UPDATED REVIEW IN
NEUROSURGICAL
ANESTHESIOLOGY AND
NEURO-CRITICAL CARE
RAMSIS F. GHALY, MD, FACS
DEPARTMENT OF
ANESTHESIOLGY AND PAIN
MANAGEMENT, ADVOCATE
ILLINOIS MASONIC MEDICAL
CENTER
GHALY NEUROSURGICAL
ASSOCIATES
CBF: METHODOLOGY
• Methodology: (Kety Schmidt Technique):
Consumption of a substance by an organ is the
product of blood flow and arteriovenous (arterial
and juglar bulb) difference for that substance with
knowledge od blood-brain partition coefficient.
Indicators: Diffusable substance e.g. N2O, Xe,
Ar133, Kr85, Non-diffusable e.g. microsphere.
Arteriovenous sampling over 10-14min Or external
detection of washout with scintillation detectors
post xenon inhalation/injection. Tomographic
method: enhancement by stable Xe. PET will
require Cyclotron-produced short lived radio
isotopes. MRSpectroscopy measures brain
substrates like ATP and others.
CEREBRAL METABOLIC
RATE
• CMR=CBF/ARTERIOVENOUS DIFFERENCE
• CMRO2 relatively stable and no change with PaCO2 2080mmHg
• COUPLING: Maintenance of CBF:CMRO2 ratio (14-18) i.e.↑
in acivated areas and ↓ in unstimulated areas)
• O2 3.3ML/100G/MIN (brain 20%O2 uptake while <2% body
weight) 60% for functional & 40% for neuronal integrity
• GLUCOSE 4.5ml/100g/min (substrate for mature brain)
95% Aerobic produces efficient energy & 5% Anaerobic
produces lactate and inefficient energy
• LACTATE 0.56ml/100g/min
• ATP 9umol/g/min
CEREBRAL METABOLIC RATE
(CMR)
•
•
CMR (CBF / Arterio-venous difference)
O2 3.3 mL/100g/min
•
Glucose 4.5 mL/100g/min
•
•
•
•
Lactate 0.56mL/100g/min
ATP 9 umol/g/min
Oxygen requirements: 60% Functional 40% integrity
Glucose, substrate for mature brain
95% Aerobic efficient energy
5% Anaerobic Lactate Lactate + inefficient energy
•
Energy stores are SCANT
•
•
ATP + ½ ADP
Energy Charge ------------------ Normal 0.87-0.96
ATP + ADP + AMP
Inadequate O2 Delivery  O2 – Glucose Index
Lactate –glucose Index
Phosphocreatine 
Global CMRO2 relatively stable (but varies with age)
No CMRO2 with PaCO2 20-80 mmHg
Coupling
Maintenance CBF:CMRO2 Ratio (14-18 normocapnia)
Regional  Activated areas and  unstimulated areas
CNS HYPOTHERMIA
• Hypothermia ↓neuronal metabolism and cellular
hemeostasis
• CO2 reactivity is maintained during moderate and
deep hypothermia
• CBF:CMR coupling is maintained during moderate
hypothermia
• Hypothermia causes relative pH alkalinity & ↓blood
gas solubility
• Brain cooling occurs faster during hypercarbia
• Prolonged hypothermia is determintal: metabolic
acidosis, ↑SVR↓COP, arrythemiacoagulopathy,
infection, shivering, irreversible shock in
rewarming
• Prolonged drug effects by hypothermia
HYPOTHERMIC BRAIN
• Q10= ratio of two metabolic rates
separated by 10ºC. A ration of 2 means
that a 10ºC decrease in temp. result in a
50% decrease in metabolism (animal=2-3,
human>2). It is non-expotential: Q10 of
28ºC-18ºC doubled (isolectric EEG)
• Tolerance to ischemia:
37ºC→5min 28ºC→12min (2.4/5)
18ºC→60min(5/12) 12ºC-15ºC→>60min
* Hypothermia 30ºC+hypoxia→↓rate of
energy depletion (1/2 normothermic with
unchanged energy stores
HYPOTHERMIC BRAIN
• OXYGEN CONSUMPTION & HYPOTHERMIA
30ºC-28ºC→↓50% O2 consumption
25ºC→
↓75%
20ºC→
↓85%
18ºC-15ºC→↓90%
• Hyperthermia 37ºC-42ºC→↑CBF >42ºC→ ↑CBF (toxic)
