This document discusses anesthesia considerations for neurosurgery patients. It covers common neurosurgical procedures, intracranial hypertension, cerebral edema, and the goals of anesthesia which include maintaining stable intracranial pressure and hemodynamics. It then focuses on anesthesia management for patients undergoing craniotomy for mass lesions, including preoperative evaluation and preparation, induction, maintenance with goals of optimal surgical conditions and neurological protection, and controlled emergence.

1. Presenter: Mohd Nizamuddin Ismail
Moderator: Dr Wan Nazarudin

2. Contents
 Introduction
 Intracranial Hypertension
 Aims of anaesthesia
 Anaesthesia for patients with mass lesions
 Anaesthesia for posterior fossa surgery
 Anaesthesia for pituitary surgery
 Anaesthesia for head trauma
 Anaesthesia for awake craniotomy

3. Introduction
 Anaesthesia for neurosurgical procedures requires
understanding of the normal anatomy and physiology of the
CNS and the likely changes that occur in response to the
presence of space occupying lesions, trauma or infection.
 In addition to balanced anaesthesia with smooth induction
and emergence, particular attention should be paid to the
maintenance of an adequate cerebral perfusion pressure
(CPP), avoidance of intracranial hypertension and the
provision of optimal surgical conditions to avoid further
progression of the preexisting neurological insult.

4. Common neurosurgical procedures
 Drainage
VP shunt, EVD, Evacuation of EDH/SDH via burr hole or
craniotomy.
 Craniotomy for excision / debulking of tumour
 Cerebrovascular surgery
Excision of cerebral aneurysm or AVM
 Surgery of the spine or spinal cord
 Surgery on the skull
Cranioplasty, elevation of depressed fractures

5. Intracranial Hypertension
 Defined as a sustained increase in ICP above 15mmHg.
 Uncompensated increases in tissue or fluid within the rigid
cranial vault produce sustained ICP elevations.
 If ICP exceeds 30 mmHg, CBF progressively decreases and
vicious circle is established: ischaemia causes brain
oedema, which increases ICP hence more ischaemia.
 Cycle continues – pt dies of progressive neurological
damage or catastrophic herniation.

6. Cerebral Oedema
 Increase in brain water content- produced by several
mechanisms:
1)Vasogenic  Disruption of BBB. Most common & allows
entry of plasma-like fluid into the brain.
 Causes Mechanical trauma, inflammatory
lesion, tumours, hypertension & infarction.
2)Cytotoxic  Following metabolic insults- hypoxaemia or
ischaemia, results from failure of brain cells to actively
extrude sodium & progressive cellular swelling.

7. Treatment
 Directed at underlying cause.
 Metabolic disturbances are corrected & operative
intervention undertaken whenever possible.
 Vasogenic oedema (tumours) responds to steroids
(dexamethasone). A single 10 mg dose can significantly
increase blood glucose concentrations in non-diabetic
patients.
(Pasternak J et al. Effect of single dose dexamethasone on blood
glucose concentration in patients undergoing craniotomy. J
Neurosurg Anesthesiol 2005; 16: 122–5)
 There is evidence to support tight glycaemic control in
critically ill, neurologically impaired patients

8.  Fluid restriction, osmotic agents & loop diuretics usually
effective in temporarily decreasing oedema.
 Moderate hyperventilation (PaCo2 30-33) – may aggravate
ischaemia in patients with focal ischaemia.
 Mannitol 0.5-1gm/kg effective in rapid reduction in ICP

9. Aims of anaesthesia
 Optimal operating conditions
 Maintenance of stable ICP
 Stable haemodynamics, oxygenation and ventilation
parameters
 Appropriate CPP and oxygenation while minimising CMRO2
to protect against ischaemia
 Early detection & prompt management of intra-op
complications- VAE in post fossa surgery, intracranial
bleed during cerebral aneurysm rupture
 Controlled but rapid emergence to enable early assessment
& monitoring of neurological status.

