NEUROANESTHESIOLOGY
PART THREE
RAMSIS F. GHALY, MD,
FACS
Table 54-3. Most Likely Complications by
Time Interval After Aneurysmal
Subarachnoid Hemorrhage
Interval After Hemorrhage
0-3 days
Major Complications
Brain edema and shift
Rebleed
Acute hydrocephalus
Cardiac dysrhythmias
Respiratory pattern abnormalities
4-14 days
and/or arrest, pulmonary
edema
Cerebral vasospasm
Rebleed
Hypovelmia
Hyponatremia
Subacute hydrocephalus
Pneumonia
Chronic hydrocephalus
Pneumonia, pulmonary emboli
Rebleed
Cerebral vasospasm
Water and electrolyte
disturbances
>15 days
ANESTHETIC CONSIDERATION FOR
INTRACRANIAL ANEURYSM CLIPPING
• AVOIDANCE OF HYPERTENSION especially before
aneurysm clipping
• AVOIDANCE OF HYPOTENSION to avoid ischemia (↑ICP
and ↓CBF)
• ADEQUATE BRAIN RELAXATION “notorius tight brain”,
CSF drainage via lumbar drain or EVD
• INDUCED HYPERTENSION: during temporary clipping
• NEUROPROTECTION during the perioperative time
especially temporary clipping time: titerate to burst
suppression EEG , mild hypothermia
• INTRAOPERATIVE ANGIOGRAPHY for adequate clip
application
• SMOOTH EMERGENCE AND BRIEF NEUROLOGIC
EXAMINATION (REOPEN, ANGIOGRAPHY/CTSCAN)
• POSTOPERATIVE HYPERVOLEMIA, HYPERTENSION AND
HEMODILUTION
INTRAOPERATIVE
ANEURYSM RUPTURE
•
•
•
•
CELL SAVER
LARGE AND MULTIPLE IV BORE
INDUCED HYPOTENSION
PROXIMAL CONTROL:
ADENOSINE PLANNED CARDIAC
ARREST, MAUAL PRESSURE TO
ICA IN THE NECK
INTRACRANIAL
HEMORRHAGE
ANEURYSMAL HEMORRHAGE
• Surgical clipping is superior to
Endovascular coiling; re-rupture &
retreatment: 1.1% & 1.7% vs 3.3% &
11% (The Cerebral Aneurysm re-rupture
After Treatment (CARAT), Johnston et al,
2006
• Rebleeding most commonly occurring
within 30 days of the procedure
Respiratory failure, Pneumonia, brainstem
herniation. Increase glucose burden
increased risk of death.
ANEURYSMAL
HEMORRHAGE
• Intravenous Magnesium, a cerebral
vasoldilator (500mg/30min followed
by 2000mg/day for 14days) when test
agonist the traditional nimodipine,
can prevent vasospasm after SAH
• Prognostic role of S100B proteins,
LMW intracellular proteins found in
glial cells) can be spilled to
extracellular space and be detected
in the serum with half life 97min
(poor outcome, new onset CVA.
Vascular Malformation
• A Group of Vascular Abnormalities
•
•
•
•
•
Arteriovenous malformation (highest mortality)
Cavernous malformation (subcortal)
Dural arteriovenous malformation (no nidus)
Venous malforamtion (most common – benign)
Capillary telangiectasia (pons – benign)
• Clinical Findings
• Asymptomatic
• Chronic Headache (unilateral – exertional –
intermittent)
• Seizures
• Hemorrhage (SAH – IVH – ICH)
ANESTHETIC
CONSIDERATION FOR
AVM SURGERY
ANESTHESIA FOR EMBOLIZATION:
• GA OR MAC
• CONTRAST DYE ANAPHYLAXIS,
OSMOTIC LOAD AND CHF
• VESSEL PERFORATION: IMMEDIATE
NEUROLOGIC DETERIORATION,
BLOOD LOSS, EMERGENCY
CRANIOTOMY AND EVD
• CONTROLLED HYPOTENSION
ANESTHETIC
CONSIDERATION FOR
AVM RESECTION
• BLOOD PRESSURE CONTROL:
HYPOTENSION →ISCHEMIA TO THE
HYPOPERFUSED AREA
HYPERTENSION OR EVEN HIGH NORMAL
BP →PERFUSION PRESSURE
BREAKTHROUGH, BRAIN SWELLING AND
ICH (BARBITURATES, HYPOTHERMIA AND
MODEST LOWERING OF BP)
• POTENTIAL FOR LARGE BLOOD LOSS
• POSTOPERATIVE ANGIOGRAPHY
Intracerebral Hemorrhage
• Blood pressure control
controversial
• Modest reduction of
blood pressure if significant systemic effects
• Use - and -blocker or
calcium channel
blocker
• Consultation for
possible clot removal
INTRAVENTRICULAR
HEMORRHAGE
• Hemorrhge inside the ventricular
system with potential hydrocephalus
• Intraventricular hemorrhage is a
predictor of worse outcome when
present in ICH (5 fold increase).
rAFVIIa improved recovery in 39%
and overall mortality 22%. It was
given within 96hr iv and via EVD.
PREOPERATIVE CAROTID
ENDARTERECTOMY
• WIDESPREAD ATHEROSCLEROTIC DISEASE OFTEN
PRESENT.
• CAD 40-80% OF VASCULAR PATIENTS AND CAUSE OF
MORBIDITY AND MORTALITY (MI CAUSES 50% OF THE
EARLY POSTOP DEATHS). CARDIAC RISK FACTORS: CHF,
MI, HTN, VALVULAR HEART DISEASE, ANGINA,
DYSRHYTHMIAS.
