Transcript 2 MB - supratentorial tumours MGMC

Anaesthesia for supratentorial
tumours
Dr. S. Parthasarathy
MD., DA., DNB, MD (Acu),
Dip. Diab.DCA, Dip. Software statistics,Phd (physio)
Mahatma Gandhi Medical college and research institute
puducherry , India
What is it ??
Supratentorial means
• Cerebral hemispheres and diencephalon
Thalamus and hypothalamus
Incidence
35, 000 new cases /year in USA
Majority are supratentorial – more in adults
Glioma
Mengioma
Astrocytoma
Pitutatry adenoma
Brain abscess
Metastasis
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Glial tumors disrupt the blood-brain barrier
More edema
More bleeding
hypertension
• Meningiomas,
• 15% of primary brain tumors,
• slow growing and very vascular and can be
difficult to dissect.
• They may require multiple attempts at resection
and this may be preceeded by embolisation of
the tumor.
Secondaries
• secondary neoplasms arising predominantly
from the lung (50%) and breast (10%).
• The incidence of secondary tumors rises with
increasing age.
• Excision of solitary lesions is justified in
patients in whom the underlying disease is
well controlled.
brain abscesses
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local spread from sinuses or ear infections
especially common in immuno compromised
and diabetic patients,
those with right-to-left cardiac shunts,
intravenous drug abusers
Three preoperative questions
• (a) Where is the mass lesion?
• (b) Is ICP already elevated?
• (c) What is the patient’s current neurologic
status?
Question number 1 -Where is the
mass lesion?
• surgical position and position of monitors
• the potential for blood loss,
• Predict Post op deficit ( if occurs ) where ?
• occasionally reveal a risk of air embolism. Risk of
VAE is quite low for most supratentorial tumors.
• However, lesions (usually convexity meningiomas)
that encroach on the sagittal sinus may convey a
substantial risk of VAE
Question no. 2 _ ICP
• Headache caused by traction or distortion of
cerebral blood vessels and dura mater. exacerbated
by recumbency, movement, and straining,
Classically, it is worse on waking up.
• Nausea and vomiting
• Papilledema
• Cushing s ulcers
• Hypertension , bradycardia, and widening pulse
pressure – ( cushing triad)
• Neuro deficit
• Respiratory changes
ICP ???
• Not all mass lesions cause increase ICP
• Not all asymptomatic patients have normal
ICP
Question 3
Mental status, level of consciousness
GCS
Pupil size, reaction
Speech defect
Neuro deficit
Any concurrent diseases
Preoperative work up !!
Hydration: duration of bed rest, fluid intake, diuretics,
syndrome of inappropriate secretion of antidiuretic
hormone
Medication: steroids, antiepileptic drugs
Associated illnesses, trauma
Patients with pan hypopituitarism will need hormone
replacement,
including
cortisol,
levothyroxine,
and
possibly DDAVP. These medications should be continued
in the perioperative period.
Investigations
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Routine investigations – electrolytes
Coagulation
Platelets
Drugs and their side effects
Neuro imaging
Blood grouping
Hydration
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Calculate
Maintenance + Fluid loss due to urine output
500 ml negative
No fasting calculations for adults
Glucose ( slow) + nonglucose (fast to counter
blood loss) – alternate
• Add 5% dextrose to NS , RL ? is just ok
• Keep hyper osmolar
Mannitol
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0.25 gm – 1 gm/ kg IV boluses
Reduce edema
Better access
Reduce ICP
But dehydration , Urine output, serum
osmolality and serum electrolytes must be
monitored
• Use it in all Vs selected cases – controversial
• Rebound edema due to chloride influx
• Blocked by frusemide
Premedication
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Preferably no sedatives
Inj Dexamethasone 10 mg tds 48 hours prior
Antiepileptic medication to continue
Formulate a plan
What position, surgery, blood loss, monitors
where, IV access where ?? ( micro planning)
• patients with mass lesions be transported
with the head of the bed elevated 15–30
Routine monitoring during brain
tumour surgery should include
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ECG,
invasive and noninvasive blood pressure,
pulse oximetry, capnography,
nasopharyngeal temperature and
urine output.
