Hyponatraemia is a common medical problem, which refers to a low plasma sodium (Na+) concentration.
It is defined as a serum sodium concentration less than 135 mmol/L.
The normal range for serum sodium is 135-145 mmol/L. Hyponatraemia can be classified according to the severity of the biochemical value or the rate of onset.
Hyponatraemia is considered the most common electrolyte disturbance that is encountered in primary and secondary care.
The incidence and prevalence of hyponatraemia is variable dependent on the data quoted, but has been suggested to account for up to 15% of hospital admissions.
The concentration of serum sodium is determined by the content of water.
The content of water within blood increases by water intake or decreases by insensible losses (i.e. sweating) and urination. Water content is further adjusted by a process known as osmoregulation. Antidiuretic hormone (ADH), which is also known as vasopressin, is central to osmoregulation.
Osmolality refers to the concentration of a solution. The normal plasma osmolality is 275–295 mOsm/kg whereas pure water has an osmolality of 0 mOsm/kg.
ADH is produced by the hypothalamus. It is subsequently stored and released from the posterior pituitary gland. Release of ADH occurs in response to a rising plasma osmolality. ADH release begins at a plasma osmolality of around 280 mOsm/kg and thirst is felt at around 290 mOsm/kg. Both of these lead to a reduction in plasma osmolality.
ADH acts on the distal convoluted tubule and collecting duct to increase water reabsorption independent on sodium. It prevents excessive loss of water from the body and helps to restore total body water (TBW) if plasma osmolarity rises.
Hyponatraemia occurs due to a relative excess of total body water compared to sodium.
It is associated with disturbances in ADH secretion, which as discussed, is critical to control of water content through osmoregulation. There may be an excess intake of water or an excessive release of ADH leading to an increase in total body water and subsequent hyponatraemia. ADH disturbances can be physiological (i.e. hypovolaemia), pathological (i.e. heart failure) or iatrogenic (i.e. diuretics).
The underlying mechanisms leading to hyponatraemia depends on the underlying aetiology, which is discussed below.
There are an extensive number of causes of hyponatraemia and the condition is usually multi-factorial in clinical practice.
The aetiology of hyponatraemia can be broadly divided into three categories based on fluid status: hypovolaemia, euvolaemia, hypervolaemia.
Hypovolaemia refers to a reduction in extracellular fluid status. If there is a greater loss of sodium relative to total body water then hyponatraemia will ensue.
The three most common categories of hypovolaemic hyponatraemia are gastrointestinal losses, skin losses and renal losses.
Euvolaemia refers to a normal extracellular fluid status. The main cause of euvolaemic hyponatraemia is SIADH. This is considered a diagnosis of exclusion and discussed further below.
The causes of euvolaemic hyponatraemia include:
Hypervolaemia refers to an increase in extracellular fluid status. If there is an increase in total body water relative to sodium then hyponatraemia will ensure.
The main causes of hypervolaemic hyponatraemia are the ‘failures’ and nephrotic syndrome.
Hyponatraemia can occur as an artifactual result due to a significant rise in serum proteins or serum lipids. This is termed pseudohyponatraemia.
The assessment of fluid status is critical to determine the underlying cause of hyponatraemia.
Assessment of fluid status is done clinically at the bedside. It involves looking for features that are suggestive of dehydration (i.e. hypovolaemia) or features suggestive of overload (i.e. hypervolaemia). If neither are present, then the patient is likely euvolaemic.
Clinical features of hyponatraemia are usually vague and non-specific.
There are a certain collection of features that are more specific to hyponatraemia, however, these are commonly present in severe hyponatraemia and reflect cerebral oedema due to changes in plasma osmolality and fluid shifts.
More focused clinical features depend on the underlying aetiology of hyponatraemia (i.e. shortness of breath in heart failure, abdominal pain in pancreatitis).
Hyponatraemia is diagnosed based on the finding of a low serum sodium concentration on blood testing. Consequently, the majority of cases of hyponatraemia are picked up incidentally.
Investigating the cause of hyponatraemia is largely dependent on the suspected underlying cause. Some of the key investigations required in all cases can be divided into blood tests and urinary tests.
A paired serum and plasma osmolality are important in determining the cause of euvolaemic hyponatraemia. In SIADH, the plasma osmolality is typically low (i.e. < 275 mOsm/kg), urine osmolality high due to an inability to dilute urine (i.e. > 100 mOsm/kg) and the urinary sodium is high (> 30 mmol/L). However, it is important to remember that SIADH is diagnosis of exclusion.
The management of acute hyponatraemia largely depends on the presence or absence of neurological symptoms.
Patients with acute hyponatraemia should be managed in a high-dependancy unit (HDU), especially in the presence of neurological symptoms and have their sodium levels checked regularly.
Management should be directed at the underlying cause. Medications should be reviewed to identify possible causes of hyponatraemia and non-essential parental fluids should be stopped.
Patients require rapid correction of serum sodium concentration to reduce the risk of complications with the use of hypertonic saline (i.e. 1.8-3% sodium chloride).
The management of chronic hyponatraemia is broadly divided by the aetiology. Importantly, sodium correction should never exceed 8-10 mmol/L per 24 hours to prevent osmotic demyelination syndrome.
Patients who are fluid deplete require intravenous replacement with normal saline (0.9%).
As fluid is given, there should be a correction in the serum sodium concentration. A medication review should also be completed to identify any drugs contributing to or directly causing hyponatraemia (i.e. diuretics, SSRIs).
The most common cause of euvolaemic hyponatraemia is SIADH. Therefore, patients are usually managed with fluid restriction in accordance with SIADH management unless another cause is identified.
Patients with SIADH may require medical treatment to prevent the action of ADH on the distal coveted tubules. Options include Demeclocycline or Vaptans (e.g. tolvaptan). Demeclocycline works as an inhibitor of ADH and the Vaptons act as a vasopressin receptor antagonist. If no clear cause is identified on initial investigations then patients should be investigated for underlying malignancy with CT or MRI.
Patients with hypervolaemic hyponatraemia require treatment of the underlying cause.
As a general rule, these patients are typically managed with fluid and salt restriction and the use of diuretics, especially in heart failure. As the fluid is off-loaded from the body, there should be an improvement in sodium levels.
Hyponatraemia is a potentially life-threatening condition, especially with a rapid decline in sodium levels, or serum levels that fall < 125 mmol/L.
The main problem with hyponatraemia is fluid shifts due to changes in osmolality. The most significant of this is fluid shifts into cells of the central nervous system leading to cerebral oedema. Cerebral oedema causes raised intra-cranial pressure, which can lead to altered mental status, seizures, coma and death.
If hyponatraemia is more chronic, it can predispose to issues with falls, gait disturbance, concentration problems and cognitive deficits.
The condition is also termed cerebral pontine myelinolysis and is caused by rapid correction of hyponatraemia.
A rapid correction of sodium levels leads to large shifts of intracellular water affecting the pons and other parts of the central nervous system. This can then precipitant irreversible neurological damage, which usually occurs 2-4 days following rapid correction.
Osmotic demyelination syndrome typically results in the development of quadriplegia and pseudo-bulbar palsy although other neurological features can occur.
To prevent this complication, in absence of severe neurological features from hyponatraema that might require more rapid correction, sodium correction should not exceed 8-10 mmol/L per 24 hours.
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