Anatomy

Spinal Cord

The spinal cord is approximately 45 cm long and passes from the foramen magnum, where it is continuous with the medulla, to a tapered end termed the conus medullaris at the level of the first or second lumbar vertebrae. At each spinal level, paired anterior (motor) and posterior (sensory) spinal roots emerge on each side of the cord. Each posterior root has a ganglion containing the cell bodies of the sensory nerves. The two roots join at each intervertebral foramen to form a mixed spinal nerve.

Intracranial Pressure

With normal cerebral compliance (the correct physiological parameter is elastance, which is the reciprocal of compliance), the intracranial pressure (ICP) is 7–15 cmH₂O (5–11 mmHg) in the horizontal position. When moving to the erect position, the ICP decreases initially, but then, because of a decrease in reabsorption of CSF, the pressure returns to normal. ICP is related directly to intrathoracic pressure and has a normal respiratory swing. It is increased by coughing, straining and positive end-expiratory pressure. In the presence of reduced cerebral compliance, small changes in cerebral volume produce large changes in ICP. Such critical changes may be induced by drugs used during anaesthesia (e.g. volatile anaesthetic agents and vasodilators), elevations in PaCO₂ and posture, as well as by surgery and trauma (Fig. 32.2).

Cerebral Blood Flow

Under normal conditions, the brain receives about 15% of the cardiac output, which corresponds to a cerebral blood flow (CBF) of approximately 50 mL 100 g^– 1 tissue min^– 1 or 600–700 mL min^– 1. The cerebral circulation is able to maintain an almost constant blood flow between a mean arterial pressure of 60 and 140 mmHg by the process of autoregulation. This is mediated by a primary myogenic response involving local alteration in the diameter of small arterioles in response to changes in transmural pressure. Above and below these limits, or in the traumatized brain, autoregulation is impaired or absent, so that cerebral blood flow is closely related to cerebral perfusion pressure (CPP) (Fig. 32.3). This effect is also seen in association with cerebral hypoxia and hypercapnia, in addition to acute intracranial disease and trauma. Cerebral perfusion pressure may be reduced as a result of systemic hypotension or an increase in ICP; CBF is maintained until the ICP exceeds 30–40 mmHg. The Cushing reflex increases CPP in response to an increase in ICP by producing, first, reflex systemic hypertension and tachycardia and then bradycardia, despite these compensatory mechanisms also contributing to an increase in ICP. In the treatment of closed head injuries, if both ICP and mean arterial pressure are being monitored, it is essential to maintain the resultant CPP with vasopressor therapy if cerebral perfusion is borderline because even transient absence of flow to the brain may produce focal or global ischaemia with infarction. Figure 32.3 also demonstrates that haemorrhagic hypotension associated with excess sympathetic nervous activity results in a loss of autoregulation at a higher CPP than normal, while the use of vasodilators to induce hypotension shifts the curve to the left, maintaining flow at lower levels of perfusion pressure. Vasodilators also differ in their effects; autoregulation is preserved at a lower CPP with sodium nitroprusside than with autonomic ganglionic blockade (however, vasodilators are rarely used during neuroanaesthesia). Cerebral blood flow is closely coupled to cerebral metabolic rate. Local increases in cerebral metabolic rate are associated with very prompt increases in CBF. The increased electrical activity associated with convulsions produces an increase in lactic acid and other vasodilator metabolites. This, together with an increase in CO₂ production, produces an increase in CBF. Conversely, cerebral metabolic depression, in association with either deliberate or accidental hypothermia or induced by drugs, reduces CBF.

Cerebral Metabolism

The energy consumption of the brain is relatively constant, whether during sleep or in the awake state, and represents approximately 20% of total oxygen consumption at rest, or 50 mL min^–1. Anaesthesia results in a decrease in cerebral metabolic rate. Cerebral metabolism relies on glucose supplied by the cerebral circulation because there are no stores of metabolic substrate. Other substrates which the brain can use are ketone bodies, lactate, glycerol, fatty acids and some amino acids including glutamate, aspartate and γ-aminobutyric acid (GABA). The brain can tolerate only short periods of hypoperfusion or circulatory arrest before irreversible neuronal damage occurs. The brain also releases and subsequently inactivates neurotransmitters.

