EXPLICATIVE CASESOF CONTROVERSIAL ISSUES IN NEUROSURGERY Edited by Francesco Signorelli Explicative Cases of Controversial Issues in Neurosurgery Edited by Francesco Signorelli Published by InTech Janeza Trdine 9, 51000 Rijeka, Croatia Copyright 2012 InTech All chapters are Open Access distributed under the Creative Commons Attribution 3.0 license, which allows users to download, copy and build upon published articles even for commercial purposes, as long as the author and publisher are properly credited, which ensures maximum dissemination and a wider impact of our publications. After this work has been published by InTech, authors have the right to republish it, in whole or part, in any publication of which they are the author, and to make other personal use of the work. Any republication, referencing or personal use of the work must explicitly identify the original source. As for readers, this license allows users to download, copy and build upon published chapters even for commercial purposes, as long as the author and publisher are properly credited, which ensures maximum dissemination and a wider impact of our publications. Notice Statements and opinions expressed in the chapters are these of the individual contributors and not necessarily those of the editors or publisher. No responsibility is accepted for the accuracy of information contained in the published chapters. The publisher assumes no responsibility for any damage or injury to persons or property arising out of the use of any materials, instructions, methods or ideas contained in the book.

Publishing Process Manager Bojan Rafaj Technical Editor Teodora Smiljanic Cover Designer InTech Design Team First published May, 2012 Printed in Croatia A free online edition of this book is available at www.intechopen.com Additional hard copies can be obtained from orders@intechopen.com Explicative Cases of Controversial Issues in Neurosurgery, Edited by Francesco Signorellip.cm.ISBN 978-953-51-0623-4 Contents PrefaceIX Section 1Anaesthesia and Neurocritical Care1 Chapter 1Trigeminocardiac Reflex in Neurosurgery Current Knowledge and Prospects3 Amr Abdulazim, Martin N. Stienen, Pooyan Sadr-Eshkevari,Nora Prochnow, Nora Sandu, Benham Bohluli and Bernhard Schaller Chapter 2Anesthesiologic Management for Awake Craniotomy19 Roberto Zoppellari, Enrico Ferri and Manuela Pellegrini Chapter 3Anaesthetic Management of Patients Undergoing Intraventricular Neuro-Endoscopic Procedures 35 A.F. Kalmar and F. Dewaele Chapter 4Neurocritical Care47 Mainak Majumdar Section 2General Topics63 Chapter 5Decompressive Craniectomy for Refractory Intracranial Hypertension65 Michal Bar, Stefan Reguli and Radim Lipina Chapter 6Suboccipital Concentric Craniotomy as Variant for Posterior Cranial Fossa Surgery87 Abraham Ibarra-de la Torre,Fernando Rueda-Franco and Alfonso Marhx-Bracho Chapter 7Diagnostic Evaluation of the Lesions of the Sellar and Parasellar Region97 Roberto Attanasio, Renato Cozzi, Giovanni Lasio and Regina Barb Chapter 8Pineal Region Tumors167 Paolo Cipriano Cecchi, Giuliano Giliberto,Angelo Musumeci and Andreas Schwarz VIContents Section 3Management of Neurovascular Diseases187 Chapter 9Cerebral Aneurysms189 Mohammad Jamous, Mohammad Barbarawiand Hytham El Oqaili Chapter 10Ruptured Cerebral Aneurysms: An Update217 Ming Zhong, Bing Zhao, Zequn Li and Xianxi Tan Chapter 11Surgical Management of Posterior Circulation Aneurysms: Defining the Role of Microsurgeryin Contemporary Endovascular Era235 Leon Lai and Michael Kerin Morgan Chapter 12Skull Base Approaches for Vertebro-Basilar Aneurysms257 Renato J. Galzio, Danilo De Paulisand Francesco Di Cola Chapter 13Endovascular Approaches to the CarotidCavernous Sinus for Endovascular Treatmentof Carotid Cavernous Fistulas and Hormone Sampling289 Akira Kurata Section 4Spinal Issues319 Chapter 14Craniovertebral Junction Chordomas321 Pratipal Kalsi and David Choi Chapter 15Anatomical and Surgical Perspectiveto Approach Degenerative Disc Hernias337 H. Selim Karabekir, Nuket Gocmen-Mas and Mete Edizer Chapter 16Balloon-Kyphoplasty for Vertebral Compression Fractures363 Luca Arpino and Pierpaolo Nina Section 5Functional Neurosurgery383 Chapter 17Cognitive and Behavioural ChangesAfter Deep Brain Stimulation of theSubthalamic Nucleus in Parkinsons Disease385 Antonio Daniele, Pietro Spinelli and Chiara Piccininni Chapter 18Targeting the Subthalamic Nucleus forDeep Brain Stimulation in Parkinson Disease:The Impact of High Field Strength MRI413 Dirk Winkler, Marc Tittgemeyer, Karl Strecker, Axel Goldammer, Jochen Helm, Johannes Schwarz and Jrgen Meixensberger ContentsVII Section 6Advanced Techniques in Neurosurgery431 Chapter 19An Assistive Surgical MRI Compatible Robot First Prototype with Field Tests433 Tapio Heikkil, Sanna Yrjn, Pekka Kilpelinen, John Koivukangas and Mikko Sallinen Chapter 20Robotic Catheter Operating Systemsfor Endovascular Neurosurgery457 Shuxiang Guo, Jian Guo, Nan Xiao and Takashi Tamiya Chapter 21The Role of Neural Stem Cells in Neurorestoration479 E.O. Vik-Mo, A. Fayzullin, M.C. Moe, H. Olstorn and I.A. Langmoen Section 7Appendix503 Chapter 22Hemostatic Agents in Neurosurgery505 F. Lapierre, S. DHoutaud and M. Wager Chapter 23Use of Physical Restraints in Neurosurgery:Guide for a Good Practice519 Ayten Demir Zencirci Preface Neurosurgeryisarapidlydevelopingfieldofmedicine.Therefore,stayingkeeping track of the advancements in the field is paramount for trainees as well as fully trained neurosurgeons.Thisbook,fullyavailableonline,isapartofoureffortofimproving availability of medical information for anyone who needs to keep up-to-date. Medicalinformationneedtobefreeandwestronglysupportthisobjective.Nevertheless, the biggest risk open access is inaccuracy for lack of control so in order to overcome this, each chapter of the book has been carefully reviewed to provide the reader with the complete, accurate and reliable information. Wewishtoofferourappreciationtoourcolleagueswhoconsistentlycontributedto the genesis of this book and shared their expertize with the readers. We welcome any suggestion and feedback the reader will give us through the web site of the publisher. Finally,IwishtothankVanessa,mywife,andAlice,mydaughter:yoursupport always goes beyondmy expectations. Francesco Signorelli, Lyon,France Section 1 Anaesthesia and Neurocritical Care 1 Trigeminocardiac Reflex in Neurosurgery Current Knowledge and Prospects Amr Abdulazim1, Martin N. Stienen1, Pooyan Sadr-Eshkevari2,Nora Prochnow1, Nora Sandu4, Benham Bohluli3 and Bernhard Schaller4 1Department of Neuroanatomy and Molecular Brain Research, Ruhr-University Bochum, Bochum,2Farzan Clinical Research Institute,Teheran, 3Department of Oral and Maxillofacial Surgery, Tehran Azad School of Dental Medicine, Tehran,4Department of Neurosurgery, University of Paris, Paris,1Germany 2,3Iran 4France 1. Introduction Suddendevelopmentofcardiacarrhythmiaasfarascardiacarrest,arterialhypotension, apnea and gastric hypermobility as manifestations of the trigeminocardiac reflex (TCR) were initiallydescribedin1870byKratschmeretal.(Kratschmer,1870)afternasalmucosa manipulationincatsandrabbits.In1908,AschnerandDagninipresentedtheoculocardiac reflex(OCR)-nowadaysconsideredasinitialdescriptionofaperipheralsubtypeofTCR- which gained broad attention by ophthalmologist (Blanc, et al., 1983). In 1977 Kumada et al. (Kumada,etal.,1977)describedsimilarautonomictrigeminaldepressorresponsesafter lowfrequencyelectricalstimulationwithinportionsofthetrigeminalcomplexin anaesthetizedordecerebratedrabbits,indicatingthatnotonlyperipheralbutalsocentral stimulation of parts of the trigeminal pathway results in autonomic reflex responses. In 1988 thetermtrigeminocardiacreflexwasintroducedbytheanaesthetistsShellyandChurch (Shelly and Church, 1988). In 1999, Schaller et al. (Schaller, et al., 1999) initially described the occurrence of central TCR in human after stimulation of central parts of the trigeminal nerve during cerebellopontine angle and brain stem surgery. It was then Schaller who merged the twoentitiesofperipheralandcentralTCRtoacommonconcept,whichisnowgenerally accepted. ThischapterintroducestheTCR,whichhasgainedbroadattentioninthefieldof neurosurgery.Inthepastyears,TCRhasbeenreportedtooccurduringseveralother neurosurgicalproceduressuchastranssphenoidalsurgery(Schaller,2005a),Jannetta microvasculardecompression(Schaller,2005b),percutaneousradiofrequency thermocoagulation and percutaneousmicrocompression ofthe trigeminalganglion (Meng, et al.,2008),neuroendovascularapproachesinneurosurgery(Amiridze,etal.,2009,Lv,etal., Explicative Cases of Controversial Issues in Neurosurgery 4 2010, Lv, et al., 2007, Ong, et al., 2010), and during aneurysm clipping (Spiriev, et al., 2011a). As theTCRmayhavedecisiveimpactonthesurgicalcourseaswellasthepostoperative functional outcome of neurosurgical patients with skull-base pathologies, the awareness of the TCRisessentialforeveryoneinvolvedinthetreatmentofthosepatients.Therefore,inthe followingchapterweprovidethecurrentknowledgeonTCRwithrespecttoitsriskand predisposing factors, its clinical implementation in neurosurgery, preventive and therapeutical means and its influence on functional outcome. Above that, we delineate the role of the TCR as an oxygen-conserving reflex and present future aspects on TCR research. 