• The intracranial compartment has fixed volume.
• Increases in volume of brain, blood, or CSF can lead to raised ICP,
compromising blood flow or causing herniation.
• Both IV & volatile anesthetic agents reduce brain metabolism. Balance of this
effect with blood flow, because of flow metabolism coupling, determines
extent of increase/decrease in CBF with a particular anesthetic agent.
• Cerebral preconditioning & augmentation of endogenous processes of repair,
including both neurogenesis & diaschisis, are promising approaches to
• Electrophysiologic & cerebral oxygenation/metabolism monitors are used
perioperatively to assess cerebral function & to detect cerebral ischemia.
• Image-guided neurosurgical procedures used for diagnosis, 3D localization, &
resection of intracranial lesions.
• Anesthesia for neurosurgical patients requires understanding of basic
principles of neurophysiology & effects of anesthetic agents on intracranial
• Supratentorial tumors (meningiomas, gliomas, and metastatic
lesions) change intracranial dynamics predictably.
• initially, when lesion is small & slowly expanding, volume-spatial
compensation occurs by compression of CSF compartment &
nearby cerebral veins.
• As lesion grows, compensatory mechanisms become exhausted, &
further increase in tumor mass causes progressively greater rise
• Primary or metastatic tumors or chronic SDH can present as chronic
• Due to ability of intracranial compartment to compensate up to a
point, patients may exhibit minimal neurologic dysfunction despite
large mass, elevated ICP, & shifts in the position of brain structures.
• As the tumor enlarges - outstrip its BS, developing central
hemorrhagic area that may expand rapidly, increasing ICP.
• Brain edema surrounding tumor increases effective bulk of tumor &
represents additional portion of the brain that is not
• In such situations (compromised compliance), small increases in
arterial pressure may produce large increases in CBF, which can
markedly increase intracranial volume & ICP & cerebral
• In addition to HTN, other causes of increased CBV such as
4. jugular venous obstruction,
can adversely affect cerebral hemodynamics & must
be avoided perioperatively.
• Intracranial tumors may be classified as
1.primary (those arising from the brain and its coverings)
• Tumors can originate from any cell type within CNS.
• Supratentorial tumors more common in adults & often
present with headache, seizures, or new neurologic deficits,
whereas infratentorial tumors are more common in children
& present with obstructive hydrocephalus & ataxia.
• Treatment & prognosis depend both on tumor type &
• Treatment may consist of surgical
• Often present in young adults with new-onset seizures. Upon
imaging, they generally show minimal enhancement with
• Surgical or radiation treatment of low-grade gliomas usually
results in symptom-free long-term survival.
• Usually appears as a contrast-enhancing, well-demarcated
lesion with minimal to no surrounding edema.
• Because of its benign pathologic characteristics, prognosis
following surgical resection is generally very good; however,
the location of the lesion, such as within the brainstem, may
• Gliobastoma multiforme (grade IV glioma) accounts for 30%
of all primary brain tumors in adults.
• Imaging usually reveals a ring-enhancing lesion due to central
necrosis as well as surrounding edema.
• Treatment typically involves debulking combined with
radiation and chemotherapy.
• Due to microscopic infiltration of normal brain by tumor cells,
resection alone is usually inadequate.
• Instead, treatment usually consists of surgical debulking
combined with chemotherapy and radiation and is aimed at
palliation, not cure. Despite treatment, life expectancy is
usually on the order of weeks.
• Arising from myelin-producing cells within CNS, account for only 6%
of primary intracranial tumors.
• Classically, seizures predate appearance of tumor on imaging, often
by many yrs.
• Calcifications are common & visualized on CT imaging.
• Usually consists of mixture of oligodendrocytic & astrocytic cells.
• Treatment & prognosis depend on the pathologic features.
• Initial treatment involves resection since, early in the course,
consists of primarily oligodendrocytic cells, which are
• Due to presence of astrocytic cells, they commonly behave like
anaplastic astrocytomas or glioblastoma multiforme later in their
• Arising from cells lining ventricles & central canal of spinal cord,
ependymomas commonly present in childhood & young adulthood.
• Most common location is floor of 4th ventricle.
• Symptoms include
• Treatment consists of resection and radiation. Tumor infiltration
into surrounding tissues may preclude complete resection.
