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You are in Home >> Exams >> Mitchell Anaesthetic Notes


Created: 22/6/2006
Updated: 8/1/2007

Positioning for neurosurgery

  • General considerations
    • Usually prolonged surgery
    • Careful identification of pressure areas
    • Avoidance of traction on nerves
    • Thromboembolic precautions
  • Supine
    • Used for frontal, temporal or parietal access
    • Extreme of head rotation may cause venous obstruction, carotid dissection
    • Slight head-up usually desirable for venous drainage
    • Hip and knee flexion reduces back strain: beach-chair position
  • Semilateral (“Jannetta”)
    • Used for retromastoid procedures
    • Table tilted 10-20°, shoulder roll, head rotation
    • Avoid extreme head rotation
  • Lateral
    • Used for posterior parietal and occipital access
    • Axillary roll to prevent brachial plexus injury
    • Stabilization with vacuum bean-bag or lateral rests (potential pressure areas)
  • Prone
    • Used for spinal, occipital, cranial suture and posterior fossa procedures
    • For cervical spine and posterior fossa usually head-up and neck flexed
    • Requires planning for turning
      • Secure airway and lines, 100% O2, removal of most monitoring
      • Unstable cervical spine may require awake intubation and positioning
    • Facial support much not cause eye compression and retinal ischaemia
    • Other pressure areas: elbows, breasts, iliac crests, genitalia, knees, toes
    • Avoid pressure on abdomen: increased PAW, IVC obstruction
    • Neck flexion may cause compression of base of tongue and pharynx
      • Especially with instrumentation: ETT, TOE
  • Sitting
    • Used for some posterior fossa and cervical spine surgery
    • Possibly greater dangers than alternative positions
      • Hypotension, cerebral ischaemia (decreased venous return, decreased CPP)
        • Perfusion pressure should be measured at ear level
        • Lightly anaesthetized patients may compensate with increased SVR, decreased CO
        • Volume loading and pressors to maintain CPP ≥60 mmHg
        • TEDs stockings or calf compression devices
      • Tongue and pharynx compression or spinal injury from neck flexion
      • Pressure areas: buttocks, potential brachial plexus distraction
      • Venous air embolism ± paradoxical embolism
      • Pneumocephalus
        • May be worsened by N2O diffusion after dural closure
        • Cease N2O with dural closure
      • PA catheter tip may be in West’s zone 1 (alveolar pressure > PA pressure)
      • Surgery in this position may involve the brainstem
        • Haemodynamic, respiratory, homeostatic disturbance
    • Some advantages
      • Better venous and CSF drainage, possibly better access


Venous air embolism

  • Incidence
    • Depends on procedure, position and method of detection
    • Sitting position posterior fossa surgery with TOE: 76%
    • Less for other positions, surgery and monitors
  • Aetiology
    • Open vessels at lower than ambient pressure
      • Cerebral sinuses, emissary veins, diploic vessels in head-up position
      • Gas under pressure in ventricles, subdural space
      • Gas under pressure in non-neurosurgical procedures: laparoscopy, hysteroscopy, gas-cooled lasers
  • Detection
    • High sensitivity
      • TOE, praecordial Doppler (right sternal edge 3rd-6th intercostal spaces)
    • Lower sensitivity, indication of severity and recovery
      • ETCO2, PAP
    • Low sensitivity, indication of incipient arrest
      • BP, ECG, SpO2
  • Management
    • ABC
    • Prevent further air entry
      • Notify surgeon, flood field
      • Jugular compression, lower head
    • Manage intravascular air
      • 100% O2, cease N2O, cease PEEP
      • Aspirate right heart catheter if present
      • Circulatory support: fluid, pressors, chest compression
      • Head-down right lateral position theoretically advantageous
        • Not feasible in most neurosurgery, no evidence for efficacy
  • Paradoxical embolism
    • Requires PFO (25% prevalence) and transient RAP > LAP
      • PFO may be detected by TOE after induction
    • RAP to LAP gradient
      • Transiently positive during cardiac cycle
      • Increased by PEEP, greatest with release of Valsalva manoeuvre
      • Reduced by fluid loading

