NEURO anesthesie

4 Neuroanesthesia
4.1 General information
Table 4.1 sh ow s th e Am er ican Societ y of An est h e siologists (ASA) gr ad in g system t o est im ate an e s-
thetic risk for various conditions.
For issu es relat e d t o in t r acran ia l p ressu re (ICP), cerebral p e r fusion p ressu re (CPP), in t r a cran ial
constituents, etc., see ICP principles (p.856). For cerebral blood flow (CBF) and cerebral metabolic
rate ofoxygen consumption (CMRO2), see CBF and oxygen utilization (p.1264).
Param eters of primary relevance to neurological surgery that can be m odulated by the
anesthesiologist:
1. blood pressure: one of the factors that determines CPP as well as spinal cord perfusion. May
need to be manipulated (e.g. reduced when working on an aneurysm, or increased to enhance
collateral circulation during cross clamping). Measurement by arterial line is most accurate and
depending on the patient’s presentation and the planned procedure, often should be placed pri-
or to induction of anesthesia. For intracranial procedures, the arterial line should be calibrated
at the external auditory meatus to most closely reflect intracranial blood pressure
2. jugular venous pressure: one of the factors that influences ICP
3. arterial CO2tension (PaCO2): CO2is the most potent cerebral vasodilator. Hyperventilation
reduces PaCO2(hypocapnea) which decreases CBV but also CBF. Goal is generally end tidal
CO2(ETCO2) of 25–30 mm Hg with a correlating PaCO2of 30–35. Use with care for stereo-
tactic procedures to minimize shift of intracranial contents when using this method to con-
trol ICP4
4. arterial O2tension
5. hematocrit: in neurosurgery it is critical to balance oxygen carrying capacity (decreased by ane-
mia) against improved blood rheology (impaired byelevated Hct)
6. patient temperature: mild hypothermia provides some protection against ischemia by reducing
the cerebral metabolic rate of oxygen (CMRO2) by ≈7% for each 1° C drop
7. blood glucose level: hyperglycemia exacerbates ischemic deficits5
8. CMRO2: reduced with certain neuro-protective agents and by hypothermia which helps protect
against ischemic injury
9. in cases where a lumbar drain or a ventricular drain has been placed: CSF output
10. elevation of the head of the patient: lowering the head increases arterial blood flow, but also
increases ICP by im pairing venous outflow
11. intravascular volume: hypovolemia can impair blood flow in neurovascular cases. In surgery in
the prone position, excessive fluids may contribute to facial edema which is one of the risk fac-
tors for PION (p.1056)
12. positioning injuries: during the procedure, the patient’s position may change and be unnoticed
due to draping. Careful and frequent examination of the patient’s position may prevent injuries
associated with prolonged malpositioning
13. post operative nausea and vomiting (PONV): may adversely a ect ICP and may negatively
impact recent cervical surgical procedures. Avoidance of anesthetic agents know n to cause
PONVor pretreatment to prevent PONV m ay be prudent
4.2 Drugs used in neuroanesthesia
4.2.1 Inhalational agents
Ge n e ra l in fo rm a t io n
Most reduce cerebral metabolism (except nitrous oxide) by suppressing neuronal activity.
Th ese agen t s d ist u rb cer ebr al a u t or e gu lat ion a n d cau se cer eb r al vaso d ilat at ion w h ich
increases cerebral blood volume (CBV) and can increase ICP. With adm inistration >2 hrs they
increase CSF volum e which can also potentially contribute to increased ICP. Most agents
increase the CO2reactivity of cerebral blood vessels. These agents a ect intra-operative EP
monitoring (p.107).
Gene ra l a n d Ne uro lo gy
4
104
Ebooksmedicine.net

Drug info : Nitrous oxide
A p o t e n t va s o d ila t o r t h a t m a r ke d ly in c r e a s e s CBF a n d m in im a lly in c re a s e s c e re b r a l m e t a b o lis m . Co n -
tributes to post-op N/V.
Nitrous oxide, pneum ocephalus and air em bolism : Th e solub ilit y of nit ro u s o xid e (N2O) is ≈34
times that of nitrogen.6When N2O comes out of solution in an airtight space it can increase the pres-
sure which may convert pneumocephalus to “tension pneumocephalus.”It m a y also a g g ra va t e a ir
embolism. Thus caution must be used especially in the sitting position where significant post-op
pneumocephalus and air embolism are common. The risk of tension pneumocephalus may be
reduced by filling the cavity with fluid in conjunction with turning o N2O about 10 minutes prior to
completion of dural closure. See Pneumocephalus (p.887).
