TREATMENT OF HYPOVOLEMIA IN HEAD TRAUMA P ATIENTS

The appropriate administration of intravenous fluids in neurosurgical patients remains an area of disagreement between neurosurgeons and ana esthetists. Fluid restriction has long been advocated by the former an d is widely believed to reduce or prevent the formation of cerebral oe dema. However, such restriction can lead to hypovolaemia which in turn can result in haemodynamic instability. Thus, brain homeostasis shoul d be aimed for through adequate fluid administration and normal or sli ghtly elevated mean arterial pressure. The properties of the endotheli um differ between the brain and the remainder of the body. In most non CNS tissues the size of the junctions between endothelial cells avera ges 65 angstrom. Proteins do not cross these gaps while sodium does. I n the brain, the junction size is only 7 angstrom, which is too small to allow crossing by sodium. Investigations with changes in osmotic an d oncotic pressure have demonstrated that : 1) reducing osmolality res ults 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 osmo lality elicits oedema in the part of brain which remained normal ; 4) similarly, a decrease in oncotic pressure does not cause an increase i n brain oedema in the injured part of the brain. Thus, a major reducti on in oncotic pressure is unimportant for the brain, whereas changes i n total osmolality are the dominant driving force at this level. To co nclude, in a hypovolemic patient with severe head injury, the cristall oid of choice is NaCl 0.9 % and the colloid of choice is hydroxyethyls tarch, both with an osmolality > 300 mosm . kg-1. Ringer-lactate is hy poosmotic (255 mosm . kg-1) and may cause or increase cerebral oedema. Mean arterial pressure should be maintained above 80 mmHg.