INTERNAL ENVIRONMENT AND INTRACRANIAL HYP ERTENSION

Intracranial pressure depends on cerebral tissue volume, cerebrospinal fluid volume (CSFV) and cerebral blood volume (CBV). Physiologically, their sum is constant (Monro-Kelly equation) and ICP remains stable. When the blood brain barrier (BBB) is intact, the volume of cerebral t issue depends on the osmotic pressure gradient. When it is injured, wa ter movements accross the BBB depend on the hydrostatic pressure gradi ent. CBV depends essentially on cerebral blood flow (CBF), which is st rongly regulated by cerebral vascular resistances. In experimental stu dies, a decrease in oncotic pressure does not increase cerebral oedema and intracranial hypertension (ICHT). On the other hand, plasma hypoo smolarity increases cerebral water content and therefore ICP, if the B BB is intact. If it is injured, neither hypoosmolarity nor hypooncotic pressure modify cerebral oedema. Therefore, all hypotonic solutes may aggravate cerebral oedema and are contra-indicated in case of ICHT. O n the other hand, hypooncotic solutes do not modify ICP. The osmotic t herapy is one of the most important therapeutic tools for acute ICHT. Mannitol remains the treatment of choice. It acts very quickly. An IV perfusion of 0.25 g.kg(-1) is administered over 20 minutes when ICP in creases. Hypertonic saline solutes act in the same way, however they a re not more efficient than mannitol. CO2 is the strongest modulating f actor of CBF. Hypocapnia, by inducing cerebral vasoconstriction, decre ases CBF and CBV. Hyperventilation is an efficient and rapid means for decreasing ICP. However, it cannot be used systematically without an adapted monitoring, as hypocapnia may aggravate cerebral ischaemia. Hy perthermia is an aggravating factor for ICHT, whereas moderate hypothe rmia seems to be beneficial both for ICP and cerebral metabolism. Hype rglycaemia has no direct effect on cerebral volume, but it may aggrava te ICHT by inducing cerebral lactic acidosis and cytotoxic oedema. The refore, infusion of glucose solutes is contra-indicated in the first 2 4 hours following head trauma and blood glucose concentration must be closely monitored and controlled during ICHT episodes.