Hyponatraemia

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Hyponatraemia\: relative excess of water compared to sodium; most common electrolyte abnormality; serum sodium
\<135mmol/L, severe \<120mmol/L.
Causes\:
Hypovolaemic\: renal (urine sodium >20mmol/L) - renal failure, Addison's, diuretics, osmotic diuresis; non-renal (urine
sodium \<20mmol/L) - GI losses, skin losses.
Hypervolaemic\: CCF, liver cirrhosis, end-stage renal failure, nephrotic syndrome.
Euvolaemic\: SIADH, primary polydipsia, endocrine disturbances.
Investigations\:
Blood tests\: U&Es, serum osmolality, LFTs, serum lipids, serum glucose, serum cortisol, thyroid function tests.
Urine tests\: urine osmolality, urine sodium.
Symptoms\: mild to moderate (anorexia, headache, nausea, lethargy, confusion, ataxia); severe (seizures, cerebral
obtundation/coma).
Examination\: assess
brainstem herniation).
Management\:
Acute severe\: IV hypertonic saline bolus (100ml 3% NaCl), close monitoring.
Hypovolaemic\: IV 0.9% normal saline.
Hypervolaemic\:
Euvolaemic\:
General goal\: correct by no more than 6mmol/L in
Complications\: gait disturbance, falls, cerebral oedema, osmotic demyelination syndrome.
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Introduction

Hyponatraemia occurs when there is a relative excess of water in the body compared to sodium. It is the most common
electrolyte abnormality encountered in clinical practice. However, it can be challenging to diagnose and treat e
Hyponatraemia is a serum sodium concentration \<135mmol/L, with severe hyponatraemia being a serum sodium
concentration \<120mmol/L. It is often further categorised into acute (\<48h duration) or chronic hyponatraemia.
Acute hyponatraemia can be life-threatening due to cerebral
The key to appropriate management of hyponatraemia is understanding the di
and how these relate to the patient's hydration status.Normal physiology
Serum osmolality measures the concentration of solutes in the blood, and sodium is the most important determinant of
serum osmolality.
Serum osmolality determines the osmolar concentration of plasma. The law of osmosis states that water will
compartments with lower osmolality to compartments with higher osmolality, so long as the membrane separating the two
compartments is permeable. In the body, this will occur between the plasma and interstitial (extracellular)
compartments, and also between the extracellular and intracellular compartments.
Any alteration in sodium concentration will a
between the intracellular and extracellular compartments.
Serum sodium regulation is maintained by a complex homeostatic mechanism involving thirst, anti-diuretic hormone
1
(ADH), the renin-angiotensin-aldosterone system (RAAS) and renal sodium excretion. Dysfunction at any stage of this
mechanism can lead to the development of hyponatraemia.
In healthy individuals, ADH is released in response to increased serum osmolality, leading to increased water retention in
the collecting ducts of the kidney. This leads to a corresponding fall in serum osmolality.
An illustration of how serum osmolality is regulated in healthy individuals.
By the same mechanism, water ingestion will not lead to hyponatraemia as the fall in osmolality leads to suppression of
ADH secretion, allowing water to be excreted in dilute urine.
2
Note\: One mechanism by which hyponatraemia can develop is inappropriate ADH secretion, i.e. ongoing secretion of ADH
when osmolality is low or normal. This is a common cause of hyponatraemia, known as SIADH.

