lOutline lIntroduction lAims of neuroanaesthesia lPhysiological principles lPharmacology lTreatment of raised ICP lCerebral protection lPreoperative evaluation lPremedication

lOutline contd. lMonitoring lConduct of neuroanaesthesia lPostoperative care lComplications and management lSpecific neurosurgical procedures lRecent advances in management

l l lIntroduction lIn the field of neuro-sugery today, more complex and intricate surgical techniques are being developed these include minimal invasive neurosurgery, functional neurosurgery (tx epilepsy, Parkinson dx), interventional neuro radiology, stereotactics surgery etc. lNeuroanaesthesia is also keeping the pace with development of newer anaesthetic techniques (e.g l mgt of awake craniotomy), and newer anaesthetic agents e.g sevoflurane, desflurane, remifentanil and the recent advances in neuro monitoring. lIntroduction contd. lAnaesthesia for neurosurgical procedures require understanding of the normal anatomy and physiology of the central nervous system and the likely changes that occur in response to the presence of SOL, trauma or infection and the effect of anaesthestic interventions on cerebral function. lIntroduction contd lIn addition to balance anaesthesia with smooth induction and emergence, particular attention should be paid to the maintenance of adequate cerebral perfussion presure (CPP), avoidance of intracranial hypertension, its proper management when already present and the provision of optimal surgical condition to avoid further progression of the preexisting neurological insult. lAims of neuroanaesthesia lThe ultimate goal of any neurosurgical procedure is to bring about a patient with an improved functional ability and psychosocial status. lThe aims of neuroanaesthesia therefore entails the following: lAims of neuroanaesthesia lTo maintain an adequate CPP and oxygenation, while minimizing cerebral metabolic rate for oxygen (CMR02) l To maintain a stable ICP or reduce elevated ICP by physical or pharmacological means lTo create optimal surgical conditions lTo ensure an adequately anaesthetized patient who is not coughing or straining. lAims of neuroanaesthesia lEarly detection and prompt management of intra-operative complications such as venous air embolism esp in posterior fossa surgery.

lTo enable rapid return to consciousness thereby allowing early neurological assessment postoperatively. lPhysiological principles l20-25ml/100g/min cerebral impairment l15-20ml/100g/min flat (isoelectric) EEG l< 10ml/100g/min are usually associated with irreversible brain damage. lPhysiological principles in NA Cranial Vault-Rigid with a fixed total volume lCPP = MAP (ICP + CVP) lAUTOREGULATION lCerebral vasodilatation rapidly adaptive to changes in CPP lNormal individuals CBF near constant between MAP 60-160mmHg lBeyond this Blood flow becomes pressure[CPP] dependent l. AUTOREGULATION Autoregulated b/twn 60-160mmHg. Attenuated by cerebral ischemia, trauma, hypoxia, hypercarbia, edema, volatile anaesthetics l l l l lArterial Oxygen and Carbon-dioxide lCarbon dioxide in the blood has a marked effect on the cerebral vasculature. lIn a patient with raised ICP,it is vital to control the PACO2 to normal and to ensure provision of adequate oxygen to avoid hypoxia. lA rise in arterial carbon dioxide(PaCO2) causes cerebral vasodilatation, increased intracranial volume and subsequent reduction in CPP. This effect is magnified in the presence of a reduced arterial oxygen tension. lPaCO2 CBF increases linearly with CO2 between 20-80mmHg: 1-2 ml/100g/min for each 1mm Hg in PaCO2 lPaO2 CBF is not affected by PaO2 until it drops to 50mmHg when CBF then begins to rise. lICP relationship between intracranial contents and cranial vault volume (Normal is 5-15 mmHg) l l l lPharmacology lInhalational agents All Vol.AA CBF,sevof least Isoflurane most potent in CMR02 lIntravenous AA Most cause CBF & CMR02 except for ketamine. Lidocaine CBF & CMR02 . Autoregulation and CO2 responsiveness is preserved. lMuscle relaxants No direct effect on CBF & CMR02 b/c they dont cross the blood brain barrier l l lPharmacology; peculiarities lThiopentone Causes a dose dependent fall in CMR02 and CBF

