Aneurysm Flashcards
Obsolete theory
underlying weakness of the media layer at site of bifurcation
Pseudoaneurysm
blood clot adjacent to a rent in the arterial wall.
Age of anurysum
40-60 🔛AVM
Common female
Most common occurs during
Sleep
sentinel headaches befor aSAH
by 2-8 weeks
SDH associated with
PCOM anurysum
interhemispheric subdural hematoma
Distal ACA aneurysm
Seizure occurs in
🥇 24hr associated MCA or acom anurysum
Causes of mortality
Medical condition ( neurogenic pulmonary edema, stress cardiomyopathy)
,
Major cause of mortality
Rebleedign > early tx to reduce risk of rebleeding
Risk of rebleeding
15-20% from first 2 weeks
Cause of sever deficit
Vasospams
Most predictive of long term outcomes
WFNS
strongest prognostic indicator
Severity of clinical presentation
MCC etiology
Truma
spontaneous SAH” causes
80% rupture of aneurysm
AVM
Vasculitis
Dissection VA ➡️ IVH 3,4 ventricle
Rupture of Small VBV
SVT
pretruncal nonaneurysmal SAH (p.1496) (perimesencephalic hemorrhage
SCD
pituitary apoplexy
Rupture of infundibulum
Spinal AVM mc
Cervical and thoracic
RF aSAH
Behavior ➡️ HTN , 🚬, 🍺,drugs
Sports, vaslalva
Gender ➡️👩🦰
Hx of aneurysm ➡️ rupture of unrupture ( sx, large, posterio) bottleneck
FHX 1 st degree and > 2 affected
Syndrome PCKD , type IV Ehlers-Danlos syndrome
Pregnancy 🤰🏼
Headache MCC sx DDX paroxysmal headache
aSAH ➡️ warnings 🛑 H/A , seizure and diplopia
Benign thunderclap headaches” (BTH) or crash migraine. 5➡️ intensity < 1 m , 🤮 ,
reversible cerebral vasoconstrictive syndrome (RCVS) 55(AKA benign cerebral angiopathy or vasculitis56)➡️ string beads angio , clear 1-3 m , Hx of vasoconstriction drugs
Airplane ✈️ H/A assistance nasal congestion
benign orgasmic cephalgia:sever throbbing during sexual
Post partum complication
During 🥇 week SAH, ICH , RPLS
During 🥈 week TIA , Strok
Meningismus occurs
6-24 hr
Postive Kernig ( flex hip and knee pain in hamstring
Brudzinski( hip flex after ( neck flex ion )
Cause of coma in SAH
⬆️ ICP , damage brain 🧠 ICH , HC , ischmic due to ⬆️ ICP , seizure , ⬇️ CBF ( ⬇️ CO )
Ocular hemorrhage 👀 🩸 type
1-subhyaloid (preretinal)➡️ RBC neear optic disc ➡️ obscures retinal BV ➡️⬆️ mortality
2- intra-retinal hemorrhage ➡️ surround the fovea
3- 🩸 vitreous humor (Terson syndrome➡️ vitreous opacity , common ACoA . Develop 12 days post SAH associated rebleeding , , ⬆️ mortality rate ,
Clear after 6-12 months long term vision good
Vitrectomy consider ➡️ vision final to improve or for rapid improvement
.
pathomechanics OH
Extension of blood 🩸 subarachnoid space to vitreous space
No complication how .
