Anesthetic management of supratentorial tumuors

1. ANAESTHETIC MANAGEMENT OF
SUPRATENTORIAL SPACE
OCCUPYING LESIONS

2. Anatomy of supratentorial space
Falx cerebri
Tentorium
cerebelli

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

4. NEOPLASMS OF BRAIN
• PRIMARY (85%)
• METASTASIS (12%)

5. 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

6. Meningioma
• Slow growing benign tumor
• Well circumscribed
• Arise from arachnoid cap cells
• Most common sites–near sagittal sinus,
falx cerebri, cerebral convexity
• Good prognosis
• Some tumors may recur

7. Astrocytoma
• Low grade-young adults,good prognosis
• Pilocytic-children ,good prognosis
• Anaplastic-poorly differentiated,intermediate
prog
• Glioblastoma multiforme

8. Glioblastoma multiforme
• 30% of all brain tumors in adults
• Central necrosis and surrounding edema
• Resection inadequate due to microscopic
infiltration of normal brain
• Treatment surgical debulking + RT + Chemo
• Life expectancy in the order of weeks

9. Oligodendroglioma
• Arise from myelin producing cells
• Treatment- resection

10. Pituitary tumors
• Arise from cells of anterior pituitary
• May occur with MEN 1
• Hormone secreting
• Microadenomas(<1 cm)functional
• macroadenomas
• Compression of ICA
cavernous sinus or 3rd
nerve or optic chiasma
nonfunctional
ACTH,TSH,FSH,
LH,PRL

11. Clinical features
Raised ICP—headache –
worst,bursting or throbbing,awaken from
sleep,aggrevated by change of posture/cough/strain
Vomiting , papilloedema
Seizures
Focal neurologic signs-
sensory deficits /hemiparesis/cranial nerve palsies

12. Frontal-hemiparesis
subtle personality changes, cognitive dysfunction
Parietal-sensory changes
Temporal lobe-focal seizures
Sellar and parasellar-visual field changes
Hypopituitarism
Features of Cushing syndrome or acromegaly

14. Anaesthetic management of supratentorial trs
problems and concerns
1. Intracranial pathophysiology of trs
2. Effect of anaesthetics on brain
3. Surgical position & concurrent medications
4. Measures to decrease ICP & brain bulk
5. Complications

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

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

18. Subfalcine
Uncal or
transtentorial
Cerebellar
Trans calvarial

19. Subfalcine
• Asymmetrical supratentorial trs
• Herniation across midline beneath falx
• Anterior cerebral artery may be compressed
Transtentorial
• Central portion is forced out of supratentorial
compartment
• DURETS HAEMORRHAGE-brain stem
haemorrhage

20. cerebellar herniation
• Compression of 3rd cranial nerve
• Dilated pupils,ptosis,lateral deviation of eye
• Anisocoria-most important early sign

21. Recurrent Issues In Neuroanesthesia
• Brain relaxation/ control of ICP
• Management of PaCO2
• Management of arterial blood pressure
• Use of steroids
• Use of Osmotherapy and Diuretics
• Use of anticonvulsants
• Patient positioning
• Pnemocephalus
• Venous air embolism
• Hypothermia
• Monitoring
• I/V fluid management
• Glucose management
• Emergence

22. Intraoperative Management
Anaesthetic goals
• Maintain CPP
• Prevent brain herniation
• Maintain O2
• Maintain CO2
• Provide lax operative field
• neuroprotection

23. 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

24. D o s e b e y o n d 1 M A C
CMR reduced; but vasodilatory effect
predominates
CBF increases
LUXURY PERFUSION
@ 1 M A C
CMR suppression = vasodilation CBF unchanged
@ 0 . 5 M A C
CMR suppression predominates So net CBF decreases

25. • Order of vasodilatory potency
• Halothane.>Enflurane>desflurane&Isoflurane>
Sevoflurane
• CO2 responsiveness preserved
• Autoregulation in response to rising arterial
pressure is impaired
• Sevoflurane cause least impairment

26. Net CBF determining factors
• Conc of the anesthetic agent
• Extent of previous CMR depression
• Extent of blood pressure changes caused by
the previous or anesthetic induced
autoregulation disturbances
• Simultaneous changes in Pa CO2 due to
disease related impairment in CO2
responsiveness

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

28. N2O
• Can cause significant increase in CBF, CMR, &
ICP
• Most extensive increase when used alone
• With IV agents, CBF effect considerably
reduced
(Thiopentone, Propofol, Benzodiazepines,
Narcotics)
• With volatile agents, CBF increase is
exaggerated.

