by DR RANJEET KUMAR PDCC NEUROANESTHESIA AT RIMS RANCHI

1. Anaesthetic management of
Supratentorial tumours
Dr Ranjeet(SR)
Moderator:Dr Saurabh (Asst.Proff.
RIMS)

2. Demography
• Incidence of CNS tumors ranges from 10 to 17 per
100,000
• Half to three-quarters are primary tumors, rest are
metastatic
 In childhood tumors are likely to arise in the
posterior fossa
 In adults - supratentorial

3. Tumors of the nervous system may arise from
Cells of the coverings
Cells intrinsic to the brain
Other cell populations within the skull
Metastasis (spread from elsewhere in the body )

4. Intracranial
neoplasm
space occupying
Raised ICP
Obstruction to
CSF flow
hydrocephalous
oedema
Raised ICP
destruction
neurological deficit
compression
neurological deficit
irritation
seizures
Patho- physiological affects of
intracranial neoplasms

5. Pathophysiologic consideration of
brain tumors
• Intracranial pressure
• Munroe kellie doctrine
CSF COMPARTMENT
BLOOD
COMPARTMENT
CELLULAR
COMPARTMENT
FLUID COMPARTMENT
ICP

6. Increase in ICP leads to
1. cerebral ischemia(CPP=MAP-ICP)
2. Brain herniation
1. Subfalcine herniation
2. Transtentorial
3. Cerebellar
4. Transcalvareal

7. Subfalcine
Uncal or
transtentorial
Cerebellar
Trans calvarial

8. CLASSIFICATION OF TUMOURS
1. TUMOURS OF THE GLIAL TISSUE – (GLIOMAS)
2. TUMOURS OF NEURONS
3. MIXED TUMOURS WITH GLIAL & NEURONAL COMPONENTS
4. POORLY DIFFERENTIATED AND EMBRYONAL TUMOURS
5. TUMOURS OF THE MENINGES
6. PERIPHERAL NERVE SHEATH TUMOURS
7. METASTATIC TUMOURS
8. PRIMARY CNS LYMPHOMA
9. Miscellaneous TUMOURS

9. CLASSIFICATION
MIXED TUMOURS WITH
GLIAL & NEURONAL
COMPONENTS
Ganglioglioma
Dysembryoplastic
Neuroepithelial tumour
(DNT)
POORLY DIFFERENTIATED
AND EMBRYONAL
TUMOURS
Medulloblastoma
Atypical teratoid/rhabdoid
tumour
Medulloepithelioma
Dysplastic Gangliocytoma of
the cerebellum (Lhermitte
–Duclos disease)
Polar spongioblastoma
TUMOURS OF THE GLIAL
TISSUE – (GLIOMAS)
Astrocytoma
Oligodendroglioma
Ependymoma
TUMOURS OF NEURONS
Gangliocytoma
Neuroblastoma
Ganglioneurocytoma
Gliomatosis cerebri
Cerebral neuroblastoma
Central neurocytoma
TUMOURS OF
THE MENINGES
Meningioma
PERIPHERAL
NERVE
SHEATH
TUMOURS
Schwannoma
Neurofibroma
Malignant
nerve sheath
tumour-
(Malignant
Schwannoma)
Miscellaneous
TUMOURS
Hemangioblastoma
Craniopharyngioma
Pituitary tumours
Mesenchymal
tumours
METASTATIC
TUMOURS
PRIMARY CNS
LYMPHOMA

10. Briefanatomy

11. Brief anatomy

12. SUPRATENTORIAL
TUMOURS
CLASSIFICATION
INTRA AXIAL
BRAIN PARENCHYMA
GLIOMA(35%)-
ASTROCYTOMA
OLIGODENDROGLIOMA
PINEALOMA
INTRAVENTRICULAR
EPENDYMOMA
CHOROID PLEXUS
PAPILLOMA
EXTRAAXIAL
MENINGIOMA(15%)
PITUITARY
ADENOMA(8%)
SCHWANOMMA
DERMOID
CRANIOPHARYNGIOMA
CHORDOMA

13. Anaesthetic management of
supratentorial tumours
Problems and concerns
1. Effect of anaesthetics on brain
2. Surgical position & concurrent medications
3. Measures to decrease ICP & brain bulk
4. Complications

14. • What are the goal of anesthesia
in supratentorial tumor

15. 1)Global maintenance of cerebral homeostasis by
● normovolemia andnormotension
● normoglycemia
● mild hyperoxia andhypocapnia
● mild hyperosmolality andhypothermia
2) Minimization of need for surgical retraction by using chemical
brain retraction.
3) Maximize therapeutic modalities that ↓intracranialvolume.
4) Provision of early neurosurgicalawakening
5) Providing lax field to surgeon