Compression central retinal V & retinochoroidal Anastomosis ➡️ ⬆️ CSF pressure ➡️ venous HTN ➡️ disruption of rerinal vein
DX for SAH
CT if -ve
LP
Dx location of anurysum
MRA no contrast but poor to detect anurysum early
CTA
DSA anatomy , filling and flow
Total contrast for healthy
Iodine< 90gm in 24 hr
CTA 65-75 cc = 21 g
if an angiogram is needed after a CTA, in most cases you do not have to wait 24 hours®
CT sensitivity
Within 6 hr ➡️ sensitivity and specificity100 %
< 12 hr sensitivity < 98%
After 12 hr sensitivity;
< 24 hr 93%
< 72 hr 80%
1 week 50%
Blood 🩸 in cisterns predict
Vasospasm
Things to look Ct
Ventricle size
Hematoma ➡️ MCA
Location of aneurysm
Location of anurysum depend on CT
IHF ➡️ ACOM,
SF ➡️ PCOM , MCA
IPC ➡️ SCA , BA
IVH 3,4 ➡️ PICA , VA dissection
IVH 3 ventril BA
CTA
Detect anurysum size > 3 mm
Detect vaspasm
LP aSAH
🚫 ⬇️ CSF pressure ➡️ ⬆️ trans mural pressure ➡️ risk of bleeding ➡️ minimum amount with < 20 GA
OP will ⬆️
xanthochromia (XTC): will paean after 2-4 hr and till 3-4 weeks
Spectrometry sensitive than inspection
RBC> 100,000, ⬆️ protein ,
If ⬇️ RBC > 70% from 🥇 to last tube ➡️ traumatic tap
MRI and MRA
Low sensitivity in 🥇 24-48 hr ( low met HG )
After 4-7 days can’t detect
Excellent 10-20 days )
FLAIR is the best to detect
MRA
Sensitivity ⬇️ if size < 3 mm
Useful as screening ( 2 🥇 degree relative IA and HTN , 🚬 )
DSA
Gold stander
If SAH but no DSA sorice ➡️ SAH of unknown etiology
4 vessels angio
Infundibulum
MC found PCOM
⬆️ multiple or familial aneurysm
< 3 mm less risk of bleeding ,
no true neck
TX
Warping or clipping
Favor clipping
Large anurysum > 15 mm
BroAED neck > 5 mm
ICH > 50 ml , MCA anurysum
Coiling
Neck narrow < 5 mm
Dome : neck > 2
Elderly
Poor WFNS 4-5
BA anurysum
partially thrombosed aneurysm
best detect by CT or MRI
Grading system
4
Most widely use H&H and WFNs
Radiological modified fisher
Hunt and Hess
Grade 1 and 2 are =
Tx grade 1 and 2 surgical
Grade 3 medical
Mortality with H&H
Grade 1-2 ➡️ 20%
Of taken OR ➡️ 14%
Major cause of death grade 1-2 rebleedign
Meningial irritation ⬆️ surgical risk
Risk of vasospasm H& H
1 ➡️25%
2➡️ 33%
3➡️ 52%
4 ➡️ 53%
5➡️ 74%
WFNS
Most predict long term outcomes
Modified fisher
ICHOP Intracranial hemorrhage of pregnancy
MC occurs in settings of eclampsia, ICH
VS HELLP ( hemolysis, ⬆️ LFT , ⬇️ palt,) ➡️ sever form of pre-eclampsia
Sx ICHOP or eclampsia alon ➡️ H/ A , 🔺 LOC , seizure
Risk of bleeding in pregnancy 🤰🏼
3.5% if no Hx of hemorrhage
5.8% w/ Hx of hemorrhage
Risk of ICHOP during pregnancy 🤰🏼 33-50%
DX aSAH in pregnancy 🤰🏼
CTA with shielding
Angio with shield 🛡️
🚫 aSAH pregnancy 🤰🏼
🚫 mannitol, nitroprusside, nimodipine
Risk of fetal exposure ☢️ during aSAH in pregnancy 🤰🏼
Absorption rate 0.17-2.8 mGRY =➡️ fetal risk of hereditary disease at birth and fetal cancer ♋️ which lower than ⬇️⬇️ natural Hx
Obstetric aSAH
If fetus < 24 ➡️ treat aneurysm and maintain pregnancy
If fetus 24-28 ➡️ weight risk and benefit
CS better fetal salvage for a moribund mother in the third trimester.
During SVD ➡️ ⬇️⬇️ risk of rebleeding by epidural anesthesia , shortening 🥈 stage , low forceps delivery
Factor ⬆️ incidence oF HC in aSAH
IVH
Diffuse , thick SAH ,m fisher 3-4
⬆️ age
HTN
Posterior circulation anurysum
⬇️ na
⬇️ GCS
Low incidence of HCP in
MCA aneurysms
EVD in HC with aSAH
⬆️ risk of rebleeding if done eralyer and fast ⬇️ ICP ➡️ ⬆️ trnasmural pressure
Keep ICP 15-25 mmhg to avoid this
Causes of Chronic HC
pia-arachnoid adhesions and
impairment of the arachnoid granulations.
