and
receive intravenous vitamin
K.
Class I, Level C
K.
Patients with ICH should have
intermittent pneumatic
compression for prevention of
venous thromboembolism in
addition to elastic stockings.
Class I, Level B
Inpatient management
and prevention of
secondary brain injury
General monitoring Initial monitoring and Initial monitoring and
management of ICH
patients should take
place in an intensive
care unit, preferably
one with physician and
nursing neuroscience
intensive care
expertise.
Class I, Level B
Management of
glucose
Glucose should be
monitored and
normoglycemia is
recommended
Class I, Level C
Seizures and
antiepileptic drugs
Patients with clinical
seizures should be
Class I, Level A
antiepileptic drugs seizures should be
treated with
antiepileptic drugs.
Patients with a change
in mental status who
are found to have
electrographic seizures
on EEG should be
treated with
antiepileptic drugs
Class I, Level C
Patients with cerebellar
hemorrhage who are
deteriorating
neurologically or who
Procedures/surgery—clot
removal
neurologically or who
have brainstem
compression and/or
hydrocephalus from
ventricular obstruction
should undergo surgical
removal of the
hemorrhage as soon as
possible.
Class I, Level B
Prevention of
recurrent ICH
After the acute ICH,
absent medical
contraindications, BP
should be well
controlled,
particularly for
Class I, Level A
particularly for
patients with ICH
location typical of
hypertensive
vasculopathy.
(Class II a; Level of Evidence:
B).
(Class II b; Level of Evidence:
B)
CT angiography, CT
venography, contrast-
enhanced CT, CEMRI, MRA &
CT angiography and contrast-
enhanced CT may be
considered to help identify enhanced CT, CEMRI, MRA &
MRV can be useful to
evaluate for underlying
structural lesions when there
is clinical or radiological
suspicion
considered to help identify
patients at risk for hematoma
expansion
(Class IIa; Level of Evidence: B)
PCCs have not shown improved outcome compared with FFP but may have fewer
complications compared with FFP and are reasonable to consider as an alternative
to FFP
(Class IIb; Level of Evidence: B)
The usefulness of platelet transfusions in ICH patients with a history
of antiplatelet use is unclear and is considered investigational
After documentation of cessation of bleeding, low-dose
subcutaneous low-molecular-weight heparin or unfractionated
heparin may be considered for prevention of venous
thromboembolism in patients with lack of mobility after 1 to 4 days
from onset
(Class III; Level of Evidence: A)
rFVIIa does not replace all clotting factors, and although the INR may be lowered,
clotting may not be restored in vivo; therefore, rFVIIa is not routinely
recommended as a sole agent for OAC reversal in ICH
Although rFVIIa can limit the extent of hematoma expansion in
noncoagulopathic ICH patients, there is an increase in thromboembolic risk with
rFVIIa and no clear clinical benefit in unselected patients.Thus rFVIIa is not
recommended in unselected patients
In patients presenting with a systolic BP of 150 to 220 mm Hg, acute lowering of systolic BP to 140 mm Hg is probably safe (Class IIa; Level of Evidence: B).(New recommendation)
� If SBP is 200 mm Hg or MAP is 150 mm Hg
� Aggressive reduction and frequent monitoring (5 minutes)
� If SBP is 180 mm Hg or MAP is 130 mm Hg with elevated ICP
� Monitoring ICP
� Reducing BP to keep CPP >60 mm Hg
� If SBP is 180 mm Hg or MAP is 130 mm Hg no ICP issues,
� Modest reduction of BP (~MAP of 110/BP 160/90)
� Using intermittent or continuous IV meds
� Evaluate every 15 minutes.
(Class II a; Level of
Evidence: B)
(Class III; Level of
Evidence: B)
Continuous EEG
monitoring is probably
Prophylactic
anticonvulsantmonitoring is probably
indicated in ICH patients
with depressed mental
status out of proportion
to the degree of brain
injury
anticonvulsant
medication should not be
used
(Class II a; Level of Evidence: B)
Ventricular drainage as treatment
for hydrocephalus is reasonable in
patients with decreased level of
consciousness
(Class II b; Level of Evidence: C)
Patients with a GCS score of 8,
those with clinical evidence of
transtentorial herniation, or those
with significant IVH or
hydrocephalus might be considered
for ICP monitoring and treatment. for ICP monitoring and treatment.
(Class IIb; Level of Evidence: B)
Although intraventricular
administration of rtPA in IVH
appears to have a fairly low
complication rate, efficacy and
safety of this treatment is uncertain
and is considered investigational
(Class IIb; Level of Evidence: B) (Class IIb; Level of Evidence: C)
For patients presenting with lobar
clots >30 mL and within 1 cm of the
surface, evacuation of
For most patients with ICH, the
usefulness of surgery is uncertain .
Specific exceptions to this surface, evacuation of
supratentorial ICH by standard
craniotomy might be considered
Specific exceptions to this
recommendation have been
described.
The effectiveness of minimally
invasive clot evacuation utilizing
either stereotactic or endoscopic
aspiration with or without
thrombolytic usage is uncertain and
is considered investigational
(Class III; Level of Evidence: B) (Class III; Level of Evidence: C)
Although theoretically
attractive, no clear evidence
at present indicates that
ultra-early removal of
Initial treatment of these
patients with ventricular
drainage alone rather than
surgical evacuation is not ultra-early removal of
supratentorial ICH improves
functional outcome or
mortality rate. Very early
craniotomy may be harmful
due to increased risk of
recurrent bleeding
surgical evacuation is not
recommended
(Class IIa; Level of Evidence: B)
Aggressive full care early after ICH onset and
postponement of new DNR orders until at
least the second full day of hospitalization is least the second full day of hospitalization is
probably recommended
� (Class II a; Level of Evidence: B)
Risk factors for recurrence: lobar location of the initial
ICH, older age, ongoing anticoagulation, presence of
the apolipoprotein E 2 or 4 alleles, and greaterthe apolipoprotein E 2 or 4 alleles, and greater
number of microbleeds on MRI
After the acute ICH period, a goal target of a normal
BP of <140/90 (<130/80 if diabetes or chronic kidney
disease) is reasonable
Avoidance of long-term anticoagulation as treatment
for nonvalvular atrial fibrillation is probably
recommended after spontaneous lobar ICH because of
the relatively high risk of recurrence
(Class IIa; Level of Evidence: B)
Avoidance of heavy alcohol use can be beneficial
(Class IIb; Level of
Evidence:B)
(Class IIb; Level of
Evidence:C)
Anticoagulation after
nonlobar ICH and
antiplatelet therapy after all
ICH might be considered,
particularly when there are
definite indications for these
agents
There is insufficient data to
recommend restrictions on
use of statin agents or
physical or sexual activity