91. Abnormal serum sodium

Question 1

Approach to working out what is the cause of low sodium

Answer 1

1. is it true hyponautraemia?
2. What is their fluid status?
   hypovolemic - more sodium out
   euvolemic - more water in
   hypervolemic - water retention>sodium retention
3. What is their urine osmolality?
   high/not adequately responded - something going wrong at the level of the kidneys eg low alodosterone, high ADH, diuretics
   low - kidneys working, problem is somewhere else

Question 2

where is sodium found

Answer 2

main cation in ECF

Question 3

how to know if it is true hyponautraemia?

Answer 3

Check serum osmolality
- in true hyponautraemis this will be low
- in pseudohyponautraemia this will be normal (hyperlipidaemia, hyperproteinemia)
- in hyperglycaemia this will be high

calcualte the osmolar gap
- 2Na + 2K + urea + glucose
- this should be <10mmol difference to serum osmolality
- if >10 pseudohyponautraemia

Question 4

causes of hypovolemic hyponautraemia

Answer 4

too much sodium lost:

• decreased aldosterone = decreased reabsorption of sodium eg ADDISONS
• diuretics = decreased resorption of sodium
• sweating/vomiting/burns
• cerebral salt wasting

Question 5

causes of euvolemic hyponautraemia

Answer 5

to much water in/retianed:

• SIADH
• water intoxication
• hypothyroidism

Question 6

causes of hypervolemic hyponautraemia? mechanism?

Answer 6

heart failure
liver failure
nephrotic syndrome

fluid leaks out of intravasucalr space –> hypotension –> reduced perfusion to kidneys –> RAAS activation –> retain more water than sodium

Question 7

how does hypothyroidism cause hyponautraemia

Answer 7

decreased CO –> decreased volume cirucalting to brain –> hypothalamus increased ADH –> dilutional hypoNa

Question 8

define mild/moderate and severe hyponautraemia

Answer 8

mild: 130-134 mmol/L
moderate: 120-129 mmol/L
severe: < 120 mmol/L

Question 9

when should someone with hyponautraemia be referred from priamry care?

Answer 9

Have acute onset (duration for less than 48 hours) or severe (serum sodium concentration of less than 125 mmol/L) hyponatraemia.
Are symptomatic.
Have signs of hypovolaemia.

Question 10

early symptoms and late symptoms hyponautraemia

Answer 10

early symptoms may include: headache, lethargy, nausea, vomiting, dizziness, confusion, and muscle cramps

late symptoms may include: seizures, coma, and respiratory arrest

Question 11

Management severe hyponautraemia/severe symptoms

Answer 11

hypertonic saline SLOWLY in HDU

eg NaCl 3%

Question 12

management of hypovolemic hyponautraemia

Answer 12

IV fluids 0.9% NaCl trial

• if increased then this supports diagnosis of hypovolemic hyponautraemia

Question 13

management of SIADH

Answer 13

fluid restrict to 500-1000ml per day

find and treat cause

tolvaptan (vasopressin antgaonist) initiated by a specialist endocrinologist and require close monitoring, for example 6 hourly sodium levels.

Question 14

management of hypervolemic hyponautraemia

Answer 14

fluid restrict to 500-1000ml per day?

treat undelrying cause

Question 15

complication of correcting sodium too fast

Answer 15

Osmotic demyelination syndrome (Central Pontine Myelinolysis)

It is usually a complication of long term severe hyponatraemia (< 120 mmols/l) being treated too quickly (> 10 mmol/l increase over 24 hours)

To avoid this, Na+ levels are only raised by 4 to 6 mmol/l in a 24-hour period

Question 16

presentation osmotic demyelination syndorme

Answer 16

symptoms usually occur after 2 days and are usually irreversible: dysarthria, dysphagia, paraparesis or quadriparesis, seizures, confusion, and coma, patients are awake but are unable to move or verbally communicate, also called ‘Locked-in syndrome’

Question 17

where is ADH produced? where is it secreted from?

