Anesthesia for Neurosurgery

Chapter 26

Morgan and Mikhail 2nd edition

Jacqueline Proper M.D.

 Introduction
 Anesthesia record developed by Harvey
Cushing
 Neurosurgery requires modification of
anesthetic techniques
 Patient positioning complicates
management
 Intracranial Hypertension
 Sustained increase in ICP > 15 mmHg
 ICP increase caused by
– Expanding tissue or fluid mass
– Interference with CSF absorption
– Excessive CBF
– Brain edema from systemic disturbance
 Symptoms: HA, N&V, visual change, focal
neuro deficits, altered consciousness
 Intracranial Hypertension
 ICP >30mmHg  ischemia  brain edema 
increased ICPischemia brain edema 
progressive neuro damage or herniation
 Cushing response: periodic increase in ABP with
reflex bradycardia
– Cerebral ischemia  autoregulation decreases CVR 
 CBV  ICP, then Cushing reflex increases BP over
ICP
– Severe ischemia and acidosis abolish autoregualtion,
ICP and CBF become passively related to ABP
 Cerebral Edema
 Increase in brain water content
– Vasogenic edema: disruption of blood brain
barrier allows entry of plasma-like fluid
 Mechanical trauma, inflammatory lesions, brain
tumors, hypertension, infarction
– Cytoxic edema: metabolic insults - brain
cells fail to maintain ionic gradient
 Ischemia, hypoxemia
 Cerebral Edema
– Interstitial cerebral edema: obstructive
hydrocephalus, entry of CSF into brain
interstitium
– Acutely decreased serum osmolality:
intracellular movement of water caused by
rapid change in serum osmolality (water
intoxication)
 Treatment
 Dexamethasone
 Fluid restriction, osmotic agents, loop diuretics
Mannitol 0.25-1.0 g/kg
– Transient increase in intravascular vol can ppt
pulmonary edema
– Do not use with aneurysm, AV malformation until
head opened
 Furosemide: diuretic and decreases CSF
formation
 Hyperventilation (paco2 25-30) reduces CBF
 Craniotomy
 Most commonly done for neoplasm
 HA, seizure, focal deficits, cognitive change
 Preanesthetic evaluation
– ?? Elevated ICP
– CT/MRI: ? brain edema – midline shift > 0.5cm
and size of ventricles
– Neurologic assessment
– Labs: ADH, glucose, electrolytes
 Premed: avoid if ICP
 Craniotomy
 Monitoring: standard plus
– A-line: optimize cerebral perfusion, ABG’s
– CVP: long arm/ median basilic vein, EJ, SC
– Foley: long surgery, diuretics, fluid
management
– ICP: ventriculostomy, subdural bolt, saline
filled tubing with pressure transducer
 Craniotomy
 Slow controlled induction and intubation
– avoid  ICP, CBF compromise
– Steroids, osmotic diuresis, CSF drainage
– Cerebral HTN  ICP, CPP, herniation
– Preinduction hyperventilation
– Thiopental, propofol, etomidate with NDMR
– Treat HTN with deepening anesthetic or
esmolol or labetalol; avoid vasodilators
until dura open
 Craniotomy Positioning
 Frontal, temporal, occipital-parietal
craniotomy: supine 15-30° head elevation
 Head position: if neck turned excessively
can impede venous drainage, increase ICP
 Maintainance: low dose IH, narcotic; TIV;
NDMR
 Hyperventilation: maintain PaCO2 25-
30mmHg, avoid PEEP
 Craniotomy
 Maintainance IVF: avoid glucose,
hypotonic fluid
 Minimal redistributive fluid loss
 Occult blood loss common
 Emergence: lidocaine, propofol for
smooth extubation
 Posterior Fossa Surgery
 Obstructive hydrocephalus
– Obstruction of CSF outflow @4th ventricle
– Increased ICP- ventriculostomy
 Brainstem injury:
– Damage to respiratory centerabrupt
circulatory changes
– Cranial nerve damage – monitor AEP’s
-CNVIII, EMG – CN VII
 Posterior Fossa Surgery
 Sitting position – back @60, legs
elevated, knees flexed to heart level,
neck flexed
 Pad pressure points: elbows, ischial
spines, forehead
 Pneumocephalus: air enters SA space as
