SURGERY FOR INTRACRANIAL ANEURYSM

SURGERY FOR INTRACRANIAL ANEURYSM ALEX ZONSHAYN MD. QUESTION 35 y.o. female developed severe headache and drowsiness while having sex. The pt. was taken to the ER, and CT scan showed SAH. Most likely cause is: 1.Rupture A-V malformation 2.Rupture of small vessel (of no major importance) 3.Rupture of IA 4.Acute migraine 5.Stroke OBJECTIVES Understanding the incidence and pathophysiology of aneurysms Considerations in management of aneurysms. Anesthetic management. New consideration in management of aneurysms. WHAT IS ANEURYSM? AN ANEURYSM IS AN ABNORMAL LOCALIZED DILATATION OF ANY VESSEL. PREVALENCE RECENT STUDY INVOLVING MORE THAN 56,000 PATIENTS FOUND THAT UNRUPTURED INTRACRANIAL ANEURYSM OCCURS IN 3.6 - 6% OF GENERAL POPULATION. PREVALENCE INCIDENTAL INTRACRANIAL ANEURYSM DISCOVERY AMONG ADULTS UNDERGOING CEREBRAL ANGIOGRAPHY IS 0.5-1%. BETWEEN 1MILLION AND 12 MILLION AMERICANS HAVE INTRACRANIAL ANEURYSM INCIDENCE 75% of subarachnoid hemorrhages 27,000 Americans/year have ruptured IA,which is fatal in 14,000 cases. Each year, new aneurysms develop in at least 2% of patients with previously ruptured aneurysms.(In this group of patients, the incidence of aneurysmal rupture is 6 per 10.000 per year.) 12% die before receiving medical help. 40% of hospitalized patients die within 1 month. More than 1/3 live with major neurologic deficits. INCIDENCE 20-25% of all individuals have or will develop an IA during their lifetime (autopsy series data) - SAH lifetime incidence 11:100,000 -28,000 SAH cases/year in the US -Mortality of SAH remains near 50% -Two major causes of morbidity and mortality are rebleeding and vasospasm *Many never reach the hospital *Of the initial survivors, 20% will rebleed in the 1st 2 weeks and 50% of those will die *40% of pts. with SAH will develop vasospasm, half of those will become symptomatic INCIDENCE - RUPTURED IA 20% morbidity 20% mortality -UNRUPTURED IA 4% morbidity 0.2% mortality INCIDENCE Causes of early morbidity : -cardiac arrhythmia/ hypoxia -increased ICP *intraparenchymal hemorrhage *intraventricular hemorrhage *hydrocephalus CAUSES OF MORBIDITY/MORTALITY in survivors of initial bleed 1.Rebleeding 2.Vasospasm 3.Hydrocephalus INTRACRANIAL ANEURYSM IN SPITE OF DIAGNOSTIC,MEDICAL,AND SURGICAL ADVANCES OVER THE PAST SEVERAL DECADES,THE CASE FATALITY RATE FOR ANEURYSMAL SUBARACHNOID HEMORRHAGE HAS NOT CHANGED. RISK FACTORS GENETIC Autosomal dominant polycystic kidney disease. Ehlers-Danlos syndrome. Pseudoxanthoma elasticum. Hemorrhagic telangectasia. Neurofibromatosis type1. Alpha1-antitrypsin deficiency. Coarctation of the aorta. Fibromuscular displasia. Pheochromocytoma. RISK FACTORS OTHER Age over 50 years. Female gender. Cigarette smoking. Cocaine use. Infection of vessel wall. Head trauma. Intracranial neoplasm/neoplastic emboli. HTN. (Significance is being studied.) Alcohol. (Significance is being studied.) PATHOLOGY Aneurysms arising from the intracranial arteries are much more common then those arising from extracranial arteries of similar size. - ICA have an attenuated tunica media. -ICA lacking an external elastic lamina. Thus, the wall of the aneurysm is composed of only intima and adventitia with minimal amount of fibrohyaline between. PATHOPHYSIOLOGY CLASSIFICATION: 1.Saccular. 2.Fusiform. 