• AGGRESSIVE MEDICAL TREATMENT WITH BETA
BLOCKING AGENTS IN STABLE ANGINA LOWERS
MORBIDITY AND MORTALITY. BUT NOT CORONARY
REVASCULARIZATION IN ELECTIVE VASCULAR
SURGERY.
• DOCUMENT BASELINE BP AND HR. BP DIFFERENCE IN
EACH ARM (SUBCLAVIAN/ AORTIC ATHEROSCLEROSIS)
PREOPERATIVE CAROTID
ENDARTERECTOMY
• OPTAMIZATION FOR RESPIRATORY FUNCTION STATUS:
SMOKING, COPD, EMPHYSEMA
• RENAL INSUFFICIENCY: RISK FACTORS DM, HTN,
ATHEROSCLEROSIS, VOLUME DEPLETION, DYE, ATN
• ENDOCRINE DM: RETINOPATHY, AUTONOMIC
NEUROPATHY, CAD, DIFFUSE ACCELERATED
ATHEROSCLEROSIS, SMALL VESSEL DISEASE, SILENT
ISCHEMIA. METFORMIN DISCONTINUED 48HRS PRIOR
TO CONTRAST DYE TO PREVENT SEVERE LACTIC
ACIDOSIS
• HEMATOLOGIC: WORK-UP FOR BLEEDING DISORDER,
HYPERCOAGULABLE STATE, HEPARIN ANTIBODIES,
ANTICOAGULANT INTAKE
• PRIOR TO REGIONAL, WITHHOLD: TICLODIPINE 1014DAYS, CLOPIDOGREL 7DAYS, LMWH 24HRS,
UNFRACTIONATED HEPARIN 4HRS.
PREOPERATIVE CAROTID
ENDARTERECTOMY
• INFECTION: HIGH MORTALITY WITH VASCULAR
GRAFT INFECTION, UNDERLYING POOR HEALING
• DOCUMENT PREEXISTING NEUROLOGIC DEFICIT
(TO COMPARE WITH NEW POSTOP DEFICIT)
• EXAMINE NECK MOTION AND IF PRODUCES
NEUROLOGIC SYMPTOMS PREOPERATIVE
• A-LINE IS PLACED. PA CATHETER IF UNDERLYING
CARDIAC IMPAIRMENT
• EEG IS RECORDED AND FINDING DURING CAROTID
CROSS CLAMPING
GENERAL ANESTHESIA
FOR CEA
• CONTROL VENTILATION, OXYGENATION AND REDUCE
CRMO2
• A PREINDUCTION EEG
• BP MAINTAINED AT PATIENT’S HIGH NORMAL AND
VASOPRESSORS PRN
• SMOOTH INDUCTION, GRADUAL TITRATION TO
MINIMIZE HEMODYNAMIC ALTERATION
• AVOID HYPOCARBIA
• SMOOTH RAPID EMERGENCE TO PROVIDE EARLY
NEUROLOGICAL ASSESSMENT WITH NO HYPO- OR
HYPERTENSION
• PRIOR TO EXTUBATION SEARCH FOR AIRWAY
IMPAIRMENT e.g RECURRENT LARYNGEAL NERVE
INJURY, HEMATOMA, ALTERED MENTAL STATUS AND
POOR AIRWAY PROTECTION
GENERAL ANESTHESIA
FOR CEA
• CAROTIS SINUS LOCAL ANESTHETIC iv
ANTICHOLINERGIC INFILTERATION TO AVOID
BRADYCARDIA AND HYPOTENSION SECONDARY
TO SURGICAL MANIPULATION ON CAROTID SINUS
ESPECIALLY IF UNDERLYING CONDUCTION DELAY,
AORTIC STENOSIS, UNSTABLE ANGINA
• HEPARIN 5000UNITS PRIOR TO CROSS CLAMPING
• SHUNT PLACED IF NEUROLOGIC OR EEG
ALTERATION. BP INCREASE BY VASOPRESSOR TO
INCREASE COLLATERAL CIRCULATION
• UNCLAMPING MY PRODUCE VASOLDILATION AND
BRADYCARDIA. VASOPRESSORS MAY BE NEEDED
AS BARORECEPTORS ADAPT CHANGE
• PROTAMINE IS NOT NEEDED UNLESS IT IS
REQUESTED OTHERWISE
REGIONAL ANESTHESIA
FOR CEA
•
•
•
•
SUPERFICIAL CERVICAL PLEXUS BLOCKADE
‡DEEP CERVICAL PLEXUS BLOCKADE
SURGICAL SUPPLEMENTATION
COOPERATIVE, TOLERATE LATERAL HEAD
POSITION UNDER SURGICAL DRAPES
• ACCESS TO THE HEAD AND LMA HANDY
• PROVIDES CONTINUOUS NEUROLOGICAL
ASSESSMENT DURING STAGES OF SURGERY AND
PROVIDES ADEQUATE INDICATION OF PERFUSION
ESPECIALLY DURING CROSS CLAMPING.
