Telechargé par Ghassen Souissi

NEURO anesthesie

General and Neurology
4 Neuroanest hesia
4.1 General inform at ion
Table 4.1 sh ow s th e Am erican Society of An esth esiologists (ASA) gradin g system to estim ate an esth etic risk for various con dition s.
For issues related to in tracran ial pressure (ICP), cerebral perfusion pressure (CPP), in tracran ial
con stituen ts, etc., see ICP prin ciples (p. 856). For cerebral blood flow (CBF) an d cerebral m etabolic
rate of oxygen con sum ption (CMRO2 ), see CBF an d oxygen utilization (p.1264).
Param eters of prim ar y relevan ce to n eurological surger y th at can be m odulated by th e
an esth esiologist:
1. blood pressure: on e of th e factors th at determ in es CPP as w ell as spin al cord perfusion . May
n eed to be m an ipulated (e.g. reduced w h en w orking on an an eurysm , or in creased to en h an ce
collateral circulation durin g cross clam ping). Measurem en t by arterial lin e is m ost accurate an d
depen din g on th e patien t’s presentation an d th e plan n ed procedure, often sh ould be placed prior to in duct ion of an esth esia. For in tracran ial procedures, th e ar terial lin e sh ould be calibrated
at th e extern al auditor y m eatus to m ost closely reflect in tracran ial blood pressure
2. jugular ven ous pressure: on e of th e factors th at in fluen ces ICP
3. ar te rial CO2 te n sion (PaCO2 ): CO2 is t h e m ost p ot en t cerebral vasod ilator. Hyp er ven t ilat ion
red u ces PaCO2 (h yp ocap n ea) w h ich d ecreases CBV bu t also CBF. Goal is gen e rally en d t id al
CO2 (ETCO2 ) of 25–30 m m Hg w it h a correlat in g PaCO2 of 30–35. Use w it h care for stereot act ic p roced u res to m in im ize sh ift of in t racran ial con ten t s w h en u sin g th is m et h od to con t rol ICP4
4. arterial O2 ten sion
5. h em atocrit: in n eurosurger y it is critical to balan ce oxygen carr ying capacit y (decreased by an em ia) again st im proved blood rh eology (im paired by elevated Hct )
6. patien t tem perature: m ild hypotherm ia provides som e protect ion again st isch em ia by reducing
th e cerebral m etabolic rate of oxygen (CMRO2 ) by ≈ 7% for each 1° C drop
7. blood glucose level: hyperglycem ia exacerbates isch em ic deficits 5
8. CMRO2 : reduced w ith cer tain n euro-protect ive agen ts an d by hypotherm ia w h ich h elps protect
again st isch em ic injur y
9. in cases w h ere a lum bar drain or a ven tr icular drain h as been placed: CSF out put
10. elevation of th e h ead of th e pat ien t: low erin g th e h ead in creases arterial blood flow, but also
in creases ICP by im pairin g ven ous outflow
11. in travascular volum e: hypovolem ia can im pair blood flow in n eurovascular cases. In surgery in
th e pron e position , excessive fluids m ay con tribute to facial edem a w h ich is on e of th e risk factors for PION (p. 1056)
12. position in g injuries: during th e procedure, th e patien t’s position m ay ch ange an d be un n ot iced
due to drapin g. Careful an d frequen t exam in ation of th e patien t’s position m ay preven t injuries
associated w ith prolonged m alposition in g
13. post operative n ausea an d vom it in g (PONV): m ay adversely a ect ICP an d m ay n egatively
im pact recen t cer vical surgical procedures. Avoidan ce of an esth etic agen ts kn ow n to cause
PONV or pretreatm en t to preven t PONV m ay be pruden t
4.2 Drugs used in neuroanest hesia
4.2.1 Inhalat ional agent s
General inform at ion
Most r e d u ce ce r eb r al m et ab olism (exce p t n it r ou s oxid e ) by su p p r essin g n e u r on al act ivit y.