10. ANAESTHESIA & CRANIOTOMY
FOR PATIENTS WITH MASS
LESIONS

11.  Comfirm diagnosis,indication and consent
Routine pre-op assessment
 Airway, CVS and respiratory system
 Details of concomitant medical illnesses,nature of
treatment and compliance to therapy
 Investigations appropriate for age, general status of
patient and type of surgery

12. Detailed CNS assessment
 Level of consciousness, presence and extent of neurological
deficit(clear documentation)
 Observe respiratory effort in terms of tachypnoea,
laboured breathing or Cheyne-Stokes pattern of breathing
Assess the presence of cough/gag reflex if bulbar
involvement is suspected.
 Look for clinical manifestation of raised ICP:
headache,vomiting,focal neurological signs and papilloedema
 Late signs: deteriorating GCS, Cushing's reflex,dilated
pupils,decorticate then decerebrate posturing and coma

13. Review CT scan or MRI:
 Size and location of the SOL, size of ventricles, presence
of midline shift and evidence of generalised/peri-tumour
cerebral oedema.
Other considerations
 Assess the fluid status: possibility of dehydration and
electrolyte imbalance in patient who has been
vomiting, fluid restricted/receiving diuretic therapy
 Assess glycaemic status: rule out hyperglycemia in diabetic
patient/patient treated with dexamethasone
 Rule out endocrine dysfunction esp in pituitary tumours:
hypo/hyperthyroidism, acromegaly, hypo/hyperadrenalism

14. Based on overall assessment, identify patients who would
requires post-op ventilation in ICU
 GCS</=6
 Evidence of raised ICP
 Large or deep seated tumour
 Presence of midline shift and/or significant cerebral
oedema

15. Premedication
 Opiod premedication often avoided: hypercarbia
increasedCBF and ICP and possibility of disrupting early
postop neurological assessment
 For patient who is going for spine surgery who is
alert, conscious and anxious: Small dose of benzodiazepine
may be prescribed
 Alternatively a small IV dose of benzodiazepine can be
administered in OT prior to induction
 Effect of benzodiazepines are not detrimental as long as
hypotension is avoided

16. Other preparation
 GXM
 Fasting instruction for the patient
 Serve the patients medications on the morning of
surgery

17. Anaesthetic Management
 Reassess the patient's neurological status before induction
 Confirm availability of ICU or HDU
 Establish venous access w large bore IV cannulae.
 Monitors: ECG, non-invasive BP, pulse oximetry, and
capnography for minor cases (VP
shunt, EVD, Burrhole, cranioplasty)
 Additional monitors: u/o, temperature, neuromascular
blockade, invasive BP and CVP (Major)

18.  Preoxygenation
Common drugs at induction:
 Fentanyl, Thiopentone or Propofol
 Atracurium, Vecuronium or Rocuronium
 Lignocaine or Esmolol may be used to obtund sympathetic
reflex during airway manipulation
 Propofol has many theoretical advantages by reducing CBV
and ICP and preserving both autoregulation and vascular
reactivity. In healthy subjects, propofol reduced CBF, as
measured by positron emission tomography (PET), more
than sevoflurane at equipotent concentrations.
(Maksimow A et al. Correlation of EEG spectral entropy with
regional cerebral blood flow during sevoflurane and propofol
anaesthesia. Anaesthesia 2005; 60: 862–9)

19.  Suxamethonium transiently increases ICP and best avoided
in elective cases (except in difficult intubation)-should not
be withheld in emergency cases
 Monitor the degree of neuromuscular blockade with
peripheral nerve stimulator
 Allow non-depolarising NMB take effect
 Laryngoscopy and intubation should be attempted when
patient is adequately paralysed

20.  Maintain head-up tilt of 15-20 deg and avoid extreme neck
flexion or rotation
 Re-check placement of ETT after positioning
 Head is often secured in place using Mayfield3-point
fixator
 An additional dose of Fentanyl before the pins inserted
helps to prevent marked hypertension and tachycardia
 In cases of intracranial HTN lower ICP by administering
mannitol 0.5-1g/kg and/or frusemide 0.5mg/kg
 Maintain PaO2>100mmHg and PaCO2 between 30-35 mmHg.
 Avoid overventilation since hypocarbia may result in
cerebral vasoconstriction and reduce cerebral perfusion

