Syndrome of inappropriate antidiuretic hormone secretion is characterized by excessive secretion of the antidiuretic hormone, dilutional hyponatremia, reduced serum osmolality, relatively increased values of urine osmolality, and elevated levels of urinary sodium in patients with a normal plasma volume. Diagnosis is based on excluding other causes of hyponatremia.
Syndrome of inappropriate antidiuretic hormone secretion (SIADH) can be primary or secondary to various etiologies ranging from drugs to tumors. It is characterized primarily by hyponatremia and low serum osmolality. The syndrome is caused by the inappropriate synthesis of the antidiuretic hormone (ADH) in patients with normal plasma volume levels . Risk factors for SIADH include advanced age as aging is associated with elevated levels of ADH and atrial natriuretic peptide (ANP), and increased susceptibility to osmotic stimulation  . In addition, the elderly may be on several medications which can cause SIADH. Postoperative patients, patients with head injury or those on mechanical ventilation, as well as individuals with tumors secreting ADH, are other groups who are at high risk of developing SIADH. Factors like stress, low blood pressure, severe pain, and general anesthesia can also predispose to SIADH.
Clinical presentation of SIADH depends on the severity and rate of hyponatremia development. Slowly progressive hyponatremia is usually asymptomatic while manifestations in acute, rapidly progressing hyponatremia include confusion, tremors, ataxia, myoclonus, asterixis, abnormal reflexes, dysarthria, seizures, coma. Neurological features appear as intracranial pressure increases and cerebral edema develops. Chronic moderate hyponatremia is associated with a poor reaction time, cognitive dysfunction, and ataxia with frequent falls  .
The diagnosis of SIADH is based on laboratory findings but patient history can raise suspicion of the condition and its underlying etiology. The onset of the manifestations is an indicator of whether the condition is acute or chronic. History may also provide information about a head injury, drug abuse, long-standing pain, neurological symptoms, and features of lung tumors or pathology such as dyspnea, chronic cough, and hemoptysis. It is essential to elicit whether the patient has consumed excessive fluids (an indicator of psychogenic polydipsia) or has received hypotonic fluids.
Laboratory tests include serum electrolytes, bicarbonate, creatinine, blood urea nitrogen, uric acid, cortisol, and thyroid stimulating hormone (TSH). Once the tests reveal hyponatremia, the urine and plasma osmolality is determined along with urine sodium. SIADH is confirmed using Bartter and Schwartz criteria :
Imaging studies like chest X-ray may show a lung tumor as the underlying cause of SIADH while computed tomography (CT) of the head and magnetic resonance imaging (MRI) of the brain may reveal features of cerebral edema or may detect an underlying brain tumor.
Patients who are already hospitalized may develop SIADH. Diagnosis of the condition in such patients may be challenging especially if they are on diuretics . Fractional excretion of uric acid (FE-UA) is very useful in these patients to diagnose SIADH .