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Intracranial aneurysms-anaesthesia PowerPoint Presentation

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Tags : anaesthesia | loss of sensation | intensive care

Published on : Mar 14, 2014
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Slide 1 -

Anesthesia For Intracranial Aneurysms

Slide 2 -

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

Slide 3 -

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

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

Slide 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

Slide 6 -

Circle Of Willis

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Classification Small – less than 12 mm Large – 12-24 mm Giant - 24mm

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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

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

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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

Slide 11 -

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

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Vasospasm High incidence angiografically Clinical symptoms 4 – 11 days post bleed

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Vasospasm Free hemoglobin - activates cascade Histamine, serotonin, catecholamines, prostaglandins, angiotensin, and free radicals Blood vessel walls abnormal

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Vasospasm Treatment Triple H therapy Calcium channel blocker - nimodipine Early surgery with aggressive removal of blood

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

Slide 16 -

Rebleed and Vasospasm

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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

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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%

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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)

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

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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

Slide 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

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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

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

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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

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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

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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

Slide 28 -

Maintenance Goals Cerebral relaxation and protection Hemodynamic stability Normovolemai to hypervolemia Control ICP … and wake up on a dime

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Maintenance Agents Inhalational agents, narcotics, oxygen, N2O controversial Can increase CBF Glucose management Hyperventilation

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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

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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

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

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Emergence Anticipate stimulating events Keep beta blockers and vasodilators on hand

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

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

Slide 36 -

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

Slide 37 -

4 causes of aneurysmal rupture

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