21. Maintenance of anesthesia
 TIVA with propofol
 Inhalation technique with volatile agent
 NMB administered by continuous infusion or intermittent
boluses
 Analgesia maintained with intermittent boluses of Fentanyl
or infusion of Remifentanyl
 Isoflurane and Sevoflurane are preferred:
 Maintenance of cerebral auto-regulation up to MAC 1.5
 Maintenance of CO2 reactivity of cerebral blood vessels

22.  Sevoflurane gives smooth induction, rapid onset and offset
of action
 In a study comparing desflurane, isoflurane, and sevoflurane
in a porcine model of intracranial hypertension, at
equipotent doses and normocapnia, CBF and ICP were
greatest with desflurane and least with sevoflurane.
(Holmstrom A et al, J Neurosurg Anesthesiol 2004; 16: 136)
 Nitrous oxide causes cerebral vasodilatation, increased CBV
and ICP. Also contribute to development of
pneumoencephalocele.
 Should be avoided:
-in patient with cerebral ischaemia/reduced intracranial
compliance
-Surgery with significant risk of VAE (posterior fossa
surgery)

23. Fluid management
 IV fluid used judiciously and be sufficient to maintain IV
volume and hemodynamic stability
 Dextrose-containing solutions should be avoided unless
indicated
-Hypo-osmolar causing fluid shift
-Hyperglycemia can cause impaired neurological recovery
 Ringer's lactate is also hypo-osmolar and can cause
increase plasma glucose via lactate metabolism
 0.9% saline is the preferred crystalloid but may cause
hyperchloraemic acidosis when large doses are infused
 Blood loss may be torrential.

24. Temperature control
 Permissive hypothermia 33-35 deg celcius decreases
CMRO2 and may increase the period of ischaemia tolerated
intra-op
 Normothermia should be achieved before patient awakens
to avoid shivering which markedly increases O2 demand
Thromboembolic prophylaxis
 Neurosurgical patients are at risk for DVT and PE
 Heparin should not be used because of risk of bleeding in
confined cavity
 Mechanical means  graduated compression stockings and
intermittent pneumatic leg

25. Emergence
 The patient should not be allowed to cough through
ETT(tachycardia, hypertension and increased ICP)
 Systemic hypertension is common and may contribute to
the development of post-op haematomas.
 The increased use of remifentanil may be associated with
more postoperative hypertension  avoided with effective
transitional analgesia
 The a-2 agonist dexmedetomidine has been shown to
provide good haemodynamic stability during intracranial
tumour surgery, attenuating the response to intubation and
emergence.
(Tanskanen PE et al. Dexmedetomidine as an anaesthetic
adjuvant in patients undergoing intracranial tumour surgery. Br J
Anaesth 2006; 97: 658–65)

26. Post-op ventilatory support
 Patients's pre-op neurological status
 Intra-op events (duration and complexity of
surgery, hemodynamic
stability, complications, hypovolemia, massive transfusion)
 Evidence of raised ICP(tense dura/tight brain)

27. Post-op
 Regular neurological observations
 Any neurological deterioration should raise suspicion of
ICB/ oedema. Urgent CT should be considered.
Other aspects:
 Hemodynamic should be closely monitored to maintain
adequate CPP.
 Post-op pain often not severe and can be managed by
intermittent bolus doses or morphine infusion
 Electrolyte imbalance(esp sodium)
 U/o should be monitored(diabetes insipidus)

28. Posterior Fossa Surgery

29. Anatomy
 Lies between tentorium cerebelli and foramen magnum
 Contains cerebellum and brainstem
 Cranial nerve IX (glossopharyngeal), X(vagus),
XI(accessory), XII(hypoglossal)
 Emissary veins (valveless veins that drain external veins of
skulls into dural venous sinuses)

30. Indications:
 Resection or biopsy of tumours (glioma, astrocytoma,
meningioma, medulloblastoma, acoustic neuroma,
hemangioblastoma)
 Resection of vascular lesion (aneurysm, angioma, AVM)
 Abscess, haematoma, congenital lesions (Arnold-chiari
malformation