POSTOPERATIVE AFTER CEA
POSTOPERATIVE MANAGEMENT
• NEUROLOGICAL ASSESSMENT
• TIGHT CONTROL OF BP’ BARORECEPTOR RESPONSE
CHANGE BY PLAQUE REMOVAL (VASOPRESSORS
PHENYLPHRINE AND VASODILATOR NTG/NTP iv HANDY
(HYPOTENSION → GRAFT THROMBOSIS,
HYPERTENSION→CEREBRAL AND LOCAL NECK
HEMORRHAGE
• HYPOTENSION SHOULD NOT BE MANAGED BY FLUID
VOLUME SINCE THE PROBLEM IS BARORECEPTOR
ADAPTATION
POSTOPERATIVE NEW NEUROLOGIC DEFICITS
• HYPOPERFUSION
• EMBOLI (ESPECIALLY DURING SHUNTING)
• SUDDEN MAJOR DEFICIT→ IMMEDIATE EXPLORATION
INTRAOPERATIVE ANGIOGRAM
CAROTID
ENDARTERECTOMY
• Regional cervical anesthesia and
dexmedetomidine infusion for CEA. Criteria
for shunting (5%-12.5%): contralateral
weakness, slurred speech, confusion
nausea. Another study using regional
cervical anesthesia and dexmedetomidine
based with fentanyl and midazolam.
Suggestions that dexmedetomidine does not
increase brain ischemia.
• Postoperative neurocognitive dysfuction
25% after CEA with majority no radiographic
evidence (perhaps, hypoperfusion). Risk
factor longer cross clamp time 61 (16.9)min
vs 44 (16.2) min, ? Older 73 vs 69 and DM.
CAROTID
ENDARTERECTOMY
• CAVATAS, 2001, indicated surgical carotid
endarterectomy vs endovascular stent placement
were similar in major complications. Risks of restenosis is common after endovascular and risks of
minor (cranial nerve deficit) is common after CEA.
• Mas et al 2006, disabling stroke or death was 3.4%
in stenting and 1.5% after CEA in a month and in 6
months
• CEA perioperative rate was 3.8% stroke, 1.6% TIA,
1.6% MI and 1.4% death
• Hyperglycemia independent predictor for stroke, MI
and death
POSTERIOR FOSSA
SURGERY
• LOWERE CRANIAL NERVE PALSIES (RISK OF
ASPIRATION), HYDROCEPHALUS (OBSTRUCTION TO
FOURTH VENTRICLE)
• RESPIRATORY CENTER IMPAIRMENT AND EDEMA OF
FLOOR FOURTH VENTRICLE
• CARDIOVASCULAR INSTABILITY: surgical manipulation
of Trigeminal nerve →bradycardia and hypertension
Glossopharyngeal or Vagus nerve →bradycardia, asystole
or hypotension. Cessation of manipulation and administer
atropine, glycopyrrolate or ephedrine
POSTERIOR FOSSA
SURGERY
• SITTING POSITION: AIR EMBLOISMCARDIOVASCULAR COLLAPSE,
CRANIOCERVICAL AND CERVICAL CORD
COMPRESSION AND QUADRIPLEGIA,
EXTREMITY NERVE/PLEXUS
ENTERAPMENT, PNEUMOCEPHALUS,
MACROGLOSSIA, MASK HEMEOSTASIS)
• IF IN DOUBT KEEP PATIENT INTUBATED
• POSTOPERATIVE HEMORRHAGE→
IMMEDIATE HERNIATION AND DEATH
WITHOUT PRIOR WARNING (OPEN WOUND
AT BEDSIDE AND DRAIN HEMATOMA)
VENOUA AIR EMBOLISM
(VAE)
• SURGERY CLOSE TO VENOUS
SINUSES
• HEAD ELEVATION ABOVE THE
HEART e.g. SITTING POSITION (76%)
• CRANIOSYNOSTOSIS
• SKULL PIN SITE
• CERVICAL LAMINECTOMY (25%)
PREVENTION OF SIDE
EFFECTS
•
•
•
•
•
RESTRICT USE OF SITTING POSITION TO ALTERNATIVES
SEMISITTING POSITION WITH LOWERING THE HEAD LEVEL
ADEQUATE HYDRATION, WRAPPING LEGS AND OTHER
PNEUMATIC ANTISHOCK TROUSERS, MAST UNIT (DECREASE
COP BY 15%, INCREASE SVR, CAUTION WITH CARDIAC
PATIENTS), INCREMENTAL ADJUSTMENT AND INCREASE
VENOUS RETURN
MEASURE PERFUSION PRESSURE TRANSDUCER AT THE HEAD
LEVEL (ALLOW FOR THE HYDROSTATIC DIFFERENCE BETWEEN
ARM/ HEART AND OPERATIVE FIELD
PNEUMOCEPHALUS (TENSION PNEUMOCEPHALUS CAUSE
DELAY AWAKENING OR NO AWAKENING) IS MINIMIZED BY
ADEQUATE INTRACRANIAL IRRIGATION OF SALINE, SYSTEMIC
HYDRATION, OFF N2O, HIGH FIO2 1.0 AND LOWER HEAD. IT
WORSEN BY DRYNESS OF THE BRAIN, USE OF N2O AND HEAD
ELEVATION. PERCUTANEOUS ASPIRATION OF AIR IS
RECOMMENDED
PREVENTION OF SIDE
EFFECTS
• MACROGLOSSIA AND DELAYED AIRWAY OBSTRUCTION
DUE TO OROPHARYNGEAL STRUCTURES SWELLING
AND ISCHEMIA (NECK FLEXION, TUBES, DRAINS),
MAINTAIN THREE FINGER BREADTHS
• QUADRIPLEGIA MAY BE CAUSED BY LOW BP/CPP, NECK
FLEXION AND UNDIAGNOSED CERVICAL STENOSIS.
