- What is Hyponatraemia
- Statistics on Hyponatraemia
- Risk Factors for Hyponatraemia
- Progression of Hyponatraemia
- Symptoms of Hyponatraemia
- Clinical Examination of Hyponatraemia
- How is Hyponatraemia Diagnosed?
- Prognosis of Hyponatraemia
- How is Hyponatraemia Treated?
- Hyponatraemia References
What is Hyponatraemia
Hyponatraemia is defined as low levels of sodium in the serum, that is less than 135mmol/L (normal range is between 135mmol/L and 145mmol/L). Sodium is the predominant positively charged ion (cation) in the body’s extracellular fluid. Severe hyponatraemia is when the serum sodium levels are below 125mmol/L.
Statistics on Hyponatraemia
Hyponatraemia occurs in approximately 1% of hospitalised patients. Incidence rates can be much higher in cancer patients, for example between 15-50% in small cell lung cancer. Decreased serum sodium levels in cancer patients usually occur due to fluid overload, which is caused by inappropriate levels of hormone that prevents excretion of free water (antidiuretic hormone – ADH). This is known as the syndrome of inappropriate secretion of ADH (SIADH), and is easily the most common cause of hyponatraemia in cancer patients.
Risk Factors for Hyponatraemia
Malignant illness can cause hyponatraemia in a variety of ways. These include:
- Decreased kidney (renal), adrenal or thyroid function (insufficiency)
- Factors relating to medical treatment (iatrogenic factors)
- Central nervous system (CNS) lesions, lung disease or nausea causing physiologic increases in ADH secretion.
- Adaptive circulatory mechanisms such as low blood pressure, heart failure or liver cirrhosis.
SIADH is the most common cause of hyponatraemia in patients with cancer.
Other Mechanisms that can cause hyponatraemia include:
- Increased thyroid hormones (hyperthyroidism) and adrenal insufficency.
- Excessive salt excretion (salt-wasting) in drug-induced kidney damage, adrenal insufficiency or use of specific medications that increase urine excretion (thiazide diuretics).
- Chemotherapy and associated nausea and vomiting.
- Overhydration with fluids containing less sodium than normal blood (hypotonic fluids).
Progression of Hyponatraemia
Hyponatraemia is usually caused by an excess of total body water relative to sodium levels. It is most often caused by water retention combined with excessive administration of fluids.
Water retention usually occurs as a result of increased ADH secretion due to a reduced volume of blood within the vessels (intravascular volume). This decreased intravascular volume may be due to excessive swelling when the body’s fluid has shifted outside of the blood vessles (oedematous state) or true volume depletion (e.g. from blood loss).
The syndrome of inappropriate ADH secretion (SIADH) involves the inability of the kidney to dilute urine even though the plasma has become less concentrated. It is defined as an inappropriately high urine concentration (osmolality) at the same time as decreased serum osmolality.
How is Hyponatraemia Diagnosed?
As the early stages of hyponatraemia may be asymptomatic, laboratory findings are useful in making the diagnosis. Diagnosis of SIADH is made by finding low serum sodium and low serum concentration (osmolality) (20 mmol/L) in a patient with normal intravascular volume.
Kidney, liver, heart, adrenal and thyroid function must all be normal for the diagnosis of SIADH to be made.
Prognosis of Hyponatraemia
Hyponatraemia results in primarily brain-related (neurological) symptoms. If serum sodium levels fall quickly, brain swelling (cerebral oedema), fits (seizures), coma and even death may result. Fortunately, serum sodium can be easily monitored, and this complication can be prevented in many patients.
How is Hyponatraemia Treated?
Treatment depends on patient symptoms and the underlying cause of the hyponatraemia. Life-threatening situations must be treated supportively; an airway tube (intubation) may be necessary and medications to stop fits (anticonvulsant medications) should be considered in patients with seizures. Low sodium (hypotonic) IV fluids should be avoided, as these worsen the condition.
Serum sodium must be corrected at the appropriate rate; asymptomatic patients require slow (0.5mmol/L/hr) replacement, whereas patients who show symptoms require more rapid intervention (1-2mmol/L/hr). This rapid correction is only indicated for the first 1-3 hours of treatment, with the remainder of correction (aim is to increase serum sodium levels by 12-15mmol/L) occurring over 24 hours.
Most cases of hyponatraemia due to SIADH develop gradually, and gradual correction is appropriate unless there are neurological symptoms. The central nervous system reacts to hyponatraemia in a specific way. If levels change too quickly, nerve cell swelling and damage may occur. Slow sodium replacement is required to prevent fluid shifting rapidly from the cells, which can cause a specific type of damage to the brain (cerebral pontine myelinolysis). Treatment of the underlying cancer may or may not be successful in reducing the ectopic ADH secretion, and this is not considered treatment enough on its own.
The other important factor in the management of hyponatraemia is fluid management. If the cause is decreased blood volume, this must be addressed appropriately. Administration of normal saline (salt water with the same sodium concentrations as blood) corrects both the fluid loss and the low sodium levels, whilst suppressing ADH secretion and encouraging free water excretion. Salt and water restriction are appropriate in cases of hyponatraemia due to oedematous states. This must be accompanied by treatment of the underlying cause of the oedema.
Because SIADH is a state of excess free water, it is treated initially by limiting the total free water intake. If limiting free water is unsuccessful, a specific type of antibiotic (demeclocycline, a tetracycline antibiotic), can be used to inhibit the activity of ADH on the kidney, but it is relatively slow to take action. Treatment with 3% saline +/- a medication to increase fluid excretion (diuretic – frusemide) is recommended if CNS symptoms are present. If the syndrome is chronic, frusemide or salt tablets may be used for long term treatment. The underlying tumour must also be treated.
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