Disorders of sodium and water: hyponatraemia and hypernatraemia

Assessment— look, ask, measure

• Understand what you are measuring: the plasma sodium is a ratio — exchangeable sodium plus potassium divided by total body water — so a disorder of the plasma sodium is almost always a disorder of water balance, not of salt balance; a patient at 118 mmol/L may have a total body sodium that is low, normal or frankly increased.
• Hyponatraemia is a plasma sodium below 135 mmol/L, the commonest electrolyte abnormality in practice, occurring in up to 22% of hospitalised patients with some series reporting that up to 35% of inpatients develop it during admission; graded mild 130–134 mmol/L, moderate 125–129 mmol/L and severe below 125 mmol/L (Davidson's uses below 124 mmol/L for severe).Not available at your setup — Serum electrolytes.
• Duration matters more than depth: acute means present for less than 48 hours, chronic means longer — roughly how long the brain takes to adapt to hypotonicity and to reverse the adaptation. The single most useful piece of history is the date of the last normal plasma sodium. When duration is unknown, treat as chronic.
• Hypernatraemia is a plasma sodium above 145 mmol/L, always implying hyperosmolality and nearly always a deficit of water rather than an excess of sodium; it is much less common but is associated with mortality of up to 40–60%.Not available at your setup — Serum electrolytes.
• Ask the brain question first — the only thing that justifies emergency treatment: seizure; coma, obtundation or a falling Glasgow Coma Scale score; vomiting with headache and drowsiness; or cardiorespiratory distress or respiratory arrest. Their absence is what permits slow, calculated correction, however alarming the number.
• The number alone never places a patient in the emergency category, and never keeps them out of it: a patient who has fallen from 140 to 126 mmol/L in twelve hours after transurethral resection may be convulsing, while one who has lived at 118 mmol/L for six months on a thiazide may be ambulant and merely tired.
• Map the symptom ladder onto the grade: mild 130–134 mmol/L usually none (but in the elderly, increased falls risk and subtle cognitive impairment even here); moderate 125–129 mmol/L nausea without vomiting, headache, unsteadiness, impaired concentration, delirium; severe below 124–125 mmol/L vomiting, cardiorespiratory distress, somnolence, seizures, coma, respiratory arrest.
• Assess extracellular volume status clinically, because it determines treatment: postural drop, dry axillae and mucous membranes and reduced turgor for hypovolaemia; oedema, raised JVP, ascites and crackles for hypervolaemia; neither for euvolaemia.
• Read the drug chart and the fluid chart first — most sodium disorders encountered in hospital were caused there: thiazides (much the most important single drug cause), SSRIs and other antidepressants, carbamazepine, antipsychotics, cyclophosphamide, opiates, chlorpropamide, oxytocin and desmopressin, NSAIDs, proton-pump inhibitors, MDMA, and hypotonic maintenance fluid.
• Exclude the two false hyponatraemias before treating: pseudohyponatraemia (a laboratory artefact of severe hyperlipidaemia or hyperproteinaemia, tonicity normal, no treatment required) and hypertonic or translocational hyponatraemia (glucose or mannitol drawing water out of cells — treat the glucose, not the sodium). True hypotonic hyponatraemia has an effective osmolality below 275 mOsm/kg.Not available at your setup — Serum electrolytes.
• Correct for glucose: plasma sodium falls by approximately 1.6–2.4 mmol/L for every 5.6 mmol/L (100 mg/dL) rise in glucose, and this variety resolves with treatment of the hyperglycaemia; cerebral oedema does not occur in hypertonic hyponatraemia because intracellular volume is reduced rather than increased.
• Score the risk of osmotic demyelination before you correct anything: sodium below 120 mmol/L, alcohol use disorder, chronic liver disease, malnutrition or cachexia or anorexia nervosa, hypokalaemia especially below 3.0 mmol/L, hypoxaemia and previous cranial irradiation. A malnourished patient with alcohol use disorder, a sodium of 108 mmol/L and a potassium of 2.4 mmol/L is the archetype of iatrogenic brain injury.Not available at your setup — Serum electrolytes.
• Send a paired urine sodium and osmolality before any fluid or diuretic — the single most informative test and the one most often omitted — with serum osmolality, glucose, urea, urate, potassium, magnesium, calcium, phosphate, liver function, cortisol and thyroid function.Not available at your setup — Serum electrolytes, Liver function tests.
• In hypernatraemia the first aetiological question is always why could this person not drink: the frail or demented elderly patient, the sedated or intubated patient, dysphagia after stroke, the infant, the patient kept nil by mouth, or the rare patient with hypodipsia from a hypothalamic lesion — thirst is blunted in old age.
• Recognise severe hypernatraemia: above 160 mmol/L causes lethargy, irritability and weakness progressing to hyperthermia, delirium, seizures and coma, with irreversible neurological damage if untreated; look also for dry mucous membranes, reduced turgor, sunken eyes, tachycardia, postural hypotension and oliguria, remembering that the circulation is defended and the patient may look less unwell than the biochemistry suggests.
• Know the two paediatric traps: in children the brain occupies a larger fraction of the intracranial volume so hyponatraemic encephalopathy occurs at higher sodium values and progresses faster (a child may herniate at a concentration that would leave an adult merely nauseated); and the infant with hypernatraemic dehydration from gastroenteritis or inadequate breastfeeding in the first fortnight of life has characteristic doughy skin with relatively preserved perfusion — a reassuring-looking circulation that is a trap.