Syndrome of Inappropriate Vasopressin Sexretion (Siadh)

SYNDROME OF INAPPROPRIATE
VASOPRESSIN SECRETION (SIADH)
UNIVERSITY OF HEALTH SCIENCES

FACULTY OF MEDICINE
IM BUNTHOEUN
2017
OBJECTIVES
- Review physiology of ADH
- Define SIADH
- Enumerate the clinical presentation of SIADH
- Describe etiology of SIADH
- Explain the pathophysiology of SIADH
- Describe clinical manifestations of SIADH

Osmoreceptor
Osmotic pressure
Hypothalamic
Posterior pituitary
ADH
Kidneys (V2 receptor)

Water reabsorption
distal tubule
> 10 liters / day
Collecting duct
Barroreceptor • Hemorrhage
• Blood pressure
Hypothalamus
Blood pressure
ADH
Blood vessel
V1receptor Vasoconstriction
DEFINITION
- SIADH is one of several causes of a hypotonic

state and due to the secretion of vasopressin in
excess what is appropriate for hyperosmolality
or intravascular volume depletion.
The hypotonic syndromes
1 Excessive water ingestion
2 Decreased water excretion
a- Vasopressin excess
SIADH
Drug induced vasopressin secretion
b-Vasopressin excess with decreased distal solute delivery
Heart failure
Cirrhosis of the liver
Nephrotic syndrome
Cortisol deficiency
Diuretic use
Renal failure
CLINICAL PRESENTATION
- Hyponatremia without edema.
- Depending on the rapidity and the severity, the

neurologic consequences of hyponatremia include
• confusion,
• lethargy and weakness,
• myoclonus,
• asterixis,
• generalized seizures, and
• coma.
ETIOLOGY
- Vasopressin secreting tumors
- Central nervous system disorder
- Pulmonary disorder and drugs
- Nephrogenic SIADH (V2 receptors mutation)

ETIOLOGY
- Tumors
• Bronchial carcinoma (particularly small cell type)
• Other carcinoma: duodenum, pancreatic, bladder,..
• Leukemia, lymphoma
- Central nervous system disorders

• Mass lesions: tumors, abscess, hematoma
• Infection: encephalitis, meningitis
• Cerebrovascular accident
• Trauma
• Inflammatory disease
ETIOLOGY
- Pulmonary disorders:
• infection: tuberculosis, pneumonia, abscess
• acute respiratory failure
• positive pressure ventilation
- Drugs:
• vasopressin, chlorpropamide, clofibrate, carbamazepine
• others : general anesthesia, vincristine
PATHOPHYSIOLOGY
- The serum sodium level: determined by

• the balance of water intake,
• renal solute delivery (a necessary step in water
excretion)
• vasopressin
- Hyponatremia occurs:
• when disorder exceeds the capacity of homeostatic
mechanisms
• Adrenal insufficiency, hypothyroidism
PATHOPHYSIOLOGY
- Despite hyponatremia occurs: urinary excretion of

sodium was preserved because of
• Hypervolemia
• No action of renin angiotensin system
• Increase GFR
• Decrease renal tubular reabsorption of sodium
• Increase ANP (FNA)

PATHOPHYSIOLOGY
- Pseudohyponatremia
• infusion of hyperosmolar solutions
• nonacqueous fraction of plasma is large than normal
- In most cases the hyponatremia of SIADH is partialy

limited by secretion of atrial natriuretic peptide
Causes of pseudohyponatremia
- Elevated plasma osmolality

• Hyperglycemia
• Manitol administration
- Normal plasma osmolality

• Hyperproteinemia (multiple myeloma)
• Hyperlipidemia
PATHOPHYSIOLOGY
- SIADH and post surgery

• After surgery
- ADH secretion increased within 3 to 5 day
- Hyponatremia occurs within 48 H
- Surgical stress or/and organism reply to the pain
due to:
• hypovolemia
• general anesthesia or hypotonic fluid
CLINICAL MANIFESTATIONS
- The pathophysiologic mechanism behind most cases of