• EEG & HYPOTHERMIA
37ºC-27ºC→↓EEG frequency (5.7% per 1ºC) ↑amplitude
27ºC-23ºC→ Burst Suppression
<21ºC
→ Isolectric
• EVOKED POTENTIAL & HYPOTHERMIA
35ºC-23ºC→ progressive ↑ latency
<20ºC-23ºC→potential loss
CEREBRAL
TEMPERATURE
• SITE
BRAIN- TYMPANIC- NASOPHARYNGEAL
(32ºC-34ºC)
• METHODS OF COOLING
ROOM
BLANKETS
INTRAVENOUS FLUID
IRRIGATION OF CENTRAL CAVITY
CEREBRAL DYNAMICS
• CVR=CPP/CBF
• CPP=MAP-ICP
• A-VO2=ARTERIO-VENOUS
(JUGLAR BULB OR SAGITTAL
SINUS OXYGEN CONTENT
DIFFERENCE
• CMRO2=CBF/A-VO2
(MAP-ICP)
CBF=
CVR
FACTORS AFFECTING
CBF: AUTOREGULATION
•
•
•
•
AUTOREGULATION: MYOGENIC INTRINSIC CAPACITY TO
MIANTAIN CBF CONSTANT OVER A WIDE RANGE OF CPP
(PRODUCT OF CVR AND BP=50-150mmHg in normotensive
patients under normal physiologic condition
IMPAIRED IN PATHOLOGICAL CONDITIONS e.g. brain tumors,
trauma, hemorrhage, metabolic, infection, encephalopathy,
ischemia, hypoxia, pharmacological
HYPERTENSION: normal autoregulation if BP controlled,
Subacute increase cause slight shift to the right, chronically
untreated causes complete shift to the right. Vascular changes
occur 1-2months and tolerance to high BP and higher ischemic
threshold. Malignant hypertension may lead to acute
hypertensive encephalopathy.
Drug-induced hypotension lower the ischemic threshold &
hypovolemic hypotension elevates the ischemic threshold
FACTORS AFFECTING
CBF
• METABOLIC (CMR)
Coupling with CMR status e.g.
sleep decrease CMR and CBF & seizure, motor activity and
intellectual exercises elevate CMR and CBF
• NEUROGENIC:
Sympathetic elevate CBF 10-15% &
parasympathetic depresses CBF.
• CO2(MOST POTENT): Mediated through
hydrogen ion in the extracellular fluid of
the vascular smooth muscle. Hyperventilation
decreases CO2 via vasoconstriction(PaCO2 20mmHg halve CBF)
& CO2 retention increases CBF (double CO2 doubles CBF) via
vasodilation
FACTORS AFFECTING
CBF
• O2: hyperoxia >300mmHg decreases CBF & hypoxia <5060mmHg increases CBF (doubles at PaO2 30mmHg via
arteriolar dilation) 1 Atmospheric O2 decrease 10-15%
CBF, hyperbaric O2 decreases CBF
• TEMPERATURE: Hypothermia reduces CBF For each 1◦C
decrease CMRO2 decrease 7%
• CEREBRAL DYNAMICS (CPP, CVR, CBV): Cardiac output
improves CBF
• RHEOLOGIC FACTORS: VISCOSITY IS DETERMINED
PRIMARILY BY HCT. HCT 33-45% normal CBF, Anemia
increases CBF and decrease CVR, Polycythemia
increases CVR and decreases CBF. Optimal O2 delivery
at HCT 30-34%
• PHARMACOLOGY: Dose-related anesthetic or drug
effects can alter vasoactive response just as BP & CO2
VOLATILE INHALED
ANESTHETIC EFFECTS
ON BRAIN METABOLISM
• HALOTHANE, ISOFLURANE, SEVOFLURANE AND
DESFLURANE ↓CMRO2 , ↓CSF PRODUCTION, AND DO NOT
ABOLISH CEREBROVASCULAR RESPONISEVENESS TO
CO2. HALOTHANE LACK BURST SUPPRESSION
• NEUROPROTECTION FOCAL AND INCOMPLETE GLOBAL
ISCHEMIA
• ↑CBF HALOTHANE>ISO-SEVO OR DESFLURANE
• In normocapnic, 0.6MAC cerebral vasodilatation
• Biphasic dose dependent effect on CBF:At 0.5MAC
↓CMRO2 counteracts the vasodilatation with no changes
on CBF. At >1 MAC→vasodilatation→↑CBF
VOLATILE
ANESTHETICS & BRAIN
• VOLATILE ANESTHETICS ↑ICP AT DOSES
>1MAC AND AUTOREGULATION IS
IMPAIRED
• ISOFLURANE, DESFLURANE &
SEVOFLURANE PRODUCE BURST
SUPPRESSION ON EEG AT 1.5-2MAC.
