By A Hollingworth Contents · By A Hollingworth Contents ... Anaesthesia with ↑ICP • signs of ↑ICP: ‣ early = - headache - vomiting - seizures - focal neurology - papiloedema

By A Hollingworth

Contents General Principles 3 .................................

Intracranial Pressure 3Causes of ↑ICP 3 .........................................................................................CPP 4 .............................................................................................................CBF 4 .............................................................................................................Measuring ICP 5 ............................................................................................Anaesthesia with ↑ICP 6Prevent Secondary Brain Injury/↓ing ICP 6Neuro Monitors & Equipment 7Jugular Bulb Oximetry 7 ................................................................................Transcranial Doppler Ultrasonography 7 .......................................................Near-Infrared Cerebral Spectroscopy (NIRS) 8 .............................................Invasive Brain Tissue Oximetry 8 ..................................................................Microdialysis 8 ...............................................................................................

Anaesthesia by Case 8 .............................Craniotomy 8Ventriculo-Peritoneal Shunt 9Evacuation of Traumatic ICH 10Anaesthesia for Regular Surgery with TBI Pt 10Post Op Rx of Head Injured Patient 11Patients with Acute Ischaemic Stroke 12Pituitary Surgery 13Posterior Fossa Surgery 14Awake Craniotomy 16Vascular Lesions 19Intracranial Aneurysm 19 ...............................................................................Ruptured Aneurysm 19 ..................................................................................Surgical Clipping Aneurysm 22 .....................................................................Interventional Radiological Coiling of Aneurysm 24 ......................................ArterioVenous Malformations 25 ....................................................................

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Surgical Clipping AVM 25 ..............................................................................Interventional Radiological Embolisation of AVMs 25 ...................................Scalp Blocks 26Deep Brain Stimulators 26Venous Air Embolism 27Paradoxical Air Embolism 28 .........................................................................

Medical Problems 29 ................................Cardiovascular Complications of Brain Injury 29Pathophysiology 29 .......................................................................................Clinical Course 29 .........................................................................................

Anatomy of Regions 31 ............................Head 31Brain 31 .........................................................................................................Skull 32 ..........................................................................................................Circle of Willis 33 ...........................................................................................Spinal Cord Circulation & Perfusion 34

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General Principles Intracranial Pressure • Norm ICP = 5-10mmHg• ICP >15 = pathological;• Head injury patients = normally Rx’ed if >20mmHg• ICP is pulsatile with 3 distinct waveforms:

‣ A = plateua = cerebral vasodilation‣ B = resp pattern changes‣ C = blood pressure & systemic vasomotor tone

• Contents of skull vault=‣ Brain = 1500mls‣ blood = 150‣ CSF = 150‣ ECF <75ml

• Compensatory mechanisms to ↑ICP from SOL:‣ displace CSF into Sub arach space in spine‣ ↑absorption of CSF‣ ↓intracranial bood

• Mechanisms can be overwhelmed ⟹ ↑ICP ↳ speed of onset depends on size required to ↑ICP

Causes of ↑ICP (>20mmHg)• ↑brain substance

‣ tumour‣ abscess‣ haematoma

• ↑CSF volume:‣ hydrocephalus‣ benign intracranial HTN‣ blocked shunt

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• ↑blood volume:‣ ↑CBF:

- (↓PO2 <50)- ↑PCO2- volatiles

‣ ↑cerebral venous volume:- ↑ITP- venous obstruction at neck- head tilt- coughing

• ↑ECF: ‣ cerebral oedema

CPP • = defines delivery of blood to brain

CPP = MAP - (ICP +CVP)

• CVP at jugular is normally zero or less• CPP varies with MAP but CBF is maintained constant by autoregulation

• ICU studies show:‣ target 60-70‣ harm ≤50‣ no evidence of benefit >70

CBF • Autoregulation (all else being normal) between 50-150mmHg• Outside this CBF varies with CPP• Factors effecting autoreg boundaries:

‣ ↑ed boundaries:- chronic HTN

‣ abolished:- hypoxia- ↑CO2- acute intracranial disease- post head injury

• Factors affecting CBF:‣ metabolism =

- most impt determinant of CBF- eg of ↑CBF = epilepsy, pain- eg ↓CBF = unconciousness, hypothermia, anaesthetic agents (TIVA>volatile)

‣ CO2- at 40mmHg a change of 7.5mmHg ⟹ 30% change in flow- eg ↑CBF = ↑CO2- eg ↓CBF = ↓CO2- MAP also effects response to CO2 - a high MAP will increase effects of ↓CO2 but if ↓MAP

to 50mmHg will nullify CO2 effects‣ O2

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- not an impt determinant- sig hypoxia <53 needed before see change in CBF

‣ Temp:- 1deg C ⟹ ↓CMRO2 by 75%

‣ Viscosity:- no effect between 30-50%

‣ Anaesthetic Agents:- Volatile agents:

• uncouple flow & metabolism = ↓CMRO2 & ↑CBF• in sufficient doses will abolish autoreg altogether• persistent post anaesthetic hyperaemia• halothane = greatest effect; isoflurane the least• ICP is unaffected in iso, sevo, des if <1 MAC• Volatiles not used =

‣ Enflurane = seizures‣ N2O = weak cerebral vasodilator ⟹ ↑CBF & ↑CMRO2

- TIVA:• propofol ⟹ ↓CMRO2, ↓CBF, ↓ICP, CO2 reactivity & autoreg maintained• ketamine traditionally thought contraindicated but now widely used

- Sux:• causes transient ↑ICP via fasciculation ↑ing venous pressure. But not clinically relevant

- Opioids:• little effect on CBF & ICP if CO2 is kept normal (CO2 reactivity is maintained)• remifentanyl - it’s removal must be supplemented with longer acting opioids

Measuring ICP • Ventricular:

‣ = Gold standard‣ catheter inserted into lat ventrical via Burr hole‣ connected to saline manometer or transducer‣ reference point is Foramen of Munro = close to centre of head

