A Presentation on Anaesthetic Management of Supratentorial Tumors

1. Anaesthetic Management
of Supratentorial Tumours
Presenter: Dr S. N. Bhagirath
Moderator: Dr Sanjaya Banakal

2. Brief anatomy

3. Brief anatomy

4. Parenchymal
Tumours
Meningioma
Glioma
Pituitary
60%
8%
15%
35%
Distribution
Others
Dermoid & Epidermoid tumours, Metastatic disease,
Extradural & Subdural Hematoma and intracerebral
abscesses

5. Surgeries commonly involved
Craniotomy
Trans-Sphenoidal
approaches

6. What to expect..?
Pituitary
Dissection around hypothalamus
Water Imbalance
Diabetes Insipidus
Cerebral Salt Wasting Syndrome
Temperature Disturbance

7. What to expect..?
Subfrontal Approach
Post-operative disturbance in
consciousness
Lethargy
Delayed Emergence

8. Understanding Neurophysiology
a. Cerebral Metabolism
O2 Glucose
Consumes 20% of total body O2
CMRO2 indicates O2 consumption
CMRO2 = 3 – 3.8 mL/100g/min
50 mL/min
Consumes mainly Glucose
Glucose Consumption
= 5 mg/100g/min
45 mL/min
Cerebral Blood Flow

9. Understanding Neurophysiology
b. Cerebral Blood Flow
Avg. CBF = 50 mL/100g/min
750 mL/min
(15 – 20%
Cardiac Output)
CBF below 25 mL/100g/min
Cerebral Impairment
So what
regulates
CBF..?

10. Understanding Neurophysiology
b. Cerebral Blood Flow Regulation
CPP = MAP – ICP (or CVP) ICP = 10 mm Hg
So CPP is more reliant on MAP and normally is 80 – 100 mm Hg
Regulation Mechanisms involved
Intrinsic Extrinsic
Vasodilatation, Vasoconstriction
Myogenic mechanism
Metabolic mechanism
NO, Adenosine, PGs,
Ionic gradients
Resp. Gas Tensions
Temperature
Viscosity
Autonomic influences

11. Understanding Neurophysiology
Respiratory Gas Tension on CBF
Ions do not cross BBB, but CO2 does
So, CBF depends on PaCO2 but not HCO3
Metabolic
Acidosis has
no immed.
effect
CBF is directly proportionate
to PaCO2
(between 20 – 80 mm Hg)
CBF changes 1 -2
mL/100g/min for every mm
of Hg change in PaCO2

12. Understanding Neurophysiology
Temperature on CBF
Hypothermia
Hyperthermia
Cerebral
Blood Flow
For every 100C increase, CMR doubles
For every 100C decrease, CMR falls by 50%

13. Understanding Neurophysiology
Viscosity on CBF
Hypo viscous (reduced Hematocrit)
Hyper viscous
(increased
Hematocrit)
Cerebral
Blood Flow
But O2
delivery
comes
down
Optimal O2 delivery occurs at a Hematocrit of 30%

14. Understanding Neurophysiology
Autonomic Influences on CBF
Sympathetic Parasympathetic
Vasoconstrictive Vasodilation
Initially increase in CBF
But intense stimulation
decreases CBF
CBF

15. Understanding Neurophysiology
Role of Anaesthetics
Cerebral Blood
Flow
Cerebral
Metabolic Rate
UNCOUPLED
I.V. Anaesthetics
CBF CMRO2
STILL
COUPLED..!!
Volatile Anaesthetics
CBF CMRO2
NO LONGER
COUPLED
Hence
Cerebro-protective
Hence
Cerebro-protective

16. Understanding Neurophysiology
Blood Brain Barrier
CO2, O2, water, lipid soluble substances
(anaesthetics) move freely
Ions, proteins & large substances such as
Mannitol penetrate poorly
Hypertonicity
H2O moves
out of cell
Hypotonicity
H2O moves
into cell
Correct Na,
Glucose
abnormalities
slowly.

17. Understanding Neurophysiology
Cerebrospinal Fluid
Formed from choroid plexus in lateral ventricles
About 500 mL/day
Total volume is 150 mL
Isotonic with plasma (despite low conc.
of K+, HCO3 and Glucose)
Carbonic anhydrase inhibitors,
Corticosteroids,
Spironolactone,
Furosemide,
Isoflurane &
Vasoconstrictors
CSF production

18. Understanding Neurophysiology
Intracranial Pressure
80% 12% 8%
Normal
ICP is
10 mm Hg
or less
Compensatory Mechanisms
• Displacement of CSF to spinal cord,
• Increase or Decrease in CSF production,
• Decrease in total cerebral blood volume (primarily venous)