ENFLURANE AND SEVOFLURANE
PRODUCE EPILEPTOFORM ACTIVITY.
• VOLATILE AGENTS PRODUCE LATENCY
DELAY AND AMPLITUDE DEPRESSION ON
SSEP ARE DOSE-DEPENDENT (0.2-0.5MAC
NITROUS OXIDE AND
BRAIN METABOLISM
• N2O →↑CMRO2- ↑CBF (Cerebral vasodilation)- ↑ICP.
Coadministration of opoids, barbiturate, or propofol
• NEUROLOGIC DEFICITS IN B12 DEFICIENT PATIENTS
• HYPERHOMOCYSTEINEMIA ASSOCIATED WITH
DEMENTIA AND CEREBROVASCULAR DISEASE
• NEURODEGENERATION IN NEONATES
• SURGICAL WOUND INFECTION
• NAUSEA AND VOMITING
• INCREASE PRESSURE IN AIR CONTAINING CLOSED
SPACES
• REGARDLESS, IT IS USED DAILY WITH NO OBVIOUS ILL
EFFECT. NO WELL DOCUMENTED DETRIMENTAL OR
BENEFICIAL IMPACT ON NEUROLOGIC OR
NEUROPSYCHOLOGICAL OUTCOMES.
INTRAVENOUS
BARBITURATES &
BRAIN METABOLISM
•
•
•
•
•
•
•
•
•
•
BARBITURATES, IDEAL NEUROANESTHETIC FOR YEARS
Dose-dependent CNS depression, potent vasoconstrictor and
↓CBF, ↓CMRO2,↓ CBV & ↓ICP
MAXIMUM ↓ICP & ↓CMRO2 ACHIEVED WITH BURST
SUPPRESSION EEG.
Suppression of seizures
Membrane stabilizer and free radical scavenger
Cerebral edema, CSF secretion
NEUROPROTECTION FOR FOCAL (stroke, surgical retraction,
temporary clipping) but not for global (cardiac arrest) ischemia.
Long acting and strong hemodynamic suppressant
METHOHEXITONE activates epileptic foci and used for
electroconvulsive therapy.
MAJOR CARDIOVASCULAR AND RESPIRATORY DEPRESSANT
ESPECIALLY IN HIGH ANESTHETIC DOSES.
INTRAVENOUS
ETOMIDATE & BRAIN
METABOLISM
• NON-BARBITURATE CARBOXYLATED IMIDAZOLE
• POTENT CEREBRAL VASOCONSTRICTOR, ↓CBF, ↓CBV,
↓CMRO2 &↓ICP
• PRESERVE CO2 REACTIVITY
• FAVORABLE CBF REDISTRIBUTION
• MEMBRANE STABLIZER
• SHORT DURATION OF ACTION
• HEMODYNAMIC STABILITY
• NEUROPROTECTIVE (BURST SUPPRESSION EEG), BUT
DATA IS LACKING
• EXCITATORY SPIKES ON EEG
• MYOCLONIC MOVEMENT AND TWITCHING 50% OF
PATIENTS WITH SEIZURE LIKE ACTIVITY ON EEG
• ADRENOCORTICAL SUPPRESSION
INTRAVENOUS
BENZODIAZEPINES &
BRAIN METABOLISM
• BENZODIAZEPINES ↓CMRO2, ↓CBF
(25%-34%)
• CEILING EFFECT IN CMRO2 BY NO
BURST SUPPRESSION EEG
• NO DEMONSTRABLE EFFECT IN ICP
• PRESERVE VASOREACTIVITY
• NO DEMONSTRABLE
NEUROPROTECTIVE EFFECT
• POTENT ANTICONVULSANT EFFECT
INTRAVENOUS OPIODS
AND LIDOCAINE AND
BRAIN METABOLISM
• INTRAVENOUS OPIODS:
PRODUCE MINIMAL CHANGES
IN CMRO2 & CBF
• INTRAVENOUS LIDOCAINE ↓CBF
& ↓CMRO2
• BRAIN AUTOREGULATION IS
PRESERVED
INTRAVENOUS
DEXMEDETOMIDINE &
BRAIN METABOLISM
• SELECTIVE ALPHA 2
ADRENERGIC AGONIST, ↓CBF
WITH SIGNIFICANT CHANGES
ON CMRO2 OR ICP
• TOLERANCE AND DEPENDANCE
INTRAVENOUS
KETAMINE & BRAIN
METABOLISM
• KETAMINE, DISSOCIATIVE
ANESTHETIC
• CEREBRAL VASODILATOR,
↑CMRO2, CBF, CBV, ICP
• NORMOCAPNIA BLUNTS CBF
EFFECTS
