Anaesthetic Management of Supratentorial Tumours

Anaesthetic Management of Supratentorial Tumours

Presenter: Dr S. N. Bhagirath

Moderator: Dr Sanjaya Banakal

Brief anatomy

Brief anatomy

Parenchymal Tumours

Glioma

Meningioma

Pituitary

60%

8%

15%

35%

Distribution

OthersDermoid & Epidermoid tumours, Metastatic disease, Extradural & Subdural Hematoma and intracerebral abscesses

Surgeries commonly involved

CraniotomyTrans-Sphenoidal

approaches

What to expect..?

PituitaryDissection around hypothalamus

Water Imbalance

Diabetes Insipidus

Cerebral Salt Wasting Syndrome

Temperature Disturbance

What to expect..?

Subfrontal Approach

Post-operative disturbance in consciousness

Lethargy

Delayed Emergence

Understanding Neurophysiology

a. Cerebral Metabolism

Consumes 20% of total body O2

CMRO2 indicates O2 consumption

CMRO2 = 3 – 3.8 mL/100g/min

50 mL/min

O2 Glucose

Glucose Consumption= 5 mg/100g/min

Consumes mainly Glucose

45 mL/min

Cerebral Blood Flow


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..?


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


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


Temperature on CBF

Hypothermia

Hyperthermia

Cerebral Blood Flow

For every 100C increase, CMR doubles

For every 100C decrease, CMR falls by 50%


Viscosity on CBF

Hypo viscous (reduced Hematocrit)

Hyper viscous (increased Hematocrit)

Cerebral Blood Flow

Optimal O2 delivery occurs at a Hematocrit of 30%

But O2

delivery comes down


Autonomic Influences on CBF

Sympathetic Parasympathetic

Vasoconstrictive Vasodilation

Initially increase in CBFBut intense stimulation decreases CBF

CBF


Role of Anaesthetics

Cerebral Blood Flow

Cerebral Metabolic Rate

COUPLEDUN

I.V. Anaesthetics

CBF CMRO2

STILL COUPLED..!!

Volatile Anaesthetics

CBF CMRO2

NO LONGER COUPLED

Hence Cerebro-

protective

Hence Cerebro-

protective


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.


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


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)


Intracranial Pressure - Compliance

B.P. Reflex vasoconstriction

Cerebral blood volume

B.P. Reflex vasodilatation

Cerebral blood volume

Cingulate gyrus

Uncinate gyrus(tentorium)

Cerebellar tonsils

Transcalvarial

Anaesthetic Considerations

What are the concerns..?

Pressure (localized/ generalized)

Slowlyexpanding

Minimal Neurologic Dysfunction

Fastexpanding

Central area of hemorrhagic necrotic tissue

ICP

Hemorrhage

Seizures

Air Embolism

Sitting/ Head elevated position

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

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)

-↑CBF by 5% and ↓ in ICP 18 % at 25 min (impaired auto-regulation). Rebound

increase in

ICP

Generation

of Idiogenic

osmoles

Later sequale

Reducing brain bulk, reducing tension

Osmotic agents

Hypertonic Saline

Concentrations of 3%, 7.5%, 23.4%

Decrease ICP

No deleterious diuresis and undesired hypovolemia.

Useful in patients refractory to Mannitol.

Increase CPP

CNS Systemic

Decreased consciousness Hyperosmolality, Hypernatremia

Seizures CHF, Hypokalemia

Central Pontine Myelinolysis Hyperchloremic Acidosis

Subdural/parenchymal hemorrhage

Coagulopathy, Phlebitis

Rebound edema Renal Failure

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

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

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

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%

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.

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

Position

Intense Nociceptive stimulation during pin application

Response can be blunted with additional doses of Fentanyl/ Propofol

Sitting PositionGood 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.

Sitting PositionVeins 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

Sudden drop in right heart CO

Acute Cor Pulmonale

Arterial hypoxemia

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

Neurologic damage follows air embolism to brain

Sitting Position

Doppler USG

Not adequate for quantification of air

TEE is particularly useful

Can quantify and detect

Sudden Drop in EtCO2

Sudden rise in right atrial and pulmonary pressures

Change in end-expired nitrogen conc. precedes drop in CO2

Sudden attempt to initiate spontaneous breaths

“Gasp Reflex”Late Signs

Hypotension,

Tachycardia,

Cardiac

Arrhythmias,

Cyanosis

Millwheel murmur

What to do upon detection of Venous air embolism..?

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.

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.

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.

Premedications

Depression of Consciousness

Sedative Premedication

Airway Obstruction

HypoxiaHypercapnia

Anxiolysis

Continuation of concurrent medications like Steroids, anticonvulsants, antacids, antihypertensives..

Monitoring

ECG

NIBP

Pulseoximetry

Capnography

CVP

ABP

Glucose

Electrolyte

Osmolality

Transducers at level of brain

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 ICPEpileptogenic

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.

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.

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.

● 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.

Maintenance

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%

Delayed Awakening

Large intracranial tumor

Residual anesthetics

Metabolic or Electrolyte disturbances

Residual hypothermia

Surgical complications

Seizures

Cerebral Edema

Hematoma

Pneumocephalus

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

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.

Health & Medicine

Anaesthetic Management of Supratentorial Tumours