3.Dissecting. PATHOPHYSIOLOGY 90% are SACCULAR ANEURYSMS (berry). Responsible for most morbidity and mortality. Develop at the sites of vessel bifurcation. (BF is most turbulent and shear forces against arterial wall are greatest.) PATHOPHYSIOLOGY FUSIFORM ANEURYSMS develop from tortuous cerebral arteries, most often in the vertebrobasilar system. Can reach several centimeters. Patients present with symptoms of cranial nerve or brain stem compression. Usually symptoms are not associated with bleeding. PATHOPHYSIOLOGY DISSECTING ANEURYSMS are the result of traumatic tear of an artery. They form as blood courses through a false lumen, while the true lumen is collapsed upon itself. OTHER CLASSIFICATION 1.Small- less then 12mm 78% 2.Large-12-24mm. 20% 3.Giant- 24mm. 2% CIRCLE OF WILLIS CIRCLE OF WILLIS CIRCLE OF WILLIS CIRCLE OF WILLIS -90% occur in the anterior circulation. -39% occur at the junction of the anterior communicating artery and anterior cerebral artery. -30% located along the carotid artery. -22% located along the middle cerebral artery. CLINICAL PRESENTATION Most IA are asymptomatic and undetected until the time of rupture. Symptoms of unruptured aneurysm(111 pts): 1.Acute Severe headache 7 Transient ischemia 7 Seizures 3 Oculomotor nerve palsy/ vision loss 2 CLINICAL PRESENTATION Symptoms of unruptured aneurysms(111 pts) 2.Chronic Noncatastrophic headache 18 Chronic loss of vision 10 Unilateral optic neuropathy 7 Motor weakness/cranial neuropathy 4 Facial pain 3 ONLY 41% OF ANEURYSMS CAUSED SYMPTOMS WHY DO UNRUPTERED IA BECOME SYMPTOMATIC? 1.MASS EFFECT. (large or giant) Symptoms depend on location (headache, cranial nerve palsy, brainstem dysfunction, visual field defects, trigeminal neuralgia, cavernous sinus syndrome, seizures, hypothalamic-pituitary dysfunction. 2.CEREBRAL ISCHEMIA. Symptoms referable to vascular territory. Can be result of embolization of intraaneurysmal thrombus. RISK OF IA RUPTURE ISUIA-International study of unruptured IA (1998).Examinaton of 2,621 pts. records. Conclusion: -Aneurysms less then 10mm had an average annual rupture rate of 0.05%. -The annual rupture rate for lager IA approaches 1%. -Rupture rate was 10 times higher for IA of a similar size in pts with hx. of subarachnoid hemorrhage. RISK OF IA RUPTURE FACTORS ASSOCIATED WITH AN INCREASED RISK OF RUPTURE: - HTN - Pregnancy - Smoking - Heavy drinking - Strenuous activity IA RUPTURE Increased ICP ICP greater than MBP 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. IA RUPTURE Increase of intracranial volume due to the accumulation of blood in the subarachnoid space leads to increase in ICP IA RUPTURE Increase in ICP produces a reduction of CPP. The increase of ICP is the factor that reduces or stops bleeding within the intracranial space. The clinical consequence is reduction in consciousness due to global cerebral ischemia. IA RUPTURE The ICP rises toward the mean BP, causing reduction of CBF, followed by reduction of ICP and increase of CBF. This leads to improvement of the cerebral function. IA RUPTURE Persistent increase of ICP with lack of recovery may be due to: Alteration in the dynamics of CSF, caused by thrombi in the basal cisterns. Cerebral swelling. Vasospasm. IA RUPTURE The reduction of CPP can produce ischemia, alteration of auto regulation and ICP increase due to rupture of the brain-blood barrier. IA GRADING - Grade 0. Perioperative mortality 0.5% IA not ruptured - Grade 1.Perioperative mortality 0-5% asymptomatic, min. headache, sl. nuchal rigidity -Grade 2.Perioperative mortality 2-10% mod.