Primitive Neuroectodermal Tumor
• Diverse class of tumors including retinoblastoma,
medulloblastoma, pineoblastoma, & neuroblastoma, all
believed to arise from primitive neuroectodermal cells.
• Medulloblastoma is the most common pediatric primary
malignant brain tumor & may disseminate via CSF to
encompass spinal cord.
• Presentation of medulloblastoma is similar to ependymoma.
• Treatment usually involves a combination of resection &
radiation given its high radiosensitivity.
• Prognosis is very good in children, if there is disappearance of
tumor celIs within CSF.
• Usually extra-axial (arising outside of the brain proper),
slow-growing, well-circumscribed, benign tumors
arising from arachnoid cap cells, not dura mater
• Due to slow-growing nature, they can be very large at time of
• Occur anywhere arachnoid cap cells exist, most common near
sagittal sinus, falx cerebri, & cerebral convexity.
• Usually apparent on plain radiographs & CT due to presence of
• On MRI & conventional angiography, these tumors often receive
their blood supply from external carotid artery.
• Surgical resection is mainstay of treatment.
• Prognosis is usually excellent; however, some tumors may be
recurrent and require additional resection.
• Arise from cells of anterior pituitary gland.
• May occur along with tumors of parathyroids & pancreatic islet
cells as part of MEN 1.
• Usually divided into functional (hormone secreting) &
• Former usually present due to endocrine disturbance related to
hormone secreted by the tumor.
• Functional tumors are usually smaller (<1 cm in diameter) at the
time of diagnosis (microadenomas).
• Macroadenomas are usually nonfunctional, present with symptoms
related to their mass (headache/visual changes due to compression
of optic chiasm), larger at diagnosis, usually >1 cm in diameter.
• Panhypopituitarism may be caused by either (compression of
normal functioning pituitary).
• Apoplexy - abrupt onset of headache, visual changes,
ophthalmoplegia, & altered mental status secondary to
hemorrhage/necrosis/infarction within the tumor.
• Can invade cavernous sinus/ICA/compress various cranial
nerves, causing an array of symptoms.
• Treatment depends on tumor type.
• Prolactinomas are often initially treated medically with
• Surgical resection transsphenoidally/open craniotomy
approach is often curative for most pituitary tumors.
• Benign schwannoma involving vestibular component of cranial
nerve VIII within internal auditory canal.
• Bilateral tumors may occur as part of neurofibromatosis type 2.
• Common presenting symptoms - hearing loss, tinnitus &
• Larger tumors, which grow out of the internal auditory canal & into
CP angle, may cause symptoms related to compression of cranial
nerves, most commonly facial nerve (cranial nerve VII) & brainstem.
• Treatment usually consists of surgical resection +/- radiation.
• Surgery usually involves intraoperative cranial nerve monitoring
with electromyography or brainstem auditory evoked potentials.
• Prognosis is usually very good; however, recurrence of tumor is not
• Rare tumor that can arise as primary brain tumor, also known
as microglioma, or via metastatis from systemic lymphoma.
• Primary CNS lymphoma can occur anywhere, most common
in supratentorial locations (deep gray mater /corpus
• Primary CNS lymphoma thought to be associated with a
variety of systemic disorders - SLE, Sjögren's syndrome, RA,
immunosuppressed states, EBV.
• Symptoms depend on location of tumor.
• Reasonable to wait to administer CTS, until after pathologic
findings are obtained as may be sensitive to steroids.
• CTS-associated tumor lysis prior to performing biopsy may
result in failure to obtain an adequate sample to make
• Mainstay of treatment is chemotherapy (including
intraventricularly delivered drugs) & whole-brain radiation.
• Prognosis is poor despite treatment.
• Originate most often from primary sites in lungs or breasts.
• Malignant melanoma, hypernephroma, & Ca colon also likely
to spread to brain.
• Metastatic brain tumor is likely diagnosis when more than
one intracranial lesion is present.
• Lab tests should be ordered based on history & clinical findings,
considering disease & complexity of Sx.
• Following are preoperative tests ordered:
– Hb, TC
– Platelet count
– PT/APTT & INR [individualized]
– Serum electrolytes, Blood sugar
– Glycosylated hemoglobin (HbA1c) in patients with long standing
– BUN, Creatinine
– TEE in patients scheduled for tumors in sitting position.
