Sodium and Fluid Balance Flashcards
Hyponatraemia is…
less than 135 mmol/L
increased extracellular water (NOT a salt problem)
commonest electrolyte abnormality in hospitalised patient
we target excess water not salt
What controls water balance
ADH (vasopressin) promotes water retention = inserts AQP2 channels into CD of nephron.
- released from posterior pituitary and acts on kidneys
- almost all causes of hyponatraemia are due to excess ADH
ADH
Acts on V2 receptors (on collecting duct cells)
- Leads to insertion of aquaporin-2 channels
NOTE: V1 receptors
- Found on vascular smooth muscle
- Causes vasoconstriction (at higher concentrations)
- Hence the alternative name vasopressin
2 main stimuli for ADH secretion
Serum osmolality (mediated by hypothalamic osmoreceptors)
- As serum osmolality increases, this is detected by osmoreceptors
- These signal to the posterior pituitary gland to release ADH
- The result is a greater retention of water
- ADH also stimulates thirst, so that you ingest more water as well as retain it
Blood volume/pressure (mediated by baroreceptors in the carotids, atria and aorta)
- If the blood volume/blood pressure drops, this is detected by baroreceptors
- Baroreceptors are located in carotids, atria and aorta
- They signal to the hypothalamus to release more ADH and retain more water
what is the first step to clniical assessment of a patient with hyponatraemia
assess volume status = hypo/eu/hypervolaemic
- examine hands, neck and chest
- look for peripheral oedema
Clinical features of hypovolaemia
what is the most reliable clinical sign of hypovolaemia + exceptions to this sign
- tachycardia
- postural hypotension
- dry mucous membranes
- reduced skin turgor
- confusion/drowsiness
- reduced UO
- LOW URINE Na+ (<20)
LOW urinary sodium
- shows that kidneys are trying to retain fluid as patient is hypovolaemia
- if patient is taking diuretics or hypovolaemia 2o to SIADH = HIGH urinary sodium regardless of volume status
- diuretics mean we cannot interpret urine sodium for 48 hours after stopping drug
- order urinary sodium when patient first presents with low sodium, before they receive any fluid correction
clinical features of hypervolaemia
raised JVP
bibasal crackles (heard on chest examination)
peripheral oedema
causes of hyponatraemia
Explaining hyponatreaemic hypovolaemia
Hypovolaemic patients can still have excess water
Let’s start with a patient who is euvolaemic, who loses water and sodium
E.g. diarrhoea or vomiting can cause a patient to lose a lot of salt and water
This leads to a low perfusion pressure and, consequently, an increase in ADH release
The patient then reabsorbs more water than salt (not enough resorption for euvolaemia)
The increased water retention without simultaneous salt retention results in hyponatraemia
The patient is not euvolaemic – they still have less salt and water (just some more water than salt)
how does cirrhosis lead to hyponatraemia
cirrhosis causes hyponatraemia because it leads to the release of various vasodilators, which leads to a drop-in perfusion pressure.
Mx of hypovolaemia hyponatraemia
volume replacement with 0.9% saline
what are the causes of hyponatraemia in a hypovolaemia patient
Renal causes: diuretics and salt losing nephropathy – in these, urinary sodium will be high
Extra-renal causes: diarrhoea and vomiting
SIADH
SIADH results in euvolaemia and not hypervolaemia
In SIADH, excess ADH is released, resulting in the excess retention of water
For a patient to become hypervolaemic, they must retain both excess water and salts
An SIADH patient retains excess water and initially becomes hypervolaemic
However, the expanded volume stimulates the release of natriuretic peptides
This results in natriuresis (loss of sodium via the urine), and water follows
The end volume status is euvolaemia
Causes of SIADH
SIADH is NOT a diagnosis -> it is a description of a cause
CNS pathology (tumour, abscess, stroke)
Lung pathology (tumour, pneumothorax, PE, chest infection)
Drugs (SSRI, TCA, opiates, PPIs, carbamazepine)
Tumours
Surgery
How do we diagnose SIADH?
No hypovolaemia
No hypothyroidism
No adrenal insufficiency
Reduced plasma osmolality (hyponatraemia) AND
Increased urine osmolality (> 100) – due to natriuresis
Euvolaemia hyponatraemia mx
fluid restriction, treat the underlying cause
What are the causes of hyponatraemia in a hypervolaemic patient?
Cardiac failure
Cirrhosis
Renal failure (not excreting water -> excess water due to reduced excretion)
What are the causes of hyponatraemia in a euvolaemic patient?
Hypothyroidism – perform TFTs
Adrenal insufficiency – perform a short synACTHen test (absence of cortisol surge)
SIADH – check plasma and urine osmolality (low plasma osmolality, high urinary osmolality)
Why do hypothyroid patients become hyponatraemic
LOW BP
Hypothyroidism causes a reduced cardiac output (reduced cardiac contractility). This is detected by baroreceptors; more ADH is released to correct the blood pressure, resulting in increased water retention.