• PRODUCES MYCLONIC
MOVEMENT BUT IT IS
ANTICONVULSANT
MUSCLE RELAXANTS
AND BRAIN
METABOLISM
• SUCCINYLCHOLINE PRODUCES
TRANSIENT ICP AND CAN BE
ATTENUATED BY
BARBITURATES OR
DEFASCICULATING DOSE OF A
NONDEPOLARIZING MUSCLE
RELAXANT
• OTHER MUSCLE RELAXANTS
HAVE NO EFFECT
CEREBRAL PERFUSIONRESERVE-STEAL
• HYPERPERFUSION AND CIRCULATORY REAKTHROUGH:
if CPP exceeds upper limit of autoregulation may lead to
arteriolar dilatation and fall in resistance and may result
in brain swelling and hemorrhage e.g. postoperative brain
swelling and ICH after AVM resection (normal pressure
perfusion breakthrough)
• HYPOPERFUSION: may lead to ischemia. CBV increases
as arterioles dilates until is exhausted and CBF decline
passively as CPP decreases. Oxygen extraction increase
to maximum as CMRO2 declines. Synaptic transmission
and neuronal function shuts down and energy is barely
enough for neuronal survival. Then membrane failure (Na,
Ca, H2O enter cell and K exit and cytotoxic edema takes
place. At such low CBF, irreversible injury and infarction
takes place and can not be corrected. Penumbra (almost
shadow) area around the infarcted portion that is
salvageable if flow restored soon
HYPERPERFUSION
• HYPERTENSION AND ↑COP →↑CBF
• INDICATIONS:
Dysautoregulated ischemic region
CBF pressure dependent
SAH-induced vasospasm, focal ischemia
• METHODS
IONOTROPES
INCREASE CARDIAC OUTPUT
VOLUME EXPANDERS (HYPERVOLEMIA)
• Deleterious if used post-injury (HTN-hemorrhage
NEUROPROTECTION
RAMSIS F. GHALY, MD,
FACS
NEUROPROTECTION
• INCREASE TOLERANCE OF NEURAL TISSUE TO
ISCHEMIA
• IMPROVED OUTCOME AS EVIDENCED BY
ELECTROPHYSIOLOGIC, METABOLIC, OR HISTOLOGIC
INDICES OF RECOVERY OR ULTIMATELY BY IMPROVED
CLINICAL NEUROLOGIC RECOVERY
• PROTECTION CAN BE ACHIEVED BY PRETREATMENT (in
anticipation of ischemia), DURING or AFTER ISCHEMIA
• MAXIMUM COUPLED SUPPRESSION OF CMRO2 & CBF
WITH CEILING EFFECT ONCE BURST SUPPRESSION EEG
• FOCAL ISCHEMIA PROTECTION ACHIEVED BY
OPTIMIZING SUBSTRATE/DEMAND RATIO
• GLOBAL ISCHEMIA, NO PROTECTIVE MEASURES IS
LIMITED AND AIMED AT SECONDARY PROCESSES
(EDEMA, HYPOPERFUSION, MEMBRANE DAMAGE.
NEUROPROTECTION
•
NEUROPROTECTION IS SEEN WITH AGENTS INDUCE CMR
DEPRESSION, GABA AGONISM, ADENOSINE A1 RECEPTOR
AGONISM, NMDA RECEPTOR ANTAGONISM. For example
protective effect of isoflurane (GABA receptor Agonist was
reversed by trimethaphan (GABA receptor antagonist)
•
Isolflurane protective effect dose-dependent <1.5MAC and above
0.5MAC
•
Neuroprotective effects being stipulated for Desflurane via CMR
depression and enhanced cerebral perfusion, Propofol via
mitochondrial swelling and morphine via protien kinase C and
NMDA receptors.