2. DefinitionThetrigeminocardiacreflexisconsideredtobeabrainstemreflex,andhascurrentlybeen definedasadecrease inheartrate(HR)andmeanarterialbloodpressure(MABP)ofmore than20%ascomparedwithbaselinevaluesbeforeapplicationofthestimulusand coinciding with the surgical manipulation at or around any branches of the trigeminal nerve (Schaller,2005a,Schaller,etal.,2007).However,thisdefinitionseemstobeproblematicas the 20% benchmark is somewhat arbitrary and implies that alterations of less than this value arenotdefinedasTCR,whichblursthetrueincidenceandleadstoanunderestimationof TCRindailyoperativeclinicalpractice.Anyway,fromastatisticalpointofview,sucha definition makes sense and therefore should be used for large series having in mind that the incidencemightbeunderestimatedbythisdefinition.Thus,itseemsmorereasonableto definetheTCRasanycardiacreflextriggereduponstimulationofthetrigeminalnerve anywherethroughoutitscourse.Clinically,however,TCRmightbebestdescribedas suddenonsetofrelativebradycardiauponthestimulationofthetrigeminalnerve, anywherethroughoutitscourse.Thisseemstobearatherinclusiveandsimplified definition for TCR. Any abrupt autonomic reflex response, additional to or without a cardiac response, upon stimulation of the trigeminal nerve anywhere throughout its course may be subsumed as trigeminovagal reflex (TVR). As for the further classification, subtypes of TCR may be defined based on triggerpoints at the proximity of the central nervous system or at peripheralnervebranches.Central(proximal)TCRistriggereduponstimulationofthe intracranialcourseofthetrigeminalnerve,namelyfromtheGasseriangangliontothe brainstem.Peripheral(distal)TCR iseliciteduponstimulationofthetrigeminalnerve anywherethroughoutits courseoutsidethecraniumtotheGasserianganglion.Peripheral TCRisfurthersubdividedbasedonthebranchoftheaffectedtrigeminalnerve distinguishing ophthalmocardiac reflex (OCR) and maxillomandibulocardiac reflex (MCR).3. Etiology and pathophysiology Stimulationofanyofthetrigeminalbranchesornerveendingsissuggestedtosendthe afferentsignalviatheGasseriangangliontothesensorynucleusofthetrigeminalnerve within the vicinity of the floor of the fourth ventricle. Small internuncial nerve fibers of the reticular formation connect the afferent to the efferent pathway, originating from the motor nucleus of the vagal nerve. The efferent pathway sends depressor fibers to the myocardium, thuscomplementingthereflexarc(Figure1)(Lang,etal.,1991,Schaller,2004).Ascardiac responses to TCR are still maintained in decerebrated animals, its circuitry is considered to belocatedinthebrainstem(ElsnerandGooden,1983,Schaller,2004).Experimentalresults Trigeminocardiac Reflex in Neurosurgery Current Knowledge and Prospects 5 Fig. 1. The anatomy of trigeminocardiac reflex arc representing the three branches of the trigeminal nerve namely ophthalmic nerve (CN V1) responsible for OCR mediation, maxillary (CN V2) and mandibular (CN V3) nerves responsible for what the authors of the present review intend to call maxillomandibulocardiac reflex (MCR). The asterisk shows the origin of anterior ethmoidal nerve, a branch of the ophthalmic nerve, which descends into and innervates the nasal mucosa and is suggested to be responsible for the diving reflex (DR). The Gasserian ganglion, CN V root (blue arrow), the main sensory nucleus of CN V (1), internuncial fibers (upper red arrow), motor nucleus of CN X (2), and vagal myocardial depressor fibers (lower red arrow) complement the reflex arc. Further, the parabrachial nucleus (a), trigeminal nucleus caudalis (b), dorsal medullary reticular field (c), and rostral ventrolateral medulla (d) are shown for they are putatively involved in the reflex circuitry. Explicative Cases of Controversial Issues in Neurosurgery 6 suggestthattheTCRresponseisinitiallymediatedfromthetrigeminalnucleuscaudalis, withsubsequentinclusionoftheparabrachialnucleus,therostralventrolateralmedulla oblongata,the dorsalmedullaryreticularfield,andtheparatrigeminalnucleus(Ohshita,et al.,2004,Schaller,B.,etal.,2009a,SchallerandBuchfelder,2006).However,regardingthe afferent pathway, there are marked differences between subtypes of TCR, which also lead to differentreflexarcs.WhereastheperipherallystimulatedTCRisrelayedviathespinal nucleus of the trigeminal nerve to the Klliker-Fuse nucleus, the centrally stimulated TCR is conveyed via the nucleus of the solitary tract to the lateral parabrachial nucleus (Schaller, B., et al., 2009a). Previous studies have revealed that peripheral stimulation (anterior ethmoidal nerveinthenasalmucosa)co-activesvagalandsympatheticnerves,resultinginboth sympatheticallymediatedperipheralvasoconstriction(hypertension)and parasympatheticallymediatedbradycardia(DutschmannandHerbert,1996,McCulloch,et al., 1999). This is in contrast to central stimulation of TCR where profound activation of the cardiacvagalbranchanddistinctinhibitionoftheinferiorcardiacsympatheticnerveis observed (Nalivaiko, et al., 2003, Schaller, B., et al., 2009a). 3.1 Subtypes of TCR BasedonthecommondefinitionoftheTCR,Schallerhasincludeddifferentperipherally and centrally stimulated subtypes into the TCR concept (Table 1) (Cornelius, et al., 2010).3.1.1 Oculocardiac Reflex (OCR) OCR has frequently been the substrate of case series reporting severe bradycardia or asystole causedbyocularsurgery(Blanc,etal.,1983).MostcommonlyOCRoccursinstrabismus surgery, resulting from traction on the extraocular muscles. However, it can also be observed during other operations and manipulations of ocular and periocular structures innervated by theophthalmicdivisionofthetrigeminalnerve(Anderson,1978,Blanc,etal.,1983,Chesley and Shapiro, 1989, Kerr and Vance, 1983, Robideaux, 1978, Schaller, 2004, Stott, 1989).3.1.2 Maxillomandibulocardiac Reflex (MCR) AsthoroughlyreviewedbyLangetal.(Lang,etal.,1991)andBohlulietal.(Bohluli,etal., 2009), bradycardic reflex responses have also been observed and described for the maxillary and mandibulary divisions of the trigeminal nerve during maxillofacial surgery. 3.1.3 Diving Reflex (DR) DR constitutes an intrinsic brain stem reflex that is characterized by breath-holding, slowing of the HR, reduction of limb blood flow and gradually rises of the MABP. It is elicited by the combinationofwatertouchingthefaceandtheeithervoluntaryorinvoluntary(reflex) arrestofbreathing(Gooden,1994).Functionally,theDRhasbeendemonstratedtobea mechanism for conserving oxygen (Gooden, 1993, 1994). 3.1.4 Central vs. peripheral Both OCR and MCR are considered to represent peripheral physiological subtypes of TCR. The literature supports the hypothesis of differentially induced peripheral and central TCR (Schaller,2004,2005a,Schaller,B.,etal.,2009a,Schaller,etal.,1999,Schaller,etal.,2007). Trigeminocardiac Reflex in Neurosurgery Current Knowledge and Prospects 7 OCRforexampleiswellassociatedwithbradycardiabut,incontrasttocentralTCR,not with hypotension (Blanc, et al., 1983, Schaller, et al., 1999). Likewise, MCR has mainly been observedwithoutaccompanyinghypotension,eventhoughthisunderstandinghasbeen challengedbyarecentstudyindicatingdecentdecreaseofMABPinMCR(Bohluli,etal., 2009, Bohluli, et al., 2010). From a physiologic point of view, TCR and DR seem to be closely linked,fortheybothunderliesimilarbrainstemreflexarcs.Thebradycardicefferent responses of both reflexes are attributed to centers located in the medulla oblongata and are mediatedbyparasympatheticpathways.Equally,peripheralvasoconstrictionisconducted via efferent sympathetic pathways (Cornelius, et al., 2010, Khurana, et al., 1980, Schaller, B., etal.,2009a,Schaller,etal.,1999).However,inTCRtheMABPdecreases,whereasit graduallyincreasesinDRassimilarlyobservedforperipheralTCR(Schaller,B.,etal., 2009a,Schaller,etal.,2008a).ThesefindingssuggestthatDRmightconstituteafurther peripheral subform of TCR and is a phylogenetic old reflex that is onlypresent in aberrant form in adults (Cornelius, et al., 2010, Schaller, B., et al., 2009a, Schaller, et al., 2008a). Peripheral TCR Central TCR Ophthalmocardiac Reflex Maxillomandibulo-cardiac Reflex Diving ReflexTriggered bypressure on ocular bulb, traction on extrinsic muscles of the eye, intraorbital injections or haematomas, acute glaucoma, stretching of the eyelids muscles maxillary and mandibulary branches and innervated tissues stimulation of anterior ethmoidal nerve in the nasal mucosa stimulation of central divisions of the trigeminal nerve including Gasserian ganglion Afferent path LCN/SCN -> CG -> O -> GG -> MSN Vth -> SIF VII/VIII -> GG -> MSN Vth -> SIF AEN -> GG -> Sp5C -> KF -> SIF TN -> GG -> NTS -> LPBN -> SIF Efferent pathMN Xth -> CDN MN Xth -> CDN MN Xth -> CDN MN Xth -> CDN Heart RateBradycardia BradycardiaBradycardiaBradycardia Respiration ApneaApnea Apnea(Gooden, 1993, 1994) Apnea Mean arterial blood pressureNormotension Normotension/ Hypotension Hypertension Hypotension LCN long ciliary nerves; SCN short ciliary nerves; CG ciliary ganglion; O ophthalmic branch of the Vth cranial nerve; GG Gasserian ganglion; MSN Vth main sensory nucleus of the Vth nerve; SIF short internuncial fibres; MN X th motor nucleus of the Xth nerve; CDN cardiac depressor nerve; AEN anterior ethmoidal nerve; Sp5C spinal trigeminal nucleus, pars caudalis; KF Klliker-Fuse nucleus; TN trigeminal nerve; NTS nucleus tractus solitarii; LPBN lateral parabrachial nucleus Table 1. Summary of the trigeminocardiac reflex subtypes according to points of elicitation, afferent and efferent paths, heart rate, respiratory alterations, and mean arterial blood pressure changes. Explicative Cases of Controversial Issues in Neurosurgery 8 3.2 TCR as an oxygen-conserving reflex Besidetheclinicalimplementation,theTCRmustbeseenasaphysiologicaland phylogenetically-inheritedoxygenconservingreflexasitinducesanincreasedcerebral blood flow (CBF) without changing cerebral metabolic rates of oxygen and glucose (Sandu, etal.,2010,Schaller,B.J.,etal.,2009).AnincreaseinCBFwithoutchangeofcerebral metabolicratesprovidesthebrainwithoxygenrapidlyandefficiently.Cerebrovascular vasodilatationmaythereforepossiblybeasecondaryresponsetoamendhypoxiaand trigeminovagallyinducedhypotension.Carbondioxide(CO2)whichisincreasedin hypno/apneicstatesmightbeamaincontributorininducingtheTCRandthesubsequent protective cerebral vasodilatation, as described for oxygen conserving reflexes (Wolf, 1966). PreviousstudiesintheanatomicalcircuitryoftheTCRandoxygenconservingreflexes revealedtheactivationofbrainstemareaswhichoverlapwiththosedescribedforhypoxic vasodilatation (Schaller, 2004). The latter was initially supposed to be elicited by direct effect of hypoxia on blood vessels and stimulation of arterial chemoreceptors (Schaller, 2004). TCR thereforeneedstobereconsideredintermsofbrainhypoxiaprevention.Thatwould, theoretically,openthedoorforTCRasatreatmentoptionforexampleininducing tolerance for hypoxemia during stroke and similar ischemic conditions. 4. Epidemiology As the TCR has been demonstrated to be triggered at any point throughout the course of the trigeminal nerve it can be observed during several different surgical approaches in the fields ofcraniofacial-andneurologicalsurgerywhichinvolvemanipulationofstructures innervated by the trigeminal nerve or the trigeminal nerve itself. 4.1 Risk factors and predisposition Generally accepted predisposing factors for the occurrence of intraoperative TCR constitute hypercapnia, hypoxemia, light general anaesthesia, young age (higher resting vagal tone in children),aswellasstrongand/orlong-lastingprovokingstimulus.Interestingly,bilateral stimulationoftrigeminallyinnervatedstructuresoroftrigeminalnervefibersresultsina moreprofoundreflexthanobservedinunilateralstimulation(Bauer,etal.,2005).Even thoughthepreviouslymentionedriskfactorsarebasedonresearchdonenearly30years ago,theycouldagainbeidentifiedinourrecentpublicationsonthistopic.Inaddition, Spirievetal.