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Intracerebral Hemorrhage
Dr Shaheer Anwar
Resident Neurosurgeon.
Objectives:
• Case Scenario.
• Introduction.
• Intracerebral hemorrhage.
• Epidemiology.
• Sites of hemorrhage.
• Etiology.
• Cerebral Amyloid Angiopathy.
• Clinical Presentation.
• ICH score.
• How to Investigate?
• How to Manage?
Case Scenario:
• This is a 21-year-old right-handed male, with a past medical history
significant for asthma and Attention Deficit Disorder (ADD), treated
with methylphenidate, who was found in a gym bathroom with left
sided weakness and urinary incontinence shortly after lifting weights.
Upon arrival to the emergency department (ED), he was following
commands with left hemiparesis. He complained of severe headache.
Initial laboratory studies revealed a normal platelet count,
coagulation profile, and negative toxicology screen.
• Emergent non-contrast CT scan brain revealed a right frontal
intracranial hemorrhage
CT scan Plain brain:
Introduction:
Intracerebral hemorrhage
• Brain parenchyma.
• Intraventricular.
Meningeal Space
hemorrhage
• Extradural hematoma(EDH).
• Subdural Hematoma(SDH).
• Subarachnoid Hemorrhage(SAH).
Intracerebral hemorrhage (Definition):
Hemorrhage within the brain parenchyma. Formerly referred to as
“hypertensive hemorrhage”, but hypertension is a debatable etiology in
many cases.
Epidemiology:
• The second most common form of stroke (≈ 15–30% of all strokes)
(earlier estimates: 10%1), and the most deadly.
• Approximately 12–15 cases per 100,000/yr.
• Onset is usually during activity (rarely during sleep), which may be
related to elevation of BP or increased CBF.
Risk Factors:
• Age, Incidence significantly increases after the age of 55yrs of age.
• Gender, men are affected more.
• Race, Affects black more as compared to white.
• Previous Stroke, of any type increases the risk to 23:1.
• Alcohol Consumption, ICH in patients with high ethanol consumption were
more commonly lobar than the typical“hypertensive hemorrhages” in the
basal ganglia.
• Cigeratte Smoking, increases the risk of SAH and ischemic infarction but
probably does not increase the risk of ICH.
• Street drugs: cocaine, amphetamines, phencyclidine.
• liver dysfunction: hemostasis may be impaired on the basis of
thrombocytopenia, reduced coagulation factors, and hyperfibrinolysis.
Common locations Of hemorrhages:
% Location
50% striate body (basal ganglia); putamen most
common; also includes: lenticular nucleus,
internal capsule, globus pallidus.
15% Thalamus.
10-15% Pons.
10% Cerebellum.
10-20% Cerebral white matter.
1-6% Brainstem.
Etiology:
1. Hypertensive ICH:
• Essential.
• Pregnancy related: the risk of pregnancy in pregnancy is 1 in 9500
2. Non-hypertensive ICH
• Vascular malformation: AVM, Aneurysm, Cavernous hemangioma
• Bleeding disorders/anticoagulant
• Amyloid angiopathy
• Trauma
• Tumor
• Drug abuse: amphetamine, cocaine,
Cerebral Amyloid Angiopathy:
• Cerebral amyloid angiopathy (CAA) AKA congophilic angiopathy.
Pathologic deposition of beta amyloid protein within the media of
small meningeal and cortical vessels without the evidence of systemic
amyloidosis. Some vessels may show fibrinoid necrosis of vessel wall.
• Incidence increases with age: CAA is present in ≈ 50% of those over
70 years of age.
• CAA is probably responsible for ≈ 10% of cases of ICH
Diagnostic Criteria for CAA:
Diagnosis Criteria
Definite CAA Full postmortem exam showing all 3 of the following:
a) lobar, cortical, or corticosubcortical hemorrhage
b) severe CAA
c) absence of another diagnostic lesion
Probable CAA with
supporting
pathological
evidence
Clinical data & pathological tissue showing all 3 of the following:
a) lobar, cortical, or corticosubcortical hemorrhage
b) some degree of vascular amyloid deposition in specimen
c) absence of another diagnostic lesion
Probable CAA Clinical data and MRI findings showing all 3 of the following:
a) age ≥ 60 yrs
b) multiple hemorrhages restricted to the lobar, cortical, or corticosubcortical
region
c) absence of another cause of hemorrhage
Possible CAA Clinical data and MRI findings:
a) age ≥ 60 yrs
b) single lobar, cortical, or corticosubcortical hemorrhage without another
causea, or multiple hemorrhages with a possible but not a definite causea or
with some hemorrhages in an atypical location (e.g. brain stem)
Pathophysiology:
• Primary immediate effect
Hemorrhage growth
Increase ICP
• Secondary effect
Downstream effect
Edema
Ischemia
Clinical Presentation:
• Alteration in level of consciousness (approximately 50%).
