This document discusses considerations for anesthesia management of supratentorial brain tumors. It begins by describing the anatomy of the supratentorial and infratentorial compartments. Common tumor types in the supratentorial compartment include gliomas, meningiomas, pituitary adenomas and metastases. Key goals for anesthesia include maintaining adequate brain perfusion and oxygenation, facilitating tumor resection, and allowing for rapid emergence. Monitoring includes standard ASA monitors plus ICP monitoring if elevated preoperatively. Positioning can affect ventilation and ICP, so padding pressure points is important. Induction aims to avoid ICP elevations while maintaining cerebral perfusion pressure. Maintenance involves propofol, opioids and muscle relaxation to prevent movements

1. Supratentorial masses-
anaesthetic considerations.
Dr. ZIKRULLAH.

2. Introduction
• Brain tumors constitute the majority of neurosurgical
conditions that present for elective operations.
• The Brain can be divided into two parts by the tentorium
cerebeli –
1.) Supratentorial Compartment.
2.) Infratentorial Compartment.
• About 80% of the tumors are located in the supratentorial
compartment and about 20% in the posterior fossa.

3. • SUPRATENTORIAL COMPARTMENTS –
• largest part of the brain.
• It is divided by falx cerebri, is contributed to by the
anterior cranial fossa and middle cranial fossa.

4. • INFRATENTORIAL COMPARTMENTS -
• It includes ?
• Brain stem & Cerebellum.
• Brain Stem- It includes the mid brain, the pons and the
medulla.

5. • SUPRATENTORIAL MASSES
• 1. INFECTION – Subdural abscess – Epidural abscess
• 2. HEMATOMA – SDH, EDH, Intracranial bleed
• 3. HYDROCEPHALUS
• 4. NEOPLASMS
• 5. ANEURYSMS & AV MALFORMATIONS

6. NEOPLASMS OF BRAIN ?
• PRIMARY (85%) – most of the tumors are primary.
1).Benign--
Meningiomas, PitutaryAdenomas, Craniopharyngioma,
Neurocytoma, Haemangioma, Pilocytic astrocytoma.
2).Malignant --
Astrocytoma/Glioma , Ependymoma , Medulloblastoma ,
Lymphoma, Germ cell tumor.
• METASTASIS (15%)– secondary tumors.

7. Classify supratentorial masses ?

8. Specific tumor types
• Astrocytoma
• Often present in young adults with new-onset seizures.
• Upon imaging, they generally show minimal enhancement
with contrast.
• 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.

9. • 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.
• 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.

10. • Oligodendroglioma
• Arising from myelin-producing cells within CNS, account
for only 6% of primary intracranial tumors.
• Classically, seizures predate appearance of tumor on
imaging.
• Calcifications are common & visualized on CT imaging.
• consists of mixture of oligodendrocytic & astrocytic cells.

11. • Treatment & prognosis depend on the pathologic features.
• Initial treatment involves resection since, early in the
course, consists of primarily oligodendrocytic cells, which
are radioresistant.

12. • Ependymoma
• Arising from cells lining ventricles & central canal of
spinal cord, commonly present in childhood & young
adulthood.
• Most common location?
• floor of 4th ventricle.
• Symptoms include: obstructive hydrocephalus, headache
,nausea, vomiting, ataxia .
• Treatment consists of resection and radiation.

13. • Meningioma
• Usually extra-axial (arising outside of the brain proper),
• slow-growing, well-circumscribed, benign tumors
• arising from arachnoid cap cells, not dura mater
• slow-growing nature, can be very large at time of
diagnosis.

14. • 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. • 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.

16. • 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

17. • 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, EBV.
• Symptoms depend on location of tumor.

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.

20. Pituitary tumors

21. • Anaesthetic management of supratentorial tumors.

22. problems and concerns ?
• Effect of anaesthetics on brain.
• Intracranial pathophysiology of tumors.
• Surgical position & concurrent medications
• Measures to decrease ICP & brain bulk.
• Intraoperative monitoring requirements.
• Implications of fluid therapy
• Perioperative haemodynamic management.
• Complications

23. • Preop knowledge of Surgery to plan technique,
Position.
Intraop monitoring.
Neurophysiological monitoring.
Blood conservation strategies.