19. Understanding Neurophysiology
Intracranial Pressure - Compliance
B.P. Reflex
vasoconstriction
Cerebral blood
volume
B.P. Reflex
vasodilatation
Cerebral blood
volume
Cingulate gyrus
Uncinate gyrus
(tentorium)
Transcalvarial
Cerebellar
tonsils

21. Anaesthetic Considerations

22. What are the concerns..?
Pressure
(localized/
generalized)
Slowly
expanding
Minimal
Neurologic
Dysfunction
Fast
expanding
Central area of
hemorrhagic
necrotic tissue
ICP
Hemorrhage
Seizures
Air Embolism
Sitting/ Head
elevated
position

23. What are the anaesthetic goals..?
1)Global maintenance of cerebral homeostasis by
● normovolemia and normotension
● normoglycemia
● mild hyperoxia and hypocapnia
● mild hyperosmolality and hypothermia
2) Minimization of need for surgical retraction by using chemical
brain retraction.
3) Maximize therapeutic modalities that ↓intracranial volume.
4) Provision of early neurosurgical awakening

24. Reducing brain bulk, reducing tension
Osmotic agents
Mannitol
20%(1098 mOsm/L) mol wt. 182
-↑ blood osmolality
- ICP effect within 4 -5 min, lasts 3-4 hrs., dose 0.5-2 g/kg.
- No change in CBF and
↓ICP by 27% at 25 min. (auto-regulation intact)
Generation
of Idiogenic
osmoles
-↑CBF by 5% and
↓ in ICP 18 % at 25 min (impaired auto-regulation). Rebound
increase in
ICP
Later sequale

25. Reducing brain bulk, reducing tension
Osmotic agents
Hypertonic Saline
Concentrations of 3%, 7.5%, 23.4%
Decrease ICP
Increase CPP
No deleterious diuresis and undesired hypovolemia.
Useful in patients refractory to Mannitol.
CNS Systemic
Decreased consciousness Hyperosmolality, Hypernatremia
Seizures CHF, Hypokalemia
Central Pontine Myelinolysis Hyperchloremic Acidosis
Subdural/parenchymal
hemorrhage
Coagulopathy, Phlebitis
Rebound edema Renal Failure

26. Loop diuretics
● ICP reduction is small and less effective.
● Isosmotic reduction of the extracellular space i.e.
↓ICP without ↑ CBV and osmolality.
● In patients with impaired cardiac reserve
Mechanism:
1) Systemic diuresis.
2) ↓cerebral edema by improving cellular water transport.
Dose 0.5-1 mg/kg iv alone or 0.15 -0.3 mg/kg with Mannitol

27. Steroids
● ↓ Peritumoral vasogenic edema
● effect may take 12-36 hrs.
Mechanism:
1)repair of abnormal BBB
2)prevention of lysosomal activity
3)enhanced cerebral electrolyte transport
4)promotion of water and electrolyte secretion
5)Inhibition of Phospholipase activity

28. Hyperventilation
● Cerebral vasoconstriction → ↓CBF
● Δ1 mm Hg PaCO2 → 1-2 ml /100 gm./min ΔCBF
● Duration of effectiveness → 4-6 hrs.
● Impaired responsiveness →ischemia, tumors, infection etc.
● Target PaCO2 30 -35 mm Hg

29. Fluids
● Restricted fluid intake → traditional approach
● Can cause hypovolemia, hypotension , ↓renal perfusion,
electrolyte and acid base disturbances.
● Glucose free iso-osmolar solution
● Hourly maintenance fluids and replacement of losses.
● Hematocrit 25 -30%

30. PEEP
● ↑ICP by ↑ mean intra-thoracic pressure , impairing cerebral
venous outflow and cardiac output .
● used cautiously and with monitoring
● 10 cm H2O or less have been used without significant rise in ICP
or ↓CPP.

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

32. Position
Intense Nociceptive
stimulation during
pin application
Response can be
blunted with
additional doses of
Fentanyl/ Propofol

33. Sitting Position
Good surgical exposure, enhanced CSF
& venous drainage, minimal blood loss
Unstable hemodynamics and potential
for Venous air embolism
Macroglossia Excessive neck flexion
Use of multiple
instruments such as ET
Tube, Oral Airway,
Esophageal
stethoscope
simultaneously.

