Neurosurgical Anaesthesia

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Neurosurgical Anaesthesia

Ne urosurgical procedures include elective and emergency surgery of the central nervous system, its vasculature and the cerebrospinal fluid (CSF), together with the surrounding bony structures, the skull and spine. Almost all require general anaesthesia. In addition to a conventional anaesthetic technique which pays meticulous attention to detail, the essential factors are the maintenance of cerebral perfusion pressure and the facilitation of surgical access by minimizing blood loss and preventing increases in central nervous tissue volume and oedema.

APPLIED ANATOMY AND PHYSIOLOGY

Anatomy

Brain

The brain comprises the brainstem, the cerebellum, the midbrain and the paired cerebral hemispheres. The brainstem is formed from the medulla and the pons, with the medulla connected to the spinal cord below and to the cerebellum posteriorly. The medulla contains the ascending and descending nerve tracts, the lower cranial nerve nuclei and the respiratory and vasomotor (or ‘vital’) centres. Running through the brainstem is the reticular system which is associated with consciousness. A lesion or compression of the brainstem secondary to raised intracranial pressure produces abnormal function of the vital centres which is rapidly fatal (‘coning’). The cerebellum coordinates balance, posture and muscular tone. The midbrain connects the brainstem and cerebellum to the hypothalamus, the thalamus and the cerebral hemispheres. The cerebrum consists of the diencephalon containing the thalamus, hypothalamus and the two cerebral hemispheres. The thalamus contains the nuclei of the main sensory pathways. The hypothalamus coordinates the autonomic nervous system and the endocrine systems of the body. Below the hypothalamus is the pituitary gland. Pituitary tumours may produce the signs of a space-occupying lesion, restrict the visual fields by compressing the optic chiasma or give rise to an endocrine disturbance. The cerebral hemispheres comprise the cerebral cortex, the basal ganglia and the lateral ventricles. A central sulcus or cleft separates the main motor gyrus (or fold) anteriorly from the main sensory gyrus posteriorly. Each hemisphere is divided into four areas or lobes. The function of the different lobes is incompletely understood. However, the frontal lobe contains the motor cortex and areas concerned with intellect and behaviour. The parietal lobe contains the sensory cortex, the temporal lobe is concerned with auditory sensation and the integration of other stimuli, and the occipital lobe contains the visual cortex. Lesions of the cerebral hemispheres give rise to sensory and motor deficits on the opposite side of the body.

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.

Meninges

Three meninges or membranes surround the brain and the spinal cord. These are the dura mater, the arachnoid mater and the pia mater. Around the brain, the dura mater is a thick, strong, double membrane which separates into its two layers in parts to form the cerebral venous sinuses. The outer or endosteal layer is adherent to the skull bones and is the equivalent of the periosteum. The inner layer is continuous with the dura which surrounds the spinal cord. The major artery supplying the dura mater in the head is the middle meningeal artery, which may be damaged in a head injury and skull fracture, leading to the formation of an extradural haematoma. The arachnoid mater is a thin membrane normally adjacent to the dura mater. Cortical veins from the surface of the brain pass through the arachnoid mater to reach dural venous sinuses and may be damaged by relatively minor trauma, leading to the formation of a subdural haematoma. The pia mater is a vascular membrane closely adherent to the surface of the brain and follows the contours of the gyri and sulci. The space between the pia and arachnoid maters is the subarachnoid space and contains CSF.

The dura mater forms a sac which ends below the cord, usually at the level of the second sacral segment. The dura extends for a short distance along each nerve root and is continuous with the epineurium of each spinal nerve. There is an extensive subarachnoid space between the arachnoid mater and the pia mater. The space between the dura and the bony part of the spinal canal (the extradural or epidural space) is filled with fat, lymphatics, arteries and an extensive venous plexus.

Vascular Supply

The arterial blood supply to the brain is derived from the two internal carotid arteries and the two vertebral arteries. The vertebral arteries are branches of the subclavian arteries and pass through foramina in the transverse processes of the upper six cervical vertebrae. They join together anterior to the brainstem to form the single basilar artery, which then divides again to form the two posterior cerebral arteries. These vessels and the two internal carotid arteries form an anastomotic system known as the circle of Willis at the base of the brain. The main arteries supplying the cerebral hemispheres are the anterior, middle and posterior cerebral artery for each hemisphere. The majority of cerebral aneurysms are of vessels that are part of, or very close to, the circle of Willis. Other important vessels supplying the brainstem and the cerebellum branch from the basilar artery. Venous blood drains into the cerebral venous sinuses, whose walls are formed from the dura mater. These sinuses join and empty into the internal jugular veins.

The blood supply to the spinal cord comes from the single anterior spinal artery formed at the foramen magnum from a branch from each of the vertebral arteries, and from the paired posterior spinal arteries derived from the posterior inferior cerebellar arteries. The anterior artery supplies the anterior two-thirds of the cord. There are additional supplies from segmental arteries and also a direct supply from the aorta, usually at the level of the eleventh thoracic intervertebral space. The blood supply to the spinal cord is fragile, and infarction of the cord may result from even minor disruption of the normal arterial supply.

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.

GENERAL PRINCIPLES OF NEUROSURGICAL ANAESTHESIA

Most intracranial operations involve a craniotomy, i.e. removal of a piece or flap of bone to gain access to the meninges and brain substance beneath. In many procedures, the size of the craniotomy can be 4–5 cm diameter or less (for example, for tumour biopsy, evacuation of a chronic subdural haematoma, insertion of an external ventricular drain or ventricular shunt catheter). Some procedures still require a large craniotomy (e.g. evacuation of acute subdural, extradural or intracerebral haematoma, meningioma resection, aneurysm surgery). A smooth anaesthetic technique is essential, avoiding increases in arterial and venous pressures and changes in carbon dioxide concentration while at the same time avoiding a decrease in cerebral oxygenation.

Most anaesthetists maintain hypnosis with either an inhalational anaesthetic agent, usually sevoflurane, or with a continuous infusion of propofol. Intra-operative analgesia is provided by a short-acting opioid such as remifentanil by infusion or intermittent doses of fentanyl (for short or minor procedures). Neuromuscular blockade and IPPV are usually employed. It is extremely important to ensure adequate fixation of the tracheal tube and intravascular cannulae and to protect the eyes, because access to the head and limbs is severely restricted during the operation. Continuous monitoring of the electrocardiograph and arterial pressure is essential; direct arterial pressure and temperature monitoring are normally used, together with continuous measurement of oxygen saturation, and end-tidal carbon dioxide and inspired anaesthetic agent concentrations. At the end of the procedure, the patient must be transferred to the recovery room with no residual neuromuscular blockade or opioid-induced respiratory depression because both may produce critical increases in ICP related to hypercapnia and hypoxaemia. Long-acting drugs with a marked sedative action are used with caution perioperatively so that a pathological failure of return to consciousness is not masked.

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.

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