•
Ischemic models examined were for focal cerebral ischemia
TEMPORARY FOCAL
ISCHEMIA
ANTICIPATED TEMPORAY
CLIPPING:
MAINTAIN BURST SUPPRESSION
DURING ISCHEMIC PERIOD
THIOPENTAL 3-5mg/kg (5min)
10-15mg/kg (10min) then 35mg/kg/hr
CSF REGULATION
•
•
•
•
•
•
•
•
CSF (Vf)is formed at a rate 0.4ml/min (500-600cc/day) Total CSF
volume is replaced 4 times/day. 60-70% formed actively at the
choroid plexus and 30% at extrachoroidal sites across
ependyma and pia. CSF reabsorption (Va) via arachnoid villi and
granulations.
EQUILIBRIUM: Vf balance with Va /ICP . Vf relatively constant.
ICP<7cmH2O minimal Va, ICP>7cmH2O linear ↑Va. Vf↓ when
CPP<70mmHg
NEURAL: Choroid plexus richly supplied by adrenergic,
cholinergic and peptidergic affecting CSF rate formation.
TEMPERATURE: hypothermia ↓ CSF formation (1C→11%)
CO2: Hypocarbia ↓CSF transiently
METABOLIC ALKALOSIS: ↓CSF formation
OSMOLARITY: ↓CSF formation
↓CSF formation →↓CPP
PHARMACOLOGICAL
ALTERATIONS OF CSF
DYNAMICS
• N2O has no effect
• ISOFLURANE: ↓Ra and no change to Vf
• ENFLURANE transiently ↑Vf 80% and Ra(resistance
to reabsorption)
• HALOTHANE ↓Vf and ↑Ra
• KETAMINE: ↑Ra no change Vf
• ETOMIDATE and BARBITURATE (HIGH DOSE) ↓Vf
and Ra
• OPOID↓Ra
• BENZODIAZEPINE↓Vf, ↑Ra
• DIURETICS ↓Vf. Acetazolamide reduces by 50%
(carbonic anhydrase inhibitor)
INTRACRANIAL
PRESSURE
• ICP is determined by the raltionship of the volume
of intracranial contents(brain+blood+CSF=12001500cm3) and the volume of the cranial vault (fixed
by rigid dura and skull bone).
• ELASTANCE is the relationship of pressure and
volume (dP/dV). In normal condition a small
increase in intracranial volume will not result in
↑ICP.
• COMPLIANCE is the relationship of volume and
pressure (dV/dP) i.e. inverse of Elastance.
• Initially, as intracranial volume increases, no
change in ICP occurs (point A, well compensated)
until point B where any further increase will cause
dramatic increase in ICP (point C).
INTRACRANIAL
PRESSURE
• CPP=MAP-ICP (zero point at foramen of Monro)
• Normal ICP <10-14 mmHg during no stimulation
• INTRACRANIAL CONTENTS AND CRANIAL VAULT
VOLUME: brain matter and intracellular water (13501450g) 80-85%. Cerebral blood volume (CBV) 3-7ml/100g
3-6%. Cerebrospinal fluid (450cc/day) 5-15%. CBV:CBF
homogenous changes but not always and inhomogenous
in pathological condition.
• VPR Pressure change per 1 ml fluid injection (0.7% total
CSF) Normal <2mmHg (plateau). Pathological >4-5mmHg
(↑ steepness small segment)
• VPI (index)=P/V-(logPp/P0). Volume addition required to
change ICP by 10 folds (normal 25ml poor<15ml). Surgical
intervention before steep portion of VP curve.
ANESTHETIC INDUCTION IN
NEUROANESTHESIA: GOALS
• Deep anesthetic level with
adequate muscle relaxation and
blunting response to intubation,
pins and craniotomy
• No increase ICP, CBV, BP and
No decrease in CPP, CBF, BP
• No hypoxia
• No coughing
ANESTHETIC
INDUCTION IN
NEUROANESTHESIA
• Thiopental (3-7mg/kg, Propofol 22.5mg/kg, Midazolam 0.2-0.4mg/kg,
Etomidate 0.2-0.4mg/kg, Fentanyl 510ug/kg, Lidocaine 1.5mg/kg prior to
intubation (Lidocaine oral and
laryngeal spray)
• Adquate airway ventilation
• Non-depolarizing muscle relaxant
intubating dose or succinylecholine
1.5mg/kg after defasciculating dose
of non-depolarizer
ANESTHETIC
INDUCTION IN
NEUROANESTHESIA
•
•
•
•
•
Thoroughly securing the Airway
Eye protection watertight
Adequate positioning and padding
Avoid head down position
Avoid pressure over the neck or tight tape
around
• Keep access to the patient and lines
• Recheck tubes and lines after positioning
• Lidocaine at the Pin sites before head pins
placement
ASA TASK FORCE IN
POSITIONING 2000
• ASA TASK FORCE ON PREVENTION OF PERIOPERATIVE
PERIPHERAL NEUROPATHIES; PRACTICE ADVISORY IN
POSITIONING 2000.
