Southern Derbyshire Shared Care Pathology Guidelines Hyponatraemia in Adults Purpose of Guideline The investigation and management of adult patients with newly diagnosed hyponatraemia. Hyponatraemia can be defined as a plasma sodium below 133 mmol/l. The clinical significance of hyponatraemia depends on its severity, its speed of onset and its underlying cause. It is usually due to an excess of water, not a deficiency of sodium. The laboratory will telephone new sodium results below 125 mmol/l during GP practice opening hours and 120 mmol/l or below to Derbyshire Health United out of hours. Symptoms These are primarily neurological and reflect changes in brain volume. They range in severity and include: Headache Confusion Nausea and vomiting Lethargy Irritability Seizures Loss of consciousness Coma There is no specific concentration at which they may occur and hyponatraemia developing over days to weeks may be relatively asymptomatic, even with Na <115 mmol/l. There may be additional symptoms which reflect the underlying cause. Outline investigation and management of hyponatraemia is shown in the following flow chart with more detailed information in the following text. Authorised by Julia Forsyth Page 1 of 6
Acute Symptomatic Hyponatraemia Rapid onset (fall of >10 mmol/l in 48 h) with CNS disturbance, confusion, headache, nausea and vomiting should be treated as a medical emergency Hyponatraemia Na <133 mmol/l Review culprit medications and consider risk/benefit of stopping e.g. Thiazides, SSRI, anticonvulsants, ACE inhibitors, amlodipine, loop diuretics, PPIs esp. omeprazole Further tests Serum: Glucose Lipids Osmolality TFTs, LFTs 9am Cortisol Urine: Osmolality Na Assess Fluid Status Euvolaemia Pseudohyponatraemia excluded i.e. Not grossly elevated trigs or protein Hypotonic hyponatraemia confirmed i.e. Serum osmo <270 mosm/kg Urine osmo >100 mosm/kg Hypovolaemia Tachycardia Hypotension, postural BP drop Dry mucous membranes Reduced skin turgor Consider fluid loss from: Gut: D&V, fistula, stoma Kidneys: Diuretics, renal disease, adrenal insufficiency Hypervolaemia Oedema Ascities Treat underlying cause e.g. heart, renal, liver failure Consider hyperglycaemia, excess drinking, hypothyroidism, adrenal insufficiency. SIADH is a diagnosis of exclusion Check urine Na Urine Na <30 mmol/l. Reconsider hypo/hypervolaemia With oedema: CCF, nephrotic syndrome, cirrhosis Without oedema: GI fluid loss, third space loss, previous diuretics Urine Na >30 mmol/l Likely SIADH Investigate underlying cause e.g. Malignancy, Cerebral/Pulmonary causes. See page 4 for details Consider fluid restriction if symptomatic Treatment of hyponatraemia See page 5 for information Note that: The use of Demeclocycline, urea or vaptans should only be considered on the advice of a specialist Authorised by Julia Forsyth Page 2 of 6
When is hyponatraemia a medical emergency? Hyponatraemia of rapid onset (fall of >10 mmol/l within 48 h) if associated with any of the symptoms above may indicate acute hyponatraemic encephalopathy and should be treated as a medical emergency. It is, however, rare in primary care. Potential causes of acute hyponatraemic encephalopathy include: Inappropriate IV fluids: 5% dextrose or dextrose-saline (unlikely in primary care) Psychogenic polydipsia Other types of excessive water drinking: habit, unconventional diets, recreational drugs (ecstasy) Beer or tea drinkers potomania: high fluid intake plus minimal food intake (eg tea and toast) Drugs: if recently started particularly diuretics, SSRIs, carbamazepine What are the main causes of hyponatraemia? Hyponatraemia is categorised according to extracellular fluid volume status. Clinical assessment of this together with fluid balance information is vital in determining the likely cause. However, clinical assessment may be unreliable and should be aided by spot urine osmolality and sodium. Hypovolaemia: Extracellular fluid loss from Gut: diarrhoea/vomiting, fistula, stoma, etc Kidneys: adrenal insufficiency, renal disease, diuretics Euvolaemia: Gain of water Excess drinking SIADH Hyperglycaemia (Na falls approx 5 mmol/l per 11 mmol/l rise in glucose) Hypervolaemia (oedema states): Nephrotic syndrome Cardiac failure Ascites Pseudohyponatraemia This is an artefactually low sodium due to the presence of grossly elevated levels of triglycerides (eg >30 mmol/l) or protein (eg >100 g/l). The laboratory can check for these and measure sodium by an alternative method (direct ion selective electrode), which is not affected. Authorised by Julia Forsyth Page 3 of 6
