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

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 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 Routine investigations – electrolytes Coagulation Platelets Drugs and their side effects Neuro imaging Blood grouping

Hydration 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 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 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 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 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

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. 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 ICP reduction

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 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 √ But 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 Blood loss Narcotics ( sedation Vs pain relief ) Paracetomol No cough, straining Steroids Antiepileptics Normoglycemia Other systemic illness

Summary Supratentorial means ?? Preop three questions Monitoring Premedication Anaesthetic techniques Early Vs delayed awakening Postop ventilation when ??

Thank you all