Problems associated with raised ICP

  • ICP
    • Intracranial pressure
    • Usually measured with LP in lateral position or intraventricular catheter
    • Used to calculate cerebral perfusion pressure
      • CPP = MAP - greater of JVP and ICP
    • Rises with intracranial expansile mass
      • Monro-Kellie Doctrine: volume of cranium is constant
      • Initial compensation by reduced venous blood volume
      • Then rapidly rising ICP, increased capillary pressure increases cerebral oedema
      • CBF becomes pressure-passive
      • Potential for herniation through tentorium
  • Cerebral blood flow (CBF)
    • Autoregulated under normal conditions
      • CPP 60-160 mmHg
      • Affected by PaO2, PaCO2, cerebral metabolic activity (CMRO2)
  • Surgery
    • To relieve intracranial pressure
      • Craniotomy, resection of lesion, drainage of haematoma
    • Incidental
      • Trauma patient with head injury and other injuries
      • Chronic intracranial hypertension
  • Assessment
    • Routine, plus
    • Neurological findings
      • Headache, nausea, vomiting, visual disturbance, cranial nerve lesions, irritability and confusion
      • Intracranial pathology: malignancy, haemorrhage
      • Time course of symptoms
    • Cardiorespiratory history
      • Usual blood pressure (baseline for autoregulation of CBF)
    • Specific diseases
      • Diabetes, pituitary dysfunction, trauma
    • Medications
      • Steroids, anticonvulsants, antihypertensives, mannitol, frusemide
    • Airway assessment, risk of aspiration
    • Usual investigations plus imaging
  • Preoperative
    • Premedication
      • Avoid hypercapnia, so no opiates
    • Usual machine and equipment checking
    • Monitoring
      • Routine, plus
      • ECG arrhythmias common
      • Arterial line, CVC or long line
      • IDC, temperature
  • Intraoperative
    • Induction
      • Most agents suitable except ketamine
      • Barbiturates, propofol reduce CMRO2, CBF and ICP
      • Non-depolarizing relaxants safe
        • Histamine release should be avoided
      • Suxamethonium relatively contraindicated
        • ICP rise is small and blocked by pre-dosing with NDB
      • Lignocaine 1.5 mg/kg may reduce ICP rise at intubation
      • Protect eyes and face
      • Use armoured tube
    • Maintenance
      • Continuous deep muscle relaxation
      • TIVA or inhalational techniques
        • All agents except ketamine cause decreased CMR, decreased CBF in parallel
        • High concentration of volatiles impair autoregulation (H >> E > I, S, D)
        • N2O is a cerebral vasodilator alone (increased CBF, decreased CMRO2)
          • Probably safe in balanced techniques
        • Propofol TIVA is probably best
      • Techniques to reduce ICP (in consultation with surgeon)
        • Cellular
          • Surgical resection
        • ICF, ECF
          • Osmotic diuretics (mannitol 0.25-2 g/kg)
            • Limited by serum osmolarity ≤320 mOsm/L
            • May cause rebound swelling, hypovolaemia, hypotension
          • Loop diuretics
            • Decresed ECF and impair idiogenic osmole formation
            • May reduce rebound swelling
          • Fluid restriction
          • Steroids
            • Decreased ICP over 48-72 h, may worsen outcome overall
        • CSF
          • Surgical drainage
        • Blood
          • Head-up position (also reduces perfusion pressure)
          • Lower CMR (with intact autoregulation)
            • Barbiturates, anticonvulsants, hypothermia
          • Acute hyperventilation (controversial)
            • Transient response, risk of ischaemia, rebound on cessation
          • Avoid agents which impair autoregulation
            • High dose volatiles, vasodilators
          • Avoid coughing, straining or high PAW --> venous pressure
          • Hypotension for vascular lesions
            • Worsens cerebral perfusion
        • Once the head is open, CPP is a higher priority
          • Support MAP
      • Neuroprotection
        • Drugs: barbiturates
        • Hypothermia

