Presentation on theme: "Neuro Protective Anesthesia During Cerebral Aneurysm Repair"— Presentation transcript:
1 Neuro Protective Anesthesia During Cerebral Aneurysm Repair Jon Jordan CRNA, MSNAStaff CRNA Providence Anesthesia
2 ObjectivesIdentify mechanisms of brain injury during intracranial aneurysm surgery.Compare and contrast current therapeutic modalities used to reduce brain injurySelect an anesthetic plan utilizing medications and or therapies designed to reduce brain injury during cerebral aneurysm repair.
3 Neuronal injury and death Delayed death is caused by apoptosisEarly ischemic neuronal death is primarily caused by excitotoxicity.Mitochondrial function lostCottrell, J. & Young, W. Neuroanesthesia (5th ed.).
4 Brain IschemiaGlobal ischemia, cessation of blood flow for greater than 8 minutes.Focal ischemia, contains three regions.1st region receives no blood flow.2nd Penumbra, receives collateral flow and is partially ischemic.3rd Area surrounding penumbra that receives normal blood
6 Goals of Neuro protective Anesthesia Maintain cerebral perfusion.Utilize an anesthetic plan that prevents cerebral ischemia, limits excitotoxicity processReduce the risk of pre and intra operative rupture.Facilitate surgical exposure ( relax the brain).Minimize reperfusion injury.Plan for prompt awakening to facilitate neurological exam (good grade SAH only)
7 Cerebral Blood flow 20%-25% of cardiac output goes to the brain Circle of Willis is primary collateral blow flow pathway.Complete circle with well developed collaterals present in only 18%-20% of population.Deliberate hypertension , 30%-40% above baseline is indicated in acute arterial occlusion or vasospasm.Szabo and Colleagues concluded increases in BP upon induction of up to 37% above baseline did not cause AVM rupture, (MAP mmHg)
9 SAH Grading Assessments Grades CriteriaHunt and Hess, a modification of Botterells original grading system.Grading of SAHMost commonly used system.Evaluates LOC comparatively to degree of SAH and operative riskUnruptured aneurysmAsymptomatic or slight HA or slight nuchal rigidtyModerate to severe HA, nuchal rigidity. No neuro deficit other than cranial nerve palsy.Drowsiness, conusion, or mild focal deficits.Stupor, mild or severe hemiparesis, possible early decerebrate rigidity, vegetative disturbance.Deep coma, decerebrate rigidity, moribund appearanceSerious co-morbidities such as HTN, diabetes, severe arteriosclerosis, chronic pulmonary disease or severe vasospasm result in patient being upgraded to more severe classification.Pong,R. Lam, A. Cottrell and Young’s Neuroanesthesia 2010
10 57 yo FemaleA 57 yo female presents to the ED with a c/o of recent onset of headache along with visual changes. An angio CT performed demonstrates no embolic or hemorrhagic stroke ; yet displays a 5mm cerebral aneurysm in the anterior circulation, Hunt Hess grade o. The question now becomes do we prepare to coil or clip, and what are the differences?
12 Coiling means a trip to INR Can we safely administer general anesthesia outside of the operating room.Need for invasive monitoring remains the same.Now were going to introduce medications that can definitely effect neuro protection.a. Systemic heparinization / reverasal.b. Contrast media (anaphylactoid reaction)c. Need for neuro muscular blockaded. Need for rapid reversal and emergence for detailed exam .
13 Communication with the Surgeon Unruptured AneurysmRuptured Aneurysm with SAHBaseline Neuro examWhere is the aneurysm located?How large is it?Difficulty of surgical exposure?Will temporary clips be used, if so how long is anticipated clip time?Baseline Neuro exam.Onset time of injury?Clinical grading of SAH.Size and location of aneurysm?Stability of the patient for surgery?Assessment of other confounding co-morbidities
15 Maintaining Autoregulation Aneurysm with SAH presents an impairment in autoregulation and a rightward shift in the lower limit of autoregulation.Grade of SAH correlates directly with degree of autoregulatory impairment.Degree of autoregulation impairment closely correlates with incidence of vasospasm.May result in delayed ischemic injury and deficits.
16 Autoregulation MAP of 50-60/150-160 mmHg Negated by hypercapnia, arterial hypoxemia and the use of volatile anesthetic gases.Also attenuated in the area surrounding an acute cerebral infarction as vessels are typically maximally vasodilated
17 Timing of SurgeryInternational Cooperative study on the timing of aneurysm surgery (1990)Same day as SAH found 50% of brains to be tight.Only 20% found to be tight after 10 days.North American results showed outcomes were best when surgery performed within 3 days, differing for overall results which showed no difference between early or late surgery.
