Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

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Basics

Syndrome of inappropriate secretion of antidiuretic hormone secretion (SIADH) is a common cause of hyponatremia in hospitalized patients. It was first described by Bartter and Schwartz in 1967 in two patients with lung cancer.

Description

  • SIADH is a disorder with impaired water excretion (concentrated urine), caused by the inability to suppress the secretion of antidiuretic hormone (ADH). If water intake is in excess of urine output, this results in hyponatremia.
    • Decreased urinary electrolyte-free water excretion leads to dilutional hyponatremia (total body sodium [Na] levels may be normal or near-normal, but the patient’s total body water is increased).
    • Often secondary to medications but may be associated with an underlying disorder, such as neoplasm, a pulmonary disorder, or CNS disease
  • Synonym(s): syndrome of inappropriate secretion of ADH; syndrome of inappropriate antidiuresis

Epidemiology

Incidence
  • Often found in the hospital setting, where incidence can be as high as 35%
  • Predominant age: elderly
  • Predominate sex: females > males

Prevalence
It is also prevalent in hospitalized postoperative patients in response to stress, hypotonic fluids, and drugs.

Etiology and Pathophysiology

  • Drugs:
    • Antidepressants (e.g., SSRIs, tricyclics, monoamine oxidase inhibitors [MAOIs])
    • Antineoplastic drugs (e.g., vincristine, vinblastine, cisplatin, cyclophosphamide)
    • Antipsychotic agents (e.g., risperidone, quetiapine, phenothiazines, haloperidol)
    • Analgesics (e.g., duloxetine, pregabalin, tramadol, NSAIDs)
    • Anticonvulsants (e.g., carbamazepine, oxcarbazepine, valproic acid, phenytoin)
    • Others (e.g., vasopressin, DDAVP, oxytocin, ciprofloxacin, α-interferon, ecstasy)
  • Malignancies (ectopic ADH production):
    • Bronchogenic carcinoma
    • Lymphoma
    • Mesothelioma
    • Small cell carcinoma of the lung
    • Pancreatic carcinoma
    • Thymoma
  • Pulmonary conditions:
    • Asthma/COPD/pneumothorax
    • Atelectasis
    • Cystic fibrosis
    • Positive pressure mechanical ventilation
    • Pneumonia (viral, bacterial)
    • Pulmonary tuberculosis (TB)
    • Sarcoidosis
  • Neurologic causes:
    • Brain tumor
    • CNS injury (i.e., SAH, trauma, stroke, surgery)
    • CNS lupus
    • Meningitis, encephalitis
    • Epilepsy
    • Multiple sclerosis, Guillain-Barré syndrome
  • Other:
    • Acute intermittent porphyria
    • Delirium tremens
    • HIV infection/AIDS
    • Rocky Mountain spotted fever
  • Hormone deficiency—hypopituitarism and hypothyroidism
  • Hereditary SIADH—a gain of function mutation in the gene for the renal V2

Genetics
  • Hereditary SIADH patients have an X-linked mutation of V2R.
  • Polymorphisms in TRPV4 gene

Risk Factors

  • Advanced age
  • Postoperative status
  • Institutionalization

General Prevention

  • Search for the cause, if unknown.
  • Reduce/change medications, if drug-induced.
  • Lifelong restriction of fluid intake

Commonly Associated Conditions

See “Etiology and Pathophysiology.”

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Basics

Syndrome of inappropriate secretion of antidiuretic hormone secretion (SIADH) is a common cause of hyponatremia in hospitalized patients. It was first described by Bartter and Schwartz in 1967 in two patients with lung cancer.

Description

  • SIADH is a disorder with impaired water excretion (concentrated urine), caused by the inability to suppress the secretion of antidiuretic hormone (ADH). If water intake is in excess of urine output, this results in hyponatremia.
    • Decreased urinary electrolyte-free water excretion leads to dilutional hyponatremia (total body sodium [Na] levels may be normal or near-normal, but the patient’s total body water is increased).
    • Often secondary to medications but may be associated with an underlying disorder, such as neoplasm, a pulmonary disorder, or CNS disease
  • Synonym(s): syndrome of inappropriate secretion of ADH; syndrome of inappropriate antidiuresis

Epidemiology

Incidence
  • Often found in the hospital setting, where incidence can be as high as 35%
  • Predominant age: elderly
  • Predominate sex: females > males

Prevalence
It is also prevalent in hospitalized postoperative patients in response to stress, hypotonic fluids, and drugs.

Etiology and Pathophysiology

  • Drugs:
    • Antidepressants (e.g., SSRIs, tricyclics, monoamine oxidase inhibitors [MAOIs])
    • Antineoplastic drugs (e.g., vincristine, vinblastine, cisplatin, cyclophosphamide)
    • Antipsychotic agents (e.g., risperidone, quetiapine, phenothiazines, haloperidol)
    • Analgesics (e.g., duloxetine, pregabalin, tramadol, NSAIDs)
    • Anticonvulsants (e.g., carbamazepine, oxcarbazepine, valproic acid, phenytoin)
    • Others (e.g., vasopressin, DDAVP, oxytocin, ciprofloxacin, α-interferon, ecstasy)
  • Malignancies (ectopic ADH production):
    • Bronchogenic carcinoma
    • Lymphoma
    • Mesothelioma
    • Small cell carcinoma of the lung
    • Pancreatic carcinoma
    • Thymoma
  • Pulmonary conditions:
    • Asthma/COPD/pneumothorax
    • Atelectasis
    • Cystic fibrosis
    • Positive pressure mechanical ventilation
    • Pneumonia (viral, bacterial)
    • Pulmonary tuberculosis (TB)
    • Sarcoidosis
  • Neurologic causes:
    • Brain tumor
    • CNS injury (i.e., SAH, trauma, stroke, surgery)
    • CNS lupus
    • Meningitis, encephalitis
    • Epilepsy
    • Multiple sclerosis, Guillain-Barré syndrome
  • Other:
    • Acute intermittent porphyria
    • Delirium tremens
    • HIV infection/AIDS
    • Rocky Mountain spotted fever
  • Hormone deficiency—hypopituitarism and hypothyroidism
  • Hereditary SIADH—a gain of function mutation in the gene for the renal V2

Genetics
  • Hereditary SIADH patients have an X-linked mutation of V2R.
  • Polymorphisms in TRPV4 gene

Risk Factors

  • Advanced age
  • Postoperative status
  • Institutionalization

General Prevention

  • Search for the cause, if unknown.
  • Reduce/change medications, if drug-induced.
  • Lifelong restriction of fluid intake

Commonly Associated Conditions

See “Etiology and Pathophysiology.”

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