– USG abdomen for polycystic kidney, pheochromocytoma
1.Anti-convulsants 2. Antihypertensives
3.Steroids 4. Hypoglycaemic agents
5.Diuretics 6. Hormonal therapy
7.Anticoagulants / antiplatelets
• Requirement of nondepolarizing muscle relaxants is increased
in patients on anticonvulsants
• Lethargic patients do not receive premedication.
• Patients who are alert and anxious may receive an anxiolytic
(e.g., midazolam 5 mg po) before coming to OR.
Evidence of midline shifts (>0.5 cm) on CT /MRI
suggests raised ICP.
• Patients with intracranial pathology may be extremely
sensitive to CNS depressant effects of opioids & sedatives.
• Drug-induced hypoventilation - accumulation of arterial CO2
increases in ICP.
• Considering potential adverse effects of preop medication,
pharmacologic premedication should be used sparingly, if at all, in
patients with intracranial tumors.
• Preop depressant drugs best avoided in patients with diminished
levels of consciousness.
• In alert adult patients with intracranial tumors, BZDs in small doses
can provide anxiety relief without meaningfully affecting
• Decisions to administer anticholinergic drugs or H2-receptor
antagonists not influenced by presence/absence of increased ICP.
• ECG monitoring : necessary to detect responses related
to intracranial tumors/ surgery.
• ECG changes can reflect increased ICP or, more importantly,
surgical retraction or manipulation of the brainstem or cranial
• CVS centers, RS control areas, nuclei of lower cranial nerves lie in
close proximity in brainstem.
• Manipulation of brainstem may produce systemic HTN &
bradycardia/ hypotension & tachycardia.
• Cardiac arrhythmias range from acute sinus arrhythmias to
ventricular premature beats/VT.
• Pulse oximetry is of obvious importance.
• Capnography : can facilitate ventilation & PaCO2 management
as well as detecting VAE.
• In elderly & those with V/Q mismatch, et CO2 may correlate
poorly with PaCO2.
• Nasopharyngeal /esophageal temperature monitored to prevent
• Urine output also measured as indicator of perioperative fluid
• Diuresis occurs following administration of osmotic/loop diuretics.
• Reduced urine output – hypovolemia/release of ADH.
• Needed in pts with diabetes insipidus/SIADH/aberrations of salt or
water physiology/ lengthy Sx anticipated & bladder distention is
• IV access with large-bore catheters , given likelihood
of bleeding & need for transfusion/
rapid administration of fluids.
• Measurement of intra-arterial blood pressure, ABG, CVP,
recommended for major neurosurgical procedures.
• Arterial cannula is inserted before induction of anesthesia to
continuously monitor ABP & estimate CPP.
• When pressure transducer is at midhead level (level of external
auditory meatus), MAP approximates MAP at level of circle of
• CPP = difference btwn MAP & CVP in pts without intracranial HTN/
ICP in those with intracranial HTN.
• When cranium is open, ICP = atm pressure & CPP = MAP.
• With direct arterial pressure monitoring, hemodynamic
consequences of pharmacologic agents administered during
anesthesia recognized instantly.
Arterial catheter access for intraop ABG, hct, serum
electrolytes, glucose, & osmolality. (to verify
adequacy of hyperventilation).
Radial/femoral/brachial arteries suitable for
short-term; after ulnar artery collateral blood flow is
tested, cannulation of radial artery preferred.
• CVP - reliable means of large-bore IV, monitor of fluid status.
• When possible, CVP catheter should be inserted through
antecubital vein instead of jugular/subclavian veins.
• Avoids increased ICP from both head-down position & decreased
cerebral venous outflow.
• Position of antecubital central venous pressure verified by CXR,
transducer pressure waveform, or ECG.
• TEE & PAC selectively used, eg. In pts with IHD.
• Peripheral nerve stimulator : monitoring persistence of drug-
induced skeletal muscle weakness/paralysis.
• If paresis/paralysis of an extremity is associated with brain tumor, it
is important to appreciate resistance (decreased sensitivity) to
NDMR in paretic extremity, compared with normal extremity.
• Therefore, monitoring skeletal muscle paralysis on paretic limb may
• In these instances, the altered muscle response to relaxants may
reflect the proliferation of acetylcholine-responsive cholinergic
receptors that can occur after denervation.
