ChemPath - Sodium and Fluid Balance Flashcards
(34 cards)
What is the most common electrolyte abnormality in hospitalised patients
Hyponatraemia (25%)
How is water regulated
ADH
1. ADH synthesised in the hypothalamus
2. Secreted from the posterior pituitary
3. Acts on the V1 receptors in the collecting duct in the kidney
4. Insertion of aquaporin 2 (AQA2) into the collecting duct
5. Increased water resorption (NOT sodium → hyponatraemia)
+ ADH acts on V1 receptors in vascular smooth muscle → vasoconstriction
What are the stimuli for ADH secretion and what is it mediated by
Serum osmolality (high) – mediated by hypothalamic osmoreceptors
Blood volume/pressure (low) – mediated by baroreceptors in carotids, atria, aorta
What is the initial assessment for a patient who is hyponatraemic
Assessment of serum osmolality - is it true hyponatraemia?
Clinical assessment of volume status (hypo-, euvo-, or hypervolaemic)
- Check pulse
- JVP
- BP
- Skin turgor
- Signs of oedema
- Mental state
- Urine output
+ Urine electrolytes
Assessment of serum osmolality - is it true hyponatraemia?
Why does hypovolaemic hyponatramia occur (mechanism)
There is a loss of water AND sodium
hypovolaemia → baroreceptors detect the loss in volume → ADH secretion → reabsorption of water → dilution → hyponatraemia (more sodium than water loss)
What are the causes of hypovolaemic hyponatraemia
Anything that causes loss of both water and sodium
urine Na >20: renal causes
Diuretics
Salt-losing nephropathy
Addison’s
urine Na <20: non-renal
Diarrhoea and vomiting
Excess sweating
Third space loss (ascites, burns)
What are the clinical signs of hypovolaemia
Tachycardia
Postural hypotension
Dry mucous membranes
Reduced skin turgor
Confusion/drowsiness
Reduced urine output
What is the best investigation to detect hyponatraemia in hypovolaemia
Urine sodium (<20) (due to larger loss of water which dilutes the urine)
What are the causes of euvolaemic hyponatraemia
SIADH (AQA2 insertion → water retention → increased volume → RAAS suppression → less aldosterone → reduced Na absorption
Hypothyroidism (→ reduced contractility → reduced BP → ADH release)
Adrenal insufficiency (→ less aldosterone → less Na+ reabsorption)
Urine sodium always >20
What are the causes of SIADH
CNS pathology – stroke, haemorrhage, tumour
Lung pathology – small cell lung cancer, pneumonia (Legionella), pneumothorax
Drugs – SSRI, TCA, PPI, carbamazepine, opiates
Tumours - small cell, pancreas, prostate, lymphoma
Surgery
What investigations should be ordered in someone with euvolaemic hyponatraemia
Hypothyroidism → thyroid function tests
Adrenal insufficiency → short SynACTHen test
SIADH → plasma and urine osmolality → low plasma and high urine osmolality
How is SIADH diagnosed
True hyponatraemia <135
Reduced plasma osmolality (resorbing lots of water) <270
Increased urine osmolality >100
High urine sodium >20
No hypovolaemia (euvolaemia)
No hypothyroidism
No adrenal insufficiency
What are the clinical signs of hypervolaemia hyponatraemia
Raised JVP
Bilateral crackles
Peripheral oedema
What are the causes of hypervolaemic hyponatraemia
Urine Na >20: renal
AKI
CKD
Renal failure → not excreting enough water, not retaining sodium
Urine Na <20: non-renal
Cardiac failure → low pressure → detected by baroreceptors → ADH release
Cirrhosis → vasodilated due to excess NO → low BP → baroreceptors → ADH releasea
What is the management for hypovolaemic hyponatraemia
Volume replacement with 0.9% saline - SLOWLY and check Na regularly
Treat the underlying cause
What is the management for euvolaemic hyponatraemia
Fluid restriction (<750ml/day)
Treat underlying cause
What is the management for hypervolaemic hyponatraemia
Fluid restriction (<750ml/day)
Treat underlying cause
What medications can be used to treat SIADH when fluid restriction is insufficient
Demeclocycline → induce nephrogenic diabetes insipidus
- Reduces responsiveness of collecting tubule cells to ADH
- Monitor U&Es as risk of nephrotoxicity
Tolvaptan – V2 receptor antagonist
What are the signs of severe hyponatraemia and how is it treated (+ the consideration for this treatment)
Reduced GCS
Seizures
Management: hypertonic 3% saline
If sodium is corrected too quickly → central pontine myelinolysis (osmotic demyelination)
Signs/symptoms: Quadriplegia, dysarthria, dysphagia, seizures, coma, death
What are the hypovolaemic causes of hypernatraemia
Urine sodium <20
GI: D&V
Skin loss: excessive sweating, burns
Urine sodium >20
Loop diuretics
Osmotic diuresis e.g. uncontrolled DM, glucose, mannitol
Diabetes insipidus
Renal disease e.g. renal artery stenosis
Why does diabetes insipidus cause hypernatraemia
insensitivity to/lack of ADH → water loss → hypovolaemia → Na resorption to compensate → hypovolaemia hypernatraemia
What is nephrogenic DI and what are the causes
Receptor defector → insensitivity to ADH
Hypercalcaemia
Hypokalaemia
Lithium
Sickle cell
What investigations should be done for suspected diabetes insipidus
Serum glucose – exclude diabetes mellitus → osmotic diuresis
Serum potassium – exclude hypokalaemia → nephrogenic DI
Serum calcium – exclude hypercalcaemia → nephrogenic DI
Plasma and urine osmolality – exclude hyperaldosteronism (high plasma osmolality, low urine osmolality, U:P ratio <2)
Water deprivation test (normal = concentrated urine, no ADH = carry on passing water – dilute urine)
What is the management for hypernatraemia
Fluid replacement → 5% dextrose (if the patient is also hypovolemic, then 0.9% saline and 5% dextrose water)
Treat underlying cause