CSF lost during surgery
– DC N2O prior to dural closure
 Posterior Fossa Surgery
 Postural hypotension common
– Fluid restriction and diuresis
– GA blunts compensatory sympathetic reflex
– Worsened by sitting position
– Vasopressors, light anesthesia preferable
to increased IVF
 Venous Air Embolism
 Open vein with subatmospheric pressure
– Wound above level of heart
 Highest incidence with sitting position
– Low CVP, poor surgical technique
 Volume, rate of air entry
– Entrained air exceeding rate of pulmonary clearance
 Paradoxical air embolism
– PFO and reversal of normal transatrial gradient
– Air passes into arterial circulation
– Hypovolemia and PEEP
 Venous Air Embolism
 Dose for lethal VAE in animals on N2O is
1/3 –1/2 of control
 Signs/symptoms:
  ETCO2 ( pulmonary dead space),  PaCO2
  N2 on mass spec,  PAP
– Sudden hypoxia, hypotension
– Sudden circ arrest / RV outflow obstruction
 Venous Air Embolism
 Monitor with TEE and/or precordial
doppler
– 0.25ml lower limit
– TEE – can also eval cardiac function, ID
transatrial passage of bubbles
– Precordial doppler:R sternum, ribs 3-6,
VAE = loud roar
 Treatment of VAE
 Notify surgeon – saline, packing, bone wax
 DC N2O
 Aspirate CV catheter
  CVP with IV fluid infusion and jugular vein
compression  air entrainment
PEEP contoversial: CVP, but reversal of
transatrial gradient
 Vasopressors - correct hypotension
 L lateral decubitus plus T-bird to dislodge air lock
 If circ arrest, supine and CPR
 Sterotactic Surgery
 Aneurysms, vascular malformations,
movement disorders, intractable pain,
epilepsy, deep tumors
 Usually local/MAC to allow patient eval
introp
 Have fiberoptic ready
 Head Trauma
 50% of trauma deaths involve head injury
 Goal is prevention of secondary insults-
hypoxia, HTN, hypercapnia, hypotension
 Glasgow Coma Scale–morbity and outcome
 GCS<8, 5mm midline shift, CT: ventricular
compression, > 25 ml lesion:  morbidity
 Skull fracture increases likelihood of
significant intracranial lesion
 Head Trauma
 ICP monitoring: contusions,
intracerebral hemorrhage, tissue shifts
 Treat  ICP with head elevation,
hyperventilation, mannitol, barbiturates
 ICP > 60mmHg sustained – irreversible
brain edema
 Preop for Head Trauma
 Assure adequate ventilation and oxygenation
– give O2 during eval
– Avoid sedation – hypercapnia and hypoxia  ICP
 Assume C-spine injury (10% incidence)-use
in-line stabilization during intubation
 Intubate if absent gag or GCS < 8
– Cricoid pressure, preO2, pentothal, NDMR
– Fiberoptic or trach if difficult intubation
 Head Trauma
 Hypotension – blood loss vs spinal cord
injury and sympathectomy
– Correct hypotension, control bleeding –
SBP < 80mmHg  poor outcome
 Dysrrythmias common – may represent
altered autonomic function
– Abnormal T wave, U wave, ST segment,
QT interval
 Head Trauma Intraop
 Same principle as mass lesion
 Barbiturate, N2O, NDMR, opioid
 Hypertension – deepen anesthesia, -block
 CPP between 70 and 110mmhg
 Associated findings
– Brain thromboplastin – DIC and ARDS
– Polyuria – diabetes insipidus with pituritary
stalk injury
– GI bleed – stress ulcer, steroid therapy
Extubation after Head Injury
 Severity of injury – diffuse vs. local,
extent
 Concomitant abdominal, thoracic injury
 Pre-op LOC
 Preexisting disease
 Intracranial Aneurysm
 Most at bifurcation of large arteries ;
incidence 5%
 Acute mortality following rupture – 10%
– 25% of survivors die within 3 months
– 50% of survivors have significant neuro defecit
 Larger than 7mm – surgery
 Unruptured prodromal symptoms: CN III, VI
palsy, headache visual field defect, eye/neck
pain
– To OR for elective clipping
– Often otherwise healthy
 Intracranial Aneurysm