31. Special problems :
 Confined space-not much room for oedema/ bleeding which
if uncontrolled can cause coning through foramen magnum
 Main motor and sensory pathways are in close proximity to
op site (lower cranial nerve nuclei and vital centres
controlling respiratory and CVS functions in brainstem)
 Obstruction to CSF flow at the aqueduct/ forth ventricle
results in hydrocephalus
 Patient may have altered conscious level with impaired
airway reflexes leading to silent aspiration

32. Position:
 Prone, lateral or semiprone (park-bench). Sitting is rarely
adopted.
 Extreme care must be taken while turning the patient
 Avoid extreme neck flexion which may cause
-venous and lymphatic obstruction (can cause upper airway
oedema)
-Cord hypoperfusion (resulting in quadriparesis) esp in elderly

33. If there is possibility of lower cranial nerve dysfunction with
bulbar paresis:
 Gag reflex, swallowing and laryngeal function may be
impaired
 InsertRT
Nitrous oxide should be avoided
 Increase CMRO2 and CBF
 Aggravate VAE or pneumocephalus
 TIVA is preferred

34. Close monitoring of CVS for interference of vital centers
 Arrhythmia or hypertension
 Precipitous decrease in HR often signifies brainstem
ischaemia and should be notified to the surgeon
 Resolves spontaneously when surgical retraction is removed
 Atropine is required in severe bradyarrythmias
 Close communication with surgeon is essential

35. Post-op ICU with mechanical ventilation is often
indicated:
 In patients with low GCS
 There is evidence of airway oedema or bulbar paresis
 The surgical resection is extensive or complicated
 There are intra-op complications

36. Pituitary Surgery

37.  The pituitary gland consists of 2 histologically distinct
parts: the large anterior lobe or adenohypophysis and the
smaller posterior lobe or neurohypophysis.
 It lies within the pituitary fossa or sella turcica, a
depression in the skull base lined with dura mater.
 The anterior pituitary synthesizes and secretes
GH, TSH, ACTH, FSH, LH, Prolactin
 Posterior pituitary stores and secretes oxytocin and ADH

38.  Most pituitary tumours arise from the anterior part of the
gland & mostly are benign adenomas
 Mass effect :
Headache, visual disturbances (bitemp. Hemianopia), Cr N
palsies, hyposecretion of hormones
 Hormone hypersecretion syndrome :
Hyperprolactinaemia, acromegaly, cushing’s
dx, thyrotoxicosis
 Surgery transphenoidal or transcranial

39. Pre-op assessment
 In addition to the usual general pre‐anaesthetic
assessment of a neurosurgical patient, we should include an
assessment of: visual function; signs and symptoms of
raised ICP; the patient’s endocrine studies; and the
effects of hormonal hypersecretion.
 Those with acromegaly or Cushing’s syndrome are
particularly likely to have co‐morbidities and pre-op
assessment should be directed accordingly.

40.  Acromegaly
 Difficult intubation, incidence of
OSA, hypertension, cardiomyopathy, glucose intolerance.
 Cushing’s dx
 Hypertension, cardiac disease, glucose
intolerance, electrolyte imbalance, osteoporosis.
 ACTH hyposecretion
 Requirement for steroid replacement perioperatively

41. Anaesthetic management
 Pre-op hormone replacement therapy should be continued
into the operative period.
 In general, hydrocortisone 100 mg should be administered
at induction of anaesthesia in all patients undergoing
pituitary surgery
 Careful pre-op assessment alerts to the possibility of
difficulties with airway management and tracheal
intubation. Ventilation with a bag and mask is generally
straightforward in acromegalic patients although an oral
airway may be required.

