SIADH

Question 1

Where is ADH (anti-diuretic hormone) produced and where is it secreted?

Answer 1

produced by the hypothalamus

secreted by the posterior pituitary

Question 2

What does ADH do?

Answer 2

it stimulates water reabsorption from the collecting ducts in the kidneys

Question 3

What is SIADH?

Answer 3

SIADH is there there is inappropriately large amounts of ADH

Question 4

What causes the excess ADH?

Answer 4

posterior pituitary secreting too much

or ADH may be coming from another source e.g small cell lung cancer**, (also prostate and pancreas)

Question 5

Besides malignancy, what are other causes of SIADH?

Answer 5

Infections: e.g Pneumonia, TB

Neurological e.g: stroke,, haemorrhage, menigits/encephalitis/abscess

Drugs e.g SSRIs, duiretics, carbamazepine (and others)

others: Positive end expiratory pressure (PEEP)

Question 6

What does the excess ADH lead to?

Answer 6

> water reabsorbtion in the collecting duct

which dilutes the sodium in the blood leading to hyponatraemia

Excessive water reabsorption usually not enough to lead to fluid overload so: EUVOLAEMIC HYPONATRAEMIA

Urine becomes more concentrated - high urine osmolality, high urine sodium

Question 7

How does SIADH present?

Answer 7

non specific symptoms

• headache
• fatigue
• muscle aches and cramps
• confusion
• if severe hyponatraemia: seizures and reduced consciousness

Question 8

How do you diagnose SIADH?

Answer 8

diagnosis of exclusion - do not test ADH

clinically:
- euvolaemic
- U+Es: hyponatraemia
- Urine sodium and osmolality = high
- CXR to establish if pneumonia, lung abscess/cancer
- if malignancy suspected: CT

other causes of hyponatraemia to exclude:

• Negative short synacthen test to exclude adrenal insufficiency
• No history of diuretic use
• No diarrhoea, vomiting, burns, fistula or excessive sweating
• No excessive water intake
• No chronic kidney disease or acute kidney injury

Question 9

What is the management of SIADH?

What is a key thing to remmeber?

Answer 9

Correction must be slow to avoid central pontine myelinolysis

• fluid restriction
• Tolvaptan (vaptan) - ADH receptor blockers initiated by endocrinologist, close monitoring needed
• Demeclocyline - inhibits ADH

Question 10

What is central pontine myelonolysis / osmotic demyelination syndrome

Physiology?

Answer 10

complication of long term severe hyponatraemia (<12 mmols/l) when treated too quickly (>10mmol/l increase in 24hrs)

• As blood sodium level falls, water moves across the BBB into the brain, causing brain to swell
• brain responds by reducing solutes so water can leave and brain does not become oedematous
• if hyponatraemia has been present for a long time, brain cells will have low osmolality
• when blood sodium level rise due to treatment - water will shift out of the brain cells rapidly
  leads to

Phase 1: encephalopathic and confused, maybe N+V+ Headache (due to electrolyte imbalance) symptoms often resolve before 2nd phase

Phase 2: demyelination of neurons esp pons - few days after rapid Na+ correction - spastic quadraperesis, pseudonulbar palsy, behavioural changes, risk of death

Question 11

What is the prognosis for central pontine myelinolysis?

Answer 11

supportive

most left with neurological deficits