best tests, September 2011: A primary care approach to sodium and potassium imbalance

A primary care approach to
sodium and potassium imbalance

Full colour PDF of the pages as they appeared in ‘best tests’.

Interpreting and managing a laboratory result of abnormal sodium or potassium levels is a common scenario in general practice. The following series is a guide to the evaluation of abnormal sodium and potassium levels. Treatment of the electrolyte imbalance or the causes is not covered.

Serum sodium imbalance

Key concepts:	rapidly decreasing or increasing levels, if neurological symptoms are present or if the patient is systemically unwell Further laboratory investigations may be appropriate if the clinical assessment and patient history do not reveal the cause of the sodium imbalance The normal reference range for serum sodium for adults is 135 – 145 mmol/L
Serum sodium imbalances are more prevalent in older people and hyponatraemia is more commonly seen in general practice than hypernatraemia The cause of the sodium imbalance is usually clinically apparent, e.g. fluid depletion or overload Urgent referral to secondary care is recommended for patients with serum sodium < 120 mmol/L or > 150 mmol/L,

Understanding sodium imbalance

Sodium is essential in the human body. It has a vital role in maintaining the concentration and volume of the extracellular fluid and accounts for most of the osmotic activity of plasma. Serum sodium levels are maintained by feedback loops involving the kidneys, adrenal glands and hypothalamus.

When serum sodium is low (usually because total body water is high), antidiuretic hormone (ADH) is suppressed and a dilute urine is excreted.¹ In addition, the kidney produces renin, which stimulates aldosterone production, which decreases the excretion of sodium in the urine, therefore increasing sodium levels in the body.

When serum sodium is high (usually because total body water is low), ADH is released, causing the kidneys to conserve water and therefore a concentrated urine is excreted.¹ In addition, atrial natriuretic peptide (ANP) is secreted by the heart (in response to high blood pressure caused by increased sodium levels) and promotes loss of sodium by the kidney (by inhibiting renin and therefore aldosterone secretion).

In people with normal renal function and adequate aldosterone production, fluid and electrolyte balance is able to be maintained in the body through these compensation processes. Sodium imbalances can indicate the presence of an underlying medical condition or the affect of a medicine.

Elderly people are more susceptible to sodium imbalances due to age-related decrease or decline in:¹

Total body water
Thirst mechanism
Maximal urinary concentrating ability
Ability to excrete water load
Renal function

Elderly people also commonly have multiple co-morbidities that can affect sodium levels and renal function. In addition, use of medicines that affect electrolyte excretion or retention, e.g. diuretics, also commonly causes sodium imbalance.¹

Low serum sodium levels – Hyponatraemia

Hyponatraemia is defined as a serum sodium concentration < 135 mmol/L

Severe hyponatraemia is defined as a serum sodium concentration ≤ 120 mmol/L

Hyponatraemia is the most common electrolyte disorder and is often an incidental finding on routine blood tests.

Hyponatraemia describes a serum sodium concentration which is lower than normal (< 135 mmol/L). It is most commonly a result of excess water diluting the serum sodium levels in the body (e.g. as seen in congestive heart failure), but hyponatraemia can also exist with normal or decreased water levels.

Mild, asymptomatic hyponatraemia does not usually require corrective measures except for treatment of the underlying factors. Correction of hyponatraemia, when required, is usually done in secondary care. Treatment must be gradual to avoid the risk of both fluid overload and cerebral demyelination, which can be fatal.

Signs and symptoms of hyponatraemia

Signs and symptoms of hyponatraemia are generally related to the underlying cause, whether or not it is associated with fluid loss or dehydration, the degree of hyponatraemia and the rate at which it develops.

The signs and symptoms of mild hyponatraemia are usually non-specific, e.g. nausea and lethargy. People with mild, long-term hyponatraemia are often asymptomatic.² Severe (serum sodium < 120 mmol/L) or rapid-onset hyponatraemia can be associated with disorientation, agitation, unsteadiness, seizures, coma and death, due to cerebral oedema.^1,2

When hyponatraemia is associated with decreased extracellular fluid then signs and symptoms can include dizziness, postural hypotension and dry mucus membranes.

