1. Anesthesia For Intracranial Aneurysms

2. Objectives Understand the incidence and pathophysiology of aneurysms
Considerations in management of aneurysms
Anesthetic management
New considerations in management of intracranial aneurysms

3. Incidence 75% of subarachnoid hemorrhages 27,000 American/year
6-49 per 100,00 year depending on location
Female predominance
Age 40-60

4. Incidence Ruptured intracranial aneurysm (IA) Unruptured IA
20% morbidity
20% mortality
Unruptured IA
4% morbidity
0-2% mortality

5. Pathophysiology Arterial wall abnormalities
Saccular, occur at bifurcations
Disease processes associated with an increased risk of IA
Polycystic kidney
Erloh Danlos
Fibromuscular disease
Coarctation of the aorta
Weakness of elastic layer

6. Circle Of Willis 90m % occur in the ant. Circaltion
39 % are at the junction of the anterior communicating artery and the anterior cerebral artery.
30 % along the carotid artery.
22 % along the middle cerebral artery.
8 % in the posterior circulation.

7. Classification Small – less than 12 mm Large – 12-24 mm Giant - 24mm
78%
20% 2%

8. IA Rupture Increase ICP ICP greater than DBP
Bleeding stops with decreased CBF
Decreased consciousness
2 clinical scenarios typical
1. Return to normal ICP and CBF with return of function
2. High ICP continues with low CBF
increase of the intracranial volume due to the accumulation of blood in the subarachnoidal space.
intracranial pressure (ICP) increases.
The increase of ICP produces a secondary reduction of cerebral perfusionpressure (CPP) (13). The increase of ICP is the factor that reduces or stops bleeding within the intracranial space. The clinical consequence is a reduction in consciousness due to global cerebral ischemia (14).
Cerebral hemodynamics can be altered in two different ways (15):
The ICP rises toward the diastolic arterial pressure causing a reduction of the CBF. This is followed by a reduction of the ICP, resulting in an increase of the CBF with subsequent hyperemic reaction which improves the cerebral function.
Persistent increase of ICP with lack of recovery of CBF and subsequent loss of consciousness may be due to alterations in the dynamics of cerebrospinal fluid (CSF) caused by thrombi in the basal cisterns. The lack of recovery of CBF has been associated with cerebral swelling and vasospasm.
The reduction of CPP can produce ischemia in the insufficiently perfused zones, alteration of autoregulation and increase in ICP due to rupture of the blood-brain

9. Factors associated with an increased risk of rupture
Hypertension
Pregnancy
Smoking
Heavy drinking
Strenuous activity

10. IA Grading Grade Criteria Perioperative Mortalit
0 Aneurysm is not ruptured
I Asymptomatic, min. headache and sl. nuchal rigidity 0-5
II Moderate to severe headache, nuchal rigidity, but no neurologic deficit other than cranial nerve palsy
III Somnolence, confusion, medium focal deficits
IV Stupor, hemiparesis medium or severe, possible early decerebrate rigidity, vegetative disturbances
V Deep coma, decerebrate rigidity, moribund appearance

11. World Federation of Neurologic Surgeons (WFNS) SAH grade
WFNS grade GCS Score Major focal deficit*
(0 intact aneurysm) - -
absent
absent
present
present or absent
present or absent

12. Vasospasm High incidence angiografically Clinical symptoms
4 – 11 days post bleed
Vasospasm is the most important cause of mortality and morbidity after SAH. Vasospasm can be seen angiographically in 60 % of the patients, but only half of these suffer a clinic syndrome. Approximately 35 % of the patients with SAH have a secondary neurological deterioration due to vasospasms.
The clinical picture of vasospasm is completed with an increase of headache, meningism, fever and tachycardia

13. Vasospasm Free hemoglobin - activates cascade
Histamine, serotonin, catecholamines, prostaglandins, angiotensin, and free radicals
Blood vessel walls abnormal
The following can be found in the vessel walls: red cells, leukocytes, macrophages, mediators such as interleucin-1, eicosanoids and immuno complexes, which show the presence of a swelling process (63).

14. Vasospasm Treatment Triple H therapy
Calcium channel blocker - nimodipine
Early surgery with aggressive removal of blood
Hypervolemia/hypertension/hemodilution
Hct – 30-35
SBP 160
Cvp – 8-10 with PAP 15-16
Pulm. Edema most common complication
Overall mortality was slightly reduced in the nimodipine group, but the trend was not statistically significant. The rebleeding rate was not increased by nimodipine.

