4. Existing guidance
• Complex
• Difficult to implement -
emphasis on clinical
assessment of volume state
• Fail to place clinical status
above biochemical
parameters
6. Pseudohyponatraemia
• Serum is 7% solid by volume (solid-phase)
• Samples are diluted prior to analysis (reduced
volume of blood needed)
• If solid-phase is elevated same added volume
will have a greater impact on dilution of the
water-phase
7.
8. Clinical proof of
pseudohyponatraemia
• Measure serum osmolality
- non diluted sample
- will be normal if pseudohyponatraemia
• ABG
- sodium is measured in undiluted sample
9. Adjustment for
hyperglycaemia e.g. DKA
• For every 5.5mmol/L increase in
glucose above normal value of
5.5mmol/L add 2.4mmol/ to
measured sodium concentration
- e.g. measured Na = 130mmol/L
with glucose 17mmol/L. Adjusted
Na = 135mmol/L
16. Osmolality:
total vs. effective
• Total osmolality - the concentration of all solutes in
a given weight of water
• Effective osmoles - contribute to water movement
between intra-cellular and extra-cellular
compartments
- urea is an example of an ineffective osmole as it
readily crosses cell membrane and equilibrates
- (2*Na) + K + Glucose
17. Increased effective osmoles
• Draw water into the
circulating volume
• Results in a dilutional
hyponatraemia (i.e. total
sodium normal)
• Effective osmolality is also
termed tonicity
- hence isotonic / hypertonic
hyponatraemia
19. Key features
• Imbalance in homeostasis of water and sodium
• Normally mediated by sodium loss and
vasopressin (ADH) activity
• Consequence is reduced effective osmolality and
hypotonic hyponatraemia
20. Implications of
low effective osmolality
• Inter-cellular compartment becomes relatively
hypertonic
• Osmotic gradient established
• Water shift into cells
• Occurs over 24 - 48 hours
25. Severe symptoms
• Immediate treatment
• 150ml 3% saline i.v. over 20 minutes
• Wait 20 minutes
- send repeat serum sample
- give further 150ml 3% saline
• May require further hypertonic saline
- aim is for 5 mmol/L increase in first hour
26. Severe symptoms
• Improving
- 0.9% saline at lowest possible rate to maintain access
- do not aim for >10 mmol/L increase in first 24 hours
• No clinical improvement
- continue 3% saline
- aim for a 1 mmol/L/hour increase no more than an
overall 10 mmol/L increase or increase to 130 mmol/L
27. Moderate symptoms
• Immediate treatment
• 150ml 3% saline i.v. over 20 minutes
• Wait 20 minutes
- send repeat serum sample
- give further 150ml 3% saline
• May require further hypertonic saline
- aim is for 5 mmol/L (max 10mmol/L) increase in 24 hours
28. “No” symptoms
• Stop provoking factors
• If >10mmol/L acute drop consider 150ml 3%
saline infusion
• Treat cause
• Limit daily increases in Na to <10 mmol/L
29. Improving too quickly
• Expert advice
• Consider 10ml/kg 5% dextrose (over 1 hour)
• Potential role for desmopressin
31. Osmotic demyelination
• Remains a risk but less that cerebral oedema
• Very poor quality data
• Threshold values appear to be >12mmol/L
increase in first 24 hours and >20mmol/L
increase in first 48 hours.
• Risk largely confined to patients with initial value
<120 mmol/L
32. Hyponatraemia Check glucose / K
Are there symptoms? Serum and urine osmolaltiy
Serum >275 - iso /
hypertonic
Serum <275 - hypotonic
MODERATE
1x 150ml 3%
saline
SEVERE
1x 150ml 3%
saline
34. Division by ECF volume
Hypotonic hyponatraemia
Decreased ECF
Normal ECF
Increased ECF
- Non-renal Na loss
- Renal sodium loss
- Third space loss
Kidney disease -
Heart failure -
Liver failure -
Nephrosis -SIADH
Primary polydipsia
(20 adrenal insufficiency)
(Hypothyroidism)
35. Volume status
• Badly assessed in clinicians
• Sensitivity 0.5 - 0.8
• Specificity 0.3 - 0.5
• Hence biochemical parameters used
- urine osmolality
- urinary sodium concentration
36. Urinary osmolality
• If <100mOsm/Kg
Cause is excess water intake
- primary polydipsia
- beer potomania
37. Hyponatraemia Check glucose / K
Are there symptoms? Serum and urine osmolaltiy
Serum >275 - iso /
hypertonic
Serum <275 - hypotonic
MODERATE
1x 150ml 3%
saline
SEVERE
1x 150ml 3%
saline
Urine <100 - water excess
38. Urinary sodium
• If <30 mmol/L there is a physiological attempt to
retain salt and expand the circulating volume
Cause is low effective circulating volume
ECF EXPANDED ECF CONTRACTED
Heart failure D & V
Liver failure
Third space loss
Nephrotic
39. Urinary sodium
• If >30 mmol/L and not in the context of diuretics /
kidney disease
Effective circulating volume is probably normal
ECF CONTRACTED ECF NORMAL
Primary adrenal insufficiency SIAD
Renal salt wasting Small print stuff
- secondary adrenal failure
- hypothyroidismCerebral salt wasting
40. Urinary sodium
• If >30 mmol/L and in the context of diuretics /
kidney disease
41. Hyponatraemia Check glucose / K
Are there symptoms? Serum and urine osmolaltiy
Serum >275 - iso /
hypertonic
Serum <275 - hypotonic
MODERATE
1x 150ml 3%
saline
SEVERE
1x 150ml 3%
saline
Urine <100 - water excess
Urine >100 -
check urinary Na
Na <30 -
Circulating
volume
Na >30 -
?Salt loss / SIAD
43. Pretentious kidney
doctors
• In SIADH vasopressin secretion is independent of
volume / osmolality
• Actions of vasopressin can be increased by gain of
function mutations / factors potentiating effects
• Hence “Syndrome of inappropriate antidiuresis”
is more correct
44. What to do and what
not to do
• DO
- assess SIAD diagnostic criteria
- realise there are lots of causes!
• DON’T
- measure vasopressin (almost impossible to interpret)
- attempt water loading tests (risk of increasing
hypotonicity)
49. Water intake
• Sodium concentration is determined by the relative
amount of extracellular water
• Regulated by intake (thirst) and output (vasopressin)
- anterior hypothalamus sensitive to cell stretch. Reduced
stretch increases thirst and vasopressin.
- persistent thirst vasopressin threshold lower than for thirst
- vasopressin inserts aquaporin-2 channels increasing
water reabsorption from collecting duct
Biochemical definition uses “profound” to avoid confusion with symptomatic classification
Acute and chronic definitions relate to risk for cerebral oedema
Argument is that asymptomatic hyponatreamia does not exist - just very mild symptoms that are not properly assessed….
Limitation here is that acute and chronic symptoms can overlap; clinical picture can rapidly change; symptoms are non-specific and can be ascribed to other conditions
