SEPT 10 Built from the handwritten pages you uploaded on 10 September 2026.
Sodium & fluid compartments
The 42-litre man, the water deficit calculation, and SIADH versus cerebral salt wasting.
Body fluid compartments — the 70 kg adult
Where infused fluid goes
5% dextrose — the glucose is metabolised, leaving free water that distributes across all 42 L. Only about 1/14 stays intravascular. Useless for resuscitation.
0.9% saline / Hartmann's — distributes through the extracellular 14 L, so about a quarter stays intravascular.
Colloid — in theory stays intravascular, but a damaged glycocalyx in sepsis lets it leak.
Water deficit
Water deficit (L) = 0.6 × weight (kg) × [ (measured Na⁺ / normal Na⁺) − 1 ]
Use 0.6 for men, 0.5 for women and the elderly, 0.45 for elderly women. Normal Na⁺ is taken as 140.
Worked example: a 70 kg man with Na⁺ 160 → 0.6 × 70 × (160/140 − 1) = 42 × 0.143 = 6 L deficit.
Replace slowly. Correct hypernatraemia at no more than about 10 mmol/L per 24 hours, or the brain — which has adapted by generating idiogenic osmoles — will swell.
Remember this is the free water deficit only; add ongoing losses and any separate volume deficit on top.
SIADH vs cerebral salt wasting
Both present after neurosurgery, subarachnoid haemorrhage or head injury with hyponatraemia, urine osmolality > 100 and serum osmolality < 280. The biochemistry alone will not separate them.
SIADH
Cerebral salt wasting
Volume status
Normovolaemic
Dehydrated / hypovolaemic
Urine sodium
> 30 mmol/L
>> 30 mmol/L — markedly raised
Urine output
Low or normal
HIGH
Urine osmolality
> serum osmolality
> serum osmolality
24 h urinary Na⁺
Normal
Raised
CVP / haematocrit / urea
Normal or low
Low CVP, raised haematocrit and urea
Primary problem
Water retention
Salt loss (natriuretic peptides)
Treatment
Fluid restriction · demeclocycline · vaptans
Salt and volume replacement · fludrocortisone
Why the distinction matters so much
The treatments are opposites. Fluid restricting a salt-wasting patient after subarachnoid haemorrhage worsens hypovolaemia and precipitates cerebral vasospasm and infarction.
Volume status is the discriminator — assess it clinically and with CVP, haematocrit, urea and urine output, not from the sodium alone.
Urine output is the most useful single bedside clue: high in CSW, low or normal in SIADH.
Treating symptomatic hyponatraemia
Seizures or a falling GCS demand hypertonic saline, whatever the cause. 3% NaCl, aiming to raise sodium by 4–6 mmol/L to stop the seizure — not to normalise it.
3% NaCl at about 100 ml/h, or a correction of 6–8 mmol/L in 24 hours where symptoms are milder.
Do not exceed 8–10 mmol/L per 24 hours in chronic hyponatraemia — osmotic demyelination (central pontine myelinolysis) is the consequence, and it is irreversible.
Acute hyponatraemia (under 48 hours, as in TURP syndrome or exercise-associated) tolerates faster correction, because the brain has not yet adapted.
Quick recall
42 L = 28 ICF + 14 ECF
ECF = 11 interstitial + 3 plasma
0.6 × wt × (Na/140 − 1)
SIADH euvolaemic · restrict
CSW dry · high UO · give salt
<8–10/day or demyelination
Built from your body fluid compartments and SIADH/CSWS pages. See also Renal physiology.