Th ese age n t s d ist u rb ce r eb r al au t or e gu lat ion an d cau se ce r eb r al va sod ilat at ion w h ich
in cr e ase s ce r eb r al blood volu m e (CBV) an d can in cr e ase ICP. W it h ad m in ist r at ion > 2 h rs t h ey
in cr e ase CSF volu m e w h ich can a lso p ot e n t ia lly con t r ib u t e t o in cr e ase d ICP. Most age n t s
in cr e ase t h e CO2 r e act ivit y of ce r eb r al blood ve ssels. Th ese age n t s a ect in t r a- op e r at ive EP
m on it or in g (p . 10 7).
Neuroanest hesia
Drug info : Nit rous oxide
A potent vasodilator that markedly increases CBF and m inim ally increases cerebral metabolism. Contributes to post-op N/V.
Nit rous oxide, pneum ocephalus and air em bolism : The solubilit y of nitrous oxide (N2 O) is ≈ 34
times that of nitrogen.6 When N2 O com es out of solution in an airtight space it can increase the pressure which m ay convert pneumocephalus to “tension pneumocephalus.” It m ay also aggravate air
embolism. Thus caution must be used especially in the sit ting position where significant post-op
pneum ocephalus and air embolism are common. The risk of tension pneumocephalus may be
reduced by filling the cavit y with fluid in conjunction with turning o N2 O about 10 minutes prior to
completion of dural closure. See Pneumocephalus (p. 887).
Halogenat ed agent s
Agen ts in prim ar y usage today are sh ow n below. All suppress EEG activit y an d m ay provide som e
degree of cerebral protect ion .
Drug info : Isoflurane (Forane®)
Can produce isoelectric EEG without m etabolic toxicit y. Im proves neurologic outcome in cases of
incomplete global ischem ia (although in experim ental studies on rats, the am ount of tissue injury
was greater than with thiopental7 ).
Drug info : Desflurane (Suprane®)
A cerebral vasodilator, increases CBF and ICP. Decreases CMRO2 which tends to cause a compensatory
Drug info : Sevoflurane (Ult ane®)
Mildly increases CBP and ICP, and reduces CMRO2 . Mild negative inotrope, cardiac output not as well
maintained as with isoflurane or desflurane.
4.2.2 Int ravenous anest het ic agent s
Agent s generally used for induct ion
1. propofol: exact m ech an ism of action un kn ow n . Sh ort h alf–life w ith n o act ive m etabolites. May
be used for in duct ion an d as a con tin uous in fusion durin g total in traven ous an esth esia (TIVA).
Causes dose depen den t decrease in m ean arterial blood pressure (MAP) an d ICP. See also in form ation oth er th an use in in duct ion (p. 106). Is m ore rapidly cleared th an , an d h as largely
replaced, th iopen tal
2. barbiturates: produce sign ifican t reduct ion in CMRO2 an d scaven ge free radicals am ong oth er
e ect s (p. 1202). Produce dose-depen den t EEG suppression w h ich can be taken all th e w ay to isoelect ric. Min im ally a ect EPs. Most are an ticonvulsan t, but m eth oh exital (Brevital®) (p. 132) can
low er th e seizure th reshold. Myocardial suppression an d periph eral vasodilatat ion from barbiturates m ay cause hypoten sion an d com prom ise CPP, especially in hypovolem ic pat ien ts
sodium th iopen tal (Pen toth al®): th e m ost com m on agen t. Rapid on set, sh ort acting. Min im al
e ect on ICP, CBF an d CMRO2
3. etom idate (Am idate®): a carboxylated im idazole derivative. An esth etic an d am n estic, but n o
an algesic properties. Som etim es produces m yoclon ic act ivit y w h ich m ay be con fused w ith seizures. Im pairs ren al fun ct ion an d sh ould be avoided in patien ts w ith kn ow n ren al disease. May
General and Neurology
produce adren al in su cien cy. See Miscellan eous drugs in n euroan esth esia (p. 106) for in form ation oth er th an use in in duction .