Transsphenoidal surgery in acromegaly

  • Acromegaly
    • Excessive growth hormone secretion
    • >99% due to pituitary adenomas
    • Gradual onset of clinical features
      • Pre-puberty: pituitary giantism, increased linear growth plus adult features
      • Adult
        • Continued growth of facial, hand and foot bones
        • Hypertrophy of soft tissues, viscera, skin tags, mucosal polyps
        • Cardiomyopathy, hypertension, IHD
        • Diabetes
        • Proximal myopathy
        • Local effects
          • Failure of other pituitary secretion: LH, FSH, ACTH…
          • Headache
          • Bitemporal hemianopia
    • Usually diagnosed in 3rd or 4th decade
    • Medical therapy with bromocriptine, octreotide, radiation
    • Surgical excision usually curative
  • Surgery
    • Elective, moderate risk
    • Performed through the nose or an incision under the upper lip
    • Shared airway, commonly soiled by surgery
  • Preoperative
    • Assessment
      • Routine, plus
      • Features of acromegaly
        • Airway compromise: large tongue and jaw, nasal polyps, mucosal folds, recurrent laryngeal nerve palsy
        • Cardiorespiratory complications
      • Other disease complications
        • Diabetes, IHD
      • Pituitary tumours
        • Commonly secrete prolactin, occasionally GH, ACTH or TSH
        • Compress normal tissue with loss of other hormone secretion
          • Supplement hypoadrenalism (hyponatraemia, hypovolaemia) or hypothyroidism
    • Investigation
      • Routine bloods, glucose, crossmatch
      • Imaging of the head may give information about the airway
    • Premedication
      • Important if fibreoptic intubation planned
  • Intraoperative
    • Monitoring
      • Routine plus arterial line, but 50% positive Allen test
      • Large IV
    • Induction
      • Large mask required, mask ventilation may be difficult
      • Oral intubation, consider awake FOB if likely to be very difficult
      • Small tube due to incidence of subglottic narrowing
      • Armoured tube plus throat pack
      • Positioning
        • May be heavy, nerve hypertrophy increases risk to ulnar nerve
        • Head-up reduces bleeding but may cause air embolism
    • Maintenance  
      • Neuro-type balanced technique
      • Vigilance for complications
        • Disconnection
        • Dissection into cavernous sinus with haemorrhage
        • Pressure on face or eyes
      • Antiemetic
    • Emergence
      • Clear blood or CSF from airway
      • Aim to minimize coughing
  • Postoperative
    • Ward care
    • Attention to complications
      • Diabetes insipidus (usually transient)
      • Panhypopituitarism
    • Analgesia
      • Oral ± IM narcotic

Paediatric neurosurgery


  • Supine, prone, sitting, lateral/park bench, knee-chest
  • Purpose
    • Surgical access, physiological effect (ICP, bleeding control)
  • Considerations
    • Airway
      • Usually IPPV with oral ETT
        • Raises CVP, ICP
        • Compensate with head-up, minimize airway P using deep
        • Paralysis, long inspiratory time, improve compliance with
        • Position (e.g. pressure off abdomen)
      • SV occasionally in brainstem surgery, still ETT
    • Access
    • Monitoring
    • Pressure areas
      • Especially eyes
    • Specific complications
      • Air embolism in sitting position
        • Diagnosis by TOE, fall in CO2, fall in SpO2, calibrate arterial
        • Pressure at head level for hypotension
        • Manage Valsalva, 100% O2, flood field, neck tourniquet, aspirate
        • CVC

