Anesthesia For Intracranial Aneurysms

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

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

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

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

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.

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

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

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

IA Grading Grade Criteria Perioperative Mortalit 0 Aneurysm is not ruptured 0-5 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 2-10 III Somnolence, confusion, medium focal deficits 10-15 IV Stupor, hemiparesis medium or severe, possible early decerebrate rigidity, vegetative disturbances 60-70 V Deep coma, decerebrate rigidity, moribund appearance 70-100

World Federation of Neurologic Surgeons (WFNS) SAH grade WFNS grade GCS Score Major focal deficit* (0 intact aneurysm) - - 1 15 absent 2 13-14 absent 3 13-14 present 4 7-12 present or absent 5 3-6 present or absent

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

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).

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.

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

Rebleed and Vasospasm

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

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%

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)

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

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).

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

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

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

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

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

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 )..

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.

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 CO@ 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 ).

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.

Hypothermia Moderate hypothermia determined to be protective in some animal studies (33-35 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

Intraoperative hemorrhage Hypotension to control 40 -50 mmHG Temporary clips Pressure on ipsilateral carotid for anterior circulation

Emergence Anticipate stimulating events Keep beta blockers and vasodilators on hand

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

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

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

4 causes of aneurysmal rupture