The energy production of the brain is related directly to its rate of oxygen consumption, and the cerebral metabolic rate for oxygen (CMRO₂) is often used to quantify cerebral activity. By the Fick principle, CMRO₂ is equal to the CBF multiplied by the arteriovenous oxygen content difference. Barbiturates have been used to reduce cerebral metabolic rate, and propofol and benzodiazepines have a similar, although less profound, effect. All are used in the sedation of patients with head injury, and the choice is related more to the anticipated duration of sedation than to differences in the effects of the drugs, with the exception of prolonged barbiturate coma induced by infusion of thiopental.

Hypothermia is associated with a reduction in cerebral metabolic rate, with a decrease of approximately 7% for every 1 °C decrease in temperature.

Effects of Oxygen and Carbon Dioxide on Cerebral Blood Flow

Physiologically, carbon dioxide is the most important cerebral vasodilator. Even small increases in PaCO₂ produce significant increases in CBF and, therefore, ICP. There is an almost linear relationship between PaCO₂ and CBF (Fig. 32.4). Over the normal range, an increase of PaCO₂ by 1 kPa increases CBF by 30%. Conversely, hyperventilation to produce a PaCO₂ of 4 kPa produces cerebral vasoconstriction and a decrease in ICP, although this is compensated for by an increase in CSF production over a more prolonged period of hyperventilation, such as that used in the treatment of head injuries. This is why there is no advantage in aggressive hyperventilation regimens in head injury management. Hypocapnia below a PaCO₂ of 4 kPa has little acute effect on ICP, and hyperventilation beyond this point to lower ICP should be avoided except as a last resort because the vasoconstriction induced may be associated with a reduction in jugular bulb oxygen saturation, suggesting hypoperfusion and ischaemia. At a PaCO₂ above 10 kPa, the vessels are maximally dilated and there is little, if any, further increase in CBF.

Reduction in blood oxygen content also leads to cerebral vasodilation such that cerebral oxygen delivery remains approximately constant. In the normal physiological range, alterations in PaO₂, have little effect on CBF over the normal range. It is only when PaO₂ decreases below about 7 kPa that cerebral vasodilatation occurs. Reduction in cerebral blood oxygen content due to anaemia has similar effects.

Induction of Anaesthesia

An intravenous infusion of an isotonic electrolyte solution should be started through a large-gauge intravenous cannula before induction. Intravenous induction should be used whenever possible. However, inhalational induction may be appropriate in children if the risk of a crying, distressed child is more likely to increase ICP than the vasodilator effects of a high inspired concentration of a volatile anaesthetic agent. Both thiopental and propofol reduce ICP and are suitable induction agents. The intravenous anaesthetic should be given with an appropriate dose of short-acting opioid and a neuromuscular blocking agent to facilitate a smooth induction and tracheal intubation, avoiding hypoxaemia and hypercapnia. A nerve stimulator should be used to ensure complete muscle paralysis before attempting direct laryngoscopy, to prevent any coughing or straining. It is important to remember that cerebral perfusion may be reduced when the ICP is raised, and an induction technique which produces significant hypotension may critically reduce cerebral perfusion in patients with a space-occupying lesion (SOL) or an intracranial or subarachnoid haemorrhage associated with vasospasm.

The most commonly used techniques to reduce the hypertensive response to laryngoscopy and tracheal intubation are supplementary short-acting opioids (fentanyl, alfentanil) or short-acting β-adrenoceptor blockade (e.g. esmolol). If remifentanil is used as a co-induction agent, an infusion is usually started immediately after the induction dose and acts to control the hypertensive response; alternatively, a target-controlled infusion (TCI) is used for both induction and maintenance during the intubation. A reinforced disposable tracheal tube is used. Careful positioning of the tube is vital because any intraoperative flexion of the neck may result in intubation of the right main bronchus if the tip of the tube is initially placed too close to the carina. After the tube has been secured, the neck should be flexed gently while listening for the presence of breath sounds in both axillae. The tube should be secured in place with several layers of sticky tape to prevent it peeling away after application of surgical ‘prep’ solution to the scalp. Cotton ties should not be used because they may compress the internal jugular veins, increasing venous pressure and leading to a reduction in cerebral perfusion pressure and increased intraoperative haemorrhage. Many anaesthetists routinely insert a pharyngeal throat pack to help to stabilize the tracheal tube in the mouth, but it is only essential if transnasal surgery (e.g. trans-sphenoidal hypophysectomy) is planned. A nasogastric tube is inserted in patients who are going to be prone for prolonged periods, or if surgery around the brainstem is planned (which might lead to a postoperative bulbar palsy).

