Saturday, November 29, 2014

1. Aneurysm rupture rates: ISUIA 1998 data (1970-1991, n~2600)
- Group 1 = no prior hemorrhage from another aneurysm, group 2 = prior hemorrhage from anther aneurysm
- In sum - people with no hx of hemorrhage, the annual bleed risk of a <1cm aneurysm is essentially 0. A 1-2.5 cm aneurysm is around 1%. Giant aneurysms (>2.5cm have a 6% bleed risk the first year) 
2. Aneurysm rupture rates: ISUIA 2003 data (1991-1998, N~4000) 
-
-Aneurysms <7 - essentially 0% rupture rate if no hx of ruptured aneurysm; 1-3% 5-year cumulative rupture rate if hx of ruptured aneurysm.
-Aneurysms 7-12 - 1-2% per year
- 13-24 - 5-10% first year depending on location- posterior circulation >> anterior circulation >>> cavernous carotid 
- giant aneurysms (>25mm) - 15-20% first year depending on location 

 3. New analysis of ISUIA 2003 data in JNS this month -- analysis of 1-year outcomes by age.

In sum: 
- Hemorrhage rate lower in surgery than in endovascular treatment for all 3 age groups (woooo) 
- Mortality rate lower in young people (<50) who get surgery compared to endovascular or non-treatment; and this is likely due to hemorrhage. NO DIFFERENCE in mortality rate between surgery, endovascular, and no treatment in all 3 age groups.
- Why people died: 3/4 people who died in endovascular group (n=451) and 22/27 people who died in non-treatment group (n=1691) hemorrhaged-- although it doesn't say that was the cause of death in every case, its likely a significant contributor in each case. None of the 4 people who died in the surgery group (N=1917) hemorrhaged.
- If you look at morbidity as well as mortality combined outcome, surgery is only associated with worse outcomes in older people (>65).
4. ISUIA caveats: 
- Old data -- the management of aneurysms is very different now than it was between 1991-1998. Not only the improvement of endovascular techniques and technologies and the invention of pipelines, but the widespread use of aspirins and statins have no doubt altered the natural history of these lesions.
- Not randomized -- treatment assignments were made based on clinical judgment not randomization.
5. Posterior reversible encephalopathy syndrome 
- Hypertensive, eclampsia, uremic, or drug induced (chemo) 
- Failure of autoregulation of arteries, leading to vasogenic edema, predilection for occipital lobes
- Will show up as FLAIR signal in occipital lobes without contrast enhancement or diffusion restriction 
- Resolves with treatment of original problem/withdrawal of offending drug 
- DDx: status, venous infarct, hypoglycemia 
6. CNS vasculitis: 
- Disseminated T2/FLAIR/DWI hyperintensity representing ischemia/infarct 
- Attenuated 2nd and 3rd order branches of major cerebral vessels on CTA/DSA
7. Cysts: 
- Arachnoid : looks just like CSF, does not restrict
- Ependymal: identical to arachnoid, except in ventricles (lateral > third >>> subarachnoid) 
- Epidermoid: cloudier than CSF, diffusion restricts 
8. Cavernous angiolipoma
- Benign tumor of fat and vascular tissue
- T1 bright, contrast enhancing on fat-sat imaging
- Typically occurs in thoracic spine as extradural mass (ddx: lymphoma, met, vascular malformation) 
9. Spinal epidural abscess: 
- From discitis/osteomyelitis: anterior epidural space, smoldering infection
- From hematogenous spread: posterior epidural space, rapid onset 
10. Hypertensive intercranial hemorrhage 
- Most common locations: putamen/external capsule (65%), thalamus (25%), pons (10%)
- 80% mortality with large IPH with IVH 
- DDx: bleeding AVM, hemorrhagic met, amyloid angiopathy