History and exam
Key diagnostic factors
common
presence of risk factors
Including age >50 years, nursing home residence, the presence of a postoperative state, pulmonary conditions (e.g., pneumonia), malignancy, central nervous system disease or trauma, medicine associated with SIADH induction, and a history of endurance exercise.
absence of hypovolaemia
Hypovolaemia 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 hyponatraemia.
absence of hypervolaemia
Patients with congestive heart failure (crackles, cardiac gallops, jugular vein distension, lower extremity oedema), cirrhosis of the liver (ascites, lower extremity oedema), or nephrotic syndrome (anasarca, lower extremity oedema) are more likely to have an alternative cause for hyponatraemia.
Pregnancy is another cause of hypervolaemic hyponatraemia.
absence of signs of adrenal insufficiency or hypothyroidism
Adrenal insufficiency (pigmentation of skin and mucosa, weight loss, hypotension) or hypothyroidism (dry coarse skin, myxoedema, hair loss, weight gain) are ruled out during patient evaluation.
nausea
May be related to brain oedema.
vomiting
May be related to brain oedema.
uncommon
altered mental status
May be related to brain oedema; needs rapid correction of hyponatraemia.
headache
May be related to brain oedema; needs rapid correction of hyponatraemia.
seizure
May be related to brain oedema; needs rapid correction of hyponatraemia.
coma
May be related to brain oedema; needs rapid correction of hyponatraemia.
Other diagnostic factors
common
no history of recent diuretic use
Diuretics, particularly thiazides, may cause hyponatraemia.
Risk factors
strong
age >50 years
Increasing age is associated with hyponatraemia.[10][13]
No mechanism has been delineated, but water-excretory capacity is increasingly impaired in ageing patients.
Many older people have underlying conditions which cause SIADH and are also treated with medicines associated with SIADH, including selective serotonin-reuptake inhibitors (SSRIs) and non-steroidal anti-inflammatory drugs (NSAIDs).[10]
pulmonary conditions (e.g., pneumonia)
A study found that 23% of 71 patients with pneumonia and Streptococcus pneumoniae bacteraemia presented with a serum sodium <135 mmol/L (<135 mEq/L).[14]
Inappropriate arginine vasopressin (AVP) release signalled 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 mmol/L (≤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]
medicine 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 analogues 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 haematoma, subarachnoid haemorrhage, stroke, brain tumours); 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 non-osmotic arginine vasopressin release and associated hyponatraemia, often complicated by hypotonic fluid administration.[14]
More common after organ transplantation and cardiovascular, gastroenterological, 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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