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SUBARACHNOID
HEMORRHAGE
Dr.Rahaf Nizar AlShamali
BLOOD SUPPLY TO THE BRAIN
BLOOD SUPPLY TO THE BRAIN
Normal Angiogram
• SAH a type of:
Hemorrhagi
c
stroke
SPONTANEOUS SAH
causes
80%
5%
• *OTHER CAUSES: brain tumor, vasculitis , cong &blood
disorder , spinal AVM, dural sinus thrombosis , infection.
Aneurysmal
SAH
INTRACRANIAL ANEURYSMS
• Incidence depends on many factors like
in Japan 22/100,000
in Finland 19/100,000
in world average 9/100,000
• Main factors : Racial & genetics
• Low incidence in middle east due to genetics
& lack of reporting
In gender:
>
3:2
BACK
A CASE
TYPES of aneurysms(shape):
AKA sacular and congenital
•Vary in size, giant cell (size=2.5 cm )
•Produce their signs : As tumor that
affect by pressure on the adjacent
structures ophthalmic a.
Giant Anterior Communicating Artery
Aneurysm
Ophthalmic artery with berry aneurysm
back
TYPES of aneurysms(shape):
• : (mostly the post circulation
(basilar artery))
• atherosclerotic process , emboli &
dissection , DON’T RUPTURE.
fusiform
back
•Case seen in
clinic
Female patient came with headache>>
here angiogram shows the following :
back
TYPES of aneurysms (origin):
:result of infective process
Infective embolus emerging from bacterial endocarditis(strep &
staph. )  weaken of peripheral cerebral vessel  mycotic
aneurysm
back
TYPES of aneurysms (origin):
• injuries with sever basilar fractures
• Suffered bullet injuries
 traumatized vessel became weak develop
aneurysm
• ICA  develop aneurysm in the cavernous sinus
( due to basilar trauma )
 This does not produce SAH  but lead to carotid
cavernous fistula ??
back
CT SCAN ,Bilateral cavernous
sinus aneurysm
Natural history;
• Factors for aneurysms :
• Anatomical congenital defect (75% OF
CASES, the wall seem weaker than other vessel
in the body : 1.defect in elastic element (defect in tunica media &
adventitia).
*specially at the site of vessel bifurcation
add stress ( Hemodynamic stress at
bifurcation)
OTHER Risk Factors:
HTN, Atherosclerosis, smoking ,OCP, pregnancy, vigorous
exercise & hemodynamic stress
• Spontaneous SAH
• In adults , aneurysmal rupture present with pressure
symptoms lead to neurological manifest
• In children , rupture of AVM come with epilepsy
• Mortality And Morbidty
10-15% die immediately
10 – 15% die within first 24 h.
40% succumbed to disease in 1st
week
50% die at 6 months
40% will have permanent disability
Clinical Presentation :
• Vary from symptoms confused with an influenzal
disease to very sever lead to immediate die, acute
rise in ICP
• The classical triad :
HEADACHE
DECREASED LEVEL OF CONSCIOUSNESS
MENINGISM
Other symptoms :vomiting, seizures, photophobia,
drooping eye-lid, sciatica.
• Headache :
“the worst headache of my life” sudden, with or without other
manifestation.
• Decreased level of consciousness :
In 50% of cases. due to sudden inc. in ICP & dec. in CPP …
ischemia … coma … die
A good indicator of the severity
• Meningism :
In 75% of cases, irritation of meninges, symptoms : neck rigidity,
photophobia, vomiting, low grade of fever
In case of nerve roots irritation may cause sciatica & low back
pain.
• Other manifestations
• Seizures :
20% of cases due to cortex irritation not the site
of aneurysm
• Mass effect :
Due to association with intracerebral hematoma &
infarction , complicated with edema, commonly
AVM
• Neurological deficits :
Result from the effect of the mass or ischemia
• Visual manifestation :
Papilledema following the ictus or , from 6th
nerve
palsy
Diagnosis :
• When the patient come to the ER with the
clinical triad so it’s SAH until proven otherwise.
• Next step ?
Non-contrast CT-scan
Non-contrast CT-scan :
• High accuracy 95% become undetectable after 72h.
• The blood appear as white streaks in the sulci replacing the black
CSF
• Could be found in :
Parenchyma
The ventricles
Subdural space
In case of negative CT
due to
late investigation the
next step
is ????
Lumber Puncture (LP) :
• Positive blood in CSF from 4 hs. after SAH and
remain 14 days and later as xanthochromia
• Which is a yellowish discoloration
“spectrophotometry”
due to breakdown of RBC
& release of pigment
• Must be distinguished
from traumatic LP
by bring3-4 tubes tests
-at SAH :all homogenous
red color
-traumatic LP: not homo.