(Spiriev,etal.,2010,Spiriev,etal.,2011b)observedperioperativeTCRonthe basis of a subdural empyema or exposure to H202, indicating that chemical or inflammatory stimuli may constitute predisposing factors. Even antecedent transient ischemic attacks less thansixweeksbeforeanoperationrepresentasignificantriskfactorforsubsequent intraoperativeoccurrenceoftheTCR(Nothen,etal.,2010).Furthermoredrugs,including potentnarcoticagentslikesufentanilandalfentanil,beta-blockersandcalciumchannel blockers, have been reported to predispose for TCR as they inhibit the sympathetic nervous system (potent narcotics), decrease the sympathetic response of the heart (beta-blockers) and causeperipheralarterialvasodilatationresultinginreducedHRandMABP(Arasho,etal., 2009,Blanc,etal.,1983,Bohluli,etal.,2009,Campbell,etal.,1994,Lang,etal.,1991, Lubbers,etal.,2010,Schaller,etal.,1999).However,evidenceforimpactofthosedrugsis low, as effects could not be confirmed in newer literature. Trigeminocardiac Reflex in Neurosurgery Current Knowledge and Prospects 9 Basedonthesefindings,wehavedevelopedtheconceptthatmostriskfactorsleadtoa sensitizationofthetrigeminalnerveandmakeitmorepronetotriggerTCRduring intraoperativestimulation(Schaller,B.,etal.,2009a,Spiriev,etal.,2011b).However,as predisposing drugs actively influence the balance of the autonomic outflow, we believe, that theireffectisratherexertedviamodulationoftheefferentreflexpathwaythaninthe reduction of the reception threshold of the afferent pathway.5. Clinical presentation Clinically,TCRhasgainedenormousattentionandimportanceduetoitspotentiallylife-threateningcomplicationwhichmayincludesuddenonsetofbradycardiaculminatingin asystole,asystolewithoutprecedingbradycardiaorapnea(Campbell,etal.,1994,Schaller, 2004).Duringseveraldifferentsurgicalprocedures,includingocular-andorbitalcavity surgery,maxillofacialsurgeryandvariousneurosurgicalprocedures,TCRhasbeen observed subsequently to manipulation of either peripheral or central parts of the trigeminal nerve,thusaffectingtheongoingoperationandrequiringimmediateandappropriate interventiontoservethepatientfromdevastatingcardiovasculardeterioration.Inthe followingsectiontheneurosurgicalproceduresinwhichTCRhasbeendescribedandthus in which TCR needs to be attended are introduced. 5.1 Cerebellopontine angle surgery In 1999, Schaller et al. (Schaller, et al., 1999) for the first time reported TCR after stimulation ofcentralpartsofthetrigeminalnerveduringsurgeryinthecerebellopontineangle,and thusintroducedTCRtotheneurosurgicalcommunity.Atotalof125patientswho underwentsurgeryinthecerebellopontineangleduetoneoplasmsweremonitoredwith respecttotheoccurrenceofautonomiccardiovascularresponsesconsistentwithTCR. Indeed,11%ofthepatientsshowedresponsesmostlikelyattributabletoTCR.While dissecting the tumor near the trigeminal nerve at the brainstem, the patients HR and MABP decreasedsignificantly.ThemeanHRfell38%fromameanof76beats/minutebefore manipulationtoameanof47beats/minuteduringtheprocedure,andreturnedtoamean of 77 beats/minute after manipulation. The MABP fell 48% from a mean of 84 mmHg before manipulationto44mmHgduringtheprocedure,andreturnedto82mmHgafter manipulation.BothHRandMABPreturnedtonormal(pre-manipulative)valuesafterthe dissection.Inthreecases,therewasanasystole,withdurationof30to70secondsanda return to a normal cardiac rhythm within 90 to 180 seconds after termination of the surgical manipulation (Schaller, et al., 1999). In each of the 14 cases, the surgical manipulation of the trigeminalnervenearthebrainstemelicitedaspecificandunequivocaleffect(sudden bradycardiaandarterialhypotension).Eliminationoftheinducingstimulus,suchas manipulationsnearoratthetrigeminalnerve,resolvedtheeffectandrepetitionofthe stimulus lead to the same effect each time (Schaller, et al., 1999). 5.2 Transsphenoidal surgery Todeterminethenatureandtheextentof TCRduringtranssphenoidalsurgery,Schalleret al.(Schaller,2005a)reviewedaconsecutiveseriesof117patientswith immunohistochemicallyand/orelectronmicroscopicallydiagnosedandtranssphenoidally operatedpituitaryadenomaswithspecialemphasizeonincidenceandriskfactorsofTCR. Explicative Cases of Controversial Issues in Neurosurgery 10TheincidenceforTCRinthisserieswas10%withlackingstatisticaldifferencebetween TCR-andnon-TCRsubgroupsfortheparametersage,gender,tumorhistology,orthe durationanddistributionofpreoperativesymptoms.Duringthepreparationofthenasal septumnoneofthepatientsrevealedTCR.However,asignificantdecreaseinHRand MABP was observed during lateral tumor resection near the cavernous sinus. The mean HR decrease was 43% from a mean of 78 13 beats/minute before manipulation to a mean of 45 13 beats/minute. The mean MABP decrease was 54% from a mean of 86 8 mmHg before to4013mmHgduringthemanipulation.Withintenminutesaftercessationofthe stimulusandwithoutadministrationofanticholinergicsHRandMABPvaluesreturnedto 779beats/minuteand828mmHg.Thepost-proceduralvalueswerenotsignificantly different from preoperative baseline values. Two patients revealed asystole lasting 25-63 sec andasinusrhythmresumedwithin75-135secaftertheendofthesurgicalmanipulation. The follow-up of these two patients was uneventful. Interestingly, TCR occurred significantly moreofteninpatientswithinvasiveadenomasgradeIII/IV,accordingtoHardys classificationasmodifiedbyWilson(83%versus22%;p30seconds(15.7%)andshortdurationseizures(14.3%).Allcomplicationswere easily handled: nausea was treated with ondansetron 4 mg intravenously, seizures with cold irrigationofthecortex,andoxygendesaturation,beingalmostconstantlytheconsequence ofoversedation,wastreatedbyloweringpropofolorremifentanilinfusion.Noneofthese eventsdidaffectthecourseofsurgery.Postoperativepain,assessedat2-6-12-24hours postoperatively, was 30 seconds. Patients Ramsay score was 4, he was stimulated intensely and allowed tobreathdeeplypureoxygenthroughafacialmaskforsomeminutes,regainingrapidly SpO2>95%.Thiseventinducedtolowerremifentanilinfusionrateto0.1mcgKg-1min-1, after which no respiratory complications were seen until the end of surgery. Total operating room time was 475 minutes; propofol effect site concentration and remifentanil infusion rate reached0.8mcgml-1and0.2mcgKg-1min-1respectivelyduringskinincisionandbone opening,twoamongthemostpainfulphasesofcraniotomy.AtthatpointPaCO2was43.2 mmHg.Comment:Oversedationoccurredbecausepainfulstimulationwasexpectedtooccurand analgesiaandsedationwereprobablyresumedtoopromptlycomparedtotheonsetof surgicalstimulation.Infactanevenhigherdosageofthesamedrugsdidnotproducethe same effect during the opening phase, when it was adequate to pain. Lowering remifentanil infusion rate and breathing pure oxygen through a facial mask for a few minutes are simple maneuvers that immediately resolved the complication. Excellent view and access to patient face is crucial to prevent more serious events. Case 2 A58-year-oldman,ASAphysicalstatus2,weight70kg(BMI23.7)wasscheduledto undergoawakecraniotomyforarecidivatingleftfrontotemporalastrocytoma.Hispast medicalhistoryrevealedgastritisandcraniotomyforthesametumouroneyearbefore. Surgery was foreseen to last 10 hours, and the patient, although willing to collaborate, was deemednotabletocopewithsuchalongprocedureduetoanxiety.Thereforehewas candidatefortheasleep-awaketechnique.Anesthesiawasinducedwithpropofol100mg and remifentanil 0.1 mcg Kg-1 min-1 in neutral supine position, an i-gel supraglottic airway device # 3 was inserted and lungs were mechanically ventilated to maintain a PaCO2 around 35mmHg(Vt700ml;RR13breathspermin).Mayfieldheadrestwaspositionedafter performingthescalpblock,thenhewasflippedtorightlateralposition,andtheopening phase took place. Anesthesia was maintained with propofol 2.5-3 mcg ml-1 at the effect site andremifentanil0.15-0.2mcgKg-1min-1.Threehourslater,uponcompletionofdura opening,anesthesiawasdiscontinued,thepatientwasawakenedandtheLMAremoved. Fifteenminuteslaterbrainmappingstarted.Intraoperativemonitoringwascarriedout without complications for the following 2 hours, then the patient became very anxious and restless,andheclaimedtobeverytiredandnottobeabletocompletethelastpartofthe procedure in the awake state. A shift to asleep-awake-asleep was decided and anaesthesia wasinducedagain.Reinsertionofi-gelairwaydevicewassmoothdespitethelateral position.I-gelwaschosenbecauseinsertionandtightadherencetothelaryngeal frameworkinanon-supinepatientcouldhavebeencumbersomeusingastandardLMA. Four hours later, surgery ended and the patient was successfully awakened. Anesthesiologic Management for Awake Craniotomy 31 Comment.Thiscaseisdescribedtoshowhowoneshouldbeabletomodifyhisstandard techniquetoadaptittodifferentsettings.Airwaymanagementisoneofthemajor drawbacksofAAA,andtheanesthesiologistshouldbefamiliarwithalargespectrumof devices to choose from in each particular case. 10. Acknowledgement We would like to thank Dr. Anna Matina for her precious help.11. References [1]AlfonsiP.Postanestheticshivering.Epidemiology,pathophysiologyandapproachesto prevention and management. Drugs 2001; 61: 2193-205. [2] BalkiM,ManninenPH,McGuireGP,El-BeheiryH,BernsteinM.Venousair embolismduringawakecraniotomyinasupinepatient.CanJAnesth2003;50 (8): 835-8. [3]BerkenstadtH,PerelA,HadaniM,UnofrievichI,RamZ.Monitoredanesthesiacare usingremifentanilandpropofolforawakecraniotomy.JNeurosurgAnesthesiol 2001; 13 (3): 246-9. [4]Blanshard HJ, Chung F, Manninen PH, Taylor MD, Bernstein M. Awake craniotomy for removalofintracranialtumor:considerationsforearlydischarge.AnesthAnalg 2001; 92: 89-94. [5]Bloomfield E.L, Schubert A, Secic M , Barnett G, Shutway F, Ebrahim Z.Y. The Influence of scalp infiltration with bupivacaine on hemodynamics and postoperative pain in adult patients undergoing craniotomy. Anesth Analg 1998; 87: 579-82. [6]Bonhomme V, Born JD, Hans P. Anaesthetic management of awake craniotomy. Ann Fr Anesth Reanim 2004; 23: 389-94. [7]ConteV,BarattaP,TomaselliP,SongaV,MagniL,StocchettiN.Awakeneurosurgery: an update. Minerva Anestesiol 2008; 74: 289-92. [8]ConteV,MagniL,SongaV,TomaselliP,GhisoniL,MagnoniS,BelloL,StocchettiN. Analysisofpropofol/remifentanilinfusionprotocolfortumoursurgerywith intraoperative brain mapping. J Neurosurg Anesthesiol 2010; 22:119127. [9]Costello TG, Cormack JR. Anaesthesia for awake craniotomy: a modern approach. J Clin Neurosci. 2004; 11: 169.