Hypokalaemia is almost always the result of potassium depletion due to renal or intestinal losses. Renal losses are most frequently due to metabolic alkalosis whereas intestinal losses are due to diarrhoea. Occasionally drugs are responsible for an acute shift from extra- to intra-cellular spaces.
Intestinal potassium losses
Potassium loss in normal stools is very low. However, in diarrhoea the potassium concentrations is approximately 80-90 mmol/L.
Hypokalaemia in acidosis (rare)
- Type 1 renal tubular acidosis (see acidification protocols)
- In uncontrolled diabetes esp DKA, the high urine glucose will cause an osmotic diuresis resulting in considerable sodium delivery to the distal tubules. This causes marked urinary potassium loss which in the presence of relative haemoconcentration with elevated plasma potassium concentration may mask a reduced total body potassium. However, with treatment the hypokalaemia will become apparent.
Hypokalaemia in alkalosis
- This is most commonly due to vomiting in which there is considerable chloride loss. The hypokalaemia is due to renal potassium loss as part of the regeneration of bicarbonate.
- Excess mineralocorticoid action (primary or secondary)
- Genetic abnormalities of renal ion transporters
Oral potassium replacement
Ideally potassium is replaced as the chloride salt (viz most therapeutic preparations) as most losses are associated with chloride loss eg diuretics, vomiting or nasogastric aspiration. Many fruits have a high potassium content eg figs, other dried fruits, nuts, avocados, bran cereals but these are phosphate salts and will need to be accompanied by extra sufficient chloride intake.
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- Halperin ML, Kamel KS. Potassium. Lancet 1998;352:135-140.
- Sayer JA, Pearce SHS. Diagnosis and clinical biochemistry of inherited tubulopathies. Ann Clin Biochem 2001; 38: 459-470.