SUBARACHNOID HEMORRHAGE AND ANEURYSMS Flashcards

14379650016	ANEURYSMAL SUBARACHNOID HEMORRHAGE	ETIOLOGY --saccular ("berry") --(rarely) a blood blister-like aneurysm --rarest - intracranial dissections and dissecting aneurysms LOCATION --suprasellar cistern, sylvian fissures and inferior interhemispheric fissures --frontal lobe ICH: apex of an anterior communicating artery (ACoA) aneurysm points upward CLINICAL ISSUES --10-12/100 000 --40-60 godina --M:F - 1:2 --10% of all childhood hemorrhagic "strokes" --SENTINEL HEADACHE - najavljuju SAH ++10-25% ++days or up to 2 weeks before the onset of overt SAH ++sudden, intense, persistent, and may represent minor bleeding prior to aneurysm rupture SCALES --Hunt and Hess scale --WFNS scale --modified Fisher scale UNFAVORABLE OUTCOME --increasing age --worsening neurologic grade --aneurysm size --large amounts of SAH on initial NECT scan --parenchymal hematoma --intraventricular hemorrhage (IVH) --vascular risk factors such as hypertension and myocardial infarction --increased lifetime risk of developing new ("de novo") intracranial aneurysms and new episodes of SAH, estimated at 2% per year DDG --Traumatic SAH (tSAH) --perimesencephalic nonaneurysmal SAH (pnSAH) --Convexal SAH (cSAH) --Pseudo-SAH --Sulcal-cisternal FLAIR hyperintensity	0
14379655702	SCREENING FOR SUSPECTED ANEURYSMAL SAH	CLINICAL ISSUES •Causes 3-5% of "strokes" •"Thunderclap" headache (aSAH 4-12%) •Peak age = 40-60 years, M:F = 1:2 NECT •Sensitivity ≈ 100% if performed in first 6 hours •Lumbar puncture unnecessary if --CT negative --Neurologic examination normal CTA --If NECT shows aSAH	1
14379661279	IMAGING OF ANEURYSMAL SAH	NECT •Hyperdense basal cisterns, sulci •Hydrocephalus common, onset often early MR •"Dirty" CSF on T1WI •Hyperintense cisterns, sulci on FLAIR +++BUT - nonspecific - other causes of "bright" CSF on FLAIR include hyperoxygenation, meningitis, neoplasm, and artifact LOCATION <--> LOCATION OF ANEURYSM •ACoA aneurysms tend to rupture superiorly into the interhemispheric fissure •MCA bifurcation aneurysms usually rupture into the sylvian fissure •Internal carotid-posterior communicating artery (ICA-PCoA) aneurysms generally rupture into the suprasellar cistern •Vertebrobasilar aneurysms often fill the fourth ventricle, prepontine cistern, and foramen magnum with blood •Bleeding from the "culprit" (krivac) aneurysm - focal hematoma in the subarachnoid space forms ANGIOGRAPHY •CTA positive in 95% if aneurysm ≥ 2 mm •DSA reserved for complex aneurysm, CTA negative •"Angiogram-negative" SAH (15%; 5% if 3D used) •Repeat "second look" DSA positive (5%)	2
14379822708	POST-aSAH CEREBRAL ISCHEMIA AND VASOSPASM	1. immediate cerebral ischemia --within the first 3 days --associated with higher death rates and poor outcome 2. delayed cerebral ischemia --two-thirds of all patients --30% become symptomatic IMAGING POST-ASAH COMPLICATIONS --CT perfusion - CBF (cerebral blood flow) decrease of 7.6 mL/min/100 g or an MTT (mean transit time) increase of 0.91 seconds at day 4 compared with day 0 predicts DCI (delayed cerebral ischemia) with 100% and 84% sensitivity, respectively --DSA - multiple segments of vascular constriction and irregularly narrowed vessels are typical findings DDG --RCVS (reversible cerebral vasoconstriction syndrome) --vasculitis TREATMENT --triple H" therapy - hypervolemia, hypertension, and hemodilution OTHER COMPLICATIONS OF aSAH 1. Obstructive hydrocephalus 2. Neurodegeneration 3. Terson syndrome - intraocular hemorrhage + SAH 4. Ischemia (early or delayed) +intraocular hemorrhage +12-13% of patients with aSAH +caused by a rapid increase in intracranial pressure +subhyaloid (most common), retinal, or vitreous	3