Main concern regarding aSAH management
1-rebleeding RF ➡️ F , high grade SAH , large anurysum, SBP > 175
2- HC
3- DIND , vasospasm
4- hyponatremia and hypovomia
5- DVT, PE
6- augmenting cerebral O 2delivery
7- seizure
8- determine the source of anurysum
Target SBP aSAH un secure anurysum
< 160 mmgh
Target 🎯 o2 saturation
Patient at risk of DCI 100%
Other patient > 92%
Target hg
8-10
Pressors
If HR ⬇️ norepinephrine
If HR ⬆️ phenylephrine
EVD indication in aSAH
Acute HC
Significant IVH
H&H 3+
It improve sx in 2/3 patient
Anti HTN in aSAH
Nimodipone 60 mg q4
Avoid vasodilation ➡️➡️⬆️ CBV ➡️⬆️ ICP
BP mangment in aSAH
Tharget < 160 un secure
> 175 ⬆️ rebleeding
If BP 🔺 use clevidipine > nicardipine if volume overload is concerning
Long acting ACE inhibitors PRN and labetalol
Hyponatremia
3times risk to develop DIND
RF ; DM , CHF, cirrhosis, Adrenal insufficiency, use NSAID , acetaminophen, narcotics, thiazide diuretics.29
CSW more common in aSAH than SIADH
CSW ECFV low , diuresis
SIADH ⬆️ ADH
Seizure in aSAH
Early within 2 wk
Late after 2 wk
RF ;
Age > 60 , MCA anurysum, thicSAH , clots MF 3-4 ,ICH , SDH , poor neurological grade , rebleeding, infraction, vasospasm, ⬇️ na , HC , HTN
Keppra > PHT
Keppra ⬆️ recurrent in short term but improve longe term outcome
Use unsecured and 1 wk after
Longe term ASM use in Hx seizure , ICH , HTN , infraction , MCA anurysum
Risk of rebleeding aSAH
First day 4-13% 1/3 within 3 hr , 1/2 within 6 hr
15-20 % in the 13 days
50% 6 months
3%/y
RF highH &H , large anurysum, HTN SBP > 160 , EVD
Prevention rebleeding in aSAH
Early colling or clipping
TXA ⬇️ early rebleedign , ⬆️ DIND and function
Dose TXA 1 g then 1 g q6 hr for 72 hr
Neurogenic stress cardiomyopathy NSC AKA reversible postischemic myocardial dysfunction, 64neurogenic stunned myocardium.
⬇️ CO and EF due to aSAH ➡️ hypothalamic ischemia ➡️ sympathetic activation and ➡️ catecholamine surge➡️ subendocardial ischemia or coronary artery vasospasm
NCS vs MI ➡️ trop normal to low in NCS
Peak 2 days to 2 weeks
RF H&H >3
ECG ➡️ broad or inverted T-waves, Q-T prolongation, S-T segment elevation or depression, U-waves, premature atrial or ventricular contraction, SVT, V-flutter or V-fib, 73bradycardia
TX NCS if low SVF and SBP < 90
dobutamine
TX NCS if SBP > 90 , normal SVR
milrinone
Neurogenic pulmonary edema Pathophysiology
1- ⬆️ ICP , hypothalamic ➡️ sympathetic discharge ➡️ redistribution of blood in pulmonary circulation ➡️ ⬆️ PCWP ⬆️ permeability
2- surge of catecholamines directly disrupts the capillary endothelium ➡️ ⬆️ alveolar permeability.