Medical disorders that can cause hyponatraemia

Conditions that can cause hyponatraemia include: gastroenteritis, pneumonia, anorexia nervosa, renal disease, hypothyroidism, Addison’s disease, congestive heart failure, liver disease, myeloma, small cell lung cancer, lymphoma, stroke, tumour, meningitis.^4,5

Assessing a patient with hyponatraemia

Assess the level of severity
Refer the patient to secondary care for treatment if sodium < 120 mmol/L.

Assess the trend
Check for previously low serum sodium measurements or repeat the test if time permits. A rapid decrease in sodium warrants referral to secondary care even if the actual degree of hyponatraemia is only moderate.³

N.B. changes of up to 5 mmol/L in two sequential individual results can reflect non-significant variation in sodium levels.³

Assess clinical status
Assess for signs and symptoms indicative of cerebral oedema, e.g. increasing confusion, decreasing consciousness, seizures. If present, urgent transfer to hospital is indicated.³

Assess if there is any acute illness, e.g. pneumonia, gastroenteritis.

Assess hydration status. Check for dehydration, postural changes in blood pressure, jugular venous pressure, peripheral oedema and ascites. Ask about fluid intake/loss and increased/decreased thirst.

Consider known conditions that may have caused the hyponatraemia, e.g. congestive heart failure, renal or liver disease.

Assess the medication history
Look for medicines usually implicated in hyponatraemia, e.g. diuretics, selective serotonin reuptake inhibitors (SSRIs).

Determining the cause of hyponatraemia

After assessing the patient, the cause of the hyponatraemia is usually evident.

Patient is hypervolaemic (i.e. fluid overload): consider possible causes such as liver cirrhosis, congestive heart failure, renal failure and nephrotic syndrome.

Patient is euvolaemic (i.e. normal fluid status): consider possible causes such as medicines, water intoxication, renal failure, hypothyroidism, glucocorticoid deficiency, syndrome of inappropriate anti-diuretic hormone secretion (SIADH).¹

If the patient is hypovolaemic (i.e. fluid depletion): consider possible causes such as vomiting, diarrhoea, renal disease, diuretics, pancreatitis, burns, disorders of CNS causing salt wasting.

Additional laboratory tests may be useful if no obvious cause is found

If no obvious cause for the hyponatraemia can be found, additional blood and urine tests may be useful. Discussion with a renal physician is recommended.

Normal results of lipids, glucose, protein and albumin can help exclude rare causes of low sodium levels, which can occur with marked hypertriglyceridaemia, hyperglycaemia and hyperproteinaemia. A TSH may reveal hypothyroidism which can also be a rare cause of hyponatraemia. Abnormal LFTs may indicate cirrhosis.

Urinary sodium concentrations may be useful to help determine if the loss is renal or extra-renal.

Medicines that can cause hyponatraemia

Medicine-induced hyponatraemia usually develops within the first few weeks of starting treatment. Once the medicine is stopped, the hyponatraemia will usually resolve within two weeks (levels can then be rechecked).⁶ In many cases, a combination of medicines is responsible for the hyponatraemia rather than just one implicated agent.

Diuretics cause hyponatraemia in approximately 20% of people who take them,⁷ although severe hyponatraemia is nearly always seen with thiazide rather than loop diuretics.⁸

Selective serotonin reuptake inhibitors (SSRIs) cause hyponatraemia in up to one-third of people who take them. Risk factors include older age, female gender, concomitant use of diuretics, low body weight and lower baseline serum sodium concentration. Serum sodium level should be checked before and several weeks after starting a SSRI in older patients and in those taking other medicines associated with hyponatraemia.⁹

Antipsychotics are associated with polydipsia (increased thirst), which in turn can cause hyponatraemia. A history of polydipsia has been found in 67% of people taking antipsychotic medicines.¹⁰

Non-steroidal anti-inflammatory drugs (NSAIDs) can cause water retention by increasing water permeability across the renal collecting ducts.¹¹

Other medicines associated with hyponatraemia include: carbamazepine, tricyclic antidepressants, ACE inhibitors, angiotensin II receptor blockers (ARBs), proton-pump inhibitors, sulphonylureas, dopamine agonists, opiates, amiodarone, some chemotherapy medicines, e.g. vincristine, vinblastine, and high dose cyclophosphamide.¹¹

High serum sodium levels – Hypernatraemia

Hypernatraemia is defined as a serum sodium level of > 145 mmol/L

Severe hypernatraemia is defined as a serum sodium level of > 155 mmol/L

Hypernatraemia is much less commonly encountered in general practice than hyponatraemia but when it does occur it is associated with a high mortality rate.

