SIADH (Syndrome of Inappropriate ADH secretion) - mechanism, pathophysiology, treatment

Summary

This video explains the Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH), a condition caused by excessive ADH release, leading to water retention and low sodium levels (hyponatremia). The script explores the physiology behind ADH, how it regulates water reabsorption in the kidneys, and how SIADH disrupts this balance. It also highlights the causes of SIADH, including brain trauma, CNS disorders, infections, and ectopic ADH production from cancers. Treatment involves managing hyponatremia, restricting fluid intake, and using medications like hypertonic saline and loop diuretics. Additionally, it discusses complications such as central pontine myelinolysis from rapid sodium correction.

Takeaways

• 😀 SIADH (Syndrome of Inappropriate Antidiuretic Hormone Secretion) is a disorder involving excessive secretion of ADH, leading to water retention and low sodium levels in the blood.
• 😀 ADH is produced in the hypothalamus and acts to increase water reabsorption in the kidneys through aquaporin channels, mainly in the collecting ducts.
• 😀 In SIADH, excessive ADH secretion results in **hyponatremia** (low sodium) and **hypoosmolarity**, causing fluid imbalance in the body.
• 😀 Causes of SIADH include brain trauma, CNS infections, lung cancer (ectopic ADH production), and medications such as chemotherapy, antidepressants, and diuretics.
• 😀 Acute hyponatremia, defined as a sodium level below 120 mmol/L, can cause severe complications such as cerebral edema, seizures, and even coma.
• 😀 Chronic hyponatremia allows for cerebral adaptation, preventing brain swelling, but still causes symptoms like headache, nausea, and vomiting.
• 😀 Diagnosing SIADH requires criteria such as hyponatremia with a normal extracellular fluid state, increased urine osmolality, and urine sodium > 20 mmol/L.
• 😀 Management of SIADH includes fluid restriction, administration of hypertonic saline for symptomatic patients, and medications like demeclocycline for chronic cases.
• 😀 One of the key mechanisms in SIADH is the inhibition of the renin-angiotensin-aldosterone system (RAAS), which leads to natriuresis (sodium excretion) and water loss.
• 😀 Rapid correction of hyponatremia can cause central pontine myelinolysis, a dangerous condition that leads to neurological deficits like quadriplegia and pseudobulbar palsy.

Q & A

What is SIADH and how is it defined?

SIADH, or Syndrome of Inappropriate Antidiuretic Hormone Secretion, is a condition where there is excessive release of ADH, leading to water retention and hyponatremia (low sodium levels in the blood).

What is the role of ADH in the body?

ADH, produced by the hypothalamus and released by the posterior pituitary, regulates water balance by increasing water reabsorption in the kidneys, specifically in the collecting ducts, via the aquaporin-2 channels.

How does ADH affect the kidneys?

ADH increases the expression of aquaporin-2 channels in the collecting ducts of the nephron, allowing more water to be reabsorbed into the bloodstream, which helps to maintain blood volume and reduce serum osmolarity.

What happens during SIADH in terms of water retention?

In SIADH, excessive ADH secretion causes increased water retention by the kidneys, leading to increased blood volume and decreased serum osmolarity (hypoosmolarity). This results in dilution of sodium in the blood, causing hyponatremia.

What are the main causes of SIADH?

SIADH can be caused by trauma, infections, or diseases affecting the central nervous system (like meningitis or stroke), malignancies producing ectopic ADH (e.g., small cell lung cancer), and certain medications (e.g., SSRIs, diuretics, chemotherapy drugs).

What are the symptoms of acute hyponatremia due to SIADH?

Acute hyponatremia can lead to dangerous symptoms like cerebral edema (brain swelling), seizures, neurogenic pulmonary edema, and even coma, due to rapid shifts of water into brain cells as a result of low sodium levels.

How does chronic hyponatremia differ from acute hyponatremia in terms of brain adaptation?

In chronic hyponatremia, the brain adapts by shifting electrolytes like sodium and potassium into circulation, preventing cerebral edema. This allows for safer water balance despite low sodium, unlike acute hyponatremia, which causes rapid cerebral edema.

What diagnostic criteria are used to diagnose SIADH?

The diagnostic criteria for SIADH include hyponatremia with a normal extracellular fluid state (euvolemia), urine osmolality higher than plasma osmolality, urine sodium greater than 20 mmol/L, and the exclusion of other causes like diuretics, thyroid, or adrenal issues.

What is the role of the renin-angiotensin-aldosterone system in SIADH?

In SIADH, increased blood volume and natriuresis (sodium excretion) result in decreased activity of the renin-angiotensin-aldosterone system (RAAS). This leads to decreased aldosterone secretion and promotes further sodium excretion through the kidneys.

How is SIADH managed clinically?

Management of SIADH includes fluid restriction (500 mL to 1 liter per day), the administration of hypertonic saline for symptomatic hyponatremia, and the use of vaptans (ADH receptor antagonists) in chronic cases. It is also essential to treat the underlying cause of SIADH.