Acute metabolic derangements - hypo- and hypernatraemia
Description
- Sodium concentration is a water problem, not a sodium problem
- Total body sodium determines volume status; water handling determines the concentration
- Both disorders are almost always disorders of ADH and of thirst/water access
Hyponatraemia
- Na <135; severe <125. Symptoms track the rate of fall, not the absolute value
- Mild: nausea, headache, unsteadiness, falls, poor concentration
- Severe: vomiting, confusion, seizures, coma, respiratory arrest (cerebral oedema)
- Chronic "asymptomatic" hyponatraemia still causes falls, fractures and osteoporosis
Hypernatraemia
- Na >145. Almost always inadequate water intake - the thirsty patient who cannot reach a glass
- Thirst, lethargy, irritability, weakness, seizures, coma
Epidemiology
- Hyponatraemia: the commonest electrolyte abnormality - 15-30% of hospital inpatients
- SIADH accounts for ~1/3 of inpatient hyponatraemia
- Independently associated with inc mortality across almost every diagnosis
- Hypernatraemia: ~1-3% of admissions, mostly elderly, dependent, or ICU; community-acquired hypernatraemia in a frail person carries mortality up to 40%
Aetiopathogenesis
Hyponatraemia - work in three steps
- 1. Is it truly hypotonic? Measure serum osmolality
- Normal osm = pseudohyponatraemia - severe hyperlipidaemia or paraproteinaemia (artefact of indirect ion-selective electrodes; direct ISE/blood gas gives the true value)
- High osm = translocational - hyperglycaemia (correct ~2.4 mmol/L Na per 10 mmol/L glucose above normal), mannitol, glycine irrigation
- In DKA the sodium is "diluted" by osmotic water shift - total body sodium is normal or high
- 2. Volume status
- 3. Urine sodium and urine osmolality
| Volume | Urine Na | Causes |
|---|---|---|
| Hypovolaemic | <20 | GI losses, burns, third-spacing, pancreatitis |
| Hypovolaemic | >20-30 | Diuretics (thiazide), mineralocorticoid deficiency, salt-wasting nephropathy, cerebral salt wasting |
| Euvolaemic | >30-40 | SIADH, glucocorticoid deficiency, hypothyroidism, non-osmotic ADH release (pain, nausea, stress, post-operative) |
| Euvolaemic | <20 | Primary polydipsia, beer potomania, "tea and toast" (low solute intake) - urine osm is also low, <100 |
| Hypervolaemic | <20 | Cardiac failure, cirrhosis, nephrotic syndrome |
| Hypervolaemic | >20 | Renal failure |
- Thiazides are the classic drug cause - act distally, so concentrating ability is preserved (unlike loop diuretics, which rarely cause hyponatraemia)
Causes of SIADH
- Malignancy - small cell lung cancer above all; head and neck, others
- Pulmonary - pneumonia, TB, abscess, positive pressure ventilation
- CNS - stroke, haemorrhage, meningitis, trauma, tumour, GBS
- Drugs - SSRIs, carbamazepine/oxcarbazepine, TCAs, antipsychotics, MDMA, cyclophosphamide, vincristine, NSAIDs, PPIs, desmopressin
- Pain, nausea, surgery - the commonest inpatient trigger and the most reversible
- Nephrogenic syndrome of inappropriate antidiuresis - gain-of-function V2 receptor, ADH undetectable**
Hypernatraemia
- Water deficit - impaired thirst or access (elderly, dementia, intubated, infants), hypodipsia from hypothalamic lesion
- Renal water loss - AVP deficiency (cranial DI) or resistance (nephrogenic DI), osmotic diuresis (glucose, urea, mannitol), post-obstructive diuresis
- Non-renal water loss - diarrhoea (commonest in children), burns, fever, sweating
- Sodium gain - hypertonic saline, sodium bicarbonate, salt poisoning, primary hyperaldosteronism (mild only)
Diagnosis
Essential first tests
- Serum osmolality, urine osmolality, urine sodium - simultaneously, before any fluid is given
- Volume assessment; TSH and 09:00 cortisol in every euvolaemic hyponatraemia
SIADH - diagnostic criteria (Bartter-Schwartz)
- Effective plasma osmolality <275 mOsm/kg
- Urine osmolality >100 mOsm/kg despite hypotonicity
- Clinical euvolaemia - no oedema, no postural drop
- Urine sodium >40 mmol/L on normal salt and water intake
- Normal thyroid and adrenal function
- No recent diuretic use
- Supportive: low urate, low urea, fractional Na excretion >1%, fractional urea excretion >55%
- No correction with 0.9% saline; corrects with fluid restriction (giving saline to SIADH can lower the sodium further - the salt is excreted and the water retained)
Distinguishing traps
| SIADH | Cerebral salt wasting | Hypovolaemic | |
|---|---|---|---|
| Volume | Euvolaemic | Hypovolaemic | Hypovolaemic |
| Urate | Low | Low | Normal |
| Response to saline | None/worse | Improves | Improves |