34. Sitting Position
Veins in the skull may not collapse due
to adherence to bone or dura.
Cut edge of skull may also admit air
Air enters the pulmonary circulation
and creates a vapor lock
Sequale Pulmonary edema
Patent Foramen Ovale leads
to Paradoxical embolism
Patent Foramen Ovale and
other cardiac effects are
contraindications.
Obstruction in coronaries
leads to myocardial ischemia
and ventricular fibrillation
Sudden drop in right heart CO
Neurologic damage follows air
embolism to brain
Acute Cor Pulmonale
Arterial hypoxemia

35. Sitting Position
Sudden Doppler Drop USG
in EtCO2
TEE is particularly
useful
Not adequate for
quantification of air
Sudden rise in right
atrial and pulmonary
pressures
Can quantify and
detect
What to do upon detection of
Venous air embolism..?
Change in end-expired
nitrogen conc.
precedes drop in CO2
Sudden attempt to
initiate spontaneous
breaths
Late Signs
“Gasp Reflex”
Hypotension,
Tachycardia,
Cardiac
Arrhythmias,
Cyanosis
Millwheel murmur

36. Sitting Position
• Surgeon should flood the site with fluid
• Occlusive material to bone edges
• Aspirate air through right atrial catheter
• Discontinue Nitrous Oxide (for fear of increasing bubble size)
• Direct Jugular Venous compression
• Sympathomimetic drugs to treat hypotension
• β-adrenergic agonists (dopamine/ dobutamine) for low CO.
• β2-agonists for bronchospasm
• In severe cases, shift patient to Hyperbaric chamber.

37. Hemodynamics
Cerebral Blood Flow (CBF) is pressure dependent
Adequate preoperative blood pressure control in hypertensives
Desist from acute normalisation of B.P. in a hypertensive patient
Induced Hypotension is no longer favoured
Direct Vasodilators – SNP, NTG & CCBs may actually increase CBF &
ICP
β-Blockers and ACE Inhibitors are preferred.

38. Implications of concurrent medications
Common medications – anticonvulsants & steroids
Anticonvulsant agent, phenytoin may decrease the duration of
action of non-depolarising muscle relaxants.
Adrenocortical suppression due to prolonged steroid therapy may
cause unexpected hypotension intraoperatively.

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

40. Monitoring
ECG
NIBP
Pulseoximetry
Capnography
CVP
ABP
Glucose
Electrolyte
Osmolality
Transducers at level of brain

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

42. Intubation
Control ICP rise on induction
1) Narcotics
2) Lidocaine
3) Short-acting β-blocker
4) Deepen plane of anesthetic
5) Quick intubation
Relaxant
1) Succinylcholine – modest rise in ICP
2) NDMRs can be used.

43. Maintenance
● Goal : control of brain tension via control of CBF and CMR (as
shown before)
● mild hyperosmolality
● iv anesthetic , adequate depth
● mild hyperventilation (EtCO2 < 35), Mild hyperoxygenation
● mild controlled hypotension
● normovolemia , no vasodilators
● Minimal PEEP
● Avoidance of brain retractors.

44. Maintenance
● Fentanyl 1-2 μg/kg/hr, alfentanil 5-10 μg/kg/hr, remifentanil 0.2-
0.5 μg/kg/hr, sufentanil 0.1-0.3 g/kg/hr.
● Volatile anaesthetic 0.5-1% Isoflurane (MAC 1.0 – 1.2).
● NDMRs like Vecuronium/ Atracurium used with neuro-muscular
monitoring
● Controllability, predictability and early awakening.

45. Maintenance
● In brain tumors , infusion of propofol with fentanyl or
remifentanil has shown to ↓ ICP more effectively than either
isoflurane or sevoflurane alone
● However the risk of cerebral hypoperfusion has been questioned
with propofol (↓CBF/CMR ratio)
● If severe intracranial hypertension persists despite
hyperventilation and other maneuvers, and the brain is tight a
total intravenous technique is preferred.

46. Emergence
● Routine craniotomy: extubated at the end of surgery – this
permits assessment of results of surgery and provide a baseline
for continuing post-op neurologic follow up.
Preconditions for Early Emergence :
● Systemic homeostasis :
1)normovolemia , normothermia
2)Normotension (MAP=80 mmHg)
3)Mild hypocapnia (PaCO2=35 mmHg)
4)Normoglycemia
5)Mild hyperosmolality
6)Hematocrit approx. 30%

47. Delayed Awakening
Large intracranial tumor
Residual anesthetics
Metabolic or Electrolyte disturbances
Residual hypothermia
Surgical complications
Seizures
Cerebral Edema
Hematoma
Pneumocephalus

48. Early Vs. Delayed Awakening
● Early awakening :
Advantages:
1)Earlier neurologic examination and intervention if necessary
2)Earlier indication of further investigation
3)Less stress response
Disadvantages :
1) ↑risk of hypoxemia and Hypercapnia
2) Monitoring in ICU

49. Early Vs. Delayed Awakening
● Delayed awakening :
Advantages:
1)Less risk of hypoxemia or Hypercapnia
2)Better respiratory and hemodynamic control
3)Earlier transfer to ICU
Disadvantages:
1)Less neurologic monitoring
2)Larger hemodynamic changes
3)More catecholamine release.