Control of ICP

  • Monro-Kellie doctrine
    • Volume of cranium is constant
    • True after closure of sutures
  • Physiological control
    • Normal 5-15 cm CSF
    • Remains constant due to redistribution of CSF and venous blood volume
    • Rises sharply after critical point in elastance curve as intracranial "mass" expands
  • Physiological interventions
    • Positioning
      • Head up reduces both ICP and CPP
    • Hypovolaemia, hypotension
    • PCO2
      • Fall causes transient fall in ICP due to vasoconstriction
      • Not used below 30 mmHg as may impair CPP
      • Effect is transient
    • Opening the cranium: surgery
  • Pharmacological interventions
      • Reducing mass effect
        • Steroids reduce reactive oedema
      • Diuretic agents
        • Mannitol (acute volume-expanding effect)
        • Frusemide
        • IDC required
        • Can also reduce MAP
      • Agents to reduce CBF, CMRO2
        • General anaesthesia, barbiturates
      • Avoiding agents which raise ICP
        • high PCO2, Valsalva, coughing
        • Drugs: suxamethonium (but commonly indicated in trauma etc.)
        • Agents which impair autoregulation: volatiles

Protection of the patient

  • Positioning
    • Pressure areas, joint hyperextension or malposition
    • Vascular compromise
    • Neuropraxia
  • Temperature
    • Conservation and warming
  • Neuroprotection
    • Drugs
    • Maintain cerebral autoregulation, reducing CMRO2
    • Barbiturates, volatiles, propofol
    • Hypothermia

Surgery following subarachnoid haemorrhage

Subarachnoid haemorrhage 

  • Aetiology, natural history
    • Rupture of arterial aneurysm or bleed from AVM
    • 40% immediate major morbidity or mortality
    • 30% major morbidity or mortality after surgery
  • Grading

Grade GCS ICP (cmH2O) Mortality
I 15 <10 2%
II 13-14 without motor deficit <10 5%
III 13-14 with motor deficit 15-20 5%
IV 7-12 >25 35%
V 3-6 >25 50%

  • Surgical management
    • Operation before 72 h or after 14 days (reduced risk of vasospasm)
    • Ischaemia managed with fluid loading and hypertension
    • Nimodipine
      • Believed to reduce vasospasm, probably cell protection
      • Requires CVC administration
      • May cause hypotension

Anaesthetic priorities

  • Avoid acute hypertension
  • Intraoperative brain “relaxation”
  • Maintain high-normal CPP
  • Preparation for BP manipulation at clipping or rupture


  • Assessment
    • Routine, plus
    • Neurological assessment
    • Complications of SAH
      • SIADH or salt-wasting (hyponatraemia, hypovolaemia, high urine Na+)
      • Vasospasm related to clot around Circle of Willis
      • ECG abnormalities: T inversion, QT prolongation, ST depression, U waves
        • No correlation with LV function
        • No specific therapy unless ischaemic pattern
  • Premedication
    • No sedation (may raise PCO2)
  • Monitoring
    • Routine, plus
    • Arterial line, long line for central venous access, large bore IV, IDC, temperature, nerve stimulator


  • Induction
    • Aim to minimize BP rise
      • Rebleeding at induction (1%) is usually fatal
      • Vasodilator and pressor agents drawn up
      • Topical anaesthesia to airway
      • Lignocaine, β-blocker, narcotic to smooth intubation
      • Suxamethonium probably safe
  • Maintenance
    • Air, O2, propofol probably causes least cerebral vasodilation in “tight” cases
      • Volatile, N2O probably safe for elective cases
      • Maintain low-normal PCO2, check on ABG
    • BP manipulation
      • Blunting response to pinning (as for intubation)
      • Maintained planned CPP (e.g. 70 mmHg)
      • Induced hypotension for uncontrolled bleeding: SNP fastest agent
      • Induced hypertension for temporary occlusion: metaraminol or phenylephrine
    • ICP manipulation
      • Hypocapnia controversial
      • Lumbar CSF drain, mannitol may be requested by surgeon
    • Cerebral protection
      • Propofol commonly used
      • Thiopentone proven effective but delays awakening so not common
        • Consider bolus 5 mg/kg for temporary occlusion
      • Mild hypothermia 32-34°C
    • AVM surgery
      • “Perfusion pressure breakthrough”
        • Closure of AVM and loss of shunt causes sudden increase in perfusion of adjacent brain which has always been vasodilated
        • Failure of autoregulation response causes rapid oedema of brain
    • Other considerations
      • EEG monitoring, angiography with femoral access
  • Emergence
    • Avoidance of hypertension, coughing
      • Consider extubation deep if fasted


