History and exam
Key diagnostic factors
common
absence of hypovolemia
Hypovolemia is ruled out during patient evaluation.
Patients with tachycardia, orthostatic hypotension, dry mucous membranes, and poor skin turgor are more likely to have an alternative cause for hyponatremia.
absence of hypervolemia
Patients with congestive heart failure (crackles, cardiac gallops, jugular vein distention, lower extremity edema), cirrhosis of the liver (ascites, lower extremity edema), or nephrotic syndrome (anasarca, lower extremity edema) are more likely to have an alternative cause for hyponatremia.
Pregnancy is another cause of hypervolemic hyponatremia.
absence of signs of adrenal insufficiency or hypothyroidism
Adrenal insufficiency (pigmentation of skin and mucosa, weight loss, hypotension) or hypothyroidism (dry coarse skin, myxedema, hair loss, weight gain) are ruled out during patient evaluation.
nausea
May be related to brain edema.
vomiting
May be related to brain edema.
uncommon
altered mental status
May be related to brain edema; needs rapid correction of hyponatremia.
headache
May be related to brain edema; needs rapid correction of hyponatremia.
seizure
May be related to brain edema; needs rapid correction of hyponatremia.
coma
May be related to brain edema; needs rapid correction of hyponatremia.
Other diagnostic factors
common
no history of recent diuretic use
Diuretics, particularly thiazides, may cause hyponatremia.
Risk factors
strong
age >50 years
Increasing age is associated with hyponatremia.[10][13]
No mechanism has been delineated, but water-excretory capacity is increasingly impaired in aging patients.
Many older people have underlying conditions which cause SIADH and are also treated with medications associated with SIADH, including selective serotonin-reuptake inhibitors (SSRIs) and nonsteroidal anti-inflammatory drugs (NSAIDs).[10]
pulmonary conditions (e.g., pneumonia)
A study found that 23% of 71 patients with pneumonia and Streptococcus pneumoniae bacteremia presented with a serum sodium <135 mEq/L.[14]
Inappropriate arginine vasopressin (AVP) release signaled by pulmonary process, plus osmostat resetting for AVP secretion, are likely mechanisms.
nursing home residence
About 18% of nursing home residents have been found to have serum sodium levels ≤135 mEq/L compared with 8% of age-matched ambulatory individuals.[15]
Coupled with impaired water-excretory capacity with advancing age, many of the patients also receive hypotonic fluids or low-sodium diets/tube feeds.
malignancy
Typically lung malignancy (especially small cell lung cancer), gastrointestinal or genitourinary malignancy, lymphoma, or sarcoma.[4]
medication associated with SIADH induction
Drugs that are associated with development of SIADH include antidepressants such as SSRIs, tricyclic antidepressants, monoamine oxidase inhibitors, and venlafaxine; anticonvulsants such as carbamazepine, oxcarbazepine, valproate, and lamotrigine; antipsychotics such as phenothiazines (e.g., chlorpromazine) and butyrophenones (e.g., haloperidol); antidiabetic agents such as first-generation sulfonylureas (e.g., chlorpropamide, tolbutamide); chemotherapeutic agents such as vinca alkaloids, platinum compounds, ifosfamide, melphalan, cyclophosphamide, methotrexate, and pentostatin; vasopressin analogs such as desmopressin, oxytocin, terlipressin, and vasopressin; other drugs such as opioids, methylenedioxymethamphetamine (MDMA), levamisole, interferon, clofibrate, nicotine, amiodarone, proton-pump inhibitors, monoclonal antibodies, and NSAIDs.[4]
central nervous system (CNS) disorder
CNS causes of SIADH include infections (encephalitis, meningitis, brain abscess, Rocky Mountain spotted fever, HIV-associated opportunistic CNS infections, malaria); vascular causes and masses (brain trauma, subdural hematoma, subarachnoid hemorrhage, stroke, brain tumors); and other CNS disorders (hydrocephalus, cavernous sinus thrombosis, multiple sclerosis, Guillain-Barre syndrome, Shy-Drager syndrome, delirium tremens, acute intermittent porphyria).[4]
weak
postoperative state
About 4.4% of postoperative patients have been found to have developed nonosmotic arginine vasopressin release and associated hyponatremia, often complicated by hypotonic fluid administration.[14]
More common after organ transplantation and cardiovascular, gastroenterologic, or trauma surgery. Mechanism unknown, but possibly mediated by postoperative pain and nausea.
endurance exercise
Excessive fluid intake is the main cause.
Elevated arginine vasopressin has been observed in some cases.
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