Hyponatraemia Flashcards
How is sodium regulated?
Thirst
ADH
- Made in the hypothalamus and secreted from the posterior pituitary
- Works on DCT and reabsorbs water (through insertion of aquarporins)
- —> produce concentration urine
Aldosterone
- Made in the adrenal gland
- Works on CT and reabsorbs Na+ and water, and excretes K+ and H+
- —> produce concentrated urine
Difference between osmolality and osmolarity
Osmolality is number of osmoles of solute per kg of solvent
Osmolarity is number of osmoles of solutes per litre of solvent
How do you work out osmolar gap?
Osmolar gap = measured osmolality - calculated osmolarity
Calculated osmolarity mOsm/L = (2xserum Na) + glucose + urea
> 10 = wide osmolar gap and indicates the presence of extra osmotically active particles (e.g. glycine test post TURP, mannitol post IVIG)
Symptoms and complications of acute hyponatraemia
Acute cerebral oedema and subsequent raised ICP
> 125: asymptomatic
115-125: lethargy, anorexia, nausea, vomiting, headache, disorientated, decreased attentiveness, neurological dysfunction causing falls
<115: muscle cramps and weakness, confusion, seizures, coma, brainstem herniation, death
Also non-ischaemic STE on ECG
Speed of onset if more important than the level
Medications causing hyponatraemia
Diuretics - thiazides, loop, indapamide, amiloride
Omeprazole
ACEI, ARB
Amlodipine
Haloperidol
Drugs that stimulate ADH release: carbamazepine, SSRIs, TCA, MAOI, opioids
Drugs that potentiate ADH in the kidneys: NSAIDs, cyclophosphamide
Initial investigations in hyponatraemia
Repeat UEC Serum osmolality Urine osmolality, Na+, K+ TFTs BSL Lipids Morning cortisol LFTs
How do diuretics cause hyponatraemia?
Particularly thiazides
Block Na Cl cotransported in DCT –> no sodium reabsorption –> natriuresis –> water follows –> diuresis
=Increased urinary sodium
= Hyponatraemic hypovolaemia
Body will trigger ADH release to try and retain water however its role can only reabsorb 10% of water –> outcome is still hypovolaemia + hyponatraemia
How does Addison’s cause hyponatraemia?
Low aldosterone –> decreased Na+ and water reabsorption in DCT and CD
= Increased urinary sodium
= Hyponatraemic hypovolaemia
How does SIADH cause hyponatraemia?
Excess SIADH –> increased aquaporin insertion in CT –> increased water reabsorption –> fluid overload –> increased GFR + ANP/BNP (heart) –> decrease RAAS –> decreased aldosterone –> decreased Na+ and water reabsorption from DCT and CD
= Euvolemic (fluid overload from high ADH counteracted by lack of water reabsorption from low aldosterone; overtime kidneys also adapt and reduce the number of aquarporins)
= Hyponatraemia (dilution and lack of Na reabsorption)
= High urinary sodium
= Urine osmolality > serum osmolality
How does beer protomania cause hyponatraemia?
Drink a lot of beer and not a lot of solutes/proteins –> fluid overload –> suppress ADH –> water excretion but at the same time, the body will try and retain solutes and water
= Euvolemic hyponatraemia
= Serum osmolality > urine osmolality
How does psychogenic polydipsia cause hyponatraemia?
Drink a lot –> fluid overload –> suppress ADH –> increase water excretion
= Euvolemic hyponatraemia
= Serum osmolality > urine osmolality
How does CCF, liver cirrhosis and nephrotic syndrome cause hyponatraemia?
CCF = low effective circulating volume due to low CO
Cirrhosis, nephrotic syndrome = low albumin; fluid leaks out into interstitium so there is low effective circulating volume
–> increased ADH + increased thirst –> increase water reabsorption and intake –> fluid overload
= Hypervolemic hyponatraemia (low serum osmolality)
= Low serum osmolality
How does chronic renal failure cause hyponatraemia?