↳ ease of use ext auditory meatus often used‣ 1-5% infection rate‣ allows drainage of CSF as Rx option‣ risks:

- haemorrhage at insertion- ventriculitis- difficult procedure esp if oedema/small effaced ventricles

• Intraparenchymal:‣ micro-miniature silicone strain gauge monitor inserted into parenchyma‣ accurate & easy to insert‣ commonest technique used‣ disadv:

- cannot be recalibrated in vivo- measure localised pressure - may not = global ICP- CSF drainage not possible- subject to drift over long periods

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Anaesthesia with ↑ICP • signs of ↑ICP:

‣ early =- headache- vomiting- seizures- focal neurology- papiloedema

‣ late =- Cushings Reflex = ↑bp & ↓HR- agitation ⟹ drowsy ⟹ coma- Cheyne stokes breathing ⟹ apnoea- ipsilat then bilat pupillary dilatation- decorticate then decerebrate posturing

• Rx aims = do not ↑ICP further:‣ avoid ↑CBF:

- avoid 4 Hs: ↑CO2, ↓O2. ↑bp, ↑temp- done by oxygenation, adequate analgesia & depth

‣ avoid ↑Venous pressure:- avoid cough, head down, obstructing ETT ties

‣ prevent further cerebral oedema:- fluid restrict but maintain adequate intravascular volume to maintain CPP- avoid hypotonic solutions eg D5W

↳ fluid across bbb is driven by plasma osmolality not oncotic pressure‣ maintain CPP -

- ↓bp in presence of ↑ICP = ↓↓CBF- target should be CPP >60mmHg (∴ if ICP is 20 = MAP 80)

‣ avoid deleterious anaesthetic agents

Prevent Secondary Brain Injury/↓ing ICP • osmotic diuretic = mannitol 0.25-1g/kg over 15mins

‣ must expect ↑UO & adjust fluid input accordingly‣ higher doses of mannitol >2mg/kg may cause rebound ↑ICP

• loop diuretic = furosemide 0.25-1mg/kg• hypertonic solutions

‣ eg 0.25mls/kg 23.4% Saline over 20mins‣ benefits:

- faster expansion of intravascular volume- ↑CO & pulmonary gas exchange- ↓CSF production - ↓ICP

‣ SEs:- sudden ↓MAP- ↑Na- ↓GCS- seizures

• ↓CO2 to 35mmHg = transient effect on ICP for ~24hrs ↳ CO2 <30mmHg ⟹ loss of autoreg ⟹ ischaemia

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• steroids - ‣ used in tumours & abscesses but have no role in TBI‣ take hrs to work‣ dexamethasone 4mg 6hrly

• Drain CSF - via drain eg ventricular or lumbar• 30deg head up• Ensure normal MAP• Adequate pain relief/depth anaesthesia• Hb Targets:

‣ Pre-op >120‣ intra-op >90

• BSL <10

Neuro Monitors & Equipment Jugular Bulb Oximetry • bulb is cannulated with cannula containing

‣ lumen for aspiration‣ fibreoptic probe:

- IR light measures Hb conc & O2 sats• norm value SjVO2 = 55-71%• injured brain has lost autoregulation thus ↓ability to vary CBF/O2 uptake • SjVO2 depends on:

‣ arterial O2 Sats‣ CBF‣ cerebral metabolic rate

• Not widely used:‣ needs frequent recalibration‣ protein deposits ↑error with time‣ invasive‣ too rapid aspiration can indraw extracerebral blood‣ affected by other variables than just O2 uptake‣ global rather than regional reading

Transcranial Doppler Ultrasonography • = measures blood velocity in cerebral arterial system - generally MCA• signal transmitted through temporal bone• Doppler shift used to measure systolic, diastolic & mean flow• Normal flow = 55cm/sec• waveform pulsality

‣ = shape of difference from peak systolic flow to end diastolic flow‣ = cerebral vascular resistance

• Uses:‣ differentiate between vasospasm & hyperaemia

- uses Lindegaard ratio to determine (flow velocitys of MCA divided by extracranial internal carotid)

‣ determine adequacy of collat circulation during carotid surgery- to decide if shunt needed post clamping- fall to ⅓-50% of baseline indicates need for shunt

‣ post stroke/TIA -

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- can see microemboli in order to predict further stroke/efficacy of antiplatelet agents‣ estimation of CPP - based on pulsatility index

Near-Infrared Cerebral Spectroscopy (NIRS) • non invasive monitor of brain oxygenation• forehead sensor shines IR light through brain• dual detector:

‣ First - placed 3cm from light source ↳ closer ∴ reflected light more scalp & subcut tissue

‣ second- placed 4cm from light source ↳ distant ∴ ↑ed path of light through brain• difference between detectors ∴ assumed to = oxygenation of brain 2.5cm below surface• Beer-Lambert law used to display O2 saturation of Hb• advs:

‣ realtime, dynamic readings‣ correlates with jugular bulb saturations

• disadvs:‣ sig error‣ metabolism - unable to account for O2 delivery & uptake‣ no targets set‣ No defined relationship in how FiO2 affects it‣ How does trend change effect management‣ no info on cognitive outcome

Invasive Brain Tissue Oximetry • 2 fibreoptic probes• placed into brain tissueMicrodialysis • fine coaxial catheter inserted into brain• dialysis membran on outer surface & low flow rates of dialysis fluid are passed through catheter

using pump• samples taken every 10-60mins• can measure substances in cerebral ECF

Anaesthesia by Case • overall goals:

‣ prevent ↑ICP during induction & maintainence‣ maintain adequate CPP‣ avoid interference with cerebral autoregulation‣ achieve rapid & smooth induction & emergence from anaesthesia

Craniotomy Preoperative

• Document signs of ↑ICP• Document any neurology• Check routine bloods esp if on dex/diuretics• Restrict IV fluids to 30ml/kg/d if oedema present