14379873415	PERIMESENCEPHALIC NONANEURYSMAL SAH	DEFINITION --anatomically confined to the perimesencephalic and prepontine cisterns --clinically benign ETIOLOGY / CLINICAL ISSUES --mostly unknown --investigators implicate venous—not aneurysmal—rupture as the most likely cause --between 40 and 60 years --no sex predilection --vasospasm and delayed cerebral ischemia are rare IMAGING --focal accumulation of subarachnoid blood around the midbrain (in the interpeduncular and perimesencephalic cisterns) and in front of the pons --90% of patients with pnSAH have negative DSAs --5-10% of cases, a ruptured posterior circulation aneurysm or vertebrobasilar dissection results in a pnSAH pattern of bleeding --CTA is recommended DDG --atraumatski SAH --traumatski SAH --SAH na konveksitetu	4
14379916252	CONVEXAL SAH	DEFINITION --cSAH is restricted to the hemispheric convexities, sparing the basal and perimesencephalic cisterns CLINICAL ISSUES --nonspecific headache --focal or generalized seizures --neurologic deficits --between the fourth and eighth decades --peak age is 70 years --but mean age of cortical vein thrombosis accompanied by cSAH is 33 years IMAGING --NECT - unilateral, involving one or several dorsolateral convexity sulci.; basal cisterns are typically spared --FLAIR --T2* (GRE, SWI) --CTA, MRA, or DSA - vaskulitis, RCVS, dural sinus/cortical sinus occlusion	5
14379666085	ETIOLOGY OF NONTRAUMATIC CONVEXAL SAH	COMMON •Reversible cerebral vasoconstriction syndrome (RCVS) •Mean age ≈ 50 years •Typical presentation = thunderclap headache •Cerebral amyloid angiopathy (CAA) --Mean age ≈ 70 years --Symptoms = confusion, dementia, sensorimotor dysfunction LESS COMMON •Endocarditis •Cortical vein thrombosis ± dural sinus occlusion RARE •Vasculitis	6
14379674319	NONTRAUMATIC SAH: ANEURYSMAL VS. NONANEURYSMAL	ANEURYSMAL SAH •Widespread; basal cisterns •Arterial origin •Complications (vasospasm, ischemia) common PERIMESENCEPHALIC NONANEURYSMAL SAH •Focal; perimesencephalic, prepontine cisterns •Probably venous origin •Clinically benign; complications, recurrence rare CONVEXAL SAH •Superficial (convexity) sulci •≥ 60 years? Think cerebral amyloid angiopathy (CAA)! •≤ 60 years? Think RCVS! •All ages: venous occlusions, vasculitis	7
14379681744	SUPERFICIAL SIDEROSIS (SS)	CLASSICAL SS •Posterior fossa > > supratentorial •Brain (typically cerebellum), cranial nerves coated with hemosiderin •Chronic repeated SAH •Cause undetermined in ≈ 50% •Sensorineural hearing loss •Trauma and surgery - most common CORTICAL SS •Cortex over hemisphere convexities •Most common etiology = CAA •Transient focal neurologic episodes •Parallel "track-like" hypointensities on T2* •High risk of future intracerebral hemorrhage •Lobar hemorrhages, microbleeds IMAGING CT - normal / advanced iron depositions -- hyperdensities MR - T2* (GRE, SWI) - bilinear "track-like" appearance with cortical SS DDG --"bounce point" artifact --cerebral veins --Sturge-Weber syndrome --hemorrhagic subarachnoid metastases --neurocutaneous melanosis --meningioangiomatosis	8