ICP monitoring.-Currently rare for elective
neurosurgery due to improvements in peri operative
ICP control
• SSEP, EEG , transcranial doppler in specific instances
Monitoring
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Glucose
Coagulation
Blood gases
Chemistry
CVP monitoring ( diabetes insipidus producing
craniopharyngomas, VAE )
• PAC – medical indications
Unilateral frontotemporal (pterional) approach
Bifrontal approach
Inter hemispheric approach
• Trans sphenoidal
• Extra cranial
Goals of GA
• Smooth induction
• Hemodynamic stability
(hypotension can lead to ischemia in areas of impaired
autoregulation; hypertension increases the risk for
hemorrhage and vasogenic edema)
• Relaxed brain (for optimal surgical access and to reduce
the risk for retractor damage)
• Rapid and smooth emergence from anesthesia to allow
early neurologic assessment
• Induced hypo – no longer favourable
• NTG , SNP not preferred to decrease BP –
increase CBF
• Beta blockers and ACE inhibitors preferred
Anaesthetic
management
Induction
• 10 degree head up
• Narcotics,
• Propofol (Hypo??)or thio in liberal doses
• Nondepolarizers but Scoline ok in difficult airways because
hypercapnia and hypoxemia worse than I ICP by scoline
• IV lignocaine or esmolol for intubation
• fix the tube, eye pad, some more monitors
• Positions
Numerous positions
Numerous positions
Maintain ??
• Air , oxygen isoflurane , sevo
• Or
• fentanyl +
• propofol infusion 50 – 150 mic. gm /kg/min.
• Mild hypocapnia
Intra op events
• Neurosurgical procedures are often associated
with “occult” blood loss (underneath surgical
drapes or on the floor).
• Nasogastric tube
• Axilla auscultation after flexion of tube
• Prone for DVT but ?? Chemical prophylaxis ??
• Nerve stimulator
• Later part of surgery ? – painful - ? Opioids
Intra operative techniques
• Fix the tube very well –
• LA and fentanyl shot before pin.
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ICP
reduction
Flex or turn the head carefully
---- tube kink
----- ICP rise
Osmotic diuretics (mannitol, hypertonic saline);
steroids for tumor
• Loop diuretics (furosemide)
• No PEEP
• Maintain BP
Intra op key points
• Increased intracranial pressure can result from
increased abdominal pressure,
• venous congestion, and positioning of the head
below the level of the heart.
• Venous congestion can result from venous
outflow obstruction caused by hyper rotation or
hyperflexion of the neck.
• Increased PEEP and airway compromise can
result from kinking of the endotracheal tube
caused by neck flexion.
Brain suddenly swells
• Is this a major ventilatory disaster?
• Is the brain swollen because of a disconnect, severe
hypoxia, hypercapnia?
• Is the chest moving appropriately?
• Does the patient have a reasonable expired CO2 waveform ?
• What is ETCO2 ? What is the SpO2?
• Is the swelling related to impaired cerebral venous
drainage?
• Anaesthesia , analgesia ??
Brain swelling continues
• Mannitol
• Frusemide
• Hypertonic saline : Various conc and doses
have been used 3%, 7.5%, 23.4% : all show
↓ICP and ↑CPP. No deleterious diuresis and
undesired hypovolemia.
• Cannulate ventricles
• NO nitrous
• No agent
• Thio 250 mg
Delayed awakening
Recovery
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Simple case
Small lesion
Preop and intra op period uneventful
No brain swelling
• Extubate on table – continue monitoring
Delay awakening
• Hypoxemia – less
• Hypercapnia – less
• Hemodynamic stability √
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• Less neurologic monitoring
• More hypertension, catecholamine release
• bleeding
“frontal lobey.”
• Bi frontal approach
• Brain retraction
• immediate postoperative period
• Delayed awakening or disinhibition or both
Other post op issues
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Blood loss
Narcotics ( sedation Vs pain relief )
Paracetomol
No cough, straining
Steroids
Antiepileptics
Normoglycemia
Other systemic illness
Summary
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Supratentorial means ??
Preop three questions
Monitoring
Premedication
Anaesthetic techniques
Early Vs delayed awakening
Postop ventilation when ??
Thank you all