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• Avoid glucose solutions ⟹ hypotonic, risk of ↑BSLPerioperative • Induction:

‣ A line +/- CVP (CVP useful if VAE but not significant problem if not sitting position)‣ TIVA & Remi with NDNMB & Remi‣ Use remi to blunt HTN response to laryngoscopy

↳Alternative = lignocaine1.5mg/kg or labetalol 5mg increments‣ Armoured ETT‣ Waterproof eye tapes‣ Use tube tape not tie to prevent jugular compression‣ Mayfield 3 point fixator screws can ⟹ severe HTN

- ↑remi- infiltrate with LA- scalp blocks

• Maintenance:‣ Avoid N2O‣ Remi/fentanyl/alfentanil infusion‣ Cox 2 inhibitors do not effect platelets of bleeding but should be discussed. Non specific Cox

inhibitors should be avoided‣ Further mm relaxants uncommonly required ‣ Aim for normotension, PaCO2 35mmHg, normovolaemia, normothermia‣ Pneumatic compression stockings

• Extubation:‣ Avoid HTN, coughing on extubation by using remi/morphine

↳ rescue with labetalolPostop • surgeons check for lateralising neurology immed post op• should not require a PCA• neuro obs on neurosurg ward• if obtunded preop - may need ICU

Ventriculo-Peritoneal Shunt • used for hydrocephalus to divert CSF away from ventricles• usually a VP shunt but could be V-atrial or V-pleural• occipital Burr hole used to place tube in lat ventricle• tube then tunneled s/c down neck/trunk & inserted into peritoneal cavity via small incision• flushing system & valves used to prevent clotting & back pressure• quicker op than craniotomyPreoperative • commonly done in children• often ↑ed ICPPerioperative • Induction

‣ A line & CVL usually not required• Maintenance

‣ tunnelling shunt is very painfulPostop

• ↓GCS = indication for CT scan to exclude shunt malfunction or subdural haematoma

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Special Points • if CSF drained too rapidly risk of ICH• shunt infection & revision is common• watch for PTX as trocar placed

Evacuation of Traumatic ICH • types:

‣ extradural - - tear in middle meningeal artery due to skull # (except in children)- must be done <1hr of pupillary dilation

‣ subdural -- bleeding from bridging veins between cortex & dura- early evac of an acute SDH ⟹ better outcome- chronic SDH in elderly can be evac with burr hole under LA

‣ intracranial -- in HTN people with warfarin or intracranial aneurysm

• overall goals:‣ optimisation CPP & prevention of intracranial HTN‣ Intubate if GCS ≤8 or ↓≥2 in any one hour‣ adequate anaesthesia & analgesia‣ prevention of secondary injury

Preoperative • ↓GCS & ↑ICP• watch for assoc injuries esp spinalPerioperative • Induction

‣ as for craniotomy‣ A line, +/- CVL‣ Assume ICP = 20 thus MAP target >80-90mmHg

↳ intra-op hypotension assoc ↑x3 mortality• Maintenance

‣ once decompression may be ↓SBP which can be treated with volumePostop • protocol to maintain ↓ICP and required CPP

Anaesthesia for Regular Surgery with TBI Pt • timing to consider:

‣ life threatening injury eg rupture intra ab organ‣ non life threatening injury eg max fax injury

• CPP target in TBI >60• admission GCS as risk stratifier:

‣ mild TBI = 15-13‣ mod TBI = 9-13↳ >8 are considered to have low risk of ↑ICP‣ severe TBI = ≤8

- ≤8 = 25% pt’s have ↑ICP (absent of surgical lesions)- 50% will have major extra-cranial injuries

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• tourniquet use:‣ inflated: ↑VR ⟹ ↑MAP ⟹ (depending on autoreg) ⟹ ↑ICP‣ release = ↓CBF:

- (systemic) ↑PaCO2 ⟹ vasodilation ⟹ ↓MAP ⟹ ↓CPP- (cranial) ↑PaCO2 ⟹ cerebral vasoD ⟹ ↑ICP & ↓CBF

• in a trauma pt should always consider a craniotomy if:‣ lateralising signs‣ depressed skull #

↳ also consider placement of ICP monitor• non life threatening injury:

‣ if operated on within 1st 24 hrs - risk period for ↓MAP & ↓PaO2‣ should prioritise excellent head injury care

Post Op Rx of Head Injured Patient • Aim to minimise secondary brain injury• use protocol to prevent, identify & treat causes of secondary brain injury:

‣ Intracranial:- haematoma

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- oedema- seizures- hydrocephalus- abscess- hyperaemia

‣ Systemic:- sepsis/fever- ↓PO2, ↑PCO2- ↑BSL, ↓Na, ↓Hb

• should not get steroids - assoc with ↑infection & worse outcome• should not cool <36 - (EUROTHERM) -

‣ ↓temp in ICU does lead to ↓ICP but probs with VAP/LRTI ‣ if cold already, do not warm

• MAP >80-90• avoid albumin (SAFE)• consider reversal of warfarin immediately regardless of INR or CT

Patients with Acute Ischaemic Stroke • ↑ing use of endovascular therapy for Rx of stroke• Indications:

‣ Proximal large occlusion‣ <6hrs since onset‣ Ischaemia

• options:‣ LA +/- sedation‣ GA

• advs of GA:‣ immobility‣ pain control‣ airway protection

• disadvs:‣ CVS instabiliy‣ delayed time to recanalisation (ischaemic brain ages 3.5yrs/hour untreated)

Preoperative • CVS response to stroke:

‣ 1st 24hrs: initial HTN:- Cushing response to mass effect- autoreg response to effect ↑CPP- neuroendocrine response from stress

‣ >24hrs - bp ↓s by ~25% in most patients• Difficult targets for bp:

‣ low = ↓CPP & CBF‣ high = risk of haemorrhagic transformation

• Aim should be:‣ prior to revascularisation = SBP 140-180mmHg ‣ post recanalisation can ↓SBP