• LIMIT ARM ABDUCTION TO 90 AND CAREFUL PADDING
OF VULNERABLE PRESSURE POINTS
• CAREFFULL PAD AND ASSESS AREAS SENSITIVE TO
PRESSURE NECROSIS e.g. EYES, EARS, NOSE,
GENITALIA AND BREASTS. FEMALE BREASTS
DISPLACED MEDIAL AND INFERIOR IN RELATION TO
CHEST SUPPORTS
• PATIENTS WHO HAVE POSITION-DEPENDENT
NEUROLOGIC SYMPTOMS OR EXTREMELY OBESE
BENEFIT FROM AWAKE INTUBATION FOLLOWED BY
AWAKE POSITIONING
PROBLEMS RELATED TO
PRONE POSITION
•
•
•
•
BRACHIAL PLEXUS INJURY
AIR EMBOLI AND CV COLLAPSE
BLINDNESS
OBSTRUCTION OF FEMORAL VEINS AND IVC→↓VR→↓CVP
AND ↓COP
• ENGORGEMENT OF PERIVERTEBRAL VENOUS
PLEXUSES→DIFFICULT SURGICAL EXPOSURE AND
↑BLOOD LOSS
• ABDOMEN HANG FREE→NEGATIVE PRESSURE WITHIN
IVC→ PERIVERTEBRAL VENOUS PLEXUSES-→ AIR
EMBOLIZATION
• FROM SUPINE TO PRONE→↓SV AND↓ CI AND↑ PVR AND
↑SVR. LEAST CHANGES WITH JACKSON SPINE AND
LONGITUDINAL BOLSTERS. CARDIAC PATIENTS MAY
NOT TOLERATE AND SWAN-GANZ CATHETER MAY BE
NEEDED
ROBLEMS RELATED TO
PRONE POSITION
• CABG PATIENTS MAY OCCLUDE BYPASS GRAFTS
• ABDOMINAL PRESSURE → DISPLACE DIAPHRAGM→
REDUCE LUNG COMPLIANCE→ POSITIVE PRESSURE
VENTILATION→BAROTRAUMA.
• POSITIVE INSPIRATORY EFFECT ON DIAPHRAGM-→
INCREASE FRC AND DESRIABLE EFFECT ON GAS
EXCHANGE
• VISUAL LOSS 1:100 SPINE SURGERIES DUE TO
ISCHEMIC OPTIC NEUROPATHY (↑FLUID, ↑BLOOD LOSS,
↑IOP , ↓PERFUSION PRESSURE)
• FACIAL EDEMA
PERIPHERAL NERVE
INJURY
•
•
•
•
•
IMPROPER INTRAOPERATIVE POSITIONINGT
REGIONAL ANESTHETIC TECHNIQUES
INJECTION SITES
DIRECT SURGICAL RETRACTION OR DAMAGE
RISK FACTORS: BODY HABITUS, PREVIOUS H/O
NEUROPATHY, SMOKING, DIABETES
• ULNAR NERVE INJURY 1/3 OF ASA CLOSED CLAIM
ANALYSIS
• BRACHIAL PLEXUS AND PERONEAL NERVE
FOLLOWED
PERIPHERAL NERVE
INJURY
• OTHER SITES: MEDIAN AND ULNAR NERVE AT
WRIST, RADIAL NERVE AT INNER ARM, VII NERVE
AT EXIT SITE COMPRESSED BY MASK AIRWAY
• PROLONGED OR IMPROPER LITHOTOMY SCIATIC,
FEMORAL, COMMON PERONEAL, SAPHENOUS
NERVES
• COMPRESSION OR STRETCHING OF NERVE WITH
DEMYELINATION
• REMYELINATION OCCURS 6-8WEEKS
• IMMEDIATE DIAGNOSIS, EARLY NEUROLOGY
CONSULTATION AND REHABILITATION ARE
CRUCIAL FOR FULL RECOVERY
NEUROANESTHETIC
MAINTENANCE
ADEQUATE BRAIN RELAXATION
• Adequate oxygenation and
ventilation (PaCO2 3335mmHg),, venous return,
muscle relaxation, anesthetic
depth
• Furosmide 10-20mg iv, Mannitol
0.5-1.5g/kg iv, iv thiopental, CSF
drainage
NEUROANESTHETIC
MAINTENANCE
STABLE ANESTHETIC STATE AND
RAPID SMOOTH EMERGENCE
• Low after the craniotomy (brain is
devoid of sensation)
• Isoflurane, Sevoflurane or Desflurane
0.5MAC & Propofol 50-150 ug/kg/min
and Remifentanil 0.1-0.5ug/kg/min
• Muscle relaxant maintaining
2twitches (phenytoin may increase
requirment of muscle relaxants)
NEUROANESTHETIC
EMERGENCE
• AVOID COUGHING STRAINING OR
BP INCREASE
• Normalize gradually PaCO2
• Full reversal of muscle relaxant
• IV Lidocaine
• IV labetolol, Nicardpine, NTP, NTG
• Brief neurological Assessment
before leaving OR
Pre emergence
• 1-2 hr before end
• Gradual decrease anesth aiming
for bis 80 at end
• Treat post op htn before hand, I
aim for SBP 110
• Maintain solid reversible NMB!!