Causes of hyponatraemia

Hyponatraemia can develop by many di
is determining whether the patient is\:
Hypovolaemic (dehydrated)
Hypervolaemic (‘overloaded’)
Euvolaemic
This is primarily achieved by clinical examination of hydration status.
Hypovolaemic hyponatraemia
In a hypovolaemic patient, hyponatraemia may be secondary to renal sodium loss or sodium loss from elsewhere
(transdermal/gastrointestinal).
In either case, sodium is lost in association with water (which explains why the patient is hypovolaemic). Patients often
drink hypotonic
Urine sodium
Urine sodium is an important investigation in hypovolaemic hyponatraemia.In a normally functioning kidney, sodium should be conserved in the urine if serum sodium levels are low\:
Urinary sodium >20mmol/L suggests a renal cause of sodium loss (the kidney is not conserving sodium)
Urinary sodium \<20mmol/L suggests a non-renal cause of sodium loss (the kidney is conserving sodium, but the
sodium is being lost from elsewhere)
Renal causes of sodium loss (urine sodium >20mmol/L) include\:
Renal failure\: creatinine will be increased, eGFR decreased
Addison’s disease\: associated with hyperkalaemia
Excess diuretic medications\: particularly thiazide-like diuretics
Osmotic diuresis\: severe hyperglycaemia
Non-renal causes of sodium loss (urine sodium \<20mmol/L) include\:
Gastrointestinal losses\: vomiting, diarrhoea, small bowel obstruction,
Skin losses\: excess sweating, burns
Hypervolaemic hyponatraemia
In a
e
sodium de
It is important to diagnose and treat the underlying cause of
Congestive cardiac failure
In cardiac failure,
angiotensin-aldosterone system. There is also increased venous capillary pressure, encouraging
oedema.
Liver cirrhosis (liver failure)
Decreased albumin synthesis leads to hypoalbuminaemia. This causes reduced oncotic pressure in the bloodstream,
leading to
hypertension) leads to
End-stage renal failure
In end-stage renal failure, the kidney loses the ability to e
decreases. This leads to signi
oedema (end-stage renal failure).
Nephrotic syndrome
In nephrotic syndrome, inappropriate loss of albumin through the glomerulus leads to hypoalbuminaemia, which
decreases plasma oncotic pressure, and
Euvolaemic hyponatraemia
In euvolemic hyponatraemia, the diagnosis is most commonly SIADH. Less common causes include primary polydipsia or
severe endocrine disturbances (hypothyroidism/cortisol de
2
Urine osmolality
In euvolaemic hyponatraemia, it is important to check the urine osmolality. Urine osmolality measures the concentration
of solutes in the urine, including sodium and urea, and will often be measured in conjunction with serum osmolality.
Under normal conditions, urine osmolality should be decreased when serum sodium (and serum osmolality) is low, as the
body attempts to conserve sodium by producing dilute urine.
If the urine osmolality is raised (>300mOsm/kg - concentrated urine with high sodium levels), the diagnosis is likely SIADH.
The key concept to understand is that a raised urine osmolality in the presence of low serum osmolality suggests SIADH,
as the kidney is inappropriately producing concentrated urine despite low serum osmolality.
If the urine osmolality is decreased (\<300mOsm/kg - dilute urine), water intoxication may be the cause (primary
polydipsia). This can be seen in patients with psychiatric disturbances or users of the recreational drug ecstasy. Rarer
causes include severe hypothyroidism or glucocorticoid de
Hyponatraemia Once the patient's hydration status has been determined and urine osmolality/urine sodium has been checked, the

Assessment of hyponatraemia

Clinical features

The clinical features of hyponatraemia are primarily neurological, developing due to the e
which can occur secondary to
3
Clinical features depend on the severity of hyponatraemia and the rate of change in sodium concentration, as the brain
can adapt to a slowly developing chronic hyponatraemia.
1
Some patients with chronic hyponatraemia of 120mmol/L (severe) may be relatively asymptomatic. However, others with
acute hyponatraemia of 130mmol/L (mild) may have severe symptoms.
History
Mild to moderate symptoms of hyponatraemia include\:
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Anorexia
Headache
Nausea/vomiting
Lethargy
Confusion
Ataxia
Severe symptoms of hyponatraemia include\:
Seizures
Cerebral obtundation / coma
Clinical examination
The key to clinical examination in hyponatraemia is an accurate assessment of , as this will help to
classify the likely cause of hyponatraemia and guide initial management.
It is important to check for neurological signs that would indicate severe hyponatraemia.
Signs of hypovolaemia include\:
Tachycardia, hypotension (late sign)
Dry mucous membranes
Reduced skin turgor
Signs of hypervolaemia include\:
Peripheral oedema
Raised jugular venous pressure (JVP)Bibasal lung
Neurological signs of severe hyponatraemia include\:
Cognitive impairment
Drowsiness
Signs of seizure activity/brainstem herniation (indicate life-threatening hyponatraemia with cerebral oedema)

