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
“clinical studies”
“Cardiac Injury after Subarachnoid Hemorrhage Is Independent of the Type of Aneurysm Therapy”
Neurosurgery Online, Vol55(6), December 2004, p 1244-51.
CONCLUSION: Surgical & endovascular therapies were associated with similar risks of cardiac injury & dysfunction after SAH
Timing of surgery
0-3 days post bleed appears to be optimal
Improved outcome within 6 hours of rupture
If delayed, 2 weeks post bleed after fibrinolytic phase
Transfusion of Intraoperative PRBC’s after SAH Worsens Outcome
Outcomes Study performed by the Neurosurg dept. at the University of Pennsylvania…
J. of Neurosurgery, 2004
Review of Article
Aneurysm Coiling
Endovascular therapy is a minimally invasive procedure that accesses the treatment area from within the blood vessel. In the case of aneurysms, this treatment is called coil embolization, or “coiling”.
In contrast to surgery, endovascular coiling does not require open surgery.
Coiling
Real-time X-ray to visualize the patient’s vascular system and treat the disease from inside the blood vessel.
The aneurysm is packed with material that doesn’t allow arterial blood to flow into it. embolization.
Materials used for aneurysm embolization include platinum coils…
risk of death/disability lower by 22.6%
Anesthetic goals
Avoid abrupt changes in BP
Maintain CBF with normal to high blood pressure
Be prepared for disaster
Monitors intraop
A-line PRE- INDUCTION
CVP as indicated
Triple H therapy may be used postop
Neurologic Monitoring
SSEP’s & BAER’s are useful for posterior circulation aneurysm
Induction
Prompt induction without ICP elevation
Muscle relaxant to facilitate endotracheal intubation and mechanical hyperventilation
(BEWARE: coughing causes marked increases in ICP) succinylcholine does not significantly alter CBF or ICP in patients with neurological injury *
Induction (cont.)
REBLEEDING IS LETHAL
- careful BP control
- weigh risk of full stomach vs. adequate depth of anesthesia & relazation
- titrate induction agent
- blunt response to intubation with fentanyl and LTA
Need supplemental agents:
Beta blockers, vasodilators, Nicardipine on hand
Opioids and/or lidocaine 1-2 minutes prior to direct larynogoscopy
Maintenance
Goals:
Hemodynamic stability (Rupture risk)
Normovolemia to hypervolemia
Control ICP
…Wake up on a dime
Remember-No one game plan can apply to all situations
Mannitol
As discussed previously, be careful about timing of administration due to changes in transmural pressure
Given till serum osmolarity is 300
Many advocate administration after dura is opened…
NOT the practice at many institutions
Lumbar Spinal Drainage
Placed after patient is ASLEEP to minimize B/P fluctuations and increased ICP
- Review article: “Neurologic Complications After Placement of Cerebrospinal Fluid Drainage Catheters & Needles in Anesthetized Patients: Implications for Regional Anesthesia” from Regional Anesthesia & Pain Management
At a lot of hospitals resident will place-be patient advocate
*Check coags
CSF Drainage Catheter
- Additional brain relaxation/promote surgical exposure & improve visualization of IC contents
- After final positioning-check patency
- Gradually withdrawn only after the dura is opened (to minimize chance of rupture)
- Usually 30-50cc is withdrawn
Maintenance cont.
+/-Steroids… Glucose management
Get Baseline ABG and Glucose prior to Incision.
Mild hyperventilation (effect wanes in 6-8 hours)
* PaCO2 30-35 mmHg probably safest (too much vasoconstriction with risk of cerebral ischemia)
Agents
* Inhalational agents, narcotics
Maintenance cont.
+/-Steroids… Glucose management
Get Baseline ABG and Glucose prior to Incision.
Mild hyperventilation (effect wanes in 6-8 hours)
* PaCO2 30-35 mmHg probably safest (too much vasoconstriction with risk of cerebral ischemia)
Agents
* Inhalational agents, narcotics
“Temporary Clip” placement
Communication with Surgeon is essential
If temporary clip utilized:
1. If a long segment of ICA is being trapped-consider 5,000u heparin to prevent thrombosis & subsequent emboli
2. <5 min: No intervention***
3. Up to 10-15 min: Consider Propofol load, f/b gtt-titrated to burst suppression
4. >20 min: not tolerated (except possibly ICA proximal to p-comm), terminate operation & plan repeat operation utilizing
a. deep hypothermic circulatory arrest
b. Endovascular techniques
c. Bypass grafting around the segment to be occluded
Disaster Management: massive blood loss
- Rupture on induction
- Rupture intraoperatively
- Blood IN ROOM, checked & ready to go…
- NTG/Nicardipine/Propofol mixed & ready to go
- May need to lower SBP
- Maintaining b/p with neosynephrine while giving medications to lower the BP carries the risk of ischemia if fluid resuscitation has not been adequate
Intraop aneurysm rupture
- M & M for IAR is 30-35%
- IMPORTANT NOTE: IAR primarily affects outcome when it occurs during induction of anesthesia or opening of dura
- Rupture likely to occur during any of the 3 following stages:
1. Initial exposure
2. Dissection of aneurysm
3. Clip application
Intraop Hemorrhage
- Hypotension to control: 40-50 mm Hg
- Burst suppression vs incremental doses of Propofol
- Temporary clips
- Pressure on ipsilateral carotid for anterior circulation
Disaster Management…
Arrhythmia’s from Surgical Manipulation (Bradycardia)
Runaways…
*Dilantin Runaways…
Load slowly 1gm/250cc NSS ONLY
ECG -can cause lengthening of Q-T interval
Do not exceed 50mg/min
Emergence
Anticipate stimulating events
Close B/P control
Keep beta blockers & vasodilators on hand
Delayed return to consciousness or neurologic deterioration: CT or MRI
Higher grade bleeds may need to stay intubated… avoid coughing, straining- pretx with lidocaine
Anesthetic ConsiderationsGiant Aneurysms >24mm
Hypothermic Circulatory Arrest
* Mild Hypothermia: Core Temp down to 33C
* Moderate Hypothermia: 32.5-33C
* Deep Hypothermia: to 18C-Permits the brain to tolerate up to 1 hour of circulatory arrest
* Profound hypothermia:<10C-Allows several hours of complete ischemia
*Review article: “Anesthetic Management of Deep Hypothermic Circulatory Arrest for Cerebral Aneurysm Clipping” Anesthesiology: Volume 96(2) February 2002 pp 497-503 *
Arteriovenous Malformation
Arteriovenous malformations (AVMs) complex tangles of dilated, thin-walled blood vessels.
O2-ated blood is pumped by the heart to arteries to capillaries = nourished tissues
De-O2ated blood passes back via veins
AVM’s LACK the tiny capillaries
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
AVM Tx options
RADIATION:If there is a very small AVM: focused beam radiation to the malformation
Within two years the malformation will most likely disappear.
&
EMBOLIZATION: Larger malformations
Fill the malformation with agents which help decrease the blood supply to the malformation
Coils, glues, plastic spheres, balloons
This makes surgery easier in some cases
The technique has been used as the primary treatment as well.
Radiation + and - ‘s
*Advantages *
Can be done without a craniotomy
Some small deep lesions can be most safely treated this way
*Disadvantages *
Lesions larger than 2.5cm are unlikely to be treated effectively
It takes two years for protection from bleeding after radiation
Summary…Management of Anesthesia
Goals:
* prevent increased blood pressure
* facilitate surgical exposure
* maintain euvolemia
* temporary occlusive clips on afferents with normal or slightly
* elevated blood pressure probably better than controlled hypotension (and no clips)
* cerebral “protection”