The eyes are protected by applying paraffin gauze, padding with a folded swab and then covering with a waterproof tape. Skin cleaning (‘prep’) solutions must be prevented from entering the eyes. Low-molecular-weight heparin is not used preoperatively, but is started after surgery when the risk of perioperative haemorrhage has reduced. There is a significant risk of deep venous thrombosis (DVT) in this group of patients. Thromboembolism (TED) stockings are used pre- and postoperatively and intermittent pneumatic compression devices are used intra-operatively.

Positioning

Many neurosurgical operations are long and positioning of the patient to facilitate optimal access, while preventing hypothermia, pressure sores and peripheral nerve injury, is important. Supratentorial cranial surgery involving the frontal or frontotemporal areas is performed with the patient supine, while parietal and occipital craniotomies are carried out in the lateral or three-quarters prone (‘park bench’) position. In all cases, care must be taken to avoid neck positions such as marked rotation or flexion which might impede venous drainage. The fully prone position is used for surgery on the posterior fossa and around the foramen magnum, and the spine. The prone position is discussed in more detail in the section on spinal surgery (page 652). For some procedures, it is necessary to tilt or roll the table during the operation. The patient must be positioned securely with supports to prevent slipping if the table is moved. Some neurosurgical operations are prolonged and, whatever position is used, it is essential that all pressure points are protected adequately. During long operations, the pulse oximeter probe should be moved every 4 h, at least.

Heat Loss

Temperature should be maintained using a forced warm air blanket. It is important to prevent heat loss during prolonged surgery. Although there are theoretical benefits of allowing the body to cool intra-operatively (to around 35 °C) if cerebral ischaemia is likely or after head injury, well-controlled studies have failed to support such an approach. However, hyperthermia should be avoided.

Maintenance of Anaesthesia

The basis of anaesthesia for neurosurgery is ventilation of the lungs with air and oxygen to produce a PaCO₂ of around 4.5 kPa, using either a volatile anaesthetic agent or a propofol infusion supplemented by an opioid analgesic (remifentanil infusion or fentanyl boluses). Unless used carefully, remifentanil may produce hypotension, and when it is stopped, there may be rebound hypertension and the sudden onset of pain or agitation. Sevoflurane is the volatile agent of choice, given that its effects on the cerebral vasculature are much less than those of isoflurane. At clinical concentrations, sevoflurane has no effect on cerebral autoregulation and causes only a minimal increase in ICP. Alternatively, total intravenous anaesthesia with propofol TCI may be used. There is no evidence that one technique is associated with a better outcome compared with any other.

The choice of neuromuscular blocking agent depends usually on personal preference. In most cases, these drugs should be given by infusion. A peripheral nerve stimulator should be used and the infusion rate titrated to maintain an adequate degree of block (one twitch of the train-of-four stimulus pattern should be present), while preventing overdosage so that the block can be completely reversed shortly (10–15 min) after stopping the infusion and administering an anticholinesterase.

The initial part of a craniotomy is painful, but after the bone flap has been reflected and the dura incised, pain is not a significant feature again until closure of the wound. For this reason, supplementary intra-operative opioids in large doses are unnecessary. Use of opioids during maintenance does allow use of less hypnotic agent. Reflex vagal stimulation can occur, particularly following stimulation of the cranial nerve roots or during vascular surgery around the circle of Willis and the internal carotid artery. This may necessitate immediate administration of an anticholinergic agent to avoid severe bradycardia or even asystole.

Maintenance of normal arterial pressure is important in all patients, but may be a particular problem during induction in very sick or elderly patients. Hypotension, with the consequent reduction in cerebral perfusion, should be treated by infusion of a moderate volume of fluid, but it is advisable to administer a vasopressor such as ephedrine at an early stage.

Use of techniques permitting rapid recovery (for example sevoflurane, propofol, remifentanil) are particularly valuable in situations in which the patient is required to wake up and move to command intra-operatively, e.g. during spinal surgery or trigeminal nerve radiofrequency lesion generation.

Fluid Replacement Therapy

Most patients who present for elective intracranial operations are satisfactorily hydrated preoperatively. Patients with acute conditions such as trauma, those with a high ICP associated with nausea and vomiting and patients with general debility and cachexia may be dehydrated. The main intra-operative distinctions between patients are related to the underlying pathology. Cerebral tumours are associated with oedema and raised ICP, and therefore such patients may have been fluid-restricted preoperatively However, intra-operative hypotension must be avoided and careful perioperative fluid administration is essential. Cerebrovascular surgery is associated with vasospasm and maintaining an adequate cerebral blood flow is the prime prerequisite. A normal circulating blood volume is essential if the perfusion pressure is to be maintained, and although a slight reduction in haematocrit to about 0.30 is optimal for perfusion, adequate fluid replacement must be given.

