SIADH Flashcards
What is SIADH
syndrome of inappropriate anti-diuretic hormone (SIADH) results from excess ADH secretion.
results in reduced diuresis - water excretion and urinary output are reduced. This leads to an increase in total body water and hyponatraemia.
Epidemiology
- Hyponatraemia is the most common electrolyte disorder encountered in clinical practice
- The prevalence of hyponatraemia in the community is around 8% and increases with age (approximately 12% in people aged 75 or older)
Neurological aetiology of SIADH
- Meningitis, encephalitis or cerebral abscess
- Intracranial haemorrhage, e.g. subarachnoid or subdural haemorrhage
- Stroke
- Trauma
Cancerous aetiology of SIADH
- Small cell carcinoma of the lung most commonly
- Other cancers, e.g. breast cancer, and head and neck tumours, are rarer causes
Infectious and Endocrine aetiology of SIADH
-
Infections
- Pneumonia
- Tuberculosis
- HIV
-
Endocrine
- Hypothyroidism
- Hypopituitarism
Pneumonic for drugs that can cause SIADH
CARDISH
CARDISH
chemo, antidepressants, recreational drugs, diuretics, inhibitors e.g. ACEI & SSRIs, sulfonylurea, hormones e.g. desmopressin)
PPIs
TCAs
RFs
- Age >50
- Pulmonary conditions
- Malignancy
- Medicine associated with SIADH induction
- CNS disorder
Pathophysiology of SIADH
Increased ADHresults in increased free water retention, subsequent dilution of the blood and a decrease in solutes in the blood.
Increase in blood volume leads to stretching of heart muscle and release of ANP and BNP (natriuretic peptide) > Inhibits RAAS > promotes natriuresis (excretion of sodium). This leads to sodium and water excretion, which promotes further ADH activity.
What happens to the kidney’s in SIADH?
Overtime, the kidneys will adapt.
The number of aquaporin channels will decrease to compensate for the amount of ADH present.
This will now lead to diuresis as well as natriuresis. This is why there is there is a euvolaemic state rather than a hypervolaemic state, coupled with hyponatraemia.
Overall: patients will have high urine Na+ levels and low serum Na+ levels.
What do the clinical features in SIADH depend on?
degree of hyponatraemia and the rate of change in serum sodium levels (acute or chronic)
Large proportion asymptomatic
Key presentations for SIADH
Hyponatraemic and euvolaemic (no features of hyper- or hypovolaemia)
Symptoms of SIADH
Mild(130-135 mmol/L):
- Nausea, vomiting, headache, lethargy, anorexia
Moderate(125-129 mmol/L):
- Weakness, muscle aches, confusion, ataxia, asterixis
Severe(< 125 mmol/L):
- Reduced consciousness, seizures, myoclonus, respiratory arrest
Investigations for SIADH
Blood tests
Renal function: gives a serum sodium that confirms hyponatraemia. May also show a low serum urea consistent with mild volume expansion.
Serum osmolality: a low serum osmolality is seen, less than 280 mOsm/kg.
Urinary tests
Urinary osmolality: a high urine osmalality is seen, greater than 100 mOsm/kg.
Urine sodium: typically a high urinary sodium is seen, greater than >40 mmol/L.
Diagnostic criteria
- Low plasma osmolality: < 275 mOsm/kg
- High urine osmolality: > 100 mOsm/kg
- High urine sodium: > 30 mmol/L
- Clinical euvolaemia
- Exclusion of glucocorticoid deficiency or hypothyroidism(rare)