Fluid Balance Disturbances in Neurosurgical Patients: Physiological Basis and Definitions

Abstract

Normally, neural, hormonal, haemodynamic, and renal mechanisms all function in a highly integrated way to preserve sodium and water homeostasis. There are two major objectives. The first is to keep the concentration of sodium in the extracellular fluid (ECF) within very tight limits Together with its associated anions, sodium constitutes more than ninety per cent of the total solute in the ECF, and it controls the distribution of water between the cells and the extracellular space. Large deviations in ECF sodium concentration from normal cause the cells to shrink or swell. This can have disastrous effects, particularly on brain function. The body protects the sodium concentration constantly by finely adjusting the water content of the ECF. This is achieved through the secretion and action of antidiuretic hormone (ADH) to control water loss from the kidney. The thirst mechanism helps by controlling the fluid intake to some extent. The second objective is to keep the total sodium content of the ECF within narrow confines, and thereby to maintain a normal ECF volume. Given that sodium is the major cation of the ECF and that the body adjusts the water around it to maintain a normal sodium concentration, then the total number of sodium ions in the ECF will determine the ECF volume. Large deviations in the ECF sodium content from normal cause fluctuations in the circulating blood volume. Both volume contraction and expansion can have disastrous consequences on brain function, particularly in the presence of brain damage. Normally ECF sodium is regulated by many closely coordinated mechanisms which adjust the amount of sodium lost through the kidneys (Schrier and Anderson 1980). Minor alterations in renal tubular reabsorption can have a profound effect on sodium balance, since the filtered load of sodium is enormous in relation to the amount excreted (Leader, Lancet 1984).