The document discusses the management of intracranial pressure (ICP) in neurosurgical procedures, emphasizing the need for awareness of the effects of anesthetic agents on cerebral dynamics. It outlines various types of intracranial tumors, their treatment options, and the importance of monitoring techniques during surgery. Additionally, it covers preoperative assessment, potential complications, and specific anesthetic considerations based on patient conditions and tumor characteristics.

2. • 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
cerebral protection.
• 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
dynamics.

3. 1.Uncal
2.Central (transtentorial)
3.Cingulate (subfalcine)
4.Transcalvarial
6.Tonsillar (downward cerebellar)
5.Upward (upward cerebellar or upward
transtentorial)
Supratentorial herniation
1. Uncal – Ptosis, Hemiparesis, pupillary
asymmetry
2. Central (transtentorial) – unconsciousness,
decerebration, bradycardia, hypo/HTN
3. Cingulate (subfalcine) – leg weakness
4.Transcalvarial

4. • Hydrocephalus
– Headache
– Vomiting
– Drowsiness
– Visual disturbances
• Hemiparesis
• Cranial nerve deficits
• Gait disturbances

6. • 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
in .
• Primary or metastatic tumors or chronic SDH can present as chronic
mass lesions.
• 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.

7. • 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
autoregulating.
• In such situations (compromised compliance), small increases in
arterial pressure may produce large increases in CBF, which can
markedly increase intracranial volume & ICP & cerebral
ischemia/herniation.
• In addition to HTN, other causes of increased CBV such as
1.hypercarbia,
2.hypoxia,
3.vasodilating agents,
4. jugular venous obstruction,
can adversely affect cerebral hemodynamics & must
be avoided perioperatively.

8. • Intracranial tumors may be classified as
1.primary (those arising from the brain and its coverings)
2. metastatic.
• 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 &
location.
• Treatment may consist of surgical
resection/debulking/chemotherapy/ radiation.

9. Astrocytoma
• Often present in young adults with new-onset seizures. Upon
imaging, they generally show minimal enhancement with
contrast.
• 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
preclude resection.

10. • 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.

11. Oligodendroglioma
• 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
radioresistant.
• Due to presence of astrocytic cells, they commonly behave like
anaplastic astrocytomas or glioblastoma multiforme later in their
course.

12. Ependymoma
• 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
1.obstructive hydrocephalus,
2.headache,
3.nausea,
4.vomiting,
5.ataxia.
• Treatment consists of resection and radiation. Tumor infiltration
into surrounding tissues may preclude complete resection.

13. 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.

14. Meningioma
• 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
diagnosis.
• 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
calcifications.
• 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.

15. Pituitary Tumors
• 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) &
nonfunctional.
• 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.

16. • 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
bromocriptine.
• Surgical resection transsphenoidally/open craniotomy
approach is often curative for most pituitary tumors.

17. Acoustic Neuroma
• 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 &
disequilibrium.
• 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
uncommon.

18. CNS Lymphoma
• 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
callosum).
• 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.

19. • CTS-associated tumor lysis prior to performing biopsy may
result in failure to obtain an adequate sample to make
diagnosis.
• Mainstay of treatment is chemotherapy (including
intraventricularly delivered drugs) & whole-brain radiation.
• Prognosis is poor despite treatment.
Metastatic Tumor
• 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.

21. • 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
DM
– BUN, Creatinine
– TEE in patients scheduled for tumors in sitting position.
– USG abdomen for polycystic kidney, pheochromocytoma
(Hemangioblastoma) .

23. 1.Anti-convulsants 2. Antihypertensives
3.Steroids 4. Hypoglycaemic agents
5.Diuretics 6. Hormonal therapy
7.Anticoagulants / antiplatelets
NOTE:
• 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.

25. 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
ventilation.
• Decisions to administer anticholinergic drugs or H2-receptor
antagonists not influenced by presence/absence of increased ICP.

26. • 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
nerves.
• 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.

27. • 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
hyperthermia/uncontrolled hypothermia.
• Urine output also measured as indicator of perioperative fluid
balance.
• 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
concern.
• IV access with large-bore catheters , given likelihood
of bleeding & need for transfusion/
rapid administration of fluids.

28. • 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
Willis.
• 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).

29. 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.

30. • 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
be misleading.
• 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
infection.
• When performed with LA before induction, can be uncomfortable to
pt.

31. Hazards of Positioning Prone
• Pressure over the eyeballs, pinna , genitalia
• Kinking of the neck veins
• Extreme flexion – endobronchial migration of the tube,
kinking
• Brachial plexus , ulnar and sciatic nerve injuries

32. • Ventilation perfusion
mismatch
• Common peroneal nerve
injury
• Dependent pinna injury

33. • 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)

34. • 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
cerebral edema.
• 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.