• GA or sedation or local is fine, key is bp controlNeuroprotective Agents • None proven:

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‣ Mg‣ Hypothermia‣ Different anaesthetic agents eg barbituates, xenon

Pituitary Surgery • pituitary tumours = 15% of intracranial tumours• presentation either:

‣ asymptomatic (up to 1:7 have a pituitary tumour but only 1:1000 have clinical symptoms)‣ Acromegaly/Cushings = hypersecretion of hormones (if functionning adenoma)‣ mass effects = headache, visual field defect (bitemporal hemianopia (periph field loss),

hydrocephalus, hypopituitarism• Operation done urgently if sight is deteriorating rapidly• surgical access via sphenoidal air sinuses

Preoperative • If acromegaly - (see medical notes)

‣ macroglossia, prognathism & hypertrophy of epiglottis/vocal cords ⟹ airway compromise ↳ low threshold for VL or AFOI

‣ CVS problems: HTN, LVH, cardiomyopathy, arrhythmias, heart failure‣ sleep apnoea (in 70%)‣ DM

• If Cushings:‣ truncal obesity & ↑reflux‣ CVS disease eg IHD & HTN‣ ↓K, ↑BSL‣ steroid cover required peri-op

• If Diabetes Insipidus:‣ ↑Nawith hypo/euvolaemia

• If multiple endocrine neoplasia may see ↑Ca• Endocrine evaluation required:

‣ prolactin, TSH, FSH& LH, Testosterone, ACTH, cortisol, ILGF (surrogate marker for GH)Perioperative • Induction

‣ throat pack‣ nasal vasoconstrictors

• A line & good access - ‣ chance of major haemorrhage if disruption of cavernous sinus/carotids (both lie lateral to pit

gland)‣ should check ulnar/radial insufficiency - Allens Test:

- make fist for 30seconds with hand elevated- apply pressure to ulna & radial- hand opened while elevated & ulna is released- colour should return within 15secs

↳ if not ulna insufficiency and should caution about placing radial A line• Permissive hypotension & ↓HR to improve surgical field• Maintenance

‣ if suprasellar extension -

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- to improve surgical field: • lumbar drain inserted into CSF

↳ May have to instil volume of sterile saline into CSF to advance tumour into operative field

• controlled hypercapnia (40-45mmHg)• ExtubationPostop • no CPAP• Pain

‣ generally not severe‣ bilat infraorbital nerve blocks an option

• Diabetes Insipidus occurs in up to 50%:‣ can normally be managed with free oral intake‣ generally self limiting‣ monitor Na & K & Rx with desmopressin (0.25-1mcg) if required

↳ watch for overshoot• CSF rhinorrhoea is possible - usually self limitingSpecial Points • Pan-hypopituitarism patients should be referred to endocrinologist for hormone replacement:

‣ hydrocortisone ⟹ ACTH adrenal insufficiency‣ thyroxine ⟹ TSH hypothyroidism‣ testosterone ⟹ GnRH male hypogonadism‣ Oestradiol + progesterone ⟹ GnRH femal hypogonaisdm‣ Growth hormone - injection‣ DDAVP nasal spray ⟹ ADH central diabetes insipidus

Posterior Fossa Surgery

• surgery:

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‣ foramen magnum decompression‣ vascular procedures‣ debulking tumours

• Boundaries:‣ Anterior: dorsum sellae & occiptal bone‣ Lat: temporal bone‣ Superiorly: dura (tentorium cerebelli)‣ Post & inf: occipital bone

• Contents of fossa =‣ pons - resp control centre‣ medulla - CVS & resp control centre‣ cerebellum‣ motor & sensory ascending & descending tracts‣ lower CN nerve nuclei‣ cerebral aqueduct for CSF flow

• Signs of ↑pressure in this area:‣ LOC‣ HTN & ↓bp‣ Resp depression & apnoea‣ loss of airway reflexes‣ hydrocephalus

Preoperative • Should look for & assess:

‣ ?bulbar palsy - lower CN dysfunction. Ax gag: may ⟹ silent aspiration ∴ Ax chest‣ cerebellar function‣ ?↑ICP 2nd to hydrocephalus may need ventricular drainage prior to procedure‣ Ax fluid status - ?vomiting‣ If sitting position planned - must have PFO r/o with bubble contrast ECHO‣ Check routine bloods‣ Airway exam - ?atlanto-axial subluxation

• Ax CVS system ?HTN, post hypotension, CVS septal defectsPerioperative • Induction

‣ NG tube if post op bulbar dysfunction‣ A line transducer at external auditory meatus‣ CVL if sitting

• Maintenance‣ specialised monitoring:

- consider monitor for VAE eg TOE- spontaneous or evoked EMG of CN VII- somatosensory evoked potentials - ?spinal cord ischaemia- brainstem auditory evoked potentials of CN VIII

‣ Lumbar CSF drainage sometimes used to improve surgical conditions ‣ watch for sudden CVS changes - surgically caused

↳ rare to need pharmacological Rx but consider atropine & BBs‣ positonning: prone, sitting or lateral

- sitting:• avoid excessive head flexion - jugular compression, cerivcal cord ischaemia• complications:

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‣ haemodynamic instability -- surgical - working near CVS centres in brainstem- gravity effects

‣ VAE & paradoxical air embolism‣ pneumocephalus‣ macroglossia - flexed neck ⟹ obstruction of venous/lymph drainage from tongue‣ quadriplegia - flexed neck ⟹ cord ischaemia - Must maintain MAP & good

positioning• absolute contraindications:

‣ PFO‣ patent V-atrial shunt‣ cerebral ischaemia when upright

• relative Contraindications:‣ uncontrolled HTN‣ COPD‣ extreme of age

• Extubation:‣ possibility of airway obstruction due to:

