Management of Fluid and Electrolyte problems in Children

Hormones
Hormones can affect the activity of the Na⁺K⁺ ATPase by:

1. Enhancing the electroneutral entry of sodium into cells by activating the Na⁺/H⁺ antiporter.
2. Stimulate existing Na⁺K⁺ ATPase enzymes directly.
3. Stimulate the production of more Na⁺K⁺ ATPase.

The main hormones involved are insulin and catecholamines. Insulin and ß-adrenergics lead to a fall in plasma [K⁺], while alpha-adrenergics lead to movement of potassium out of cells.

Acid-Base changes
Metabolic acidosis, caused by a loss of bicarbonate or gain of HCl causes movement of potassium out of cells the K⁺ being displaced from the cell by the entry of H⁺. If the kidneys are working normally, via the action of aldosterone, the acidosis will be corrected and the plasma [K⁺] return to normal.

In contrast, accumulation of organic acids does not lead to hyperkalaemia, as the associated anions (lactate in the case of lactic acid) move into the cells alongside the H⁺ and K⁺ ions are not displaced out.

Respiratory acid-base problems do not produce any significant change in plasma potassium.

Intracellular anions
Within the cell there is a balance between negative and positive charges. Most of the anions are large molecules (organic phosphates such as DNA and RNA). The number of these molecules remains relatively constant except in specific diseases such as diabetic ketoacidosis. If there is a lack of insulin, organic phosphates are degraded to maintain protein synthesis and this fall in anions leads to a parallel loss of K⁺.

Ion Channels
Some problems of potassium homeostasis are the result of abnormalities of ion channels. Such a disease is periodic paralysis. Normally the voltage-gated Na⁺ channel in muscle cells is inactive, because of the negative potential within the cell. Nerve stimulation leads to opening of these Na⁺ channels allowing Na⁺ to rapidly enter the cell. This results in a transient depolarization of the muscle cell. There is a rapid restoration of the resting potential because:

1. the fall in the negative charge within the cell switches off the Na⁺ channels
2. voltage-gated K⁺ channels open, causing K⁺ to exit cells down its concentration gradient restoring the negative charge within the cell
3. increased activity of the Na⁺K⁺ ATPase pumps Na⁺ out of the cell.

Hyperkalaemic periodic paralysis - This condition is caused by an abnormality of the skeletal muscle Na+ channel. When the [K⁺] in the ECF is raised, some of these voltage-gated Na⁺ channels remain active and the cell becomes inexcitable.

Hypokalaemic periodic paralysis - This is an autosomal dominant condition presenting as hypokalaemia and weakness in the second decade of life. The resting membrane potential is less negative than normal. The precise molecular abnormality is unknown.

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