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