42.  4 grades of airway involvement have been described in
acromegaly: grade 1, no significant involvement; grade 2,
nasal and pharyngeal mucosa hypertrophy but normal cords
and glottis; grade 3, glottic involvement including glottic
stenosis or vocal cord paresis; and grade 4, combination of
grades 2 and 3, i.e. glottic and soft tissue abnormalities.
 Tracheostomy has been recommended for grades 3 and 4
but others have suggested that fibreoptic laryngoscopy is
a safe alternative
(60 Ovassapian A. Fiberoptic Airway Endoscopy in Anesthesia
and Critical Care. New York: Raven Press, 1990; 57–79)

43.  Following intubation, the mouth and posterior pharynx
should be packed before surgery begins
 Any anaesthetic technique suitable for intracranial
procedures is acceptable, but the presence of increased
intracranial pressure requires special attention
 In the presence of raised intracranial pressure, total
intravenous anaesthesia and the avoidance of nitrous oxide
has been recommended.
(44 Matta BF et al. Management of head injury: part 1. In:
Kaufman L, Ginsberg R, eds. Anaesthesia Review. London:
Churchill Livingstone, 1997; 163–78)

44.  Whichever technique is chosen, it is important that
short‐acting agents are used to allow rapid recovery at the
end of surgery (propofol, sevoflurane)
 During trans-sphenoidal surgery, ventilation to normocapnia
should be employed.
 Excessive hyperventilation will result in loss of brain bulk
and make any suprasellar extension of the tumour less
accessible from below

45.  Smooth and rapid emergence from anaesthesia following
neurosurgery is essential
 At the end of trans-sphenoidal surgery, extubation is
carried out after return of spontaneous ventilation,
pharyngeal suction under direct vision, removal of the
throat pack and return of laryngeal reflexes.
 Smooth emergence can be facilitated by placing the
patient in a semi‐seated position & ensuring that there is a
response to verbal commands before extubation.
 Care should be taken to ensure that nasal packs or stents,
put in place at the end of surgery, do not become dislodged
during extubation

46. Post-op care
 Consists of careful airway management, provision of
adequate postoperative analgesia, appropriate fluid and
hormone replacement and careful monitoring for
postoperative complications (DI, hyponatraemia)

47. Anaesthesia for Head
Trauma

48. Head Injury
 Contributory factors in up to 50% of deaths due to trauma
 Significance dependent not only on the extent of
irreversible neuronal damage at the time of injury but also
on secondary insults
 Systemic factors- hypoxaemia, hypercapnia, hypotension
 Formation & expansion of EDH, SDH, ICB
 Sustained intracranial HTN

49.  Surgical & anaesthetic management is aimed at preventing
secondary insults
 GCS correlates well with severity of injury & outcome.
 GCS of 8 or less assoc w approx 35% mortality.
 Evidence of >5mm midline shift, a lesion > 25ml and
ventricular compression on CT assoc w substantial
increased in morbidity

50. Anticipated problems:
Emergency surgery
 Full stomach, insufficient time for thorough pre-op
assessment
Associated injuries
 C-spine fracture dislocation may result in SC injury with
initial period of spinal shock
 Maxillofacial trauma w potential for acute upper airway
obstruction, bleeding into airway & difficult intubation
 Thoracic injuries – lungs, heart, great vessels (life
threatening)
 Intra-abdominal injury
 Pelvic / bone injuries w problems of concealed bleeding &
FES

51. Difficult intubation
 Presence of cervical or maxillofacial trauma
Presence of raised ICP
 Requires pre-op resus, urgent surgery & post-op ICU
 CP need to be instituted

52. Anaesthetic Management
 Adequate venous access and invasive monitoring
 Choice of RSI w precalculated doses of fentanyl,
thiopentone & scoline w cricoid pressure
 Scoline causes transient rise in ICP but effect is short
lived
 Cervical fracture intubation w head & neck in neutral
position & manual in-line stabilisation
 Intra-op management is similar to that of elective
procedures

53. May require ventilation post-op
 Extent & nature of head injury
 Initial GCS
 Evidence of raised ICP
 Intra-op complications
 Associated injuries esp chest injury

54. ICU Management
Position & monitoring
 Kept in slight (15-20 deg) reverse trendelenburg
 Regular neuro & haemodynamic monitoring
Resp. care
 Adequate oxygenation (PaO2 > 90mmHg)
 Normocarbia (PaCO2 30-35mmHg)
 Avoid hyperventilation & hypocarbia which result in
cerebral vasoconstriction
 Regular chest physio & tracheal suction w adequate
sedation & analgesia