Preoperative ICP monitoring
• Rarely used in patients for elective supratentorial tumor operations.
• ICP monitoring is invasive procedure that can cause bleeding or
• When performed with LA before induction, can be uncomfortable to
Hazards of Positioning Prone
• Pressure over the eyeballs, pinna , genitalia
• Kinking of the neck veins
• Extreme flexion – endobronchial migration of the tube,
• Brachial plexus , ulnar and sciatic nerve injuries
• Ventilation perfusion
• Common peroneal nerve
• Dependent pinna injury
• Achieved with drugs ( thiopental, etomidate, propofol)
produce rapid, reliable onset of unconsciousness without increasing ICP.
• In presence of raised ICP, thiopental is commonly used.
• Alternative agents : propofol / midazolam depending on pt's condition.
• Following induction sequence suggested: IV administration of thiopental
(3-5 mg/kg) or propofol (1.25-2.5 mg/kg), followed by opioid (fentanyl, 3-
5 µg/kg) & muscle relaxant.
• In pts who have been vomiting due to raised ICP, cricoid pressure is
applied during mask ventilation.
• If no airway difficulties anticipated, NDMR administered while controlled
hyperventilation with 100% oxygen is instituted, with goal of decreasing
PaCO2 to near 35 mm Hg.
• Administration of succinylcholine associated with modest, transient
increases in ICP. (risk benefit assessment)
• Adequate depth & profound skeletal muscle paralysis should be
achieved prior to laryngoscopy, (as movement can abruptly
increase CBF, CBV & ICP).
• Abrupt, sustained increases in systemic blood pressure, particularly
in areas of impaired cerebrovascular tone, may be accompanied by
undesirable increases in CBF, CBV, and ICP, and followed by
• To deepen, fentanyl administered in 50µg increments to total dose
of 10µg/kg, depending on BP.
• Lidocaine (1.5 mg/kg) also administered IV 90sec before intubation
to suppress laryngeal reflexes ( & other forms of intraop
stimulation like placement of pinions, skin incision).
• Esmolol infusion / bolus may be used to reduce HR & BP response
to DLscopy & intubation.
• Sustained hypotension must also be avoided (ischemia due to
• New-onset seizures or repeat episodes of seizures are another
possible origin of unexpected movement.
• ET intubation is performed as rapidly & smoothly as possible.
• Patient's lungs are ventilated at a rate & tidal volume that maintain
PaCO2 near 35 mm Hg.
• Routine hyperventilation no longer recommended in neurosurgical
patients due to risk of ischemia in some pathologic conditions.
(surgical conditions should define PaCO2 level for each pt).
• Eg, in pts with significant intracranial HTN / using volatile agents,
PaCO2 adjusted btwn 30-35 mmHg to reduce brain bulk.
• Opiods selected are usually fentanyl or remifentanil.
• PEPP should be used with caution, attention paid to
ICP, MAP & CPP effects.
• IV administration of succinylcholine activation of
EEG & increases in CBF / ICP.
• Cerebral effects Attributed to scoline-induced increase in
muscle afferent activity - cerebral stimulation.
• Pts with compromised intracranial compliance, scoline shown
to increase ICP.
• Not recommended for elective cases; but remains best agent
for achieving total paralysis for rapid-sequence intubation.
• Anesthetic depth required to protect against ICP-elevating
effects of such noxious stimuli as well as scoline itself.
• In Hemiplegic /paraplegic) pt, scoline avoided due to risk of
• Agents that release histamine avoided (Histamine alone may lower
BP & increase ICP, thus lowering CPP).
• When BBB disrupted, histamine can produce cerebrovasodilation &
increases in CBF.
• Most benzylisoquinolinium compounds (d-tc, metocurine,
atracurium, mivacurium) potential to release histamine.
• Doxacurium & cisatracurium produce minimal /no histamine
• Atracurium in intubating doses, reported to have no significant effect
on ICP, BP, or CPP in neurosurgical patients.
• Steroidals (pancuronium, pipecuronium, vecuronium & rocuronium)
may be better relaxants (do not directly affect ICP).
• Pancuronium does not produce an increase in CBF, CMRO2,ICP.
• However, pancuronium's vagolytic effects can increase HR & BP, &
elevate ICP in pts with disturbed autoregulation.
• Pipecuronium, reported to have no significant effect on ICP or CPP
in patients with intracranial tumors & no hemodynamic side effects.