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Subarachnoid hemorrhage

  • 2.
  • 3. BLOOD SUPPLY TO THE BRAIN
  • 4. BLOOD SUPPLY TO THE BRAIN
  • 6. • SAH a type of: Hemorrhagi c stroke
  • 7. SPONTANEOUS SAH causes 80% 5% • *OTHER CAUSES: brain tumor, vasculitis , cong &blood disorder , spinal AVM, dural sinus thrombosis , infection. Aneurysmal SAH
  • 8. INTRACRANIAL ANEURYSMS • Incidence depends on many factors like in Japan 22/100,000 in Finland 19/100,000 in world average 9/100,000 • Main factors : Racial & genetics • Low incidence in middle east due to genetics & lack of reporting
  • 11. TYPES of aneurysms(shape): AKA sacular and congenital •Vary in size, giant cell (size=2.5 cm ) •Produce their signs : As tumor that affect by pressure on the adjacent structures ophthalmic a.
  • 12. Giant Anterior Communicating Artery Aneurysm
  • 13. Ophthalmic artery with berry aneurysm back
  • 14. TYPES of aneurysms(shape): • : (mostly the post circulation (basilar artery)) • atherosclerotic process , emboli & dissection , DON’T RUPTURE.
  • 16. •Case seen in clinic Female patient came with headache>> here angiogram shows the following :
  • 17.
  • 18.
  • 19.
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  • 21.
  • 22. back
  • 23. TYPES of aneurysms (origin): :result of infective process Infective embolus emerging from bacterial endocarditis(strep & staph. )  weaken of peripheral cerebral vessel  mycotic aneurysm back
  • 24. TYPES of aneurysms (origin): • injuries with sever basilar fractures • Suffered bullet injuries  traumatized vessel became weak develop aneurysm • ICA  develop aneurysm in the cavernous sinus ( due to basilar trauma )  This does not produce SAH  but lead to carotid cavernous fistula ?? back
  • 25.
  • 26. CT SCAN ,Bilateral cavernous sinus aneurysm
  • 27. Natural history; • Factors for aneurysms : • Anatomical congenital defect (75% OF CASES, the wall seem weaker than other vessel in the body : 1.defect in elastic element (defect in tunica media & adventitia). *specially at the site of vessel bifurcation add stress ( Hemodynamic stress at bifurcation) OTHER Risk Factors: HTN, Atherosclerosis, smoking ,OCP, pregnancy, vigorous exercise & hemodynamic stress
  • 28.
  • 29. • Spontaneous SAH • In adults , aneurysmal rupture present with pressure symptoms lead to neurological manifest • In children , rupture of AVM come with epilepsy • Mortality And Morbidty 10-15% die immediately 10 – 15% die within first 24 h. 40% succumbed to disease in 1st week 50% die at 6 months 40% will have permanent disability
  • 30. Clinical Presentation : • Vary from symptoms confused with an influenzal disease to very sever lead to immediate die, acute rise in ICP • The classical triad : HEADACHE DECREASED LEVEL OF CONSCIOUSNESS MENINGISM Other symptoms :vomiting, seizures, photophobia, drooping eye-lid, sciatica.
  • 31. • Headache : “the worst headache of my life” sudden, with or without other manifestation. • Decreased level of consciousness : In 50% of cases. due to sudden inc. in ICP & dec. in CPP … ischemia … coma … die A good indicator of the severity • Meningism : In 75% of cases, irritation of meninges, symptoms : neck rigidity, photophobia, vomiting, low grade of fever In case of nerve roots irritation may cause sciatica & low back pain.
  • 32. • Other manifestations • Seizures : 20% of cases due to cortex irritation not the site of aneurysm • Mass effect : Due to association with intracerebral hematoma & infarction , complicated with edema, commonly AVM • Neurological deficits : Result from the effect of the mass or ischemia • Visual manifestation : Papilledema following the ictus or , from 6th nerve palsy
  • 33. Diagnosis : • When the patient come to the ER with the clinical triad so it’s SAH until proven otherwise. • Next step ? Non-contrast CT-scan
  • 34. Non-contrast CT-scan : • High accuracy 95% become undetectable after 72h. • The blood appear as white streaks in the sulci replacing the black CSF • Could be found in : Parenchyma The ventricles Subdural space In case of negative CT due to late investigation the next step is ????
  • 35. Lumber Puncture (LP) : • Positive blood in CSF from 4 hs. after SAH and remain 14 days and later as xanthochromia • Which is a yellowish discoloration “spectrophotometry” due to breakdown of RBC & release of pigment • Must be distinguished from traumatic LP by bring3-4 tubes tests -at SAH :all homogenous red color -traumatic LP: not homo.

Editor's Notes

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