Investigations

All patients with hyponatraemia identi
help determine the underlying cause of hyponatraemia. Blood and urine tests must be performed simultaneously to
compare urine and serum osmolality accurately.
Laboratory investigations
Relevant blood tests include\:
Serum urea & electrolyte panel\: to con
Serum osmolality\: usually decreased in hyponatraemia; if normal consider pseudohyponatraemia, if raised consider
hyperglycaemia.
Liver function tests\: assess the albumin levels in hypervolaemic hyponatraemia, and exclude obstructive jaundice if
pseudohyponatraemia is suspected.
Serum lipids\: to assess for lipaemia if pseudohyponatraemia is suspected.
Serum glucose\: signi hyperglycaemia can cause hyponatraemia, often with raised serum osmolality.
Serum cortisol/thyroid function tests\: exclude Addison’s (low cortisol level) / severe hypothyroidism (high TSH, low T3)
as rare causes of euvolaemic hyponatraemia.
Note\: calculated serum osmolality = (2 x Na) + Glu + Urea (all in mmol/L).
Relevant urine tests include\:
Urine osmolality\: required to con
osmolality suggests SIADH.
Urine sodium\: useful to di
>20mmol/L are suggestive of renal sodium loss. Urine sodium is also a useful investigation to help con
of SIADH (markedly raised in SIADH >40mmol/L).
2
Pseudohyponatraemia
Hyperlipidaemia, hyperproteinaemia or hyperbilirubinaemia (secondary to obstructive jaundice) can interrupt some
laboratory analysis methods of measuring serum sodium, leading to falsely low readings. This is known as a
pseudohyponatraemia.
Serum osmolarity is classically normal if measured. Pseudohyponatraemia is rare but important to exclude before
initiating treatment for hyponatraemia.
Hyperglycaemia associated hyponatraemia
In patients with signi
pulling water out of cells and expanding the extracellular space, causing a dilutional e
concentrations.
In this case, total body sodium remains unchanged, and sodium concentration will generally correct with the
correction of the hyperglycaemia. Calculated serum osmolality is classically raised.Management
Management aims to restore a normal serum sodium level at an appropriate pace. This is primarily achieved by treating the
underlying cause and aiming to restore normal volume status.
Acute severe hyponatraemia
Acute hyponatraemia with severe neurological symptoms (e.g. seizures, severe drowsiness) is a medical emergency.
Initial treatment involves IV hypertonic saline bolus (100ml 3% NaCl) with close monitoring of serum sodium.
5
The diagnosis and management of the underlying cause is essential once the neurological status begins to improve.
Note\: Some clinicians recommend cautious hypertonic saline use in patients with severe hyponatraemia (\<120 mmol/L),
even without neurological symptoms. However, this is usually a consultant-led decision.
5
Hyponatraemia without severe neurological symptoms5
In the absence of acute severe hyponatraemia, a cautious approach to management is taken. If the sodium is corrected too
quickly, patients are at risk of severe complications (osmotic demyelination syndrome).
The general goal of treatment is to correct by no more than 6mmol/L in the
the
1
The initial management approach depends on volume status. In all cases, identi
cause is essential.
Hypovolaemic hyponatraemia
Rehydration with intravenous 0.9% normal saline, with regular monitoring of serum sodium.
Hypervolaemic hyponatraemia
Fluid restriction (\<1.5L/24h), with regular monitoring of serum sodium.
Euvolaemic hyponatraemia
Fluid restriction (1.5L/24h), with regular monitoring of serum sodium. Oral salt tablets may be required if
alone is ine

Complications

Complications of hyponatraemia include\:
1
Gait disturbance and falls\: particularly in elderly patients
Cerebral oedema\: can lead to brainstem herniation and death
Osmotic demyelination syndrome\: severe and often irreversible neurological de
shifts caused by the rapid correction of hyponatraemia; classically occurs 2-4 days after the treatment, typically
presenting with quadriplegia and pseudobulbar palsy

References

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UpToDate. D i a g n o s t i c e v a l u a t i o n o f a d u l t s w i t h h y p o n a t r e m i a . July 2023. Available from\: [LINK].
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UpToDate. O v e r v i e w o f t h e t r e a t m e n t o f h y p o n a t r e m i a i n a d u l t s . July 2023. Available from\: [LINK].
UpToDate. T r e a t m e n t o f h y p o n a t r e m i a \: S y n d r o m e o f i n a p p r o p r i a t e a n t i d i u r e t i c h o r m o n e s e c r e t i o n ( S I A D H ) a n d r e s e t
o s m o s t a t . February 2022. Available from\: [LINK].Related notes
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