• Vecuronium has no effect on ICP, HR/BP in neurosurgical pts.
• To achieve relatively rapid airway control (within 90 seconds), a
priming dose of vecuronium (0.01 mg/kg) can be administered
followed by a higher dose (0.10 mg/kg), or high doses of
vecuronium (to 0.4 mg/kg) without hemodynamic consequence.
• Rocuronium also has no effect on ICP in neurosurgical pts, but may
have mild vagolytic activity in higher doses (0.9 mg/kg).
• Popular technique - continuous infusion of propofol with
remifentanil / fentanyl. (shown to reduce ICP more effectively than
iso/ sevo), propofol with remifentanil produced quicker emergence
• In susceptible pts, risk of cerebral hypoperfusion greater when pts
hyperventilated under propofol anesthesia.
• Nitrous oxide & volatile anesthetics potential to increase CBV & ICP
as result of direct cerebral vasodilation.
• Nitrous oxide, 50 -70% in O2, administered by some to decrease
total dose of IV agent / volatile agent.
• In elevated ICP / low compliance, some clinicians avoid nitrous
oxide / high conc of isoflurane (> 1.0%).
• Opioid ,thiopental / propofol with midazolam / low-dose iso.
• Peripheral vasodilating drugs (nitroprusside/nitroglycerin), may
increase CBV & ICP despite decrease in SBP (best used after
craniotomy & opening dura).
• Spontaneous movement by pts must be prevented (dangerous
increases in ICP/herniation/bleeding).
• In addition to adequate depths of anesthesia, skeletal muscle
MEASURES TO REDUCE ICP
• Osmotic: Mannitol (0.25-1 g/kg iv), hypertonic saline.
Furosemide: 0.5-1 mg/kg iv, or 0.15-0.3 mg/kg with mannitol.
• Dexamethasone (localized cerebral edema surrounding tumors;
requires 12-36 hrs).
• PaO2 100 mmHg, PaCO2 33-35 mmHg.
• (MAP, CVP, PCWP, HR): normotension, maintain CPP .
Fluid therapy: Normovolemia before induction - prevent hypotension.
Position improve cerebral venous return (neutral, head-up position).
Drug-induced cerebral vasoconstriction (e.g., thiopental, propofol).
Temperature control mild intraoperative hypothermia.
CSF drainage to acutely reduce brain tension.
CLINICAL CONTROL OF RAISED ICP
• Severe intracranial HTN - reflex arterial hypertension &
bradycardia (Cushing's triad).
• Reduction in SBP can further aggravate ischemia (reducing CPP).
• Rapid brain dehydration & ICP reduction produced by administering
osmotic diuretic, mannitol / loop diuretic, furosemide.
• Infusion 0.25-1.0 g/kg.
• Action begins within 10-15 mins, effective for approx 2 hrs.
• Larger doses produce a longer duration of action but do not
necessarily reduce ICP more effectively (metabolic derangement).
• Mannitol is effective when the blood-brain barrier is intact.
• By increasing osmolality of blood relative to brain,
pulls water across intact BBB from brain to blood
to restore the osmolar balance.
• Shown to cause vasodilation of VSM, dependent on dose & rate of
• Mannitol-induced vasodilation affects intracranial & extracranial
vessels & can transiently increase CBV & ICP while simultaneously
• Hence should be given slowly (10-minute infusion) in conjunction
with maneuvers that decrease ICV (steroids / hyperventilation).
• Prolonged use of mannitol may produce
4.impaired renal function.
• Currently under investigation.
• Shown to reduce ICP in animals & human studies
may be more effective than other diuretics in certain conditions
(refractory intracranial HTN/ brain debulking ).
• Alternative /adjunct to mannitol.
Potential Adverse Effects of IV Administration
CENTRAL NERVOUS SYSTEM & SYSTEMIC
1.Decreased level of consciousness 8. Hyperchloremic acidosis
2.Hyperosmolality Hypernatremia 9. Coagulopathy
3.Seizures 10. Rebound edema
4.CHF 11. Phlebitis
5.Central pontine myelinolysis 12. Renal failure
7.Subdural & intraparenchymal hemorrhagea
• better agent in pts with impaired cardiac reserve.
