Hyponatraemia

Question 1

is low sodium always drug induced

Answer 1

No - we should not always go in stopping drugs

Question 2

Where sodium goes……’ ‘ follows…..

Answer 2

water

Question 3

Sodium homeostasis is controlled by

Answer 3

• posterior pituitary (via ADH)
• kidneys (via aldosterone)
• brain
• cardiovascular system (via ANP/BNP)

Question 4

what is the plasma osmolality equation

Answer 4

(2 x (Na + K)) + urea + glucose

sodium is the main extracellular cation in the body and serves as the main plasma osmolyte

normal range 275-205 mosm/kg

Question 5

What is isosmolar hyponatraemia

Answer 5

• Low [Na+] but no change in osmolality

- can be due to a laboratory error or an appropriate physiological response

Question 6

What is hyperosmolar hypontraemia

Answer 6

• Increased osmolality despite low [Na+]

- Due to physiological compensatory mechanisms being overwhelmed

Question 7

What is hypos molar hyponatraemia

Answer 7

• Decreased osmolality in line with low [Na+]

- this is true hyponatraemia

Question 8

Isosmolar hyponatraemia - two reasons for this

Answer 8

lab error - A sodium reading for example 140 is 140 per litre of total blood volume. But actually the sodium can only be in 93% of our blood volume because the other 7% is cells etc.
if a patient has raging hypertryglyceridaemia the amount of blood volume that sodium can be in drops below 93%. So we may have a low sodium reading but actually it is fine because the volume it can be in has dropped. This is very rare

An appropriate physiological response - 
osmolality equation ( 2 x (Na + K)) + urea + glucose.
So if the glucose increases substantially due to DKA for example then the sodium will fall in order for the body to maintain osmolality. So we treat the DKA and everything should resolve. The only thing that would really increase here to effect the equation is glucose.

Question 9

Hyperosmolar Hyponatraemia

Answer 9

Osmolality high but sodium is low.

• Our boys physiological compensatory mechanisms responsible for maintaining serum osmolality becoming overwhelmed. This may happen is HHS.
• The body cannot compensate by lowering sodium. This is quite rare

Question 10

Hyposmolar hyponatraemia - true hyponatraemia

Answer 10

Must identify the cause.

Need to consider:

• volume status of the patient
• urine osmolality
• urine sodium

There are three types: hypovolaemic, hypervolaemic, euvolaemic.

Question 11

What is hypovolaemic hyposmolar hyponatraemia?

Answer 11

Patient is dehydrated
They are losing sodium faster than they are losing water
Can be caused by:
- V&D (urine sodium <10mmol/L) low shows they are not losing the sodium through urine/kidneys
- XS nature’s (thiazides), aldosterone deficiency or cerebral salt wasting (urine sodium > 20mmol/L) high shows they are losing it through their kidneys

Is it gastric loss or is it renal loss?

Treatment: Normal saline, stop diuretics, antiemetics if vomiting, never fluid restrict as they are volume deplete.

Question 12

What is hypervolaemic hyposmolar hyponatraemia?

Answer 12

Patient is overloaded
They retain water quicker than they retain sodium
-Non renal (CCF/liver failure) - resulting from falling effective circulated volume due to oedema for example which activates ADH and aldosterone
- Renal - kidney failure - inability to remove excess water

The amount of water in the body relative to the amount of sodium increases

Treatment : Fluid restriction, aquaresis (loop diuretic), tolvaptan, treat the underlying disease

Question 13

What is euvalaemic hyperosmolar hyponatraemia

Answer 13

No signs of volume change.

Patient is unable to excrete free water:

• primary polydipsia (psychogenic water intoxication, ecstasy use) - overwhelming the kidneys ability to excrete dilute urine. Kidneys dilute urine as much as possible but there comes a point where they cannot dilute anymore so they start to dilute your body.
• SIADH (inappropriate secretion of ADH) - can be due to drugs (e.g., SSRI’s or carbamazepine), malignancies or diabetes insidious and giving too much desmopressin.

Treatment

• For primary polydipsia - fluid restrict and medicate?
• For SIADH, remove cause (drugs, cancer), fluid restrict, medication (democlocycline, tolvaptan)

The way we differentiate between the two is urinary osmolality. IF we have polydipsia our urine is very very dilute as our kidneys are doing everything they can to ditch the water. If we have SIADH our urine is more concentrate & osmolality or urine will go up.

Question 14

If a patient has been > 48 hours of low sodium how should we correct it….

Answer 14

No more than 12 mmol in the first 24 hours

No more than 18 mmol in the first 48 hours

Unless someone is fitting then we would give hypertonic saline to get >120mmol in range rapidly and then replace more slowly

Question 15

Treatment of SIADH

Answer 15

1) Fluid restriction is first line

2) Demeclocycline + fluid restriction is second line
- Induces nephrogenic diabetes insipidus (body produces enough ADH but kidneys just don’t respond to it)
- initially 0.9-1.2g daily in divided doses, maintenance 600-900mg daily.

3) Tolvaptan is third line
- V2 receptor agonit
- NEVER used in combination with fluid restriction - patient must have access to water to prevent dehydration (it is contraindicated in patients who are unable to perceive thirst)
- consider if renal function is <30ml/min (demeclocycline is usually not used in poor renal function)
- Usually NHS England funded - very expensive £80 per tablet