Vasospasm duration and peak
Peak day 6-8
Duration 3-14 days
RF for vasospasm
High SAH grade and more blood in CT ( high modified fisher score. )
Clinical vasospasm DIND
Incidence 30%
Neurological deification ( motor or speech 🎤) , ⬇️ GCS by 2
Non localizing ➡️H/ A , 🔺 LOC , diorinatation,meningitis
Focal CN palsy
Resolve by 12 day
Radiological / angiographic vasospasm
Arterial narrowing in angiography ➡️ slowing contrast filling
50% in SAH
Discovered day 7
Resolve over 3-4 weeks
Vasospasm high in which artery
ACA more than MCA
anterior cerebral artery (ACA) syndrome
Associated ACOM rupture anurysum
abulia, grasp/ suck reflex, urinary incontinence, drowsiness, slowness, delayed responses, confusion, whispering)
middle cerebral artery (MCA) syndrom
hemiparesis, monoparesis, aphasia (or apractagnosia of non-dominant hemisphere—inability to use objects or perform skilled motor activities, due to lesions in the lower occipital or parietal lobes; subtypes: ideomotor apraxia and sensory apraxia)
Risk of vasospasm
Pathogenesis of vasospasm
Result in changes in the vessels
oxyhemoglobin➡️ contraction
hemoglobin➡️ vasorelaxant
platelet-derived growth factor ➡️ vascular stiffening
⬇️ NO and ⬆️ endothelin-1
nervi vasorum
⬆️ vasoconstriction tone
Loss vasodilation
Sympathetic hyper activity due to ⬆️ ICP and hypothalamic injury
obligatory role in vasodilatation factor
endothelial derived relaxant factor (EDRF):
Other cause of ⬇️⬇️ LOC 7
Low o
Infection
Low na
Seizure
Hydrocephalus
Edema
Rebleeding
Dx criteria vasospams
EEG change on vasospasm
Declaims percent of alpha ➡️ Relative alpha ( 6-14 hz)
⬇️ amplitude
Can predict vasospasm
TCD in vasospasm
Detect vasospasm be for clinical by 24-48 hr
Increase 50cm/ sec predict vasospasm
Prevention of vasospasm
Reduce risk of rebleeding by early treatment and remove blood clots
transluminal balloon angioplasty (TBA)
Complication ➡️ artery occlusion, dissection , rupture , displacement of clipping
Criteria ( indication )
1- failure triple H
2- ruptured aneurysm is repaired
3- within 12 hr form sx onset
CI 🚫🚫 Strok t/ o first by CT or MRI
Triple H
CI unsecured anurysum
Start If anurysum secure
Start pressure to ⬆️ SBP by 15% or improve neurologically or SBP reach 220
Dopamine ,
Levophed
phenylephrine ( use N HR )
dobutamine: positive inotrope
MCC 📍 Saccular aneurysm
80-90 ICA; 🥇 ➡️ 30% ACoA ➡️ 🥈 25% PCOM ➡️ 🥉 20% MCA
4-15% VBA ➡️ basillar tip ➡️ BA- SCA ➡️ BA-VA ➡️ AICA
5% VA- PICA
pathophysiology of cerebral aneurysms
⬇️ tunica media and adventitia at site of bifurcation with internal elastic lamina prominent
Fusiform aneurysms mc 📍
VBA
IVH with anurysum location
Distal PICS ➡️ 4th ventricle
ACOM ➡️ lamina terminals ➡️ 3 rd V
Distal BA , carotid terminus➡️ floor 3 rd V
Presentation of cerebral aneurysms
SAH , ICH ,IVH , SDH , intravacular ➡️ arteriovenous fistula
CN palsy aneurysmal
3rd 🥉 CN ➡️ PCOM 🚨in non aSAH ➡️ impending or enlarge aneurysm
Optic CN2
➡️ ophthalmic , ACOm, Basil’s apex ➡️ chism compression
Trigminal ( facial pain syndrom) c4 , c6
ADPKD and anurysum location and secrning
Mc location MCA
Screening cerbral angio
Q2-3 y in 1 Hx of aneurysm or 2- relative ADPKD+ anurysum
Q5-20 y patient with ADPKD with relative ADPKD 🚫 Hx of anurysum
Endovascular techniques to treat the aneurysm
Thrombosis ➡️ colling or Onyx( wide- giant ICA anurysum) , flow diversion
Traping, ligation
Surgical treatment options for aneurysms
Clipping gold stander ⭐️
Warping ➡️ fusiform or branch from dome best by plastic resin
