Dear Mohmed Ashmaig,
A possible explanation is as follows:
* Administration of large volumes of iv fluids with each visit to
theatre most of which contain 130-150 mmol/L of sodium.(Colloids, Ringers,
human albumin, plasma etc)
* Stress response due to severe illness and surgery causes sodium
retention (aldosterone release and inhibition of natriuretic peptides)
* Insensible losses of water but not sodium (e.g. pyrexia and
mechanical ventilation)
* Recognition of fluid overload: (e.g. pulmonary oedema but often too
late) and attempts to fluid restrict makes hypernatraemia worse
* Failure to realise that critically ill patients require larger than
normal urine volumes to excrete sodium and nitrogen because of reduced
renal concentrating ability.
* Increased osmotic load due to nitrogen losses (catabolism, sepsis
and melena in this case) compromises ability to excrete the large iv sodium
load usually given to surgical and ICU patients
The end result is an excessive accumulation of sodium which cannot be easily
excreted, especially if there is renal impairment.
Suggestions for treatment:
Haemofiltration: particularly if renal failure is a problem (was creatinine
of 68 umol/L without haemofiltration or dialysis ?)
Restrict sodium input as much as possible (Watch out for hidden sodium
sources e.g. antibiotics)
Increase free water input as much as possible (e.g.enteral water and/or iv
5% dextrose )
Measure urine sodium potassium, urea and osmolality, and try to promote a
diuresis, aiming for a significant negative sodium balance with urine
osmolality 500 mosm/kg or less.
If the patient is not hypovolaemic and haemodynamically stable, consider a
loop diuretic with low sodium fluid replacement
Caution, do not lower ECF sodium too rapidly, because of the risk of
cerebral oedema: opinions vary as to how fast, probably 2-4 mmol/L/24
hours if hypernatraemia is chronic seems sensible.
Good luck
Peter Gosling
Clin Biochem
University Hospital Birmingham
Birmingham UK
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