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Hemorrhagic Stroke
By: Dr-Issa Kh. Aldababseh
Outlines
● Intracerebral hemorrhage
● Subarachnoid Hemorrhage
● Introduction
● Definition
What is stroke?
It is an acute neurologic condition resulting from a disruption in
cerebral perfusion, either due to ischemia or hemorrhage.
A blocked artery: Ischemic 87%
A ruptured artery: Bleeding 13%
What is Hemorrhagic stroke?
It is the cerebral infarction due to hemorrhage.
1- Intracerebral hemorrhage 2- Subarachnoid hemorrhage
Bleeding within the brain parenchyma Bleeding into the subarachnoid space
1- Intracerebral hemorrhage
High mortality rate (50% at 30 days).
Significant morbidity.
Hematoma formation and enlargement may lead to
local injury and increase in intracerebral pressure.
Locations
Basal ganglia (66%)
Pons (10%)
Cerebellum (10%)
Other cortical areas
1- Intracerebral hemorrhage
1- Intracerebral hemorrhage
Causes?
B- Ischemic stroke A- HTN (Particularly a sudden increase in BP)
May convert to a
hemorrhagic stroke
HTN causes a rupture of small vessels deep within the brain parenchyma.
Chronic HTN causes degeneration of small arteries,
leading to microaneurysms, which can rupture easily.
It is typically seen in older patients; risk increases with age
C- Others Amyloid angiopathy (10%), Anticoagulant/Antithrombolytic use (10%),
brain tumors (5%), and AV malformations (5%)
HIT: Cocaine is one of the main causes of stroke in young patients. ICH, ischemic stroke, and SAH are all associated with cocaine use.
Clinical Features
1- Intracerebral hemorrhage
● Altered level of
consciousness, stupor,
or coma
● Headache, vomiting
● Signs of increased ICP
● Abrupt onset of a focal
neurologic deficit that
worsens steadily over
30 to 90 minutes
Diagnosis
a. CT scan of the head diagnoses 95% of ICH (may
miss very small bleeds)
b. Coagulation panel and platelets-check these to
evaluate for bleeding diathesis.
1- Intracerebral hemorrhage
Complications
1- Intracerebral hemorrhage
● Vasospasm
● Hydrocephalus
● SIADH
● Increased ICP
● Seizures
● Rebleeding
Treatment
1- Intracerebral hemorrhage
1- Admission to the ICU
2- ABC's (airway, breathing,
and circulation)-airway
management is important
due to altered mental status
and decreased respiratory
drive. Patients often require
intubation.
3- BP reduction
● Elevated BP increases ICP and can cause further
bleeding. However, hypotension can lower
cerebral blood flow, worsening the neurologic
deficits. Therefore, BP reduction must be gradual.
● Treatment is indicated if systolic BP is >180 or the
MAP is >130. Common IV agents used include
nicardipine, labetalol, nitroprusside, and others.
1- Intracerebral hemorrhage
4- Initial management of elevated ICP
includes elevating the head of the bed to
30 degrees and appropriate sedation and
pain control. Mannitol (osmotic agent) is
often used to lower ICP; other options
include hyperventilation, barbiturates,
neuromuscular blockade, and CSF drainage.
5- If the patient is on anticoagulation
or an antiplatelet agent, reversal
agents (e.g., vitamin K for warfarin,
protamine sulfate for heparin,
prothrombin complex concentrate
for warfarin and the newer oral
anticoagulants, etc.)
6- Use of steroids is harmful
and is not recommended.
7- Rapid surgical evacuation of cerebellar
hematomas can be lifesaving. However,
surgery is not helpful in most cases of ICH.
Treatment
2- Subarachnoid Hemorrhage
a. Mortality rate can be as
high as 40% to 50% at 30
days.
b. Berry aneurysms occur
at bifurcations of arteries
of the circle of Willis.
Causes
2- Subarachnoid Hemorrhage
B. Trauma is also a common cause.
C. AV malformation.
A. berry aneurysms are the most
common cause
Arteriovenous
angioma
(arteriovenous
malformation)
Clinical features
2- Subarachnoid Hemorrhage
D. Retinal hemorrhages in up
to 30% of patients.
A. Sudden, severe
(often excruciating)
headache in the
absence of focal
neurologic symptoms;
the classic description
is "the worst
headache of my life"
but may also be more
subtle.
B. Sudden, transient loss of consciousness in approximately
50% of patients.