Drugs commonly causing hyponatraemia Thiazide and thiazide-like diuretics Amiloride Carbamazepine Sulphonylureas (but not gliclazide) Proton pump inhibitors Antidepressants, particularly SSRIs ACE inhibitors and ARBs Opiates How is syndrome of inappropriate ADH (SIADH) diagnosed? SIADH is a common cause for hyponatraemia, but there is no specific test for it and the diagnosis is one of exclusion after other causes have been disproved. The criteria are: Normovolaemia Normal renal, adrenal, thyroid function Urine not maximally dilute (ie, osmolality >100) Urine Na >30 mmol/l No drugs causing hyponatraemia, e.g. diuretics Improvement in Na following water restriction What are the causes of SIADH? Malignancy: ectopic secretion o Small cell Ca bronchus Cerebral o Tumour; infection; CVA; trauma Pulmonary o Pulmonary embolus; pneumonia; trauma; tuberculosis Metabolic o Acute porphyria What other information is needed in the hyponatraemic patient? Previous sodium results Symptoms and signs of neurological disturbance Fluid balance information Volume status: hypovolaemia, euvolaemia or oedema Medical and drug and smoking history Authorised by Julia Forsyth Page 4 of 6
What other investigations are needed in the hyponatraemic patient? U&E Glucose Serum osmolality Urine osmolality and Na Ca, Mg, Phosphate (may be deranged in alcoholics) TFT Cortisol (9 am) +/- short Synacthen test Other investigations will depend on cause (eg cardiac investigations if CCF, chest, brain and possibly whole body imaging if SIADH) Interpretation of urine results At this point it is important to review all available results and information from other parts of the assessment (eg, drug history and volume status assessment) to determine the most likely cause of the hyponatraemia. Urine osmolality <100 mmol/kg: consistent with primary water overload, eg primary polydipsia, low solute intake, beer potomania >100 mmol/kg: look at urine Na Urine Na <30 mmol/l: consistent with low effective arterial blood volume o With oedema: CCF, nephrotic syndrome, cirrhosis o Without oedema: GI fluid loss, third space loss, previous diuretics >30 mmol/l: consistent with renal Na loss o Diuretics, kidney disease o Adrenal insufficiency, cerebral salt wasting, occult diuretics o SIADH Treatment In the absence of acute hyponatraemic encephalopathy, hyponatraemia should be corrected slowly. Mortality is related to the underlying cause, rather than the sodium concentration. There is a risk of central pontine myelinolysis (CPM), also known as osmotic demyelination syndrome, if correction is too rapid. Features of CPM include dysarthria, dysphagia, seizures, altered mental status and quadriparesis, which typically begin 1-3 days after plasma sodium has been corrected. Chronic, mild, asymptomatic hyponatraemia may not require treatment in its own right, as long as underlying causes have been considered and excluded. Symptomatic patients and those with sodium less than 125 mmol/l need Authorised by Julia Forsyth Page 5 of 6
treatment. Stopping hyponatraemic medications can help to confirm the cause of hyponatraemia as well as resolve the problem. The basic principle is to seek a diagnosis and treat it. If a patient is symptomatic (eg lethargy, confusion) and there is SIADH fluid restriction is indicated and this may also have a role in some other diagnoses (eg CCF). Nevertheless, fluid restriction is not a universal treatment for hyponatraemia. Other treatments such as demeclocycline, urea or vaptans should only be considered on the advice of a specialist. An important principle is regular reassessment of results and fluid balance status to guide ongoing treatment. Contacts Duty Biochemist 01332 789383 (8am to 7pm, Mon Fri) On Call Consultant Biochemist Via RDH switchboard, 01332 340131 (24/7) A&E, MAU and ACC Via RDH switchboard, 01332 340131(24/7) OR ED Nurse in Charge 07799 337674 MAU Nurse in Charge 07917 650751 Author: Dr Paul Masters, May 2012 Reviewed by: Date: Expiry date: Dr P Masters, Dr R Stanworth Feb 2015 28 th Feb 2017 Dr P Masters, Dr R Stanworth, Dr P Blackwell, Mrs H Seddon Sept 2017 30 th Sept 2019 Authorised by Julia Forsyth Page 6 of 6