Neurosurgical anaesthesia

Brain

The brain comprises the brainstem, cerebellum, midbrain and 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 diencephalon (the major components of which are the hypothalamus and thalamus) and the cerebrum (the two cerebral hemispheres and the subcortical structures such as the basal ganglia). 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, basal ganglia and 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. 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.

Cerebrospinal fluid

Cerebrospinal fluid fills the cerebral ventricles and the subarachnoid space around the brain and spinal cord. The CSF acts as a buffer, separating the brain and spinal cord from the hard bony projections inside the skull and the vertebral canal. It is produced by the choroid plexus in the lateral, third and fourth ventricles by a combination of filtration and secretion ( Fig. 40.1 ). The total volume of CSF is 150–200 ml. Cerebrospinal fluid passes back into the venous blood through arachnoid villi. Obstruction of the normal flow of CSF through the ventricular system, or reduction in reabsorption, leads to a build-up in ICP, producing intracranial hypertension, dilatation of the ventricles and hydrocephalus.

Meninges

Three meninges (or membranes) surround the brain and the spinal cord. These are the dura, arachnoid and 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 or skull fracture, leading to the formation of an extradural (epidural) haematoma ( Fig. 40.2 ). 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 ( Fig. 40.3 ). 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. Around the spinal cord 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 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. The vertebral arteries 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 ( Fig. 40.4 ).

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 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, often 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.

Autonomic nervous system

The autonomic nervous system is classified on anatomical and physiological grounds into the functionally opposing sympathetic and parasympathetic nervous systems. The central areas responsible for coordinating the autonomic nervous system are mostly in the hypothalamus and its surrounding structures and in the frontal lobes. The sympathetic nervous system cells arise from the lateral horn of the thoracic and first two lumbar segments of the spinal cord. The neurons of the parasympathetic nervous system exit the central nervous system with the third, seventh, ninth and tenth cranial nerves and from the second to the fourth sacral segments of the spinal cord.

Intracranial pressure

With normal cerebral compliance (note: the correct physiological parameter is elastance, the reciprocal of compliance, as the variable of interest is the change in pressure for a given change of volume; however, the parameter compliance is more commonly used), ICP is 7–15 cmH ₂ O (5–11 mmHg) in the horizontal position. When moving to the erect position, ICP decreases initially, but then, because of a decrease in reabsorption of CSF, the pressure returns to normal. Intracranial pressure is related to intrathoracic pressure and has a normal respiratory swing. It is increased by coughing, straining and PEEP. 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; see Chapter 3 ), elevations in P a co ₂ and posture, as well as by surgery and trauma ( Fig. 40.5 ).

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 MAP 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 traumatised brain, autoregulation is impaired or absent so that CBF is closely related to cerebral perfusion pressure (CPP) ( Fig. 40.6 ).

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 first producing 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, when both ICP and MAP are monitored, it is essential to maintain the calculated CPP with vasopressor therapy if cerebral perfusion is borderline as even transient absence of flow to the brain may produce focal or global ischaemia with infarction.

Fig. 40.6 also demonstrates that haemorrhagic hypotension associated with excess sympathetic nervous activity results in a loss of autoregulation at a higher CPP than normal, whereas the use of vasodilators to induce hypotension shifts the curve to the left, maintaining flow at lower levels of perfusion pressure.

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 CO ₂ production, produces an increase in CBF. Conversely, cerebral metabolic depression, in association with either deliberate or accidental hypothermia or induced by drugs, reduces CBF.

It is important to understand that these descriptions of autoregulation are of the ‘average’ person. There are differences between individuals and within the brains of individuals. Modern neurointensive care management attempts to target therapy to individual behaviours.

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 . General anaesthesia results in a decrease in cerebral metabolic rate. Cerebral metabolism relies on glucose supplied by the cerebral circulation as 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 energy production of the brain is related directly to its rate of oxygen consumption, and the cerebral metabolic rate for oxygen (CMRO ₂ ) is often used to quantify cerebral activity. By Fick's principle:

Barbiturates have been used to reduce cerebral metabolic rate, and propofol and benzodiazepines have a similar, although less profound, effect. All have been 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 P a co ₂ produce significant increases in CBF and therefore ICP. There is an almost linear relationship between P a co ₂ and CBF ( Fig. 40.7 ). Over the normal range an increase of P a co ₂ by 1 kPa increases CBF by 30%. Conversely, hyperventilation to produce a P a co ₂ of 4 kPa produces cerebral vasoconstriction and a decrease in ICP. 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. Thus, there is no advantage in aggressive hyperventilation regimens in head injury management. Hypocapnia below a P a co ₂ of 4 kPa to lower ICP should be avoided, except as a last resort, because the vasoconstriction induced may be associated with increased areas of hypoperfusion and ischaemia. At a P a co ₂ of 10 kPa or greater, the vessels are maximally dilated and there is little, if any, further increase in CBF.

A 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 P a o ₂ have little effect on CBF. It is only when P a o ₂ decreases below approximately 7 kPa that cerebral vasodilatation occurs. Reduction in cerebral blood oxygen content as a result of anaemia has similar effects.

Positioning

Skin cleaning (prep) solutions must be prevented from entering the eyes. For cranial or cervical spine surgery, the eyes are protected by applying paraffin gauze, padding with a folded swab and then covering with a waterproof tape.

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, whereas parietal and occipital craniotomies are carried out in the lateral or three three-quarters (‘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, around the foramen magnum and the spine. The prone position is discussed in more detail in the section on spinal surgery (see later). 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. Whatever position is used, it is essential that all pressure points are protected adequately. During long operations, the pulse oximeter probe should be moved at least every 4 h.

Blood pressure management

Maintenance of normal arterial pressure is important in all patients but may be a particular problem in very sick or frail patients. Hypotension, with the consequent reduction in cerebral perfusion, should be treated promptly by judicious use of i.v. fluids and vasopressors such as ephedrine.

Induced hypotension was formerly one of the mainstays of cerebrovascular surgery, but its use for intracranial surgery is now rare because of the appreciation that cerebral perfusion is all-important. Most open 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. The alternatives are a short-acting β-adrenoceptor blocker such as esmolol or increasing the depth of anaesthesia. 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 often 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.

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. Cerebral tumours are associated with oedema and raised ICP, and therefore such patients may have been fluid-restricted preoperatively. However, to avoid intraoperative hypotension, careful perioperative fluid administration is necessary.

Cerebrovascular surgery can be associated with vasospasm, and maintaining an adequate CBF 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.

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 80–90 g L ⁻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 oral anticonvulsant, and others may require i.v. anticonvulsant, depending on the site of surgery. Patients receiving high-dose steroids need peri- and postoperative dexamethasone; the normal dose is 4 mg every 6 h with 8–16 mg as an intraoperative bolus. Steroids should not be given to patients undergoing tumour biopsy without discussing it with the surgeon first because of possible effects on the histological diagnosis of cerebral lymphoma.