55. BP control
 Maintain BP within 20% of baseline to ensure adequate CPP
 CPP kept above 70mmHg
 Treat hyper or hypotension with vasoactive drugs & appropriate
fluid therapy
Rx of raised ICP
 Maintain on controlled ventilation w IPPV and sedation for 24-48H
 Administer diuretics  mannitol and/or frusemide
 Restrict fluid maintenance & avoid dextrose-containing solution
 Consider hypertonic saline or high dose barbiturate in selected
cases
 Use of dexamethasone
 Antiepileptic drugs for immediate or long term control of seizures

56. Awake Craniotomy

57.  Awake craniotomy is gaining popularity worldwide
 Used for the excision of tumours located in the functional
cortex, namely the motor strip, broca’s & wernicke’s
speech areas
 Intra-op testing allows optimal tumour resection while
preserving functional tissue  minimal post-op neurological
dysfunction
 The enthusiasm for awake craniotomy is such that it has
even been suggested that it could become routine for
supratentorial tumours irrespective of functional cortex.

58.  In a prospective trial of 200 patients, the procedure was
well tolerated with reduced intensive care time and
hospital stay.
(Taylor MD et al. Awake craniotomy with brain mapping as
the routine surgical approach to treating patients with
supratentorial intraaxial tumors.J Neurosurg 1999; 90: 35–
41)
Contraindications
 Patient refusal
 Communication difficulties, confused or extreme anxiety
 Obese or those with oesophageal reflux & large vascular
tumour are best excluded

59. Anaesthetic Techniques
 Neurolept anaesthesia
 Dexmedetomidine infusion
 Local anaesthesia combined with appropriate sedation and
MAC
 Asleep-awake-asleep using GA
 Important to maintain airway & ventilatory control
 BIS

60.  Dexmedetomidine provides sedation and analgesia without
respiratory depression and has been used as a sole
agent, an adjunct, and a rescue drug for awake craniotomy.
 It was used successfully for awake craniotomy in 10
consecutive patients. Five patients were sedated with
midazolam, fentanyl, or remifentanil and five had an AAA
technique using sevoflurane, spontaneous ventilation, and
LMA. All received dexmedetomidine infusions 0.01–1.0 mg/
kg/h as an adjunct.
(Mack PF et al. Dexmedetomidine and neurocognitive testing in
awake craniotomy. J Neurosurg Anesthesiol 2004; 16: 20–5)

61.  Asleep-awake-asleep techniques makes use of TIVA w
target –controlled infusion of propofol & remifentanil.
 Propofol is the most frequently used drug for both
sedation and general anaesthesia. It provides titratable
sedation and a rapid smooth recovery, decreases the
incidence of seizures and, when stopped for awakening,
minimizes interference with electrocorticographic
recordings.
 Controlled ventilation is maintained via LMA or proseal.
 Infusion rates are adjusted in response to changes in
haemodynamics & surgical stimulation- guided by BIS

62.  Remifentanil has short half-life & provides greater
haemodynamics stability but more respiratory depression
than fentanyl, thus safer to control ventilation than
spontaneous.
 When tumour is exposed, remifentanil inf is reduced until
spontaneous respiration resumes.
 Propofol inf is stopped & LMA removed as patient awakens.
 Background inf of remifentanil 0.005-0.01mcg/kg/min is
used to provide additional analgesia during awake period.

63.  A retrospective analysis of an AAA technique using
propofol and remifentanil showed that adequate conditions
were obtained in 98% of patients with a median wake-up
time of 9 min
(Keifer JC et al. A retrospective analysis of a remifentanil /
propofol general anaesthetic for craniotomy before awake
functional brain mapping. Anesth Analg 2005; 101)
 When tumour is resected, pt is re-anaethetised & LMA
inserted.

64.  LMA is superior to others because it minimizes the risk of
coughing or straining & subsequent vomiting during
lightening of anaesthesia.
 Controlled ventilation via LMA obviates problems of
apnea, hypoventilation or airway obstruction.

65. Thank You