All hypotonic fluids are avoided. Isotonic crystalloids are the standard maintenance fluids. There is no evidence for a specific role for colloid solutions, although blood is used if the haemoglobin falls below 8–9 g dL^− 1. During significant haemorrhage or in patients with multiple injuries, careful attention to haemostasis is essential.

Supplementary Drug Therapy

Patients with a tumour or some other lesions may already be receiving an antiepileptic, and others may require intravenous phenytoin perioperatively, depending on the site of surgery. Patients receiving high-dose steroids need peri- and postoperative dexamethasone; the normal dose is 4 mg 6-hourly with 8–16 mg as an intra-operative bolus. Depending on local microbiological flora and surgeons’ preferences, perioperative antibiotics are administered to many patients; a common choice is cefuroxime 1.5 g, which should be repeated 3-hourly during long operations.

Monitoring During Neurosurgical Anaesthesia

Standard monitoring should be started before induction. In patients in whom cardiovascular instability may be a problem, including the very elderly and frail or following subarachnoid haemorrhage, this should include direct arterial pressure monitoring started before induction. Arterial cannulation is now used routinely in all patients undergoing an intracranial operation, for surgery on the cervical spine, and in other situations in which rapid fluctuations in arterial pressure may occur. It also facilitates arterial sampling for blood gas analysis. Use of central venous pressure (CVP) catheters varies greatly among different practitioners and different neurosurgical units. They are used when major blood loss is expected, such as surgery for very vascular meningiomas, and for clipping of a cerebral aneurysm. They may be used in other operations in which there is a high risk of air embolism. A precordial or oesophageal stethoscope may be used to auscultate cardiac and respiratory sounds and also abnormal flow murmurs produced by air embolism. An oesophageal stethoscope is used more frequently in children.

Cerebral oximetry, transcranial Doppler, electroencephalography and evoked potentials are used in specific situations.

Mechanisms for Reducing Intracranial Pressure

The methods used commonly to reduce ICP (or to limit increases) are drugs, ventilation, posture and drainage. Adequate cerebral venous drainage must be assured by ensuring the neck veins are not compressed by ties, tapes or excessive neck rotation or flexion. Diuretics such as mannitol 10% or 20% (0.5–1.0 g kg^− 1) or furosemide (20–40 mg) deplete the intravascular fluid volume and subsequently reduce CSF production. A bolus of an intravenous anaesthetic agent such as propofol or thiopental may be used to reduce the cerebral metabolic rate, causing a reduction in cerebral blood flow and therefore decreases in cerebral blood volume and ICP. Direct drainage of CSF may be accomplished either by lumbar puncture or by direct puncture of the cisterna magna or lateral ventricles. A move to an increased head-up position reduces venous congestion and ICP, but arterial hypotension must be avoided. Hypercapnia must be prevented by the use of IPPV, while short-term use of moderate hyperventilation produces cerebral vasoconstriction and a reduction in cerebral blood volume. If in doubt, an arterial blood gas analysis should be performed to verify adequate lung ventilation.

Elective Hypotension

Induced hypotension was formerly one of the mainstays of cerebrovascular surgery, but its use has diminished considerably in recent years because of the appreciation that cerebral perfusion is all-important. Most aneurysm surgery in now carried out at normotension; indeed, if the patient has an element of cerebral vasospasm, any reflex hypertension should be maintained. Hypotension is now a therapy of last resort if bleeding is torrential and it is otherwise impossible for the surgeon to regain control. If hypotension is required, the choice of technique is determined by the anticipated duration of induced hypotension. The alternatives are a short-acting β-adrenoceptor blocker such as esmolol, or increasing the depth of anaesthesia with a volatile agent. Direct vasodilators are rarely used because of the risk of ‘steal’ away from areas of poor perfusion, and the possibility of increasing cerebral blood volume and affecting the ICP. Hypotensive anaesthesia is used more frequently in spinal surgery, although the risks of inducing ischaemia in the cord substance are the same as in the brain. In this situation, evoked potentials may be used to assess spinal cord function during periods of hypotension.