Halogenated agents
Age n t s in p rim ar y u sage t od ay a r e sh ow n below . All su p p r ess EEG act ivit y a n d m ay p r ovid e som e
degree of cerebral protection.
Drug info : Isoflurane (Forane®)
Can produce isoe lect ric EEG wit hout m et abolic t oxicit y. Im p roves neurolog ic outcom e in case s of
incom plete global ische m ia (although in experim ent al st udies on rat s, t he am ount of t issue injury
was greater than with thiopental7).
Drug info : Desflurane (Suprane®)
A c e re b r a l va s o d ila t o r, in c re a s e s CBF a n d ICP. De c r e a se s CMRO2which tends to cause a compensatory
vasoconstriction.
Drug info : Sevoflurane (Ult ane®)
Mild ly incre ase s CBP and ICP, a nd re duce s CMRO2. Mild negative inotrope, cardiac output not as well
maintained as with isoflurane or desflurane.
4.2.2 Intravenous anesthetic agents
Ag e n t s g e n e ra lly u se d fo r in d u ct io n
1. propofol: exact mechanism of action unknown. Short half–life with no active metabolites. May
be used for induction and as a continuous infusion during total intravenous anesthesia (TIVA).
Ca u se s d ose d e p en d e n t d e cr ea se in m e an a r t er ial b lo o d p r e ssu re (MAP) a n d ICP. Se e a lso in fo r -
mation other than use in induction (p.106). Is more rapidlycleared than, and has largely
replaced, thiopental
2. barbiturates: produce significant reduction in CMRO2and scavenge free radicals among other
e ects (p.1202). Produce dose-dependent EEG suppression which can be taken all the way to iso-
electric. Minimally a ect EPs. Most are anticonvulsant, but methohexital (Brevital®) (p.132) can
lower the seizure threshold. Myocardial suppression and peripheral vasodilatation from barbitu-
rates may cause hypotension and compromise CPP, especially in hypovolemic patients
sodium thiopental (Pentothal®): the most common agent. Rapid onset, short acting. Minimal
e ect on ICP, CBFand CMRO2
3. etomidate (Amidate®): a carboxylated imidazole derivative. Anesthetic and amnestic, but no
analgesic properties. Sometimes produces myoclonic activity which may be confused with seiz-
ures. Impairs renal function and should be avoided in patients with known renal disease. May
Neuroanest hesia
4
105
Ebooksmedicine.net

produce adrenal insu ciency. See Miscellaneous drugs in neuroanesthesia (p.106) for informa-
tion other than use in induction.
4. ketamine: NMDA receptor antagonist. Produces a dissociative anesthesia. Maintains cardiac out-
put. May slightly increase both heart rate and blood pressure. ICP increases in parallel with
increased cardiac output.
Narcotics in anest hesia
Nonsynthet ic narcot ics
Narcotics increase CSF absorption and m inim ally reduce cerebral m etabolism . They slow the EEG but
will not produce an isoelectric tracing. All n ar co t ics ca u se d ose- d ep e n d e n t re sp ir ato r y d e p r ession
which can result in hypercarbia and concomitant increased ICP in non-ventilated patients. Often also
contribute to post-op N/V
Morphine: does not significantly cross the BBB.
Disadvan tages in n euro patients:
1. causes histamine release which
a) may produce hypotension
b) may cause cerebrovascular vasodilation →increased ICP8(p 1593)
c) the above together may compromise CPP
2. in renal or hepatic insu ciency, the metabolite morphine-6-glucuronide can accum ulate which
may cause confusion
Synt he t ic n arcot ics
Th e se d o not cause histamine release, unlike morphine and meperidine.
Re m ife n t a n il (Ult iva ®); se e also d e t aile d in fo r m at io n (p . 1 3 3 ): r e d u ce s CMRO2, CBV and ICP.
La r g e d o s e s m a y b e n e u r o t o x ic t o lim b i c s ys t e m a n d a s s o c ia t e d a r e a s . M a y b e u s e d fo r a w a k e c r a -
niotomy (p.1432).