- macroglossia- partial vagus damage- excessive Cx flexion

‣ medulla/pons surgery can ⟹ ↓post op resp drive‣ high risk of PONV

Postop • consider ICU if

‣ preop status poor‣ extensive resection‣ cerebral oedema‣ complications

Special Points • acoustic neuroma -

‣ facial nerve vulnerable & monitored with nerve stim over face ∴ limited NMBs or remi induction‣ CNVIII monitored - keep anaesthesia depth constant & watch for changes ∴ attributable to

surgery• VAE risk is high• paeds:

‣ if VP shunt in place must establish patency‣ must screen for PFOs if planning sitting‣ Rx blood loss agressively‣ watch hypothermia - big heads‣ post fossa syndrome

- = temporary & complete loss of speech- RFs = medulloblastoma & midline tumours

Awake Craniotomy • Used for

‣ epilepsy surgery - accurate mapping of resection margins‣ excision of tumours in eloquent cortical areas (motor, speech, sensory)

• benefit = ‣ intraop Ax of neuro state

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‣ ↓ed HDU needs‣ shorter length of stay‣ ↓PONV‣ ↓post op complications‣ ↓cost

• techniques:‣ LA incl scalp blocks then sedation:

- dexmedetomidine• selective α2 agonist• anxiolysis & analgesia without resp depression• no effect on ICP• may cause ↓HR & ↓bp• load 0.5-1mcg/kg over 20mins• infusion 0.2-0.7mcg/kg/hr

‣ asleep - awake - asleep technique with LMA ↳ may be better as less oversedation, airway obstruction, ↓ventilation, unco-operationPreoperative • need experienced anaesthetist & surgeon• pt must be informed, motivated & tolerate lying still• absolute CI:

‣ confusion‣ anxiety‣ diff comms

• relative CI:‣ obesity‣ reflux‣ highly vascular tumours‣ OSA

Perioperative • Induction

‣ IV antiemetics - must avoid at all costs‣ TIVA & remi on an LMA

• Maintenance‣ ?prophylactic anti-seizures meds - phenytoin‣ adequate infiltration of LA to pins sites or scalp blocks‣ once tumour exposed:

- ↓remi to allow spont vent- then remove LMA & stop propofol

‣ Dexmedotomidine:- load 0.7mcg/kg load over 30min- infuse 0.2-0.4mcg/kg/hr

• Cortical mapping - awake:‣ most likely time for complications:

- surgical factors:• seizure:

‣ ice cold saline to brain tissue - usually resolves‣ midazolam, re-sedation may be required

• VAE• focal neuro deficit• brain swelling

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- airway compromise - usually LMA rescue- CVS- Anaesthetic technique eg LAST, N&V, pain, ↑↓sedation- Psych factors: anxiety, tiredness, revoking consent

‣ once tumour excised ⟹ restart propofol & reinsert LMA• possible complications:

‣ seizure‣ ↓resp drive/obstruction‣ restlessness‣ VAE

Special Points • calm & quiet atmosphere in theatre• drapes used to allow access to face & prevent claustrophobia• cortical mapping - need to identify:

‣ Broca’s area‣ Wernickes area‣ motor & sensory cortex

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Vascular Lesions • either

‣ intracranial aneurysms‣ AVMs

Intracranial Aneurysm • cerebral arteries have ↓elastic mm layer ⟹ weaker• Berry aneurysm occur at vessel junctions• Aneurysms account for 85% of SAHs• Systemic associations:

‣ atherosclerosis‣ familial trait‣ cocaine or alcohol abuse‣ polycystic kidneys‣ hereditary haemorrhagic telangectasia‣ co-arctation of aorta‣ Marfans‣ Ehlers Danlos - type 4‣ Klinefelters syndromes

• commonest sites: in Circle of Willis close to bifurcations:‣ ant cerebral = 34%‣ middle cerebral = 20%

• prevalence = 6% in angio studies• commoner in female (3:2) men & 40-60yrs• in 25% cases are multipleRuptured Aneurysm • rupture generally occurs only when >5mm in diameter• present as SAH or ICH• Symptoms:

‣ sudden onset severe headache +/- LOC‣ photophobia, neck stiffness, Kernigs +ve‣ focal neuro deficit = enlarging aneurysm causing localised pressure effect‣ cardiac arrest‣ APO‣ ECG changes - can be anything but esp inferior ischaemia

• Differentials:‣ migraine‣ meningitis‣ pituitary apoplexy‣ postcoital cephalgia

• Diagnosis:‣ CT highly sensitive - 95-100% on first day - if read by neuro-radiologist‣ LP can be done 12hrs after onset of bleed - test for xanthochromia‣ Ct angiogram - used to identify cause of SAH -

- NPV of 82-96%- most sensitive for aneurysms >4mm in size- Digital subtraction angiography (DSA) = gold standard

Grading • > 40grading systems exist - most impt is GCS, speech, motor deficit

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• World Federation of Neurosurgeons grading 1-5• gives value in morbidity & mortality• grade 1-2 = operate or coil early• gd 3-5 = delay intervention to within 72hrs

Acute Management • standard care to prevent secondary brain injury• indications for intubation:

‣ GCS <8‣ ↓GCS by >2 points‣ hypoventilation/hypoxia‣ refractory seizures‣ protection of airway if no bulbar reflexs

• Rx HTN with SBP target of 160mmHg & avoidance of ↑bp ↳ labetalolComplications • split:

‣ neurological complications‣ medical complications

Neurological Complications• Rebleeding:

‣ 1st 24hrs = 4% risk of rebleed‣ every day after for 4 weeks = 1.5% risk/day‣ each rebleed episode ⟹ 60% risk of death

↳ ∴ aim is to secure aneurysm by clipping or angiographically obliterating it endoluminally early ↳ coiling = now most common method used

‣ historically surgery was delayed for 10d to avoid peak of vasospam‣ nimodipine has resulted in earlier surgery