29. Muscle relaxants
• Succinylcholine
– Transient increase in ICP
– Caused by increased afferent signals from muscle
spindles
– Prevented by deep anaesthesia, defasciculation
with NDMR

30. • 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

31. • Pancuronium
Large bolus -> abrupt increase in BP -> if
autoregulation defective -> increase ICP
 Vecuronium
No variation in HR and BP
Preferred competetive blocker

32. • Benzodiazepines
– Modest parellel reduction in CBF & CMRO2
– CO2 responsiveness preserved
 Lignocaine
• Dose related reduction in CMRO2 & CBF
• Prevention or treatment of acute increase in ICP
(enotracheal suctioning)
• Large dose - seizures

33. • Opioids
– Modest reduction in CBF & CMR
– Neuroexcitatory activities & seizures reported

34. 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

35. • Physical examination
• Goal
– Assess how much permanent & reversible
neurological damage is already present

36. • 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

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

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

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

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. Anticonvulsants
• Intraop seizures—Cortical irritation, Cortical
incision, Brain surface irritation by retractors
• Levetiracetam can be safely given even in TBI

43. • Preinduction monitors
– NIBP
– SpO2
– ECG
• Vascular access
– 2 large widebore peripheral IV lines under LA

44. • Indications of Central Venous access
– Large vascular tumors
– Proximity to major arteries or venous sinus
– Extensive bone resection
– Major cardiovascular compromise present
– Vasoactive drugs are to be infused
– Risk of venous air embolism

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

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

47. • Premedication – Fentanyl 1-2 ug/kg
• Preoxygenation with 100% O2
• Induction with TPS 3-6mg/kg or Propofol 1.25-
2.5mg/kg
• Control ventilation (PaCO2~ 35mm Hg)

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

49. • 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

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. • Pressure points should be padded
• Eyes taped to prevent corneal damage from exposure or
irrigation of fluid

53. Intra op ICP reduction
1. Hyperventilation
– Lower pCO2 (1mm change in pCO2, CBF changes
by 1-2ml/100gm/min )- Cerebral ischemia in
injured brain. ICP lowering effect is not
sustained. The CSF pH and CBF returns to normal
within 8- 12 hrs.
– Maintain PaCO2 30-35 mm Hg
– If hyperventilated for long (ICU) make them
normocapnic slowly

55. 1. Drugs -Osmotic diuretics – Mannitol
– 0.25-1gm /kg over 10-15min prior to craniotomy
– Effective for ~ 2hrs
– Upper acceptable osmolality limit of 320mosm/L
Mechanism of action
– Produce osmotic gradient that draws fluid out of brain
parenchyma
– Removes ~ 90ml brain water at peak effect
Side effects
– Acute hypervolemia (due to vasodilatation)
– Electrolyte imbalance

56. Frusemide
MOA
• Hastens excretion of water from intravascular
space and maintains osmotic gradient
• Inhibit chloride channel and prevent
accumulation of idiogenic osmoles --
prevents rebound oedema
• Dose .15-.3 mg/kg

57. 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

58. Tight brain check list
Are relevant pressures controlled JVP
Airway pressure
Arterial pressure
PaCO2, PaO2
Is metabolic rate controlled Pain/arousal
Seizures
temperature
Are any potential vasodilators
in use
N2O
Volatile agents
CCB
Nitroprusside
Are there any unrecognized
mass lesions
Blood
Air with/without N2O
JVP
•Extreme head rotation
•Direct jugular
compression
•Head up posture
•Airway obstruction
•Bronchospasm
•Straining
•Coughing
•Pneumothorax

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

60. Others
• PNS
• 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

61. 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%
• Normoglycemia not recommended- injured brain
is the state of hyperglycolysis.

62. • Normal saline and ringerlactate preferred
• Normal saline-slightly hyperosmolar (308)
compared to plasma(295)
Disdvantage- hyperchloremic metabolic
acidosis
• Ringer lactate(280) hypoosmolarlarge
volume can cause cerebral edema
• Alternate NS and RL litre by litre in case of
large volume administration

63. Colloids
• TCMP gradient is mainly determined by osmolarity and
only by a smaller grade by colloid oncotic pressure
• 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.
• Keep the dose limited to the manufacturers
recommendation

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

67. Temperature
• Routine use of hypothermia not advocated
Problems– dysrhythmias and coagulation
dysfunction
Deep brain temperature- esophageal, tympanic
membrane pulmonary artery jugular bulb
temperature

69. Emergence
Goals
• Smooth emergence
• Maintain MAP, CMRO2, PaO2, PaCO2, Temp
• Avoid factors that lead to intracranial bleeding
– (coughing, bucking, intratracheal suctioning,
ventilator fight)
• Pt should be calm, cooperative, & responsive
to verbal commands soon after emergence

70. Awakening sequence
• Discontinue opioids (bolus / infusion) ~ 60 min
before planned emergence
• Progressive rise of PaCO2 to normal
• Systemic HTN during last stages of craniotomy
managed by labetelol, esmolol, enalapril,
nicardipine, diltiazem, dexmeditomedine

71. • Stop volatile anesthetics during skin closure
• Maintain with 02 +N2O with propofol either bolus
or infusion at rates of 25-100 ug/kg/min
• 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

72. Indications for late emergence
• Preop – pt obtunded
• Inadequate airway control preop
• Large risk of brain edema / raised ICP
• Extensive surgery
• Repeat surgery
• Major glioblastoma surgery
• Surgery involving/ close to vital areas
• Surgery asso with significant brain ischemia
(long vascular clipping times, extensive retractor
pressure)

73. Delayed emergence
• If pt not awake enough to obey simple verbal
commands 20-30 min after pharmacologically
adequate cessation of anaesthesia, non
anesthetic causes of delayed emergence should
be considered & ruled out like
– Seizures
– Cerebral edema
– Intracranial hematoma
– Pneumocephalus
– Ischemia
– Metabolic / electrolyte abnormalities

74. Complications
• Bleeding
• Hemodynamic instability
• Brain swelling
• Venous air embolism
• Frontal lobey
• Abnormal water balance
• Temperature disturbances