Neuro Anesthesia Part 3

Question 1

Intracranial Aneurysm Grading

Answer 1

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

Question 2

Types of Cerebral Aneurysms

Answer 2

• Saccular
• Atherosclerotic
• Mycotic
• Traumatic
• “berry”
• fusiform

Question 3

Saccular Aneurysm

Answer 3

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

Question 4

Circle of Willis - what is it and major supplying vessles

Answer 4

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

Question 5

additional circle of willis photos

Answer 5

Question 6

circle of willis man

Answer 6

Question 7

circle of willis with % of blood flow

Answer 7

Question 8

Cerebral aneurysm sizes (*memorize %’s)

Answer 8

Small: <12mm diameter, 78%
Large: 12 - 24 mm, 20%
GIANT: >24mm,** 2%**

Question 9

Presentation - ruptured (most common cause of intracranial hemorrhage):

Answer 9

headache
nausea and vomiting
focal neurological signs
depressed consciousness
ECG - sinus bradycardia, T abnormality (may mimic myocardial ischemia)

Question 10

Cerebral Vasospasm

Answer 10

occurs generally 3-4 days after bleed
major cause of morbidity ***
diagnosis
transcranial Doppler positive before symptoms:
worsening headache
hypertension

Question 11

Etiology of Vasospasm

Answer 11

• Free Hemoglobin - activates cascade
• Histamine, serotonin, catacholamines, prostaglandins, angiotensin, & free radicals
• Blood vessel walls abnormal
• Depletion or Inactivation of NO

Question 12

Traditional management & prevention of vasospasm

Answer 12

Nimodipine-a dihydropyridine calcium antagonist

Several randomized clinical trials & a metanalysis demonstrate that prophylactic nimodipine is associated with improved outcome following aneurysmal SAH

Question 13

Nimodipine

Answer 13

• 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

Question 14

Triple “H” Therapy

Answer 14

Hypervolemia
Hypertension
Hemodilution

Question 15

Recommendations for management after SAH

Answer 15

Question 16

Cardiovascular Effects

Answer 16

• 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%

Question 17

Cardiac effects cont.

Answer 17

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

Question 18

“clinical studies”

Answer 18

“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

Question 19

Timing of surgery

Answer 19

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

Question 20

Transfusion of Intraoperative PRBC’s after SAH Worsens Outcome

Answer 20

Outcomes Study performed by the Neurosurg dept. at the University of Pennsylvania…
J. of Neurosurgery, 2004
Review of Article

Question 21

Aneurysm Coiling

Answer 21

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.

Question 22

Coiling

Answer 22

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%

Question 23

Anesthetic goals

Answer 23

Avoid abrupt changes in BP
Maintain CBF with normal to high blood pressure
Be prepared for disaster

Question 24

Monitors intraop

Answer 24

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

Question 25

Induction

Answer 25

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 *

Question 26

Induction (cont.)

Answer 26

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

Question 27

Maintenance

Answer 27

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

Question 28

Mannitol

Answer 28

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

Question 29

Lumbar Spinal Drainage

Answer 29

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

Question 30

CSF Drainage Catheter

Answer 30

* 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

Question 31

Maintenance cont.

Answer 31

+/-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

Question 31

Maintenance cont.

Answer 31

+/-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

Question 32

"Temporary Clip" placement

Answer 32

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

Question 33

Disaster Management: massive blood loss

Answer 33

* 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

Question 34

Intraop aneurysm rupture

Answer 34

* 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

Question 35

Intraop Hemorrhage

Answer 35

* Hypotension to control: 40-50 mm Hg * Burst suppression vs incremental doses of Propofol * Temporary clips * Pressure on ipsilateral carotid for anterior circulation

Question 36

Disaster Management...

Answer 36

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

Question 37

Emergence

Answer 37

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

Question 38

Anesthetic Considerations**Giant Aneurysms >24mm**

Answer 38

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 *

Question 39

Arteriovenous Malformation

Answer 39

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

Question 40

AVM's

Answer 40

* 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

Question 41

AVM Tx options

Answer 41

**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.

Question 42

Radiation + and - 's

Answer 42

*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

Question 43

Summary...Management of Anesthesia

Answer 43

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"