Hyperkalaemia Essay, Research Paper
Essay
A patient in hospital presented with a serum potassium concentration of 6.6mmol/L. Discuss the possible causes, further investigation and any consequences of this finding.
Potassium is the predominant intracellular cation. This means that serum potassium concentrations are a poor indicator of total body potassium, as only 2% exists in the extracellular fluid. It is disturbances in the balance between the extracellular and intracellular concentrations that cause raised serum potassium levels, which may even occur when the total body potassium is low. As the patient has a serum potassium level of 6.6mmol/L, which is far higher than the upper limit of the reference range (3.3 4.7 mmol/L) it appears the patient is hyperkalaemic. The distribution of potassium in the body is about 150mmol/L in the intracellular fluid (ICF), and about 4mmol/L in the extracellular fluid (ECF). The ICF concentration is determined by the movement of cations across the cell membrane, so anything causing movement of potassium out of the cell will result in hyperkalaemia. The ECF concentration is determined by intake and excretion of potassium. In normal non-diseased individuals the amount of dietary potassium is equal to the amount excreted in the urine via the kidneys. This is normally between about 20-100mmol daily, but even potassium intake exceeding 100mmol will rarely result in hyperkalaemia as healthy kidneys can cope with excretion of high potassium loads, so a dietary excess rarely causes hyperkalaemia.
Firstly, before any of the causes of hyperkalaemia because of disease are considered, one important cause of hyperkalaemia diagnosis in serum must be investigated. This is artefact or pseudohyperkalaemia. As potassium is mainly intracellular, then any trauma to the blood cells which may cause cell lysis, hence release of intracellular potassium, may lead to increased potassium concentrations e.g. trauma to cells during collection and storage, a time delay in separating the serum, freezing of blood samples or the presence of potassium EDTA (an anticoagulant) in the blood collection tube. This is the most common cause of hyperkalaemia and may not always be obvious in the case of potassium EDTA, as sometimes the mistake may be realised upon collection and the sample transferred to another collection tube before arrival in the laboratory. In cases where the patient has no history of other disease and no clinical symptoms, a repeated measurement on a new sample may be advisable to rule out artefact.
As the potassium is mainly intracellular, anything which causes the movement of potassium out, or prevents entry in, to cells will cause hyperkalaemia. Factors that cause the movement of potassium out of cells are hypertonicity, acidosis, severe cell damage and cell death. Cell damage and death will release potassium out of the cell due to cell lysis. In hypertonic states, the decreased ICF volume causes increased cell potassium concentration, causing potassium to move out of the cell into the ECF. In all cases of acidosis, the hydrogen ion concentration in the blood increases. The buffering of hydrogen ions that takes place leads to a displacement of potassium ions from the ICF to the ECF. In both acidosis and diabetes, the increased potassium loss in the urine due to osmotic diuresis may lead to reduced total body potassium although the plasma potassium levels are increased. Cell damage may also prevent the uptake of potassium as will a lack of insulin. A membrane bound, ATPase dependent sodium pump actively excludes sodium from cells causing passive movement of potassium into the cell. Any cell membrane damage or impaired activity of the sodium pump will decrease the potassium uptake into cells. Insulin stimulates the cellular uptake of potassium; the
If the distribution of potassium between the ICF and ECF is normal, then the cause of hyperkalaemia may be due to an altered external balance. Any disease that can cause decreased excretion of potassium will cause the plasma serum levels to be above normal. Potassium is filtered at the glomerulus and reabsorbed in the proximal tubule, with only less than 10% reaching the distal tubule, where the main regulation of potassium ion excretion occurs. Acute renal failure or the later stages of chronic renal failure will lead to decreased renal function, hence a decreased renal excretion of potassium. If excessive dietary potassium intake occurs in renal failure the serum potassium levels will be very high. In the distal tubule, sodium reabsorption also takes place, which is an active process. The electronegativity created in the lumen by sodium reabsorption is neutralised by potassium and hydrogen ions passing into the lumen. In acidosis hydrogen ions will tend to be secreted in preference to potassium to try and decrease the hydrogen ion concentration in the blood. This means that potassium retention will occur. Aldosterone stimulates potassium secretion, indirectly by increasing active sodium reabsorption, and directly by increasing active potassium secretion, both in the distal part of the convoluted tubules. Addisons disease and secondary adrenocortical hypofunction both cause a deficiency in mineralcorticoids. Hyperkalaemia usually causes increased secretion of aldosterone, but if a deficiency is present, not enough aldosterone can be produced to increase the secretion of potassium to lower blood potassium levels and potassium retention occurs.
If artefact has been ruled out as a cause of hyperkalaemia, then further investigations must be performed. ECG monitoring is of value in the diagnosis of hyperkalaemia as changes in ECG waveform reflect changes in serum potassium. Once a definite diagnosis of hyperkalaemia is confirmed the underlying cause can also be investigated, in which patient history is important. If renal disease, diabetes etc is already previously diagnosed in the patient then the hyperkalaemia can be concluded as being a secondary problem to these diseases. In cases where the cause is unclear other tests can be carried out e.g. plasma total [CO2] can be measured to investigate acid-base imbalance, presenting as a decrease in [CO2] if acidosis is present.
The patient must be given urgent treatment to counteract the hyperkalaemia as the serum potassium levels are over 6.5mmol/L. Intravenous calcium gluconate can be given to treat the neuromuscular effects, although this is short-lived. The movement of potassium into cells can be stimulated with glucose and insulin and salbutamol can be used to activate sodium/potassium ATPase. Bicarbonate can be used for treatment if acidosis is identified as the cause of the hyperkalaemia. Treatment with ion-exchange resins or renal kidney dialysis may also be needed. Once the patient has been treated to return the serum potassium levels to normal, any further treatment, once a diagnosis of any underlying disease has been made, can be commenced.
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