lThis effect and antiConv useful in ICP lPropofol :similar effect to thiopentone but may preserve autoregulation more effectively and useful for maintainance.Its amnesic and antiemetic properties encourages smooth recovery.However,its effect on MAP may be deliterious lKetamine Traditionally avoided cos it raises ICP,CBF. Only acceptable for emergency induction and maintainance of sedation in head injury with hemodynamic compromise. l l lPharmacological peculiarities contd. lSevoflurane is d vol agent with least cerebral vasodilatory effect. lDesflurane at 1 MAC increase ICP in pts with supratentoral SOL,in contrast to isoflu. lNitrous oxide increases ICP,CBF, and CMR02. for this,and its adverse effect on closed gas spaces,its not used.Moreso when chest injury is suspectd. lRemifentanil has a rapid onset and offset which allows titration to counter stimulating events such as the application of the Mayfield clamp. .

lPharmacological peculiarities contd. lFantanyl and morphine these agents have little effect on intracranial pressure or blood flow which makes them suitable for titration to provide postoperative anagelsia. lThe non-depolarising NMBs do not have any effect on ICP lSuxamenthonium causes a transient rise in ICP. There may be a slight increase in CMR02 and CBF. These consideration must be weighed against the need for rapid airway control. lPharmacological peculiarities contd. lSuxamethonium is usually reserved for emergency anaesthesia rather than elective cases. lMannitol useful in the prevention and treatment of cerebral oedema. Causes a reduction in ICP. Also causes transient rise in CBV and CVP which may last up to 20minutes. lWorsens ICP If the BBB is damage lPharmacological peculiarities contd. lFurosemide 1mg/kg produces a reduction in ICP to the same extent as mannitol at 1g/kg. it is advantageous as it also reduces CVP. lPhenytoin can be given as IV loading dose. 15mg/kg for frontal and temporal lobe surgeries. lCan cause hypotension and arrythmia if given too fast. lPharmacological peculiarities contd. lAlphaagonists such as phenylephrine and noradranaline are use to increase blood pressure. As there are fewer alpha receptors in the cerebral vasculature, cerebral vascular resistance is relatively unaffected. lAlpha 2 antagonist e.g clonidine can be use to treat hypertension at the start of surgery. It has an analgelsic and sedative properties which may be a useful adjunct. This effect must be weighed against the need for rapid emergences l l lTreatment for raised ICP lMeticulous airway Mx. Avoid O2, CO2 Hyperventilation to a PaCO2 25 30 mmHg lVenous drainage 300 lBarbiturates

lMannitol 0.5-2.0g/kg IV l CSF vol. ventriculostomy catheter lCerebral Protection lCerebral Ischemia Focal: stroke, arterial occlusion, embolization Incomplete global ischemia:hypotension,embolization Complete global ischemia: Cardiac Arrest lAgents Isoflurane; accelerates post ischaemic neurogenesis. Barbiturates ; anaesthetic neuroprotection is sustainable for 2-4wks.[Head and Patel,Curr Opin anaeshesiogy.2007 Oct;20(5):3959] Hypothermia lLimited by CVS & resp. depression, dysrhythmias, tissue hypoperfusion and coagulopathy lCMR02 7% for every 10C in temp. l lCerebral Protection lHyperglycemia May worsen neurological outcome lNimodipine Beneficial effects on vasospasm after SAH lSteroids Not generally beneficial High dose methyl prednisolone beneficial in acute spinal injury if treatment is started within 8 hours of injury. lAnaesthetic challenges in NA

lPathology lProlonged and delicate surgery lBleeding lICP lRemote access lUnusual positions lUnusual equipment and technique e.g. stereotactic and Intraop Wake-up in epilepsy surgery.

lPreoperative evaluation

lFull History - General and Neurological -Headache, nausea, vomiting, visual disturbance, gait disturbance, ring too tight, striae, polydipsia, menstrual irregularities etc Pituitaryvisual impairment, endocrine derangement, Prolonged recumbence, electrolyte abnormalities