• Nausea and vomiting (approximately 40-50%).
• Headache (approximately 40%).
• Seizures[3] (approximately 6-7%).
• Focal neurological deficits.
Focal Neurological Deficit:
1. Putamen - Contralateral hemiparesis, contralateral sensory loss,
contralateral conjugate gaze paresis, homonymous hemianopia,
aphasia, neglect, or apraxia.
2. Thalamus - Contralateral sensory loss, contralateral hemiparesis,
gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion.
3. Lobar - Contralateral hemiparesis or sensory loss, contralateral
conjugate gaze paresis, homonymous hemianopia, aphasia, neglect, or
apraxia.
4. Caudate nucleus - Contralateral hemiparesis, contralateral conjugate
gaze paresis, or confusion.
Cont…
5. Brain stem - Quadriparesis, facial weakness, decreased level of
consciousness, gaze paresis, ocular bobbing, miosis, or autonomic
instability
6. Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial
weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis,
or decreased level of consciousness
Delayed deterioration:
Deterioration after the initial hemorrhage is usually due to any
combination of the following:
1. rebleed.
2. edema.
3. hydrocephalus: higher risk with intraventricular extension or
posterior fossa ICH
4. seizures
Rebleed:
The incidence of hematoma enlargement decreases with time:
33–38% in 1–3 hours
16% in 3–6 hrs
14% between 24 hrs of onset
Second CT scan within 24 hrs of the first should be done. Patients with
enlarging hematomas were more likely to have coagulopathy, and had a
worse outcome.
ICH Score:
Feature: Finding Points:
GCS Score 3-4
5-12
13-15
2
1
0
Age >80yrs
<80yrs
1
0
Location Infratentorial
supratentorial
1
0
ICH Volume >30ml
<30ml
1
0
Intraventricular
blood
Yes
No
1
0
ICH Score(Total
Points).
0-6
Interpretation Of ICH Score:
ICH Score 30days mortality
0 0%
1 13%
2 26%
3 72%
4 97%
5 100%
Investigation:
Laboratory studies
• CBC
• Coagulation profile.
• Electrolyte
Others
• Imaging – CT brain w/o contrast.
CT Scan:
1. Demonstrates acute hemorrhage as hyperdense signal intensity
2. Multifocal hemorrhages at the frontal, temporal, or occipital poles
suggest a traumatic etiology.
3. Hematoma volume can be approximated by (A x B x C)/2
4. Iodinated contrast may be injected to increase screening yield for
underlying tumor or vascular malformation.
Vessel Imaging:
1. CT angiography permits screening of large and medium-sized
vessels for AVMs, vasculitis, and other arteriopathies.
2. Formal Angiography for definitive treatment.
Management:
1. patients should be managed in an ICU
2. HTN: Issues: HTN may contribute to further bleeding, especially within the first
hour. However, some HTN may be needed to maintain perfusion.
CPP=MAP-ICP.
3. intubate if stuporous or comatose
4. maintain euglycemia
5. maintain normothermia
6. anticonvulsants
a) seizures are treated with appropriate AEDs
b) prophylactic AEDs: optional. May decrease risk of early seizures in patients with lobar
Hemorrhages.
7. hemostatic issues, check INR (or PT), PTT & platelet count (PC), platelet function assay
(PFA)
8. steroids: controversial. No benefit from dexamethasone in ICH, with significantly more
complications
(primarily infectious, GI bleeding and diabetogenic). Consider use if significant
perihemorrhage edema on imaging.
9. treat intracranial hypertension with mannitol and/or furosemide as tolerated.
10. external ventricular drain (EVD): for hydrocephalus, some cases of intraventricular
blood, or to
manage ICP.
11. follow electrolytes and osmolarity.
a) aggressively treat hyperglycemia.
b) watch for SIADH.