Fen t anyl: crosse s t h e BBB. Red u ce s CMRO2, CBV and ICP. May be given as bolus and/or as a contin-
uous infusion.
Sufen tan il: m ore potent th en fen tanyl. Does n ot in crease CBF. Raise s ICP (m ay be d u e t o h ypo -
ventilation –which can occur with any narcotic) and is thus often not appropriate for neurosurgical
cases. Expensive.
4.2.3 Miscellaneous drugs in neuroanesthesia
Be n zo d ia ze p in e s. Th e se d ru gs a re GABA agon ist s an d d e cr ea se CMRO2. They also provide anti-
convulsant action and produce amnesia. See also agents and reversal (p.205).
Etom id at e (p.105) .Used prim arily for induction (p.105).
●a cerebrovasoconstrictor which therefore: reduces CBFand ICP; reduces CMRO2but no longer pro-
moted as a cerebral protectant based on experimental studies9and a drop in pBtO2with tempo-
rary MCA clipping10
●does not suppress brainstem activity
●suppresses adrenocortical function cortisol production. This usually occurs with prolonged
administration, but can occur even after single dose for induction and may persist up to 8 hrs (no
adverse outcomes from short-term suppression have been reported)
●increases activity of seizure foci which may be used for mapping foci during seizure surgery but
may also induce seizures
Propofol. A se d a t ive h yp n ot ic. Usefu l fo r in d u ct ion (p . 10 5). Re d u ces ce r ebr a l m e t a bo lism , CBF
and ICP. Has been described for cerebral protection (p.1203) and for sedation (p.133). Short half–life
permits rapid awakening which may be useful for awake craniotomy (p.1434). Not analgesic.
Li d o c a i n e . Given IV, suppresses laryn geal reflexes w hich m ay help blunt ICP elevation s that n or-
mally follow endotracheal intubation or suctioning. Anticonvulsant at low doses, may provoke seiz-
ures at high concentrations.
Esm olol. Selective beta-1 adren ergic ant agon ist, blu n ts th e sym path et ic resp on se to lar yn goscopy
and intubation. Less sedating than equipotent doses of lidocaine or fentanyl used for the same pur-
pose. Half life: 9 minutes. See also dosing, etc. (p.127)
Gene ra l a n d Ne uro lo gy
4
106
Ebooksmedicine.net

Dexm edetom idin e (Precedex®). Alp h a 2 ad re n e r gic r e ce pt o r ago n ist , u se d for co n t r ol o f h yp e r -
tension post operatively, as well as for its sedating qualities during awake craniotomy either alone or
in conjunction w ith propofol (p.105). Also used to help patients tolerate endotracheal tube without
sedatives/narcotics to facilitate extubation.
4.2.4 Paralytics for intubation
Paralytics (neurom uscular blocking agents (NMBA)): adm inistered to facilitate tracheal intuba-
tion and to improve surgical conditions when indicated. Administration of paralytics ideally
should always be guided by neuromuscular twitch monitoring. Also see Sedatives & paralytics
(p.132). In addition to paralytics, all conscious patients should also receive a sedative to blunt
awareness.
Paralytics should not be given until it has been determ ined that patient can be ventilated m an-
ually, unless treating laryngospasm (may be tested with thiopental). Use with caution in non-fixated
patients with unstable C-spine.
Due to long action, pancuronium (Pavulon®) is not indicated as the prim ary paralytic for intuba-
tion, but may be useful once patient is intubated or in low dose as an adjunct to succinylcholine.
Drug info : Succinylcholine (Anect ine®)
Th e o n ly d e p ola rizin g ag en t . May b e u se d t o se cu re air wa y fo r e m e rg en c y in t u ba t io n , b ut d u e t o
possible side e ects (p.135), should not be used acutely following injury or in adolescents 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 muscle relaxant reduces muscle
fasciculations.
Int u b at in g d o se : 1 –1.5 mg/kg (supplied as 20 mg/ml →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®)
Int e rm e d ia t e act in g , a m in ost e ro id , n on -d e p o larizin g m u scle re laxa n t . Th e o nly no nd e p ola rizin g n e u-
romuscular blocking agent approved for rapid sequence intubation. Duration of action and onset are
dose dependent. (p. 135).
Drug info : Vecuronium (Norcuron®)
See det ails (p. 136).
