Intracerebral Hemorrhage & high ICP
management
Emergency Lecture Series
July 10, 2013
Abdulla Alkuwaiti R2
Content
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Pathophysiology
Epidemiology
Clinical features
Causes/Risk factors
Types of ICH
Radiological Findings
Management/ including increase
ICP
• Prognosis
Pathophysiology
• Thrombin and iron, released upon red blood
cell (RBC) lysis, are 2 major factors causing
brain injury after ICH.
• Thrombin at high concentrations kills
neurons and astrocytes in vitro.
• Hemoglobin degradation can result in iron
release. The iron causes marked brain
edema, even in small concentration.
Ya Hua, “Intracerebral hemorrhage: introduction brain injury afteriIntracerebral hemorrhage, ther
role of Thrombin and Iron” Stroke.2007; 38: 759-762
Secondary Damage
Hematoma expansion
≥ 80 ml fatal
Cerebral edema
Secondary injury
Epidemiology
• Accounts for 15% of strokes in the West and 30%
in the East
• 12-15 cases per 100,000 per year
• More common in Hispanics, Blacks, Asian than
in whites
Canada: 2008/2009
Total 11%: AGE 20-29: 17%, 30-39: 16%, 40-49:
11%, 50-59: 12%, 60-69: 12%, 70-79: 10%, 80-89:
10%, 90+: 7%
Male 53%, female 47%
The quality of stroke care in Canada, Canadian stroke network 2011
Clinical Features
• Sudden headache +/- N & V
• Smooth progressive onset over minutes
to hours
• Usually during activity
• Confusion
• Neurodeficit: hemiplegia
• Depressed level of consciousness
• Seizures
Case: 26F
Post op
Post Angio
ICH Score
Component
ICH score points
GCS
3-4
2
5 - 12
1
13 - 15
0
ICH volume
≥ 30 ml
1
≤ 30 ml
0
IVH
yes
1
no
0
Infratentorial
1
Age > 80
1
Mortality and ICH Score
Classification of ICH
SECONDARY
PRIMARY (78-88%)
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Hypertensive
angiopathy
(fibrohyalinosis)
Amyloid angiopathy
Anticoagulant
Associated
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AVM
Aneurysm
Cavernoma
Neoplasm
Coagulopathy
 Alcoholic liver
disease
 Hemophilia
Hemorrhagic infarct
Toxic-cocaine
Risk factors
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AGE: Incidence significantly doubles with each
decade after age 55. Above 80 years of age risk
increases 25 times
Gender: more common in men
Race: more common in blacks, hispanics, asians, less
in whites
Previous CVA
Alcohol consumption: >3 drinks per day increases
the risk of ICH by 7 folds
Drugs: cocaine, amphetamine
Cigarette smoking does not increase the risk of ICH
Risk Factors
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Oral Anticoagulant: warfarin risk of bleed in
afib patient is 2.2% per year
Antiplatelets: ASA alone (1.3% per year risk)
no significant increase in risk but ASA and
plavix together increase risk to 2.4% per year.
rTPA: risk of ICH is 6.4% in the next 36hrs
Genetic predisposition
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The E2 and E4 alleles of the apolipoprotein E
gene play an important role in the occurrence
of certain forms of ICH as labor hemorrhages
O’Donnel et al, 2000
Types of Intracerebral Hemorrhage
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Putaminal hemorrhage (35%)
Caudate Hemorrhage (5%)
Thalamic Hemorrhage (10-15%)
Mesencephalic Hemorrhages (rare)
Pontine Hemorrhage (5%)
Medullary Hemorrhages (rare)
Cerebellar Hemorrhage (5-10%)
Lobar Hemorrhage (25%)
IVH
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Extension of ICH to IVH is a common feature
of caudate and thalamic hemorrhages, and of
large putaminal and lobar hemorrhages
Lobar Hemorrhages
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2nd most common (25%)
Nonhypertensive mechanisms:
Young (AVM sympathomimetic agents)
Elderly: cerebral amyloid angiopathy
Usually subcortical frontal vs parietal vs
temporal vs occipital
Seizures in up to 28% of patients
Mortality rate is lower than other bleeds, and
long term functional outcome maybe better.
