12

The factors affecting potassium balance have been described previously (p. 22). Hypokalaemia may be due to reduced potassium intake, but much more frequently results from increased losses or from redistribution of potassium into cells. As with hyperkalaemia, the clinical effects of hypokalaemia are seen in ‘excitable’ tissues like nerve and muscle. Symptoms include muscle weakness, hyporeflexia and cardiac arrhythmias. Figure 12.1 shows the changes that may be found on ECG in hypokalaemia.

Diagnosis

The cause of hypokalaemia can usually be determined from the history. Common causes include vomiting and diarrhoea, and diuretics. Where the cause is not immediately obvious, urine potassium measurement may help to guide investigations. Increased urinary potassium excretion in the face of potassium depletion suggests urinary loss rather than redistribution or gut loss. Equally, low or undetectable urinary potassium in this context indicates the opposite.

Reduced intake

This is a rare cause of hypokalaemia. Renal retention of potassium in response to reduced intake ensures that hypokalaemia occurs only when intake is severely restricted. Since potassium is present in meat, fruit and some vegetables, marked potassium restriction is difficult to maintain. Hypokalaemia should, however, be a consideration when severely hypocaloric diets are prescribed to bring about rapid weight loss.

Redistribution into cells

 Metabolic alkalosis. The reciprocal relationship between potassium and hydrogen ions means that in just the same way as metabolic acidosis is associated with hyperkalaemia, so metabolic alkalosis is associated with hypokalaemia. As the concentration of hydrogen ions decreases, so potassium ions move inside cells in order to maintain electrochemical neutrality (Fig 12.2).

Fig 12.2 Hypokalaemia is associated with alkalosis.

 Treatment with insulin. Insulin stimulates cellular uptake of potassium, and plays a central role in treatment of severe hyperkalaemia (see pp. 22–23). It should come as no surprise therefore that when insulin is given in the treatment of diabetic ketoacidosis (see pp. 66–67), there is a risk of hypokalaemia. This is well recognized, and virtually all treatment protocols for diabetic ketoacidosis take this into account.

 Refeeding.

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