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The Journal publishes articles on basic or clinical research relating to nephrology, arterial hypertension, dialysis and kidney transplants. It is governed by the peer review system and all original papers are subject to internal assessment and external reviews. The journal accepts submissions of articles in English and in Spanish languages. The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. SRJ is a prestige metric based on the idea that not all citations are the same. SJR uses a similar algorithm as the Google page rank; it provides a quantitative and qualitative measure of the journal's impact. SNIP measures contextual citation impact by wighting citations based on the total number of citations in a subject field. Nuestro objetivo fue el desarrollo de dos algoritmos de tratamiento de la hiponatremia secundaria al SIADH en el paciente ingresado. Resultados: Se elaboraron dos algoritmos de tratamiento. Introduction: The syndrome of inappropriate antidiuretic hormone secretion SIADH is the most frequent cause of hyponatremia in a hospital setting. However, detailed protocols and algorithms for its management are lacking. Our objective was to develop 2 consensus algorithms for the therapy of hyponatremia due to SIADH in hospitalized patients. Material and methods: A multidisciplinary group made up of 2 endocrinologists, 2 nephrologists, 2 internists, and one hospital pharmacist held meetings over the period of a year. The group worked under the auspices of the European Hyponatremia Network and the corresponding Spanish medical societies. Results: Two algorithms were developed. Algorithm 1 addresses acute correction of hyponatremia posing as a medical emergency, and is applicable to both severe euvolemic and hypovolemic hyponatremia. Specific infusion rates are proposed, as are steps to avoid or reverse overcorrection of serum sodium levels. It addresses when and how to use fluid restriction, solute, furosemide, and tolvaptan to achieve eunatremia in patients with SIADH. Conclusions: Two complementary strategies were elaborated to treat SIADH-induced hyponatremia in an attempt to increase awareness of its importance, simplify its therapy, and improve prognosis.. The Syndrome of Inappropriate Antidiuretic Hormone Secretion SIADH is characterized by the presence of hypotonic hyponatremia in a context of inadequately diluted urine given the hypoosmolality in plasma, in the absence of a low effective circulating volume. For its diagnosis, the following conditions must be excluded: hypotension, renal failure, adrenal insufficiency, severe hypothyroidism, as well as non-osmotic physiologic stimuli of arginine vasopressin AVP secretion. In SIADH, a lowering of plasma osmolality P osm does not inhibit AVP secretion as expected, and free water is inappropriately reabsorbed at the level of the collecting duct of the nephron, thus inducing further hemodilution and hyponatremia, concomitantly with an inappropriately elevated urine osmolality U osm 1,2. Major advances have taken place over the last few years in our understanding of the negative consequences of hyponatremia. Mild, chronic hyponatremia is not asymptomatic. On the contrary, it is accompanied by mental symptoms, impaired gait, falls 6 , fractures , and possibly osteoporosis 10 , as well as increased mortality 9, Severe hyponatremia per se can be life-threatening, inducing profound cerebral edema and potentially brain herniation and death. Even once hyponatremia is corrected, complete neurologic recovery can take weeks, and some patients will have permanent neurologic sequelae as a consequence of profound hyponatremia Yet overly rapid correction of serum sodium can induce osmotic demyelination syndrome ODS. And specific treatment directed towards correcting hyponatremia is accompanied by a lower death rate. SIADH is considered to be the most frequent cause of hyponatremia in a hospital setting A new class of therapeutic agents, the vaptans, is currently available for the treatment of SIADH in the adult. They block the AVP-responsive V2 collecting duct receptors that ultimately induce apical expression of aquaporin 2 channels through which water is reabsorbed following AVP stimulus Tolvaptan is the only drug of its class authorized by the European Medicines Agency, and is a selective V2-receptor blocker. Our objective was to develop two consensus algorithms for the therapy of hyponatremia due to SIADH in hospitalized patients. These algorithms address acute correction of hyponatremia posing as a medical emergency Algorithm 1 and correction of mild or moderate, non-acute hyponatremia requiring less aggressive measures Algorithm 2. The algorithms were developed by a multidisciplinary group made up of 2 Endocrinologists, 2 Nephrologists, 2 Internists, and 1 Hospital Pharmacist. Over the period of a year, the group held meetings and worked on-line, organized under the auspices of the European Hyponatremia Network and the corresponding Spanish Medical Societies. Application of the protocol should be flexible, and adapted to the specific needs of each patient, as is always the case in clinical medicine. Explanation of the algorithms and their use. When applying either algorithm, medication that can potentially cause hyponatremia must be discontinued when feasible. Pain and nausea are potent stimuli of AVP secretion and must be adequately treated. If the underlying cause of SIADH-induced hyponatremia is not evident, a Chest x-ray, brain, cervical and thoracic CT, and abdominal ultrasound must be considered. It is applicable to severe euvolemic or hypovolemic hyponatremia per se , regardless of the cause, and thus prior to diagnosis of its origin. A central venous line is unnecessary and can only delay treatment. The resulting solution must be shaken before administration. Immediately prior to initiating