• Loop diuretic : reduces ICP by inducing systemic diuresis,
decreasing CSF production & resolving cerebral edema by
improving cellular water transport.
• lowers ICP without increasing CBV or blood osmolality; but not as
effective as mannitol.
• Can be given alone,initial dose (0.5-1 mg/kg) or lower dose with
mannitol (0.15-0.30 mg/kg).
• combination of mannitol & furosemide diuresis more effective
than mannitol alone in reducing ICP & brain bulk but causes more
severe dehydration & electrolyte imbalances.
• Thus necessary to monitor electrolytes intraop & replace K as
• reduce edema around tumors; require many hrs/days
before reduction in ICP.
• Steroids preop frequently cause neurologic improvement that
precede ICP reduction.
Postulated MOA for steroidal reduction in brain edema
• 1.brain dehydration,
• 2.BBB repair,
• 3.prevention of lysosomal activity,
• 4.enhanced cerebral electrolyte transport,
• 5.improved brain metabolism,
• 6.promotion of H2O & electrolyte excretion,
• 7.inhibition of phospholipase A2 activity.
Potential complications of continuous
• 3.gastrointestinal bleeding,
• 4.increased incidence of infection.
• 5.electrolyte disturbances
• Therefore, the potential risks and benefits of continuous steroid
administration need to be evaluated in these patients.
• reduces brain volume by decreasing CBF through
• For every 1 mm Hg change in PaCO2, CBF changes by 2 mL/100
• Duration of effectiveness for lowering ICP as short as 4-6 hrs,
depending on pH of CSF.
• Only effective when CO2 reactivity of cerebrovasculature intact.
• Impaired responsiveness to changes in CO2 in areas of vasoparalysis
(associated with ischemia, trauma, tumor & infection).
• Target PaCO2 is 30-35 mmHg.
• By monitoring global cerebral oxygenation with, for example, SjVO2,
therapeutic effectiveness of hyperventilation determined & more
• Therapeutic goals are to maintain CPP &
control intracranial dynamics so that cerebral ischemia,
edema, hemorrhage & herniation are avoided.
• Severe hypotension results in cerebral ischemia & should be
treated with volume replacement, inotropes, or vasopressors
as dictated by clinical need.
• Severe HTN, can worsen edema & cause IC hemorrhage &
• β2-adrenergic blockers propranolol & esmolol , combined αβ-
adrenergic blocker labetalol effective in reducing SBP in pts
with raised ICP with minimal or no effect on CBF / ICP.
1.Do not dehydrate
2.Avoid hypotonic solutions
• Restricted fluid intake was traditional approach to IC
decompression therapy but now rarely used.
• Severe fluid restriction over several days only modestly effective in
reducing oedema & can cause hypovolemia, hypotension,
inadequate renal perfusion, electrolyte & acid-base disturbances,
hypoxemia, reduced CBF.
• In pts who are dehydrated preop, IV volume must be restored to
normal before induction to prevent hypotension.
• Relatively iso-osmolar solutions (NS, RL) do not adversely affect
oedema (if intact BBB).
• Free water in hypo-osmolar solutions (0.45% NaCl) adversely
affects ICP management.
• Hyper-osmolar solutions, 3% NaCL, initially tend to decrease brain
water by increasing osmolarity of plasma.
• Regardless of solutions selected, any solution administered in large
amounts can increase CBV & ICP.
• Blood loss should be corrected with PRBCs/ colloids supplemented
with balanced salt solutions.
• Glucose-containing solutions should be used with caution since
hyperglycemia, in CNS ischemia exacerbates neuronal injury.
• Replacement at approx 3:1 ratio (crystalloid:blood) to hct of approx
25-30%, depending on physiologic status.
• Neutral head position, elevated 15-30° to decrease
ICP by improving venous drainage.
• Flexing /turning of head may obstruct cerebral venous outflow
(dramatic ICP elevation, resolves with neutral head position).
• Can increase ICP (increases mean intrathoracic pressure, impairing
cerebral venous outflow & CO).
• If PEEP required to maintain SpO2, applied cautiously & with
appropriate monitoring to minimize decreases in CO & increases in
• PEEP 10 cm H2O < used without significant increases in ICP /
decreases in CPP.
• If higher levels of PEEP required to optimize SpO2, both CVP & ICP
• Intraop, modest degree of hypothermia, approx 34°C, way to
confer neuronal protection during focal ischemia.