Recovery from Anaesthesia

The majority of patients are allowed to wake up as usual at the end of operation, preferably in a dedicated neurosurgical recovery room. The Glasgow Coma Scale (Table 32.1) or an equivalent for children is recorded. Patients should return rapidly to at least their preoperative level of consciousness. A failure to achieve this, or a deterioration after an initial awakening, should alert carers to possible ischaemia or raised ICP. Re-imaging or immediate wound exploration is then required. Seizures after elective intracranial neurosurgery are surprisingly rare and, if they occur, should be treated immediately and the cause identified.

Complete reversal of nondepolarizing neuromuscular blockade must be achieved and judicious use of intra-operative opioids should remove the need for administration of naloxone. Paracetamol is used, but non-steroidal anti-inflammatory drugs are avoided because of the risk of inhibiting platelet function and precipitating a postoperative intracranial bleed.

Intracranial Tumours

Gliomas usually grow quickly and the history is often short (days or weeks); meningiomas are slow-growing and the history may be slow and insidious. Unlike gliomas, the volume effect of a meningioma is usually minimal because a reduction in the volume of the other intracranial contents compensates. However, the volume effects may eventually become apparent, especially if there is bleeding into the meningioma.

Patients with an intracranial tumour are usually taking steroids (normally dexamethasone 4 mg every 6 h), which may precipitate a latent diabetic state, requiring insulin during the acute episode. Most patients have some symptoms of raised ICP, such as headache, nausea, vomiting or visual disturbances. Anticonvulsant therapy may have been prescribed to patients who have presented with fitting or who are thought to be at risk. Some patients may be frankly dehydrated, and while it is important to avoid aggressive preoperative fluid therapy, hypovolaemia must be treated before induction of anaesthesia.

For slowly growing tumours such as meningiomas and less aggressive gliomas, as near total excision as possible is attempted. However, total excision of all the macroscopically identifiable glioma tissue is now considered futile for fast-growing lesions. Large portions of tumours are excised if pressure symptoms are the main presenting feature. For aggressive tumours, the greatest need is for a tissue diagnosis. If lesions are small, deep-seated or near critical areas (such as the motor strip or speech centre), a radiologically-guided biopsy or awake surgery (see section on functional surgery below) is appropriate. Stereotactic biopsy involves a CT scan with a rigid metal frame firmly attached to the skull. Trigonometry is then used to find co-ordinates, relative to the frame, which describe the exact site of the lesion (to within 1 mm). A biopsy needle is then passed through the brain to sample tissue from this site. The frame is applied after induction of anaesthesia and, because small changes in brain volume causes the lesion to move, the PaCO₂ should be maintained at a constant level for both the CT scan and the biopsy. Frameless image-guided surgery can be performed, in which a scan of the brain (and skull) is compared with topographical features of the head in theatre to guide a biopsy needle or small craniotomy biopsy and excision.

There is a small (~ 1%) risk of haemorrhage after a biopsy. Following surgery, patients should be assessed for neurological defects related to the excised tissue. There is a risk of postoperative haemorrhage after any craniotomy and a deterioration in conscious state should be investigated urgently. After retraction of normal brain tissue to access a tumour (e.g. retraction of the frontal lobes to excise an olfactory groove meningioma), reperfusion injury can lead to swelling and infarction during the first 24 h.

Cerebrovascular Lesions

Patients with a vascular lesion such as an intracranial aneurysm or arteriovenous malformation (AVM) may present acutely with a subarachnoid or intracerebral haemorrhage. Congenital lesions are seen frequently in young and previously healthy patients. Intracranial aneurysms occur in the older age group and may be associated with other, more widespread cardiovascular disease. Subarachnoid haemorrhage is now graded using the World Federation of Neurosurgeons’ (WFNS) scale (Table 32.2). Although application of clips (‘clipping’) at craniotomy should prevent the risk of further bleeding, significant perioperative morbidity and mortality can result from vasospasm, which may occur pre- or postoperatively The current trend is to undertake emergency cerebral angiography and clipping of an aneurysm in good-grade patients, but to delay surgery in the poor-grade patients until their condition improves. The calcium channel blocker nimodipine is used to reduce or prevent vasospasm. By preference, it is given orally because the hypotensive effects are less.

An alternative method of treating intracranial aneurysms is by interventional neuroradiological ‘coiling’ (see below). This was used initially for inaccessible posterior circulation aneurysms but has now become the technique of choice for most aneurysms in many centres.