12. angiography: primarily to R/O underlying vascular malformation.
a) if urgent surgery is indicated (e.g. for herniation), angiogram may be
deferred to post operative period.
b) indications: angiography is recommended except for patients > 45
yrs of age with preexisting hypertension and ICH in thalamus, putamen
or posterior fossa.

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Intracerebral hemorrhage

  • 1. Intracerebral Hemorrhage Dr Shaheer Anwar Resident Neurosurgeon.
  • 2. Objectives: • Case Scenario. • Introduction. • Intracerebral hemorrhage. • Epidemiology. • Sites of hemorrhage. • Etiology. • Cerebral Amyloid Angiopathy. • Clinical Presentation. • ICH score. • How to Investigate? • How to Manage?
  • 3. Case Scenario: • This is a 21-year-old right-handed male, with a past medical history significant for asthma and Attention Deficit Disorder (ADD), treated with methylphenidate, who was found in a gym bathroom with left sided weakness and urinary incontinence shortly after lifting weights. Upon arrival to the emergency department (ED), he was following commands with left hemiparesis. He complained of severe headache. Initial laboratory studies revealed a normal platelet count, coagulation profile, and negative toxicology screen. • Emergent non-contrast CT scan brain revealed a right frontal intracranial hemorrhage
  • 4. CT scan Plain brain:
  • 5. Introduction: Intracerebral hemorrhage • Brain parenchyma. • Intraventricular. Meningeal Space hemorrhage • Extradural hematoma(EDH). • Subdural Hematoma(SDH). • Subarachnoid Hemorrhage(SAH).
  • 6. Intracerebral hemorrhage (Definition): Hemorrhage within the brain parenchyma. Formerly referred to as “hypertensive hemorrhage”, but hypertension is a debatable etiology in many cases.
  • 7. Epidemiology: • The second most common form of stroke (≈ 15–30% of all strokes) (earlier estimates: 10%1), and the most deadly. • Approximately 12–15 cases per 100,000/yr. • Onset is usually during activity (rarely during sleep), which may be related to elevation of BP or increased CBF.
  • 8. Risk Factors: • Age, Incidence significantly increases after the age of 55yrs of age. • Gender, men are affected more. • Race, Affects black more as compared to white. • Previous Stroke, of any type increases the risk to 23:1. • Alcohol Consumption, ICH in patients with high ethanol consumption were more commonly lobar than the typical“hypertensive hemorrhages” in the basal ganglia. • Cigeratte Smoking, increases the risk of SAH and ischemic infarction but probably does not increase the risk of ICH. • Street drugs: cocaine, amphetamines, phencyclidine. • liver dysfunction: hemostasis may be impaired on the basis of thrombocytopenia, reduced coagulation factors, and hyperfibrinolysis.
  • 9. Common locations Of hemorrhages: % Location 50% striate body (basal ganglia); putamen most common; also includes: lenticular nucleus, internal capsule, globus pallidus. 15% Thalamus. 10-15% Pons. 10% Cerebellum. 10-20% Cerebral white matter. 1-6% Brainstem.
  • 10.
  • 11.
  • 12.
  • 13. Etiology: 1. Hypertensive ICH: • Essential. • Pregnancy related: the risk of pregnancy in pregnancy is 1 in 9500 2. Non-hypertensive ICH • Vascular malformation: AVM, Aneurysm, Cavernous hemangioma • Bleeding disorders/anticoagulant • Amyloid angiopathy • Trauma • Tumor • Drug abuse: amphetamine, cocaine,
  • 14. Cerebral Amyloid Angiopathy: • Cerebral amyloid angiopathy (CAA) AKA congophilic angiopathy. Pathologic deposition of beta amyloid protein within the media of small meningeal and cortical vessels without the evidence of systemic amyloidosis. Some vessels may show fibrinoid necrosis of vessel wall. • Incidence increases with age: CAA is present in ≈ 50% of those over 70 years of age. • CAA is probably responsible for ≈ 10% of cases of ICH
  • 15. Diagnostic Criteria for CAA: Diagnosis Criteria Definite CAA Full postmortem exam showing all 3 of the following: a) lobar, cortical, or corticosubcortical hemorrhage b) severe CAA c) absence of another diagnostic lesion Probable CAA with supporting pathological evidence Clinical data & pathological tissue showing all 3 of the following: a) lobar, cortical, or corticosubcortical hemorrhage b) some degree of vascular amyloid deposition in specimen c) absence of another diagnostic lesion Probable CAA Clinical data and MRI findings showing all 3 of the following: a) age ≥ 60 yrs b) multiple hemorrhages restricted to the lobar, cortical, or corticosubcortical region c) absence of another cause of hemorrhage Possible CAA Clinical data and MRI findings: a) age ≥ 60 yrs b) single lobar, cortical, or corticosubcortical hemorrhage without another causea, or multiple hemorrhages with a possible but not a definite causea or with some hemorrhages in an atypical location (e.g. brain stem)
  • 16. Pathophysiology: • Primary immediate effect Hemorrhage growth Increase ICP • Secondary effect Downstream effect Edema Ischemia
  • 17. Clinical Presentation: • Alteration in level of consciousness (approximately 50%). • Nausea and vomiting (approximately 40-50%). • Headache (approximately 40%). • Seizures[3] (approximately 6-7%). • Focal neurological deficits.
