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Hyponatraemia
Symptoms - likely if sodium is 125 mmol/L or less
- Weakness, lassitude, headache, nausea.
- Confusion, convulsions, coma.
- Some patients may have no symptoms, especially if hyponatraemia is chronic.
Causes
- These are many and varied.
- Remember to consider factitious causes:
- Laboratory error - check anion gap and calculate osmolarity [(2 x Na) + urea + glucose] (all mmol/L).
- Hypertonic hyponatraemia is commonly seen with hyperglycaemia and reflects osmotic shifts of water from the intracellular to extracellular space.
- Drip arm specimen.
- Pseudohyponatraemia (hyperlipidaemia or hyperproteinaemia). You may need to get a direct reading of sodium (contact Biochemistry).
Approach to Hyponatraemia
Always try to assess whether the patient is volume deficient, normal or volume expanded. A good history from the patient (or the family) is important in assessing the likelihood of plasma volume depletion (e.g., history of poor salt intake, nausea, vomiting, diarrhoea, recent use of thiazide diuretic).
Assessment of Plasma Volume Status in Hyponatraemia
Volume Deficient
- History:
Renal or GI losses, burns, third space losses, diuretic use, aldosterone deficiency, cerebral salt wasting, history of heart failure, cirrhosis.
- Examination:
Volume contraction with low JVP and postural hypotension, or signs of congestive heart failure or cirrhosis
- Laboratory:
Hypo-osmolar plasma, hypo or hyperosmolar urine, urine Na <20 mmol/L (not if recent diuretics, tubular disorders, or cortisol deficient), normal or raised uric acid, urea, creatinine
Normal or Volume Expanded
- History:
Excess water ingestion, potomania (excess beer drinking), recent surgery / trauma / pain, thiazide diuretics, renal failure, SIADH (pulmonary; neurological; thyroid/adrenal insufficiency; drugs - DDAVP, oxytocin, SSRIs, tricyclics, vincristine, NSAIDs, carbamazepine).
- Examination:
Normovolaemic clinically. No postural BP fall. JVP not low.
- Laboratory:
Hypo-osmolar plasma, inappropriately concentrated urine (>100 mmol/kg), urine Na >20 mmol/L (not if water restricted), reduced uric acid, urea, creatinine.
Notes:
Management of Hyponatraemia
The brain gradually adapts to hypo-osmolality thus the presence or absence of symptoms gives some guide to chronicity and appropriate treatment. Thus rapid correction of chronic severe hyponatraemia in the 'adapted' asymptomatic patient may result in osmotic demyelination (pontine myelinolysis). Conversely, the symptomatic patient with hyponatraemia warrants urgent correction of plasma sodium (maximum increase 8-12 mmol/day) to 125-130 mmol/L.
- Withdraw inappropriate drugs.
- Exclude deficiencies of thyroid or adrenal function (FT4, TSH, Synacthen test).
- Whatever the cause, treatment and monitoring is needed if plasma sodium <130 mmol/L.
- If volume deficient give sodium chloride 0.9% IV provided congestive heart failure/cirrhosis excluded.
- If not volume deficient (e.g., SIADH), main treatment is water restriction (500-1000 mL/day; allow water intake equal to urine output). Ensure adequate sodium and potassium intake (IV saline may be needed especially if plasma sodium <120 mmol/L). Oral sodium supplements may be useful (Slow Sodium™ - 10 mmol sodium per tablet, 4-6 tablets daily) - consult Endocrinology.
- In all cases aim to restore plasma sodium to 125-130 mmol/L. The speed of correction depends on presence of symptoms and careful monitoring of clinical state and sodium level is required. In the symptomatic patient, the initial rate of correction can be 1-2 mmol/L per hour for several hours.
- Severe hyponatraemia may be life-threatening (e.g., coma or convulsions) and may require hypertonic 3% saline. Infuse 1-2 mL/kg body weight/hour and check plasma sodium every 2-4 hours to guide therapy. Consult Endocrinology before use.
- Investigate and treat underlying cause.
Topic Code: 1381