18 Reperfusion InjuryOccurs when perfusion is restored to previously ischemic tissue areas.Reduced perfusion to area due to neutrophil adhesion on vascular endothelium.Free oxygen radicals are formed which react with polyunsaturated fatty acid disrupting cell membranesFormation of free radicals is associated with both apoptosis and necrotic cell death.May be mitigated by NMDA antagonists as well as NOS inhibitors.
19 Perioperative Monitoring Standard anesthetic monitoring including twitch monitor.Intra arterial pressure monitoring. Level transducer to base of skull.Two large bore 14ga – 16ga IV cathetersConsider triple lumen or Cordis placement.Uses of jugular bulb oxygen saturation remains investigative.Trans cranial doppler use currently remains impractical.
20 Patient PositioningAnterior circulation aneurysms, patient supine for a frontal temporal incision.Basilar tip aneurysms, lateral position for a subtemporal incision.Vertebral or Basilar aneurysm, seated or park bench position for suboccipital incision.
21 Patient PositioningEnsure alignment of the neck to promote adequate venous drainage.Once positioned palpate the neck to ensure no venous obstruction.Venous outflow obstruction will cause the brain to remain tight
22 Induction Induction is a critical time period. 7% incidence of rupture during induction of anesthesia.Potential unstable hemodynamics.Blunting sympathetic responses to laryngoscopy or other painful stimulation is essential.Goal is to maintain current hemodynamics if they are stable.Abrupt increase in BP during induction with or without bradycardia could be indicative of acute rupture
23 Pharmacology of Cerebral Protection Induction / MaintenanceAdjunctive neuro protectantsThiopentalPropofolFentanyl, Sufentanil, remifentanylEtomidateAtivan vs. MidazolamRocuronium, vecuronium, vs atracurium, cisatracuriumMagnesium sulfateMethylene BlueAnti epileptic drugsMannitolSteroidsFree radical scavengersAntioxidants
24 Benzodiazepines Decrease CMRO2, CBF and minimal change in ICP. Preserved autoregulation.Potent anticonvulsants.May cause respiratory depression leading to hypercapnia and elevated ICPDiazepam; t 1/2 21 – 37 hrs. To long for quick wakeup.Lorazepam; t ½ 10 – 20 hrs. Again to long for quick wakeup and examMidazolam; t ½ 1 – 4 hrs. May have similar protective effects against hypoxia or cerebral ischemia similar to barbiturates.
25 ThiopentalOne of few drugs shown to be protective against ischemic damage in humansCerebral vasoconstrictor, reduces CMRO2 and CBF.Reduced CMRO2 ( 55% - 60%) is primary mechanism of protection.Blocks Na+, K+ and Ca++ fluxes, free radical scavenger, decreases ICPMay cause inverse steal.National shortage.Very high doses were need to demonstrate clinical improvement after cardiac surgery. Doses range from 3 – 5mg/kg every 5 – 10 minutes titrated to burst suppression up to total dose of 15 – 20 mg/kg
26 Propofol Cerebrovascular profile much like barbiturates Decreases CMRO2, CBF and ICP. Autoregulation remains intact.Chemically similar to phenol based free radical scavengersPotent antioxidant propertiesPrevents lipid peroxidationProtective against oxidative stress, hypo energy metabolism and free radical mediated injury
27 EtomidateCerebral vasoconstrictor, reduces CBF, ICP and CMRO2 35% -45%.Autoregulation is preserved.May activate seizure foci.Can cause cerebral desaturation with induction doses.Burst suppression with High doses.
28 Lidocaine Dose related reduction in CMRO2 and CBF Low dose possess anticonvulsant activities.Dose with induction augments the sedative effects of propofol.May further reduce incidence of ischema related damage when given at clinical doses (1.5mg/kg) following burst suppressive doses of barbiturates or propofol. (reduces CMRO2 by 15% -20%)High doses result in seizure activity
29 NarcoticsFentanyl. Decreases ICP and cerebral blood volume with no effect on perfusion pressure. No histamine releaseSufentanil. May cause vasodilitation which will increase cerebral blood volume and ICP. Not the best choiceRemifentanil. Ultra short acting, much like fentanyl in its ability to decrease ICP and CBV with no effect on CPP. May be best when quick wake up is needed for neuro examHigher bolus doses of Sufentanil and fentanyl have been associated with increases in ICP most likely associated with cerebrovascular autoregulation
30 DexmedetomidineProduces decrease in sympathetic activity by inhibiting norepinephrine release.Excess catecholamine levels correlate with increased ischemic neuronal damage.Decreases CBF with little or no change in CMRO2.Can be used in conjunction with volatile agents or as part of TIVA.
