Presenter: Mohd Nizamuddin IsmailModerator: Dr Wan Nazarudin
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
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.
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
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.
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.
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
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
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.
ANAESTHESIA & CRANIOTOMY FOR PATIENTS WITH MASS LESIONS
Comfirm diagnosis,indication and consentRoutine 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
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, Cushings reflex,dilated pupils,decorticate then decerebrate posturing and coma
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
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
Premedication Opiod premedication often avoided: hypercarbia increasedCBF 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
Other preparation GXM Fasting instruction for the patient Serve the patients medications on the morning of surgery
Anaesthetic Management Reassess the patients 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)
PreoxygenationCommon 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)
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
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
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
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)
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 Ringers 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.
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 demandThromboembolic 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
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)
Post-op ventilatory support Patientss 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)
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)
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)
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
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
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
If there is possibility of lower cranial nerve dysfunction with bulbar paresis: Gag reflex, swallowing and laryngeal function may be impaired InsertRTNitrous oxide should be avoided Increase CMRO2 and CBF Aggravate VAE or pneumocephalus TIVA is preferred
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
Post-op ICU with mechanical ventilation is oftenindicated: 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
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
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
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.
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
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.
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)
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)
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
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
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)
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
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
Anticipated problems:Emergency surgery Full stomach, insufficient time for thorough pre-op assessmentAssociated 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
Difficult intubation Presence of cervical or maxillofacial traumaPresence of raised ICP Requires pre-op resus, urgent surgery & post-op ICU CP need to be instituted
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
May require ventilation post-op Extent & nature of head injury Initial GCS Evidence of raised ICP Intra-op complications Associated injuries esp chest injury
ICU ManagementPosition & monitoring Kept in slight (15-20 deg) reverse trendelenburg Regular neuro & haemodynamic monitoringResp. 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
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 therapyRx 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
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.
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
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
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)
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
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.
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.
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.