Fluid and electrolyte balance
Water and sodium balance
Approximately 60% of the body weight in men and 55% in women consists of water. Most of this exists within two physiological fluid ‘spaces’ or compartments: about two-thirds within the intracellular compartment and one-third in the extracellular compartment. The extracellular compartment consists of both intravascular fluid (blood cells and plasma) and interstitial fluid (fluid in tissues, which surrounds the cells). Additionally a small amount of fluid is described as in the ‘third space’, e.g. fluid in the gastrointestinal tract, pleural space and peritoneal cavity. Pathological third space fluid is seen with gas-trointestinal obstruction or ileus and pleural effusion or ascites.
Water remains in physiological balance between these compartments because of the concentration of somatically active solutes. Osmosis is the passage of water from a low concentration of solute through a semi permeable membrane to a more concentrated solution. A proportion of the total osmotic pressure is due to the presence of large protein molecules; this is known as the colloidal osmotic pressure or oncotic pressure.
· Intracellular–extracellular fluid balance: The cell membrane acts as semipermeable to sodium and potassium because the Na+ -K+ -ATPase pump keeps moving sodium out of the cell into the interstitial fluid and moving potassium into the cell. Sodium is the main determinant of extracellular fluid volume.
· Intravascular–interstitial fluid balance: The capillary wall is semi-impermeable to plasma proteins, whereas sodium passes freely across the capillary wall. This means that proteins (through oncotic pressure), rather than sodium, exert the osmotic effect to keep fluid in the intravascular space. The hydrostatic pressure generated across the capillaries offsets this, driving intravascular fluid out into the interstitial fluid. If there is a reduction in plasma protein levels (hypoal-buminaemia), the low oncotic pressure can lead to oedema; this is where there is excess interstitial fluid at the expense of intravascular fluid.
Water is continually lost from the body in urine, stool and through insensible losses (the lungs and skin). This water is replaced through oral fluids, food and some is derived from oxidative metabolism. Sodium is remarkably conserved by normal kidneys, which can make virtually sodium-free urine, e.g. in hypovolaemia. Obligatory losses of sodium occur in sweat and faeces, but account for <10 mmol. The average dietary intake of sodium in the United Kingdom is ∼140 mmol/day, which is the equivalent of 8 g of salt. The recommended sodium in-take for a healthy diet is 70 mmol/day. Normal kidneys can easily excrete this sodium load, and in a healthy person the body is able to maintain normal fluid balance by sensing the concentration of sodium and the extracellular volume. This process is under the control of both local sensing mechanisms and more distant neurohormonal mechanisms. These drive thirst and water intake on the one hand and renal excretion or conservation of sodium and water on the other. In disease states or due to an excess or lack of salt and/or water intake, this normal balance may be disturbed.
There are essentially four patterns of water and sodium imbalance:
· Sodium depletion is usually due to excess sodium loss, e.g. due to vomiting or diarrhoea, or burns. Water is lost with the sodium, so the serum sodium usually remains normal, but hypovolaemia results. If hypertonic fluid is lost or if there has been water replacement but insufficient sodium replacement (typically in a patient who is vomiting and only drinking water or only given intravenous 5% dextrose or dextrosaline), hyponatraemia results, which can lead to confusion, drowsiness, convulsions and coma.
· Water deficiency due to inadequate intake of water leads to dehydration. The plasma osmolality rises and hypernatraemia occurs. This stimulates thirst and vasopressin release, which increases water reabsorption by the kidneys. Pure water depletion is rare, but many disorders mostly lead to water loss with some sodium loss. Initially water moves from the cells into the extra-cellular compartment, but then both the intracellular and extracellular compartments become volume depleted, causing symptoms and signs of fluid depletion.
· Sodium excess rarely occurs in isolation. It is usually found in combination with water excess, causing fluid overload with peripheral oedema, pulmonary oedema and hypertension. The effect on serum sodium and fluid balance depends on the relative excess of sodium compared to water. Sodium excess > water excess causes hypernatraemia whereas water excess > sodium excess causes hyponatraemia.
· Water excess may be due to abnormal excretion e.g. in syndrome of inappropriate antidiuretic hormone (SIADH;) or excessive intake. In normal circumstances the kidney excretes any excessive water intake, but in renal disease or in SIADH, water is retained. This invariably causes hyponatraemia. Patients often remain euvolaemic, but if there is also some degree of sodium excess there may be symptoms and signs of fluid overload.
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