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Subarachnoid hemorrhage (SAH)
Most common cause is rupture of saccularaneurysm.
Others: bleeding from vascular formation andextension from a primary intracerebralbleeding.
Most unruptured intracranial aneurysms are
asymptomatic. Symptoms are usually due to rupture and
resultant SAH.
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Subarachnoid hemorrhage (SAH)
At rupture, ICP rises.
Sudden transient loss of consciousness
Excruciating headache, worst headache of mylife, generalized, change in usual headachepattern, most important is the sudden onset ofheadache
Neck stiffness
Vomiting
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Subarachnoid hemorrhage (SAH)
Prodromal symptoms suggest location ofenlarging aneurysm.
3
rd
cranialnerve
palsy- j
unction of PC
Aand IC
A
6th nerve palsy- cavernous sinus
Occipital and cervicalpain- PICA or AICA aneurysm
Pain in or behind the eye and in the low temple-
MCA aneurysm
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Vasospasm
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Vasospasm
Pathological constriction of cerebral arteries
which can cause ischemia or stroke from 4 to21 days after SAH
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Fisher Grading
Classifies SAH according to how they appearon CT scan
To check for vasospasms most dreadedcomplication ofSAH
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Fisher Grading
Grade 1- No hemorrhage evident
Grade 2- Subarachnoid hemorrhage less than1mm thick
Grade 3- Subarachnoid hemorrhage more than1mm thick
Grade 4- Subarachnoid hemorrahge of any
thickness with intra-ventricular hemorrhage(IVH) or parenchymal extension
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Management
Maintenance of optimalperfusion withhypertension & mild hypovolemia
Administration of Nimodipine, a CCB that may
decrease the incidence % degree of spasm
Neurointerventional options for treatingsymptomatic vasospasm include intra-arterialpapaverine or nicardipine, and ballon angioplastyfor larger caliber vessels
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Etiology & Presentation
Treatment option & Timing of surgeryOutcome & Prognosis
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Hunt-Hessclinical gra ing syste f r S H
0- Assy pt atic; unrupture aneursy
1- Awake; assy pt atic r ild headache, ildnuchal rigidity
2- Awake, derate t severe headache, cranialnever palsy (e.g. CN3 r 4), nuchal rigidity
3- Lethargic; ild f calneur logic deficit (e.g.pronator drift)
4- Stupurous; significant neurologic deficit (e.g.he iplegia)
5- Comatose; posturing
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Treatment option& Timing of surgery
Diagnosis
Lumbar puncture
CT scan MRI scan
4-vessel cerebral angiography
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Patients suspected with SAH should have CT immediately. If
CT is (-), lumbar puncture (LP) should be performed. An LP with xantochromia and high RBC counts (usually
100,000/mL), which do not decrease between tubes 1 and 4,is consistent with SAH
(-) CT and LP essentially rules out SAH
Patients diagnosed with SAH require 4 vessel cerebralangiography within 24 hours to assess for aneurysm or othervascular malformation
Catheter angiography is the gold standard for assessing thepatients cerebral vasculature, relevant anomalies andpresence, location, and morphology of the cerebral
aneurysms SAHpatients should be admitted to the neurologic ICU Hunt-Hess grade 4 or 5 require intubation and hemodynamic
monitoring and stabilization. The current standard of care forruptured aneursyms requires early aneurismal occlusion
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There are 2 options for occlusion: Craniotomy & Coiling
The patient may undergo craniotomy with microsurgicaldissection and placement of a titanium clip across the
aneurysm neck to exclude the aneurysm from the circulationand reconstitute the lumen of the parent vessel
The 2nd option is to coil the aneurysm via an endovascularapproach. The patient is taken to the interventionalneuroradiology suite for placement oflooped titanium coils
inside the aneurysm dome
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The coils support thrombosis & prevent blood flow into the aneurysm
Factors favoring craniotomy & clipping:
Young age
Good medical condition
Broad aneurysm necks Factors favoring coiling:
Age
Medical comorbidities
Narrow aneurysm necks
Due to coil migration or compaction overtime, surgical clipping is believedto result in a more definitive cure
Long term outcomes may be better in younger patient with clippedaneurysms
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Outcome
Mortality rate of50% in the 1st month
Approximately 1/3 of survivors return to pre
SAH function, and the remaining 2/3s havemild to severe disability
Most require rehabilitation afterhospitalization
Long term outcomes may be better in youngerpatient with clipped aneurysms
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References
Schwartzs Principle ofSurgery. 9th ed
Harrisons Principle of InternalMedicine. 17th ed
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ClassificationEtiology
Clinical PresentationTreatmentOutcome
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Classification
Congenital
Arterio-venousMalformation
Venous Malformation
Capillary Telangiectasias
cquired
Cavernous angioma (cavernousMalformation)
DuralArteriovenous Fistula (Dural Venous Fistula)
Harrisons InternalMedicine 17th
ed
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Vascular Malformations
Hemorrhage to subarachnoid space- picturealmost identical to ruptured saccularaneurysm (SA)- less severe
Most AVMs in cerebral tissue- intracerebralbleeding more than likely
1/10 as common as SA
Avm and SA associated with 5% of cases Association increases with size ofAVM and age ofpatient
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Arterio-Venous Malformation
Tangle of dilated vessels forming an abnormalcommunication bet arterial and venous systemsacross the cortical surface or within the brain
substance. Vary in size and blood vessels usually thin and do
not have normal structures.