16. Understanding
Neurophysiology
CerebralBlood
Flow
Cerebral
MetabolicRate
UNCOUPLED
I.V.Anaesthetics
CBF CMRO2
STILL
COUPLED..!!
VolatileAnaesthetics
CBF CMRO2
NO LONGER
COUPLED
Hence
Cerebro-
protective

17. Effect of anaesthetic drugs
BARBITURATES PROPOFOL ETOMIDATE KETAMINE
CMRO2 CMRO2 CMRO2 CMRO2
CBF CBF CBF CBF
ICP ICP ICP ICP
Cerebral
protection +
CPP preserved CPP decreased No reduction in
CPP
Autoregulation
maintained
Autoregulation
maintained
Autoregulation
not evaluated
CO2
responsiveness
preserved
CO2
responsiveness
preserved
CO2
responsiveness
preserved

18. N2O HALO ISO SEVO ENFLU DES
CMRO2
CBF
ICP
CSF
production
decreas No
change
increas increas
CSF
absorption
decreas increas increas No
change

19. Reducingbrain bulk, reducingtensionOsmotic agents
Mannitol
20%(1098 mOsm/L) mol wt. 182
- ↑ blood osmolality
- ICPeffect within 4 -5 min, lasts 3-4 hrs., dose 0.5-2
g/kg.
- No change in CBFand
↓ICP by 27%at 25 min. (auto-regulationintact)
-↑CBF by 5%and
↓ in ICP18 %at 25 min (impaired auto-regulation).
Generation
of Idiogenic
osmoles
Rebound
increasein
ICPLatersequale

20. Reducingbrain bulk, reducingtension
Osmotic agents
HypertonicSaline
Concentrations of 3%,7.5%, 23.4%
DecreaseICP
IncreaseCPP• Nodeleterious diuresis and undesired
hypovolemia.
• Useful in patients refractory toMannitol.
• CNS SystemicDecreased consciousness Hyperosmolality, Hypernatremia
Seizures CHF,Hypokalemia
Central Pontine Myelinolysis HyperchloremicAcidosis
Subdural/parenchymal
hemorrhage
Coagulopathy, Phlebitis
Rebound edema RenalFailure

21. Loopdiuretics
● ICPreduction is small and lesseffective.
● Isosmotic reduction of the extracellularspacei.e.
↓ICP without ↑ CBVand osmolality.
● In patients with impairedcardiac reserve
Mechanism:
1) Systemic diuresis.
2) ↓cerebral edema by improving cellular watertransport.
Dose 0.5-1 mg/kg iv alone or 0.15 -0.3 mg/kg with Mannitol

22. Steroids
● ↓ Peritumoral vasogenic edema
● effect may take 12-36hrs.
Mechanism:
1)repair of abnormal BBB
2)prevention of lysosomalactivity
3)enhanced cerebral electrolyte transport
4)promotion of water and electrolytesecretion
5)Inhibition of Phospholipaseactivity

23. Hyperventilation
● Cerebral vasoconstriction →↓CBF
● Δ1mm HgPaCO2→1-2 ml /100 gm./minΔCBF
● Duration of effectiveness →4-6hrs.
● Impaired responsiveness →ischemia, tumors, infection etc.
● Target PaCO230 -35 mm Hg

24. CSF Drainage
• By either direct puncture of lateral ventricle by
surgeon or lumbar spinal catheter by
anaesthesiologist
• A/C brain herniation may occur
• Draining 10-20 ml CSF effectively reduces
brain tension

25. Fluids
● Restricted fluid intake →traditionalapproach
● Cancausehypovolemia, hypotension , ↓renal perfusion,
electrolyte and acid basedisturbances.
● Glucose free iso-osmolar solution
● Hourly maintenance fluids and replacement oflosses.
● Hematocrit 25-30%

26. PEEP
● ↑ICP by ↑ mean intra-thoracic pressure , impairing cerebral
venous outflow and cardiac output .
● used cautiously and with monitoring
● 10 cm H2Oor less have been used without significant rise in
ICPor ↓CPP.

