SIADH Flashcards
What is SIADH?
Increased release of ADH from the posterior pituitary
What is the impact of too much ADH?
Water reabsorption from the urine is increased (in the collecting ducts of the kidneys) - this causes hyponatraemia
What are the two potential sources of excess ADH?
Increased production by the posteior pituitary
Ecoptic ADH, most commonly from small cell lung cancer
What is serum and urine osmolality like in SIADH?
Low serum osmolality
High urine osmolality
What is the presentation of SIADH?
Headache
Fatigue
Muscle cramps
Confusion
Reduced consciousness (severe hyponatraemia)
Seizures (severe hyponatraemia)
What are the possible causes of SIADH?
Post-op after major surgery
Lung infection
Brain pathologies - head injury, stroke, meningitis
Medications - SSRIs, carbamazepine
Small cell lung cancer
HIV
Hypothyroidism
What are the diagnostic criteria for SIADH?
Low plasma osmolality - <275
High urine osmolality > 100
High urine sodium > 30 mmol/L
Clinical euvolaemia
Exclusion of glucocorticoid deficiency
What is the managment of acute SIADH?
Acute SIADH < 48 hours - treatment of hyponatraemia
- Hypertonic 3% saline
What is the management of chronic SIADH (> 48 hours)?
Maximum increase of 10mmol/L per day of sodim
- Fluid restriction for mild cases
- Demeclocycline or ADH receptor antagonists (tolvaptan) for severe cases
What are the complications of SIADH?
Cerebral oedema
Central pontine myelinolysis (due to rapid correction of sodium)
What is central pontine myelinolysis?
Demyelination (typically of the pontine white matter tracts) following rapid correction of hyponatraemia
What is the presentation of central pontine myelinosis?
Tremors
Dysarthria
Quadriplegia
Seizures
Extrapyramidal symptoms
Locked in syndrome
How is diagnosis of central pontine myelinolysis confirmed?
MRI