Occur in allparts of Cerebral hemispheres
brainstem, and Spinal cord. Largest at posterior half of hemispheres- wedge
shaped lesion extending from cortex to ventricle
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ClinicalFeatures
Bleeding & seizures
Present at birth; Onset 10-30 y/o
First clinical manifestation 50%- cerebral subarachnoid hemorrhage
30%- seizure
20%- headache
10%- progressive hemiparesis and FND
Chronic recurrent headache- migraine-like headaches- parieto-occipital
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Huge AVM- progressive FND due tocompression of neighboring structures Enlarging mass of vessels & shunting ofblood to
dilated vessels (intracerebral steel) Hydrocephalus- enlarged vein of Galen-
drainage of adjacent AVM
Pulsating carotid arteries on neck, mastoidprocess or eyeballs- pathognomonic ofAVM
Fundoscopy- retinal vascular malfomation
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DIAGNOSIS
CT- contrast infusion- 90%
MRI- shows previous bleeding AVM
Arteriography/Conventional Xray-angiography- gold standard
Autopsy- dissecting microscope
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Treatment Surgical Excision
20-40% block dissection
Endovascular Embolization- Ligation of feeding arteries
Radiosurgery Single dose of subnecrotizing stereotactically directedproton radiation.
Photon radiation, linear accelerator, gamma knife Slow scelerosis of arterial channels for 2-3 years
Complication: delayed radiation necrosis & venouscongestion
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Venous Malformation
Consist purely of distended veins deep in thewhite matter and results in an abnormalcerebral, cerebellar, or brainstem drainage.
Functional venous channels Vs AVM
Mostly seizures and headache
Little significance- ignored
Surgical resection- venous infarction andhemorrhage
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Capillary telangiectasia
True capillary malformation that formsextensive vascular networks on normalbrainstructure.
Common: Pons, deep cerebral white matter Osler-Rendu-Webber- HereditaryHemorrhagic telangiectasia
Rarely produces mass effect/ significantsymptoms
No treatment options
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Classification
Congenital
Arterio-venousMalformation
Venous Malformation
Capillary Telangiectasias
cquired
Cavernous angioma (cavernousMalformation)
DuralArteriovenous Fistula (Dural Venous Fistula)
Harrisons InternalMedicine 17th
ed
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DuralAV Fistula
May be Cranial and Spinal
Cranial- nidus of abnormal atrteries and veinswith AV shunting contained entirely within theleaflets of dura
Origin oflesion not settled- not developmental
Arise adjacent to venous sinus thrombosis or in
association with vascular atresia Transverse sigmoid sinus/ adjacent cavernous sinus
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DuralAV Fistula
Acquired connection of dural sinus todural artery
Manifestations Pulse-synchronous cephalic bruit (pulsatile
tinnitus)
Headache
Cortical ischemia, venous hypertension- >subarachnoid hemorrhage
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DuralAV Fistula
After forceful injury- remote to site of contact
Klippel-trenaunay or osler-weber rendusyndromes
Subdural hemorrhage is infrequent- dramatic mode ofpresentation
Large fatal clot
Cerebral-subarachnoid hemorrhage- antcranial fossa, tentorial incisura.
Seizures uncommon
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DuralAV Fistula
Pseudomotor cerebri- headache, vomitting,papilledema ( highflow)
High-flow shunt0- cause CHF
DX- CT & MRI- thickening or enhancement ofregion of dura generally close to a large duralvenous sinus
Injection of Gadolinium TX: Surgery- smalllesions ;Endovascular
Embolization-larger and inaccessible lesions
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Cavernous Malformation
Small hemorrhages- clinically silent
Small hamartomatous lesions of multiple
juxtaposed endothelium- lined cavites withoutinterposed neural tissues
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Cavernous Malformation
Diagnosis Clinical
MRI- cluster if vessels surrounded by zone of
hypodense ferritin on T1 weighted images-product ofprevious small episodes ofbleeding Mostly in brainstem, pons, cerebral hemispheres
and adjacent venous anomalies
Treatment: Surgical resection of cavernous angioma Low-dose proton-radiation
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Prognosis
With an overall risk of intracerebral hemorrhage of 2-4% per year,angiographic assessment is recommended to further defineprognosis for patients with AVM.
Those with superficial, moderate-sized AVMs have a good long-term prognosis and may not have any additionalbenefit with
interventional treatment. Lifetime risk of hemorrhage may be substantial for young patients
with AVM. Prognosis after AVM hemorrhage is generally better than that after
intracerebral hemorrhage from other causes. Better prognosis maybe due to the relatively younger age ofpatients and a greaterpotential for reorganization ofbrain function. More accurateprognosis awaits the results of currently active, long-term,population-based outcome studies.
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Management ofSAH
Early aneurysm repair prevents rupture and allows the safeapplication of techniques to improve blood flow (e.g. inducedhypertension & hypervolemia) should symptomaticvasospasm develop
An aneurysm can be clipped by a neurosurgeon or coiledby an endovascular surgeon
Medical management ofSAH focuses on protecting theairway, managing the BP before and after the aneurysmtreatment, prevent rebleeding prior to treatment, mnageing
vasopasm, treating hydrocephalus, treating hyponatremia &preventing pulmonary embolus