27. Positioning
• Common neurosurgical positions are
– Supine
– Lateral (park bench)
– Semilateral (Janetta)
– Prone
– Sitting

28. Position
Sitting position –
fallen in disrepute
o Air Embolism
o Severe
Hypotension
Significant Neck
Flexion
o Airway Obs.
o Obs.to cerebral
venous outflow
Headabove heart
level
Venous air embolism
Tongue
swelling

29. Position
Intense Nociceptive
stimulation during
pin application
Responsecan be
blunted with
additional dosesof
Fentanyl/ Propofol

30. Sitting Position
Good surgical exposure, enhanced CSF
& venous drainage, minimal bloodloss
Unstable hemodynamics and potential
for Venous air embolism
Macroglossia Excessiveneck flexion
Useof multiple
instruments suchasET
Tube, OralAirway,
Esophageal
stethoscope
simultaneously.

31. Sitting Position
Veins in the skull may notcollapse due
to adherence to bone ordura.
Cut edge of skull may also admitair
Air enters the pulmonarycirculation
and creates avapor lock
Sequale Pulmonary edema
Suddendrop in right heartCO
Acute CorPulmonale
Arterial hypoxemia
Patent Foramen Ovaleleads
to Paradoxicalembolism
Patent Foramen Ovaleand
other cardiac effects are
contraindications.
Obstruction in coronaries
leads to myocardialischemia
and ventricular fibrillation
Neurologic damage follows air
embolism to brain

32. Sitting Position
Doppler USG
Not adequate for
quantification of air
TEEis particularly
useful
Canquantify and
detect
SuddenDrop in EtCO2
Suddenrise in right
atrial andpulmonary
pressures
Changein end-expired
nitrogen conc.
precedes drop in CO2
Suddenattempt to
initiate spontaneous
breaths
“Gasp Reflex”
Hypotension,
Tachycardia,
Late Signs Cardiac
Arrhythmias,
Cyanosis
Millwheel murmur
What to do upon detectionof
Venous air embolism..?

33. Sitting Position
• Surgeon should flood the site withfluid
• Occlusive material to boneedges
• Aspirate air through right atrialcatheter
• Discontinue Nitrous Oxide (for fear ofincreasing bubble size)
• Direct Jugular Venouscompression
• Sympathomimetic drugs to treathypotension
• β-adrenergic agonists (dopamine/ dobutamine) for lowCO.
• β2-agonists for bronchospasm
• In severe cases,shift patient to Hyperbaricchamber.

34. Hemodynamics
Cerebral Blood Flow (CBF)is pressure dependent
Adequate preoperative blood pressure control inhypertensives
Desist from acute normalisation of B.P.in ahypertensivepatient
Induced Hypotension is no longerfavoured
Direct Vasodilators – SNP,NTG& CCBsmay actually increase CBF&
ICP
β-Blockers andACEInhibitors arepreferred.

35. Implications of concurrentmedications
Common medications – anticonvulsants & steroids
Anticonvulsant agent, phenytoin may decrease the durationof
action of non-depolarising musclerelaxants.
Adrenocortical suppression due to prolonged steroid therapymay
causeunexpected hypotension intraoperatively.

36. Preoperative asessment
• History
– Raised ICP- Headache, Nausea, vomiting, blurred
vision
– Level of consciousness
– History of seizures
– Focal neurologic signs – sensory deficits,
hemiparesis, cranial nerve palsy
– Medication – steroids, antiepileptics, mannitol

37. • GCS score
• Papilloedema
• Cushings response
– HTN, bradycardia
• Focal neurological signs-document
hemiparesis,
sensory deficits, cranial nerve palsy
• Hydration status
– Ask about duration of bed rest
– Fluid intake
– Diuretics

38. Investigations
• BRE
• URE
• RBS
• RFT
• LFT
• S.electrolytes
• Coagulation profile
• ECG all leads
• CXRAY

39. • CT/ MRI
– Look for size & location of tumor
• To assess surgical position
• Potential for blood loss
• Risk of air embolism
– Midline shift
– Effacement of ventricles
– Loss of sulci
– Obliteration of cisterns
– Cerebral edema
– Hydrocephalus

40. Preoperative Preperation
• Preop steroids
– Decreases edema
– Decreases BBB pemeability
– Improves the viscoelastic properties of intracranial
space
– Clinical improvement within 24 hrs
– Decreases ICP within 48-72 hrs
ARRANGE BLOOD

41. Premedication
Not premedicated outside operating room
– Benzodiazepines like midazolam if no signs of
raised ICP
 H2 blockers & gastric prokinetic drugs

42. Premedications
Depression of
Consciousness
Sedative Premedication
Airway
Obstruction
Hypoxia
Hypercapnia
Anxiolysis
Continuation of
concurrent
medications like
Steroids,
anticonvulsants,
antacids,
antihypertensives..