PREOP TESTING OF NECK FLEXION AND
INTRAOPERATIVE SSEP RECORDING
• PEEP IS AVOIDED FOR THE FEAR OF PARADOXICAL AIR
EMBOLISM. PFO 25% OF ADULTS AND MAY OPEN BY
ELEVATION OF R SIDED PRESSURE OF THE HEART AND
MAY CAUSE INTRA-ARTERIAL EMBOLUS FROM RIGHT TO
LEFT (SYSTEMIC)
DETECTION OF VENOUS
AIR EMBOLISM
• COMBINATION OF PRECORDIAL DOPPLER AND EXPIRED
CO2 MONITORING IS THE CURRENT STANDARD
• DOPPLER PLACEMENT IN A LEFT OR RIGHT
PARASTERNAL LOCATION IN SECOND TO FOURTH
INTERCOSTAL SPACE
• TEE (76% REPORTED INCIDENCE) IS MORE SENSITIVE
THAN PRECORDIAL DOPPLER (40% REPORTED
INCIDENCE)
MANAGEMENT OF ACUTE AIR
EMBOLIC EVENTS
PREVENT FURTHER AIR ENTRY
• FLOOD/ PACK SURGICAL FIELD
• JUGLAR COMPRESSION (INFLATABLE NECK
TOURNIQUET)
• LOWER HEAD
• G-SUIT (INCREASE RAP)
TREAT THE INTRAVASCULAR AIR
• ASPIRATE VIA CVC
• DISCONTINUE N2O
• FIO2 1.0
• PRESSORS/INOTROPES
• CHEST COMPRESSION
• LEFT LATERAL DECUBITUS (AIR REMAIN IN THE R
CHAMBER)
ALTERNATIVE POSITIONING
SODIUM AND VOLUME
IMBALANCE
•
•
•
•
DI
SERUM NA
↑→
URINE NA
→
URINE OSMO
↓
VASCULAR VOL→↓
SIADH SAH-SALT WAST
↓
↓→
→↑
↑
↑
→↑
→↑
↓
TRANSSPHENOIDAL
SURGERY COMPLICATIONS
• CRANIAL NERVE DYSFUNCTION
(II, III, V1, V,VI)
• HEMORRHAGE (SINUS, ICA
INJURY) AND CVA
• CSF RHINORRHHEA (LUMBAR
DRAIN)
• HYPOTHALAMIC INJURY AND
COMA
HYPOTHYROIDISM
• CHRONIC THYROIDITIS, FOLLOWING RADIOIODINE
TREATMENT FOR HYPERTHYROIDISM
• LETHARGY, FATIGUE, INTOLERANCE TO COLD,
BRADYCARDIA, DECREASED COP, PERIPHERAL
VASOCONSTRICTION, HYPONATREMIA
• MILD TO MODERATE HYPOTHYROIDISM NO
INCREASE RISK UNDERANESTHESIA
(PEROPERATIVE EUTHYROID)
• 7-10 DAYS REQUIRED FOR EFFECT OF T4 ONCE PO
AND 3-4 WEEKS FOR STABLE STATE
• RAPID TREATMENT MAY PRECIPTATE CARDIAC
ISCHEMIA
HYPOTHYROIDISM
• AIRWAY CHALLENGES; ENLARGED TONGUE,
RELAXED OROPHARYNGEAL TISSUE, GOITER AND
POOR GASTRIC EMPTYING
• SENSITIVE TO VOLATILE ANESTHETIC, OPIODS
AND NEUROMUSCULAR BLOCKADE
• PRONE TO HYPOTENSION (HYPOVOLEMIA AND
BLUNTED BARORECEPTOR REFLEXES ESP. TO
CARDIAC DEPRESSANTS AND VASODILATORS
• USE SYMPATHOMIMIETIC DRUGS: PANCURONIUM,
KETAMINE, N2O
• PRONE TO HYPOTHERMIA, CHF, HYPOGLYCEMIA,
HYPONATREMIA
• STERIOD SUPPLEMENT
• DELAY EMERGENCE/ AWAKENING
MYXEDEMA COMA
• SEVERE HYPOTHYROIDISM : MYXEDEMA COMA,
MENTAL STAUS OBTUNDATION,
HYPORESPONSIVENESS TO CO2, PERICARDIAL
EFFUSION, CHF, HYPOTHERMIA PLUS
EXAGGERATED SYMPTOMS OF HYPOTHYROIDISM.
• SURGERY, DRUGS, TRAUMA, INFECTION MAY
PRECIPTATE DECOMPENSATED STATE.
• DELAY SURGERY AND START SLOW THYROID
REPLACEMENT TO AVOID CARDIAC ISCHEMIA.
