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The question as to whether the head and trunk of neurosurgery patients should be elevated remains controversial. This question is particularly important when intracranial hypertension is present. Head up position may have beneficial effects on intracranial pressure (ICP) via changes in mean arterial pressure (MAP), airway pressure, central venous pressure and cerebro spinal fluid displacement. However, in some circumstances, head up position may decrease MAP which in turn will result in a paradoxical rise in ICP through autoregulation mechanisms. Therefore, the degree of head elevation has to be titrated by evaluating the most adequate cerebral perfusion pressure (CPP) for each patient by means of transcranial Doppler or measurement of jugular venous blood oxygen saturation. Head elevation above 30 degrees should be avoided in all cases. In most patients with intracranial hypertension, head and trunk elevation up to 30 degrees is useful in helping to decrease ICP, providing that a safe CPP of at least 70 mmHg or even 80 mmHg is maintained. Patients in poor haemodynamic conditions are best nursed flat. CPP is thus the most important factor in assessment and monitoring when considering head elevation in patients with increased ICP.

The prone position is commonly used for surgery of the spine and the posterior fossa, and is well tolerated by the majority of patients. As long as the abdomen is not compressed, the physiologic impact of this position on cardiorespiratory function is minor, in some cases even less than with the supine position. However extremes of position, particularly of the head and neck, are poorly tolerated and may lead to a variety of severe neurological complications. In addition, several specific forms of pre-existing pathology may predispose the prone patient to major cardiorespiratory complications. In this paper we have systematically reviewed the English and French literature from 1991 to 1997 using Medline Search of peer reviewed journals for the search terms "prone position" and "prone position and venous air embolism". The 330 collected references were reviewed for quality. In combination with review of current standard textbooks these references form the basis for the current report.

Following subarachnoid haemorrhage, delayed cerebral ischaemia from cerebral vasospasm remains the most important cause of mortality and morbidity in patients with surgically secured aneurysms. Therapy with haemodilution, hypertension and volume expansion has been recommended to prevent and treat delayed cerebral ischaemia in these patients on the basis of uncontrolled clinical series (level of evidence III to V, grade C recommendation). Despite the lack of controlled studies, the maintenance of a cardiac index3.5 L.min-1.m-2 and a systolic arterial pressure between 120 and 150 mmHg before clipping and 160 to 200 mmHg thereafter is recommended as a prophylactic or therapeutic measure for vasospasm. Close monitoring of neurological and cardiorespiratory status is important to avoid neurologic and systemic complications.

Mannitol, the osmotic diuretic used in neuroanaesthesia and neurointensive care, has, in addition to its osmotic properties, various effects upon haemodynamics, cerebral blood flow and cerebral blood volume. Three factors are proposed to contribute to mannitol's capacity to lower intracranial pressure and to improve cerebral compliance: cerebral dehydration, and two forms of autoregulation-mediated vasoconstriction. In the case of viscosity autoregulation, it is admitted that changes in blood viscosity after mannitol result in reflex vasoconstriction to maintain cerebral blood flow constant. It has also been proposed that when mannitol administration results in increased cerebral perfusion pressure, vasoconstriction may occur in vascular beds in which autoregulation to perfusion pressure is preserved. On the basis of its effects on cerebral blood flow and free radical scavenging properties, mannitol has recently been investigated as a cerebral protective agent, with the capacity to reduce or prevent damage due to cerebral ischaemia. Finally, mannitol may be injected into a carotid or a vertebral artery to produce blood-brain barrier breakdown, thus improving the brain penetration of chemotherapeutic agents.

Most of the adverse effects of cerebral injury derive result from the formation of cerebral oedema, which causes brain swelling, brain shift and intracranial hypertension. The mechanisms of cerebral oedema are specific of the type of cerebral injury and the effectiveness of treatments such as corticosteroids depend on the type of cerebral oedema. Recent magnetic resonance imaging studies of the brain in patients with acute intracranial injury have confirmed that anatomical brain shifts accompany the clinical syndromes of brain herniation. In particular, specific neurological syndromes can effectively identify rostro-caudal herniation, both transtentorially (uncal and central syndrome) and through the foramen magnum. Signs of upward transtentorial herniation are less specific. Early detection of these syndromes is essential if therapeutic measures to reduce intracranial pressure are to be taken before secondary neurological injury occurs.

By a variety of mechanisms, the cerebral endothelium isolates the extracellular fluid space in the central nervous system from the plasma. The combination of physical and enzymatic mechanisms which prevent macromolecules, polar solutes, neurotransmitters, peptides, and electrolytes from passively entering the brain has been termed the blood-brain barrier (BBB). Specific mechanisms provide facilitated transport across the BBB and active secretion of extracellular fluid and CSF maintain homeostasis for nutrients and for cation and H+ respectively. Consequently, interstitial fluid volume in the CNS does not increase when the total extracellular fluid volume is increased. Total tissue volume is sensitive to osmotic forces, while oncotic forces are relatively unimportant. Most anaesthetic drugs are sufficiently lipid soluble that they enter the CNS easily by passive diffusion. Differences in the rates of CNS penetration between drugs can be predicted from their lipid solubility. Anaesthetic drugs have little effect on BBB permeability and their effects on brain oedema formation derive principally from their haemodynamics effects.

The appropriate administration of intravenous fluids in neurosurgical patients remains an area of disagreement between neurosurgeons and anaesthetists. Fluid restriction has long been advocated by the former and is widely believed to reduce or prevent the formation of cerebral oedema. However, such restriction can lead to hypovolaemia which in turn can result in haemodynamic instability. Thus, brain homeostasis should be aimed for through adequate fluid administration and normal or slightly elevated mean arterial pressure. The properties of the endothelium differ between the brain and the remainder of the body. In most non CNS tissues the size of the junctions between endothelial cells averages 65 A. Proteins do not cross these gaps while sodium does. In the brain, the junction size is only 7 A, which is too small to allow crossing by sodium. Investigations with changes in osmotic and oncotic pressure have demonstrated that: 1) reducing osmolality results in oedema formation in all tissues including normal brain; 2) a decrease in oncotic pressure is only associated with peripheral oedema but not in the brain; 3) in case of brain injury, a decrease in osmolality elicits oedema in the part of brain which remained normal; 4) similarly, a decrease in oncotic pressure does not cause an increase in brain oedema in the injured part of the brain. Thus, a major reduction in oncotic pressure is unimportant for the brain, whereas changes in total osmolality are the dominant driving force at this level. To conclude, in a hypovolaemic patient with severe head injury, the crystalloid of choice is NaCl 0.9% and the colloid of choice is hydroxyethylstarch, both with an osmolality300 mosm.kg-1. Ringer-lactate is hypoosmotic (255 mosm.kg-1) and may cause or increase cerebral oedema. Mean arterial pressure should be maintained above 80 mmHg.