[10] DanksRA,AglioLS,GuginoLD,BlackPM.Craniotomyunderlocalanesthesiaand monitoredconscioussedationfortheresectionoftumoursinvolvingeloquent cortex. J Neurooncol 2000; 49 (2):131-9. [11] EganT,LemmensHJM,FisetP,HermannDJ.PharmD,MuirK.T,StanskiD.R,Shafer S.L.Thepharmacokineticsofthenewshort-actingopioidremifentanil(GI87084B) in healthy adult male volunteers. Anesthesiology: 1993; 79 (5): 881-92. [12] Egan, Talmage D. Pharmacokinetics and pharmacodynamics of remifentanil: an update in the year 2000. Curr Opin Anaesthesiol 2000; 13 (4): 449-55. [13] FrostE,BooijL.Anesthesiainthepatientforawakecraniotomy.CurrOpin Anaesthesiol 2007; 20 (4): 331-5. Explicative Cases of Controversial Issues in Neurosurgery 32[14] GadhinglajkarS,SreedharR,AbrahamM.Anesthesiamanagementofawake craniotomy performed under asleepawakeasleep technique using laryngeal mask airway: report of two cases. Neurol India 2008; 56: 657. [15] GonzalesJ,LombardFW,BorelCO.Pressuresupportmodeimprovesventilationin asleep-awake-asleep craniotomy. J Neurosurg Anesthesiol 2006; 18 (1): 88. [16] GrossmanR,RamZ,PerelA,YusimY,ZaslanskyR,BerkenstadtH.Controlof postoperativepainafterawakecraniotomywithlocalintradermalanalgesiaand metamizol. Isr Med Assoc J 2007; 9 (5): 3802. [17] HansP,BonhommeV.Anestheticmanagementforneurosurgeryinawakepatients. Minerva Anestesiol 2007; 73 (10): 507-12. [18] HerrickIA,CraenRA,Gelb AW,MillerLA,KubuCS,GirvinJP,ParrentAG,Eliasziw M,KirkbyJ.Propofolsedationduringawakecraniotomyforseizures:patient-controlledadministrationversusneuroleptanalgesia.AnesthAnalg1997;84(6): 1285-91.[19] Herrick IA, Craen RA, Gelb AW, McLachlan RS, Girvin JP, Parrent AG, Eliasziw M, KirkbyJ.Propofolsedationduringawakecraniotomyforseizures: electrocorticographic and epileptogenic effects. Anesth Analg1997; 84 (6): 1280-4.[20] Hol JW, Klimek M, van der Heide-Mulder M, Stronks D, Vincent AJ, Klein J, Zijlstra FJ, FekkesD.Awakecraniotomyinducesfewerchangesintheplasmaaminoacid profilethancraniotomyundergeneralanesthesia.JNeurosurgAnesthesiol2009; 21: 98107. [21] HunckeK,VandeWieleB,FriedI,RubinsteinE.TheAsleep-Awake-Asleep anesthetictechniqueforintraoperativelanguagemapping.Neurosurgery1998; 42 (6): 1312-6. [22] HunckeT,ChanJ,DoyleW,KimJ,BekkerA.Theuseofcontinuouspositiveairway pressureduringanawakecraniotomyinapatientwithobstructivesleepapnea.J Clin Anesth 2008; 20 (4): 297-9. [23] JohnsonKB,EganTD.Remifentanilandpropofolcombinationforawakecraniotomy: case report with pharmacokinetic simulations. J Neurosurg Anesthesiol 1998; 10 (1): 25-9.[24]KeiferJC,DentchevD,LittleK,WarnerDS,FriedmanAH,BorelCO.Aretrospective analysis of a remifentanil/propofol general anesthetic for craniotomy before awake functional brain mapping. Anesth Analg. 2005; 101 (2): 502-8. [25] KlimekM,HolJW,WensS,Heijmans-AntonissenC,NiehoffS,VincentAJ,KleinJ, ZijlstraFJ.Inflammatoryprofileofawakefunction-controlledcraniotomyand craniotomy under general anesthesia. 2009; 2009: 670480. [26] Lobo,FranciscoMD;Beiras,AldaraMD.Propofolandremifentanileffect-site concentrationsestimatedbypharmacokineticsimulationandbispectralindex monitoringduringcraniotomywithintraoperativeawakeningforbraintumour resection. J Neurosurg Anesthesiol 2007, 19 (3): 183-9. [27] ManninenPH,BalkiM,LukittoK.BernsteinM.Patientsatisfactionwithawake craniotomyfortumoursurgery:acomparisonofremifentanilandfentanylin conjunction with propofol. Anesth Analg 2006; 102: 237-42. Anesthesiologic Management for Awake Craniotomy 33 [28] ManninenPH,RamanSK,BoyleK,EI-BeheiryH.ReportsofInvestigation.Early postoperativecomplicationsfollowingneurosurgicalprocedures.CanJAnesth 1999; 46 (1): 7-14. [29] Manninen PH, Tan TK. Postoperative nausea and vomiting after craniotomy for tumour surgery:acomparisonbetweenawakecraniotomyandgeneralanesthesia.JClin Anesth 2002; 14 (4): 279-83. [30] Mirski MA, Lele AV, Fitzsimmons L, Toung T. Diagnosis and treatment of vasculair air embolism. Anesthesiology 2007; 106 (1) : 164-77. [31] MurataH,NagaishiC,TsudaA,SumikawaK.LaryngealmaskairwaySupremefor asleep-awake-asleep craniotomy. Br. J. Anesth. 2010; 104 (3): 389-90. [32] PalmonSC,MooreLE,LundbergJ,ToungT.VenousAirEmbolism:AReview.JClin Anesth1997;9(3):251-7.ParatiG,LombardiC,NarkiewiczK.Sleepapnea: epidemiology,pathophysiologyandrelationtocardiovascularrisk.AmJPhysiol Regul Integr Comp Physiol 2007; 293 (4): R1671-83.[34] Perks A, Chakravarti S, Manninen P. Preoperative Anxiety in Neurosurgical Patients. J Neurosurg Anesthesiol 2009; 21 (2): 127-30. [35] PeruzziP,BergeseSD,ViloriaA,PuenteEG,Abdel-RasoulM,ChioccaEA.A retrospectivecohort-matchedcomparisonofconscioussedationversusgeneral anesthesia for supratentorial glioma resection. J Neurosurg 2011; 114 (3): 633-9. [36] PiccioniF,FanzioM.Managementofanesthesiainawakecraniotomy.Minerva Anestesiol 2008; 74 (7-8): 393-408.[37] PichtT, Kombos, HJ,Brock M,SuessO. Multimodalprotocol forawakecraniotomyin language cortex tumour surgery. Acta Neurochir 2006; 148: 127-38. [38] SaltariniM,ZorziF.Awakecraniotomy.MinervaAnestesiol2005;71(suppl1,n10): 183-5. [39] Sarang A, Dinsmore J. Anaesthesia for awake craniotomy-evolution of a technique that facilitates awake neurological testing. Br J Anaesth 2003; 90 (2): 161-5. [40] SartoriusCJ,BergerMS.Rapidterminationofintraoperativestimulation-evoked seizureswithapplicationofcoldRingerslactatetothecortex.Technicalnote.J. Neurosurg 1998; 88: 349-51. [41] See JJ, Lew TW, Kwek TK, Chin KJ, Wong MF, Liew QY, Lim SH, Ho HS, Chan Y,Loke GP,YeoVS.Anaestheticmanagementofawakecraniotomyfortumourresection. Ann Acad Med Singapore 2007; 36 (5): 319-25. [42] SkucasAP,ArtruAA.Anestheticcomplicationsofawakecraniotomiesforepilepsy surgery. Anesth Analg 2006; 102: 882-7. [43] SuarezS,OrnaqueI,FbregasN,ValeroR,CarreroE.VenousAirEmbolismDuring ParkinsonSurgeryinPatientswithSpontaneousVentilation.AnesthAnalg2010; 110: 1138-45. [44] Verchre E, Grenier B, Abdelghani M, Siao D, Mussa S, Maurette P. Postoperative Pain ManagementAfterSupratentorialCraniotomy.JNeurosurgAnesthesiol2002;14 (2): 96-101. [45] WhittleIR,MidgleyS,GeorgesH,etal.Patientperceptionsofawakebraintumour surgery. Acta Neurochir 2005; 147: 275-7. Explicative Cases of Controversial Issues in Neurosurgery 34[46] ZorziF,SaltariniM,BonassinP,VecilM,DeAngelisP,DeMonteA.Anesthetic management in awake craniotomy. Signa Vitae 2008; 3 (1) S: 28 32. 3 Anaesthetic Management of Patients Undergoing Intraventricular Neuro-Endoscopic ProceduresA.F. Kalmar1 and F. Dewaele2

1University Medical Centre Groningen 2Ghent University Hospital 1The Netherlands 2Belgium 1. IntroductionEndoscopic neurosurgery has a long history of solid progression of over a century (Enchev etal.,2008).Inthisperiod,severalneuroendoscopicproceduresweredescribed,but althoughsteadytechnicalimprovementsincreasedtheendoscopicfunctionalityand indications,poormagnificationandilluminationkeptneuroendoscopydifficultand unreliable,keepingitoutofroutinepracticeuntiltheendofthe1980s.Onlyafterthe invention of new lenses, electronics and fiberoptics allowed for the manufacturing of a new generationofendoscopesgrantingbrighterilluminationandimprovedresolution, neuroendoscopycameforwardasroutinetreatmentinneurosurgery(Lietal.,2005). Initially,neuroendoscopywasalmostexclusivelyperformedforendoscopicthird ventriculostomy (ETV) for the treatment of obstructive hydrocephalus, and still the majority of neuroendoscopies is performed for ETV. Recently however, it is increasingly used for the managementofalltypesofneurosurgicallytreatabledisorders(Enchev&Oi,2008),either asaprimarysurgicalapproachorasanadjunct,suchthatendoscopicproceduresare commoninmostneurosurgicaldepartments.Acontinuedevolutionoftechnological advances, introduction of robotic technology, steerable endoscopes and novel neurosurgical techniques are expected to increase its applications even further. These newly implemented surgicalpracticesofferimprovedtreatmentoptions,commonlyreferredtoasminimally invasiveinmanyclinicalconditions.Sinceendoscopictechniquesallowforintracranial interventions with minimal damage to healthy brain tissue, these advances are obviously a majorbenefit.Additionally,someinterventionshaveabetteroutcomewhenperformed endoscopically.However,inseveraloftheseinterventions,directsurgicalmanipulationof cerebralstructuresandparticularitiesoftheendoscopictechniquesareaconstanthazard sincetheycanseverelydisturbintracranialpressure,cerebralperfusionandoxygenation. Thisperturbationofcerebralhomeostasismayimplyimportantrisksforirreversiblebrain damage, and severe haemodynamical effects which, if not taken proper care of, make these surgicalimprovementsmuchlessminimalinvasivethanpreviouslysupposed.Aproper understandingofthephysiologicalchangesinducedbyandduringtheseproceduresis essentialforoptimalpatientcare.Neuroendoscopyhasbeensuccessfullyusedforthird Explicative Cases of Controversial Issues in Neurosurgery36ventriculostomy,tumorbiopsyorresection,cystfenestrationorremoval,evacuationof intraventricularhaemorrhageandplexuscoagulation.Thetechniquehashaditsgreatest application in the treatment of noncommunicating hydrocephalus by third ventriculostomy (Shubertetal.,2006).Thesurgeonestablishesaconnectionbetweenthethirdventricle and theprepontinesubarachnoidspacebyendoscopicallyfenestratingthefloorofthethird ventricle to allow the cerebrospinal fluid to flow directly from the third ventricle to the basal subarachnoidspaces,thusbypassingtheaqueductandtheCSFpathwaysoftheposterior fossa. 2. Key steps of the procedure Inmostcasespatientsarepositionedinthesupineorsemisittingpositionwiththehead flexed, so that the burr hole is located at the apex. This helps to minimize loss of CSF and air entrapmentintotheventriclesorthesubduralspace(Amini&Schmidt,2005).During neuroendoscopy,theendoscopeisoperatedcarefullyinordertominimizebraintissue damage and to allow precise manipulation of the working instruments. The presence of the shaftthroughthebraintissuemandatesabsoluteimmobilityofthepatientduringthe procedure. To ensure this precondition, the patients head is fixated with neurological head pinsinmostcases.Afterinfiltrationwithalocalanaesthetic,aburrholeismadeatan appropriatelocationforaccesstotheintendedtrajectory.Forendoscopicthird ventriculostomy, this is mostly a right precoronal burr hole, 2-3 cm lateral to the midline. In mostcases,thiswillprovideadirecttrajectoryfromtheentrysitethroughtheforamenof Monro into the third ventricle. Then preferably a rigid endoscope is introduced through the frontal cortex into the lateral ventricle (Caemaert et al., 1992), the mandrins of the irrigation channel(s)andoftheworkingchannelareretracted.Thentheendoscopeisadvancedinto the lateral ventricle and through the foramen of Monro into the third ventricle. A connection betweenthethirdventricleandthesubarachnoidspaceisestablishedbyendoscopically fenestratingthefloorofthethirdventricle.Thefloorofthethirdventricleisperforated bluntly,oftenusingthetipofaFogartyballooncatheterorcoagulationprobe.Theinitial fenestrationisthenenlargedtoapproximatelya4-mmopeningbyinflatingtheFogarty catheter.Afterfenestration,thecerebrospinalfluidcandrainintothebasalcistern, bypassingtheaqueductalstenosis.IfanimperforatemembraneofLiliequistispresent beneath the floor of the third ventricle, which would obstruct CSF outflow, it can be opened underdirectvisionwithaglassfiberorballooncatheter(Amini&Schmidt,2005).During fenestration of the ventricle, there is a risk of injury to the basilar artery, which can result in fatal haemorrhage or brainstem infarction. Adequate