ORAL IS 50% BIOAVAILABILITY AND ↓BY HALF FOR
IV ONLY IN MYXEDEMA COMA (T3 i.v. 25Ug BID),
HYDROCORTISONE 50MG IV Q8HRS AND
SUPPORTIVE CARE
HYPERTHYROIDISM
• ANXIETY-FATIGUE-MUSCLE WEAKNESSTACHYCARDIA-TACHDYSRHYTHMIASEXOPHTHALMOS
• THYROID STORM; STATE OF PHYSIOLOGICAL
DECOMPENSATION (SURGERY EVEN 6-18HRS
POSTOP, STRESS, EXCESS IODINE OR IV
CONTRAST MY PRECCIPTATE) DIARRHEA,
VOMITING, HYPERPYREXIA, TACHYCARDIA,
HYPOVOLEMIA, CHF, SHOCK, WEAKNESS,
IRRITABILITY, DELIRIUM, COMA
• DD OF THYROID STORM: PHEOCHROMOCYTOMA
CRISIS, MH, NEUROLEPTIC MALIGNANT
SYNDROME, SEPSIS, HEMORRHAGE,
TRANSFUSION/ DRUG REACTION
HYPERTHYROIDISM
• B-BLOCKERS SELECTIVE B1 e.g. PROPRANOLOL 1-2mg
iv, 40-80mg po q6hrs, ATENOLOL OR METOPROLOL
(CONTROL HYPERDYNAMIC STATE, RESTING HR
<85BBM AND PREVENT PERIPHERAL T4 TO T3
CONVERSION)- VERAPAMIL 5-10mg iv
• ANTITHYROID MEDS 2-6WKS, PROPYLTHIOURACIL
200mg q6hrs, METHIMAZOLE 20mg po q4hrs
(PREFERRED, RAPID ONSET AND LESS COMPLICATIONS
URTICARIA, HEPATITIS & AGRANULOCYTOSIS). IT
BLOCK NEW THYROID HORMONE SYNTHESIS AND BE
GIVEN I HR PRIOR TO IODINE THERAPY
• IODIDES (BLOCK RELEASE OF THYROID HORMONES
FROM THE GLAND) Iopanoic acid 500mgbid po
• PRN; ACTIVE COOLING, HYDRATION, MEPERIDINE,
STERIODS dexamethasone 2mg bid.
• THYROID GLAND ABLATION WITH SURGERY OR
RADIOACTIVE IODINE
HYPERTHYROIDISM
• EUTHYROID PROOR ELECTIVE SURGERY
• PREOPERATIVE BENZODIAZEPINE FOR
ANXIOLYSIS
• GENEROUS DEEP PREOP SEDATION AND DEEP
ANESTHETIC LEVEL. REGIONAL BLOCKADE IS
ENCOURAGED. INCREASE IN DRUG METABOLISM
AND ANESTHETIC REQUIREMENTS.
• ESMOLOL INFUSION TITRATE 100-300 Ug/kg/min
• THIOPENTONE ATTRACTIVE ITS THIOUREA
STRUCTURE SIMILAR TO ANTITHYROID MEDS
• AVOID SYMPATHETIC STIMULATION i.e. PAIN,
ANTICHOLINERGICS, EPINEPHERINE IN LOCAL
ANESTHETICS, PANCURONIUM AND KETAMINE
HYPERTHYROIDISM
• CHECK FOR THROMBOCYTOPENIA, HYPOVOLEMIA
• USE DIRECT ACTING AGENTS AND FLUID FOR
HYPOTENSION
• PROTECT THE PROPTOTIC EYES
• AIRWAY ASSESSMENT (COMPRESSION OF AIRWAY AND
GREAT VESSELS BY ENLARGED THYROID GLAND)
CTSCAN AND EVIDENCE OF ORTHOPNEA.
• RECURRENT LARYNGEAL N MONITORING (NO
NEUROMUSCULAR BLOCKADE
• MYASTHENIA GRAVIS 30 FOLD INCREASE. TITRATE
MUSCLE RELAXANTS.
• WATCH FOR RECURRENT LARYNGEAL N PALSY,
PHRENIC NERVE INJURY, HYPOPARATHYROIDISM,
HYPOTHYROIDISM, PNEUMOTHORAX, THYROID STORM,
TRACHEOMALACIA, HEMATOMA INDUCED TRACHEAL
COMPRESSION
PHEOCHROMOCYTOMA
• CATECHOLAMINE-SECRETING (EPINEPHRINE,
NOREPINEPHRINE, DOPAMINE) TUMORS OF
ADRENAL MEDULLA, 10% BILATERAL, 10% EXTRAADRENAL, 10% METASTATIC, 10% FAMILIAL (PART
OF MEN IIa & Iib). CAUSE OF HTN IN 0.1%
• PALPITATION, H/A, DIAPHORESIS EPISODIC HTN,
TREMORS, HYPERGLYCEMIA, ANXIETY, WT LOSS,
ORTHOSTATIC HYPOTENSION (DEHYDRATED AND
HEMOCONCENTRATED)
• PREOPERATIVE DX SINCE INTRAOPERATIVE DX
CARRIES MORTALITY 50%
• 24-HOUR URINE FOR CATECHOLAMINES AND
METABOLITES
PHEOCHROMOCYTOMA
• CATECHOLAMINE INDUCED CARDIOMYOPATHY,
CHF, HYPOVOLEMIA, ICH, HYPERGLYCEMIA,
RENAL FAILURE, COMORBID ENDOCRINOPATHIES
(MEDULLARY THYROID CA,
HYPERPARATHYROIDISM, MARFANOID, TUBEROUS
SCLEROSIS, NEUROFIBROMATOSIS, VON HIPPELLINDAU OR STURGE WEBER SYNDROME.
