4. Sodium fluid balance Flashcards
What is the usual reference range for serum sodium?
135-145mmol/L
What is the serum sodium range for hyponatraemia?
<135mmol/L
What is the most common electrolyte abnormality in hospitalised patients?
Hyponatraemia
What is the underlying pathogenesis of hyponatraemia?
Increased cellular water. Water balance is controlled by vasopressin (ADH) released from posterior pituitary and acts on the V2 receptors in collecting duct cells to increase water retention by increasing AQP-2 channel insertion.
Where are V1 receptors found and what does it do?
Found in vascular smooth muscle and causes vasoconstriction at higher concentrations.
What are the 2 main stimuli for secretion of ADH?
Serum osmolality mediated by hypothalamic osmoreceptors. Blood volume or pressure mediated by baroreceptors in carotids, atria and aorta.
How does increased ADH secretion affect serum sodium
Decreases
First assessment of a patient with hyponatraemia is to clinically assess volume status. What would you notice on examination?
O/E: tachycardia, low BP, dry mucous membranes, reduced tissue turgor, confusion, drowsiness, reduced urne sodium output (<20 - reliable way of telling that this is hypovolaemia as the kidneys are trying to retain fluid). NOTE: If the patient is on diuretics they will have high urine sodium regardless.
Clinical features of hypervolaemia
Raised JVP, bibasal crackles, peripheral oedema
Causes of hyponatraemia
Common cause of low sodium is hypervolaemia.
Renal cause: diuretics.
Extra-renal causes: diarrhoea, vomiting.
Other causes: cardiac failure (low cardiac output, low BP), cirrhosis, renal failure
What are causes of hypovolaemic hyponatraemia?
Diarrhoea, vomiting, diuretics, salt losing nephropathy
What are causes of euvolaemic hyponatraemia?
Hypothyroidism, adrenal insufficiency, SIADH
What are causes of hypervolaemic hyponatraemia?
Cardiac failure, cirrhosis, nephrotic syndrome
How does diarrhoea and vomiting cause hypovolaemic hyponatraemia?
Hypovolaemic patients still have excess water. D+V leads to a loss of salt and water. This leads to low perfusion pressure and consequently increased ADH release. The patient will then reabsorb more water than salt leading to hyponatraemia.
Why is there hyponatraemia in cirrhosis?
It leads to the release of various vasodilators like nitric oxide which lower blood perfusion pressure.
What investigations to do for a patient with hyponatraemia who is euvolaemic?
Hypothyroidism -> thyroid function tests; adrenal insufficiency -> short synacthen test; syndrome of inappropriate ADH (SIADH) -> low plasma osmolality, high urine osmolality
What are causes of SIADH?
CNS pathology, lung pathology (e.g. lung tumour secreting ADH), drugs (e.g. SSRIs, TCA, opiates, PPIs, carbamazepine), tumours, surgery
A diagnosis of SIADH is only made if:
No hypovolaemia, no hypothyroidism, no adrenal insufficiency, reduced plasma osmolality AND increased urine osmolality (>100)
How does euvolaemic hyponatraemia work?
The initial increase in ADH release will cause water retention. Then atrial expansion caused by increased circulating volume will lead to atrial natriuretic peptide (ANP) release causing sodium (+water) loss.
Management of hypovolaemic hyponatraemia
Volume replacement with 0.9% saline to replenish circulating fluid volume to normal levels and switch off the stimulus for ADH release.
However, you need to be sure that the patient is in fact hypovolaemic because giving 0.9% saline to euvolaemic patient can worse hyponatraemia.
Management of hypervolaemic hyponatraemia
Fluid restriction and treat underlying cause
Management of euvolaemic hyponatraemia
Fluid restriction and treat underlying cause
How does severe hyponatraemia present?
Reduced GCS, seizures
How to manage severe hyponatraemia?
Requires expert help, treat with hypertonic 3% saline. When treating hyponatraemia, serum sodium should NOT be corrected too rapidly as it can cause osmotic demyelination (central pontine myelinosis).
What does osmotic demyelination (central pontine myelinosis) lead to?
Quadriplegia, dysarthria, dysphagia, seizures, coma and death. These Sx only manifest a few days after sodium has been corrected too quickly, by which point it is too late and cerebral damage has been done.
How to treat SIADH?
If water restriction is insufficient, give demeclocycline, which reduces responsiveness of collecting tubule cells to ADH. Monitor U+Es for in case there is a risk of nephrotoxicity.
Could give tolvaptan,
V2 receptor antagonist – causes aquaresis, loss of water without salt
What is the serum sodium range for hypernatraemia?
> 145mmol/L
What are the main causes of hypernatraemia?
Unreplaced water loss. This includes GI losses (common), sweat losses. Renal losses e.g. osmotic diuresis, reduced ADH release or action (diabetes insipidus). NOTE: tends to happen in patients who don’t drink when they are dehydrated e.g. elderly, children
Investigations for diabetes inspidus
Serum glucose 🡪 exclude diabetes mellitus
Serum potassium 🡪 exclude hypokalaemia.
NOTE hypokalaemia can induce a nephrogenic diabetes insipidus
Serum calcium 🡪 exclude hypercalcaemia
Plasma and urine osmolality
Water deprivation test
What is Tx for hypernatraemia?
Fluid replacement -> use dextrose as this replaces fluid without giving excess salt. Treat underlying cause. Take serial Na+ easurements, every 4-6 hours.
What to do if someone is hypovolaemic and hypernatraemic?
You may initially give 0.9% saline to treat hypovolaemia followed by dextrose for the hypernatraemia. Take serial Na+ easurements, every 4-6 hours.
How can diabetes mellitus affect serum sodium?
Variable effects on serum sodium depending on dominating mechanisms. Hyperglycaemia will draw water out of cells leading to hyponatraemia
However, osmotic diuresis in uncontrolled diabetes leads to loss of water and hypernatraemia.