  • 18. Focal Neurological Deficit: 1. Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, aphasia, neglect, or apraxia. 2. Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion. 3. Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, aphasia, neglect, or apraxia. 4. Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion.
  • 19. Cont… 5. Brain stem - Quadriparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability 6. Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousness
  • 20. Delayed deterioration: Deterioration after the initial hemorrhage is usually due to any combination of the following: 1. rebleed. 2. edema. 3. hydrocephalus: higher risk with intraventricular extension or posterior fossa ICH 4. seizures
  • 21. Rebleed: The incidence of hematoma enlargement decreases with time: 33–38% in 1–3 hours 16% in 3–6 hrs 14% between 24 hrs of onset Second CT scan within 24 hrs of the first should be done. Patients with enlarging hematomas were more likely to have coagulopathy, and had a worse outcome.
  • 22. ICH Score: Feature: Finding Points: GCS Score 3-4 5-12 13-15 2 1 0 Age >80yrs <80yrs 1 0 Location Infratentorial supratentorial 1 0 ICH Volume >30ml <30ml 1 0 Intraventricular blood Yes No 1 0 ICH Score(Total Points). 0-6
  • 23. Interpretation Of ICH Score: ICH Score 30days mortality 0 0% 1 13% 2 26% 3 72% 4 97% 5 100%
  • 24. Investigation: Laboratory studies • CBC • Coagulation profile. • Electrolyte Others • Imaging – CT brain w/o contrast.
  • 25. CT Scan: 1. Demonstrates acute hemorrhage as hyperdense signal intensity 2. Multifocal hemorrhages at the frontal, temporal, or occipital poles suggest a traumatic etiology. 3. Hematoma volume can be approximated by (A x B x C)/2 4. Iodinated contrast may be injected to increase screening yield for underlying tumor or vascular malformation.
  • 26. Vessel Imaging: 1. CT angiography permits screening of large and medium-sized vessels for AVMs, vasculitis, and other arteriopathies. 2. Formal Angiography for definitive treatment.
  • 27. Management: 1. patients should be managed in an ICU 2. HTN: Issues: HTN may contribute to further bleeding, especially within the first hour. However, some HTN may be needed to maintain perfusion. CPP=MAP-ICP. 3. intubate if stuporous or comatose 4. maintain euglycemia 5. maintain normothermia 6. anticonvulsants a) seizures are treated with appropriate AEDs b) prophylactic AEDs: optional. May decrease risk of early seizures in patients with lobar Hemorrhages.
  • 28. 7. hemostatic issues, check INR (or PT), PTT & platelet count (PC), platelet function assay (PFA) 8. steroids: controversial. No benefit from dexamethasone in ICH, with significantly more complications (primarily infectious, GI bleeding and diabetogenic). Consider use if significant perihemorrhage edema on imaging. 9. treat intracranial hypertension with mannitol and/or furosemide as tolerated. 10. external ventricular drain (EVD): for hydrocephalus, some cases of intraventricular blood, or to manage ICP. 11. follow electrolytes and osmolarity. a) aggressively treat hyperglycemia. b) watch for SIADH.
  • 29. 12. angiography: primarily to R/O underlying vascular malformation. a) if urgent surgery is indicated (e.g. for herniation), angiogram may be deferred to post operative period. b) indications: angiography is recommended except for patients > 45 yrs of age with preexisting hypertension and ICH in thalamus, putamen or posterior fossa.