- Cerebral salt wasting is over-diagnosed - it needs genuine, documented volume depletion in the setting of intracranial disease
Hypernatraemia
- Paired serum and urine osmolality
- Urine osm >600-800 with high serum Na -> appropriate renal response: extrarenal loss or inadequate intake
- Urine osm <300 -> diabetes insipidus (see AVP deficiency and AVP resistance)
- Urine osm 300-600 -> partial DI or osmotic diuresis (check urine glucose and urea)
Management
Hyponatraemia - severity decides, not aetiology
### A. Severe symptoms (seizure, coma, vomiting, GCS drop) - treat before diagnosing
- Hypertonic 3% saline: 100-150 mL IV bolus over 10-20 min, repeat up to 3 times
- Target an immediate rise of 4-6 mmol/L - that is enough to stop seizures and reverse herniation
- Rapid intermittent bolus is now preferred to a continuous infusion - as effective, less overcorrection
- Recheck sodium after each bolus
### B. The correction limit - the thing that kills
- *Maximum 8-10 mmol/L in 24 h, and <=18 mmol/L in 48 h*
- <=8 mmol/L/24h if high risk of osmotic demyelination: Na <=105, hypokalaemia, alcoholism, malnutrition, advanced liver disease
- Anticipate auto-correction: once the stimulus is removed (fluid replaced, drug ceased, cortisol given), ADH switches off and a water diuresis overshoots
- Watch for a sudden rise in urine output with dilute urine
- Rescue: desmopressin 1-2 microg IV +/- 5% dextrose to re-lower the sodium - this works and should not be delayed
- Osmotic demyelination presents 2-6 days later: dysarthria, dysphagia, quadriparesis, locked-in syndrome. Often irreversible
### C. By cause
- Hypovolaemic - 0.9% saline, stop diuretic, treat the loss
- Hypervolaemic - fluid AND salt restriction, treat the heart/liver/kidney disease, loop diuretic; tolvaptan for refractory cases
- SIADH
- Fluid restriction 500-1000 mL/day first line - fails in almost half
- Predictors of failure: urine osmolality >500, urine Na + K > serum Na, urine output <1.5 L/day
- Remove the cause - drug, pain, nausea
- Second line: oral urea 15-30 g/day (osmotic diuresis; well tolerated, cheap) or tolvaptan (V2 antagonist)
- Tolvaptan corrects faster; both overcorrect - urea in up to 14-37% depending on baseline severity, so monitor sodium 6-hourly on starting
- Do not fluid-restrict while on tolvaptan; hepatotoxicity limits duration
- Salt tablets + loop diuretic as an alternative
- Fluid restriction 500-1000 mL/day first line - fails in almost half
- Adrenal insufficiency - hydrocortisone. Hypothyroidism - thyroxine
Hypernatraemia
- Calculate the free water deficit: `0.6 (0.5 in women/elderly) x weight x (Na/140 - 1)`
- Restore circulation first with isotonic fluid if shocked, then replace water with 5% dextrose or enteral water
- Correct no faster than 10-12 mmol/L per 24 h (<=0.5 mmol/L/h); chronic hypernatraemia slower
- Too-fast correction -> cerebral oedema and seizures - the mirror image of ODS
- Add ongoing losses to the deficit - the calculation always underestimates
- Treat the cause: desmopressin for AVP-D, stop the offending drug, relieve obstruction, ensure water access
Associations
- Small cell lung cancer - SIADH; also ectopic ACTH
- SSRIs and thiazides in the elderly - the two commonest drug causes; check the sodium 2 weeks after starting either
- Marathon running and MDMA use - exercise-associated hyponatraemia from excess hypotonic intake plus non-osmotic ADH
- Chronic hyponatraemia -> falls, fractures, osteoporosis (bone releases sodium), gait and attention deficits
- Beer potomania and "tea and toast" - low solute intake limits free water excretion
- Adrenal insufficiency, hypothyroidism - always exclude before labelling SIADH
- Hypernatraemic dehydration in infants - diarrhoea, breastfeeding failure
Natural history & complications
- Acute (<48h) hyponatraemia -> cerebral oedema - the brain has not yet extruded organic osmolytes
- Chronic (>48h) hyponatraemia -> brain adapted -> fewer symptoms but far greater risk from rapid correction
- Osmotic demyelination syndrome - 2-6 days after overcorrection; central pontine and extrapontine; often permanent
- Hypernatraemic dehydration -> brain shrinkage tears bridging veins -> subdural and intraparenchymal haemorrhage (classically in infants with diarrhoea or burns)
- Hyponatraemia is an independent marker of severity in heart failure, cirrhosis and pneumonia - correcting the number does not correct the prognosis
- SIADH from a reversible cause resolves in days; paraneoplastic SIADH tracks the tumour
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