Quick tip: The most dangerous aspect of hyponatraemia is correcting it too quickly. In critical situations make sure you are counting ALL fluids – inc antibiotics, other electrolytes. It may be possible to reduce volume of these (inc with help from your pharmacist).
The terminology surrounding hyponatraemia can be very confusing as it is classified in many ways. Hyponatraemia can be broadly classified depending on onset time, severity of symptoms, plasma sodium level, plasma osmolality and volume status:
- Onset time – acute (<48hrs) v chronic (>48hrs)
- This is because the brain takes 24-48h to compensate for the drop in sodium levels which can lead to raised intracranial pressure.
- Severity of symptoms –
- Moderately symptomatic – headache, nausea, confusion
- Severely symptomatic – vomiting, coma, seizures, cardiorespiratory distress
- Sodium level
- Mild – 130-134 mmol/L
- Moderate- 125-129 mmol/L
- Profound (cf severe above) - <125 mmol/L
Hyponatraemia towards the more severe end has a link with morbidity and mortality.
Evaluation and management of patients with hyponatraemia can be challenging – it is well recognised that clinical evaluation of volume status is often inaccurate.
Patients with chronic hyponatraemia tend to undergo adaptations so may have mild symptoms despite significant biochemical derangement.
Approach to hyponatraemia – a few general points
When it comes to work-up, our first aim is to distinguish ‘true’ (by this I mean hypotonic) from ‘other’ hyponatraemia as the risks and management are different
The traditional method of classifying hyponatraemia by clinical assessment of volume status is fraught with difficulty and has now been superseded by analysis of urinary sodium
Differential diagnosis of hyponatraemia
- ‘False’ or ‘other’ hyponatraemias (the term is of course inaccurate as hyper/isotonic hyponatraemia isn’t ‘false’ but it can help with the process)
- Pseudohyponatremia: effectively a lab artefact caused by the effect of very high levels of protein or lipids. The patient is not hyponatraemic.
- Hypertonic (aka hyperosmolar) hyponatremia: the patient is hyponatraemic but the serum osmolality is normal or high, usually for obvious reasons (e.g. hyperglycaemia) Na drops in order to keep osmolality normal when another solute is in excess – this should correct itself as the other solute is lowered and there are not the same concerns around fluid shifts in the brain.
- ‘True’ hyponatraemia i.e. Hypotonic (aka hypo-osmolar) hyponatraemia: serum osmolality is low. This can be further subdivided depending on volume status into:
- Hypovolaemic hyponatraemia: dehydration states e.g. vomiting & diarrhoea,
- Euvolemic hyponatraemia: includes SIADH, endocrine causes (esp cortisol deficiency)
- Hypervolemic hyponatraemia: decompensated heart or liver disease or nephrotic syndrome
Aims of assessment:
- Assess severity (most important)
- And therefore guide initial management
- Establish diagnosis
- Which will guide ongoing management
The current approach relies more on analysis of biochemistry than clinical evaluation (which can be misleading)
Simultaneous blood and urine tests for sodium and osmolality are most helpful.
Current recommended approach (as per EJE) is as follows:
- Is the patient severely symptomatic (regardless of cause)? If yes – follow the emergency guidance below
- If no:
- Confirm ‘true’ hypo-osmolar hyponatraemia by measuring serum osmolality
- NB there are calculators available online which can correct Na for hyperglycaemia
- Measure urine osmolality (≤ or > than 100 mOsm/kg) – unfortunately this is often done late or not at all – be pro-active to get a urine result asap
- Urine osmo ≤100 mOsm/kg – dilute urine, ADH not acting. This implies water intoxication or low solute intake (e.g. beer potomania)
- Urine osmo >100 mOsm/Kg – concentrated urine, ADH is acting (?appropriately or inappropriately). Go on to compare urinary Na:
- Urine Na ≤30 mmol/L – implies renal compensation for low arterial perfusion (e.g. heart failure, liver failure, nephrotic syndrome) or dehydration
- Urine Na >30 mmol/L – implies hypoadrenalism, diuretic use, SIADH, (rarely hypothyroidism)
*Notice the picture of hypoadrenalism is the same as SIADH – hyponatraemia with low serum osmolality, high urine osmolality and high urinary sodium – it’s not ‘SIADH’ if you don’t know cortisol is normal*
Obvious caution should be taken interpreting urine Na on diuretics
Other investigations will depend on the identified mechanism of hyponatraemia e.g. echo, urinary protein, CT CAP…..etc
Clues to cause from history and examination:
- History of dehydrating illness/event (e.g. sport)
- Previous available Na results
- History of excessive fluid intake (e.g. for sports event)
- Underlying pathology associated with SIADH – neurological (e.g. head trauma), respiratory (e.g. pneumonia or other suppurative lung disease), malignancy
- Known cardiac, renal or liver disease (esp causing fluid overload)
- Medications (e.g. diuretics, anti-epileptic agents, antidepressants ACE-inhibitors) – esp if newly introduced
It is strongly advised to follow the local guidelines and ask for specialist input in case of uncertainty.
Severe symptomatic hyponatremia is a medical emergency. You should consider:
- Bolus of hypertonic saline to raise plasma sodium by 5 mmol/L (available % may vary locally – refer to your local guidelines or pharmacist) – may need repeating to meet this target
- Intensive monitoring – hypertonic saline should usually be given in a critical care environment and involving local Endocrine team is advisable.
- Frequent blood testing – EJE has specific advice on frequency of testing depending on response – see link below
The targets for avoidance of osmotic demyelination are a MAXIMUM rise in plasma sodium of <10 mmol/L in the first 24 h, and <8 mmol/L in the second 24h – NB this is a limit, not a target.
The risk of overcorrection is higher if: long duration, profound hyponatraemia, liver disease, alcohol excess, causative medications.
NB – if hyponatraemia is correcting too quickly, treatment should be stopped and a specialist consulted re use of sodium-lowering therapies.
- Treatment of the underlying disorder often resolves hyponatraemia.
- If hypovolaemic – rehydrate with normal saline
- If hypervolaemic (e.g. heart failure) - may require a combination of fluid restriction and diuretics
- If hypoadrenal – will likely require fluid resuscitation and hydrocortisone (see adrenal crisis guidance) – d/w/ endocrinology if new diagnosis +/- crisis suspected
- For SIADH
- Typically improves as the underlying condition is treated
- Stop causative drugs if possible (may need to consult specialist for some medications re risk of stopping e.g. for psychiatric or neurological disease)
- Fluid restriction (500 – 1000 ml in 24 hours) is recommended as first line treatment of SIADH
- Other treatment options should be considered under specialist advice and with close monitoring e.g. demeclocycline
- Vasopressin antagonists (“vaptans”) have been approved by NICE for SIADH in patients requiring chemotherapy but use is limited by risk of overcorrection (leading to potential of central pontine myelinolysis) and hepatotoxicity. This is a specialist only prescription in most hospital and it is recommended that this is not prescribed without involving the local Endocrine team
NB - Mild hyponatraemia >130mmol/l does not usually require any specific treatment.
European Society of Endocrinology. Clinical practice guideline on diagnosis and treatment of hyponatraemia (2014) URL: https://eje.bioscientifica.com/view/journals/eje/170/3/G1.xml
NICE Clinical Skill Summary on Hyponatraemia: https://cks.nice.org.uk/topics/hyponatraemia/diagnosis/assessing-a-person-with-hyponatraemia/