Dear Phil,
It depends why they are on TPN. However it is extremely rare for post
op patients to be sodium depleted, even with fistulae: the majority
have sodium overload. Serum sodium does not tell you how much sodium is
in you patient and hyponatraemia is very common in fluid and sodium
overloaded patients. This is not an easy problem to solve but here are
some suggestions:
See if the patient is clinically oedematous: do they have pitting
oedema in ankles or wrists, crackles in the chest? If they are
oedematous they have too much sodium and fluid in the interstitial
space. Sodium deficiency is almost impossible under these
circumstances. An extremely common cause is fluid and NaCl overload
causing the hyponatraemia. (remember tissue perfusion is compromised in
oedematous patients, and sick cells allow sodium in and potassium out).
Common scenarios are a combination of fluid overload (including NaCl)
and heart failure. The approach is to off load the fluid and NaCl e.g.
with diuretics and limit water and NaCl input. The patient should get
better and the serum sodium rise as they lose the fluid and sodium from
the interstitial oedema and cells and organs (especially heart lungs and
kidneys) start to work better
Check the fluid balance chart paying particular attention to the sodium
input. Remember a normal person only needs about 60-100 mmol/24 hr of
sodium. I bet your patients have had received much more than this.
NOTE apart form 5% dextrose almost all iv fluids have lots of sodium and
chloride: especially 0.9% ABnormal saline (154 mmol/l of both Na and
Cl) So for example 2L of ABnormal saline gives the patient 308 mmols of
NaCl equivalent to 3-4 days intake in a normal person. Sodium loading
leads to simultaneous water loading because the body tries to keep the
osmolality of the ECF constant.
OK so there are GI losses, is the patient hypovolaemic? (low BP,
postural hypotension (if they can stand up) rapid pulse, poor urine
output and increasing serum urea with near normal creatinine) If they
are, then consider filling the vascular space with a colloid which will
remain in the vascular space in an ill patient (medium Mol wt
hydroxyethyl starch) as well as red cells etc if needed. You cannot
effectively treat hypovolaemia with ABnormal saline or Hartmanns
solutions: they leak into the interstitium and make the oedema even
worse.
Daily urine U/E is essential for managing these patients. If you are
successfully mobilising oedema you should have a massive naturesis -
high urine sodium is usually good sign under thee circumstances. Low
urine sodium suggest under renal perfusion due for example to
hypovolaemia, heart failure or occasionally severe intrarenal oedema.
Good luck
Peter
Peter Gosling BSc MSc PhD FRCPath
Consultant Clinical Scientist and Honorary Senior Clinical Lecturer
Clinical Biochemistry
Selly Oak Hospital
University Hospital Birmingham NHS Trust
Birmingham B29 6JD
Tel 0121 627 1627 Ex 52272
Mobile 07771647586
-----Original Message-----
From: Clinical biochemistry discussion list
[mailto:[log in to unmask]] On Behalf Of Wills Philip
(Queen Elizabeth Hospital NHS Trust)
Sent: 23 November 2005 16:10
To: [log in to unmask]
Subject: [Maybe spam]80% high Old chestnut
Does anyone have any working experience of biochemical
monitoring of patients on parenteral nutrition? A frequent
finding recently in many patients in this hospital is
continuing hyponatraemia (<130mmol/L) with or without
abnormal potassiums. It ought to be easy to assess whether it
is primary sodium loss or water retention but with so many
variables that is not always so.
For example, somebody with a fistula (or fistulae) in small
and large bowel, losing maybe 1.5+ litres, taking (variable
volumes of) dioralyte and various sips as well as IV 2L PN
and 2L 0.9% NaCl and alternating daily positive/negative
fluid balances .CVP doesn't seem to be helpful nor are
osmolalities.Electrolyte measurements on drainage fluids are
not technically possible. Everything is a moving feast (bad
pun).
Does anyone have a "magic formula", as our Dieticians are
always very anxious to give additional sodium by means of
altering the "Kabi" prep. or flow rate but I'm not always so
sure. This replacement would be over and above that provided
by the "Kabi" formula that meets their daily nutritional
requirements.
I know we should treat the patient and not the numbers, but
if we do treat the numbers, do we add sodium or take water
away?Or shoud we leave "well" alone? These patients do not
seem to obey the rules, which we find easier in non-PN
patients.What do other colleagues advise? Any observations or
protocols would be much appreciated. Thanks, Phil Wills QEH
Woolwich
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