- gd 1-2 = immediately- gd 3-5 = within 72hrs

‣ minimise re-bleed by preventing large ↑SBP & fluctuations in ICP:- avoid cough/valsalva- effective analgesia, antiemetics

• Delayed neuro deficit (DND):‣ =any clinically detectable neuro deficit caused by:

- delayed cerebral ischaemia (DCI) & vasospasm

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- hydrocephalus - in 30% pts - Rx with EVD- cerebral oedema- fevers- seizures -

• in 1-7% patients. • Assoc with rebleed• prophylactic anticonvulsants are not used esp phenytoin

- electrolyte abnormalities‣ major cause of morbidity‣ 2nd common cause or mortality‣ DCI & Vasospasm:

- DCI can occur without vasospasm- DCI often affects more than 1 vascular territory- definitions:

• DCI = deterioration related to ischaemia which persists >1hr with no other cause• vasospasm = arterial narrowing shown on angio/doppler with corresponding signs

- Vasospasm risks:• poor SAh grade• large SA blood load on CT - defined by Fischer Grade 3-4• Intraventricular haemorrhage• smokers

- Pathophysiology:• Subarach blood undergoes haemolysis• released substances eg oxyHb ⟹ vasospasm

‣ peaks 3-14days after initial bleed - with early surg now common to see post op‣ angiographic anatomical vasospasm occurs in up to 75% but only 50% will get DND‣ 20% may suffer stroke or die 2nd to vasospasm despite best Rx‣ Treatment:

- nimodipine:• selective dihydropyridine CCB with good bbb penetration• prevents Ca influx to cells via L type Ca channels• started at diagnosis & continued for 3weeks • 60mg NG/PO 4hrly or 1mg/hr IV• SEs = ↓bp which must be overcome with fluid or vasopressors

- Triple H therapy:• Hypertensive:

‣ = ↑CPP ⟹ ↑CBF‣ suggested target =

- normal MAP +15% OR - graduated increase in bp until resolution of symptoms

• Hypervolaemia - no longer‣ euvolaemia is better to prevent pulmonary oedema etc

• Haemodiltion - no longer‣ ↓HCT = ↑CBF but ↓O2 delivery

- Medical therapies:• Normal Mg• Rx fever - TTM• BSL <10

- Ballon angioplasty- Intra-arterial targetted papverine

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• Hydrocephalus:‣ blood in subarach space may obstruct drainage of CSF ⟹ hydrocephalus‣ note draining with ventricular drain must be done slowly to avoid chance of rebleed by ↑transmural pressure across aneurysm

‣ CT is required to rule this out before treating as DND/rebleed• seizures• cerebral oedemaMedical Complications• severe complications seen in 40% patients• account for 23% of deaths• pathophys is massive sympathetic surge & catecholamine release which follows SAH• include:

‣ severe LV dysfunction/cardiogeneic shock- 45% of patients see EF <50% or RWMA

‣ ECG abnormalities (27%) - assoc with higher grades- T wave inversion- ST segment changes- Q waves- QTc prolongation

‣ neurogenic pulmon oedema:- hydrostatic effect - initially:

• ↑in pulmon artery pressure ⟹ damage to microvasculature ⟹ ↑permeability‣ electrolyte disturbances:

- ↓Na:• ?caused by: ↑ANP release & SIADH ⟹ hypovolaemia & ↓Na. • Should give Na back

- ↓K, ↓Mg‣ DVT- medical treatment only after aneurysm is secured‣ pneumonia‣ hepatic, renal, GI dysfunction

Prognosis • SAH leads to:

‣ initial bleed = 20% death‣ reach hospital =

- 15% die within 24hrs- 40% good recovery

Anaesthesia • 2 options:

‣ clipping‣ coiling

• overall goals:‣ optimum operating conditions for surgeon‣ prevent transmural changes which may lead to aneurysm rupture & rebleed‣ keep adequate CPP & cerebral oxygenation

Surgical Clipping Aneurysm • microsurgery to apply spring clip across neck of aneurysm

‣ post fossa craniotomy if vertebral or basilar artery aneurysm‣ often need to control bleeding prior to clipping by clamping more proximal vessels temporarily

• ISAT - International Subarach Aneurysm Trial

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‣ absolute risk reduction of 6-9% favouring coiling:clipping‣ but coiling need higher re-treatment & slightly ↑ed chance of rebleed

• clipping only used for:‣ wide neck aneurysms‣ locations in MCA

Preoperative • Neuro exam to document effects on brain• Ax volume status/bleeding• start nimodipine• prophylactic anti seizure meds:

‣ levotericetam‣ phenytoin - 15mg/kg loading then 3-4mg/kg daily as single dose

• discuss surgical difficulty - will affect need for anaesthetic adjuncts:‣ induced ↓temp‣ deep anaesthesia/barbituates

Perioperative • Induction

‣ consider CVL - useful to maintain MAP‣ good access - potential for catestrophic bleeding‣ stable induction (use lignocaine, opioids, adequate induction, preop BBlocker)

- ↑in MAP may ⟹ rupture- ↓MAP risk ↓CPP

↳ ∴ aim for bp +/- 10% preinduction

• Maintenance‣ ventilate to normal PaCO2 to avoid ischaemia‣ gd 1-3 patients = use norm core temp ‣ induced hypotension is not commonly used - instead use temp spring clips

↳ if required SBP 60-80mmHg using ↑volatile, labetalol ↳ if vasospasm already present must avoid ↓bp

‣ temporary spring clips:- surgeon may request temp ↑in MAP (10%) after placement of clip to drive collateral flow

‣ if rupture:- replace blood with blood- ↓MAP will ⟹ ↓bleeding- ipsilateral carotid compression

‣ cerebral protection:- thiopentone to EEG burst supression - 3-5mg/kg bolus then 3-5mg/kg/hr- ↓temp to 32deg

• = reserved for complex procedures• done using surface cooling devices

‣ Lumbar drainage:- may be requested by some surgeons- only open drain when skull is open- drainage should be limited to max 5ml/min