• Hypothermic techniques for febrile neurosurgical patients.
• Hyperthermia particularly dangerous as it increases brain
metabolism, CBF & cerebral edema.
• To acutely reduce ICP, CSF drainage either by direct surgical
puncture of lateral ventricle /lumbar spinal catheter employed.
• Lumbar CSF drainage used cautiously & only when dura open & pt
mildly hyperventilated to prevent acute brain herniation.
• Brain tension can be effectively reduced by draining 10-20 mL of
Neurologically intact preop & uneventful Intraop
• Smooth emergence
• No coughing or straining
Neurologically compromised & extensive manipulations
• Continue intubation & ventilation
• Also if there is facial or neck swelling
Causes of Delayed Awakening
1.Preoperative low GCS 6.Surgical complications
2.Large tumor 7.Cerebral edema
3.Residual anesthetics 8.Hematoma
4.Metabolic / electrolyte disturbances 9. Pneumocephalus
5.Residual hypothermia 10.Vessel occlusion/ischemia
• IC hematoma & major cerebral edema most
• Emergence from anesthesia should be as smooth as possible,
avoiding straining/ bucking.
• Bucking can cause HTN & elevated ICP, leading to postop hge &
• Relaxants not reversed until head dressing applied. IV lidocaine (1.5
mg/kg) 90 seconds before suctioning & extubation .
• Extubated only when fully reversed or awake & following
commands. If not responsive, not extubated.
• Brief neurologic exam performed before & after extubation.
• Pt positioned with head elevated 15-30°, shifted to recovery room
with oxygen by mask & SpO2 monitoring.
• General assertion states that larger the resection, lower the risk of
recurrence of lesion & higher chance of pt's survival.
• But extensive tissue excision may favor occurrence of unpredictable
degree of functio laesa, (depending on location).
• Neurological sequelae due to tumor excision may cause severe
disability compromising pt's social life.
• Therefore, aim to remove max amount of lesion without impairing
neurological function has pushed physicians & industry to develop
sophisticated approaches performed in awake & responding pts, to
evaluate neurological dysfunction before tissue removal.
• Awake craniotomy dates back to 2nd half 19th century, when only
indication was epilepsy & Sx done under LA.
• Subsequently, surgical practice extended to resection of tumors
involving functional cortex.
• In more recent years, indications further extended to removal of
supratentorial tumors, regardless of cortical involvement.
• Awake Craniotomy evolved as direct consequence of following:
1.huge improvement of diagnostic tools;
2.impressive development of intraoperative functional neurosurgical
3.enhancement of anesthesia monitoring devices,
4.Pharmacokinetic & dynamic properties of new anesthetic agents &
• Main advantage : intraop electrocorticography & mapping for
accurate identification of brain areas controling motor function &
• Allows maximal tumor resection with minimal postop deficits from
retraction, edema &/or resection of eloquent tissue.
• Other advantages include :
1.avoidance of GA
2. avoidance of more intensive monitoring intra-op & postop,
3. low complication rate,
4.reduction in resource utilization (shorter ICU & hospital stay).
• Functional mapping performed by stimulating brain with small
• Neuropsychologist then performs neurocognitive testing &/or
monitors motor responses during mapping & later tumor resection.
• Intraop testing of language & motor function gold std.
• Intraop monitoring severely inhibited by GA: some higher cortical
brain functions (i.e. speech) cannot be monitored during surgery.
• "Awake craniotomy" is misleading term, as different Sx phases
require various levels of sedation & pt maintained completely
awake only during mapping procedure & early resection of tumor.
• Preop selection, evaluation & preparation of pts different than GA.
• Cooperative, able to participate in neurocognitive testing.
• Must have uncomplicated airway, also candidate for GA.
• Accurate detailed explanation of procedure (i.e. intraop sounds of
surgical instruments, head immobilization, voices...).
• Regarding sequence of events during Sx & possible complications,
to minimize fear. (pt's confidence & agreement,
cooperation fundamental factor for successful
• Like any craniotomy, adequate surgical exposure & brain relaxation
• Providing appropriate sedation & analgesia greatest challenge.
• Continuous, rapid modulation of sedation & analgesia level
necessary to manage painful stimuli & cortical testing.
• Adequate analgesia & sedation needed for head frame application,
skin incision, craniotomy & opening of dura.