visualization often requires continuous irrigationoftheventricleswithwarmednormalsalineorpreferablylactatedringers accompanied by drainage of cerebrospinal fluid and irrigating fluid through the scope or the burr hole. Therefore, the inlet irrigation tubes are connected to the rinsing fluid bags, either withorwithoutpressurisingequipmentforactiverinsing.Ifanysignificanthaemorrhage occurs in the ventricle as a result of the procedure, copious irrigation must be possible until thehaemorrhageiscleared.Theunrestrainedeffluxofrinsingfluidneedstobeassuredin ordertopreventuncontrolledintracranialhypertensionduringheavyrinsing.Inorderto preventincreasedhydrostaticpressurecausedbytheshaftoftheendoscope,anoutflow tube is often connected to the outlet of the endoscope and its distal end is fixed at the same level as the burr hole, so that there is no siphoning effect or raised ICP. Anaesthetic Management of Patients Undergoing Intraventricular Neuro-Endoscopic Procedures37 3. State of the art anaesthesia Theanaestheticgoalsshouldcenteronintraoperativeimmobilization,cardiovascular stability,andrapidemergenceforearlyneurologicexamination.Sharpincreasesin intracranialpressuremustbedetectedandtreatedimmediately.Inthisview,adequate monitoring and good communication with the neurosurgeons is essential.3.1 Preoperative planning Patientspresentingforventriculostomymayhavepriorshuntplacementswithexisting shunttubingroutedfromthecraniumtoperitoneal,pleural(rarely),orcentralvascular locations. Patients may present with symptoms of elevated intracranial pressure (ICP) such as vomiting, headache, confusion or obtundation. Prolonged nausea and vomiting may have causeddehydrationorelectrolyteabnormalitiesrequiringcorrectionpriortosurgery.The patientsneurologicstatusandexaminationshouldbedocumentedpriortoinduction(Shubertetal.,2006).Hydrocephalusisoftenpartofmultisystemcongenitalsyndromes, withassociatedriskssuchashigherriskforurinarytractinfectionsorimpairedrenal function. Premedication with anxiolytics or narcotics should be titrated very carefully, since theproceduresareusuallyveryshortandfastpostoperativeneurologicassessmentisdesirable.Therefore,benzodiazepinesorotheragentsthatmaycontributetoprolonged postoperative sedation are preferably avoided (Fbregas & Craen, 2010). 3.2 Anaesthetic technique Intravenousandvolatilehypnoticsarebothroutinelyusedforneurosurgery.However,in published studies inhalation anaesthesia was the predominant technique of choice. Nitrous oxide should not be used in order to avoid elevations in ICP (Derbent et al., 2006), because of the additional risk with venous air embolism (Ganjoo et al., 2010) and the risk of diffusion intoandexpansionofventricularairbubbles(Shubertetal.,2006).Mildhyperventilation canbeperformedinordertodecreaseintracranialbrainvolume.Becauserapidemergence isofprimeconcern,wewouldrecommendtheuseofremifentanilduringtheprocedure, combined with either intravenous or volatile hypnotics. Adequate care for thermoregulation must be taken since patients especially small children - are at risk for hypothermia during neuroendoscopy, mainly because oflarge exchanges of irrigating fluid and ventricular CSF andbythewettingofdrapes(Ambesh&Kumar,2000).Prophylaxisagainstpostoperative nauseaandvomitingisadvisablebecausetheelevatedICPisoftenassociatedwith increasedgastricacidsecretion,andmayadditionallyincreasetheriskofvomiting. Prophylacticanalgesicsshouldbegivenbeforeemergenceofnarcosis.Acombinationofa low dose of opiates (such as morphine 0.03mg/kg) and paracetamol in most cases provides adequateanalgesiceffectwithoutcompromisingneurologicevaluation.Non-steroidalanti-inflammatory drugs are generally discouraged because of haemostatic concerns. 3.3 Intraoperative monitoringMostauthorsrecommendinvasivebloodpressuremonitoringbyanindwellingarterial catheterinallpatients,includingchildren.Wewouldalsostronglysuggestcontinuous measurement of the ICP and CPP. Active rinsing of the ventricles can unexpectedly increase the ICP very severely. The principal reasons for induced intracranial hypertension are high Explicative Cases of Controversial Issues in Neurosurgery38flow rinsing (used to improve visibility during bleedingor to maintain access in collapsing ventricles ) and obstruction of the outflow channel by tissue debris , blood clotsor kinking ofoutflowtubes.TheseincreasesinICPmustbedetectedassoonaspossibletoprevent severe complications such as cardiovascular instability (Fabregas et al., 2002, Handler et al., 1994),herniationsyndromes,retinalbleeding(Boogaartsetal.,2008;Hovingetal.,2009) andexcessivefluidresorption(Kalmaretal.,2009).Asidefromtheseunambiguous complicationsanimalresearchshowedthatawakeningwithoutapparentneurological deficitdoesnotprecludehistologicaldamage(Kalmaretal.2009).Itispossiblethatthe samecouldapplyforhumans.Beat-to-beat monitoringofthearterialbloodpressureoffers the most reliable warning sign for a developing Cushing reflex, which is a sign of decreased CPP(Kalmaretal.,2005a).ThisCPPshouldatalltimebemaintainedabove40mmHg. Transcranialdoppleristhefastestandmostreliablemethodtoshowabruptdecreasesin cerebralbloodflowduetoincreasedICP(Kalmaretal.,2005b).Becauseofitshigh sensitivitytoimpairedcerebralbloodflow,itmaybeconsideredasbasicmonitoring, although practical objections limit its routine use during neuroendoscopy. 3.4 Active rinsing and Intracranial hypertensionTwostrategiestoensuresufficienteffluxofrinsingfluidarecommonlyused.Thefirst option is to use a peel-away sheath with a diameter just slightly larger than the endoscope to provideaworkingportholeintotheanatomy.Asidefromallowingeasyinsertionand reducedtissuedamageduringendoscopemanipulation,itallowsforegressofirrigation fluid (Amini & Schmidt, 2005). Most surgeons however do not use an extra sheath. Effusion capacity of the rinsing fluid is consequently largely restricted to the outflow channel of the endoscope, in which case substantial intracranial pressure can emerge, mandating adequate ICPmonitoring(Fbregasetal.,2001;Kalmaretal,2005a).Themanipulationof intraventricular fluid volume and pressure by controlling the rinsing inflow and outflow is sometimesadvocatedasaparticularadvantage.Asurgicalskillconsistsofdeliberately increasing the intracranial pressure as a surgical intervention to expand collapsed ventricles. Itisalsoproposedasaninstrumenttocontrolhaemorrhage.Inthelattercase,controlled increase of the intracranial pressure at least above the venous pressure, and even higher are advocated as a tool to tamponade venous or maybe even arteriolar bleeding.This allows for moredelicateprocedurestobeperformedendoscopically.Especiallyduringcomplex operations, such as tumourresections characterized by frequent bleedings with each bite during the piece-by-piece removal, it allows to quickly regain visibility. An increase in ICP canbetolerateduptoacertainlevel,anditisofteninevitablewhileprovidingadequate rinsingtoimprovevisibility.However,therinsingactivityandICPincreaseshavetobe performedinacontrolledmanner.Particularlyinthesesituations,meticulousICP monitoring, monitoring of the haemodynamical status and optimal communication between the anaesthetist and neurosurgeon are critical (Kalmar et al., 2005a). Although the technique ofpressurefeedingtherinsingfluid(i.e.usingpressurisedrinsingfluid)ispreferredby manysurgeonstoprovidesufficientrinsingcapacity,othersprefertoperformthe endoscopicprocedurewithasteadystateinflowpressureusinggravityfeed(i.e.only usinggravityasadrivingpressureoftherinsingfluid)toavoidbarotraumatothebrain ventricles.However,evenincaseofgravityfeed,arinsingfluidbagatalevelof100cm abovetheheadstillcouldcauseanICPof~76mmHgincaseofcompletelyobstructed outflow.Incaseofasuddensevereincreaseofintracranialpressure,thesurgeonshould Anaesthetic Management of Patients Undergoing Intraventricular Neuro-Endoscopic Procedures39 immediatelystoptherinsingandremoveanyinstrumentoutoftheworkingchannel.This mostly wide channel is an additional way out for the accumulated rinsing fluid. 3.5 Intracranial pressure and the Cushing reflex Endoscopic third ventriculostomy is associated with a wide range of haemodynamic effects causedbydirectstimulationofbrainstructures,andbychangesinintracranialpressure. Severalmechanismshavebeenpostulatedtoelucidatetheneurologicaloriginofthese changes,butnoindiscriminateanatomicalsourceofthereflexeshasyetbeendetermined (Fbregasetal.,2010).Themanifestationofhaemodynamicalreflexesduringendoscopic neurosurgerydescribedinliteraturediffersbetweenauthors.Historically,theCushing reflexwasfirstdescribedbyHarveyCushingin1901asasimultaneousoccurrenceof hypertension,bradycardiaandapnoeafollowingintracranialhypertension(Cushing1901). Thisobservationhowever,wasbasedonhisexperiencesasaneurosurgeon,wherehe treatedpatientsthatwerereferredsometimeafteranintracranialbleedingorwithlonger lastingintracranialhypertension(hydrocephalus,tumors).AlthoughHeymansshowedin 1928inanimalresearchthatthereisaninitialshort-lastingtachycardiabeforetheonsetof bradycardia (Heymans1928), it is only since the introduction of neuro-endoscopy, this has become of clinical relevance. Relying on the experience in relatively slow-evolving processes likea chronic subdural hematoma, hydrocephalus or cerebral tumors, many clinicians still considerbradycardiaandhypertensionasthefirsthemodynamicsignofhyperacute intracranialhypertension.IntheliteraturedescribingtheCushingreflexduringneuro-endoscopy,theobservationofhypertensionisubiquitous.However,severalgroups observedmostlyhypertensionandbradycardiaasapredominantsign(El-Dawlatly2008, Fbregas2001),whileothers(VanAken2003,Kalmar2005a)systematicallyobserved hypertensioncombinedwithaninitialtachycardia,whichonlyoccasionallyevolvesinto bradycardia.Itisveryconceivablethatthedifferencesintheseobservationsarearesultof variationsinsurgicalpractice.Additionally,directpressureoncertainanatomicalregions seemsmainlytoprovokebradycardia(Baykanetal.,2005),whileisolatedintracranial hypertension seems rather to induce tachycardia (Kalmar et al., 2009). Al-Dawlatly suggests thatthepossibleabsenceoftachycardiafoundinmanystudiesmaybe duetotheprotocol thatallowstheirrigationfluidtoventoutduringtheprocedurewithoutnoticeable accumulationinthethirdventricle.