SIADH are not well understood.
- Clinical manifestation determined by:

• The nature and course of any underlying disorder
• The severity of hyponatremia and
• The rapidity with which hyponatremia develops
- Neurologic manifestation: confusion, myoclonus,

generalized seizures, and coma
- Serum sodium level:

• slowly decreased, but less than 110-115 meq/L: likely
severe and sometimes irreversible neurologic
damage
• rapidly decreased from 140-130 meq/L: thirst,
impaired taste, anorexia, fatigue
• from 130-120 meq/L severe gastrointestinal
symptoms (vomiting, abdominal cramps)
• less than 115 meq/L: confusion, convulsion
- Central pontine myelinolysis: due to rapid correction of

hyponatremia
• acute paralysis, dysphagia (difficulty swallowing),
and dysarthria(difficulty speaking), and other
neurological symptoms.
• Hyponatremia should be corrected at a rate of no

more than 8-10 mmol/L of sodium per day to prevent
central pontine myelinolysis.
Evaluation
• Serum hypoosmolality(<280 mOsm/kg) and

hyponatremia, sodium level <135 mEq/L);
• Urine hyperosmolarity
• Urine sodium excretion that matches sodium intake;
• Normal renal, adrenal, and thyroid function; and
• Absence of conditions that can alter volume status

(e.g.,recent diuretic use, heart failure, hypervolemia
from any cause, or renal insufficiency)
- Tumors
Syndrome of inappropriate
- CNS disorders
ADH secretion
- Pulmonary disorders
- Drugs
ADH
Dilution of serum Hypervolemia

electrolytes Highly concentrated urine
(Urine osmolality > 300 mOsm/kg)
Dilution of sodium Expanded Atrial natriuretic

circulating peptide
volume
Hypoosmolar
hyponatremia Natriuresis
Exacerbation of Symptoms of
hyponatremia hyponatremia
• Confusion
• Nausea
• seizure
REFERENCES
• S Silbernagl Florian LANG (2000), Atlas de poche de

physiopathology.
• Stephen J. McPhee et al (2014), Pathophysiology of
disease: an introduction to clinical medicine
• Thomas J. Nowak, et al, 2014. Essentials of
Pathophysiology. Concepts of Altered Health States

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SYNDROME OF INAPPROPRIATE

VASOPRESSIN SECRETION (SIADH)

UNIVERSITY OF HEALTH SCIENCES

- Review physiology of ADH

- Enumerate the clinical presentation of SIADH

- Describe etiology of SIADH

- Explain the pathophysiology of SIADH

- Describe clinical manifestations of SIADH

Kidneys (V2 receptor)

- SIADH is one of several causes of a hypotonic

- Hyponatremia without edema.

- Depending on the rapidity and the severity, the

- Vasopressin secreting tumors

- Central nervous system disorder

- Pulmonary disorder and drugs

- Nephrogenic SIADH (V2 receptors mutation)

- Central nervous system disorders

- The serum sodium level: determined by

- Despite hyponatremia occurs: urinary excretion of

• No action of renin angiotensin system

• Decrease renal tubular reabsorption of sodium

• Increase ANP (FNA)

- In most cases the hyponatremia of SIADH is partialy

- Elevated plasma osmolality

- Normal plasma osmolality

- SIADH and post surgery

- The pathophysiologic mechanism behind most cases of

- Clinical manifestation determined by:

- Neurologic manifestation: confusion, myoclonus,

- Serum sodium level:

- Central pontine myelinolysis: due to rapid correction of

• Hyponatremia should be corrected at a rate of no

• Serum hypoosmolality(<280 mOsm/kg) and

• Urine sodium excretion that matches sodium intake;

• Normal renal, adrenal, and thyroid function; and

• Absence of conditions that can alter volume status

Dilution of serum Hypervolemia

Dilution of sodium Expanded Atrial natriuretic

• S Silbernagl Florian LANG (2000), Atlas de poche de

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