Hypernatraemia describes a serum sodium concentration which is higher than normal (>145 mmol/L). It is characterised by a deficit of water in relation to sodium in the body, which can result from either a net water loss (which would usually be corrected by increased fluid intake via the thirst mechanism) or less commonly, a hypertonic sodium gain. In most cases the cause of the hypernatraemia will be apparent from the clinical setting. Common causes include kidney disease, inadequate water intake and loss of water through vomiting or diarrhoea.

People at highest risk of hypernatraemia include:

Infants and elderly people who cannot maintain adequate fluid intake without assistance
People with impaired mental status who are unable to ask for water
People with uncontrolled diabetes
People with an impaired thirst mechanism
Hospitalised patients receiving hypertonic infusions, tube feedings, osmotic diuretics, lactulose or mechanical ventilation

Signs and symptoms of hypernatraemia

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.¹

Clinical evidence of dehydration may be evident, e.g. tachycardia, low blood pressure and decreased urine output. Symptoms in older people may be non-specific.¹

Assessing a patient with hypernatraemia

Assess the severity
Refer the patient to secondary care for treatment if the serum sodium is ≥ 155 mmol/L.³

Assess the trend
Check for previous results or if time permits, repeat levels. Refer to secondary care if levels are rapidly increasing.

Assess clinical status
If neurological symptoms are present, if the patient is systemically unwell or if oral rehydration is not possible, refer to secondary care for treatment.³

Assess if there is any acute illness, e.g. gastroenteritis.

Assess hydration status (Above).

N.B. Most patients with mild hypernatraemia caused by fluid loss or decreased fluid intake can be managed in primary care with oral rehydration (with a balanced electrolyte solution). It is important that rehydration is performed slowly. Excessively rapid correction or overcorrection of hypernatraemia increases the risk of iatrogenic cerebral oedema.

Assess the medication history
Look for medicines that may be implicated in hypernatraemia, e.g. loop diuretics, lithium.³

Determining the causes of hypernatraemia

The cause of hypernatraemia is usually derived from the clinical assessment and the patient’s history.

Net water loss can be due to:^12,13

Unreplaced insensible loss (dermal and respiratory)
Inadequate fluid intake/impaired thirst – typically in elderly people
Neurogenic diabetes insipidus – post-trauma, idiopathic, caused by tumours, sarcoidosis
Nephrogenic diabetes insipidus – congenital or acquired (e.g. renal disease), medicines such as lithium, amphotericin B

Hypotonic fluid loss can be due to:^12,13

Renal causes, e.g. osmotic diuresis in uncontrolled diabetes
Medicines, e.g. loop diuretics, mannitol, urea, corticosteroids (increase production of urea), high protein supplements
Gastrointestinal losses, e.g. diarrhoea, vomiting, fistulae, use of osmotic laxatives (lactulose, sorbitol)
Cutaneous loss, e.g. burns, excessive sweating

Hypertonic fluid gain can be due to:^12,13

Ingestion of salt, salt water, sodium rich enemas
IV hypertonic infusions, e.g. sodium bicarbonate, sodium chloride

Additional investigations

Additional investigations are indicated by the clinical situation and may include: serum potassium, urea, creatinine, calcium and glucose.³

Osmolality testing

Serum and urine osmolality tests are frequently mentioned in the literature as part of the investigation for either hyponatraemia or hypernatraemia. However, these tests would rarely be requested in the general practice setting.

Urine osmolality is used to detect the ratio of water and solutes in the urine (using a random urine specimen). Urine osmolality is controlled by ADH and it varies over a wide range to reduce the effect of fluid intake on serum osmolality, which is tightly controlled.¹⁴ A high urine osmolality (> 600 mOsm/kg) can indicate fluid losses (e.g. gastrointestinal, diuretics) and a low urine osmolality (< 300 mOsm/kg) can indicate diabetes insipidus or water diuresis.^1,14

Serum osmolality measures the ratio of water and solutes in the serum and is used to determine hydration status. Paired serum and urine osmolality samples can be used to investigate causes of hyponatraemia. A decreased serum osmolality (i.e. < 280 mOsmol/kg) indicates true hyponatraemia. If the urine osmolality is > 100 mOsmol/kg, this can suggest SIADH.^2,14

Urine sodium concentration indicates whether losses are renal or extra-renal and can be used to further interpret results.²

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