• Of utmost importance, pt must be awake & alert during brain
mapping, able to participate in complex neurocognitive testing.
• Vital functions to be ensured, emergency support if deterioration of
clinical status occurs.
• Positioning : comfortably with bolsters & additional padding.
Technique selected requires
1.optimal analgesia during nociceptive stimulations
2.sedation/anxiolysis, immobility/comfort during mapping & resection
3. prevention of nausea, vomiting & seizures
4.Maintenance of airway & adequate ventilation
Techniques described for more secure airway
(a) ETT & awakening without tube withdrawal (disallowing vocalization
testing); extubation & re-intubation after testing
(b) placement, removal & replacement of LMA
(c) Non-IPPV has also been described (CPAP, BiPAP).
• Whichever technique used, must anticipate respiratory
complications (low SpO2, increase in EtCO2, hypoventilation/airway
obstruction) & plan of action & required equipment to deal with
difficult airway management.
• In asleep, awake, asleep techniques, initial phase of GA, with
insertion of supraglottic airway device, followed by intraop
awakening for language mapping during tumor resection & finally,
back to GA during craniotomy closure.
• Sarang & Dinsmore retrospectively examined 3 techniques:
(a)sedation with propofol, fentanyl, droperidol & midazolam
(b)propofol infusion, i.v. fentanyl & spontaneous ventilation LMA
(c) propofol & remifentani, IPPV via a LMA.
• Found that profound sedation & apnoea was possible in three
scenarios, must be vigilant to avoid.
• Limitations to NIPPV: nasal mask may be difficult to position,
interfere with surgical field; pts may find it unpleasant.
• Successful use of pressure support ventilation described for pt with
OSAS undergoing awake craniotomy.
5. Greater occipital
6. Lesser occipital
• In addition, line of scalp incision infiltrated with LA.
• Scalp blocks & infiltration with large volumes of LA carry potential
of toxicity in pts already prone to seizures.
• Studies have shown LA absorbed rapidly & potentially toxic conc
achieved in some pts.
• 1st choice hypnotic
• Can be administrated using target control infusion
• With remifentanil, which has very short t1/2, rapid & fine
modulation of sedation depth
• Accurate titration of both avoids devices for airways control.
• Highly specific α2 adrenoreceptor agonist, recommended for use.
• Advantage of providing sedation & analgesia without respiratory
• Provides sedation closer to natural sleep, anxiolysis & analgesia,
decreasing need for opioids & antiHTN drugs.
α2 agonist clonidine often used as analgesic co-adjuvant
(a).Supraorbial & supratrochear - above eyebrow at midpoint,
needle inserted perpendicular to skin, & medial margin of orbit.
(b) Auriculotemporal - 1.5cm anterior to tragus, perpendicular to skin.
(c) Zygomatico temporal - midway btwn supraorbital ridge & post
margin of Zygoma; deep infiltration within temporalis & fascia.
(d) Post auricular branches(greater auricular) - 1.5 cm posterior to ear
at level of tragus btwn skin & bone.
(e) Greater & lesser occipital- along superior nuchal line approx
halfway btwn occipital protruberance & mastoid process;
infiltration done with 22 G spinal needle.( all others with 23G)
• Remaining soultion used to infiltrate pin sites & line of incision, 15
mins before procedure & lasts atleast 4-5 hours.
• In lesions near motor cortex, electrical stimulation used to test
motor function & map area.
• With speech, considerable inter-patient variability in location &
cortical representation of speech areas.
• Intraoperative mapping of speech involves the identification of
Broca’s area by producing speech arrest with cortical stimulation, &
other speech areas by a series of naming & word/sentence
comprehension tests using books or slides.
• Computer programs available that allow dysphasic patients to
respond to images.
• In pts who are fluent in >1 language, localization problematic as
multiple representation sites.
1.Seizures 2. Decreased level of consciousness
3.Increased ICP 4. Neurological deficit
5.HTN 6. Nausea & vomiting
7.Pain & loss of patient cooperation
• Onset of new seizures common presentation, esp during brain
mapping (5-20 %), due to decreased levels of anticonvulsants /LA
• Focal / general, usually self-limiting.
• Protocols include prophylaxis with antiHTNs, anticonvulsants &
antiemetics to prevent these complications.
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