Ultra ear
Y anurysum secure by
< 24 hr
Early vs late secure aneurysm
Early 25-96 hr
Late 10- 14 d
Late associated with high mortality and poor outcomes in high grade aSAH
Favor late ⏰ surgery day 10-14
Inflammation of brain , solid clot , intra operative rupture ⬆️ early , vasospasm ⬆️ early
H&H >4
Poor medical conditions
Difficult location BA , giant
Favorable factor for early surgery
Good medical 🏥 condition
H&H < 3
Large amount of SAH / large clot
Condition ( 🔺. BP or seizure ) complicate mangment if un secure anurysum
Early rebleeding , imminent rebleeding
Imminent aneurysm rupture sign
1- progressing cranial nerve palsy
2-increase in aneurysm size on repeat angiography
3-beating aneurysm sign ➡️ pulsatile changes in aneurysm size between cuts or slices on imaging
Aneurysmal rest 🐶 ear
When a portion of the aneurysm neck is not occluded by a surgical clip,
🧠 relaxation during surgery
Hyperventilating
CSF after dura opening ➡️ EVD , LP , cinsternostomy
Cerebral protection by increasing the ischemic tolerance of the CNS
1- drug ⬇️ ischmic effect 🚫 ⬇️ CMRO➡️ CC. Nimodipine , mannitol
2- ⬇️ CMRO2 ➡️ long action barbiturates vs isoflurane and Propofol short acting
Hypothermias safe 33
< 33 moderate hypothermia TBI
Deep hypothermia < 18
Profound hypothermia < 10
Prevention of intraoperative rupture aneurysm
Prevent HTn due to pain ➡️ local anesthesia
⬇️ transmural pressure by ⬇️ MAP before dura opening
3- reduce shearing force by ⬇️ brain retraction ➡️ wide exposure remove sphenoid wing 🪽
⬇️ 🧠 volume by CSF drain or mannitol
4 ⬇️ tear aneurysm fundus or neck by sharp dissection
Intra operative rupture MC occurs during which step
Dissection blunt dissection laceration by sharp dissection
Risk of recurrence after clipping anurysum
1.5/y at 4 years
⭐️ follow up aneurysm after treatment
Anomalies of ACA are common
Azygous ACA, the “unpaired ACA” (type I anomaly) is rare.
Type II anomaly is “bihemispheric ACA” as an A2 segment of the ACA that
sends branches across the midline to both hemispheres, usually in the
presence of a contralateral A2 segment that is either hypoplastic or that terminates early
most common (type III anomaly) is the “accessory ACA,” defined as a third artery originating from the Acom, in addition to the paired A2, usually in the midline and with branches to one or both hemispheres.
Familial aneurysms most syndroms associated
polycystic kidney disease, and connective tissue disorders such as Ehlers-Danlos type IV, Marfan syndrome, and pseudoxanthoma elasticum
Risk for rupture Familial aneurysms
familial IAs tend to rupture at a smaller size and at a younger
Genetics with Familial aneurysms
Ch 9 CDKN2B; antisense inhibitor gene)
Ch8 SOX17; transcription regulator gene),
Ch4 EDNRA gene).
Cortical subarachnoid hemorrhage cSAH cause
Trauma ⭐️ MC
AVM pial
DAVF
Dissection
CVST
CAA
Coagulation
Tumors
vasculitis
posterior reversible encephalopathy syndrome (PRES)
reversible cerebral vasoconstriction syndrome (RCVS),
reversible cerebral vasoconstriction syndrome (RCVS),AKA Call-Fleming syndrome,
Groups of disorder shrink sx of reversible segmental multifocal cerebral vasoconstriction➡️ sever H/A focal ischmic and seizure
RF postpartum, certain drugs,female
DSA , CTA ➡️ beading of vessels
MCA clippings artery need to preserved
distal MCA branches, recurrent perforators
superior hypophyseal artery aneurysm sx depend on location
paraclinoid variant ➡️ 🚫 👀 visual sx
suprasellar variant ➡️ when giant, may mimic pituitary tumor on CT