• Extubation‣ standard neuro extubation

Postop • ↓GCS ⟹ needs CT to exclude haematoma, hydrocephalus, vasospasm

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Interventional Radiological Coiling of Aneurysm • most done by releasing Guglielmi detachable coils (GDCs)• microcatheters used via femoral artery access point• approach shows ↑1 & 5yr survival compared to surgical clipping• but does have slightly higher rebleed rate

Perioperative • Induction

‣ +/- CVL line. Can transduce femoral artery introducer sheath ↳ gives good MAP but overestimates DBP & underestimate SBP

‣ normal neuro care - not a stimulatin procedure‣ can use LMA or standard ETT‣ baseline ACT taken to establish clotting time

• Maintenance‣ procedure is not stimulating - maintain CVS with low dose anaesthetic‣ keep close eye on volume status - lot of contrast & flush may ⟹ hypervolaemia then

hypovolaemia‣ intraop:

- heparin 5000 IU then further boluses to keep ACT 2-3x baseline- monitor ACT hourly- protamine used to reverse heparin 1mg/100 IU of heparin- abciximab targetted thrombolysis

• Extubation‣ smooth & rapid recovery

Post Op • aspirin may be used• CT if any concerns• EVD may be required & ICU careSpecial Points • remote anaesthesia• contrast, flush, heparin, antiplatelet drugs & thrombolysis all used• complications:

‣ Occlusion - causes:

• intraop vasospasm - from manipulation of vessel. Rx by withdrawing catheter & waiting or targetted nimodipine

• thromboembolism• arterial dissection• coil misplacement

- Rx goals:• ↑MAP ⟹ ↑collateral flow• targetted therapy eg heparin, antiplatelet agents, thrombolytics

‣ Haemorrhage = rupture of aneurysm - seen by extravasation of contrast- signs = ↑ICP, ↑MAP, ↓HR- Rx =

• reverse heparin, • ↓MAP (to level before bleed), • pharmacological ↓ICP, • pharmacological metabolic suppression eg thio

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• control seizures• initiate cerebral protection ?cooling

- a rescue craniotomy & clipping may be requiredArterioVenous Malformations • = dilated arteries & veins with no intervening capillaries• present:

‣ SAH‣ seizures

• high blood flow through these lesions ⟹ stealing blood from surrounding tissues ⟹ ischaemiaSurgical Clipping AVM • surgery not urgent unless of pressure effects• surgery assoc with massive blood loss• corection of AVM ⟹ removal of blood shunted ⟹ relative hyperperfusion to surrounding tissue ⟹ ↑ICP or oedema

• no risk of vasospasm ∴ hypotension could be used if required• in paeds:

‣ AVMs can cause high output failure due to intracerebral shunt‣ heart failure can be caused by lesion excision

Interventional Radiological Embolisation of AVMs • embolisation may be used to obliterate AVM or ↓size before definitive surgery• use liquid polymer or glue• allows ↓bleeding while preserving arterial supply to brain• staged procedures common if:

‣ rapid blood flow‣ multiple fistulae‣ feeding/draining vessels‣ assoc aneurysms

Perioperative • Induction

‣ as for coiling• Maintenance

‣ ↓bp can ⟹ intracerebral steal‣ ↑ICP from haemorrhage can ↑↑bp‣ temporary controlled ↓bp used to produce flow arrest through AVM & enable glue to set

Special Points • fem artery may need cannulating multiple times ∴ angio-seal is not used ∴ need prolonged

anaesthesia to avoid coughing & pressure on hole• complications:

‣ inadvertent occlusion of norm vessels ⟹ ischaemia‣ PE from shunting of particulate matter‣ bleeding from

- incomplete embolisation- perforation of arterial feeders- rupture of assoc aneurysms- hyperperfusion (if shared venous drainage ⟹ oedema & ↑ICP)

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Scalp Blocks • anatomical block rather than a ring block• use standard max calculations for total LA dose• 7 injections:

‣ supraorbital (V1 trigeminal branch):- innervates: forehead, ant scalp, top of head- LM: palpate supraorbital notch & insert immediate superiorly perpendicular to eyebrow

‣ Supratrochlear (V1, trigeminal branch)- innervates: forehead & ant scalp- LM: just medial to supraorbital injection

‣ Zygomatico-temporal (V2 trigeminal branch):- Innervates: small area of forehead & temporal area- Nerve: nerve passes through temporalis muscle to enter fascia ∴ need to infiltrate above &

below mm- LM: infiltrate lat to supraorbital margin continuing posterior to distal zygomatic arch

‣ Auriculotemporal (V3 trigeminal):- innervates: temporal area, lower lip, lower face, auricle (ear) & scalp around- Nerve: passes close to facial nerve, should be cautious and inject more superior- LM: 1cm ant & 1cm above tragus palpate for superficial temporal artery. Inject posterior to

it aiming to deposit LA underneath it‣ Lesser Occipital Nerve (branch of 2nd or 3rd Cx spinal nerve):

- innervates: scalp in lat area of head posterior to auricle- nerve: ascends on post border of SCM- LM: infiltrate behind auricle top of ear to lobule below. Then continue posteriorly along

superior nuchal line‣ Greater Occipital Nerve (branch of 2nd Cx spinal nerve):

- Innervates: skin along post scalp +/- scalp at top of head & over auricle- Nerve: comes from 1st & 2nd Cx vertebrae- LM: palpate occipital artery (3-4cm) from occipital protuberence along superior nuchal line.