31 Neurmuscular Blockaide Vecuronium, Little to no change in CBF, ICP or CMRO2. No histamine release. Rocuronium. Much like vecuronium. Rapid onset at higher doses make it more preferable to succinylcholine for rapid sequence induction.Atracurium. No significant effect on CBF, CMRO2 or ICP. High doses may cayse histamine release. Cisatracurium. Near similar or weaker effects than atracurium with less histamine releasePatient movement, coughing or straining due aneurysmal clipping can result in catastrophic results. While succinylcholine is not completely ruled out for neuromuscular blockaide during neurosurgery its use can cause an increase in ICP. This rise is often associated with muscle faciculations, EEG arousal and potential jugular venous stasis. Pretreatment with an non depolarizing muscle relaxant will minimize these adverse reactions.
33 HyperventilationCBF has near linear relationship with arterial PaCO2 when between mmHg.CBF is altered 2-3% for every 1 mmHg change in PaCO2 or 1-2ml/100g/min.CBV will change approximately 1% for every 1 mmHg change in PaCO2Reducing PaCO2 causing cerebral vasoconstriction, reducing brain volume.
34 HyperventilationExcessive hyperventilation may lead to excessive vasoconstriction causing further brain ischemia.Vasoconstriction resulting in reduced brain tension may cause an unruptured aneurysm to rupture.Hyperventilation should be limited to a paCO2 of 25 – 35 while the dura is open.A slow return to normal CO2Rupture would be due to reduced external force applied around the aneurysm (tamponade) by the tight brain. Mild hypocapnia may be induced prior to dural opening. Normocapnia should always be the norm if utilizing a hypotensive technique
35 Mannitol Osmotic diuretic, dose of 0.25 – 1 gram/kg. Should be administered once the bone flap is removed over 15 minutes.Biphasic effect as initial increase in plasma osmolality will cause cerebral vasodilitation.May cause transient shift in serum electrolytes as intravascular volume increase. (increase in serum K+, decrease in Na+).Free radical scavenger.
36 Choice of Volatile Agents Isoflurane (0.5% - 1%). Minimal increase in CBF. Dose dependent loss of autoregulation.Desflurane (4% - 6%). Much like Isoflurane. Low blood gas solubility, high concentration may cause undesirable sympathetic stimulation.SevofluraneUnique property over other volatile agents in that autoregulation remains preserved at all concentrations.
37 IV Fluid and Blood Viscosity Crystalloids0.9 normal salineLactated RingersColloids5% Albumin. SAFE trial revealed increased mortality in patients resuscitated with albumin.Component of triple H therapy.Reduced blood viscosity reduces cerebral vascular resistance.Initial goals of 33% Hct due to concern for reduced oxygen carrying capacity.Due to increased morbidity mortality associated with transfusion an Hct of 27 – 30% could be tolerated.
38 Interfering with Excitotoxicity and Free Radical Formation
39 Magnesium Sulfate Essential element in over 300 enzyme systems Long known vasodilatory properties make peri-operative use in neuro surgery questionable.Post operative use indicated for treatment of reperfusion injury associated with vasoconstriction.Meta-analysis by Wong et al in 2011 on use of Magnesium sulfate in patients with Subarachnoid hemorrhage and delayed cerebral infarction (DCI).Six studies, 875 patients, Result was no beneficial effect of magnesium sulfate infusion on DCIMagnesium is responsible for Ca++ regulation into cell as well as action in the cell. Natural calcium antagonist. Works with most of enzymes involved in energy productionWong et al. Critical Care 2011
40 Methylene BlueAutoxidizable phenothiazine with potent antioxidant properties.Easily crosses the blood brain barrier.Animal models have demonstrated the neuroprotective effects of MB not only as an antioxidant but also by triggering functional network changes in brain metabolism.A potential valuable tool for reducing oxidative stress and energy hypometabolism(Rojas, J. Simola, N. Kermath, B. et al. Journal of Neuroscience. 2009
41 Hypothermia Mild hypothermia, temp 33c to 35 Reduces CMRO2 by 7% for each degree of changeNasopharyngeal temperature may best correlate to actual brain temperature.Deep hypothermia (13c – 21c) in conjunction with circulatory arrest may be indicated for clipping of basilar or giant aneurysms
42 IHASTMild Intraoperative Hypothermia during Surgery for Intracranial Aneurysm Trial(IHAST) 2005.30 participating centers with 2856 surgeries for SAH.1001 patients with good grade (WFNS) score of I II or III and SAH no more than 14 days prior to surgery.Intraoperative (hypothermia target temp of 33c) or normothermia (target temp of 36.5c).Pt’s evaluated at POD 90 using Glasgow Outcome scale, Rankin Scale, Barthel Index and NIH Stroke scale.