PHEOCHROMOCYTOMA
• ALPHA- RECEPTOR ADRENERGIC BLOCKADE: MINUMIM
14 DAYS BP<165/95, POSTURAL HYPOTENSION
BP>80/45, ONE PVC/5MIN, NO EKG CHANGES, NASAL
STUFFINESS
• PHENOXYBENZAMINE (STOP 48HRS PRIOR TO
SURGERY) LONG ACTING ALPHA 1 &2 ADRENERGIC
BLOCKADE20-30MG/ DAY UP TO 250MG/ DAY UNTIL BP
CONTROL, PRAZOSIN (STOP 12HRS PRIOR) 1-6mg qid,
DOXAZOSIN 4-12mg/ day
• VOLUME REPLETION REFLECTED BY WT GAIN AND
DECREASE HCT
• BETA BLOCKADE AFTER ADEQUATE ALPHA BLOCKADE
(WORSENING OF HYPERTENSION BY UNOPPOSED
ALPHA STIM. & WITH CAUTION (CARDIOMYOPATHY)
• METYROSINE, CATECHOLAMINE SYNTHESIS INHIBITOR
(1-4mg/ DAY)
PHEOCHROMOCYTOMA
• ADEQUATE PERIOPERATIVE SEDATION AND DEEP
ANESTHETIC LEVELS (BIS) INCLUDING ADDITION OF
REGIONAL BLOCKADE WITHOUT EPINEPHERINE USE
AND HYPOTENSION
• AVOID SYMPATHOMIMETICS, VAGOLYTICS, OR
HISTAMINE RELEASE AGENTS
• A-LINE FOR CONTINUOUS BP MONITORING. OTHER
INVASIVE MONITORS PER PT CONDITION
• HYPERTENSIVE CRISES AND DYSRHYTHMIAS (DURING
TUMOR MANIPULATION INTRAOP.) TREATED BY IV NTP,
NICARDDIPINE OR PHENTOLAMINE. BETA BLOCKADE BY
LABETOLOL OR ESMOLOL
• MAGNESIUM (40-60mg/kg LOADING INFUSION 2gm/hr
and prn 20mg/kg bolus) BLOCKS CATECHOLAMINE
RECEPTORS AND RELEASE FROM ADRENALS AND
PERIPHERAL TERMINALS.
PHEOCHROMOCYTOMA
• SUDDEN HYPOTENSION ONCE VENOUS SUPPLY IS
LIGATED DUE TO SUDDEN DECREASE IN
CIRCUILATING CATECHOLAMINES. VOLUME
REPLETION, PHENYLEPHERINE DIRECT
VASSOPRESSOR AND VASOPRESSIN.
• TIGHT BLOOD GLUCOSE CONTROL
PERIOPERATIVE HYPER- AND POST-TUMOR
RESCTION HYPOGLYCEMIA
• AFTER BILATERAL ADRENALECTOMY,
GLUCOCORTICOID AND MINERALOCORTICOID
REPLACEMENT.
• NORMAL SERUM CATECHOLAMINES LEVEL
RETURN IN FEW DAYS
ADRENOCORTICAL AXIS
• CUSHING SYNDROME:
↑NA ↓K, HYPERGLYCEMIA, HYPERTENSION,
INCREASED INTRAVASCULAR VOLUME, SKELETAL
MUSCLE WEAKNESS, OSTEOPOROSIS,
HYPERCOAGULABILITY AND THROMBOEMBOLISM
• HYPOADRENOCORTICISM:
CIRCUILATORY COLLAPSE, LOW CARDIAC OUTPUT
HYPOTENSION, HYPOVOLEMMIA, HYPOGLYCEMIA,
↓NA ↑K, OLIGUREA, WEIGHT LOSS
• SENSITIVITY TO ANESTHETICS, MYOCARDIAC
DEPRESSANTS AND MUSCLE RELAXANTS AND
NEED FOR STRESS CORTISOL DOSE
ANESTHESIA FOR SPINE
SURGERY
•
POSITIONING (OPTIMAL BODY POSITION, PRESSURE POINT
PADDED AND NEURAL, FACE, GENITALIA PROTECTION, LINE
AND AIRWAY SECURE)
•
FOR CERVICAL AND CRANIOCERVICAL SPINE SURGERY:
SUPINE FOR CORPECTOMY, DISCECTOMY AND FUSION
PRONE FOR LAMINECTOMY, LAMINOTOMY, MICRODISCECTOMY
AND POSTERIOR FUSION AND OCCIPITOCERVICAL FUSION
TRANSORAL APPROACH FOR C1-C2 LEVEL SURGERY
• FOR THORACOLUMBAR SPINE SURGERY
PRONE (LAMINECTOMY, DISECTOMY AND POSTERIOR FUSION
(PLIF)
SUPINE (ANTERIOR DISCECTOMY, ALIF
LATERAL, DISECEOMY, CORPECTOMY AND LATERAL FUSION
ANESTHESIA FOR SPINE
SURGEY
• INTRAOPERATIVE MOTOR AND SOMATOSENSORY
MONTORING AND ND POSSIBLE WAKE UP TEST
IF UNSURE OF NEUROLOGIC FUNCTION
PRESERVATION, PATIENT WILL BE ALLLOWED TO
WAKE UP BRIEFLY AND ASKED TO MOVE THE
LEGS AND ARMS WHILE REMAINED IN POSITION. IF
NO LEG MOVEMENT, SPINE DISTRACTION IS
RELEASED AND THEN REASSESSED. PATIENT
SHOULD BE WARN OF THIS.
• BLOOD LOSS : ↓INTRAABDOMINAL AND
INTRATHORACIC PRESSURE, PREOPERATIVE
AUTOLOGUS DONATION, INTRAOPERATIVE BLOOD
SCAVENGING TECHNIQUES AND INTRAOPERATIVE
HEMODILUTION
VISUAL LOSS AFTER
SPINE SURGERY
• Periperative visual deterioration can be caused by
corneal exposure, corneal abrasion, glaucoma,
retinal artery occlusion or venous obstruction, optic
nerve ischemia and stroke
• 93 cases reported in Spine surgery ASA registry
(males 72%, ASA 1 &2, elective surgery,
instrumented spine fusion in prone position 89%,
bilateral loss 66%; 67% due to posterior ischemic
optic neuropathy and 23% due to anterior ischemic
optic neuropathy. Visual loss is permanent, some
recovery in 42%.