Concurrent illnesses

lPreoperative evaluation contd lShould attempt to establish the presence or absence of intracranial hypertension Current drugs---dexamethasone, anticonvulsants, OHA, antacids Physical examination and investigations are exhaustive for major procedures.

lPreoperative evaluation contd lExamination should include a neurological assessment documenting mental status (COMISH) and any existing sensory or motor deficit. lCT and MRI scans should be reviewed for evidence of brain edema, a midline shift greater than 0.5cm and venticular size . lLaboratory evaluation should rule out hyperglycemia and electrolyte disturbances. lHyperglycemia = corticosteroid, ED = diuretic lPreoperative evaluation contd lPoserior fossa tumors ocassionaly cause bulbar palsies and lower cranial nerve lesions which increase the risk of laryngeal incompetence and thus chronic or acute aspiration of gastric contents and hypoxia. lSubarachnoid haemorrhage can cause massive release of catecholamines which can cause acute heart failure, malignant arrythmias, T-wave and ST abnormalities on EEG. lPreoperative evaluation contd lThe patients general medical condition must be stabilized, especially any respiratory or cadiovascular disease, as hypoxia, hypercarbia or failure to maintain blood pressure will be detrimental. lAirway assessment is important because prolonged attempts at laryngoscopy are extremely stimulating and increase cerebral oxygen demand and ICP. lPreparation lSome procedures do not require more than the usual basic monitoring e.g. VP shunts and repair of congenital defects lIntracranial procedures -ABP and CVP for intracranial procedures that may be associated significant fluid shifts lNeuro-monitoring imperative for extensive spinal procedures but these require expertise for their interpretation

lPremedication lPatient are often anxious. lThose with normal ICP are usually given a benzodiazepine (oral diazepam or iv/im midazolam. lThis is best avoided when raised ICP is suspected as this might be due to hypercapnia from respiratory depression. lMonitoring lBasic Plus

Temperature PNS UO ABP CVP ABG, Blood Glucose, E&U, PCV, Clotting profile Neuromonitoring Cerebral oxygenation and metabolism lElectrophysiologic monitoring lElectroencephalography(EEG) Measures electrical activity of the neurons of the cerebral cortex. Used when the possibility of cerebral ischemia is high. E.g. CEA lEvoked potential monitoring (EP) Electrical potentials generated within the neuraxis in response to stim. of a peripheral or central nerve Damage to pathway is evident by in amplitude or a prolongation of latency Examples include SSEPs, VEPs lElectrophysiologic monitoring lMotor evoked potentials (MEP) Useful in detecting threatened motor function of the spinal cord. Affected by anesthesia making interpretation difficult. l l lElectromyography (EMG) Records muscle response to stimulation of motor nerves lBispectral Index monitoring l lConduct of Anaesthesia: Induction lIV Agents Barbiturate/Methohexiton Propofol Ketamine Benzodiazepines Suxamethonium NDM relaxants

lVolatile agents Halothane

Enflurane Isoflurane N2O Sevoflurane Desflurane

lIdeal induction agent for neuro-anaesthesia lDecrease the cerebral metabolic rate of oxygen (CMRO2) lMaintain adequate balance between cerebral blood flow (CBF) and tissue metabolic requirements lMaintain cerebral perfusion pressure (CPP) and CBF lMaintain cerebral autoregulation and vascular reactivity to CO2 lHave anticonvulsant action lHave a short and easily reversible action. lConduct of Anaesthesia: Induction lWide-bore cannulae, (sudden massive heamorrhage can occur IV fluids- N/S or R/L. Avoid glucose containing fluids-euglyc, lMonitors lEnsure smooth Induction and intubation: to ensure that the blood pressure and thus CBF is maintained near preoperative values. a bolus of either propofol (0.5-1mg/kg) should be given immediately prior to larygoscopy. lAdequate time should be allowed for non deplorising muscle relaxant to work before intubation is attempted. lIV or Inhalational (if ICP allows) lReinforced endotracheal tube may needs to reposition,, awkward positioning, shared field. lThroat Pack lConduct of Anaesthesia: Induction lObtund the CVS responses to ETT lPrevent rises in ICP lSECURE the TUBE lWhat position??? Supine, prone, sitting, l15 degree head elevation lIPPV 30mmHg etCO2 lOxygenation lMannitol to reduce cerebral oedema lPOSITIONING lFor many procedures patient is placed in a particular position or posture only after the induction of anaesthesia. lThis is especially true for procedures done with patient pronated e.g posterior fossa surgeries. lAttention must be paid to patient position, protection of pressure areas, including the eyes, and to ensure unrestricted venus drainage from the head. lPOSITIONING lFor most craniotomies, the skull is often pinned into a clamp (Mayfield clamp) to maintain optimal surgical positioning. lThis is stimulating and so a pre-emptive bolus of propofol or an opioid should be given to prevent a sudden rise in blood pressure. lPOSITIONING lSupine lProne

