Clinical management of SIADH

Abstract

Hyponatremia is the most frequent electrolyte disorder and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) accounts for approximately one-third of all cases. In the diagnosis of SIADH it is important to ascertain the euvolemic state of extracellular fluid volume, both clinically and by laboratory measurements. SIADH should be treated to cure symptoms. While this is undisputed in the presence of grave or advanced symptoms, the clinical role and the indications for treatment in the presence of mild to moderate symptoms are currently unclear. Therapeutic modalities include nonspecific measures and means (fluid restriction, hypertonic saline, urea, demeclocycline), with fluid restriction and hypertonic saline commonly used. Recently vasopressin receptor antagonists, called vaptans, have been introduced as specific and direct therapy of SIADH. Although clinical experience with vaptans is limited at this time, they appear advantageous to patients because there is no need for fluid restriction and the correction of hyponatremia can be achieved comfortably and within a short time. Vaptans also appear to be beneficial for physicians and staff because of their efficiency and reliability. The side effects are thirst, polydipsia and frequency of urination. In any therapy of chronic SIADH it is important to limit the daily increase of serum sodium to less than 8-10 mmol/liter because higher correction rates have been associated with osmotic demyelination. In the case of vaptan treatment, the first 24 h are critical for prevention of an overly rapid correction of hyponatremia and the serum sodium should be measured after 0, 6, 24 and 48 h of treatment. Discontinuation of any vaptan therapy for longer than 5 or 6 days should be monitored to prevent hyponatremic relapse. It may be necessary to taper the vaptan dose or restrict fluid intake or both.

Description of Three Female 24-h Ultra-Endurance Race Winners in Various Weather Conditions and Disciplines

“…By contrast, post-race TTKG increased and was >10 in Cases 2 and 3, suggesting an increased activity of aldosterone (16,22,67 (43). The urinary free water conservation occurred in Case 2 and Case 3, as shown by an increase in urine osmolality, and simultaneously urinary [Na + ] losses, therefore we assume they have an inappropriate release of ADH in response to exercise (24). This is in accordance with previous findings in hot conditions, where a significant negative correlation between performance times and urine osmolality results was observed (11).…”

Evidence for the use of demeclocycline in the treatment of hyponatraemia secondary to SIADH : a systematic review

“…There is a clinical need to treat HN and manage patients with SIADH appropriately 3; in particular, the management of patients with cancer. For example, chemotherapy may need to be delayed until the normalisation of these patients' sodium levels 43, and delays to chemotherapy negatively influence outcomes 44.…”

“…Clinical criteria for the syndrome of inappropriate antidiuretic hormone secretion (SIADH) were established by Bartter and Schwartz 2 and have remained largely unchanged ever since 1. SIADH accounts for one‐third of all cases of HN 3.…”

A Single Case Report on Hyponatremia Seizure Induced by Acetylcholinesterase Inhibitors

“…Clinically hyponatremia may be "silent" or may present with malaise, muscle ache, nausea, vomiting or can occur with severe manifestations such as seizures, delirium, coma and even death. Syndrome of inappropriate antidiuretic hormone (SIADH) is the most common cause of hyponatremia in almost one-third of all cases [8][9]. Drugs such as selective serotonin reuptake inhibitors, tricyclic antidepressants, monoamine oxidase inhibitors, diuretics and antiepileptic drugs are known to cause hyponatremia, mostly by inducing the syndrome of inappropriate antidiuretic hormone (SIADH) [10][11].…”