Akutní onemocnění mozku– poruchy vodního a natriovéhohospodářství, natriuretické peptidy

Acute Brain Disease – Disturbances of Water and SaltMetabolism, Natriuretic Peptides

Disturbances of water and sodium ion (Na+) metabolism in acute brain diseases are presented.Hyponatraemia accompanies two etiopathogenetically quite different syndromes, the cerebralsalt wasting syndrome (CSWS) and the syndrome of inappropriate secretion of natriuretichormone (SIADH). The first one is caused by increased urinary Na+ loss and accompanied byincreased loss of water and elevated plasmatic atrial and brain natriuretic peptides (ANP,BNP). The second one is caused by water retention with subsequent dilutional hyponatremia,caused by an increased antidiuretic hormone (ADH) level.The CSWS was discovered and described more than 50 years ago, SIADH a few years later.During the approximately 30 years there after the hyponatraemic states developing in acutebrain diseases were considered to be SIADH and treated by water restriction and diuretics.Only 10 years ago renal functional parameters were introduced as part of the differentialdiagnosis between both syndromes. Since that time, CSWS is much more frequently diagnosedas the cause of hyponatraemia. In therapy intensive supplementation of Na+ salts and fluidsis required.The third disturbance of Na+ metabolism is the diabetes insipidus centralis with typicaldevelopment of hyponatraemia. The paper also describes parameters typical for its diagnosis.Attention is also paid to the possible share of renal diabetes insipidus in polyuria in criticallyill patients.Data about the frequency and time-dependency of development of hyper- or hyponatraemia arepresented. Hyponatraemia is more frequent and usually accompanied by hypernatriuria andby depletion of the circulating volume. Hypernatraemia is prognostically more serious. Hyponatraemia treated by fluid restriction and diuretics was complicated by a higher frequency ofcerebral vasospasms and infarctions. Increased water nad salt supplementation rectified thesituation.PlasmaticADH elevation is usually described during days 0–2 after onset of acute brain diseaseor closely to neurosurgical operation. During the following days, when natriuresis and hyponatraemiadevelops, the ADH values return into the reference ranges. In the CSWS pathogenesisno significant role of digoxin-like-substances was found. Unambigous are the increased plasmaticANP and BNP levels. This elevation lasts up to two weeks (when monitoring is unfortunatelyusually stopped). So far the origin of natriuretic peptides in acute brain disease is notknown, but most authors place it into the cardiac tissue. However possible mechanisms of theirliberation are only discussed. Significant correlations are found between natriuretic peptidechanges and hyponatremia, natriuresis and intracranial pressure.

Key words:
hypernatraemia, hyponatraemia, natriuretic peptides, syndrome of inappropriateantidiuretic hormone secretion (SIADH), cerebral salt wasting syndrome (CSWS).