CURRENT RECOMMENDATIONS FOR
VISUAL LOSS DURING SPINE
SURGERY
• Normalize BP and avoid overzealous
fluid and hemoglobin management
and vasopressors, patient
positioning and the use of staged
surgeries.
• Preoperative consent and discussion
should include visual loss.
ACUTE SPINAL CORD
INJURY
PREVENT SECONDARY INJURY
• CERVICAL SPINE STABILIZATION AND
REDUCATION
• ADEQUATE AIRWAY AND VENTILATION AND
OXYGENATION(LESIONS ABOVE C3 →IMMEDIATE
INTUBATION (LOSS OF DIAPHRAGMATIC
INNERVATION) LESION AT C5-6 →↓70% OF VC AND
FEV1
• MAINTAIN SPINAL CORD PERFUSION PRESSURE
• NEUROPROTECTIVE (HIGH 30MG/KG OVER 15MIN
THEN 5.4MG/KG FOR THE NEXT 23HOURS
METHYLYPREDINSOLONE INFUSION)
• ASSOCIATED SERIOUS INTERNAL INJURIES
ACUTE SPINAL CORD
INJURY
• SPINAL SHOCK→ SUDDEN SYMPATHETIC
LOSS→ VASOLDILATION AND
HYPOTENSION
• T1-T4 INJURY → DAMAGE CARDIAC
ACCELERATORS AND UNOPPOSED VAGAL
TONE → BRADYCARDIA, ASYSTOLE AND
AV BLOCK
• ATROPINE, DOPAMINE, IV CRYSTALLOIDS
RESUSCITATION
• ATONY OF GASTROINTESTINAL TRACT
AND URINARY BLADDER (NG TUBE AND
FOLEY INSERTION)
Spinal Trauma: Indication of
Surgical Intervention
• Documented neurological deterioration and
spinal canal compromise (disk, bone
fragments, hematoma, subluxation)
• Incomplete cord injury with ongoing cord
compromise (?)
• Complete injury with possibility of some
recovery (?) Spinal canal realignment with
8 hr of injury
• Increasing bony deformity and pain despite
conservative therapy
• Unstable spine - malalignment
CHRONIC SPINAL CORD
INJURY
AUTONOMIC DYSREFLEXIA
•
•
•
•
•
INJURY AT OR ABOVE T6
FEW MONTHS TO YEARS AFTER INJURY
DISORGANIZED AFFERENT/SYMPATHETIC NEURONAL
CIRCUITS
STIMULATION (e.g. CUTANEOUS, VISCERAL, BLADDER
DISTENSION) INDUCES HYPERTENSION (SEVERE),
SWEETING, HEADACHE, FLUSHING OR PALLOR,
BRADYCARDIA
TREATMENT: REMOVAL OF THE STIMULUS, ADEQUATE
DEPTH OF ANESTHESIA (INCLUDING NEURAXIAL
ANESTHESIA) AND PROMPT LOWERING OF THE BP (IV
NTG/NTP, SUBLINGUAL NIFIDPINE)
SPINAL CORD ISCHEMIA DURING
THORACOABDOMINAL AORTIC
ANEURYSM REPAIR
• INCIDENCE 6%-40% SPINAL CORD ISCHEMIA
• MEP, SEP AND H-REFLEX MONITORING
• DECREASE DURATION OF ISCHEMIA: CRAWFORD
AORTIC INLAY TECHNIQUE, SINGLE-CLAMP
REPAIR TECHNIQUE, SEQUENTIALAORTIC
CLAMPING TECHNIQUE
• INCREASE MAP AND PERFUSION PRESSURE
• INTRATHECAL PAPAVERINE
• CSF DRAINAGE DURING CROSS CLAMP TO
DECREASE PRESSURE AND INCREASE PERFUSION
• REGIONAL EPIDURAL SPINAL CORD 9T12-L4-L5)
COOLING 28ºC
• SYSTEMIC HYPOTHERMIA
POSTOPERATIVE NAUSEA &
VOMITING IN
NEUROANESTHESIA
• PONV Common (66%) in females, use
of desflurane, cranial nerve V
decompression surgery and if
scoplamine patch was not used.
• Transsphenoidal surgery PONV
incidence was 7.5% especially if
there was CSF leak, Lumbar drain,
craniopharyngioma.
MONITORING IN
NEUROSURGERY
• MOTOR EVOKED POTENTIAL LIMITED BY THE
DEPRESSANT ANESTHETIC EFFECTS. TECHNICAL
ADVANCES REPETITIVE HIGH FREQUENCY
STIMULATION DEVICES (Multipulse TCE Stim 5 square
waves, 0.5ms duration delivered at 250Hz) AND TIVA
ANESTHETIC REGIMEN (Propofol, remifentanil ). MEP
recorded (5400ms, 500Hz, <200mA)
Sevoflurane/isoflurane 0.5 MAC, 67%N2O, propofol (BIS
40), vecuronium inducing 40% suppression of first twitch
in a train of 4.three twitch preservation
• SOMATOSENSORY EVOKED POTENTIALS, SSEP has a
role in prevention of perioperative peripheral nerve injury.