43. Monitoring
ECG
NIBP
Pulseoximetry
CVP
ABP
Glucose
Electrolyte
Capnography
Osmolality
Transducers at level ofbrain

44. Monitoring
• PR, MAP, SPO2, ETCO2
• U/O
• CVP
• Temp

45. Others
• Precordial doppler, Trans esophageal ECHO
• ICP monitor
• EEG – CMRO2, depth of anaesthesia, cerebral
ischemia
• Evoked potentials
• Jugular venous bulb monitoring – determines
adequacy of cerebral perfusion & oxygenation

46. Induction
Propofol
(1.25 - 2.5mg/kg)
Thiopentone
(3-6 mg/kg)
Etomidate
0.3 – 0.6mg/kg
Ketamine
(1.0 - 2.0mg/kg)
tends to increaseICP
Epileptogenic

47. Induction
• Avoid ICP elevations
• Preserve CPP
• Adequate depth of anaesthesia

48. Intubation
1)
2)
3)
4)
5)
Control ICPrise on induction
Narcotics
Lidocaine
Short-acting β-blocker
Deepen plane of anesthetic
Quick intubation
1)
2)
Relaxant
Succinylcholine – modest rise in ICP
NDMRscan be used.(atracurim
histamine release ,laudonosine)

49. • Lignocaine 1.5mg/kg 90sec before intubation
• Succinyl choline (transient increase in ICP)
Prevented by deep anaesthesia and NDMR
• Gentle laryngoscopy & intubation

50. Positioning
• Pin holder application
Deepen with propofol 0.5mg/kg or
TPS 1mg/kg or
Fentanyl 1-3 ug/kg
Or esmolol .5mg/kg or labetalol .075-.15 mg/kg
along with local anesthetic infiltration
• Pin insertion can be associated with venous
air embolism

51. • Mild head up positioning (15-300) to allow optimum
venous drainage
• Secure ETT tightly
• Severe flexion / lateral rotation of head should be
avoided (at least 2 finger space between chin &
nearest bone)
• If head is turned laterally, contralateral shoulder is
elevated with roll to prevent brachial plexus stretch
injury

52. • Intra Op Icp reduction
• Different mode has been discused
• Hyperventilation
• Drugs
• CSF drainage

53. 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

54. • Normal saline
• Normal saline-slightly hyperosmolar (308)
compared to plasma(295)
Disdvantage- hyperchloremic metabolic
acidosis
• Ringer lactate(280) hypoosmolarlarge
volume can cause cerebral edema

55. Colloids
• Albumin is a reasonable choice if colloid is
required
• Starch containing solutions produces
I. Dilutional reduction of coagulation factors
II. Interferes directly with platelets and factor
viii complex.

56. BP CONTROL
• Maintain cerebral perfusion pressure normal
or high normal range
• CBF is low in many regions after TBI
• Brain compressed under retractors- regional
perfusion press will be low

57. Maintenance
● Goal: control of brain tension via control of CBFand CMR (as
shown before)
● mild hyperosmolality
● iv anesthetic , adequatedepth
● mild hyperventilation (EtCO2<35), Mild hyperoxygenation
● mild controlled hypotension
● normovolemia , novasodilators
● Minimal PEEP
● Avoidance of brainretractors.

58. 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

59. ● In brain tumors , infusion of propofol with fentanyl or
remifentanil hasshown to ↓ ICPmore effectively than either
isoflurane or sevofluranealone
● However the risk of cerebral hypoperfusion hasbeenquestioned
with propofol (↓CBF/CMRratio)
● If severe intracranial hypertension persists despite
hyperventilation and other maneuvers, and the brain is tight a
total intravenous technique ispreferred.
Maintenance

60. DelayedAwakening
Largeintracranial tumor
Residual anesthetics
Metabolic or Electrolytedisturbances
Residual hypothermia
Surgical complications
Seizures
Cerebral Edema
Hematoma
Pneumocephalus

61. Early Vs.Delayed Awakening
● Early awakening :
Advantages:
1)Earlier neurologic examination and intervention ifnecessary
2)Earlier indication of furtherinvestigation
3)Lessstress response
Disadvantages :
1)↑risk ofhypoxemia and Hypercapnia
2) Monitoring in ICU

62. Early Vs.Delayed Awakening
● Delayed awakening :
Advantages:
1)Lessrisk of hypoxemia or Hypercapnia
2)Better respiratory and hemodynamiccontrol
3)Earlier transfer to ICU
Disadvantages:
1)Lessneurologic monitoring
2)Larger hemodynamic changes
3)More catecholamine release.