C. Vomiting (common).
F. Meningeal irritation, nuchal rigidity, and photophobia
can take several hours to develop Death-25% to 50% of
patients die with the first rupture. Those who survive will
recover consciousness within minutes.
Diagnosis
2- Subarachnoid Hemorrhage
c. Once SAH is
diagnosed,
order a cerebral
angiogram. It is
the definitive
study for
detecting the
site of bleeding
(for surgical
clipping).
a. Noncontrast CT
scan identifies the
majority of
subarachnoid
hemorrhages
(SAHs).
However, CT scan
may be negative in
up to 10% of cases.
b. Perform lumbar puncture (LP) if
the CT scan is unrevealing or negative
and clinical suspicion is high.
Xanthochromia (yellow color of the CSF) is
the gold standard for diagnosis of SAH.
Xanthochromia results from RBC lysis.
Xanthochromia implies that blood has
been in CSF for several hours and that it is
not due to a traumatic tap.
Complications
2- Subarachnoid Hemorrhage
c. Hydrocephalus (communicating)-
secondary to blood within the
subarachnoid
space hindering normal CSF flow.
a. Rerupture-occurs in up to 30% of
patients.
b. Vasospasm-occurs in up to 50% of
patients (more often with aneurysmal
SAH);
can cause ischemia/infarction and
therefore stroke.
d. Seizures may occur (blood acts as
an irritant).
e. Siadh
Treatment
2- Subarachnoid Hemorrhage
c. Medical-therapy reduces the risks
of rebleeding and cerebral vasospasm.
• Bed rest in a quiet, dark room.
• Stool softeners to avoid straining
(increases ICP and risk of rerupture).
• Analgesia for headache
(acetaminophen).
• IV fluids for hydration.
a. Minimally invasive-consult
interventional neuroradiology.
Recent studies have shown
endovascular coiling to have better
outcomes than surgical clipping.
b. Surgical-consult neurosurgery
Surgically clip the aneurysm to
prevent rebleeding.
2- Subarachnoid Hemorrhage
E. Calcium channel blocker
(nimodipine) for vasospasm-lowers
the incidence of cerebral infarction by
one-third.
D. Control of HTN-lower the BP
gradually because the elevation in
BP may be a compensation for the
decrease in cerebral perfusion
pressure (secondary to increased
ICP or cerebral arterial narrowing).
Treatment
Any Questions?

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Hemorrhagic Stroke.pptx

  • 2. Outlines ● Intracerebral hemorrhage ● Subarachnoid Hemorrhage ● Introduction ● Definition
  • 3. What is stroke? It is an acute neurologic condition resulting from a disruption in cerebral perfusion, either due to ischemia or hemorrhage. A blocked artery: Ischemic 87% A ruptured artery: Bleeding 13%
  • 4.
  • 5. What is Hemorrhagic stroke? It is the cerebral infarction due to hemorrhage. 1- Intracerebral hemorrhage 2- Subarachnoid hemorrhage Bleeding within the brain parenchyma Bleeding into the subarachnoid space
  • 6. 1- Intracerebral hemorrhage High mortality rate (50% at 30 days). Significant morbidity. Hematoma formation and enlargement may lead to local injury and increase in intracerebral pressure.
  • 7. Locations Basal ganglia (66%) Pons (10%) Cerebellum (10%) Other cortical areas 1- Intracerebral hemorrhage
  • 8. 1- Intracerebral hemorrhage Causes? B- Ischemic stroke A- HTN (Particularly a sudden increase in BP) May convert to a hemorrhagic stroke HTN causes a rupture of small vessels deep within the brain parenchyma. Chronic HTN causes degeneration of small arteries, leading to microaneurysms, which can rupture easily. It is typically seen in older patients; risk increases with age C- Others Amyloid angiopathy (10%), Anticoagulant/Antithrombolytic use (10%), brain tumors (5%), and AV malformations (5%) HIT: Cocaine is one of the main causes of stroke in young patients. ICH, ischemic stroke, and SAH are all associated with cocaine use.
