ChemPath: Sodium and Fluid Balance Flashcards
What is the underlying pathogenesis of hyponatraemia?
Excess water - concentration of sodium is lower
Which hormone controls water balance?
ADH (vasopressin)
Describe how ADH controls water balance.
ADH is released from the posterior pituitary gland.
It acts on V2 receptors on collecting ducts causing insertion of aquaporin-2 water channels.
This causes increased water reabsorption.
What receptors may ADH (Vasopressin) work on?
V1 receptors:
- On vascular smooth muscle
- Causes vasoconstriction
- This occurs at higher concentrations
V2 receptors:
- On kidneys
- Insertion of aquaporin-2 channels on collecting ducts
What are the two main stimuli for ADH secretion?
Where are the receptors
- high serum osmolality - mediated by hypothalamic osmoreceptors
- low blood volume/pressure - mediate by baroreceptors in carotids, atria and aorta
What is the effect of increased ADH secretion on serum sodium?
Hyponatremia
(More water = Less sodium)
What is the first step in the clinical assessment of a patient with hyponatraemia?
- Clinical assessment of volume status
- Look at hands
- Head and neck
- Peripheries
What are clinical signs of hypovolaemia?
- Dry mucous membranes
- Reduced JVP
- Reduces tissue turgor
- Tachycardia
- Postural hypotension
- Confusion/drowsiness
- Reduced urine output
- Low urine Na+ (<20)
If you are hypovolaemic, you need to hold onto sodium so urine sodium will be low → always remember to send off this test
hard to differentiate between hypo + euvolemia without urine Na+
What are clinical signs of hypervolaemia?
- Raised JVP
- Peripheral oedema
- Bibasal crackles (on chest examination)
What makes urine sodium uninterpretable?
Diuretics - these alter the kidney’s ability to retain salt. Must stop it and check 48 hours after.
What are causes of hypovolaemia?
- Diarrhoea
- Vomiting
- Diuretics
- Salt losing nephropathy
NOTE: even though patient is hypovolemic the hyponatremia is still due to excess water because the drop in blood volume –> baroceptors –> release ADH –> reabsorb more water
What are causes of euvolaemic hyponatraemia?
- Hypothyroidism
- Adrenal insufficiency
- SIADH
What are causes of hypervolaemic hyponatraemia?
- Heart failure —> reduced CO –> low BP –> detected by baroceptors –> ADH release
- Cirrhosis –> increase NO produced –> splanchnic vasodilation –> low BP –> baroceptors –> ADH released
- Nephrotic Syndrome –> albumin lost in urine –> oncotic pressure lost from blood –> water moves into insteritium –> low BP –> baroreceptors –> ADH released
What are causes of hyponatraemia in a hypovolaemic patient?
- Renal: diuretics
- Extra-renal: diarrhoea, vomiting
What the causes of hyponatraemia in a hypervolaemic patient?
- Cardiac failure
- Cirrhosis
- Renal failure
What are causes of hyponatraemia in a euvolaemic patient?
- Hypothyroidism - due to reduction in CO detected by baroreceptors leading to ADH secretion
- Adrenal insufficiency - cortisol needed for water excretion, aldosterone needed for sodium and water retention.
- SIADH
What are the causes of SIADH?
- CNS pathology - infection, haemorrhage, stroke
- Lung pathology - PE, SCLC, pneumonia, pneumothorax
- DRUGS (SSRI, TCA, opiates, PPIs, carbamazepine)
- Tumours - don’t forget breast exam
- Surgery - acutely due to fluid adminstration during surgery
What investigation is urgently required in suspected SIADH
CT head - to exclude brain/CNS pathology
CXR - to exclude lung pathology
to identify underlying cause - if nothing with these –> CT CAP
What investigations would you order in a patient wih euvolaemic hyponatraemia?
- Hypothyroidism: Thryoid function tests
- Adrenal insufficiency: Short synacthen test
- SIADH: Paired plasma and urine osmolality (low plasma & high urine osmolality)
how does the short synACTHen test work
inject potent synthetic ACTH
if no corresponding rise in serum cortisol –> adrenal insufficiency
Will osmolality of plasma and urine be high or low in SIADH?