treatment, blood must be drawn for determination of S Na , serum potassium SK , urea, creatinine and plasma osmolality P osm. Urine for the determination of Na U Na , K U K and U osm must be obtained as soon as possible, without delaying initiation of hypertonic saline administration. Hypoxemia must be ruled out and corrected if detected, since it worsens prognosis Infusion rate. We do not advise the use of formulas to estimate the quantity and rate of infusion, since these calculations often lead to overcorrection and can needlessly complicate therapy. As previously mentioned, treatment must be particularly aggressive in children and in women of child-bearing age 27 , given that their risk of severe hyponatremic encephalopathy is higher, potentially leading to subsequent brain herniation and death, or permanent neurologic sequelae. This is also the case for patients with acute hyponatremia. Patients who have recently ingested large quantities of liquid acute water intoxication are at special risk, since their neurologic symptoms and serum sodium will often worsen as they continue absorbing water from the gastrointestinal tract HSS can induce substantial water diuresis, favoring overcorrection. These patients are also candidates to receive 1 mcg of sc or iv desmopressin directly upon detection of polyuria, thus preventing an excessive rise in serum sodium 32, Specific treatment goals of hypertonic saline infusion. Thus, our aim should be to achieve an increase in serum sodium of the order of 6 to 8 mmol over a hour period. Avoiding overcorrection is particularly important in patients at a high risk of developing the osmotic demyelination syndrome such as alcoholics, patients who are malnourished, and those presenting hypokalemia However, in patients with acute hyponatremia S Na can rise more quickly, without negative consequences. No other treatments that raise serum sodium levels should be given concomitantly with hypertonic saline, with the exception of iv furosemide in patients with a history of heart failure. Monitoring and discontinuing hypertonic saline infusion. S Na should be repeated 2 hours after initiating HSS infusion. If bolus therapy has been used, sodium levels should be monitored 30 minutes after the last bolus. S Na should once more be monitored 2 hours later 4 hours after initiation of saline infusion. If the patient presents only moderate or mild symptoms, the infusion rate can be maintained and S Na repeated hours later. One of the most important recommendations we can make in the use of hypertonic saline is that the prescribing physician personally supervise cessation of the iv infusion. Once hypertonic saline infusion has been discontinued, and until 24 hours have passed since the start of treatment, oral salt can be administered and fluid restriction initiated in patients with SIADH. Other measures that can potentially raise S Na should be avoided, to decrease the risk of overcorrection. We include potassium chloride KCl in this category: mild hypokalemia should not be corrected until the following day, since KCl administration will increase serum sodium levels. Corrective Measures to Relower Serum Sodium. Relowering of serum sodium, following an excessive rise, prevents ODS. The development of ODS has been associated with an excessive rise in serum sodium over a 24 or 48 hour period. ODS can induce death or leave permanent neurologic sequelae. However, a rapid reinduction of hyponatremia has been shown to prevent ODS symptoms 37,43,44 and has been successfully used to treat patients that have developed ODS Specific Measures. When using desmopressin, we recommend a lower initial rate of dextrose infusion: 1. The association of desmopressin to iv dextrose is particularly important in patients who will not otherwise reabsorb large quantities of water in the collecting duct, as is the case of patients with primary polydypsia, and other patients with low U osm. With low AVP levels, these patients will have few patent aquaporin-2 channels, reflected by a low U osm and desmopressin should be administered for dextrose infusion to be useful. Iv furosemide can be administered once the desired serum sodium level has been reached, to put a halt to a further reduction in S Na. Patients at high risk for overcorrection. Certain groups of patients present a higher risk of overcorrection of serum sodium than others, and must be more closely monitored. These include patients in which the cause of hyponatremia is transitory, e. Patients with an extremely low salt intake prior to admission also fall into this category. Patients with adrenal failure, either primary or secondary, are a separate case. They should receive high enough hydrocortisone doses to cover their glucocorticoid and mineralocorticoid needs. S Na can rise very quickly after initiation of steroid therapy, particularly if high doses of hydrocortisone are given, and especially if administered by iv bolus, as when treating an adrenal crisis. In many patients, however, the infusion of lower doses of hydrocortisone will be sufficient between mg daily 51 , with or without an intial bolus of 50 mg iv and will induce a slower rate of correction of S Na levels. In even milder cases, oral hydrocortisone can be given at a dose of 20 mg tid. The aim of algorithm figure 2 is to achieve eunatremia in patients with SIADH-induced mild or moderate hyponatremia not posing as a medical emergency. Correction of hypokalemia. If hypokalemia is present, Potassium Chloride supplements should be given, taking care NOT to administer potassium bicarbonate, or potassium supplements that result in the generation of bicarbonate, since the latter will increase renal sodium excretion, and can induce metabolic alkalosis A hospital diet frequently provides less than 4 grams of sodium chloride a day. Furthermore, many patients eat considerably less than what is