(Al-Dawlatlyetal.,2008).Inourexperience,we frequently observe bradycardia at the moment of balloon inflation close to the brainstem. In ordertopreventthis,weretracttheballoonsomewhatintothethirdventricleduring dilatationofthebottomofthethirdventricle.Inananalysisfocusingontheincidenceof bradycardia, Al-Dawlatly postulated that bradycardia recorded in a small series was due to directstimulationofthefloorofthethirdventricle(Al-Dawlatlyetal.,1999).Themost notable difference in surgical method is that for instance in the department of Van Aken & Kalmar,high-pressurerinsingispreferredasasurgicaltechniqueforrinsing,bleeding control and ventricular dilatation. Therefore, more swift and higher increases in intracranial pressuremayoccurwhichmayexplainthedifferencesinclinicalobservations.Inseveral neurosurgicalcentershowever,gravitationalflow,withouttheuseofpressurebags,is preferred as a method to prevent very high ICP values. In our personal experience however, whileendoscopicthirdventriculostomyprocedurescaninmostcasesbeperformedwith free flow gravitational rinsing, since bleeding is unusual and rather limited, procedures like Explicative Cases of Controversial Issues in Neurosurgery40tumorresectionorbiopsiesaremuchmoreatriskforseverebleedingandthereforemandatehigherrinsingflowsrequiringhigh-pressurerinsing.Duringsuchevents,itis usefulforthesurgeontobeattentivetothebeepsoftheanaesthesiamonitor.Changesin heartrateduringneuroendoscopyareveryinformativeforacknowledgementofthe consequencesofincreasedICPordirectstimulationofbrainstructures,inwhichcase immediate action can prevent serious complications. Typical hemodynamic reflexes such as bradycardia,tachycardiaorhypertensionassociatedwithETVaretransientandwill respondtosimplesurgicalmanoeuvressuchasreducingorstoppingtheinflowand retraction of the working instrument to allowegress of irrigant fluids through the working channel(Fbregasetal.,2010).Sinceextensivemanipulationofcerebralstructuresduring difficultsurgicalproceduresoftencoincideswithhigherrinsingflows,itisimpossibleto clearly differentiate the cause of these haemodynamic changes between direct stimulation of the brainstem and a genuine Cushing reflex. In an animal model of sudden increases in ICP devoid of any direct stimulation of brain structures severe bradycardia was never observed in the initial hypertensive phase. The haemodynamic reflex induced by isolated intracranial hypertension always consisted of hypertension, and the absence of bradycardia did not even excludeaCPPofzero.Inmanycases,aseveretachycardiaistheonlyandverydistinct constituentoftheinducedCushingreflex(Kalmar2009).Moreover,inthisanimalmodel, significantrinsingfluidresorptionwasobservedathighrinsingpressures,resultingin considerabledecreaseinhematocrit.Manyoftheanimalssuccumbedfrompulmonary edema.However,theseobservationsofexceptionalfluidresorptionorpulmonary complicationswereneverreportedinhumancases.Interestingly,althoughcerebral ischaemiawaspresentforseveralminutes,manyoftheanimalsrecoveredwithoutany apparentclinicalsignsofcerebralinsultwhilehistologicalanalysisshowedsignsof ischaemicinjurywithanincreasednumberofpinocyticneuronsinthehippocampus.This indicatesthatanormalawakeningofthepatientafteranapparentlyuneventfulnarcosis may not exclude important CPP suppression and even ischaemic injury. 3.6 ICP monitoring SeveralstrategiestomeasureICParerecommendedintheliterature.ICPmeasurements with an ICP tip sensor through the working channel have been used, but this may interfere withthesurgicalprocedure(Vassilyadi&Ventureyra,2002).AnintraparenchymalICPtip sensor will provide reliable measurements, but it is invasive and therefore less acceptable as aroutinepractice(Prabhakaretal.,2007).AnepidurallyplacedICPtipsensorisaless invasive,butalessreliablemethod.Althoughconsideredthegoldstandard,pressure measurementviaaseparatelyinsertedventricularcatheterisgenerallyunfeasibleand difficult to justify. Alternatively, an ICP Tipsensor can be advanced with the endoscope into theventricles.ThisprovidesreliableICP-readingsbutbearsanadditionalriskoftissue damage and is quite expensive. Fbregas proposed measuring the ICP by means of a fluid-filledcatheterconnectedtoastopcockconnectedtotheirrigationlumenofthe neuroendoscope (inflow channel) and attached to a pressure transducer zeroed at the skull base(Fbregasetal,2000).ThisPressureInsidetheNeuroendoscopecorrelateswiththe epiduralpressure(Salvadoretal.,2010)andwithmanifestationsoftheCushingreflex (Fbregasetal.,2010;Kalmaretal.,2005a).Alternatively,theoutletoftheendoscope-flushingsystemcanbeconnectedbyalongpressuretubetoapressuretransducerfor Anaesthetic Management of Patients Undergoing Intraventricular Neuro-Endoscopic Procedures41 continuous monitoring of the ICP (Kalmar et al., 2005a). The level of foramen of Monro was used as the zero reference point. A major pitfall in using the outflow channel to measure the ICP,isthatblockageintheoutflowlumenresultsinasevereunderestimationofthetrue intracranialpressure.MeasuringtheICPviatherinsingchannelsoftheendoscopeis preferredinliterature,althoughitisnotconvincinglydeterminedwhethertheinflowor outflowpointisthemostappropriatelocation.ICPmonitoringisthusimportant,butthe optimallocationofmonitoringiscontroversial.Sincefluidsflowdownpressuregradients, andflowingfluidsgeneratedynamicresistances,measurementattherinsinginletand outlet may at higher rinsing speeds correlate poorly with ventricular measurements. An In-vitrostudycomparingventricularpressurewithpressureattherinsinginletandoutlet showsverysignificantrespectiveover-andunderestimationsofthetrueintracranial pressure of up to 50mmHg at high rinsing flows (Dewaele et al., 2011). Measurement via a capillarytubeorelectronictipsensoradvancedthroughtherinsinginletchannelofthe endoscopeprovidesreliableICPmeasurementsandmaybasedontheseinvitro observationsbeproposedasbestpractice.Still,inordertominimallyhinderrinsing capacity,onlyverythincatheterscanbeadvancedthroughtherinsingchannel.However convincing,nohumanstudieshavepresentlybeenpublishedtoconfirmthesein-vitro findings in clinical practice. 3.7 Irrigation fluid LactatedRingersolutionatbodytemperatureisthemostfrequentlyusedirrigation fluid(Fbregas&Craen;2010).AfewstudiessuggestasignificantdisturbanceoftheCSF compositionwhenusingsalineasrinsingfluid,especiallyafterlongprocedures.Toavoid intraoperativeandpostoperativecomplicationsarisingfromtheuseofirrigatingfluids, somesurgeonstakecaretolimitthelossofCSFandtouseirrigationonlywhennecessary (Cinalli et al., 2006). 4. Complications Theincidenceofcomplicationscanvarywidelydependingontheprocedure.For endoscopicthirdventriculostomy,anincidenceof0to31.2%isreportedwithamortality rateof1%.Themostfrequentintraoperativecomplicationsarehaemostaticproblemsand infection.However,injuryofthebasilararterycomplexisthemostfearedintraoperative complicationandcancausemassiveintraventricularandsubarchnoidhemorrhage, hemiparesisandmidbraindamage(Jones&Kwok,1994).Meningealirritation,headache andhighfeverfromaninflammatoryresponsetoirrigatingfluidcanoccur(Okaetal., 1996).Uncontrolledintracranialpressurecancauseretinalbleeding,resultinginTerson syndrome(Boogaartsetal., 2008;Hovingetal.,2009).Neurologicalmorbiditycanbevery diverse,andcanoftenbeexplainedbytheapproachandtechnique,althoughaspecific incidentthatisresponsibleforthepostoperativedefectismostlyunappreciated.For example,althoughgazepalsyisreportedas acomplicationin0.60% ofpatients,innocase wasinjuryoftheoculomotornervedescribedasanintraoperativeincident(boeras& Sgouros,2011).Manystudiesreporttransientneurologicaldysfunctions,whichcanbe explained by the mechanics of the operation, such as short memory disturbances caused by irritationofthefornixbyscratchingoftheendoscopetothewallofthelateralventricleat the level of the foramen of Monro. Explicative Cases of Controversial Issues in Neurosurgery425. Postoperative care and longterm outcome Transient neurologic deficits such as delayed emergence, confusion, memory loss, transient papillarydysfunctionortransienthemiplegia-arethemostcommonpostoperative complicationoccurringin838%ofpatients(Fbregasetal.,2000).Inanextensivemeta-analysisof2985casesofETV,Bouras&Sqourosdescribedthatintheimmediate postoperativeperiodafterETV,CNSinfections(meningitis,ventriculitis)arerecordedin 1.81%ofthepatients.In2cases,aCSFinfectionisreportedtohaveevolvedtosepsis.Cerebrospinalfluidleaksarerecordedin1.61%ofcases.Postoperativehemorrhagic complicationsarereportedin0.81%ofthepatients.Theseconsistofsubduralhematoma, intraventricularhemorrhage,intracerebralhematomaandepiduralhematoma.Subdural hygromaswererecordedin0.27%ofthepatients.Therateofsystemiccomplicationswas 2.34%. Among them, hyponatremia, systemic infections, and deep vein thrombosis were the most frequent (Bouras & Sqouros, 2011). Particularly,hypothalamic or pituitary stalk injury canoccur,resultingindiabetesinsipidusorthesyndromeofinappropriatesecretionof antidiuretic hormone (SIADH) (Grant & Mclone, 1997). These cases are often not permanent, butincaseofdoubt,plasmaandurineelectrolytesshouldbeobserved.Incaseofdiabetes insipidus, desmopressin 1-4g IV (adult dose) can be administered.In case of postoperative polyuria,appropriatediagnosticmeasuresmustbeperformedaccordingly.Patientscan developtransientfeverduetoasepticirritationoftheependymaortomanipulationofthe hypothalamus. Convulsions have been reported by several authors, with one case resulting frompneumoencephalus.PersistinghighICPcanoccurpostoperatively,requiring additionaldiagnosticmeasures.Respiratoryarresthasbeenreportedininfantsduringthe firsthoursafterneuroendoscopy,necessitatingtheuseofapneamonitors(Shubertetal., 2006).Preferably,patientsarekeptintheneurosurgicalcareunitovernightforclose surveillance of vital signs, level of consciousness, change of papillary size, polyuria or other complications.InareviewofBouras&Sqouros,overallpermanentmorbidityofETVwascalculatedto be2.38%.Neurologicalmorbidity(1.44%)includesgazepalsy(0.60%),decreased consciousness(0.34%),hemiparesis(0.34%),andmemorydisorders(0.17%).Hormonal morbidity(0.94%)compriseddiabetesinsipidus(0.64%),weightgain(0.27%),and precocious puberty (0.04%).Theoverallmortalityratewas0.28%,alloftheminthepostoperativeperiodbecauseof sepsis or hermorrhagic incidents. Global good long-term outcome after ETV is between 70-80% in most series (Gangemi et al., 2007)6. Explicative cases In2003,a56yearoldwomanpresentingwith asubependymaltumourintherightlateral ventricle, was being operated on for an endoscopical biopsy and resection. Haemodynamic monitoring consisted of invasive arterial blood pressure (IABP), NIBP, ECG, pulse oximetry,and ICP-monitoring at the outflow-channel of the endoscope. After an uneventful induction and maintenance of narcosis with propofol, remifentanil and cisatracurium, classical patient positioningandintroductionoftheendoscope,thesurgicalprocedurefortumourremoval was performed. Anaesthetic Management of Patients Undergoing Intraventricular Neuro-Endoscopic Procedures43 Becauseofminorbleedingfromthetumoursurface,rinsingwasperformedmore elaborately than usual. The heart rate and IABP revealed stable haemodynamics but without any other warning signs, anisolated increase in blood pressure of 30 mmHg was observed withinless than ten seconds, followed by the onset of distinct tachycardia from 65 up to 105 bpm and a further increase of the systolic blood pressure to 180mmHg within a few seconds. AlthoughmonitoringshowedalowICP-level,thesurgeonwasinformedofahigh probability of severe intracranial hypertension, who instantly removed an instrument from theworkingchannelinordertoprovideanadditionaloutflowchannel.Immediately,a floodofrinsingfluidgushedoutoftheworkingchanneloftheendoscope.Withinfifteen seconds, the heart rate and IABP were stabilizing and after two minutes they had returned to normal levels. The procedure was resumed and completed without further events and the patient recovered without complications. Interestingly,thecollectedrinsingfluidshowedalotoftumourdebrisfloating,which probablyhadobstructedtheoutflowchanneloftheendoscope.Thisexplainsthe inaccurately low ICP-level on the monitor. This case shows the importance of adequate haemodynamic monitoring and comprehension of the Cushing reflex during neuroendoscopy. If in such a case the haemodynamic changes areperceivedasasignofarousal,painoridiopathichypertension,thepatientwouldbe treatedincorrectly,whiletheintracranialpressurewouldcovertlyincreasetodeleterious levels. On the other hand, swift adequate action may have prevented severe complications. Bothfortheanaesthetistandtheneurosurgeon,itisimportanttobeconstantlyawareof sudden changes in heart rate and blood pressure. Therefore, the sound level of the monitor shouldbeadequatelyhigh.Duringactiverinsing,especiallywithpresenceoftissuedebris intherinsingfluid,thesurgeonshouldbeparticularlyattentivetosuchchangesandact accordingly. 