IMMEDIATE
POSTOPERATIVE CARE
IN NEUROANESTHESIA
•
•
•
•
•
ADEQUATE VENTILATION AND OXYGENATION
HEAD OF BED (10-25C0
NEUROLOGIC FUNCTION
CEREBRAL DYNAMICS MONITORING AND CONTROL
SERUM ELECTROLYTE: SIADH (↓Na, ↓serum osm, ↑urine
osmo) Treatment restrict water intake ‡meds
DI (polyuria, ↑Na, ↑serum osmo, ↓urine osmo) Treatment
Aqueous vasopressin 5-10USP units sq or 3units iv OR
desmporessin 1-2 ug iv sq q6-12hr. Plus adequate fluid
replacement
• SEIZURE (adequate oxygenation, ventilation and airway
protection: midazolam (2-4mg), thiopental (100-150mg),
fosphenytoin 15-20mg/kg, 100 mg/min)
• POSTOPERATIVE IMAGING (CTScan, MRI, Angiography)
TRANSPORT FROM
OPERATING ROOM
TRANSPORT FROM OPERATING ROOM TO NEURO-ICU OR PACU:
• PRIOR COMPLETE REPORT TO ACCEPTING UNIT WITH SET-UP
NEEDED
• TRANSPORT ONLY WHEN PATIENT IS STABLE OR AS STABLE
AS CAN BE
• DIRECT SUPERVISION OF ANESTHETIST
• HEMODYNAMIC AND RESPIRATORY SYSTEMS MONITORED AND
CONTROLLED
• O2 SUPPLEMENT
• WORKING IV AND RUNNING INFUSION PUMPS
• BLANKETS AND HEAT LOSS PREVENTION
• EMERGENCY MEDS AND INTUBATION KIT
• ENDORSEMENT IS NOT COMPLETE UNTIL PATIENT IS STABLE
AND COMPREHENSIVE REPORT HAS BEEN DELIVERED
CAUSES OF POSTANESTHETIC HYPOTENSION
•
•
HYPOVOLEMIA
↑HR, RR, SKIN TURGOR, DRY MUCOUS MEMBRANE, OLIGURIA
AND THIRST.
INADEQUATE FLUID REPLACEMENT, ONGOING LOSS, OSMOTIC
POLURIA, FLUID SEQUESTRATION (ASCITIS, INTESTINAL
OBSTRUCTION
A MEANINGFUL VOLUME CHALLENGE AND FURTHER
ASSESSMENT (CAUTIOUS IN IMPAIRED BBB)
IMPAIRED VENOUR RETURN
JUGLAR VEIN DISTENTION, ↑CVP, ↓BREATH SOUNDS AND
↓HEART TONES.
