NephrologyTier 1Disease (DEADMAN)

Electrolyte abnormalities - hypo- and hypernatraemia

Description

Both reflect water balance disorders, not Na+ balance disorders (except rare pure Na+ loss/gain)
Hyponatraemia - relative water excess (Na+ <135 mmol/L)
Hypernatraemia - relative water deficit (Na+ >145 mmol/L)
Classify both by extracellular volume status - hypo/eu/hypervolaemic - this drives management more than the Na+ level itself

Hyponatraemia - commonest electrolyte abnormality in hospitalised patients (~15-20%)
Hypernatraemia - less common, concentrated in patients who cannot access water independently (elderly, infants, ICU)

Hyponatraemia by volume status

Volume status	Causes
Hypovolaemic	GI loss, diuretics (esp. thiazide), cerebral/renal salt wasting, Addison's
Euvolaemic	SIADH, hypothyroidism, glucocorticoid deficiency, psychogenic polydipsia, low solute intake (beer potomania)
Hypervolaemic	Heart failure, cirrhosis, nephrotic syndrome, advanced CKD

SIADH diagnosis: hyponatraemia + urine osm >100 mOsm/kg + urine Na+ >30-40 mmol/L + clinically euvolaemic + normal thyroid/adrenal/renal function
- Causes: malignancy (esp. SCLC), CNS disease, pulmonary disease, drugs (SSRIs, carbamazepine, opioids)

Hypernatraemia

Hypovolaemic - GI/renal/insensible water loss exceeding Na+ loss
Euvolaemic - diabetes insipidus (central or nephrogenic), insensible losses
Hypervolaemic - hypertonic saline/bicarbonate administration
Requires impaired thirst or restricted access to water to become established - rarely develops if both intact

Hyponatraemia work-up

Exclude pseudohyponatraemia (severe hyperlipidaemia/paraproteinaemia) and translocational (hyperglycaemia - correct Na+ by ~1.6-2.4 mmol/L per 5.5 mmol/L glucose above normal)
Serum + urine osmolality, urine Na+, clinical volume assessment, TFT, cortisol
Severity by symptoms, not number alone: moderate (nausea, confusion) vs severe (seizure, coma, respiratory arrest)

Hypernatraemia work-up

Urine osmolality - <300 mOsm/kg despite hypernatraemia = diabetes insipidus
Water deprivation + desmopressin trial distinguishes central from nephrogenic DI

Hyponatraemia - correction rate is the safety-critical number

Severe/symptomatic acute hyponatraemia: 3% hypertonic saline bolus (100-150 mL), repeat if needed until symptoms improve
Maximum correction rate: 8 mmol/L per 24h (10 mmol/L in first 24h as an upper ceiling), lower (<=6-8 mmol/L/24h) if additional risk factors for osmotic demyelination (alcoholism, malnutrition, liver disease, hypokalaemia)
- Over-correction -> osmotic demyelination syndrome - if it occurs, can consider re-lowering Na+ with desmopressin + free water
Chronic, asymptomatic - treat cause: fluid restriction (SIADH), stop offending diuretic, treat heart failure/cirrhosis
Vasopressin receptor antagonists (tolvaptan) - selected refractory euvolaemic/hypervolaemic hyponatraemia; avoid in liver disease (hepatotoxicity) and rapid correction risk

Hypernatraemia

Correct free water deficit slowly - max fall ~8-10 mmol/L per 24h (chronic)
Fluid type by volume status: isotonic first if hypovolaemic, then hypotonic; desmopressin if central DI

Hyponatraemia - falls, fractures (even "asymptomatic" mild hyponatraemia impairs gait/attention), inc mortality marker of underlying illness severity
Hypernatraemia - seizures, intracranial haemorrhage if acute/severe
Both - iatrogenic harm from over-rapid correction is a major preventable complication

Chronic adaptation occurs for both (brain accumulates/loses osmolytes over 48h) - this is exactly why correction rate, not the absolute number, determines neurological safety
Recurrent SIADH - screen for underlying malignancy if no drug/CNS/pulmonary cause found
Osmotic demyelination syndrome - potentially irreversible if it occurs; prevention (slow correction) is the entire strategy, there is no reliable treatment

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