4. ketam in e: NMDA receptor an tagon ist. Produces a dissociative an esth esia. Main tain s cardiac output. May sligh tly in crease both h eart rate an d blood pressure. ICP in creases in parallel w ith
in creased cardiac out put.
Narcot ics in anest hesia
Nonsynthet ic narcotics
Narcotics in crease CSF absorpt ion an d m in im ally reduce cerebral m etabolism . Th ey slow th e EEG but
w ill not produce an isoelect ric t racin g. All n arcotics cause dose-depen den t respirator y depression
w h ich can result in hypercarbia an d con com itan t in creased ICP in n on -ven tilated pat ien ts. Often also
con tribute to post-op N/V
Morph in e: does n ot sign ifican tly cross th e BBB.
Disadvan tages in n euro patien ts:
1. causes h istam in e release w h ich
a) m ay produce hypoten sion
b) m ay cause cerebrovascular vasodilation → in creased ICP8 (p 1593)
c) th e above togeth er m ay com prom ise CPP
2. in ren al or h epatic in su cien cy, th e m etabolite m orph in e-6-glucuron ide can accum ulate w h ich
m ay cause con fusion
Synthetic narcot ics
Th ese do not cause h istam in e release, un like m orph in e an d m eperidin e.
Rem ifen tan il (Ultiva®); see also detailed in form ation (p. 133): reduces CMRO2 , CBV an d ICP.
Large doses m ay be n eurotoxic to lim bic system an d associated areas. May be used for aw ake cran iotom y (p. 1432).
Fen tanyl: crosses th e BBB. Reduces CMRO2 , CBV an d ICP. May be given as bolus an d/or as a con tin uous in fusion .
Sufen tan il: m ore poten t th en fen tanyl. Does n ot in crease CBF. Raises ICP (m ay be due to hypoven tilation – w h ich can occur w ith any n arcotic) an d is th us often n ot appropriate for n eurosurgical
cases. Expen sive.
4.2.3 Miscellaneous drugs in neuroanest hesia
Ben zod iazep in es. Th ese drugs are GABA agon ists an d decrease CMRO2 . Th ey also provide an ticonvulsan t action an d produce am n esia. See also agen ts an d reversal (p. 205).
Etom id at e (p. 105) . Used prim arily for in duct ion (p. 105).
a cerebrovasocon strictor w h ich th erefore: reduces CBF an d ICP; reduces CMRO2 but n o lon ger prom oted as a cerebral protectan t based on experim en tal studies 9 an d a drop in pBtO2 w ith tem porar y MCA clipping 10
does n ot suppress brain stem act ivity
suppresses adren ocort ical fun ction cort isol product ion . Th is usually occurs w ith prolonged
adm in istration , but can occur even after single dose for in duct ion an d m ay persist up to 8 h rs (n o
adverse outcom es from sh ort-term suppression h ave been reported)
in creases activit y of seizure foci w h ich m ay be used for m appin g foci durin g seizure surger y but
m ay also in duce seizures
Prop ofol. A sedative hypn otic. Useful for in duct ion (p. 105). Reduces cerebral m etabolism , CBF
and ICP. Has been described for cerebral protect ion (p.1203) an d for sedation (p. 133). Sh ort h alf–life
perm its rapid aw aken in g w h ich m ay be useful for aw ake cran iotom y (p. 1434). Not an algesic.
Lid ocain e. Given IV, suppresses lar yn geal reflexes w h ich m ay h elp blun t ICP elevation s th at n orm ally follow en dotrach eal in tubation or suct ion in g. An t iconvulsan t at low doses, m ay provoke seizures at h igh con cen tration s.
Esm olol. Selective beta-1 adren ergic an tagon ist, blun ts th e sym path et ic respon se to lar yn goscopy
and in tubation . Less sedating th an equipoten t doses of lidocain e or fen tanyl used for th e sam e purpose. Half life: 9 m in utes. See also dosin g, etc. (p.127)
Neuroanest hesia
Dexm ed et om id in e (Preced ex®). Alph a 2 adren ergic receptor agon ist, used for con trol of hyperten sion post operat ively, as w ell as for its sedatin g qualit ies durin g aw ake cran iotom y eith er alon e or
in conjun ct ion w ith propofol (p.105). Also used to h elp patien ts tolerate en dotracheal t ube w ith out
sedatives/n arcotics to facilitate extubation .
