JANUARY 2011 H HYPONATRAEMIA yponatraemia or low serum sodium is a common electrolyte disorder in the older person with significant morbidity and mortality. Hyponatraemia may be present in up to 20% of residents in aged care facilities. It is also present in up to 30% of patients with depression on selective serotonin reuptake inhibitors (SSRIs). Hyponatraemia is generally defined as a plasma sodium level of less than 135 mmol/L. The normal reference range for serum sodium is between 135 and 145mmol/L. Other laboratory tests that may be considered are serum osmolality and urine osmolality, urine sodium concentration, other electrolytes (potassium, chloride, bicarbonate), urea, glucose, uric acid, total proteins and triglycerides. Serum levels of thyroid-stimulating hormone (TSH) are needed to identify hypothyroidism. Age-related changes Hyponatraemia is more common in older people because they have an increased incidence of comorbid conditions (heart failure, renal failure) that can be complicated by it. As the body ages there is a decrease in total body water that makes the older person susceptible to electrolyte disturbances such as hyponatraemia. In addition, the thirst mechanism diminishes with age and increases the risk of dehydration. There is also an agerelated decrease in the ability to concentrate urine, which also increases the risk of dehydration. The ability to excrete a water load is delayed in the elderly. Age-related changes to the kidneys occur, with decreased kidney mass, decreased renal blood flow and glomerular filtration rate, as well as impaired responsiveness to sodium balance in the body. Causes Most of the water in the body is in the cells. If water moves from the cells to the plasma, it dilutes the plasma, resulting in hyponatraemia. Antidiuretic hormone (ADH) prevents the clearance of water from the body. This hormone is appropriately released in older people who are hypovolaemic as a way to encourage the body to conserve water. In contrast, ADH © Manrex Pty Ltd (ABN: 63 074 388 088) t/as Webstercare - 2011 may be inappropriately released in response to cancer, certain medications, or diseases such as hypothyroidism. Hyponatraemia usually occurs when elimination of total body water decreases and the kidneys retain too much water or if there is increased oral intake of water. This may be due to medications and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Types of hyponatraemia Hyponatraemia reflects the fluid status of the person and can be classified as: ■■ Hypervolaemic (or dilutional) - excess water dilutes the sodium concentration, causing low sodium levels ■■ Hypovolaemic (or depletional) - water and sodium levels are both low ■■ Euvolaemic - normal water levels are combined with low sodium levels Hypervolaemic hyponatraemia can be caused by retention of excessive water and occurs in heart failure, liver cirrhosis and kidney disease (renal failure or nephrotic syndrome). The person shows oedema or fluid overload due to an increase in total body water. Hypovolaemic hyponatraemia may be due to gastrointestinal loss (diarrhoea, vomiting), excessive loss of sodium through the skin (burns, excessive sweating), sodium loss by kidneys (diuretics) or poor water intake. To distinguish between hypovolaemic and euvolaemic hyponatraemia plasma osmolality and urinary sodium concentration need to be measured also. Increased plasma osmolality may be caused by severe hyperglycaemia that may occur in a person with diabetes and diabetic ketoacidosis. Low plasma osmolality with a high urine sodium level may be due to hypothyroidism, SIADH or medications. A urine sodium level greater than 40mmol/L is suggestive of SIADH or hypothyroidism. Low urinary sodium concentration is caused by severe burns, gastrointestinal losses from vomiting and diarrhoea and acute water overload. Medication causes Onset of drug-induced hyponatraemia usually occurs within Hyponatraemia, continued the first month of treatment. Medications that cause hyponatraemia include: ■■ Thiazide diuretics (eg hydrochlorothiazide) ■■ Thiazide-like diuretics (eg indapamide) ■■ Carbamazepine (Tegretol) ■■ Chlorpromazine (Largactil) ■■ Vasopressin (Pitressin) ■■ Indapamide (Natrilix, Dapa-Tabs) ■■ SSRI and SNRI antidepressants ■■ Theophylline (Nuelin SR) ■■ Amiodarone (Aratac, Cordarone X, Cardinorm) ■■ Ecstasy Frusemide is not likely to cause hyponatraemia. NSAIDs, corticosteroids (eg prednisone) and fludrocortisone (Florinef) can cause increase salt and fluid retention. Common medication causes of SIADH include amiodarone, carbamazepine, chlorpromazine, SSRI and SNRI antidepressants and theophylline. Medications most commonly reported are hydrochlorothiazide, indapamide, paroxetine, venlafaxine and sertraline. Non-drug causes include cerebral disorders (tumor, meningitis) and chest disorders (pneumonia, empyema). Symptoms Most people with hyponatraemia do not show any signs or symptoms. Symptoms do not generally appear until the plasma sodium level drops below 120mmol/L. Early signs include headache, lethargy, malaise and nausea. Confusion, agitation, irritability and disorientation may also occur. In cases of severe hyponatraemia (less than 115 mmol/L), neurologic and gastrointestinal symptoms occur. It can cause significant and permanent neurological injury and death. If hyponatraemia develops rapidly, muscular twitches, irritability and convulsions can occur. The risk of seizures and coma increases as the sodium level decreases. Levels of serum sodium only slightly below normal are associated with increased mortality and increased length of stay in hospital. Falls and fractures Older people even with mildly decreased levels of sodium in the blood experience increased rates of falls and fractures. They are twice as likely to experience a major fracture as those who do not have low sodium blood levels. The risk of vertebral fracture and vertebral compression fractures is about 60% higher in adults with hyponatraemia. Hip fractures are also considerably increased, with a 39% difference. © Manrex Pty Ltd (ABN: 63 074 388 088) t/as Webstercare - 2011 However hyponatraemia does not appear to affect bone mineral density (BMD) nor the risk of osteoporosis, the most common cause of fractures in older people. Management Identifying the cause of hyponatraemia is the first step in the treatment plan. Patients with hyponatraemia from any cause require close attention to their electrolyte and fluid status. Acute severe hyponatraemia (less than 125mmol/L) is usually associated with seizures and should be treated urgently with hypertonic saline, with or without loop diuretics (frusemide). Diuretics may be necessary when significant oedema is present. In persons with chronic hyponatraemia, rapid correction should be avoided. In most cases, removing the underlying cause or medication is sufficient. Fluid restriction (less than 1 to 1.5 litre per day) is the main treatment and the preferred mode of treatment with SIADH. It is generally effective and inexpensive, although compliance can be poor unless supervised. Other less common treatments include lithium and demeclocycline. A new class of medications called vaptans or vasopressin receptors antagonists increase the elimination of electrolyte-free water, but are currently not available in Australia. The addition of salt tablets is not appropriate. Summary Hyponatraemia is a common electrolyte disturbance in older people. In all residents with hyponatraemia the cause should be identified and treated. Treatment of even mild hyponatraemia should be considered. Hyponatraemia can result in changes in cognition and seizures. Even mild levels of chronic hyponatraemia may contribute to an increased rate of falls. References American Family Physician 2004;69:2387-94. Australian Adverse Drug Reactions Bulletin 2008;27(5):19-20.
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