24. • Major goals during anesthesia include ?
maintenance of adequate perfusion & oxygenation of
normal brain.
optimizing operative conditions to facilitate resection.
ensuring a rapid emergence for neurologic assessment.
accommodating intraoperative electrophysiologic
monitoring.

25. Preanesthetic evaluation?
• Assess neurological status, deficit to be documented.
• Routine pre-op assessment.
• Airway, cvs and respiratory system.
• Evaluate hydration status.
• Investigations appropriate for age, general status of
patient and type of surgery .
• The preanesthetic evaluation should attempt to establish
the presence or absence of intracranial hypertension.

26. • Computed tomographic (CT) and magnetic
resonance imaging (MRI) scans should be reviewed
for evidence of brain edema, ventricular size and
midline shift greater than 0.5 cm.
• Medications should be reviewed with special
reference to corticosteroid, diuretic, and
anticonvulsant therapy.

27. Monitoring ?
• Standard ASA monitoring devices.
• 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 cranium is open, ICP = atm pressure & CPP =
MAP

28. • Capnography : can facilitate ventilation & PaCO2
management as well as detecting VAE
• Urine output also measured as indicator of perioperative
fluid balance.
• IV access with large-bore catheters , given likelihood
• of bleeding & need for transfusion.
• rapid administration of fluids.

29. • CVP - reliable means of large-bore IV, monitor of fluid status.
• Avoids increased ICP from both head-down position & decreased
cerebral venous outflow.
• Neuromuscular function should be monitored.
• Peripheral nerve stimulator : monitoring persistence of drug-
induced skeletal muscle weakness/paralysis

30. • Preoperative ICP monitoring
• Management of patients with intracranial hypertension is
greatly facilitated by monitoring ICP perioperatively.
• A ventriculostomy or subdural bolt is commonly
employed and is usually placed by the neurosurgeon
preoperatively under local anesthesia.
• A ventriculostomy has the added advantage of allowing
removal of CSF to decrease ICP.

31. Brain monitoring ?
• Electroencephalogram,
• Evoked potentials,
• Jugular venous bulb oxygen saturation (Sjo2),
• Flow velocity measured by transcranial Doppler (TCD),
• Brain tissue Po2 (btPo2),
• ICP

32. POSITIONING & ITS PROBLEMS ?
• Common neurosurgical positions are:
• Supine
• Lateral (park bench)
• Semilateral (Janetta)
• Prone
• Sitting

33. 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.

34. • avoid extreme flexion or rotation of the neck as it impedes
jugular venous drainage and can increase ICP
• The head is elevated 15°–30° to facilitate venous and CSF
drainage.
• Pressure points should be padded
• Eyes taped to prevent corneal damage from exposure or
irrigation of fluid
•

35. • Re-check placement of ETT after positioning.
• During positioning, the tracheal tube should be well
secured and all breathing circuit connections checked.
• Risk of unrecognized disconnection as the patient's
airway is not easily accessible.
• Head is often secured in place using Mayfield 3-point
fixator

36. HAZARDS OF POSITIONING LATERAL
• Ventilation perfusion mismatch.
• Common peroneal nerve injury.
• Dependent pinna injury.

37. Preoperative Preperation ?
• Preop steroids
• -Decreases edema.
• -Decreases BBB permeability.
• -Improves the viscoelastic properties of intracranial
space.
• -Clinical improvement within 24 hrs
• -Decreases ICP within 48-72 hrs
• Arrange blood .

38. • Premedication
• Benzodiazepines like midazolam if no signs of raised ICP.
• H2 blockers & gastric prokinetic drugs.
• Anticonvulsants
• Intraop seizures—Cortical irritation, Cortical incision,
Brain surface irritation by retractors.
• Levetiracetam can be safely given even in TBI

39. • Vascular access
• 2 large widebore peripheral IV lines.
• Central Venous access :
• Large vascular tumors
• Extensive bone resection
• Major cardiovascular compromise present
• Vasoactive drugs are to be infused
• Risk of venous air embolism

40. • Arterial cannulation
• Preinduction is appropriate.
• Need for close monitoring & control CPP
• (transducer at level of external auditory meatus / circle of
willis)
• ABG.
• RBS or S. electrolytes.