-severe headahe, nuchal rigidity, cranial palsy. - Grade 3.Perioperative mortality 10-15% somnolence, confusion, medium focal deficits. IA GRADING - Grade 4.Perioperative mortality 60-70% Stupor, hemiparesis, early decerebrate rigidity, vegetative disturbances. - Grade 5.Perioperative mortality 70-100% deep coma, decerebrate rigidity, moribund appearance. CAUSES of morbidity from SAH vs. time after initial hemorrhage VASOSPASM Abnormal narrowing of arteries surrounded by blood (focal, segmental, or diffuse) VASOSPASM Angiographic vasospasm: 40-70% incidence Clinical vasospasm: 20-30% incidence Usually associated with aneurysmal SAH 4 – 11 days post bleed Result of vasospasm: ischemia and infarction VASOSPASM Vasospasm is the most important cause of morbidity and mortality after SAH. The clinical picture of vasospasm is completed with : increase of headache, meningismus, fever, and tachycardia. VASOSPASM – Free hemoglobin - activates cascade – Histamine, serotonin, catecholamines, prostaglandins, angiotensin, and free radicals – Blood vessel walls abnormal VASOSPASM Treatment – Triple H therapy (hypertensive hypervolemic hemodilution) “Push” blood into narrowed vessels -Push CO -Increase BP Cerebral blood vessels don’t have many alpha/beta receptors – Calcium channel blocker - nimodipine – Early surgery with aggressive removal of blood/angioplasty TRIPLE “H” THERAPY Hct – 30 – 35 SBP - 160 CVP – 8-10 PAP – 15-16 Most common complication is pulmonary edema. TRIPLE “H” THERAPY THE SCIENCE BEHINED THIS THERAPY IS SOFT. EMPIRICALLY, IT APPEARS TO WORK. NEW IN VASOSPASM THERAPY Tirilazad – Antioxidant – Appears to decrease need for HHH therapy in men – No improved outcome NEW IN VASOSPASM THERAPY TAK-044 – endothelin antagonist. Endothelin is potent vasoconstrictor. Demonstrates small, but statistically significant reduction in delayed ischemic deficits. Hypotension is a side effect. NEW IN THERAPY OF VASOSPASM Magnesium sulfate therapy revealed a nonsignificant trend toward improved neurological outcome. NEW IN THERAPY OF VASOSPASM Anti – fibrinolytics. Recent results of brief administration of tranexamic acid prior to early surgery suggest a decreased rate of rebleeding without any apparent increase in ischemic complications. NEW IN VASOSPASM THERAPY Vasospasm – Intraventricular SNP used in severe refractory cases, however effects are highly variable REBLEED 14-30 % Peak incidence first few days post bleed and second week post bleed High risk of rebleed during angiography REBLEED ONLY RELIABLE PREVENTION FOR REBLEEDING IS THE EXPEDITIOUS PLACEMENT OF A SURGICAL CLIP (OR ENDOVASCULAR PROCEDURE) IA WITH HYDROCEPHALUS Indications for ventricular drainage: -high clinical grade (grade 3 or higher) -increased ICP enlarged ventricles “tight” ventricles with diffuse blood over convexity -thick subarachnoid clot 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 increased myocardial wall tension CARDIOVASCULAR EFFECTS -Significance of EKG changes associated with SAH Originally, EKG changes were thought to be unrelated to cardiac disease. Now multiple studies suggest otherwise. -Normal EKG= No cardiac problems -EKG changes may have clinical significance Clinical significance much more likely with postmenopausal women CARDIOVASCULAR EFFECTS Cardiac dysfunction does not appear to affect morbidity or mortality (studies from Zaroff and Browers) CARDIOVASCULAR EFFECTS SAH induced myocardial dysfunction Similar to “stunned” myocardium -may be caused by massive catecholamine release -associated with elevation in CPK-MB -not associated with CAD – but may occur coincidentally More common in post menopausal women Does not occur in the absence of EKG changes Resolves over several week time course ENDOCRINE EFFECT SIADH ( fluid restriction is the mgmt.) Cerebral salt wasting syndrome – release of naturetic peptide. – hypovolemia, volume contraction, high urine sodium concentration. While the clinical distinction may be difficult mgmt is simple: ISOTONIC FLUID INFUSION USING INTRAVASCULAR VOLUME AS THE ENDPOINT. ENDOCRINE EFFECT Dehydration along with hypotension increases the risk