7. Expert suggestion Forstableanaesthesiaandfastrecoveryinoptimalconditions,werelyonbalancedtotal intravenous anaesthesia with propofol TCI 2-5 g/ml and remifentanilTCI 2-6 ng/ml. As a rinsingfluid,Ringerslactatesolutionatbodytemperatureisfavourableinorderto maximallypreserveelectrolytehomeostasis.Monitoringoftheintracranialpressureis currentlyperformedateithertheinfloworoutflowchanneloftheendoscopewithboth havingtheirdrawbacks.Optimalpressuremonitoringwilllikelyprogresstowards noninvasivetransendoscopicICPmeasurementbutthisremainstobeinvestigatedmore thoroughly.WeexpectmostaccurateICPmeasurementviaacapillarythroughtherinsing inletchannel.Studiesonthistopicarebeingperformedcurrently.Asemphasizedmany times,itisimperativetohavebeat-to-beatinformationonchangesinblood-pressureand heartratewheneversuddenincreasesinICParepossible.Sinceevengravitationalrinsing withtherinsingfluidpositionedatonly1meterabovethepatientcancauseanICPof 76mmHg,everyendoscopyholdssucharisk.Thereforewealwaysuseinvasiveblood pressure monitoring, but advanced noninvasive alternatives for beat-to-beat haemodynamic monitoring may become a fine alternative. In the postoperative period, short term memory can be disturbed due to tissue damage and irritationofthefornixattheleveloftheforamenofMonro,causedbyfrictionofthe Explicative Cases of Controversial Issues in Neurosurgery44endoscopicshaft.Inordertolimitthiscomplication,wefavourusinganendoscopewitha diameter of 6mm. 8. References (6pt) AmbeshSP,KumarR.Neuroendoscopicprocedures:anestheticconsiderationsfora growing trend: a review. J Neurosurg Anesthesiol 2000; 12:262270. AminiA,SchmidtRH.Endoscopicthirdventriculostomyinaseriesof36adultpatients. Neurosurg Focus. 2005;19:E9. BaykanN,IsbirO,GerekA,DagnarA,OzekMM.Tenyearsofexperiencewith pediatricneuroendoscopicthirdventriculostomy.JNeurosurgAnesthesiol. 2005;17:33-7. BoogaartsH,GrotenhuisA.Tersonssyndromeafterendoscopiccolloidcystremoval. Minim Invasive Neurosurg 2008; 51: 3035BourasT,SgourosS.Complicationsofendoscopicthirdventriculostomy.JNeurosurg Pediatr. 2011;7:643-9. 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El-DawlatlyA,ElgamalE,MurshidW,AlwatidyS,JamjoomZ,AlshaerA.Anesthesiafor thirdventriculostomy.Areportof128cases.MiddleEastJAnesthesiol.2008 Feb;19(4):847-57. Enchev Y, Oi S. Historical trends of neuroendoscopic surgical techniques in the treatment of hydrocephalus. Neurosurg Rev. 2008; 31: 249-62. HandlerMH,AbbottR,LeeM.Anear-fatalcomplicationofendoscopicthird ventriculostomy: case report. Neurosurgery 1994; 35: 5257 Heymans C. The control of heart rate consequent to changes in the cephalic blood pressure and in the intracranial pressure. Am J Physiol 1928; 85: 498505 HovingEW,RahmaniM,LosLI,RenardeldeLavaletteVW.Bilateralretinalhemorrhage afterendoscopicthirdventriculostomy:iatrogenicTersonsyndrome.JNeurosurg 2009; 110: 85860 Anaesthetic Management of Patients Undergoing Intraventricular Neuro-Endoscopic Procedures45 FbregasN,LpezA,ValeroR,CarreroE,CaralL,FerrerE..Anestheticmanagementof surgicalneuroendoscopies:usefulnessofmonitoringthepressureinsidethe neuroendoscope. 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VassilyadiM,VentureyraEC.Neuroendoscopicintracranialpressuremonitoring.Childs Nerv Syst 2002; 18: 147148. 4 Neurocritical Care Mainak MajumdarCritical Care Physician, Peninsula Health, VictoriaAustralia 1. Introduction Neurocritical care is at the forefront of bringing effective new therapies to patients with life threatening neurological diseases. Neurocritical care units have evolved from neurosurgical unitsfocusedprimarilyonpostoperativemonitoringtounitsthatprovidecomprehensive medical and specialized neurological support for patients with life-threatening neurological diseases.Inadditiontostandardinterventions,areasofexpertiseuniquetoneurocritical care include management of intracranial pressure, hemodynamic augmentation to improve cerebralbloodflow,therapeutichypothermia,andadvancedneuromonitoring. Neurointensivists defragment care by focusing on the interplay between the brain and other systems,andbyintegratingallaspectsofneurologicalandmedicalmanagementintoa singlecareplan.Outcomesresearchhasestablishedthatvictimsoftraumaticbraininjury andhemorrhagicstrokeexperiencereducedmortality,betterfunctionaloutcomes,and reducedlengthofstaywhencaredforbyneurointensivistsinadedicatedneurointensive care unit (Rincon & Mayer 2007). This chapter aims to provide an overview of global organ support of the critically ill neurosurgical patient.2. Critical care for neurosurgical patients Theneurocriticalcareunitprovidesavenuewhereadvancedmonitoringenables optimisation of oxygen and metabolite delivery to the neurons by aggressive, often invasive interventions within a controlled environment.2.1 Brain monitoring ThewordmonitororiginatesfromtheLatinmonere(towarn).Monitoringmerely provideswarningofpathologyandmaytrackitsprogressionlongbeforeitbecomes clinicallyobviousthusallowingearlieraggressivemanagementofunderlyingdiseaseand assessmentofresponsetotherapy.Thesuperiorityofanyonemodeofmonitoringover another has never been proven. Available forms of brain monitoring include Measurementofintracranialpressure(ICP):ICPhastraditionallybeenmeasuredbya ventricular drain connected by a fluid coupled system to an external strain gauge.Currently,availableoptionsincludesystemswithmicrostraingaugesorfibreopticsbuilt intothetip.Cathetersmaybeplacedintheparenchyma,subarachnoid,epiduralor Explicative Cases of Controversial Issues in Neurosurgery48subduralspacesinadditiontotheventricles.Generally,parenchymalcatheterswithmicro straingaugesinthetiphavegoodcorrelationwithventriculardrainpressures. Subarachnoid, subdural and epidural catheters are thought to be less accurate.Microstraingaugeandfibreopticcathetersneedtobecalibratedpriortoinsertionand cannotberecalibratedinsitu.Theoreticalconcernshavebeenraisedaboutmeasurement drift and resulting inaccuracy of measurement. There is little by way of published literature and the actual device selection is guided by institutional preference. Measurement of cerebral blood flow: Transcranial Doppler monitoring is an easily available, reproducible,noninvasiveandinexpensivemeansofmeasuringcerebralbloodflowby measuring flow velocity in the middle cerebral artery (MCA). It has been used to assess for cerebralvasospasm,toassesscerebralautoregulation(Reinhardetal,2010)anddiagnose traumatic dissection of the internal carotid artery (Bouzat et al, 2010). Measurement of brain oxygenation: Jugular venous oxymetry (SjO2) has been used to assess oxygendeliverytothebrain.Bothlow(75%)SjO2havebeenassociated with poor outcomes. The arterio jugular difference in oxygen content has been measured to assess cerebral oxygen extraction.Brain tissue oxygenation (PBrO2) can be directly measured by placing catheters into affected areasofthebraintodetectfocalischaemia.PBrO290mmHg,PaO2>70mmHg)andnormocapnia (PCO2 35-45 mmHg) Liberal opiate analgesiaLiberal sedation targeting Richmond Agitation and Sedation Scale (RASS) -4 or lower.Neuromuscular blockade if frequent shivering or coughing Prompt treatment of any seizure activity Addition of phenobarbitone Hyperosmolartherapy(either0.5-1gm/kgofmannitolor3%NaCltotargetserum sodium ~150) Hyperventilation to PCO2300)isassociatedwith increased risk of in hospital mortality (Kilgannon et al, 2010). Historically,aggressivehyperventilationtoinducehypocapnia(PaCO250)causescerebralvasodilation,increasingcerebralbloodvolumeand thereby ICP. The optimal strategy would be to aim for normocapnia (PaCO2 35-45).Positiveendexpiratorypressure(PEEP)improvesoxygenationandformspartofroutine lung protective ventilation strategies. Traditionally, concerns have been raised regarding the useofPEEPinventilatingneurosurgicalpatientasitmayincreaseICPand,byextension, reducecerebralperfusionpressure(CPP).LowlevelsofPEEPtoimprovealveolar recruitmenthavebeenshowntonotchangeICP(Masciaetal2005).IncreasingPEEPtoas highas15cmH2Otoimproveoxygenationwasparadoxicallyassociatedwithdecreasesin ICP and improved CPP (Huynh et al 2002).Reasonable goals of ventilation would be to achieve SaO2>90, PaO2>70, PCO2 35-45. Lung protective ventilator strategies (low tidal volumes 6-8 ml/kg, judicious use of PEEP) would meettheventilatoryrequirementsofthemajorityofneurosurgicalpatients.Additional measuressuchaslooseningtapessecuringendotrachealtubesandoptimumhead positioning and head elevation to prevent jugular outflow obstruction would be of benefit to maintaining adequate CPP. 3.2 Cardiovascular support Thegoalofallresuscitationisthedeliveryofoxygenandmetabolitestoendorgans. Hypotension,definedasasystolicbloodpressurelessthan90mmHg,hasbeenshownto Neurocritical Care53 worsen outcomes from acute brain injury. Even isolated episodes of in hospital hypotension havebeenassociatedwithincreasedmortalityandmorbidity(Jonesetal,1994).Dueto ethicalconsiderations,thereisnoClassIevidenceontheeffectofhaemodynamic resuscitationonoutcomes.However,raisingthebloodpressureimprovesoutcomein proportion to the efficacy of the resuscitation (Vassar et al 1993).The ideal fluid for volume resuscitation remains controversial. 