Am in o s t e ro id w it h a c t ivit y s im ila r t o t h a t o f ro c u r o n iu m , h o w e ve r, d o e s n o t c a u s e h is t a m in e
release and is not approved for rapid sequence intubation. .
Drug info : Cisat racurium (Nim bex®)
See det ails (p. 136).
Met ab o lize d by Ho man degradation (temperature dependent), intermediate acting, no signifi-
cant increases in histamine. 
4.3 Anesthetic requirements for intra-operative evoked
potential monitoring
For d et ails of in t ra-op er a tive e voked p ot e n t ial (EP) m on it or in g it self, se e In tra-operative evoked
potentials (p.239).
Neuroanest hesia
4
107
Ebooksmedicine.net

All volat ile a n e st h et ics p r o d u ce d ose - d e p e n d e n t r e d u ct ion in SSEP p e a k am p lit u d e an d a n
increase in peak latency. Adding nitrous oxide increases this sensitivity to anesthetic agents.
An esth esia issu e s r ela t e d t o in t r a -op er at ive e voke d p ote n t ia l (EPs) m on it or in g:
1. induction: minimize pentothal dose (produces ≈30 minutes of suppression of EPs), or use eto-
midate (which increases both SSEP amplitude and latency11)
2. total intravenous anesthesia (TIVA) is ideal (i.e. no inhalational agents)
3. nitrous/narcotic technique is a distant second choice
4. if inhalational anesthetic agents are required:
a) use <1 MAC (maximal alveolar concentration), ideally <0.5 MAC
b) avoid older agents such as Halothane
5. nondepolarizing muscle relaxants have little e ect on EP (in monkeys12)
6. propofol has a mild e ect on EP: total anesthesia with propofol causes less EP depression than
inhalational agents at the same depth of anesthesia13
7. benzodiazepines have a mild-to-moderate depressant e ect on EPs
8. continuous infusion of anesthetic drugs is preferred over intermittent boluses
9. SSEPs can be a ected by hyper- or hypo-thermia, and changes in BP
10. hypocapnia (down to end tidal CO2=21) causes minimal reduction in peak latencies14
11. antiepileptic drugs: phenytoin, carbamazipine and phenobarbital do not a ect SSEP15
4.4 Malignant hyperthermia
4.4.1 General information
Malignant hyperthermia (MH) is a hypermetabolic state of skeletal muscle due to idiopathic block of
Ca ++ re-entry into sarcoplasmic reticulum. Transmitted by a multifactorial genetic predisposition.
To t a l b o d y O 2consumption increases ×2–3.
In cid en ce: 1 in 15,000 an esthetic adm inistration s in p ed s. 1 in 40,000 adu lts. 50% h ad previous
anesthesia without MH. Frequently associated with administration of halogenated inhalational
agents and the use of succinylcholine (fulminant form: muscle rigidity almost immediately after suc-
cinylcholine, may involve masseters →di culty intubating). Initial attack and recrudescence may
also occur post-op. 30% mortality.16
4.4.2 Presentation
1. earliest possible sign: increase in end-tidal pCO2
2. tachycardia (early) and other arrhythmias
3. with progression:
a) coagulation disorder (DIC) (bleeding from surgical wound and body orifices)
b) ABG: increasing metabolic acidosis & decreasing pO2
c) pulmonary edema
d) elevated body temperature (may reach ≥44° C (113° F) at rate of 1° C/5-min) (normal patients
become hypothermic with general anesthesia)
e) limb muscle rigidity (common, but late)
f) rhabdomyolysis →elevated CPK & myoglobin (late)
4. terminal:
a) hypotension
b) bradycardia
c) cardiac arrest
4.4.3 Treatment
1. eliminate o ending agents (stop the operation, D/C inhalation anesthesia and change tubing on
anesthesia machine)
2. dantrolene sodium (Dantrium®) 2.5 mg/kg IV usually e ective, infuse until symptoms subside,
up to 10 mg/kg
3. hyperventilation with 100% O2
4. surface and cavity cooling: IV, in wound, per NG, PR
5. bicarbonate 1–2 mEq/kg for acidosis
6. IV insulin and glucose (lowers K
+, glucose acts as energy su bstrate)
7. procainamide for arrhythmias
8. diuresis: volume loading+osmotic diuretics
Gene ra l a n d Ne uro lo gy
4
108
Ebooksmedicine.net