15. Rebleed
14-30 %
Peak incidence first few days post bleed and second week post bleed
High risk of rebleed during angiography

16. Rebleed and Vasospasm

17. Cardiovascular effects
ECG abnormalities
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

18. Cardiovascular effects
Cardiac dysfunction does not appear to affect morbidity or mortality (studies from Zaroff and Browers)
Prolonged Q-T with increased incidence of ventricular arrhythmias
PVC’s are seen in 80%

19. QTdc
Difference between the longest and shortest QT interval on a 12 lead
Increase reported to be associated with cardiorespiratory compromise and need for inotropes (Br. J Anesth. 82:454p-455p, 1999)

20. Neurologic effects Hydrocephalous Seizures
13%
Vasospasm may be cause
Increased risk of rebleed
Treat and prophylaxis
Headache, visual field changes, motor deficits

21. Endocrine Effects SIADH Cerebral salt wasting syndrome
release of naturetic peptide
hypovolemia, increased urine NA and volume contraction
Distinguish between the two and treat accordingly
Hyponatriemia lowers of the level of consciousness, leads to muscular weakness, seizures and coma. Dehydration along with hypotension increases the risk of vasospasm (29,30).

22. Pulmonary Effects Neurogenic pulmonary edema 1-2% with SAH
Hyperactivity of the sympathetic nervous system
Pneumonia in 7-12% of hospitalized patients with SAH

23. Timing of surgery 0-3 days post bleed appears to be optimal
Improved outcome within 6 hours of rupture despite high H/H grade
If delayed, 2 weeks post bleed after fibrinolytic phase

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

25. Monitors Arterial line preinduction CVP as indicated
Triple H therapy may be used post op
Neurologic monitoring
SSEPs and BAERs useful for posterior circulation aneurysm

26. Induction REBLEEDING IS LETHAL!!! Careful blood pressure control
Weigh risk of full stomach vs. adequate depth of anesthesia and relaxation
Titrate induction agent
Blunt response to intubation

27. Induction
Thiopental 3-6mg/kg reduces CBF and O2 consumption but does not blunt hemodynamic response. Need supplemental agents
Propofol and etomidate good alternates
Succinylcholine controversy ….
Beta blockers and vasodilators on hand
Succinylcholine is reported to produce an increase in ICP ( 104 , 105 ), attributed to its activity at the muscle spindle. It can be reduced by defasciculation. Succinylcholine can also produce hyperkalemia. Serious arrhythmia have been reported after administration of succinylcholine in cerebral aneurysm surgery ( 106 )..

28. Maintenance Goals Cerebral relaxation and protection
Hemodynamic stability
Normovolemai to hypervolemia
Control ICP
… and wake up on a dime
Cerbral protection – decrease CMRO2, Maintain CPP, drainage of csf
Avoid increase in BP at critical periods,
Hypertonic or isotonic solution. Osmolality has more effect on cerbral edema than oncotic pressure.

29. Maintenance Agents Glucose management Hyperventilation
Inhalational agents, narcotics, oxygen,
N2O controversial
Can increase CBF
Glucose management
Hyperventilation
Stu
CO2 40 to 80 doubles CBF
CO2 40 to 20 halves CBF
lower than 20 changes auotregulation and can lead to ischemia
Normaocapnia should be maaintained for
1 A reduction of cerebral mass due to reduction of the cerebral blood volume with a reduction of the CBF.
Redistribution of blood flow from normal regions to ischemic regions.
A compensating effect for cerebral acidosis due to an increase of extracellular pH ( 125 ).
Hyperventilation has two practical applications in neuroanesthesia:
As an specific or prophylactic treatment of intracranial hypertension during induction and during the surgical period prior to the opening of the dura mater.
After the opening of the dura mater in order to provide better surgical access and less pressure on the separators on the cerebral tissue. There is no established method to quantify the degree of relaxation obtained. It as been proposed to measure pressure on the separators but it has not been developed ( 126 , 127 ).

30. Fluids Isotonic or hypertonic solutions Mannitol
Increase intravascular volume
Effect in 5-15 min. with peak at 30-45
Careful administration in those with reduced cardiac function
Hypertonic or isotonic solution. Osmolality has more effect on cerbral edema than oncotic pressure.

31. Hypothermia
Moderate hypothermia determined to be protective in some animal studies ( degrees)
Mild hypothermia (35.5) found to improve outcome but not statistically significant
Deep hypothermic arrest for giant aneurysms
Neurosurgery 1999 Jan; 44(1):23-32; discussion 32-3
Mild hypothermia as a protective therapy during intracranial aneurysm surgery: a randomized prospective pilot trial.
N=32
Although not achieving statistical significance, patients with SAH randomized to the hypothermic group, when compared with patients in the normothermic group, had the following: 1) a lower frequency of neurological deterioration at 24 and 72 hours after surgery (21 versus 37-41%), 2) a greater frequency of discharge to home (75 versus 57%), and 3) a greater incidence of good long-term outcomes

32. Intraoperative hemorrhage
Hypotension to control
mmHG
Temporary clips
Pressure on ipsilateral carotid for anterior circulation

33. Emergence Anticipate stimulating events
Keep beta blockers and vasodilators on hand

34. Extubation
Decision to extubate made by anesthesia provider and surgeon
Higher grade bleeds may need to go to ICU intubated

35. New management Endovascular balloon placement Tirilazad Antioxidant
Appears to decrease need for HHH therapy in men
No improved outcome

36. New Management Vasospasm
Intraventricular SNP used in severe refractory cases, however effects are highly variable

37. 4 causes of aneurysmal rupture