Water and Sodium Metabolism

Water and Sodium Metabolism:
Water makes up about 60% of body weight – about 2/3rd is intracellular fluid (ICF) – rest is in extracellular fluid (ECF), which includes the plasma and interstitial fluid.

Fluid exchange between the ECF and ICF is regulated by osmotic and hydrostatic pressure:
• hydrostatic pressure forces filtrate out of the capillaries and osmotic pressure pulls it back in
• water moves freely between the compartments by osmosis
• movement of solutes is restricted by their size, their electrical charges and if they depend on active transport
• water will flow in response to changes in the osmolarity of the ECF

Sodium (Na) is the major osmotically active cation in extracellular fluid compartment – body content is regulated by dietary intake and renal excretion.

Water intake depends on the thirst mechanisms:
• triggered by increased plasma osmolarity or decrease in the plasma volume  mediated by the osmoreceptors in the hypothalamus
• inhibited by osmotic signals or GI tract distension

Extracellular fluid volume depletion:
• decrease in extracellular fluid volume due to a net decrease in total sodium content
• due to GI loss (vomiting, diarrhoea, obstruction); loss via urine (diuretics, osmotic diuresis, metabolic acidosis, adrenocortical insufficiency, renal diseases); loss via sweat (fever, high temperature); loss from body surface (burns, severe dermatitis); loss into body tissues (ascites, peritonitis, rhabdomyolysis)
• clinical features – if mild  thirst; if moderate  thirst, concentrated urine, weakness, dizziness, oliguria, postural hypotension; if severe  confusion, hypotension, cold extremities, reduced skin turgor (‘doughy’)
• management – IV saline

Extracellular fluid volume excess/generalised oedema:
increase in extracellular fluid volume due to a net increase in body sodium content
occurs when renal excretion of Na+ does not keep pace with ingestion  increase in extracellular fluid so the concentration of Na+ does not change  becomes clinically evident when increase is above 15%
associated with oedema formation in cardiac failure, nephrotic syndrome, renal failure, liver disorders, starvation, premenstrual fluid retention, pregnancy, drugs (calcium channel blockers, vasodilators, corticosteroids, NSAID’s, oestrogens)
management – dietary sodium restriction, diuretics, treatment of cause

• decrease in the sodium plasma concentration caused by an excess of water
• seen in SIADH, adrenocortical failure, hypothyroidism, uncontrolled diabetes mellitus, cardiac failure, liver failure, nephrotic syndrome, cirrhosis, renal failure

• increase in plasma sodium plasma concentration caused by a deficit of water – common in hospitalised elderly
• caused by excessive water loss – fever, high temperature, reduced intake, diabetes insipidus
• develop thirst, restlessness, irritability, disorientation, dry mouth and fever

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