of vasospasm. IA SURGERY AN AREA OF CONTINUING CONTROVERSY IN THE MANAGEMENT OF RUPTURED IA IS THE TIMING OF SURGERY. IA SURGERY Early surgery ( within 48 to 72 hrs. of hemorrhage )- contemporary mgmnt. - decreased risk of rebleeding - allows aggressive mgmt. of vasospasm - reduces the incidence of medical complications (DVT, pneumonia…) IA SURGERY Disadvantages of early clipping: - more difficult surg. approach(edema). - higher risk of intraop. aneurysmal rupture. ENDOVASCOLAR THERAPY Insertion of metallic coils within the lumen of IA, which are detached after placement. Then, through the electrothrombosis, a local thrombus forms around coils within aneurysm,obliterating aneurysmal sac Early experience suggests that procedural risks are low, but the long term effectiveness has not yet been proven COILING COILING PERIOPERATIVE ISSUES - Transport to OR/ Premedication - The patient with a ventriculostomy 1.CLOSE ventriculostomy prior to transport 2.If ventriculostomy bag falls to the floor with the system open to the pt., fluid will drain rapidly causing fall in CSF pressure 3.This fall may cause the IA rupture TEMPERATURE MANAGEMENT Previously thought that mild to moderate hypothermia would be protective to the brain. - Much animal data to support this. - Preliminary human data supported this practice - Large randomized trial FAILED to support the use of mild to moderate hypothermia ( T= 34 degrees ) for improving outcome following IA clipping ANESTHETIC TECHNIQUE NO DATA TO SUPPORT THE USE OF ONE TECHNIQUE OVER ANOTHER. IA (MAP – ICP)/CVR =CBF MAP, ICP, and CVR: all can be altered by anesthesiologist! ANESTHETIC GOALS Avoid abrupt changes in BP Maint. CBF with normal to high blood pressure Be prepared for disaster MONITORING Arterial line preinduction CVP as indicated ( triple H therapy) Neurologic monitoring (SSEP, BAER) 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 MAINTENENCE Goals – Cerebral relaxation and protection – Hemodynamic stability – Normovolemia to hypervolemia – Control ICP – … and wake up on a dime MAINTENENCE Agents – Inhalational agents, narcotics, oxygen, – N2O controversial Can increase CBF Glucose management Hyperventilation BRAIN RELAXATION Ventriculostomy / spinal drain Mannitol Head up position Mild hyperventilation ( not< 35 p a CO2 ) - Hyperventilation should NOT be used any longer than absolutely needed. BRAIN RELAXATION Lumbar CSF drainage. Extremely effective ( to the point that other techniques are unnecessary). - avoid excess loss of CSF. - discontinue drain after clipping of IA. HYPERVENTILATION pCO2 40 to 80 doubles CBF pCO2 40 to 20 halves CBF pCO2 < 20 changes autoregulation and can lead to ischemia. CEREBRAL PROTECTION Thiopental, 10-15 mg/kg loading dose followed by infusion @ 15 mg/kg/hr - Reduce dose with age - Phenylephrine will likely be needed - Hypertension may be needed during temporary vessel occlusion 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 Osmolality has more effect on cerebral edema than oncotic pressure. INTRAOP. HEMORRHAGE – Hypotension to control – Temporary clips – Pressure on ipsilateral carotid for anterior circulation INDUCED HYPOTENSION The choice of agent should be made based on expertise. ( I prepare nipride drip and bolus plus deepen anesthesia with isoflurane). 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 Depends on the grade of aneurysm CONCLUSIONS Rapid advances in technology and pharmacology have led to some improvement in outcome following surgical or endovascular mgmt. of a ruptured IA. Much room for improvement remains. Endovascular mgmt. provides treatment options for high-risk patients previously denied treatment.