Why?
Plasma osmolality - LOW
Urine osmolality - HIGH (>100)
High ADH –> resorbing lots of water
Circulating volume increase –> atria stretches –> ANP release –> excrete more Na+
What does a diagnosis of SIADH require?
- No hypovolaemia - urine Na+ has to be normal
- No hypothyroidism - TFTs normal
- No adrenal insufficiency - rise in cortisol following short synACTHen test
- Reduced plasma osmolality
- Increased urine osmolality (>100)
How would you manage a hypovolaemic patient with hyponatraemia?
Volume replacement with 0.9% saline - this removes the stimulus for ADH secretion
How can saline be used for diagnostic purposes in hyponatremia
Give a very small amount of saline
If Na+ continues to fall –> indicates it is SIADH
If it starts to increase –> indicates its hypovolemic
How would you manage a hypervolaemic patient with hyponatraemia?
Fluid restriction and treat the underlying cause.
Do NOT give saline as the patient will just hold onto the water and exacerbate the hyponatraemia → giving saline won’t address the issue causing ADH secretion if it’s a tumour etc.
How would you manage a euvolaemic patient with hyponatraemia?
Fluid restriction and treat the underlying cause (same as hypervolaemic patient with hyponatraemia)
What are clinical symptoms of severe hyponatraemia?
- Reduced GCS
- Seizures
Seek expert help (treat with hypertonic 3% saline)
How is severe hyponatraemia managed?
Can give boluses of hypertonic 3% saline but only if patient has low GCS or fitting.
DO NOT GIVE 3% saline if alert and orientated.
What is an important point to remember while correcting hyponatraemia?
- Serum Na must NOT be corrected >4-6 mmol/L in the first 24 hours
- Risk of osmotic demyelination (central pontine myelinolysis)
- Presents a few days later with quadriplegia, dysarthria, dysphagia, seizures, coma, death
What is the treatment for SIADH?
Water restriction
PLUS (but both used rarely)
- Demeclocycline - reduces responsiveness of collecting tubule cells to ADH - but caution because nephrotoxic - monitor U&Es
OR - Tolvaptan (V2 receptor antagonist) - use cautiously as they work rapidly
What are the main causes of hypernatraemia?
- Unreplaced water loss
- Gastrointestinal losses, sweat losses
- Renal losses: osmotic diuresis, reduced ADH release/action (Diabetes insipidus/Vasopressin deficiency/resistance)
- Patient cannot control water intake e.g. children, elderly
- Diabetes insipidus
- Not enough ADH
- Resistant to ADH
- Osmotic diuresis in uncontrolled diabetes mellitus
- Loss of water leads to HHS
What investigations would you order in a patient with suspected vasopressin deficiency/resistance?
Prev known as diabetes insipidus
- Serum glucose (exclude diabetes mellitus)
- Serum potassium (exclue hypokalaemia) - low K+ reduces action of ADH (vasopression resistance)
- Serum calcium (exclude hypercalcaemia) - high Ca2+ reduces action of ADH (vasopressin resistance)
- Plasma and urine osmolality
- Water deprivation test - urine osmolality will fail to increase
What do patients with diabetes insipidus present with?
Polyuria and polydipsia
How would you treat hypernatraemia?
- Fluid replacement (not normal saline!!)
- Treat the underlying cause
What is the management of hypernatraemia?
- Correct water deficit
- 5% DEXTROSE (free water)
- May need to correct extracellular fluid volume depletion/hypovolemia (especially if they’ve been vomiting)
- 0.9% saline
- Serial Na+ measurement
- Every 4-6 hours
- Risk of cerebral oedema is correction is too rapid –> seizures –> coma –> death
normal saline will NOT treat hypernatremia
What are the effects of diabetes mellitus on serum sodium?
Variable:
- Hyperglycaemia draws water out of the cells leading to hyponatraemia
- Osmotic diuresis in uncontrolled diabetes leads to loss of water and hypernatraemia
This varies from person to person - based on which factor is pre-dominating
What is the definition of hyponatraemia?
Sodium concentration <135 mmol/L