Decrease in GFR –> activate RAAS –> raised aldosterone –> increase Na+ and water reabsorption –> fluid overload
= Hypervolaemic hyponatraemia (low serum osmolality)
= Low urinary osmolality
How does hypothyroidism cause hyponatraemia?
Hypothyroidism –> bradycardia –> reduced CO –> reduced effective circulating volume –> increased ADH –> increased water reabsorption
Reduced –> reduced GFR –> activates RAAS –> increased aldosterone –> increased Na+ and water reabsorption
= Hypervolemic hyponatraemia (low serum osmolality)
= Low urinary osmolality
How does hyperglycaemia cause hyponatraemia?
High BSL –> pulls water out of cells –> expands extracellular water –> lowers serum Na+ through dilution
Increased tonicity –> increase ADH and thirst –> further water retention
Don’t correct hyperglycaemia too rapidly and given too much IVT –> drive water back into cells –> cerebral oedema
How does IV mannitol, glycerol or IVIG cause hyponatraemia?
IV mannitol, IV glycerol, IVIG –> pulls water out of cells –> increase extracellular water –> lowers serum Na+ through dilution
Increased tonicity –> increase ADH and thirst –> further water retention
Similar mechanism to hypglycaemia
What is pseudohyponatraemia?
Extreme hyperlipidaemia (especially TG), hyperproteinaemia –> reduces plasma water –> thus plasma [Na+] that is measured per L of plasma is artificially low
Serum osmolality is normal
Definition of chronic hyponatraemia
Lasting >48h
Why is chronic hyponatraemia usually asymptomatic?
Brain has adapted to the surrounding hypotonicity
What’s pontine demyelinosis?
When sodium is corrected too quickly. More likely in chronic hyponatraemia
Develops 3-5 days post treatment
Demyelination of nerve cells in central pons, corticobulbar and corticospinal tracts
Starts with lethargy and affect changes (generally after initial improvement of neurological symptoms with treatment), followed by acute paralysis, problems with speech and swallow, pseudobulbar palsy, altered mental state
How much sodium should be corrected per day?
No more than 8mmol/L first 24 hours. Can go up to 10mmol/L if acute.
To avoid pontine demyelinosis
Management of acute (<48h) symptomatic hyponatraemia, Na <125mmol/L
Raise 1-2mmol/L/hr. No more than 8-10mmol/L for the first day, and no more than 18-25mmol/L for the first 2 days.
Hypertonic (3%) saline +/- frusemide
Check serum sodium level Q2H and just infusion rate. Stop when symptoms improve.
Management of hypovolaemic hyponatraemia
Normal saline
Management of hypervolaemic hyponatraemia
Fluid restrict
Causes of SIADH
Lots of causes!!
SIADH –> release ADH
Atypical pneumonia (legionella)
Brain dysfunction (meningitis, SAH)
Drugs such as carbamazepine, SSRIs
How to diagnose SIADH?
Diagnosis of exclusion
Essential features
- Decreased serum osmolality
- High urine osmolality, urine sodium
- Clinical euvolemia
- Normal thyroid and adrenal function
- No recent diuretics
Management of chronic/unclear duration asymptomatic SIADH
Don’t correct too quickly! Risk of demyelination
Fluid restrict!!!
Adequate intake of protein and salt
Oral urea 30g/day is effective but poorly tolerated
Demeclocycline reduces urine osmolality and increases serum Na+. Effects are variable, nephrotoxic.
Vasopressin-receptor antagonist activity (VAPTANS) can be considered in hospitalised patients who have moderate-severe hyponatraemia and symptoms but NOT seizure, delirium or coma, which would warrant the use of hypertonic saline. Risk of rapid correction. Don’t use it in acutely unwell patients.
Management of chronic symptomatic SIADH
Don’t correct too quickly! Risk of demyelination
Increase serum sodium by 0.5-1mmol/L/hr, using slow normal saline infusion
No more than 8mmol/L over 24h and 18mmol/L over 48 hours