4.2.4 Paralyt ics for int ubat ion
Paralyt ics (n eu rom u scu lar blockin g agen t s (NMBA)): ad m in istered t o facilit ate t rach eal in t u bat ion an d to im p rove su rgical con d it ion s w h en in d icated . Ad m in ist rat ion of p aralyt ics id eally
sh ou ld alw ays be gu id ed by n eu rom u scu lar t w itch m on itor in g. Also see Sed at ives & p aralyt ics
(p. 132). In ad d it ion to p aralyt ics, all con sciou s p at ien t s sh ou ld also receive a sed at ive to blu n t
aw aren ess.
Paralytics sh ould n ot be given un t il it h as been determ in ed th at patien t can be ven tilated m an ually, un less t reatin g lar yn gospasm (m ay be tested w ith th iopen tal). Use w ith caution in n on -fixated
patien ts w ith un stable C-spin e.
Due to lon g action , pan curon ium (Pavulon ®) is n ot in dicated as th e prim ar y paralyt ic for in tubat ion , but m ay be useful on ce patien t is in t ubated or in low dose as an adjun ct to succinylch olin e.
Drug info : Succinylcholine (Anect ine®)
The only depolarizing agent. May be used to secure airway for em ergency intubation, but due to
possible side e ect s (p. 135), should not be used acut ely following injury or in adolescent s or
children (a short acting nondepolarizing blocker is preferred). May transiently increase ICP. Prior
dosing with 10% of the ED95 dose of a non-depolarizing m uscle relaxant reduces m uscle
Intubating dose: 1–1.5 mg/kg (supplied as 20 m g/m l → 3.5–5 cc for a 70 kg patient), onset 60–
90 sec, duration 3–10 min, may repeat same dose × 1.
Drug info : Rocuronium (Zem uron®)
Intermediate acting, am inosteroid, non-depolarizing muscle relaxant. The only nondepolarizing neurom uscular blocking agent approved for rapid sequence intubation. Duration of action and onset are
dose dependent.
(p. 135).
Drug info : Vecuronium (Norcuron®)
See details (p. 136).
Aminosteroid with activit y sim ilar to that of rocuronium , however, does not cause histamine
release and is not approved for rapid sequence intubation. .
Drug info : Cisat racurium (Nim bex®)
See details (p. 136).
Metabolized by Ho man degradation (tem perature dependent), intermediate acting, no significant increases in histamine.
4.3 Anest het ic requirem ent s for int ra-operat ive evoked
pot ent ial m onit oring
For details of in t ra-operative evoked poten tial (EP) m on itoring itself, see In t ra-op erat ive evoked
p oten t ials (p. 239).
General and Neurology
All volatile an esth etics produce dose-depen den t reduct ion in SSEP peak am plitu de an d an
in crease in peak laten cy. Adding n it rous oxide in creases th is sen sitivity to an esth etic agen ts.