41. Induction goals ?
• Avoid ICP elevations
• Preserve CPP
• Adequate depth of anaesthesia

42. • Achieved with drugs ( thiopental, etomidate, propofol)
• produce rapid, reliable onset of unconsciousness
without increasing ICP.
• In presence of raised ICP, thiopental is commonly used
• 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

43. • Adequate depth & profound skeletal muscle paralysis
should be achieved prior to laryngoscopy, (as movement
can abruptly increase CBF & ICP).
• Lidocaine (1.5 mg/kg) also administered IV 90sec before
intubation to suppress laryngeal reflexes
• Administration of succinylcholine associated with modest,
transient increases in ICP. (risk benefit assessment)
• Gentle laryngoscopy & intubation.

44. • Maintenance
• Maintain with propofol infusion & opiod till dura is
opened
• N2O + O2 (50-70%)+ Propofol infusion 50-150 ug/kg)
• Muscle relaxants
• Vecuronium is ideal
• NDMR with histamine release is avoided
• Volatile anesthetics may be used once dura open.

45. • 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.
• Spontaneous movement by pts must be prevented
(dangerous increases in ICP/herniation/bleeding).
• In addition to adequate depths of anesthesia, skeletal
muscle paralysis maintained.

46. Effect of anaesthetic drugs ?

47. MUSCLE RELAXANTS
• Succinylcholine
• Transient increase in ICP
• Caused by increased afferent signals from muscle spindles
• Prevented by deep anaesthesia, defasciculation with
NDMR

48. • NDMR
• With histamine release(eg Atracurium, mivacurium)
• Cause cerebral vasodilatation & increase ICP
• Simultaneous decrease in BP & cause reduction in CPP
• Laudanosine-metabolite of atracurium -seizures

49. • Steroidals (pancuronium,vecuronium & rocuronium) may
be better relaxants (do not directly affect ICP).
• 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.

50. MEASURES TO REDUCE intra-op ICP ?
• Hyperventilation
• Hyperosmolar therapy- Mannitol, glycerol, hypertonic
saline
• Loop diuretics- furosemide.
• Corticosteroids- dexamethasone, methylprednisolone.
• Barbiturate therapy.
• Adequate sedation and analgesia.

51. • Hyperventilation
• Hyperventilation decreases PaCO2, which can induce constriction
of cerebral arteries by alkalinizing the CSF.
• The resulting reduction in cerebral blood volume decreases ICP.
• reduces brain volume by decreasing CBF through cerebral
vasoconstriction.
• Aggressive hyperventilation (PCO2<25 mm hg) should be avoided
as it may lead to cerebral ischemia.
• Maintain PaCO2 30-35 mm Hg.

52. • Mannitol: Most commonly used hyperosmolar agent.
• Infusion 0.25-1.0 g/kg.
• Intravenous bolus administration of mannitol lowers the ICP in 1
to 5 minutes with a peak effect at 20 to 60 minutes.
• The effect of mannitol on ICP lasts 1.5 to 6 hours.
• 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.

53. • By increasing osmolality of blood relative to brain,
• pulls water across intact BBB from brain to blood
• to restore the osmolar balance
• Hence should be given slowly (10-minute infusion) in conjunction
with maneuvers that decrease ICV (steroids / hyperventilation
• Side effects :
• Acute hypervolemia (due to vasodilatation)
• Electrolyte imbalance

54. • Glycerol
• Trivalent alcohol.
• Used systemically and orally to decrease the ICP.
• Not metabolically inert and is partially metabolised to CO2 and
water.
• Oral glycerol decreases the ICP in 30-60min.
• Dosage: 1-2g/kg, maintainence 0.5-1gm/kg every 3-4 hrs
• Complications: hemolysis, hemoglobinuria, renal failure and
hyperosmolar coma

55. Hypertonic saline ?
• Mechanism of action:
• Membrane stabilizing effect helps in preserving BBB.
• Direct vasodilatation of pial vessels
• Reduction of blood viscosity due to enhancement of the
intravascular volume
• Rapid absorption of cerebrospinal fluid
• Restoration of the normal membrane potentials
• Local dehydration of brain tissue

56. Loop diuretics
• furosemide
• Used in conjunction with mannitol to treat raised ICP.
• Furosemide works synergitically with mannitol
• Removes free water
• Appropriate in patients with fluid overload
• Decreases CSF production
• Decreases edema in pathological areas (disrupted
BBB)

57. • 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.