The conscious state in patients with intracerebral haemorrhage ranges from completely lucid to confused, and the preoperative assessment must take this into account. Those in the older age group may be receiving drugs with cardiovascular effects and are also frequently receiving aspirin or warfarin, which may be a contraindication to urgent craniotomy.

As flow is more pressure-dependent in areas with vasospasm, it is necessary to avoid both hypotension and hypertension. Similarly, hypocapnia should be avoided. A normal cerebral perfusion pressure should be maintained. Although fluid replacement therapy may be all that is required, the careful use of a vasopressor may be necessary in the interval between induction and incision. Nimodipine therapy interacts with inhalational anaesthetic agents to enhance their hypotensive effects. Postoperatively, nimodipine therapy is continued for several days until the risk of vasospasm has passed. Blood entering the CSF either as a result of the initial haemorrhage or during operation is an extreme irritant. Its presence may cause large increases in plasma catecholamine concentrations, with consequent hypertension and vasospasm. Blood which clots in the aqueduct of Sylvius causes obstruction to CSF flow and non-communicating hydrocephalus, necessitating temporary ventricular drainage or insertion of a ventriculo-peritoneal shunt.

Intra-operative temporary clipping of feeding vessels (or to prevent anastomotic backflow from tributaries) may be required to allow safe application of the permanent clip to the neck of the aneurysm. Temporary clips may also be required if the aneurysm bursts, to allow the surgeon to stop the haemorrhage. These clips cause temporary ischaemia in the territory supplied by that vessel. Attempts are usually made to reduce the risk of permanent ischaemic damage. Metabolic suppression with intravenous anaesthetic agents and mild hypothermia have been used. There is, however, no evidence that these techniques have any effect on outcome.

Anaesthesia for Interventional Neuroradiology

In addition to coiling of intracranial aneurysms, radiologists treat a variety of other lesions including AVMs, carotid-cavernous sinus fistulae and dural arteriovenous fistulae in the head or spine. These procedures use several techniques including detachable coils and glue placed within vessels to interrupt blood supply. The blood vessels supplying some tumours, e.g. meningiomas, may also be occluded before surgical excision. Most of these procedures are not painful, although headache may occur. However, to allow precise localization of the lesion and accurate positioning of the intravascular catheters, the patient has to lie very still, sometimes for several hours, and general anaesthesia is commonly used. Many of the risks of open aneurysm surgery apply equally in this situation, and a full, conventional neurosurgical anaesthetic technique should be used, including direct arterial pressure monitoring both to monitor arterial pressure and to enable blood sampling for coagulation studies. Heparin is used during the procedure. If thrombus starts to form in the feeding vessels, antiplatelet treatment is started. Rupture of the aneurysm may require immediate craniotomy, clot evacuation and open clipping of the neck of the aneurysm. It is important not to underestimate the need for a full neuroanaesthetic technique, simply because a craniotomy is not being performed.

Pituitary Surgery (Hypophysectomy)

The pituitary fossa is sometimes approached through a frontotemporal craniotomy for large suprasellar tumours, or more usually through the nose (trans-sphenoidal). The majority of pituitary adenomas are non-functioning and cause pressure symptoms – usually on the optic chiasm. However, there may be preoperative endocrine abnormalities such as acromegaly or Cushings’s disease. Acromegalic patients who present for pituitary surgery may pose considerable difficulties in tracheal intubation and are at risk of obstructive sleep apnoea. Glucocorticoid replacement is required in the immediate perioperative period; mineralocorticoid requirements increase only slowly over the subsequent days. Diabetes insipidus may present in the immediate postoperative period and requires stabilization with vasopressin until the degree of the imbalance is known. It usually resolves over the first few days. If the nasal approach is used, a pharyngeal pack must be inserted and the airway protected to prevent aspiration of blood and CSF.