35. • Sustained hypotension must also be avoided (ischemia due to
decreased CPP).
• 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.

37. MUSCLE RELAXANTS
SUCCINYLCHOLINE
• 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
hyperkalemia.

38. • 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
release.
• 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).

39. • 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).

40. MAINTENANCE
• Popular technique - continuous infusion of propofol with
remifentanil / fentanyl. (shown to reduce ICP more effectively than
iso/ sevo), propofol with remifentanil produced quicker emergence
than des/sevo.
• In susceptible pts, risk of cerebral hypoperfusion greater when pts
hyperventilated under propofol anesthesia.

41. • 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
paralysis maintained.

42. MEASURES TO REDUCE ICP
Diuretics:
• 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.
Corticosteroids:
• Dexamethasone (localized cerebral edema surrounding tumors;
requires 12-36 hrs).
Adequate ventilation:
• PaO2 100 mmHg, PaCO2 33-35 mmHg.
Optimize hemodynamics
• (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.

43. 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.
Mannitol:
• 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.

44. • 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
administration.
• Mannitol-induced vasodilation affects intracranial & extracranial
vessels & can transiently increase CBV & ICP while simultaneously
decreasing SBP.
• Hence should be given slowly (10-minute infusion) in conjunction
with maneuvers that decrease ICV (steroids / hyperventilation).
• Prolonged use of mannitol may produce
1.dehydration,
2.electrolyte disturbances,
3.hyperosmolality,
4.impaired renal function.

45. Hypertonic saline
• 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
6.Hypokalemia
7.Subdural & intraparenchymal hemorrhagea

46. FUROSEMIDE
• 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
indicated.

47. CORTICOSTEROIDS
• 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.

48. Potential complications of continuous
periop steroid
• 1.hyperglycemia,
• 2.glucosuria,
• 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.

49. HYPERVENTILATION
• reduces brain volume by decreasing CBF through
cerebral vasoconstriction.
• For every 1 mm Hg change in PaCO2, CBF changes by 2 mL/100
g/min.
• 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
safely applied.

50. NOTE
• 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 &
herniation.
• 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.

51. FLUID THERAPY
1.Do not dehydrate
2.Avoid hypotonic solutions
3.Colloids
4.Blood
5Avoid over-transfusion
• 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.

52. • 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.

53. POSITION
• 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).
PEEP
• 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
ICP.
• 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
monitoring indicated.

54. TEMPERATURE
• 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.
CSF DRAINAGE
• 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
CSF.

55. EMERGENCE
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

56. • IC hematoma & major cerebral edema most
feared complications.
• Emergence from anesthesia should be as smooth as possible,
avoiding straining/ bucking.
• Bucking can cause HTN & elevated ICP, leading to postop hge &
cerebral edema.
• 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.

58. • 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.

59. • 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
technology;
3.enhancement of anesthesia monitoring devices,
4.Pharmacokinetic & dynamic properties of new anesthetic agents &
delivery systems.

60. • Main advantage : intraop electrocorticography & mapping for
accurate identification of brain areas controling motor function &
speech.
• 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
electrical charge.
• Neuropsychologist then performs neurocognitive testing &/or
monitors motor responses during mapping & later tumor resection.

61. • 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
procedure).

62. • Like any craniotomy, adequate surgical exposure & brain relaxation
required.
• 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.

65. 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
5.hemodynamic stability
6.brain relaxation
Techniques described for more secure airway
protection include
(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).

66. • 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.

67. • 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.

68. 1. Supraorbital
2. Supratrochlear
3. Zygomaticotemporal
4. Auriculotemporal
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.

69. Propofol
• 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.
Dexmedetomidine
• Highly specific α2 adrenoreceptor agonist, recommended for use.
• Advantage of providing sedation & analgesia without respiratory
depression.
• Provides sedation closer to natural sleep, anxiolysis & analgesia,
decreasing need for opioids & antiHTN drugs.
α2 agonist clonidine often used as analgesic co-adjuvant

70. • Nerves blocked
1.supraorbital,
2.supratrochlear,
3.zygomatico temporal,
4.auricuculotemporal,
5.posterior auricular,
5.lesser & greater occipital.
• Total solution– 80ml
• 0.5% Bupivacaine – 40ml
• 2% Lidocaine – 20ml
• Adrenaline – 400 mcg(in
4ml saline)
• Saline – 16ml

71. (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.

72. • 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.

73. 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
toxicity.
• Focal / general, usually self-limiting.
• Protocols include prophylaxis with antiHTNs, anticonvulsants &
antiemetics to prevent these complications.