SIADH

Question 1

Causes of SIADH

Answer 1

• Post-operative from major surgery
• Infection, particularly atypical pneumonia and lung abscesses
• Head injury
• Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDSs,)
• Malignancy, particularly small cell lung cancer
• Meningitis

Question 2

Pathophysiology of SIADH

Answer 2

• ADH isproduced in thehypothalamus and secreted by theposterior pituitary gland. It is also known as vasopressin. ADH stimulates water reabsorption from thecollecting ductsin the kidneys. SIADH is a condition where there is inappropriately large amounts of ADH.
• This may be the result of theposterior pituitary secreting too much ADH or the ADH may be coming from somewhere else, for example asmall cell lung cancer.
• The excessive ADH results in excessive water reabsorption in thecollecting ducts. This waterdilutesthe sodium in the blood so you end up with a low sodium concentration (hyponatraemia). The excessive water reabsorption is not usually significant enough to cause a fluid overload, therefore you end up with a euvolaemic hyponatraemia. The urine becomes more concentrated as less water is excreted by the kidneys therefore patients with SIADH have a “highurine osmolality” and “highurine sodium”.

Question 3

Risk factors:

Answer 3

cancer risk factors (small cell carcinoma)

infection

head injury etc

Question 4

Clinical presentation of SIADH

Answer 4

symptoms are non specific:

• Headache
• Fatigue
• Muscle aches and cramps
• Confusion
• Severe hyponatraemiacan cause seizures and reduced consciousness

Question 5

Investigation/diagnosis of SIADH

Answer 5

SIADH is a diagnosis of exclusion as we do not have a reliable test to directly measure ADH activity. Clinical examination will showeuvolaemia. U+Es will show a hyponatraemia. Urine sodium and osmolality will be high.

Other causes of hyponatraemia need to be excluded:

• Negativeshort synacthen testto exclude adrenal insufficiency
• No history of diuretic use
• No diarrhoea, vomiting, burns, fistula or excessive sweating
• No excessive water intake
• Nochronic kidney diseaseoracute kidney injury

Question 6

Treatment of SIADH

Answer 6

The aim is to establish and treat the cause of the SIADH. It is most common for medications to be the cause so if possible it is best to stop the causative medication. It is essential correct the sodium slowly to preventcentral pontine myelinolysis. Aim for a change in sodium of less than 10 mmol/l per 24 hours.

• Fluid restrictioninvolves restricting their fluid intake to 500mls – 1litre. This may be enough to correct the hyponatraemia without the need for medications.
• Tolvaptan. “Vaptans” areADH receptor blockers. They are very powerful and can cause a rapid increase in sodium. Therefore they are usually initiated by a specialist endocrinologist and require close monitoring, for example 6 hourly sodium levels.
• Demeclocyclineis atetracycline antibiotic that inhibits ADH. It was used prior to the development of vaptans and is now rarely used for this purpose.

Question 7

Complication of SIADH treatment?

Answer 7

Central pontine myelinosis (CPM) - known as osmotic demyelination syndrome

• complication of long term severe hyonatraemia (<120 mmols/l) being treated too quickly