14385616037	SACCULAR ANEURYSM - GENERAL CONCEPTS AND RF	GENERAL CONCEPTS •Acquired, not congenital! •Abnormal hemodynamics, shear stresses → weakened artery wall •Underlying genetic alterations common INCREASED RISK OF SA •Anomalous vessels --Persistent trigeminal artery --Fenestrated anterior communicating artery --A1 asymmetries or infraoptic course of the A1 segment •Other vascular anomalies --Bicuspid aortic valves --Aortic coarctation •Vasculopathies, syndromes --Abnormal collagen (Marfan, Ehlers-Danlos) --Fibromuscular dysplasia --Autosomal-dominant polycystic kidney disease •Familial intracranial aneurysm --4-10x ↑ risk if first-order family member with aSAH	9
14385621478	SACCULAR ANEURYSM - PATHOLOGY	LOCATION •90% anterior circulation --Circle of Willis, MCA bifurcation --ACoA, ICA/PCoA junction most common •10% posterior circulation (basilar bifurcation) SIZE, NUMBER •Tiny (1-2 mm) to giant (≥ 2 cm) •15-20% multiple (> 2 F:M = 10:1) GROSS, MICROSCOPIC FEATURES OF SA WALLS •SAs lack internal elastic lamina, media •Variable thrombus •Inflammatory changes common	10
14385622989	SACCULAR ANEURYSM - CLINICAL ISSUE	EPIDEMIOLOGY •3% of population; F > M •Peak presentation 40-60 years (rare in children) •Causes 80-90% of all nontraumatic SAHs PRESENTATION •SAH with sudden severe "thunderclap" headache •Mass effect (CN palsy) less common --Most common - pupil-involving CN III palsy from a PCoA aneurysm	11
14385625611	SACCULAR ANEURYSM - NATURAL HISTORY	NATURAL HISTORY OF SACCULAR ANEURYSMS Most saccular aneurysms don't rupture! WHAT INCREASES RISK OF RUPTURE? •Size matters! --Rupture risk increases with size --Aneurysms ≥ 5 mm greater risk than 2-4 mm (hazard ratio = 12) --However, no absolutely "safe" minimal size with zero risk •Shape, configuration matter! --Nonround (nonsaccular shape) = ↑ rupture risk! --"Daughter" sac or "tit" = ↑ rupture risk! •Location affects rupture risk! --Rupture risk of similarly sized aneurysms changes with location --Vertebrobasilar, ICA-PCoA location highest rupture risk --MCA, ACA moderate risk --Non-PCoA-ICA aneurysms lowest •Type --Blood blister-like aneurysms rupture at smaller size PROGNOSIS •Rebleeding risk - highest in the first 24-48 hours after the initial hemorrhage •20% of ruptured but untreated SAs rebleed within 2 weeks •50% rehemorrhage within 6 months	12
14385627116	SACCULAR ANEURYSM - IMAGING AND DDG	IMAGING •Larger lesions - well-delineated hyperdense masses with rim/mural calcifications, especially thrombosed SA •Occasionally - SA as relatively hypodense filling defect within a pool of hyperdense subarachnoid blood •MR - "flow voids" on T1- and T2WI in 50% •FLAIR scans may show hyperintensity in the subarachnoid cisterns •CE - inflammatory changes in the aneurysm wall •CTA 95% sensitive if aneurysm > 2 mm •MRA 90% sensitive if aneurysm > 2 mm •Round/lobulated arterial outpouching •DSA with 3D SSD best delineates architecture DIFFERENTIAL DIAGNOSIS •Vessel loop •Arterial infundibulum --Conical --≤ 2 mm --ICA-PCoA junction •Blood blister-like aneurysm --Hemispherical bulge --Along superior surface of supraclinoid ICA •Pseudoaneurysm --Usually distal to circle of Willis, MCA bifurcation --History of trauma, drugs, infection, neoplasm	13