Answer 17

Antidiuretic hormone (ADH) is produced in the hypothalamus and secreted by the posterior pituitary gland. It is also known as “vasopressin”.

can also be produced and released from ectopic sites eg small cell lung cancers

Question 18

name some causes of SIADH

Answer 18

SIADH

Small cell lung tumours
Infection (particularly atypical pneumonia)
Abscess
Drugs (use SIADH cannot void)
Head injury
post-op from major surgery

Drugs:
SSRIs
Inhibitors (ACEi, PPI)
Antidepressants eg TCAs
Diuretics
Haloperidol
Cannot: carbamazepine
Void: vincristine

Question 19

what do you think when someone has persistent hyponatraemia with no clear cause

Answer 19

suspect malignancy

Particularly in someone with a history of smoking, weight loss or other features of malignancy.

If malignancy is suspected the NICE CKS (March 2015) recommend a CT thorax/abodmen/pelvis and MRI brain to find the malignancy.

Question 20

hypovolemia vs dehydration

Answer 20

Hypovolemia refers to a decreased volume of fluid in the vascular system with or without whole body fluid depletion. Dehydration is the depletion of whole body fluid. Hypovolemia and dehydration are not mutually exclusive nor are they always linked.

Question 21

how to ddx between cerebral salt wating and SIADH

Answer 21

both can be caused by head injury

cerebral salt wasting - hypovolemic

SIADH - euvolemic

Question 22

what kind of steroid is aldosterone, where is it produced?

Answer 22

mineralocorticoid

zona glomerulosa of the adrenal cortex

Question 23

pathophysiology addison’s disease

Answer 23

Autoimmune destruction of the adrenal glands

no adrenal glands –>
- no aldosterone - low sodium, high potassium, high H+ (metabolic acidosis

• no cortisol so low glucose

Question 24

symptoms of addisons

Answer 24

lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women,

Question 25

why do you get hypermigmentation is addisons

Answer 25

no negative feedback to decrease ACTH so is high - this stimulates melanocytes

Question 26

symptoms adrenal crisis? signs

Answer 26

collapse, shock, pyrexia

Reduced consciousness
Hypotension
Hypoglycaemia
Hyponatraemia and hyperkalaemia

Question 27

examination findings addisons

Answer 27

Hypotension (particularly postural hypotension – with a drop of more than 20 mmHg on standing)

muscle weakness

hyperpigmentation (especially palmar creases)*

medical alert bracelet worn to alert medical services that they are steroid-dependent if they become unconscious.

Question 28

U&Es addisons, glucose

Answer 28

low sodium
high potassium
metabolic acidosis
Raised creatinine and urea due to dehydration
Hypercalcaemia (high calcium)
hypoglycaemia

Question 29

test of choice for diagnosing adrenal insufficiency

Answer 29

short Synacthen test

Question 30

what does the short synthacten test involve? interpretation of short synthacten test

Answer 30

dose of Synacthen, which is synthetic ACTH. Cortisol is checked before and 30 and 60 minutes after the dose. The synthetic ACTH will stimulate healthy adrenal glands to produce cortisol. The cortisol level should at least double. A failure of cortisol to double indicates either:
Primary adrenal insufficiency (Addison’s disease)
Very significant adrenal atrophy after a prolonged absence of ACTH in secondary adrenal insufficiency

Question 31

what other test other than short synthacten has a role ?addisons

Answer 31

Early morning cortisol (8 – 9 am) has a role but is often falsely normal

Question 32

autoantibodies addisons

Answer 32

Adrenal cortex antibodies
21-hydroxylase antibodies

Question 33

why may someone go into adrenal crisis

Answer 33

It may be the initial presentation of adrenal insufficiency or triggered by infection, trauma or other acute illness in established adrenal insufficiency.

Question 34

Initial management adrenal crisis

Answer 34

IV or IM hydrocortisone

(the initial dose is 100mg, followed by an infusion or 6 hourly doses)

Question 35

management of adrenal crisis

Answer 35

dont wait for investigations

ABCDE
IV or IM hydrocortisone
IV fluids
IV dextrose to correct hypoglycaemia
Careful monitoring of electrolytes and fluid balance

Question 36

long term management addison’s disease

Answer 36

hydrocortisone: usually given in 2 or 3 divided doses. Patients typically require 20-30 mg per day, with the majority given in the first half of the day

fludrocortisone

PLUS hydrocortisone IM kit for addisons crisis

Patient education and advice about medical alert bracelt

Question 37

management of steroids addison’s disease with intercurrent illness

Answer 37

glucocorticoid dose should be doubled, with the fludrocortisone dose staying the same