Quiz Feedback: Sodium and potassium imbalance

The majority of respondents correctly identified the indications for urgent referral to secondary care, which is recommended for patients with a serum sodium <120 mmol/L, if the levels are rapidly decreasing or if neurological symptoms are present.

Often patients with mild hyponatraemia are either asymptomatic or may have non-specific symptoms, e.g. nausea and lethargy. Patients with dehydration will often display signs and symptoms consistent with hypovolaemia, e.g. dizziness.

As a general rule, mild, asymptomatic hyponatraemia does not require corrective measures except for the treatment of the underlying factors. When a patient has symptoms, then addressing the underlying cause will often help address both the symptoms and the hyponatraemia.

The majority of respondents correctly identified that the possible causes of hyponatraemia in a hypervolaemic patient were liver cirrhosis and congestive heart failure. Other causes are renal failure and nephrotic syndrome.

Pancreatitis tends to be associated with hypovolaemia. Hypothyroidism is a possible cause of hyponatraemia but is not necessary associated with hypovolaemia.

All four medicines are reported to cause hyponatraemia. Diuretics cause hyponatraemia in approximately 20% of people who take them, and severe hyponatraemia is more commonly seen in thiazide rather than loop diuretics. SSRIs cause hyponatraemia in up to one-third of people who take them. Serum sodium levels should be checked before and several weeks after starting a SSRI in older patients and those taking other medicines associated with hyponatraemia. NSAIDs can cause hyponatraemia by promoting water retention (by increasing water permeability across the renal collecting ducts). Tricyclic antidepressants are one of a number of other medicines that are associated with hyponatraemia.

A patient should be referred to secondary care for treatment if their serum sodium is ≥ 155 mmol/L, if levels are rapidly rising, if neurological symptoms are present or the patient is systemically unwell, or if oral rehydration is not possible. The signs and symptoms of hypernatraemia are primarily neurological and can include lethargy, weakness and irritability. With more severe hypernatraemia or a rapid rise in sodium level, this can progress to twitching, seizures, coma and death.

The cause of hypernatraemia is usually derived from the clinical assessment and history. When associated with a net water loss, diabetes insipidus (either neurogenic or nephrogenic) can be a cause. Osmolality tests (serum or urine) are only rarely required to be requested in the primary care setting.

The majority of respondents correctly identified the medicines that can cause hypernatraemia, which include lithium, loop diuretics (e.g. furosemide) and corticosteroids (e.g. prednisone). The most common complication of chronic lithium therapy is nephrogenic diabetes insipidus (causing a net water loss). Medicines such as loop diuretics, mannitol, urea, corticosteroids and high protein supplements can also result in hypernatraemia (by causing hypotonic fluid losses). Amoxicillin is not known to be associated with hypernatraemia.

Hypokalaemia can be associated with hypotension, bradycardia or tachycardia, premature atrial or ventricular beats, ventricular arrhythmias and cardiac arrest. Characteristic progressive ECG changes can be seen as the serum potassium level drops but there is no cut-off level at which they become apparent. However, it is recommended that an ECG be performed in patients with a serum potassium < 3.0 mmol/L.

Mild hypokalaemia is often well tolerated in otherwise healthy people, however, in people with co-morbidities, particularly those with hypertension, underlying heart disease or liver cirrhosis, it is associated with an increased incidence of life-threatening cardiac arrhythmias, sudden death, and rarely hepatic coma.

Hypokalaemia can be caused by increased losses from the gastrointestinal tract such as acute gastroenteritis, and by increased urinary potassium excretion with the use of medicines such as diuretics. Diuretic induced hypokalaemia usually occurs within the first two weeks of treatment.

Reduced dietary intake of potassium is a rare cause of hypokalaemia, but may be an important factor in patients concurrently taking diuretics, e.g. an elderly patient on a “tea and toast” diet, or in a person aiming to achieve rapid weight loss on a diet of low calorie liquid protein drinks.

Test–tube haemolysis tends to be associated with pseudohyperkalaemia, not hypokalaemia.

If no obvious cause for the hypokalaemia can be found, additional blood and urine tests may be useful. Measuring urinary potassium excretion (although rarely done in general practice) and serum magnesium concentrations (to investigate for hypomagnesaemia) can be appropriate. Serum bicarbonate levels may help determine if an acid-base disorder is present e.g. metabolic alkalosis. Unexplained hypokalaemia is not an indication to request both CRP and ESR together.

Urgent referral to secondary care is recommended for patients with serum potassium ≥ 7.0 mmol/L or potassium ≥ 5.5mmol/L with any ECG changes or symptoms.

Pseudohyperkalaemia is a common reason for an isolated raised potassium level. It is advisable to contact the laboratory for any level of potassium > 6.0 mmol/L, especially if unexpected, to discuss potential reasons such as haemolysis that may explain the raised level.

An ECG is recommended for patients with serum potassium levels > 6.0 mmol/L. ECG changes are not usually seen below this level in hyperkalaemia. A raised serum potassium level is most commonly caused as an adverse effect of a medicine or secondary to a disease process.

ECG changes that can be seen with hyperkalaemia include: progressive abnormalities including peaked T waves, flattening or absence of P waves, widening of QRS complexes and sine waves (which can indicate that arrest is imminent).

U waves are one of the characteristic ECG changes seen with hypokalaemia.