14385826061	PSEUDOANEURYSM	PATHOLOGY •Arterial wall completely disrupted •Often contained only by cavitated clot •Inflammatory changes common ETIOLOGY •Rarely form spontaneously •Trauma, infection, drugs or neoplasm LOCATION •80% extracranial --Cervical carotid, vertebral arteries •15-20% intracranial --Cavernous/paraclinoid ICA --Distal cortical branches IMAGING FEATURES •When to suspect --Unexplained enlargement of an existing parenchymal hematoma --Unusual or delayed evolution of hematoma •Irregularly shaped outpouching --"Neck" usually absent --± Surrounding avascular mass effect (cavitated hematoma) •CTA --May show "spot" sign --Pseudoaneurysms often small, easily overlooked --DSA may be required if CTA is negative •MR: Look for distal emboli --"flow void" within the hematoma •Angiography --globular, fusiform, or irregularly shaped "neckless" aneurysm with delayed filling and emptying of contrast agent DIFFERENTIAL DIAGNOSIS •Blood blister-like aneurysm --May be a form of pseudoaneurysm •Saccular aneurysm •Dissecting aneurysm •Fusiform aneurysm	14
14385914030	BLOOD BLISTER-LIKE ANEURYSM	PATHOLOGY •1% of all intracranial aneurysms and 0.5-2.0% of all ruptured aneurysms •Broad-based "blister" covered by thin friable tissue cap •Usually solitary •Can occur almost anywhere •Dorsal wall of supraclinoid ICA most common site CLINICAL ISSUES •Easily rupture, may cause catastrophic aSAH •Compared with saccular aneurysms --Rupture at earlier age --Rupture at smaller size IMAGING •Small, easy to miss on CTA •DSA with 3D shaded surface display best TREATMENT •Endovascular > surgical clipping --Flow-diverting stent --Stent-assisted coil embolization --Intraprocedural rupture is common, occurring in nearly 50% of cases	15
14385926058	ATHEROSCLEROTIC FUSIFORM ANEURYSM	TERMINOLOGY •ASVD with a focally dilated fusiform enlargement •Also called aneurysmal dolichoectasias PATHOLOGY •More common in vertebrobasilar artery •Affects long nonbranching segment •ASVD with irregular intima •Extensive loss of elastica, media •Layers of organized mural, intraluminal thrombus --Clot often much larger than residual lumen CLINICAL ISSUES •Middle-aged, older patients --Peak = 60-80 years •Presentation --History of hypertension, systemic ASVD common --Symptoms vary with location --Posterior circulation TIAs, stroke --Less common = cranial neuropathies IMAGING •CT, CTA --Generalized changes of ASVD present --Elongated vessel + fusiform or ovoid dilatation --Mural Ca++ --Partial thrombosis common •MR --Layered thrombus in wall, lumen --Signal intensity often complex --Clot surrounds variably-sized residual "flow void" •CE --variable enhancement of the vessel wall DIFFERENTIAL DIAGNOSIS •Dolichoectasia --Elongated artery --No focal fusiform or saccular dilatation •Dissection, dissecting aneurysm --Often younger patients --Also posterior circulation --ASVD changes minimal/absent •Nonatherosclerotic fusiform aneurysm --Younger patient (including children) --Inherited vasculopathy (e.g., Marfan, Ehlers-Danlos type IV) --Vascular neurocutaneous syndrome (e.g., NF1) --Acquired immune deficiency	16
14385941523	NONATHEROSCLEROTIC FUSIFORM ANEURYSM	ETIOLOGY --collagen vascular disorders (e.g., lupus) --viral infections (varicella, HIV) --inherited vasculopathies (e.g., Marfan, Ehlers-Danlos) --vascular neurocutaneous syndrome (NF1, tuberous sclerosis) PATHOLOGY --often involve nonbranching segments of intracranial arteries --multiple lesions common --carotid (anterior) = vertebrobasilar circulations CLINICAL ISSUES --children and young adults --40% of HIV-positive adults - common TIAs and strokes	17