[Osmotic cerebral oedema: the role of plasma osmolarity and blood brain barrier].

There are five types of oedema: vasogenic, cytotoxic, interstitial, hyperemic and osmotic. The differences lie on the type and localization of the oedema, the state of the blood-brain barrier (BBB) and the pathological context. Under physiological conditions, the osmolarity of extra cellular fluids (ECFs) is equal on both sides of the BBB. However, the pathophysiological variations of circulating osmolarity (including acute hyponatremia and hypernatremia) do not affect, at the same time, the osmolarity of cerebral ECFs. This situation generates an osmotic gradient on either side of the BBB. The latter, if intact, behaves like a semi-permeable membrane allowing water transport according to the osmotic laws. Depending on its direction, water movement could induce cerebral liquid inflation (i.e. osmotic oedema) or cerebral dehydration. In case of osmotic insult, cerebral cell modify their active osmotic molecular contents in order to limit volume variation. There are two types of osmoactive molecules, organic (i.e. ideogenic osmoles: amino acids, polyols and trimethylamines) and non organic (i.e. electrolytes). In the event of plasma hypotonicity, cerebral cells expel active osmotic molecules to reduce the osmotic gradient and water movement thereby reducing edema. The opposite reaction is observed in the case of hypertonic insult. This cerebral osmoregulation becomes more effective, the slower the osmotic disorder. It explains, for example, why patients with chronic and severe hyponatremia could be asymptomatic. Severe osmotic oedema is observed mainly in water intoxication, acute hyponatremia or too rapid reduction of hyperosmolarity. However, osmotic oedema is not limited to extreme clinical circumstances. Hyponatremia, even modest, could modify cerebral blood volume and impair osmoregulation. Generally these minor modifications do not affect normal brain tissue. In the presence of cerebral lesion, osmoregulation operates only in areas of preserved BBB. The pathological zones are therefore exposed to osmotic oedema (even in cases of moderate hyponatremia) with deterioration of both clinical status and intracranial pressure. This authentic phenomenon could be insidious and difficult to differentiate from osmotic central oedema. Hyponatremia constitutes an authentic secondary cerebral insult of systemic origin, an entity clearly identified by experimental studies to justify the choice between crystalloids and colloids in neuroanaesthesia and neurointensive care. These studies have revealed an increase in water content in normal brain tissues after administration of hypotonic solutions. The increase in plasma osmolarity as a treatment modality using mannitol or hypertonic saline is based on the same concepts. The most remote indication is the occurrence of a reactive mydriasis in the context of trauma for example. More recently, therapeutic hypernatremia has been proposed to control intracranial hypertension.