In 1000 cases surgical cases, 74 cases had upper
extremity nerve entrapment that was detected by SSEP
(lateral decubitus, prone). Concerns still in false
positives.
INTRAOPERATIVE EEG
MONITORING
• BISPECTRAL ANALYSIS (BIS) BIS
guided anesthesia demonstrated
superiority in monitoring depth of
anesthesia, minimize awareness
under anesthesia, reduction in
anesthetic utilization, guide delivery,
fast awakening. Spectral Entropy, a
measure of disorder in EEG activity,
is being evaluated.
ANESTHESIA FOR
NEURORADIOLOGY
ANESTHESIA SERVICE IS NEEDED OUTSIDE
THE OR IN NEURORADIOLOGY FOR:
DIAGNOSTIC: MRI/CTSCAN (CHILDREN, CLAUSTROPHOBIC AND
UNCOOPPERATIVE PATIENTS)
INTERVENTIONAL
• CEREBRAL AND SPINAL ANGIOGRAPHY
• BALLON TEST OCCULSION
• VERTEBROPLASTY AND KYPHOPLASTY
• RADIOFREQUENCY OR NEUROLYSIS FOR TRIGEMINAL
NEURALAGIA
• ENDOVASCULAR EMBOLIZATION
• ENDOVASCULAR COILING, STENTING, OBLITERATION OF
VASCULAR VISTULA
• THROMBOLYSIS FOR ACUTE CVA
• CEREBRAL VASOSPASM (STENTING OR PAPAVARINE,
NICARDIPINE OR MILRINONE USES)
• UNEXPECTED EVENT
NEURORADIOLOGY
• INCREASING NEED, FUTURE OF
NEUROSCIENCE
• OUTSIDE THE MAIN OPERATING
ROOM
• LIMITED SPACE
• RAGE FROM SEDATION TO DEEP AN
ESTHETIC LEVEL WITH MINIMAL
SEDATION
• UNCONTROLLED AND UNEXPECTED
INTRACRANIAL HEMORRHAGE
ANESTHESIA FOR
NEURORADIOLOGY
• FOR MRI MANADATORY USE OF NONFERROMAGNETIC ANESTHESIA EQUIPMENT
(MONITORS, VENTILATORS, BLADES—ETC) AND
NO METALLIC IMPLANTS. RADIOFREQUENCY
SIGNAL INTERFERENCE WITH ELECTRONIC
MONITORING, NOISE)
• LARYNGEAL MASK AIRWAY or ENDOTRACHEAL
INTUBATION: IV (PROPOFOL) or volatile (sevo- or
desflurane) anesthetics
• CONSCIOUS SEDATION AND MAC: Chloral hydrate
30-50mg/kg po/pp
• Methohexitone 25-30mg/kg PR,
ANESTHESIA FOR
NEURORADIOLOGY
IONIC AND NONIONIC CONTRAST MEDIA:
ALLERGIC REACTION (RISK FACTORS H/O ADVERSE
REACTION, ASTHMA, HAY FEVER, B-BLOCKERS,
INTERLEUKIN 2). PROPHYLAXIS: PREDNISOLONE 12
AND 2 HRS PRIOR, RANITIDINE 50mg,
DIPHENHYDRAMINE 50mg.. FOR EMERGENCY IV
HYDROCORTISONE 200MG, DIPHENHYDRAMINE
50mg. TREATMENT: O2, EPINEPHERINE, B2
AGONIST, AIRWAY PROTECTION. HYPEROSMOLAR
CONTRAST DYE DIURESIS FOLEY
AND IV REPLACEMENT
AWARENESS OF ANTICOAGULATION USE
AVOID HYPERTENSION (A-LINE INSERTION)
INTRAPROCEDURAL COMPLICATIONS (RUPTURE OF
ANEURYSM, BLOOD VESSEL) MEASURES TO ↓ICP
LENGTHY PROCEDURES
INTERVENTIONAL
NEURORADIOLOGY
• INTRODUCTION OF
MICROCATHETER/ BALLOON,
COIL TECHNOLOGY
• SELECTIVE INTRACRANIAL AND
INTRASPINAL INTRARTERIAL
AND INTRAVENOUS THERAPY
ANESTHESIA FOR
ELECTROCONVULSIVE
THERAPY
•
•
•
ELECTROCONVULSIVE THERAPY(provide amnesia, prevent damage from
tonic clonic contracture, control hemodynamic response bradycardia,
hypotension then tachycardia/hypertension, avoid interference with
initiation/duration of seizure, increase IOP, ICP, CBF, CNRO2, intragastric
pressure)
Hold benzodiazepine, lithium (post-ictal delerium),
Preoxygenate and ampu bag, bite blocks, methohexitone (lower seizure
threshold), 0.5-1mg/kg, succinylcholine 0.5-1mk/kg or , labetolol or
esmolol to blunt hypertensive response, propofol (20-50mg) reduce
seizure duration, ketorolac reduce muscle pain. Seizure monitoring by
EEG or Isolated arm technique (inflate BP cuff in the arm prior to use of
muscle relaxant and visualize seizure activity. Watch for drug interaction:
TRICYCLIC ANTIDEPRESSANT (potentiate hypotension, sedation,
tachycardia, prolonged PR and widen QRS complex, exaggerate
hypotension with spinal anesthesia and severe hypertension with
ephedrine. Meperidine with MAOI serotnin excess (hemodynamic
instability, respiratory depression, hyperpyrexia, seizure, coma, death)
THE END
THANK YOU
?QUESTIONS