  • Maintain slight head-up position or as required by surgeons
  • Close monitoring of haemodynamic and neurological status
  • ICU or HDU level of care

Awake craniotomy

  • Surgery
    • Usually for an epileptogenic focus in the temporal lobe
  • Preoperative
    • Assessment
      • Routine, plus
      • Detailed history of epilepsy
        • Nature of aura and seizures for intraoperative recognition
        • Medication and complications
      • Investigation
        • Wada test
          • Unilateral carotid injection of sodium amytal
          • Determines lateralization of speech, short term memory
        • Videotelemetry
          • Continuous EEG with subdural, parenchymal or foramen ovale electrodes to localize focus of seizures
    • Premedication
      • Anticonvulsant agents avoided (benzodiazepines)
    • Monitoring
      • Routine, plus
      • Gas analysis to confirm airway patency
      • Continuous neurological assessment
      • Careful attention to patient comfort and warming
  • Intraoperative
    • Sedation, analgesia
      • Must allow patient responsiveness during cortical stimulation
      • Must not inhibit seizure activity
    • Drug regimens
      • Local anaesthetic block and infiltration for pins and incision
      • Droperidol 2.5-7.5 mg plus narcotic
        • Alfentanil 5-10 µg/kg plus 0.25-0.5 µg/kg/min, or
        • Fentanyl 0.7 µg/kg plus 0.7 µg/kg/h
      • Propofol infusion or PCA plus narcotic
      • If provoking agent is required for seizures, methohexitone 0.3 mg/kg
      • For seizure termination if necessary, thiopentone 1 mg/kg
    • Surgery
      • Usually prolonged
      • Pin placement (if necessary) and craniotomy are painful
      • Brain parenchyma is insensate
      • Airway access may be difficult, especially if head is pinned

Fluid management in neuroanaesthesia


  • Mole
    • Quantity of a substance containing the same number of particles as in 12 g of 12C
  • Osmolality
    • Number of osmotically active particles per kilogram of solvent
    • 1 Osmolal solution = 1 mole/kg of osmotically active particles
    • Measured directly be freezing point depression
      • 1 osm/kg of water depresses freezing point by 1.86°C
    • Approximated from electrolyte results
      • 2 ([Na+] + [K+]) + [glucose] + [urea]
      • Normal 280-290 mOsm/L
      • Less than the sum of concentrations of solutes because of particle interactions
      • Approximation is an underestimate when other solutes are present in high concentrations
        • Mannitol, ketoacidosis, alcohol
  • Osmolarity
    • Number of osmotically active particles per litre of solution
    • 1 Osmolar solution = 1 mole/l of osmotically active particles
    • Theoretical value calculated from concentration of ions and molecules assuming complete dissociation
    • Measured values slightly less than calculated due to incomplete dissociation
      • e.g. LR: calculated 275 mOsm/L, measured 254 mOsm/kg
  • Osmotic pressure
    • The pressure required to prevent net diffusion of water through a membrane with differing osmolalities of the solutions on each side
    • Proportional to the number of osmotically active particles in solution
    • Calculated using van’t Hoff’s Law
      • p = CRT
        • where p is osmotic pressure, C is concentration of solutes in osmoles/L, R is the gas constant and T the absolute temperature
    • 1 mOsm/L exerts 19.3 mmHg pressure at 37°C
    • Normal osmolarity of plasma is 282 mOsm/l (5443 mmHg)
    • Whole-body equilibration of osmotic pressure takes less than 30 minutes
  • Colloid oncotic pressure
    • The osmotic pressure exerted across the capillary wall by the non-diffusible elements of plasma
    • Ions and small molecules diffuse readily across capillary walls (reflection coefficient close to 0)
    • Plasma proteins have high reflection coefficients, close to 1
    • Total plasma protein osmotic pressure is about 19 mmHg in plasma and 8 mmHg in interstitial fluid
    • Most pressure (12 mmHg) is due to albumin as it is in high concentration and is a smaller molecule than most other plasma proteins
    • The Gibbs-Donnan effect results in increased cation concentration in plasma to balance anionic non-diffusible proteins. The “excluded volume” effect results from proteins not being an “ideal solute” and increases oncotic pressure. These effects increase plasma oncotic pressure by another 9 mmHg, total 28 mmHg
  • Equivalent
    • Quantity of ions which will combine with 1 mole of H+
    • Equal to number of mole multiplied by charge
      • e.g. 1 mmol of Ca2+ = 2 mEq of Ca2+

