SIADH Flashcards

1
Q

What is SIADH

A

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.

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2
Q

Epidemiology

A
  • 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)
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3
Q

Neurological aetiology of SIADH

A
  • Meningitis, encephalitis or cerebral abscess
  • Intracranial haemorrhage, e.g. subarachnoid or subdural haemorrhage
  • Stroke
  • Trauma
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4
Q

Cancerous aetiology of SIADH

A
  • Small cell carcinoma of the lung most commonly
  • Other cancers, e.g. breast cancer, and head and neck tumours, are rarer causes
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5
Q

Infectious and Endocrine aetiology of SIADH

A
  • Infections
    • Pneumonia
    • Tuberculosis
    • HIV
  • Endocrine
    • Hypothyroidism
    • Hypopituitarism
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6
Q

Pneumonic for drugs that can cause SIADH

A

CARDISH

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7
Q

CARDISH

A

chemo, antidepressants, recreational drugs, diuretics, inhibitors e.g. ACEI & SSRIs, sulfonylurea, hormones e.g. desmopressin)
PPIs
TCAs

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8
Q

RFs

A
  • Age >50
  • Pulmonary conditions
  • Malignancy
  • Medicine associated with SIADH induction
  • CNS disorder
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9
Q

Pathophysiology of SIADH

A

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.

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10
Q

What happens to the kidney’s in SIADH?

A

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.

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11
Q

What do the clinical features in SIADH depend on?

A

degree of hyponatraemia and the rate of change in serum sodium levels (acute or chronic)

Large proportion asymptomatic

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12
Q

Key presentations for SIADH

A

Hyponatraemic and euvolaemic (no features of hyper- or hypovolaemia)

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13
Q

Symptoms of SIADH

A

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
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14
Q

Investigations for SIADH

A

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.

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15
Q

Diagnostic criteria

A
  • 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)
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16
Q

First line treatment

A

Fluid restriction

17
Q

Acute management of SIADH <48 hrs onset

A

Acute hyponatraemia must be treated urgently due to the risk of cerebral oedema and herniation

  • Hypertonic (3%) saline is preferred - slow infusion to avoid complications
  • Furosemide (diuretic) - in patients who have fluid overload. Causes an increase in water, Na+, Ka+ and Cl- excretion. (Note: KCl should be replaced)
18
Q

Chronic management of SIADH
Mild to moderate asymptomatic cases

A
  • fluid restriction to increase Na+ conc
    • Fluid restriction may not be used in SIADH secondary to subarachnoid haemorrhage as it risks lowering blood pressure which may cause cerebral vasospasm and infarction.
19
Q

Management of severe or symptomatic cases

A
  • Demeclocycline, a tetracycline antibiotic, causes an iatrogenic nephrogenic diabetes insipidus through the inhibition of ADH. Though historically popular it is rarely used today.
  • A newer class of drugs termedvaptans(e.g. tolvaptan) are now more commonly used. These ADH receptor antagonists are effective but expensive agents.
20
Q

Complications of SIADH

A
  • Cerebral oedema: hyponatraemia lowers the osmolality of the blood causing an osmotic shift of water into brain tissue with subsequent oedema and risk of herniation
  • Central pontine myelinolysis:rapid correction of sodium can cause osmotic demyelination, particularly in chronic hyponatraemia (slow correction is vital)
    • Manifests as tremors, dysarthria, quadriplegia, ophthalmoplegia, seizures and extrapyramidal symptoms
    • May result in ‘locked-in syndrome’, where patients are awake but unable to verbally communicate or move
    • Diagnosis is confirmed with MRI