  • 9. Clinical Features 1- Intracerebral hemorrhage ● Altered level of consciousness, stupor, or coma ● Headache, vomiting ● Signs of increased ICP ● Abrupt onset of a focal neurologic deficit that worsens steadily over 30 to 90 minutes
  • 10. Diagnosis a. CT scan of the head diagnoses 95% of ICH (may miss very small bleeds) b. Coagulation panel and platelets-check these to evaluate for bleeding diathesis. 1- Intracerebral hemorrhage
  • 11. Complications 1- Intracerebral hemorrhage ● Vasospasm ● Hydrocephalus ● SIADH ● Increased ICP ● Seizures ● Rebleeding
  • 12. Treatment 1- Intracerebral hemorrhage 1- Admission to the ICU 2- ABC's (airway, breathing, and circulation)-airway management is important due to altered mental status and decreased respiratory drive. Patients often require intubation. 3- BP reduction ● Elevated BP increases ICP and can cause further bleeding. However, hypotension can lower cerebral blood flow, worsening the neurologic deficits. Therefore, BP reduction must be gradual. ● Treatment is indicated if systolic BP is >180 or the MAP is >130. Common IV agents used include nicardipine, labetalol, nitroprusside, and others.
  • 13. 1- Intracerebral hemorrhage 4- Initial management of elevated ICP includes elevating the head of the bed to 30 degrees and appropriate sedation and pain control. Mannitol (osmotic agent) is often used to lower ICP; other options include hyperventilation, barbiturates, neuromuscular blockade, and CSF drainage. 5- If the patient is on anticoagulation or an antiplatelet agent, reversal agents (e.g., vitamin K for warfarin, protamine sulfate for heparin, prothrombin complex concentrate for warfarin and the newer oral anticoagulants, etc.) 6- Use of steroids is harmful and is not recommended. 7- Rapid surgical evacuation of cerebellar hematomas can be lifesaving. However, surgery is not helpful in most cases of ICH. Treatment
  • 14. 2- Subarachnoid Hemorrhage a. Mortality rate can be as high as 40% to 50% at 30 days. b. Berry aneurysms occur at bifurcations of arteries of the circle of Willis.
  • 15. Causes 2- Subarachnoid Hemorrhage B. Trauma is also a common cause. C. AV malformation. A. berry aneurysms are the most common cause Arteriovenous angioma (arteriovenous malformation)
  • 16. Clinical features 2- Subarachnoid Hemorrhage D. Retinal hemorrhages in up to 30% of patients. A. Sudden, severe (often excruciating) headache in the absence of focal neurologic symptoms; the classic description is "the worst headache of my life" but may also be more subtle. B. Sudden, transient loss of consciousness in approximately 50% of patients. C. Vomiting (common). F. Meningeal irritation, nuchal rigidity, and photophobia can take several hours to develop Death-25% to 50% of patients die with the first rupture. Those who survive will recover consciousness within minutes.
  • 17. Diagnosis 2- Subarachnoid Hemorrhage c. Once SAH is diagnosed, order a cerebral angiogram. It is the definitive study for detecting the site of bleeding (for surgical clipping). a. Noncontrast CT scan identifies the majority of subarachnoid hemorrhages (SAHs). However, CT scan may be negative in up to 10% of cases. b. Perform lumbar puncture (LP) if the CT scan is unrevealing or negative and clinical suspicion is high. Xanthochromia (yellow color of the CSF) is the gold standard for diagnosis of SAH. Xanthochromia results from RBC lysis. Xanthochromia implies that blood has been in CSF for several hours and that it is not due to a traumatic tap.
  • 18. Complications 2- Subarachnoid Hemorrhage c. Hydrocephalus (communicating)- secondary to blood within the subarachnoid space hindering normal CSF flow. a. Rerupture-occurs in up to 30% of patients. b. Vasospasm-occurs in up to 50% of patients (more often with aneurysmal SAH); can cause ischemia/infarction and therefore stroke. d. Seizures may occur (blood acts as an irritant). e. Siadh
  • 19. Treatment 2- Subarachnoid Hemorrhage c. Medical-therapy reduces the risks of rebleeding and cerebral vasospasm. • Bed rest in a quiet, dark room. • Stool softeners to avoid straining (increases ICP and risk of rerupture). • Analgesia for headache (acetaminophen). • IV fluids for hydration. a. Minimally invasive-consult interventional neuroradiology. Recent studies have shown endovascular coiling to have better outcomes than surgical clipping. b. Surgical-consult neurosurgery Surgically clip the aneurysm to prevent rebleeding.
  • 20. 2- Subarachnoid Hemorrhage E. Calcium channel blocker (nimodipine) for vasospasm-lowers the incidence of cerebral infarction by one-third. D. Control of HTN-lower the BP gradually because the elevation in BP may be a compensation for the decrease in cerebral perfusion pressure (secondary to increased ICP or cerebral arterial narrowing). Treatment