Radiological Findings
Spot
Sign
Radiological Findings
Spot sign: predictor of expansion (PREDICT 2012)
PPV 61%
NPV 78%
Sensitivity 51%
Specificity 85%
Mortality at 3 months was 43·4% (23 of 53) in CTA
spot-sign positive versus 19·6% (31 of 158) in CTA
spot-sign-negative patients (p=0·002).
Demchuk AM, Prediction of haematoma growth and outcome in patients with intracerebral haemorrhage using the
CT-angiography spot sign (PREDICT): a prospective observational study. Lancet Neurol. 2012 Apr;11(4):307-14.
MRI Brain
Management of ICH
• ABC  ICU admission
• Early control of elevated BP
• Correction of coagulopathy and platelet
abnormalities
• Identification and control of urgent surgical
issues, such as threatening mass effect,
intracranial HTN and hydrocephalus
• Definitive diagnosis of the cause of the
hemorrhage and definitive treatment of the
underling cause
General Supportive Care
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HOB 30°
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SO2 ≥ 95%
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Glucose control, hypoglycemia should be
avoided
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T° control ≤ 37.5° C
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Pain control, sedation
Prognosis and Acute Blood Pressure
↑ Early Neurological Deterioration
↓ Functional Outcome (90 days)
1 month mortality (%)
1 month mortality (%)
100
80
60
40
20
0
-117
118-132
133-144
MAP (mm Hg)
145-
Fogelhom et al, Stroke, 28: 1396-400, 1997
Okumura et al, J. Hypertension, 23: 1217-23, 2005
Blood Pressure and Hematoma Evolution
Target max
SBP
No
Enlargement
Hematoma
Enlargement
140 mmHg
16
2
150 mmHg
14
1
160 mmHg
22
8
9%
p=0.025
30%
170 mmHg
8
5
Ohwaki et al, Stroke, 35: 1353-1367, 2004
Blood pressure control
• Blood pressure on initial arrival to the ER and every 15
minutes until blood pressure has stabilized, showed be
corrected within 1 hour of presentation.
• Target < 180 mmHg
• Close blood pressure monitoring (e.g. every 30 to 60
min) should continue for at least the first 24 to 48 hours.
• There is evidence demonstrating it is safe to target
systolic blood pressure to less than 160 mmHg.
American and Best practice canadian guidelines for stroke management
BP Control Meds
• Labetalol: 10-20mg iv over 2 minutes, then 40-80mg iv
every 10 min, until BP is controlled. Max dose 300mg
per day. Fu heart rate, avoid bradycardia.
• Enalopril iv 0.625 to 1.2 mg every 4-6 hours
• Hydralazine iv 10-20mg every 4-6 hours
• Nicardipine 5mg/hr titrate by 2.5mg/hr every 5 min to a
maximum dose of 15mg/hr
• Sodium Nitroprusside: it can increase ICP so to be
avoided in neurological emergencies unless everything
else fails. Risk of cyanide toxicity can occur with rapid
and prolonged infusion. Metabolic acidosis, elevated
lactate levels and lactate/pyruvate ratios, and increased
mixed venous oxygen content suggest clinical toxicity.
Antiepileptics
• Clinical 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
• Prophylactic anticonvulsant medication should not
be used
American and Best practice canadian guidelines for stroke management
Statins
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The SPARCL trial of high-dose atorvastatin
in secondary stroke prevention reported an
excess of ICH with active treatment
compared with placebo (55 versus 33;
P 0.02).
2012 meta-analysis of 31 RCT trial on statin
and risk of intracerebral hemorrhage, there was
no significant increase
Reversing coagulopathies
 Check Coag and platelets
 Correct thrombocytopenia below 100, some references
say below 75.