lSitting lLateral lPark Bench position -MAINTAIN AN IMPECCABLE AIRWAY -ENSURE FREE RESPIRATION -PROTECT OTHER PARTS OF THE BODY FROM INJURY -ENSURE MONITORS ARE WELL APPLIED l lPOSITIONING-Sitting,Supine lPOSITIONING-Prone lMaintenance lTIVA or Inhalation: volatile agent in oxygen or propofol infusion lAdequate analgesia (short acting opioids) lRegular Muscle Relaxant dosing lMonitoring-Blood loss challenges: -Difficult to monitor intraoperative blood loss lThe patient must have a urinary catheter for lenghty procedures or if duretics is used. lCore body temperature should be measured preferebaly with an oesophageal probe. lOnce the skull is open a bolus of diuretic optimises operating conditions. lMaintenance lDuring the procedure maintain low normal end tidal CO2 (around 4.0kPa ), normotension and normal oxygen levels. lHowever, mild hypotension can help improve the surgical field if necessary. Normothermia should be maintained, especially if the procedure is long. lAllowing the patient to become hypothermic has consequences of poor clotting function, impaired cardiac contractility and postoperative shivering which increases the metabolic oxygen demand. lMaintenance lGlucose free crystalloid is appropriate for fluid replacement. Hyperglycemia can worsen neurological outcome through lactate accumulation. lHypotonic intravenous solutions e.g. DH2o of any concentration will exacerbate cerebral edema. lWatch out for intraoperative complications lBrain swelling major problem of intraoperative procedure l l l l lIntraoperative care contd. lDuring surgery, especially posterior fossa surgery the brainstem may be manipulated, which can cause profound bradycardias. If this occurs, communicate with the surgeon to release traction or pressure and treat with glycopyrrolyte 200-400 micrograms (atropine crosses the blood brain barrier) and allow surgery to resume when the heart rate normalises. lIntraoperative care contd. lOnce surgery is drawing to a close. lAim for a smooth extubation with a minimum of straining and coughing-raises ICP lRemifentanil infusion, if available, helps to smooth out the waking and extubation process , but remember to give a bolus of longer acting opioids to avoid postoprative agitation. lPostoperative

lAspirate ETT if need be before discontinuing anaesthesia lEnsure adequacy of ventilation before extubation lICU care is often necessary in intracranial procedures lContinued vigilance lOptimization of patients condition There may be a need for postop ventilation lPostoperative management lDecision for postoperative ventilatory support depends on the patients preoperative neurological status, intraoperative events (duration and complexity of surgery, hemodynamic stability, complications such as VAE, hypovolaemia, massive transfusion), and evidence of raise ICP, as shown by tense dura or tight brain. lPostoperative management lRegular neurological observations, including ICP monitoring if available, should be recorded. lAny neurological deterioration should raise the suspicion of intracranial bleeding or oedema. lAn urgent CT scan should then be considered. lPostoperative management lThe patients haemodynamic status should be closely monitored to maintain an adequate cerebral perfusion pressure. lPostoperative pain which is often not severe can be manage by intermittent bolus doses or infusion of morphine or other opioids. lNon steroidal anti-inflammatory drugs have an anti-platelet effect and should be used with caution. lPostoperative management lElectrolyte imbalance, especially abnormalities in sodium concentration, may be common in patients with neurological disorders. This should be checked and corrected if present. lUrine output should be closely monitored as diabetes insipidus may occur . lPostoperative Care lContinue sedation and analgesia if unextubated lWhich sedative agent is preferred?[flumazenil],dexmedetomidine lMaintain Close monitoring including ICP lGenerally A B C lEt CO2 lSaO2 lFluids lAnalgesics lExtubate as soon as safe l lComplications in ICU lDiabetes Insipidus lProlonged Coma-trauma patient commonly lTumour bed haematoma lIncreasing ICP,Tension pneumocephalus , Cerebral edema lElectrolyte abnormalities-SIADH lN&V lPain lSeizure lInfections l l lPostoperative Care