Starling hypothesis

  • Flow of water across a membrane is determined by hydrostatic and osmotic pressure gradients and permeability of the membrane
  • Hydrostatic pressure in capillares and interstitum
    • Pc mean capillary pressure 17.3 mmHg
    • Pi interstital pressure -3 mmHg
  • Oncotic pressure in capillaries and interstitium
    • pc plasma oncotic pressure 28 mmHg
    • pi interstitial oncotic pressure 8 mmHg
  • Mean net force is 0.3 mmHg out of capillaries
  • Filtration coefficient 7 ml/mmHg/min for whole body
    • Net lymph flow 2 ml/min at rest
    • In the CNS there is little lymphatic drainage
      • Fluid moves into CSF or via pinocytosis into vessels
  • Varies widely from tissue to tissue with capillary pressure, permeability, protein concentration changes
  • Jv = Kf (Pc - Pi - pc + pi)

Systemic Pulmonary Glomerular
Pc 30 --> 10 12 --> 6 60 --> 58
pc 28  28 21 --> 33
Pi -3 -5 15
pi 8 12 0
net +13 --> -7 +1 --> -5 +24 --> +10
Kf 0.01/100 g ? 12.5


Oedema formation

  • Depends on Starling forces and interstital compliance
    • Brain interstitum is non-compliant
    • The cranium is a non-compliant container
    • Under normal conditions, oedema does not form
  • Compliance increases with disruption of microscopic structure or craniectomy for decompression

Blood-brain barrier (BBB)

  • Cerebral vessels are relatively impermeable
    • Effective pore size 7Å vs 65Å for systemic vessels
    • So small ions can exert osmotic pressure across cerebral vessels
      • Osmotic effect of Na+, K+, Cl- etc are far greater than protein effects
    • With an intact BBB, plasma osmolality is far more important than colloid concentration
      • Small solutes are effective osmotherapy: mannitol, hypertonic saline
      • Hypotonic solutions promote edema: Lactated Ringer’s
  • Disrupted or abnormal vessels are readily permeable to both small and large molecules
    • Neither small nor large solutes exert osmotic pressure
    • Osmotic therapy is ineffective

Fluid restriction

  • No proven benefit
  • Better than administration of hypotonic solutions
  • May reduce hydrostatic pressure

Hypertonic solutions

  • Reduce cerebral oedema with an intact BBB
  • Hypertonic saline as effective as mannitol or hypertonic colloids
    • Choose the solution with least adverse effects
      • Coagulopathy with some colloids
      • Hypernatremia with saline
  • Mannitol the most common choice
    • Transient increase in perfusion pressure with rapid administration is detrimental
    • Subsequent reduction in cerebral volume is desirable
    • Gradual accumulation in interstitium may cause oedema later
  • Furosemide
    • Not a hypertonic solution, but slowly increases plasma osmolality due to water loss
    • Decreases CSF formation
    • Synergistic with mannitol

Glucose-containing solutions

  • Hyperglycaemia is proven to be harmful in cerebral ischaemia
    • Worsens neurological outcome
  • Hypoglycaemia is also harmful


  • Oxygen delivery is related to blood oxygen content and flow
    • Content falls with anaemia and hypoxaemia
    • Flow rises with anaemia
    • High PaO2 is desirable
    • Optimal Hct is about 30% (Hb 100 g/l)
      • Active haemodilution is not necessary and not of proven benefit

Kindly provided by Dr James Mitchell from his pharmacodynamics series.

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