Why do adrenal insufficient patients become hyponatraemic?
LOW ALDOSTERONE AND CORTISOL
Adrenal insufficiency results in low levels of aldosterone and cortisol. Low aldosterone results in less salt and water retention at the kidney. Cortisol is required for water clearance; low levels of cortisol results in excess ADH release and excess water retention.
In Conn’s syndrome, we see polyuria and polydipsia. This is because the hypokalaemia caused produces a nephrogenic diabetes insipidus.
What happens to urinary sodium in cardiac failure?
Urine sodium is low in cardiac failure. These patients develop secondary hyperaldosteronism to maintain blood volume (activation of the renin-angiotensin-aldosterone system as a compensatory mechanism), and aldosterone promotes water and sodium retention. This shows us that urinary sodium can be low both in hypervolaemia (cardiac failure) and hypovolaemia. Urinary sodium is only high in euvolaemic patients (e.g. in SIADH).
euvolaemia hyponagtraemia and ADH
NOTE: in euvolaemic hyponatraemia, the initial increase in ADH release will cause water retention. Then, the atrial expansion caused by the increased circulating volume will lead to natriuretic peptide release.
tx
severe hyponatreaemia: sx and tx
Reduced GCS
Seizures
Seek expert help (treat with 3% hypertonic saline)
- We have 2.7% sodium chloride currently available
- 2-3 boluses under supervision of a senior
- This is only used if the patient is fitting or if they have a reduced GCS
an important consideration when treating hyponatraemia: how quick to tx, complications if too quick (sx of this condition) and how to tx this
serum sodium must NOT be corrected faster than 8-10 mmol/L in the first 24 hours
- Water will move out of cells too quickly, which affects gap junctions in the CNS
- Inflammatory cells are able to enter cells of the CNS as a result of compromised gap junctions
- If serum sodium is corrected too rapidly -> osmotic demyelination (central pontine myelinolysis)
This leads to quadriplegia, dysarthria, dysphagia, seizures, coma and death
These symptoms only manifest a few days after the sodium has been corrected too quickly
to avoid too fast administration of sodium = small ampules of hypertonic saline granules
tx: 5% dextrose for hypernatraemia
Drugs used to treat SIADH (used if fluid restriction is insufficient)
Demeclocycline
- Reduces responsiveness of the collecting tubule cells to ADH -> less water retention
- Monitor U&Es (risk of nephrotoxicity so not used as much these days)
Tolvaptan
- V2 receptor antagonist
- This is expensive and associated with rapid rises in serum sodium
- Alternative: fluid restriction + salt tablets + frusemide
Hypernatraemia definition, cause
> 145 mmol/L
It is much less common than hyponatraemia
It is caused by unreplaced water loss
- GI losses (COMMON)
- Sweat losses
- Renal losses: osmotic diuresis, diabetes insipidus (reduced ADH release/action)
This tends to only be seen in patients who do not drink when they’re dehydrated (e.g. elderly, children)
Ix for diabetes insipidus (adrenal insufficiency in Conn’s syndrome)
What to do if the patient presents with polyuria and polydipsia…
- Serum glucose (exclude diabetes mellitus – much more common than diabetes insipidus)
- Serum potassium (exclude hypokalaemia)
- Serum calcium (exclude hypercalcaemia)
NOTE: hypokalaemia and hypercalcaemia both induce a nephrogenic diabetes insipidus
Plasma and urine osmolality
Water deprivation test (for DI)
- Ask the patient not to drink throughout the test
- Healthy: osmolality increases, increased ADH release -> retain water (concentrated urine)
- Diabetes insipidus: patient continues to produce dilute urine due to ineffective/absent ADH
Treating hypernatraemia
Fluid replacement (use DEXTROSE because this will replace the fluid without giving excess salt)
Treat underlying cause
NOTE: if someone is hypovolaemic and hypernatraemic, you may initially give 0.9% saline to treat the hypovolaemia, followed by dextrose for the hypernatraemia
A 70-year-old man presents with a 3-day history of diarrhoea. His mental status is altered. He has dry mucous membranes. On taking bloods, you see that his serum sodium is 168 mmol/L. How do you manage this patient? NOTE: diarrhoea can cause hyponatraemia, but this patient is confused, so he may not have been replacing fluids orally and hence this may explain his sodium levels.
Correct the water deficit (correct the hypernatraemia): 5% dextrose
Correct extracellular fluid volume depletion (correct the hypovolaemia): 0.9% saline
Serial sodium measurements: Every 4-6 hours
If elderly person is hypernatraemic -> check if safeguarding problem because of dehydration
Diabetes Mellitus and Serum Sodium
Diabetes has a variable effect on serum sodium
It depends on the degree to which each of the following mechanisms predominate:
- Hyperglycaemia will draw water out of cells leading to hyponatraemia
- Osmotic diuresis in uncontrolled diabetes leads to loss of water and hypernatraemia
Summary
Hyponatraemia is common
Most cases are due to increased ADH
Assess the volume status first
Treat the underlying cause