lSIADH Na, serum osmolarity,urine osmolarity Rx. Free H20 restriction lDiabetes insipidus Common after pit.surgery. Polyuria assoc. Na, serum osmolarity, urine osmolarity. Rx. fluid intake, vasopressin 5-10 IU sc. l lPostoperative Care lSeizures May indicate expanding hematoma Airway control, oxygenation and ventilation must be ensured Rx. STP 50-100mg IV.; midazolam 2-4 mg IV; Phenytoin 300-500 mg po. or IV/day lTension pneumocephephalus Suspected when there is failure to awaken from anesthesia skull X-ray Rx. Re-open the dura lManagement of brain swelling lHyperventilate with 40% oxygen and volatile agent preferably isoflurane. lMaintain arterial PCO2 between 30-32 mm Hg. lAvoid PEEP, if possible. lHead-up position lAvoid severe rotation or flexion of the neck l

l lManagement of brain swelling l lAvoid obstruction to venous drainage from the head. lTreat hypertension (measured at the level of the brain) with labetalol, esmolol lTreat hypotension with phenylephrine or a dopamine infusion. lIf not already administered, consider the use of mannitol, furosemide, and dexamethasone. l

l l?? Persistent Brain Swelling lElevate the head and check for any obstruction of venous drainage. lABG to ascertain arterial PCO2 30 mm Hg. lConsider temporarily increasing ventilation. lIs mannitol and/or furosemide working. Consider more mannitol. l lDiscuss with the surgeon the possibility of draining CSF lDecrease cerebral oxygen requirement by cooling the patient not < 34 C and consider propofol or sodium thiopental to achieve EEG burst suppression. l lConsider changing to a propofol-based, air/oxygen anaesthetic. lRemove retractors, blood clots, tumor, from edematous brain. l lConsider the possibility of an additional undetected hemorrhage or surgical vascular (arterial or venous) obstruction. l lTRAUMATIC BRAIN INJURY lTraditionally efforts focused on optimizing ICP

lCPP based management currently been appreciated ? Appropriate level of CPP One size does not fit all CPP should be optimized to maximize the cerebral oxygenation and avoid anaerobic metabolism Direct Cerebral oxygen tension and cerebral metabolite monitoring-Technology still to be deployed clinically lSpecific Neurosurgical Procedures lSAH Acute or elective Neurologic grade (I- V) Drug therapy Ca channel blockers - Nifedipine ECG changes dysrhythmias and ST- segment, QT-interval and T-wave changes Optimal timing of surgery controversial Early - re-bleeding& allows for more aggressive therapy for vasospasm but conditions are suboptimal Late optimal condition,re-bleeding, hydrocephalus & does not allow for aggressive Rx of vasospasm lClassification of patients with intracranial aneurysms according to surgical risk (Hunt and Hess) lGrade I Asymptomatic / minimal headache and slight nuchal rigidity. lGrade II - Moderate to severe headache, nuchal rigidity, no neurological deficit other than cranial nerve palsy lGrade III Drowsiness, confusion, or mild focal deficit lGrade IV Stupor, moderate to severe hemiparesis, possible early decerebrate rigidity and vegetative disturbances lGrade V Deep coma, decerebrate rigidity, moribund appearance lSAH lAvoidance of BP: opioid, blockers ,lidocaine lAvoidance of BP: maintain CPP lAdequate brain relaxation lInduced hypertension: phenylephrine lIntraop. aneurysm rupture: induced hypotension or manually compressing the carotid artery lMild hypothermia 340C lPrevention of vasospasm: BP, fluid infusion,hemodilution-tripple H therapy lArteriovenous Malformations (AVM) lDirect communications b/twn cerebral arteries and veins without an intervening capillary bed lRx. Embolization surgical removal Embolization to bld flow lPerformed under GA or sedation with MAC. lMonitored anesthetic care (MAC) Potential problem include rxn to contrast dye, osmotic load, vessel perforation neurologic changes lGA Tight blood pressure control lPosterior Fossa Surgery