43 IHAST ResultsNo significant difference in ICU Length of stay, hospitalization, death rates 6% or discharge destination.Hypothermia 66% compared to Normothermia 63% had a Glasgow Outcome score of 1. odds ratio 1.14; 95%CI P=0.32.Hypothermia showed no improvement in outcomes in patients undergoing craniotomy for good grade SAH.Increased incidence of Bacteremia in hypothermia groupResults further validated in Cochran Reviews meta analysis published in 2012.
44 Prior to Clip Placement Check BP, ETCO2 and twitch monitor.The dura is open, hyperventilation and ETCO2 should be optimal.Normotension should be the absolute lower limit unless otherwise indicated (acute rupture).Patient coughing or movement could catastrophic. Re paralyze prior to manipulation.Plan for disaster i.e. acute rupture. Need to lower MAP ASAP. Be prepared to reduce cardiac output, nitrate based vasodilators are not the best choice.
46 Cerebral VasospasmStructural and pathological changes within the vessel intima.Swelling and necrosis of smooth muscle.Hypothesized that vasoactive substances found in the blood in the cisterns induce changes.Currently thought to be oxyhemoglobin, deoxyhemoglobin in conjunction with endothelium derived relaxing factor or nitric oxide.Disruption in the balance of vasodilating and vasoconstricting factors is the postulated cause. In experimental studies the rise of oxy and deoxyhemoglobin parallel the time course of vasospasm
47 Cerebral VasospasmAccounts for 13.5% of major morbidity and mortality.Incidence and severity correlate to amount of blood found in basal cisterns40-60% occurrence rate by cerebral angiography.Clinically significant vasospasms occur in only 20-30% of patients.Angiographically detectable vasospasm is usually not detected until at least 72 hours after SAH, peaks at 7 days and usually not seen after two weeks50% of patients who develop significant vasospasm will die or develop serious neurological deficits.The difference between occurrence and clinical significance can be attributed to the spasm failing to fall to the lower limit cerebral perfusion to the of 15-20ml/100g/min
48 Putting it all together No definitive solution.Know what you have to work with before you start.Work to preserve autoregulation.Antioxidant therapyTight control of BP.Avoid histamine releasing drugs or therapiesPrepare for the worst case scenario
49 ReferencesKass, I. Cottrell, J. & Lei, B.(2010) Brain metabolism, The pathophysiology of Brain injury and potential beneficial agents and techniques. In Cottrell, J. & Young, W. Neuroanesthesia (5th ed.).(pp. 1-16). Philadelphia PA. Mosby Inc, affiliate of Elsevier. Sakabe, T. Matsumoto, M. (2010) Effects of anesthetic agents and other drugs on cerebral blood flow, metabolism and intracranial pressure. . In Cottrell, J. & Young, W. Neuroanesthesia (5th ed.).(pp ). Philadelphia PA. Mosby Inc, affiliate of Elsevier. Rusa, R. Zornow, M. (2010) Fluid management during Craniotomy. . In Cottrell, J. & Young, W. Neuroanesthesia (5th ed.).(pp ). Philadelphia PA. Mosby Inc, affiliate of Elsevier. Wong, G. Boer, R. Poon, W. Chan, M. Gin, T. Ng, S. & Zee, B. Intravenous magnesium sulphate for aneurysmal subarachnoid hemorrhage: an updated systemic review and meta-analysis. Critical Care (2011), 15: RS2 Rojas, J. Simola, N. Kermath, B. Kane, J. Scallert, T. & Gonzalez-Lima, F. Striatal Neuroprotection with Methylene Blue. Journal of Neuroscience (2009) October 20; 163 (3): 877 – 889 Newfield, P. and Bendo, A.(2006) Anesthetic Management of Intracranial Aneurysms. Cottrell, J. & Newfield, P. Handbook of Neuroanesthesia (4th ed.). (pp. 143 – 172) Philadelphia PA. Lipincott, Williams & Williams. Morales, M. Pittman, J & Cottrell, J. (2006) Cerebral Protection and Resuscitation. Cottrell, J. & Newfield, P. Handbook of Neuroanesthesia (4th ed.). (pp. 55 – 72) Philadelphia PA. Lipincott, Williams & Williams. Alderson, P. Lefebvre, C. Li, WP. Roberts, I. & Schierhout, G. (2004) Human albumin for resuscitation and volume expansion in critically ill patients. Cochrane Database Systemic Review, 2011; (10): CD Todd, M. Hindman, B. Clarke, W. & Tomer, J. (2005) Mild Intraoperative Hypothermia during Surgery for Intracranial Aneurysm. New England Journal of Medicine (2005); 352: (pp. 135 – 145) Singer, R. Ogilvy, C. & Rordorf, G. Enraptured intracranial aneurysms. Uptodate. Literature review version 19.3: January Retrieved February 13th 2012 from