CSF Shunt Insertion and Revision

The majority of patients who present for insertion or revision of a ventriculo-peritoneal shunt are children with congenital hydrocephalus, often resulting from spina bifida or from intraventricular haemorrhage after premature birth. Older patients may require a permanent shunt after intracranial haemorrhage or head injury or to treat normal pressure hydrocephalus. The major anaesthetic considerations lie in the presentation of a patient with severely raised ICP who may be drowsy, nauseated and vomiting, with resultant dehydration. Compensatory systemic hypertension to maintain cerebral perfusion may also be present. Rapid-sequence induction may be indicated to avoid aspiration; the increase in ICP caused by succinylcholine is of secondary importance. Artificial ventilation to control PaCO₂ is essential to prevent further increases in ICP, and a volatile anaesthetic agent should be used with care for the same reason. When the ventricle is first drained, a rapid decrease in CSF pressure may result in an equally rapid reduction in arterial pressure, which no longer needs to be elevated to maintain cerebral perfusion. Adequate venous access is important to allow rapid resuscitation in response to this severe but temporary hypotension. Shunt surgery may be painful, particularly at the site of insertion into the peritoneum or from the tunnelling of the catheter under the skin. Use of long-acting opioids has to be balanced against the need to have the patient achieve at least the preoperative level of consciousness.

An endoscopic technique may be used to create a new passage for the flow of CSF. The endoscope is passed through a small burr-hole into the lateral and then the third ventricles. The sudden changes in ICP from the use of irrigating fluid and the passage of the neuroendoscope near to vital structures may result in dramatic changes in heart rate and arterial pressure.

Functional Surgery

Surgery for Parkinson’s disease and epilepsy is performed in an awake patient. The initial exposure may be made under general anaesthesia, but the mapping of the brain, and the surgery itself (e.g. inducing a lesion in the basal ganglia), are performed awake under local anaesthesia only. Surgery to remove slow-growing or benign tumours from the ‘eloquent’ or critical areas near the main motor and sensory gyri may also be performed in this way, to guide the surgeon and avoid damage to these areas. Careful assessment and selection of patients is essential to ensure that patient knows what to expect and can co-operate during long periods of awake surgery. Careful positioning (to avoid neck strain), urethral catheterization and temperature control are also required.

Treatment of Trigeminal Neuralgia

This extremely debilitating condition is usually treated pharmacologically with large doses of antiepileptic drugs. However, surgical lesions of the trigeminal ganglion are performed when the side-effects of medical treatment become unacceptable. A lesions of the ganglion is induced by radiofrequency ablation or injection of either phenol or alcohol. All these techniques are very painful and require general anaesthesia. The patient is anaesthetized while the ganglion is identified radiologically, awakened to allow identification of correct positioning of the needle, and then re-anaesthetized for generation of the lesion or neurolytic injection. If the CSF is encountered during localization of the ganglion, nausea frequently occurs and vomiting with the patient in the supine position should be anticipated. Some cases of trigeminal neuralgia are caused by an abnormal vascular loop compressing the trigeminal nerve in the posterior fossa. A small craniotomy and decompression of the nerve by placing a Teflon pad between the nerve and vessel is often successful in curing the symptoms; the problems of anaesthesia and surgery in this area are highlighted below.

Posterior Fossa Craniotomy

Surgery in the posterior cranial fossa involves lesions of the cerebellum and fourth ventricle. The lateral ‘park bench’ position may be used for some lesions such as vestibular schwannoma (acoustic neuroma). The prone position facilitates operations on the cerebellum, foramen magnum and upper cervical spine. Bone is usually removed as a craniectomy in the posterior fossa rather than by raising a bone flap.

In the past, some surgeons favoured the sitting position because this produced good venous drainage, relative hypotension and excellent operating conditions. The patients were frequently allowed to breathe a volatile anaesthetic agent (usually trichloroethylene) spontaneously so that changes in the respiratory pattern could be used to monitor the progress of fourth ventricular surgery in the region of the respiratory centre. This posed several major anaesthetic problems. Patients in the sitting position are prone to hypotension, which results inevitably in poor cerebral perfusion. Air embolism is also a severe potential problem because when the skull is opened many of the veins within the bone are held open and, if the venous pressure at this point is subatmospheric, air may enter the veins, leading to systemic air embolism. For these reasons, the sitting position is no longer used other than in exceptional circumstances. Although this change has diminished the risks of cerebral hypoperfusion and consequent hypoxia, air embolism is still a potential problem. The operative site, particularly with a moderate head-up tilt, is still above the level of the heart and the veins are held open by the surrounding structures.

Anaesthesia for Cervical Spine Surgery

The cervical spine may be approached from either the anterior or the posterior route, depending largely upon the site of cord or root compression. Although the posterior approach is less likely to damage vital structures, the patient must lie prone, and hypotension, blood loss and access, particularly in a large individual, may cause problems.

