SiADH Flashcards
What is the Syndrome of Inappropriate Antidiuretic Hormone (SIADH)?
SIADH refers to increased release of antidiuretic hormone (ADH) from the posterior pituitary, which leads to water reabsorption, diluting the blood and causing hyponatraemia (low sodium).
Where is antidiuretic hormone (ADH) produced, and what is its role?
ADH is produced in the hypothalamus and secreted by the posterior pituitary. It stimulates water reabsorption in the kidneys’ collecting ducts.
What are the two main sources of excess ADH in SIADH?
- Increased secretion by the posterior pituitary
- Ectopic ADH, commonly from small cell lung cancer
What does excess ADH result in within the body?
Excess ADH causes increased water reabsorption in the kidneys, diluting the blood, leading to hyponatraemia and euvolaemic hyponatraemia (normal blood volume).
What are the typical urine characteristics in SIADH?
In SIADH, the urine becomes more concentrated with high urine osmolality and high urine sodium due to decreased water excretion by the kidneys.
What are the symptoms of SIADH due to low sodium (hyponatraemia)?
- Headache
- Fatigue
- Muscle aches and cramps
- Confusion
- Severe hyponatraemia can cause seizures and reduced consciousness.
What are the common causes of SIADH?
- Post-operative after major surgery
- Lung infection (e.g., atypical pneumonia, lung abscesses)
- Brain pathologies (e.g., stroke, head injury, meningitis)
- Medications (e.g., SSRIs, carbamazepine)
- Malignancy, especially small cell lung cancer
- HIV
What are the top three causes of SIADH to remember?
- Post-operative status
- SSRIs
- Small cell lung cancer
What tests are needed to diagnose SIADH?
Diagnosis is based on clinical features such as:
* Euvolaemia
* Hyponatraemia
* Low serum osmolality
* High urine sodium and osmolality
What other causes of hyponatraemia must be excluded when diagnosing SIADH?
- Adrenal insufficiency (short synacthen test)
- Diuretic use
- Diarrhoea, vomiting, burns, excessive sweating, or excessive water intake
- Chronic kidney disease, acute kidney injury, heart failure, or liver disease
How do you distinguish primary polydipsia from SIADH?
Primary polydipsia is characterized by excessive water intake without an underlying cause, leading to euvolaemic hyponatraemia. It differs from SIADH in that urine sodium and osmolality are low in primary polydipsia.
How do you establish the cause of SIADH?
The cause may be identified if the hyponatraemia resolves after removing the cause (e.g., stopping medications or treating infection). Imaging (e.g., chest x-ray, CT, MRI) may be used to exclude malignancies, particularly small cell lung cancer.
How is SIADH managed?
- Admission if symptomatic or severe (e.g., sodium < 125 mmol/L)
- Treating the underlying cause (e.g., stopping causative medications or treating infection)
- Fluid restriction (750-1000 mL/day)
- Vasopressin receptor antagonists (e.g., tolvaptan)
- Slow correction of sodium to avoid osmotic demyelination (max 10 mmol/L change in 24 hours)
What is Osmotic Demyelination Syndrome (ODS)?
ODS (also known as central pontine myelinolysis) is a complication of rapid correction of severe hyponatraemia. It causes brain cell damage due to water shifts, leading to neurological deficits and possible death.
What are the symptoms and stages of Osmotic Demyelination Syndrome (ODS)?
- First Phase: Electrolyte imbalance, confusion, headache, vomiting, and seizures.
- Second Phase: Demyelination of neurons, particularly in the pons, causing spastic quadriparesis, pseudobulbar palsy, and cognitive changes.
How can Osmotic Demyelination Syndrome (ODS) be prevented?
Prevention is crucial by correcting sodium slowly to avoid rapid shifts in brain water. Treatment is supportive once ODS occurs, and many patients experience neurological deficits.