 Sudden severe HA, no neuro deficit, transient

LOC from ICP, CPP
 Complications:
– Cerebral vasospasm – 4-14d post rupture
– Rerupture (10-30%) with 60% mortality rate
– Hydrocephalus – shunt or drainage
 Vasospasm therapy
– Hypertension, hypervolemia, hemodilution (triple H
therapy)
– Ca channel blockers may be effective for prevention
Aneurysm/ AV Malformation
 Preop eval for signs of ICP, coexisting
disease
 History of hypertension, cardiac, renal,
ischemic cerebrovascular disease
contraindicate controlled hypotension
 Sedation prior to surgery based on ICP
 CerebralAneurysm
Intraoperative Management
 Have blood available
 A-line and CVP – prevent rupture of
aneurysm, ischemia, vasospasm
 Avoid hyperventilation – prevent  CBF
 After dura open, mannitol to imrove
surgical exposure
 Cerebral Aneurysm
Intraoperative Management
 Controlled hypotension (MAP 60-
70mmHg)
– Decreased MAP decreases transmural P
across aneurysm
– Decreases risk of rupture
– Facilitates surgical clipping
– Decreases blood loss
– Improves surgical visualization during
bleed
 Cerebral Aneurysm
Intraoperative Management
 Hypotensive agent with slight head-up
position and volatile agent (isoflurane)
 Use thiopental and mild hypothermia for
brain protection
 Large basilar artery aneurysm may
require hypothermic arrest
 AV Malformation
 Developmental abnormalities  AV fistulas
– Size increases over time
– Intracerebral hemorrhage most common at age 10-30
– HA, seizure, high output cardiac failure
 Anesthetic management complicated by
extensive blood loss
– A-line
– Multiple large bore IV’s
 Hyperventilation and mannitol facilitate surgical
access
 AV Malformation
 Hypothermia and pharmacologic brain
protection for large lesions
 Altered autoregulation in normal brain
area  hyperemia and swelling
following resection
– Use beta blockade to control BP / minimize
hyperemia and swelling
 Spinal Surgery
 Degenerative disease of the spine with
nerve root or cord compression
– Disc herniation (L4-5, C5-6, age 30-50)
– Osteophytic bone (spondylosis, low C-
spine)
 Scoliosis, fixation following trauma, cord
decompression, abscess, tumor
 Spinal Surgery
 Preop management
– Airway/ventilatory impairment
– Neurologic deficits
– Pain associated with degenerative disease
 Intraop management
– Prone position common
– Induction in supine, neck position critical
during turn to prone
 Spinal Surgery
 Complications from prone position
– Retinal ischemia from pressure on globe
– Pressure necrosis - nose, ears, forehead, breasts,
genitalia
– Chest rolls to facilitate ventilation
– Arms at sides, elbows flexed
– Abdominal compression – increased blood loss
 Monitoring
– A-line and CVP if cardiac disease /high blood loss
– Intraop wake up test vs SSEP’s
 Pituitary Tumor Resection
 41 y.O. F, 10mm pituitary tumor,
amenorrhea, decreased visual acuity
 Pituitary gland hormones
– Anterior: ACTH, TSH,GH, FSH, LH, PRL
 Secretion regulated by hypothalamic peptides
transported via capillary portal system
 Negative feedback control by products of target
organs
– Posterior: ADH (vasopressin), oxytocin
 Hypothalamic osmoreceptors and peripheral
vascular stretch receptors regulate ADH secretion
 Surgical Approach
 Transphenoidal if tumor under 10mm
 Bifrontal craniotomy if > 10mm diameter
 Pituitary gland attached to brain by stalk
– Bordered by bone anterior, posterior,
inferior
– Cavernous sinus lateral – CN III, IV, V1, VI
and cavernous portion of carotid artery
– Superior – diaphragma sella encircles stalk
 Surgical Approach
 Risk associated with transphenoidal approach
– Epinephrine mucosal injection to decrease bleeding
– Blood and tissue debris in pharynx
– Risk of hemorrhage associated with entry of
cavernous sinus or internal carotid artery
– Cranial nerve damage
– Pituitary hypofunction
 Diabetes insipidus in 40% of patients post-op
– Supine or head up position – risk of VAE
 Monitoring
 Precordial doppler
 Visual evoked potentials if optic nerve
involved
 Assure good venous access
 Anesthetic Technique
 General principles for craniotomy
? Increased ICP
 Use of nitrous oxide controversial – risk
of pneumocephalus
 Intense muscle paralysis