An esth esia issues related to in tra-operative evoked poten tial (EPs) m on itorin g:
1. in duct ion : m in im ize pen toth al dose (produces ≈ 30 m in utes of suppression of EPs), or use etom idate (w h ich in creases both SSEP am plitu de an d laten cy 11 )
2. total in t raven ous an esth esia (TIVA) is ideal (i.e. n o in h alat ional agen ts)
3. n itrous/n arcot ic tech n ique is a distan t secon d ch oice
4. if in h alation al an esth etic agen ts are required:
a) use < 1 MAC (m axim al alveolar con cen tration ), ideally < 0.5 MAC
b) avoid older agen ts such as Haloth an e
5. n on depolarizing m uscle relaxan ts h ave litt le e ect on EP (in m on keys 12 )
6. propofol h as a m ild e ect on EP: total an esthesia w ith propofol causes less EP depression th an
in h alation al agen ts at th e sam e depth of an esth esia 13
7. ben zodiazepin es h ave a m ild-to-m oderate depressan t e ect on EPs
8. con tin uous in fusion of an esth etic drugs is preferred over in term itten t boluses
9. SSEPs can be a ected by hyper- or hypo-th erm ia, an d ch anges in BP
10. hypocapn ia (dow n to en d tidal CO2 = 21) causes m in im al reduct ion in peak laten cies 14
11. an t iepilept ic drugs: ph enytoin , carbam azipin e an d ph en obarbital do n ot a ect SSEP15
4.4 Malignant hypert herm ia
4.4.1 General inform at ion
Malign an t hyper th erm ia (MH) is a hyperm etabolic state of skeletal m uscle due to idiopath ic block of
Ca + + re-en tr y in to sarcoplasm ic reticulum . Tran sm itted by a m ultifactorial gen et ic predisposition .
Total body O2 con sum ption in creases × 2–3.
In ciden ce: 1 in 15,000 an esth etic adm in istration s in peds. 1 in 40,000 adults. 50% h ad previous
an esth esia w ith out MH. Frequen tly associated w ith adm in istration of h alogen ated in h alation al
agen ts an d th e use of succinylch olin e (fulm in an t form : m uscle rigidit y alm ost im m ediately after succinylch olin e, m ay involve m asseters → di cult y in tubatin g). In it ial attack an d recrudescen ce m ay
also occur post-op. 30% m ortalit y.16
4.4.2 Present at ion
1. earliest possible sign : increa se in en d-tidal pCO2
2. tachycardia (early) an d oth er arrhyth m ias
3. w ith progression :
a) coagulation disorder (DIC) (bleedin g from surgical w oun d an d body orifices)
b) ABG: in creasing m etabolic acidosis & decreasing pO2
c) pulm on ar y edem a
d) elevated body tem perat ure (m ay reach ≥ 44° C (113° F) at rate of 1° C/5-m in ) (n orm al pat ien ts
becom e hypoth erm ic w ith gen eral an esthesia)
e) lim b m uscle rigidit y (com m on , but late)
f) rh abdom yolysis → elevated CPK & m yoglobin (late)
4. term in al:
a) hypoten sion
b) bradycardia
c) cardiac arrest
4.4.3 Treat m ent
1. elim in ate o en din g agen ts (stop th e operation , D/C in h alation an esth esia an d ch ange t ubin g on
an esth esia m ach in e)
2. dan trolen e sodium (Dan trium ®) 2.5 m g/kg IV usually e ect ive, in fuse un til sym ptom s subside,
up to 10 m g/kg
3. hyper ven tilation w ith 100%O2
4. surface an d cavit y cooling: IV, in w oun d, per NG, PR
5. bicarbon ate 1–2 m Eq/kg for acidosis
6. IV in sulin an d glucose (low ers K+, glucose acts as en ergy substrate)
7. procain am ide for arrhyth m ias
8. diuresis: volum e loading + osm otic diuretics
Neuroanest hesia
4.4.4 Prevent ion
1. iden tification of patien ts at risk:
a) on ly reliable test: 4 cm viable m uscle biopsy for in -vitro tests at a few region al test cen ters
(abn orm al con tract ure to ca ein e or h aloth an e)
b) fam ily h istor y: any relative w ith syn drom e puts pat ien t at risk
c) related traits: 50% of MH patien ts h ave h eavy m usculature, Duch en n e t ype m uscular dyst rophy, or scoliosis
d) patien ts w h o exh ibit m asseter spasm in respon se to succinylch olin e
2. in patien ts at risk: avoid succinylch olin e (n on depolarizing blockers preferred if paralysis essen t ial), m ay safely h ave n on -h alogen ated an esth etics (n arcotics, barbiturates, ben zodiazepin es, droperidol, n it rous…)
3. prophylact ic oral dan trolen e: 4–8 m g/kg/day for 1–2 days (last dose given 2 h rs before an esth esia) is usually e ect ive
[1] Sch n eider AJ. Assessm en t of Risk Factors an d Surgical Ou tcom e. Su rg Clin N Am . 1983; 63:1113–1126
[2] Vacan t i CJ, Van Houten RJ, Hill RC. A Statist ical An alysis of th e Relation sh ip of Physical Stat us to Postoperative Mortalit y in 68,388 Cases. An esth An alg
Cu rr Res. 1970; 49:564–566
[3] Mar x GF, Mateo CV, Orkin LR. Com p uter An alysis of
Postan esth etic Death s. An esth esiology. 1973;
[4] Benveniste R, Germ an o IM. Evaluat ion of factors
predict in g accu rate resect ion of h igh -grad e gliom as
by u sin g fram eless im age-gu id ed stereotactic gu id an ce. Neu rosu rg Focus. 2003; 14
[5] Mar tin A, Rojas S, Ch am orro A, Falcon C, Bargallo N,
Plan as AM. W h y does acute h yperglycem ia w orsen
th e ou tcom e of tran sien t focal cerebral isch em ia?
