Hyponatraemia

Question 1

How common is hyponatraemia in hospitals?

Answer 1

30% of in-patients.

Question 2

Early symptoms of hyponatraemia.

Answer 2

Headache

Nausea

Vomiting

General malaise

Question 3

Late signs of hyponatraemia.

Answer 3

Confusion

Agitation

Drowsiness

Question 4

Complications of acute severe hyponatraemia.

Answer 4

Seizures

Respiratory depression

Death

Question 5

Treatment of acute severe hyponatraemia.

Answer 5

Usually IV saline

Question 6

Important history of hyponatraemia.

Answer 6

Full history and examination requried.

Drug history and hydration status are of particular importance.

Question 7

Why is drug history important in hyponatraemia?

Answer 7

Thiazide diuretics can commonly cause hyponatraemia.

Question 8

Give examples of biochemical investigations done in hyponatraemia.

Answer 8

Serum osmolality

Urine osmolality

Urine sodium

Thyroid function

Assessment of cortisol reserve (0900 cortisol or synacthen test)

Question 9

What should be given in acute severe hyponatraemia with neurological compromise, regardless of cause?

Answer 9

Hypertonic saline.

This is however a senior decision and should only be done under close supervision.

Question 10

Complication of untreated acute severe hyponatraemia with neurological compromise.

Answer 10

Cerebral oedema

Question 11

What should be followed in mild or moderate hyponatraemia?

Answer 11

Diagnostic algorithm.

Question 12

Explain the diagnostic algorithm.

Answer 12

First off you confirm low serum osmolality.

Once this is confirmed the urine osmolality is checked.

Urine osmolality puts the next step into categories of < 100 mosmol/Kkg or > 100 mosmol/kg.

If > 100 mosmol/kg you need to check urine sodium

Question 13

Why is it important to confirm low serum osmolality?

Answer 13

To exclude non-hypo-osmolar hyponatraemia

Question 14

Give an examples of a non-hypo-osmolar hyponatraemia.

Answer 14

Hyperglycaemia

Question 15

What does a urine osmolality of <100 mosmol/kg suggest?

Answer 15

Primary polydipsia

Inappropriate administration of IV fluid

Low solute intake

Question 16

What does a urine sodium < 30 mmol/l suggest?

Answer 16

A low effective arterial volume.

Question 17

When is urine sodium < 30 mmol/l with a low effective arterial volume and hyponatraemia seen?

Answer 17

True dehydration where there is GI salt loss.

When patients are clinically overloaded but have intra-vascular depletion such as congestive heart failure, cirrhosis or nephrotic syndrome.

Question 18

What should be considered if urine sodium is > 30 mmol/l and the patient is euvolaemic?

Answer 18

SIADH

AVP-like drugs

NSIAD

Question 19

What is NSIAD?

Answer 19

Nephrogenic syndrome of inappropriate antidiuresis

Question 20

What must be excluded before confirming SIADH?

Answer 20

ACTH deficiency

Question 21

What diagnosis is suggested if urine sodium is >30 mmol/l and the patient is dehydrated (low effective arterial volume)?

Answer 21

Addisons

Renal and cerebral salt-wasting

History of vomiting

Question 22

Why might vomiting cause hyponatraemia with urine sodium >30 mmol/l and dehydration?

Answer 22

Loss of hydrogen ions leading to metabolic alkalosis.

This is then corrected by renal excretion of sodium bicarbonate.

Question 23

What else might cause hyponatraemia?

Answer 23

Severe hypothyroidism

Mechanism is unclear.

Question 24

What is SIADH characterised by? (hallmarks)

Answer 24

Low serum osmolality (<275 mosmol/kg)

Urine osmolality > 100 mosmol/kg

Urine sodium > 30 mmol/l

Question 25

What needs to be excluded before confirming SIADH?

Answer 25

Hypothyroidism

Total salt depletion

ACTH deficiency

Question 26

ACTH deficiency can look identical to SIADH.

Why?

Answer 26

Because it causes reduced excretion of free water.

This is because cortisol deficiency leads to increased vasopressin activity.

This is not to be confused with hyponatraemia caused by mineralcorticoid deficiency in Addisons disease.

Question 27

Causes of SIADH.

Answer 27

Malignancy

Respiratory and CNS pathology

Drugs

Question 28

What malignancy most commonly causes SIADH?

Answer 28

Lung cancer

Question 29

Drugs that can cause SIADH

Answer 29

Anticonvulsants

Question 30

If no cause for SIADH is found, what should be done?

Answer 30

Cross-sectional maging or bowel investigation to search for an underlying malignancy.

Idiopathic SIADH is a diagnosis of exclusion.

Question 31

Management of hypovolaemic hyponatraemia.

Answer 31

Normal saline

Question 32

Management of hypervolaemic hyponatraemia.

Answer 32

Specialist treatment of cirrhosis, nephrotic syndrome or CCF is indicated.

Question 33

Management of SIADH.

Answer 33

Fluid restriction (1-1.5 litres a day)

Question 34

Why is the management of SIADH difficult?

Answer 34

Compliance to drink low amounts of water when you are thirsty is poorly tolerated.

Question 35

What can be given in SIADH instead?

Answer 35

Demeclocycline

ADH antagonists such as tolvaptan

Question 36

Question 37

Treatment of asymptomatic chronic hyponatraemia.

Answer 37

Fluid restriction is often sufficient if they are asymptomatic.

Demeclocycline (ADH antagonist) can be used if required.

If hypervolaemic as well such as in cirrhosis or CCF the underlying disorder should be treated.

Question 38

Treatment of acute or symptomatic hyponatraemia or if dehydrated.

Answer 38

Cautious rehydration with 0.9% saline but do not correct too quickly because of central pontine myelinolysis.

Maximum rise in serum Na+ should be 15mmol/L per day if chronic, or 1 mmol/L per hour if acute.

Consider using furosemide as well if not hypovolaemic in order to avoid fluid overload.

Be aware of heart failure as well.

Question 39

When might tolvaptan be used?

Answer 39

It promote water excretion without the loss of electrolytes.

It can be effective in treating hypervolaemic and euvolaemic hyponatraemia but they are expensive

Question 40

Treatment of emergency hyponatraemia.

Answer 40

Seek expert help.

COnsider hypertonic saline like 1.8% saline at 70 mmol Na+/h and add furosemide as well.

Aim for a gradual increase in plasma Na+ to around 125 mmol/l.

You need to beware of heart failure and central pontine myelinolysis.