POSITIVE PRESSURE VENTILATION, PEEP, PNEUMOTHORAX,
PERICARDIAL TAMPONADE. TREATED BY VOLUME AND THE
CAUSE
CAUSES OF POSTANESTHETIC HYPOTENSION
•
VASODILATION
REWARMING, RESIDUAL INHALATION AGENTS, NEUROAXIAL
ANESTHESIA, TRANSFUSION REACTION, ANAPHYLAXIS,
INFLAMMATION, SEPSIS, ADRENAL INSUFFICIENCY, LIVER
FAILURE
• DECREASED CARDIAC OUTPUT
MYOCARDIAL ISCHEMIA, INFARCTION, CHF, NEGATIVE
INOTROPIC DRUGS, SEPSIS, HYPOTHYRODISM, MALIGNANT
HYPERTHERMIA
DYSPNEA, DIAPHORESIS, CYANOSIS, JUGLAR VEIN
DISTENTION, OLIGURIA, RHYTHM DISTURBANCES, WHEEZING,
DEPENDENT CRACKLES, AND S3 GALLOP
INOTROPIC AGENTS (e.g. DOPAMINE)
AFTERLOAD REDUCTION (e.g.Nitrate)
DIURESIS for fluid overload
ANTIDYSRHYTHMICS OR ELECTRICAL CARDIOVERSION
CAUSES OF
POST-ANESTHETIC
DYSRHYTHMIAS
•
•
•
•
•
•
•
•
•
•
•
INCREASED SYMPATHETIC OUTFLOW (PAIN)
HYPOXEMIA, PE
HYPERCARBIA
HYPO-HYPERTHERMIA
HYPOVOLEMIA
ELECTROLYTE AND ACID-BASE IMBALANCE
DRUG TOXICITY
THYROTOXICOSIS
MALIGNANT HYPERTHERMIA
MYOCARDIAL ISCHEMIA, CHF
ELEVATED ICP
COMMON TYPES OF
POSTANESTHETIC
DYSRHYTHMIAS
SUPRAVENTRICULAR DYSRHYTHMIAS
• SINUS TACHYCARDIA
• SINUS BRADYCARDIA
• PAROXYSMAL SUPRAVENTRICULAR
TACHYDYSRHYTHMIAS
VENTRICULAR DYSRHYTHMIAS; STABLE
• PVCS
• VENTRICULAR TACHYCARDIA (NON-SUSTAINED)
UNSTABLE VENTRICULAR TACHYCARDIA AND
VENTRICULAR FIBRILLATION
GENERAL TREATMENT OF POSTANESTHETIC DYSRHYTHMIAS
•
•
•
•
•
•
•
•
•
•
•
•
O2 SUPPLEMENT
INCREASE PERFUSION
TREAT THE CAUSE (S)
Pain: Opiods
Bradycardia: Atropine 0.2-0.4mg or glycopyrrolate 0.2mg
Synchronized cardioversion if unstable arrthymia
Adenosine 6mg then 12mg rapid to convert PACS
B-adrenergic blockers (labetalol 5-20mg -2mg/min, esmolol 10100mg or 25-300ug/kg/min, propranolol 0.5-1mg iv)
Calcium-channel blockers (Verapamil 2.5-5mg increment,
diltiazem 5-20mg iv or 0.25-0.35mg/kg iv then 5-15mg/hr
Amiodarone 150mg over 10min then 1mg/min for 6hrs then
0.5mg/min
Digoxin 0.25mg increment 1.5mg
Ibutilide, Procainamide 20-30mg/min iv up 17mg/kg 1-2mg/min,
Lidocaine 1.5mg/kg then 1-4mg/min
PERIOPERATIVE FLUID
MANAGEMENT IN
NEUROANESTHESIA
• Avoid infusion of water or dextrose in water (Water
freely passes through BBB)
• BBB is impermeable to most ions. Total osmolarity
rather than oncotic pressure determine osmotic
gradient.
• Maintenance of high serum osmolality decrease
brain water content
• Large, polar substances cross poorly BBB e.g
albumin
• If BBB is disrupted, permeability to mannitol,
albumin, and saline increases and edema formation
PERIOPERATIVE FLUID
MANAGEMENT IN
NEUROANESTHESIA
• Physiologic mainenance fluid given hourly without
replacement of overnight deficit
• Third spacing is minimal during craniotomy surgery
• 2/3 of total intraoperative urine output is replaced
with crystalloid
• Iso-osmolar crystalloid sol (0.9NS, 309 mOsm.
Large quantity may cause metabolic acidosis)
• Hypokalemia secondary to steriod, porassiumwasting diuretics, hyperventilation.
• Hyponatremia caused by SIADH and diuretic used
Brain Death
• Apnea test
Determination
• Disconnect the ventilator
• Deliver 100% FIO2 via t-piece/trach collar
• Monitor for ventilatory effort until ABG
confirms a PaCO2 greater than 60 mm Hg
• Reconnect ventilator
• If patient becomes unstable, terminate
apnea test
• Patient is considered apneic if PaCO2 is >
60 and there is no respiratory effort
THE END
THANK YOU
?QUESTIONS