Role of cort icosteroids, in flam m ation , an d protein
O-glycosylation . Stroke. 2006; 37:1288–1295
[6] Raggio JF, Fleisch er AS, Su n g YF, et al. Exp an din g
Pn eu m oceph alus d ue to Nitrou s Oxide An esth esia:
Case Repor t . Neu rosurger y. 1979; 4:261–263
[7] Dru m m on d JC, Cole DJ, Patel PM, Reyn old s LW .
Focal Cerebral Isch em ia durin g An esthesia w ith Etom idate, Isofluoran e, or Th iopental: A Com parison of
th e Exten t of Cerebral Inju r y. Neurosurger y. 1995;
[8] Sh ap iro HM, Miller RD. In : Neu rosu rgical An esth esia and In t racran ial Hyperten sion . An esth esia. 2n d
ed. New York: Church ill Livingston e; 1986:1563–
[9] Dru m m on d JC, McKay LD, Cole DJ, Patel PM. Th e
role of n it ric oxid e syn th ase in h ibit ion in th e
ad verse e ects of etom idate in th e settin g of focal
cerebral isch em ia in rats. An esth An alg. 2005;
100:841–6, table of con ten ts
Ho m an W E, Ch arbel FT, Ed elm an G, Misra M, Au sm an JI. Com parison of th e e ect of etom idate and
desfluran e on brain t issue gases an d p H durin g prolon ged m id dle cerebral arter y occlu sion . An esth esiology. 1998; 88:1188–1194
Koh t A, Sch utz W , Sch m idt G, Sch ram m J, Watan abe
E. E ects of etom idate, m idazolam , an d thiopen tal
on m ed ian n er ve som atosen sor y evoked p oten t ials
an d th e add itive e ects of fentan yl an d n it rous
oxide. An esth An alg. 1988; 67:435–441
Sloan TB. Nondepolarizing n eurom uscular blockade
does n ot alter sen sor y evoked poten t ials. J Clin
Mon it. 1994; 10:4–10
Liu EH, Won g HK, Chia CP, Lim HJ, Chen ZY, Lee TL.
E ects of isofluran e and propofol on cort ical som atosen sor y evoked poten tials du rin g com p arable
dep th of anaesth esia as gu ided by bispectral in dex.
Br J An aesth . 2005; 94:193–197
Sch u bert A, Dru m m on d JC. Th e e ect of acute hypocapn ia on h u m an m edian n er ve som atosen sor y
evoked responses. An esth An alg. 1986; 65:240–244
Borah NC, Math esh w ari MC. E ect of an t iepileptic
dru gs on sh ort-latency som atosen sor y evoked
poten tials. Acta Neu rol Scand. 1985; 71:331–333
Nelson TE, Flew ellen EH. Th e Malign an t Hyperth erm ia Syn drom e. N En gl J Med . 1983; 309:416–418
Explore flashcards