 If on ASA or plavix, should be held and transfused
platelets
 Warfarin should be stopped and treated with
prothrombin complex concentrate (PCC) (contains
factor 2, 7, 9, 10, protein c and protein s) and Vitamin K
10 mg IV. Fresh-frozen plasma 2-6 units and Vitamin K
could be used as alternative if PCC is not available
 If on heparin best reversed with protamine sulfate (1.0
to 1.5 mg/1000 U heparin
American and Best practice canadian guidelines for stroke management
Reverse anticoagulation
Dabigatran reversal may benefit from PCC but
the evidence is weak and efforts should be
directed toward improving renal clearance with
consideration of hemodialysis in emergency
situations.
Rivaroxaban and apixaban are more likely to
benefit from PCC administration than
dabigatran but are unlikely to benefit from
hemodialysis.
F Robert ‘The role of anticoagulats, antiplatelets, and their reversal strategies in the management of intracerebral
hemorrhage’ Neurosurg focus 34 (5): 2013
Factor V11a
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Recombinant Factor VIIa
Within 4 hours prevents hematoma growth
Increases the risk of arterial thromboembolic
No clinical benefit for survival or outcome.
It is not recommended for use outside of clinical
trials at this time
American and Best practice canadian guidelines for stroke management
Hematoma Evolution and rFVIIa
4.5ml
5.8ml
3.3ml
rFVIIa within 4 hours:
• Dose dependent attenuation of
hematoma expansion
• no effect on mRS at 90 days
Mayer et al. NEJM 2005; 352: 777-85
Treatment of ICHT
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Intubation
Hyperventilation
Sedation
Steroids: NO role
Osmotic agents
Mannitol
 Hypertonic saline
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No Δ in outcome
Intracranial Pressure control
•Elevate the HOB to 30 degrees
•Analgesia and sedation, particularly in unstable, intubated
patients
•ICP monitor should be considered for patients with GCS
<8, those with clinical evidence of transtentorial
herniation, or those with significant IVH or
hydrocephalus.
•Osmotic diuretics (eg, mannitol and hypertonic saline
solution)
•neuromuscular blockade
•Goal of maintaining cerebral perfusion pressure (CPP) of
50 to 70 mmHg
ICP control
The ICP lowering effect of hyperventilation to a
PaCO2 of 25 to 30 mmHg is dramatic and rapid.
However, the effect only lasts for minutes to a
few hours.
ICP control
Glucocorticoids should not generally be used
to lower the ICP in patients with ICH. No
improvement in outcome
American and Best practice canadian guidelines for stroke management
Surgical Indications
• Cerebellar bleed: >3cm, and deteriorating, vs brain
stem compression, vs hydrocephalus due to
ventricular obstruction
• Supratentorial ICH evacuation: Controversial
• STICH trial: patients assigned to early (within 24hr)
surgical hematoma evacuation were slightly more
likely to have a favorable outcome at six months
compared with initial conservative treatment, but
trend did not reach statistical significance.
• It should only be considered as a life saving
procedure to treat refractory increases in ICP
American and Best practice canadian guidelines for stroke management
Surgical Indications
• Favoring surgery: obtunded-stupor patients, recent
onset of hemorrhage, ongoing clinical deterioration,
involvement the nondominant hemisphere, location
of the hematoma near the cortical surface.
• For patients presenting with lobar clots >30 mL and
within 1 cm of the surface evacuation of supratentorial
ICH by standard craniotomy might be considered
• No clear evidence at present indicates that ultra-early
removal of supratentorial ICH improves functional
outcome or mortality rate.
American and Best practice canadian guidelines for stroke management
Intra-ventricular Hemorrhage
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EVD
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Intra- ventricular rtpa (CLEAR)
Case 55F presented with
Headache and LOC
PROGNOSIS
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Mortality 35-52% in the first 30 days and half of
them in the first 2 days
Factors Affecting Prognosis
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Volume of hemorrhage
Hematoma growth
Early Neurological deterioration within 48hr
Oral Anticoaglants
GCS on presentation
Age
Hemorrhage location
Intraventricular hemorrhage
Summary ICH Management
• Early control of elevated BP
• Correction of coagulopathy and platelet
abnormalities
• Identification and control of urgent surgical
issues, such as threatening mass effect,
intracranial HTN and hydrocephalus
• Definitive diagnosis of the cause of the
hemorrhage and definitive treatment of the
underling cause
Questions
Modified Rankin Scale