Neuro Anesthesia Part 3 Flashcards
Intracranial Aneurysm Grading
0: not ruptured, 0-5% mortality
I: Asymptomatic to minimal headache, 0-5% mortality
II: mod/severe headache, nuchal rigidity, - neuro deficits other than CN palsy, 2-10% mortality
III: somnolence, confusion, moderate focal deficits, 10-15% mortality
IV: Stupor, hemiparesis, mod/severe vegetative disturbances, 60-70% mortality
V: deep coma, decerebrate rigidity, moribund appearance, 70-100% mortality
Types of Cerebral Aneurysms
- Saccular
- Atherosclerotic
- Mycotic
- Traumatic
- “berry”
- fusiform
Saccular Aneurysm
Saccular aneurysms develop from defects in the muscular layer of arteries
Tunica muscularis/media
Alterations in the internal elastic membrane (lamina elastica interna) of cerebral arteries are thought to weaken vessel walls –> renders them less resistant to changes in intra luminal pressure
Circle of Willis - what is it and major supplying vessles
Permits collateral blood flow in the event that a major blood vessel (right or left internal carotid or basilar artery) become occluded
Major vessels supplying the circle of Willis:
- Rt. & lt. Internal carotids
- Basilar
additional circle of willis photos
circle of willis man
circle of willis with % of blood flow
Cerebral aneurysm sizes (*memorize %’s)
Small: <12mm diameter, 78%
Large: 12 - 24 mm, 20%
GIANT: >24mm,** 2%**
Presentation - ruptured (most common cause of intracranial hemorrhage):
headache
nausea and vomiting
focal neurological signs
depressed consciousness
ECG - sinus bradycardia, T abnormality (may mimic myocardial ischemia)
Cerebral Vasospasm
occurs generally 3-4 days after bleed
major cause of morbidity ***
diagnosis
transcranial Doppler positive before symptoms:
worsening headache
hypertension
Etiology of Vasospasm
- Free Hemoglobin - activates cascade
- Histamine, serotonin, catacholamines, prostaglandins, angiotensin, & free radicals
- Blood vessel walls abnormal
- Depletion or Inactivation of NO
Traditional management & prevention of vasospasm
Nimodipine-a dihydropyridine calcium antagonist
Several randomized clinical trials & a metanalysis demonstrate that prophylactic nimodipine is associated with improved outcome following aneurysmal SAH
Nimodipine
- Specificity for cerebral vasculature
- Blocks dihydropyridine sensitive (L-type) channels found in the smooth muscle cells of major cerebral arteries and arterioles
- Now, looking at improving outcome after SAH
- Exact mechanism unknown… Postulated Mechanisms:
Blockage of calcium-dependent excitotoxicity
antiplatelet aggregation
dilatation of leptomenigeal arteries or collateral vessels not seen on angiogramms
inhibition of RBC product-induced-ischemia
Triple “H” Therapy
Hypervolemia
Hypertension
Hemodilution
Recommendations for management after SAH
Cardiovascular Effects
- ECG Abnormalities are very common
Many changes seen: cannon t wave, Q-T prolongation, ST changes - Autonomic surge may in fact cause some subendocardial injury from increase myocardial wall tension
- PVC’s are seen 80%
Cardiac effects cont.
Cardiac dysfunction does not appear to affect M & M
Increase m & m associated with CP compromise & need for inotropes
10% of pts demonstrate LV systolic dysfunction
Prolonged Q-T with increased incidence of ventricular arrhythmias
AVM’s
- The connection between the arterey & vein is known as the “shunt”
- The area of tissue is known as the “nidus” of the AVM
- AVM’s can be thought of as a “short circuit”- Blood is pumped through the shunt & back to the heart without giving the tissue the nourishment
- Cause: Unknown-It is thought that there is a rupture or clotting of a blood vessel that happens during development before one is born…
- Cause intracerebral hemorrhage more often than SA hemorrhage
- Typically grow in size with time
- May present at any age but bleeding is most common b/t 10-30 years of age
