Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

Etiology

Neuropschiatric Disease

Gastrointestinal Disease

Neoplastic Disease

Pulmonary Disease

Drugs

Stimulation of Vasopressin Release

  • Acetylcholine
  • Amitriptyline
  • Barbiturates (see Barbiturates, [[Barbiturates]])
  • Bromocriptine
  • Carbachol
  • Carbamazepine (Tegretol) (see Carbamazepine, [[Carbamazepine]])
  • Chlorpropamide (see Chlorpropamide, [[Chlorpropamide]])
  • Clofibrate (Atromid-S) (see Clofibrate, [[Clofibrate]])
  • Cyclophosphamide (Cytoxan) (see Cyclophosphamide, [[Cyclophosphamide]])
  • Cyclopropane
  • Desipramine
  • Halothane
  • Haloperidol (Haldol) (see Haloperidol, [[Haloperidol]])
  • Histamine
  • Ifosfamide (see Ifosfamide, [[Ifosfamide]])
  • Isoproterenol (Isuprel) (see Isoproterenol, [[Isoproterenol]])
  • Lorcainide
  • Morphine (see Morphine, [[Morphine]])
  • Nicotine (see Nicotine, [[Nicotine]])
  • Nitrous Oxide (see Nitrous Oxide, [[Nitrous Oxide]])
  • Oxcarbazepine
  • Thioridazine
  • Thiopental
  • Tranylcypromine
  • Vidarabine (see Vidarabine, [[Vidarabine]])
  • Vinblastine (see Vinblastine, [[Vinblastine]])
  • Vincristine (see Vincristine, [[Vincristine]])

Potentiation of Peripheral Activity of Vasopressin

  • Clofibrate (Atromid-S) (see Clofibrate, [[Clofibrate]])
  • Griseofulvin (see Griseofulvin, [[Griseofulvin]])
  • Hypoglycemic Agents
  • Non-Steroidal Anti-Inflammatory Drugs (NSAID) (see Non-Steroidal Anti-Inflammatory Drug, [[Non-Steroidal Anti-Inflammatory Drug]]): inhibit renal PGE2 synthesis
  • Oxytocin (see Oxytocin, [[Oxytocin]]): at high doses
  • Theophylline (see Theophylline, [[Theophylline]])
  • Triiodothyronine
  • Vasopressin Analogs

Unknown Mechanism

Other

  • Exercise-Induced Hyponatremia
  • Giant Cell Arteritis (see Temporal Arteritis, [[Temporal Arteritis]])
  • Human Immunodeficiency Virus (HIV) (see Human Immunodeficiency Virus, [[Human Immunodeficiency Virus]]): Hyponatremia has been reported in as many as 40% of adult patients with HIV infection. Patients with acquired immunodeficiency syndrome (AIDS) can have many potential causes for increased ADH secretion, including volume depletion and infection of the lungs and the CNS.[5] Although one third of the hyponatremic patients with AIDS are clinically hypovolemic, the remaining hyponatremic patients fulfill most of the criteria for SIADH.
  • Idiopathic SIADH

Diagnosis

  • In the absence of a single laboratory test to confirm the diagnosis, SIADH is best defined by the classic Bartter-Schwartz criteria, which can be summarized as follows[1] :
    Hyponatremia with corresponding hypo-osmolality
    Continued renal excretion of sodium
    Urine less than maximally dilute
    Absence of clinical evidence of volume depletion
    Absence of other causes of hyponatremia
    Correction of hyponatremia by fluid restriction

  • The following laboratory tests may be helpful in the diagnosis of SIADH:
    Serum sodium, potassium, chloride, and bicarbonate
    Plasma osmolality
    Serum creatinine
    Blood urea nitrogen
    Blood glucose
    Urine osmolality
    Serum uric acid
    Serum cortisol
    Thyroid-stimulating hormone
    The patient’s volume should be assessed clinically to help rule out the presence of hypovolemia.

  • Imaging studies that may be considered include the following:

    • Chest radiography (for detection of an underlying pulmonary cause of SIADH)
    • Computed tomography or magnetic resonance imaging of the head (for detection of cerebral edema occurring as a complication of SIADH, for identification of a CNS disorder responsible for SIADH, or for helping to rule out other potential causes of a change in neurologic status)

Clinical

Treatment

General Treatment

  • Oral Fluid Restriction

Drug Therapy

  • Conivaptan (Vaprisol) (see Conivaptan, [[Conivaptan]])
  • Tolvaptan (Samsca) (see Tolvaptan, [[Tolvaptan]])

References

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