Inject medial to artery‣ Greater auricular nerve (branch of 2nd &3rd Cx spinal nerves:

- Innervates: skin over parotid gland & mastoid process & auricle- Nerve: emerges from post border of SCM. Divides into ant & post branch- LM: should be covered by injection of lesser occipital nerve ie 2cm post to auricle at level

of tragus

Deep Brain Stimulators • aka functional neurosurgery• used to Rx chronic conditions:

‣ Parkinsonism - can decrease ‘off’ state time. ‣ tremor - used for severe disabling tremor where medication is failing‣ psychiatric disturbances - useful in OCD‣ chronic pain

• Surgical procedure:‣ electrode implantation into brain - LA or GA

- stereotactic frame placed on head with LA & sedation- CT scan- return back to theatre for implantation

‣ impulse pulse generator placed sub cut - GA

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• Mechanism of action:‣ high supressive frequency to supress overactivity in

- Parkinsons: pallidum or STN (subthalmic nucleus)- Tremor - thalamus

• Risks:‣ bleeding ⟹ stroke <1%‣ infection or migration of implant

• Side effects:‣ altered walking‣ altered speech‣ mood disturbance‣ weight gain‣ limitations on MRI

• Benefits: L dopa & dopamine agonists are reduced to 50% of preop level• Safety:

‣ MRI:- Risks incl heating, magnetic field interactions causing movement of electrodes, ↑ed

stimulation, DBS damage- strict criteria apply for use of MRI with DBS insitu

‣ Surgical diathermy:- Use bipolar where possible- Monoplar:

• use low voltage mode• lowest possible power setting• keep ground pad as far from DBS as possible (subclavicular space, neck, head)

‣ Defibrillations:- use pads as far from DBS as possible- use lowest energy output- confirm DBS working afterwards

• Programmed externally from hand held device over DBS unit

Venous Air Embolism • can occur whenever operative site is higher than RA• esp common in sitting craniotomy when veins are opened that are unable to collapse despite -ve

intraluminal pressures eg emissary veins in post fossa• N2O does not ↑risk of VAE but may worsen outcomePathophysiology

• pulmonary microvascular occlusion ⟹ ↑physiological dead space• bronchoconstriction• frothing in RA/RV & ineffective RV pumping⟹ obstruction of RV outflow tract ⟹ ↓COSigns • ↓MAP• arrhytymias• ↑pulmon art pressure• ↓EtCO2• ↓SpO2

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Detection • ETCO2 most reactive monitor - see sudden drop ↳ note differentials eg ↑ventilation, ↓CO, other types of embolism• doppler ultrasound:

‣ most sensitive non invasive monitor - probe R parasternal region‣ not quantitative - does not differentiate from clinically relevent or irrelevant emboli‣ probe position can be difficult

• TOE:‣ allows determination of amount of air aspirated‣ invasive & difficult to place, needs expertise

• PA cateters:‣ invasive but sensitive‣ ↑in PAP not specific though

• Stethoscope - millwheel murmur. Only seen in massive VAEPrevention • avoid sitting position unless essential• elevate head only as much is necessary• ensure normovolaemic to maintain +ve CVP• trendelenburg & elevate legs to minimise gradient between surg field & heart• PEEP controversial - good if no PFO otherwise may ↑risk of systemic embolism• Medical antishock trousers can ↑VR in sitting patientsTreatment • Supportive B & C care• inform surgeon - flood field with saline to stop further entrainment & identification of veins to

cauterise or wax• Stop N2O if using• 100% O2• position operation site below level of heart • aspirate air from CVP line if present• if poss: turn pt into L lateral & head down - to keep air in RA• gentle chest compressions (even if not in arrest)- can break up volume of air• consider hyperbaric referral (Rx up to 6hrs post event can be helpfulParadoxical Air Embolism • entry points:

‣ thesbian veins in heart ‣ bronchial vessels‣ PFO = VAE into pulmon circulation ⟹ PAP ⟹ pulmon HTN ⟹ ↑R heart pressures ⟹ R to L

movement encouraged• small volumes of air in systemic circulation can be disastrous• cardiac septal defects are absolute CIs to sitting position surgery

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Medical Problems Cardiovascular Complications of Brain Injury • common problem post brain injury:

‣ HTN‣ ↓bp‣ ECG changes‣ arrhythmias‣ release of cardiac biomarkers‣ LV dysfunction

• problems usually reversiblePathophysiology • related to:

‣ catecholamine effects:- TBI & SAH ⟹ catecholamine storm- levels remain high for ~10days- may be protective mechanism designed to maintain CPP- result is ↑SVR ⟹ ↑afterload ⟹ ↑myocardial work without ↑O2 supply ⟹ possible

ischaemia‣ neurogenic stunned myocardium (NSM) =

- excessive norad release from myocardial SNS independent of plasma catecholamines- severity proportional to brain injury- can be quick onset <4hrs

‣ direct effect on brain stem control centres = neurogenic ↓bp‣ neuroinflammation:

- release of central mediators ⟹ SIRSClinical Course • acute = HTN & ↑HR should treat if becomes malignant ie >180SBP and tachy >100 ↳ ß blocker good evidence for ↑mortality with ↓HR• subacute = ↓bp due to periph vasoD & ventricular dysfunction ↳ Rx with IVF & NA• ECG in SAH:

‣ generally in first few days before subsiding (can be up to 8weeks)‣ pattern:

- ST segment changes- flat Ts- prominent U waves- prolonged Qtc

‣ due to local SNS activation (not systemic catecholamine)• cardiac arrhythmias:

‣ any type but immediately life threatening is rare‣ usually in first 7 days‣ post ischaemic stroke incidence = 25%‣ should do ECG every 24hrs in first week

• ventricular dysfunction:

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‣ assoc with NSM:- RWMA in antero septal & antero ventricular walls (apex sparing)

‣ SAH:- 15% have LV dysfunction but often mild- 71% diastolic dysfunction

• Takotsubo:‣ apical & mid ventricular akinesia with basal sparing‣ causes:

- emotional of physical stressor ⟹ benign- SAH ⟹ ↑mortality

‣

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Anatomy of Regions Head Brain

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Skull

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Circle of Willis

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Spinal Cord Circulation & Perfusion

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ie CPP = MAP - (ICP + CVP)

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