SIADH Flashcards
What is ADH also called?
Vasopressin
What does ADH do?
Stimulates water reabsorption from the collecting ducts
What is the effect of excessive ADH production?
Excessive water reabsorbed
Water dilutes the sodium in the blood –> hyponatraemia
Water not usually enough to cause fluid overload so –> euvolaemic hyponatraemia
Urine becomes more concentrated –>
- high urine osmolality
- high urine sodium
What are the clinical features of SIADH?
Headache Confusion Muscle aches + cramps Fatigue Severe hyponatraemia --> seizures and reduced consciousness
What are the possible causes of SIADH?
Post-op from major surgery Infection, esp atypical pneumonia + lung abscesses Head injury Medications Malignancy esp small cell lunch cancer Meningitis
Which drugs might cause SIADH?
Thiazide diuretics Carbamazepine Vincristine Cyclophosphamide Antipsychotics SSRIs NSAIDs
How is SIADH diagnosed?
Euvolaemia
Hyponatraemia
High urine sodium + osmolality
Exclude other causes of hyponatraemia?
Which other causes of hyponatraemia should be excluded?
Adrenal insufficiency (-ve short synacthen test)
Diuretic use
Diarrhoea, vomiting, burns, fistula or excessive sweating
Excessive water intake
CKD or AKI
How is SIADH managed?
Treat the cause e.g. stop causative medications
Correct the sodium slowly:
- fluid restriction (500-1000ml) may be enough to correct
- tolvaptan (ADH receptor blocker)
Why does sodium need to be increased slowly? at what rate should it be increased?
Risk of central pontine myelinolysis
Aim for a change in sodium of < 10 per 24 hours
What is central pontine myelinolysis (CPM)?
Aka osmotic demyelination syndrome
Complication of severe hyponatraemia (< 120) being treated too quickly (> 10 per 24 hours)
What happens when hyponatraemia in reversed too quickly causing CPM?
As sodium levels rise, water shifts rapidly out of the brain cells into the blood:
- first phase due to electrolyte imbalance
- second phase due to demyelination of neurones, esp in pons
What are the features of the first phase of CPM?
Encephalopathic + confused
Headache
Nausea + vomiting
Usually resolves prior to onset of second phase
What are the features of the second phase of CPM?
Occurs a few days after rapid correction of sodium Spastic quadriparesis Pseudobulbar palsy Cognitive + behavioural changes Significant mortality
How is CPM managed?
Only supportive treatment
–> prevention is essential