lLocation Tumors may cause cranial nerve palsies, cerebellar dysfunction & hydrocephalus b/c of obst.of 4th ventricle Tumors around the 9th & 10th gag reflex Tumors at the floor of the 4th ventricle - ? Post op.ventilation lCVS / Resp. instability lSitting position lPost op Verify adequacy of respiration before extubation Close observation lTranssphenoidal Resection of Pituitary Gland lPerformed via nasal or labial route lEndocrine disorders e.g acromegaly, cushings lPotential for bleeding lMonitoring airway, IBP rarely placed lThroat packs lPost op nasal obstruction by nasal packs lDiabetes insipidus lSpinal Cord Surgery lEgs of surgical probs include spondylosis, stenosis, neoplasm, scoliosis and trauma l10 objectives are to maintain spinal cord perfusion pressure & cord compression lAreas of importance Intubation - ? Awake neurological assessment Position often prone padding, prevention of venous obst & maintenance of adequacy of ventilation Bleeding lMonitoring SSEP Wake up test lTechnique nitrous oxide- narcotic relaxant l lRecent advances in management AWAKE NEUROSURGERY-Intraoperative brain mapping aimed at aiding maximal surgical resection of tumour while minimizing functional sequelae. -Reduction in post operative morbidity -During direct stimulation of the language areas adjacent to the tumour, the patient should be able to speak and participate in language testing. l lTechnique lRange from LA Conscious sedation GA l+/- Airway device Benefits vs Potential Risks(seizure, resp depression, patients discomfort) lCareful selection of Patients;uncooperative,morbid obesity,vascular tumor,tumor+dural involvement. lNo consensus on optimal regimen lTechnique contd. lTraditionally neurolept analgesia(opioid + droperidol) lFrom 1990s Propofol sedation increasingly Popular (Propofol + Remifentanil-short acting,titratable and rapidly cleared).

ASLEEP

- AWAKE

- ASLEEP anaesth

Requires airway device/control during spont. ventilation. Dexmedetomidine-Higher level of sedation without resp depression lENDOSCOPIC NEUROSURGICAL PROCEDURES Indications lNon communicating hydrocephalus lAqueductal stenosis lIntraventricular diseases(Colloid/arachnoid cysts,periventricular tumours Endoscopic Third Ventriculostomy is rapidly becoming the treatment of choice for noncommunicating hydroceph. ltechnique lEnsure immobility of the patient lPrevent and treat sharp increases in ICP lRapid emergence lMonitor as if major rather than minimally invasive lUse of saline irrigation may cause significant changes in CSF composition lStereotactic Surgery lStereotactic Surgery Performed via a burr hole using a three dimensional reference grid attached to the head with pins placed in the outer table of the skull. Localization of discrete area of the brain for biopsy & ablation LA + IV sedation * precludes full airway access lInterventional Neuroradiology Cerebral Aneurysms lEndovascular treatment with cyanoacrylate glues, onyx liquid emboli system and detachable coils Cerebral Vasospasm Intra-arterial papavarine and nimodipine are being used in the treatment of cerebral vasospasm. GA Preferrred ? Sedation-airway obs + undesirable movement by patient

LMA as an alternative to ET lSUMMARY lNeuroanaesthesia today is in a fast-pacing evolution mandated by the rapid changes in the technology and techniques for solving diverse neurosurgical problems. lThere is need therefore , for an anaesthetist to regularly update his/her knowledge and improve the expertise as these have a direct bearing on patients outcome. lTHANK YOU ALL lA l