58. • CORTICOSTEROIDS
• Dexamethasone is the most widely used
• Steroids are effective in reducing ICP in tumors.
• Steroids preop frequently cause neurologic improvement
that precede ICP reduction.
• No proven benefit in head injury patients.

59. MOA for steroidal reduction in brain edema ?
• Reduction in CSF production
• Membrane stabilization & restoration of BBB
• Reduction in ICP secondary to antiedema action
• Improves CSF bulk outflow at arachnoid villi.
• improved brain metabolism,
• promotion of H2O & electrolyte excretion,
• inhibition of phospholipase A2 activity.

60. Barbiturate therapy
• Barbiturate protect brain from anoxic, ischemic and
vasogenic cerebral edema.
• Useful in reducing ICP resistant for other methods of
treatment.
• Mechanism of action:
• Uncouples brain metabolism and CBF
• Reduces CMRO2 permitting tolerance of a degree of
ischemia or anoxia => lower demand for CBF =>reduces
the CBV and hence reduces the ICP.
• Free radical scavenger

61. • Dosage: 10mg/kg adminstered over 30min.
• Followed by 1-5mg/kg to maintain a serum
concentration of 3.5 – 4.5mg/100ml or 10 – 20min of burst
suppression

62. Fluid management ?
• Aim---to maintain normovolemia, normotension
• Avoid reduction of serum osmolarity
• Keep hematocrit around 30 %
• Glucose containing solutions to be avoided
• Hyperglycemia -> increased lactate production ->
intracellular acidosis -> aggravate neuronal injury
• Blood glucose <140-180 mg%

63. • Normal saline and ringer lactate preferred
• 0.9% saline is the preferred crystalloid but may cause
hyperchloraemic acidosis when large doses are infused
• Normal saline-slightly hyperosmolar (308) compared to
plasma(295)
• Ringer lactate(280) hypoosmolarlarge volume can cause
cerebral edema.
• Alternate NS and RL litre by litre in case of large volume
administration

64. BP CONTROL
• Maintain cerebral perfusion pressure normal or high
normal range
• CBF is low in many regions after TBI
• Autoregulatory response may not be intact after TBI/
SAH
• Brain compressed under retractors regional perfusion
press will be low

65. PONV:
• very common after craniotomy despite the widespread use of
dexamethasone.
• Decreased incidence with Propofol anesthesia.
• Treatment / prevention:
• Ondansetron 4 mg (0.1 mg/kg in children)
• Granisetron 0.01–0.04 mg/kg
• Dolasetron 12.5 (0.035 mg/kg in children )
• Refractory cases
• Dexamethasone 4–10 mg (0.10 mg/kg in children), combined
with another antiemetic.

66. Emergence from Anaesthesia
• Aims during emergence from anaesthesia
• Smooth emergence
• Maintain MAP, CMRO2, PaO2, PaCO2, Temp
• maintenance of stable ICP, thereby adequate CPP,
• Avoid factors that lead to intracranial bleeding
• (coughing, bucking, intratracheal suctioning, ventilator fight)
• The patient must be fully awake at the time of extubation so
that neurological examination can be performed

67. • Extubate patients if normal criteria are met and if High
ICP is not out of control, patients who remain intubated
should be sedated if agitation is a problem.
• The patient should not be allowed to cough through
ETT(tachycardia, hypertension and increased ICP), it
may precipitate intracranial hemorrhage or worsen
cerebral edema.

68. Awakening sequence ?
• Discontinue opioids (bolus / infusion) ~ 60 min before planned
emergence
• Progressive rise of PaCO2 to normal
• Stop volatile anesthetics during skin closure
• Lignocaine 1.5mg/kg to be given as head dressing begins, which
decrease coughing & straining
• Adequate suctioning
• Antagonise muscle relaxant, Stop N2O
• Extubate
• Transfer to pacu/icu for post op monitoring.

69. causes for late emergence ?
Preoperative low GCS
Large tumor
Residual anesthetics
Surgical complications
Cerebral edema
Hematoma

70. PACU MANAGEMENT ?
• Regular neurological observations
• Any neurological deterioration should raise suspicion of
ICB/ oedema. Urgent CT should be considered.
• Other aspects:
• Hemodynamic should be closely monitored to maintain
adequate CPP.
• Electrolyte imbalance (esp sodium)
• U/o should be monitored(diabetes insipidus)

71. Thanks….