In most patients, the neck is relatively stable. Bony degeneration from osteoarthritis can produce severe cord compression. However, rheumatoid arthritis can produce neck instability, particularly in flexion. It is essential to assess the range of neck movement in addition to the assessment of the ease of tracheal intubation. It is doubly unlucky to have a difficult intubation in a patient with an unstable neck! If problems are anticipated, the normal ‘difficult intubation’ drill should be followed, using the methods with which the anaesthetist is most familiar. Severe ankylosing spondylitis involving the neck probably presents the most awkward problem, caused by the rigid immobility of the cervical spine. Additional factors which apply particularly in rheumatoid patients include anaemia, steroid therapy, fragile skin, and renal and pulmonary problems.

Anaesthesia for Thoracic and Lumbar Decompression

Lumbar microdiscectomy for sciatica and one-level laminectomy are usually quite minor procedures. Patients with severe sciatica may gain instant pain relief postoperatively. However, multiple-level laminectomies are more major operations and direct arterial blood pressure measurement may be required in elderly or debilitated patients. Thoracic discs and tumours such as neurofibromata are approached occasionally by the transthoracic route, involving thoracotomy and a combined approach with the patient in the lateral position. Bronchial intubation and one-lung anaesthesia may be needed to facilitate access in this situation.

Correction of spinal deformities such as scoliosis and surgery to stabilize vertebrae damaged by trauma or destroyed by metastatic tumour are often associated with significant bleeding and the need for massive blood transfusion. Hypotensive anaesthesia is used occasionally to decrease bleeding, and particularly the venous ooze in the operative field. Cell salvage reduces the need for blood transfusion, although its role in tumour surgery is unclear. Spinal cord monitoring using somatosensory- or motor-evoked potentials allows identification of spinal cord ischaemia during surgery. These potentials are affected by many anaesthetic agents, particularly the volatile anaesthetic agents, and a TIVA-based technique is preferred. Children with congenital scoliosis associated with other conditions (such as Duchenne muscular dystrophy) represent a significant anaesthetic challenge as a result of their co-morbidities, in particular their lung function, and the volume of blood loss.

1. Initial airway maintenance, remembering that patients with craniofacial injuries often have associated damage to the cervical spine. Tracheal intubation is usually necessary, must be accomplished without excessive neck manipulation and should be performed by an experienced person. It is important to make intubation as atraumatic as possible; consequently, sedation and neuromuscular blockade should be used irrespective of the level of consciousness, except in the most severe situation. The benefits of succinylcholine usually outweigh the potential risks. Nasotracheal intubation is contraindicated because of the possibility of a basal skull fracture.

2. Maintenance of adequate ventilation with oxygen-enriched air. Avoidance of hypoxaemia and hypercapnia is essential.

3. Maintenance of an adequate circulating volume and arterial pressure. Hypotension after head injury greatly worsens outcome. Other injuries which may affect the circulatory state must be identified while resuscitation is being performed.

4. Sedation and analgesia, and neuromuscular blockade, are usually continued to allow management of other injuries, CT scanning and possible inter-hospital transfer.

5. Detailed assessment of thoracic, abdominal and limb injuries and appropriate therapy to stabilize the patient’s cardiovascular and respiratory systems are required before transfer to the CT scanner and X-ray room. Other life-threatening injuries must be dealt with to prevent secondary brain injury caused by hypoxaemia or hypotension.

6. Invasive arterial pressure monitoring, together with ECG, capnography and pulse oximetry are all important in the early detection of deterioration in ICP, cardiovascular stability or respiratory function. A contused, oedematous and non-compliant brain tolerates only minimal changes in oxygen supply or carbon dioxide tension before ICP increases still further.

7. After the CT scan, many patients are transferred directly to the neurosurgical operating theatre for evacuation of haematoma or insertion of an intraventricular catheter or pressure transducer. Patients who are scanned in peripheral hospitals have their scans relayed to the main neurosurgical centre. The patient is then transferred directly by ambulance to the neurosurgical operating theatre, but both cardiovascular and neurological stability must be achieved before the journey. Realistically, this involves the transfer of a sedated, intubated and ventilated patient, often pretreated with mannitol to minimize acute increases in ICP.

Cold G.E., Dahl B.L., eds. Topics in neuroanaesthesia and intensive care. Berlin: Springer-Verlag, 2002.

Matta B.F., Menon D.K., Smith M., eds. Core topics in neuroanaesthesia and neurointensive care. Cambridge: Cambridge University Press, 2011.