3. Sodium and Fluid Balance

Question 1

Hyponatraemia is…

Answer 1

less than 135 mmol/L

increased extracellular water (NOT a salt problem)

commonest electrolyte abnormality in hospitalised patient

we target excess water not salt

Question 2

What controls water balance

Answer 2

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

Question 3

ADH

Answer 3

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

Question 4

2 main stimuli for ADH secretion

Answer 4

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

Question 5

what is the first step to clniical assessment of a patient with hyponatraemia

Answer 5

assess volume status = hypo/eu/hypervolaemic

• examine hands, neck and chest
• look for peripheral oedema

Question 6

Clinical features of hypovolaemia

what is the most reliable clinical sign of hypovolaemia + exceptions to this sign

Answer 6

• 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

Question 7

clinical features of hypervolaemia

Answer 7

raised JVP

bibasal crackles (heard on chest examination)

peripheral oedema

Question 8

causes of hyponatraemia

Answer 8

Question 9

Explaining hyponatreaemic hypovolaemia

Answer 9

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)

Question 10

how does cirrhosis lead to hyponatraemia

Answer 10

cirrhosis causes hyponatraemia because it leads to the release of various vasodilators, which leads to a drop-in perfusion pressure.

Question 11

Mx of hypovolaemia hyponatraemia

Answer 11

volume replacement with 0.9% saline

Question 12

what are the causes of hyponatraemia in a hypovolaemia patient

Answer 12

Renal causes: diuretics and salt losing nephropathy – in these, urinary sodium will be high

Extra-renal causes: diarrhoea and vomiting

Question 13

SIADH

Answer 13

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

Question 14

Causes of SIADH

SIADH is NOT a diagnosis -> it is a description of a cause

Answer 14

CNS pathology (tumour, abscess, stroke)

Lung pathology (tumour, pneumothorax, PE, chest infection)

Drugs (SSRI, TCA, opiates, PPIs, carbamazepine)

Tumours

Surgery

Question 15

How do we diagnose SIADH?

Answer 15

No hypovolaemia

No hypothyroidism

No adrenal insufficiency

Reduced plasma osmolality (hyponatraemia) AND

Increased urine osmolality (> 100) – due to natriuresis

Question 16

Euvolaemia hyponatraemia mx

Answer 16

fluid restriction, treat the underlying cause

Question 17

What are the causes of hyponatraemia in a hypervolaemic patient?

Answer 17

Cardiac failure

Cirrhosis

Renal failure (not excreting water -> excess water due to reduced excretion)

Question 18

What are the causes of hyponatraemia in a euvolaemic patient?

Answer 18

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)

Question 19

Why do hypothyroid patients become hyponatraemic

Answer 19

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.

Question 20

Why do adrenal insufficient patients become hyponatraemic?

Answer 20

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.

Question 21

What happens to urinary sodium in cardiac failure?

Answer 21

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).

Question 22

euvolaemia hyponagtraemia and ADH

Answer 22

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.

Question 23

tx

Answer 23

Question 24

severe hyponatreaemia: sx and tx

Answer 24

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

Question 25

an important consideration when treating hyponatraemia: how quick to tx, complications if too quick (sx of this condition) and how to tx this

Answer 25

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

Question 26

Drugs used to treat SIADH (used if fluid restriction is insufficient)

Answer 26

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

Question 27

Hypernatraemia definition, cause

Answer 27

> 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)

Question 28

Ix for diabetes insipidus (adrenal insufficiency in Conn’s syndrome)

Answer 28

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

Question 29

Treating hypernatraemia

Answer 29

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

Question 30

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.

Answer 30

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

Question 31

Diabetes Mellitus and Serum Sodium

Answer 31

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

Question 32

Summary

Answer 32

Hyponatraemia is common

Most cases are due to increased ADH

Assess the volume status first

Treat the underlying cause