0.9% NaCl remains the most commonlyusedfluidforthispurpose,probablyforreasonsoffamiliarity,costandeaseof use. There is little conclusive evidence to support colloid over crystalloid therapy. The SAFE studysuggestedsimilaroutcomesfromfluidresuscitationwithsalineor4%albumin.A posthocanalysisoftheSAFEstudydatasuggestedhighermortalityratesassociatedwith fluid resuscitation with albumin compared to saline in patients with traumatic brain injury (SAFEstudyinvestigators,2007).Amulticentrerandomisedtrialiscurrentlyunderway comparing outcomes of resuscitation with saline and starch. ItisreasonabletousevasopressorsandinotropesasneededtodefendMAPand,by extension,CPP.Thereisnoconclusiveevidencetoprovethesuperiorityofanyvasoactive agent over another. The use of these drugs is often determined by local critical care practice. The authors vasopressor of choice is noradrenaline. Thesystolicbloodpressureof90mmHgitselfisastatisticalratherthanaphysiological threshold. It makes more sense to try and approximate the patients baseline blood pressure with hemodynamic therapies than chase anartificial statistical target. The authors practice is to stay within 20% of the patients baseline blood pressure, where known.Cerebralperfusionisreliantmoreonthesystemicmeanarterialpressure(MAP)andICP. The MAP may be a more meaningful end point of resuscitation to aim for. Autoregulation of bloodflowbreaksdowninmostvascularbedsbelow~60mmHg.Thus,assuminga normal ICP of 10 cmH20 and intact cerebral vasculature, a MAP of 70 mmHg would be a reasonableinitialtarget.Clearly,theabovecaveatsarenotnecessarilytrueformany neurosurgicalpatientsand,inthepresenceofICPmonitoring,theMAPcanbetitratedto maintain a CPP>60 mmHg. Alternately, in the presence of cerebral oxygenation monitoring (eg. JvSO2), the MAP can be titrated to adequate cerebral oxygenation.ThereisnoconclusiveevidenceforelevatingMAPtosupranormaltargets.Thismaywell be hazardous in the context of trauma or recent surgery, with concomitant disruption of the blood brain barrier and cannot be recommended in routine neuro critical care practice. 3.3 Nutrition Thereisnodiseaseprocessthatbenefitsfromlackofnutritionalsupport.Criticallyunwell patients are hypercatabolic and at risk of losing significant lean body mass in the absence of nutritionalsupport.Currentpracticewouldbetoattempt toinitiatenutritionearly(within 72 hours) aiming to establish full calorific replacement within 7 days. Clearly this would be modified for patients presenting with evidence of poor nutritional state at baseline. Enteral nutrition, by gastric or jejunal routes, is the preferred route. In the event of inability to access thegutorfailuretoestablishenteralnutritionwithinareasonabletimeframe,parenteral nutrition should be considered. Explicative Cases of Controversial Issues in Neurosurgery54Patientswithtraumaticbraininjuriesoftenhavegastroparesis.Manydrugsroutinely administeredinacriticalcaresettingfurtheraltergutmotility.Thisisparticularlytrueof opiates.Prokinetics(egmetoclopramide10-20mg6hourly)shouldbeconsideredearlyin the establishment of enteral nutrition.Reasonablegoalsofnutritionsupportshouldaimfor25-30kcal/kg/day,ofwhich0.5-2 gm/kg/day should be protein content and 30-40% non protein content should be lipids. It is important to also supplement fat and water soluble vitamins and trace elements. 3.4 Glycemic control Hyperglycemiaiscommonincriticallyillpatientsandisassociatedwithmorbidityand mortality in varying groups of patients.In 2001, the Leuven Intensive Insulin Therapy Trial was published (van den Berghe et al, 2001), suggestingdramaticreductionsinmortalityincriticallyillsurgicalpatientswithtight glycaemiccontrol(targetbloodsugar4.4-6.1mmol/L).Subsequentstudiesfailedtoreplicate thesefindings.Concernswerealsoraisedregardingtherisksofhypoglycaemia,increased resource use and the difficulty of achieving tight normoglycemia in critically ill patients.TheNICE-SUGARstudy(Finferetal,2009)suggestedbloodglucoselevelslessthan10 mmol/Lresultedinlowermortalitythanatargetof4.5-6mmol/L.Theauthorscurrent practice is to aim for a blood sugar level of 5-10 mmol/L.3.5 Stress ulcer prophylaxis Stressulcersareaknowncomplicationofavarietyofcriticalillnesses.Theyoccurasa consequenceofhypoperfusionofthemucosaoftheuppergastrointestinaltract.Itis commonpracticetoprovideprophylaxistodecreasetheincidenceofclinicallysignificant bleeding. The most commonly used classes of drugs used for this purpose are H2 antagonists, proton pump inhibitors and sucralfate. To a large extent, the agent used is dictated by local critical care practice. H2 antagonists have been shown to be more effective than sucralfate, antacids and placebo inpreventingstressulcers(Stollman&Metz,2005).However,concernshavebeenraised regardingtheassociationbetweenacidsuppressivetreatmentandventilatorassociated pneumonia(Cooketal,1998).Ranitidinehasbeenassociatedmorestronglywith nosocomialpneumoniathansucralfate(Messorietal,2000).Furtherconcernshavebeen raisedregardingencephalopathyandcytochromeP450inductionbyH2antagonists. Omeprazolewasshowntoreduceclinicallysignificantgastrointestinalbleedingcompared toranitidine(Levyetal,1997).Arecentsinglecentrestudyfoundahigherassociationof nosocomialpneumoniawithpantoprazolecomparedtoranitidineincardiacsurgical patients(Mianoetal,2009).BothH2antagonistsandprotonpumpinhibitorshavebeen associated with increased risk of developing community and hospital acquired Clostridium difficile associated disease (CDC, 2005). Inkeepingwiththeabove,arecentsystematicreviewwasunabletofindthemost appropriateformofprophylaxisforneurocriticalcarepatients(Schirmeretal,2011).The Neurocritical Care55 mostsensibleapproachappearstobeaggressivehaemodynamicresuscitationtoimprove mucosal perfusion in the upper gastrointestinal tract and the establishment of early enteral nutrition,wherepossible.ItisstandardAustralianpracticetoprescribestressulcer chemoprophylaxisandbothH2antagonistsandprotonpumpinhibitorsarecommonly used. 3.6 Thromboprophylaxis Critically ill neurosurgical patients are at high risk of developing venous thromboembolism. Theincidenceofdeepveinthrombosis(DVT)inpatientswithtraumaticbraininjuryis estimatedtobeashighas20%(BrainTraumaFoundationGuidelines,3rded.).Pulmonary emboli(PE)areassociatedwithhighratesofmortalityandmorbidityinhospitalised patients.TreatmentofPEinneurosurgicalpatientsisoftencomplicatedbyuncertainty regarding the safety of anticoagulation soon after craniotomy or intracranial haemorrhage. It makes sense to try and prevent DVT than have to treat the PE. OptionsforDVTprophylaxisaremechanical(graduatedcompressionstockingsand sequential calf or foot compression devices) or chemical (low dose heparin or low dose low molecularweightheparin).Recentstudieshavefailedtoprovethesuperiorityoflow molecularweightheparinsoverlowdoseunfractionatedheparin(Cooketal2011, Goldhaber et al 2002) Mechanicalinterventionshavelowriskofcomplicationsandshouldbeofferedtoall patients.Cautionneedstobeexercisedinpatientswithsevereperipheralvasculardisease and limb trauma may preclude their use in some cases.Bothlowmolecularweightheparinandunfractionatedheparinhavebeenshowntobe effectiveforprophylaxisofvenousthromboembolisminelectiveneurosurgery(Ioro& Agnelli, 2000). In traumatic brain injury, the risk versus benefit analysis must be made on a casebycasebasis.ThereappearstobelittledifferenceintheincidenceofDVTorPEin patientsreceivingchemicalprophylaxisafter72hoursofadmissioncomparedtothose receivingprophylaxisearlierthan72hours(Kimetal,2002).Intheeventthatchemical prophylaxis cannot be initiated within 72 hours of admission, consideration should be given to a vena caval filter. 4. Prognostication in neurocritical care Theoutcomeofcriticallyillneurosurgicalpatientsaftersignificantbraininsultremains uncertain.Patientsmaysurvivetoacognitivelyimpaireddependentstateorworse,ina minimally conscious or persistently vegetative state with resultant implications for resource use.Predictionofoutcomeinvolvesmakingprobabilitystatementsthatdependonalogical relationship between outcome and features encapsulated in antecedent data. It still remains impossible to predict with certainty the outcomes of an individual patient. In a neurocritical care population, the groups most widely studied in this context are those with traumatic brain injury and hypoxic brain injury. Explicative Cases of Controversial Issues in Neurosurgery564.1 Traumatic brain injury Thebraintraumafoundationhaspublishedprognosticparametersfortraumaticbrain injury. The following factors have been considered Glasgow Coma Scale (GCS) score: If the initial GCS is reliably obtained and not tainted byprehospitalmedicationsorintubation,thereisincreasingprobabilityofpoor outcomewithalowGCSinacontinuousstepwisemanner.Approximately20% patients with initial GCS 3 will survive and 8-10% will have a functional survival. Age:Thereisincreasingprobabilityofpoorneurologicoutcomewithage,witha significant rise in poor outcomes in age>60 years. Bilaterally absent pupillary light reflex is a predictor of poor neurologic outcome Hypotension (systolic BP25 mm IV Midline shift >5 mm; no high or mixed density lesion >25 cc Table 1. 4.2 Hypoxic brain injury Attempts have been made to identify prognostic factors for poor outcomes in patients with hypoxic brain injuries at up to 3 days after admission (Levy et al, 1985 and Zandbergen et al, 2006).TheAmericanAcademyofNeurologyhaspublishedguidelinesforpredictionof outcomes in comatose survivors of cardiopulmonary resuscitation (Wijdicks et al 2006). Developmentofmyoclonusstatusepilepticuswithinthe1stday,bilaterallyabsentcortical responseonsomatosensoryevokedpotentials(delayedN20)atday1-3,serumneuron specific enolase (NSE) >33micrograms/L at day 1-3, absent pupillary or corneal reflexes on day3orextensororabsentmotorresponsetostimulusonday3arepredictiveofpoor neurologic outcomes. Neurocritical Care57 BurstsuppressionorgeneralisedepileptiformactivityonEEGwaspredictiveofpoor outcome but with insufficient prognostic accuracy. Imaging (CT, MRI, PET) and duration of CPR were not reliable predictors of poor outcome. 5. Determination of brain death Deathhasalwayshadimmenseculturalandreligioussignificanceforhumansocieties acrosstheworld.UntiltheRenaissance,therewasnobiologicalunderstandingofdeath. William Harveys seminal paper On the Motion of the Heart and Blood in Animals in the 17thcenturylaidthefoundationtotheunderstandingofdeathasirreversiblecessationof cardiovascularfunction.In1959,Wertheimeretalfirstdescribeddeathofthecentral nervous system as a syndrome of coma, areflexia and apnoea. Later that year, Mollaret and Goulon coined the term coma depasse to describe this syndrome.Braindeathisdefinedasirreversiblecessationofbrainfunction.Priortothediagnosisof brain death being made, the following