Post on 13-Jul-2015
transcript
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
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..?
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
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
Understanding Neurophysiology
Temperature on CBF
Hypothermia
Hyperthermia
Cerebral Blood Flow
For every 100C increase, CMR doubles
For every 100C decrease, CMR falls by 50%
Understanding Neurophysiology
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
Understanding Neurophysiology
Autonomic Influences on CBF
Sympathetic Parasympathetic
Vasoconstrictive Vasodilation
Initially increase in CBFBut intense stimulation decreases CBF
CBF
Understanding Neurophysiology
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
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.
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
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)
Understanding Neurophysiology
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.