provided, and will have an even lower sodium intake. We recommend the association of NaCl supplements, for a minimum consumption of 5 to 8 grams of salt daily. The administration of large amounts of solute can be used for the treatment of SIADH — induced hyponatremia, acting through the induction of increased renal obligatory water clearance. In this case, oral salt supplementation can range from 3 to 4 grams every 8 hours, and must be even higher in exceptional cases. Close monitoring of blood pressure is essential. Another solute that has been given for the treatment of SIADH hyponatremia is oral urea, at doses of 30 g a day, usually given in two 15 g doses However, its low palatability has limited its use. Fluid Restriction. Currently, fluid restriction is the cornerstone of treatment of SIADH-induced hyponatremia not requiring urgent intervention. By fluid restriction we mean the reduction of all liquids administered to the patient, be it with iv medication, oral liquids, or the intrinsic water content of foods. To adequately initiate fluid restriction, iv medication must be concentrated whenever feasible, and non-essential oral and iv medication discontinued. Oral liquid intake must be limited and foods with a high water content eliminated from the diet soups, mashed foods, coffee, tea, gelatins, semi-liquid desserts, melons, citric fruits, etc. Patients with a result less than 0,5 can be limited to ml of total liquid intake, whereas those between 0,5 and 1 need to be limited to ml of liquid a day. Patients with a result of 1 or more will not respond to fluid restriction, since their nephrons are not capable of eliminating electrolyte-free water. In this case fluid restriction to ml daily is used to prevent worsening of hyponatremia, not to correct it. The response of a specific patient to fluid restriction is not constant, and can vary from one day to another. Therefore, for a correct use of the Furst formula, electrolytes must be measured in serum and urine frequently. Fluid restriction is not practical in all patients, and is simply incompatible with necessary medication or artificial nutrition in others. Another group does not tolerate or does not respond to the required fluid restriction. Furthermore, fluid restriction to ml makes meals less palatable, and can worsen the nutritional status of the patient if used for more than a few days. In these cases, together with those presenting a Furst formula result of 1 or more, alternative therapies must be initiated. Furosemide can be useful as a short-term treatment for SIADH hyponatremia when the U Osm is sufficiently high, as it induces an increase in renal free water clearance. Sodium losses must be compensated by sufficient oral salt intake. Furosemide can be administered iv or orally, in doses ranging from 20 mg iv every 8 to 24 hours, or 40 mg every 8 to 24 hours p. The use of this loop diuretic is particularly helpful in patients in whom SIADH will presumably be of limited duration days , as is the case of patients with pneumonia or drug-induced SIADH when the medication can be discontinued table 3. In this case serum sodium should be repeated 3 to 6 hours after an iv dose. We recommend the use of tolvaptan, the selective V2 receptor inhibitor 58 , in patients with SIADH who are not candidates for fluid restriction or furosemide. The drug is particularly useful in patients that will need treatment of their hypotonic hyponatremia for several days, or longer, as occurs in patients with chronic SIADH. Initiation and monitoring of tolvaptan therapy. Volker Burst, University of Cologne, personal communication. Tolvaptan therapy must always be initiated while the patient is hospitalized. Care should be taken to assure that during the first day of tolvaptan administration patients not only have free access to liquids, but also are actively encouraged to drink ad libitum , since maximum aquaresis is observed precisely on day 1, when excess circulating water is greatest. Patients who have previously been on fluid restriction are prone to not drinking as much as they desire and must be closely monitored. Patients with a nasogastric tube will also need increased liquids. In these cases, diuresis is helpful in estimating increased fluid needs. The initial recommended dose is of 15 mg p. Volker Burst, personal communication. We recommend measuring serum sodium, potassium and P Osm as well as sodium, potassium and osmolality in urine at baseline, and 6 hours after the initial dose, with monitoring of fluid intake and diuresis every 6 hours. We have found the association of desmopressin iv or sc to be useful in avoiding overcorrection of S Na in spite of V2 blockade, at doses of mcg every 6 hours as needed. Not all patients drink as needed and thus some present a excessively negative fluid balance. They will also require a new 12 h measurement of S Na. The drug can be reintroduced on the following day. Experience with tolvaptan in Europe is still somewhat limited, and its use will surely undergo modifications in the future, particularly regarding doses. Tolvaptan: General Considerations. Tolvaptan has important drug interactions which must be taken into account before and during its use Table 4. As a substrate for cytochrome P 3A4, circulating levels of tolvaptan will increase when used with inhibitors, and will drop when associated with inducers. Tolvaptan at high doses 60 mgday can increase serum digoxin concentrations. Tolvaptan should be used as monotherapy for SIADH, and never be administered jointly with hypertonic saline. On day 1 of use, it is preferable not to associate potassium supplements, nor furosemide. Tolvaptan should never be administered to a hypovolemic patient, underlying the importance of a correct diagnosis of SIADH. Tolvaptan is usually well tolerated, and in our experience is very effective for attaining strict eunatremia. However, intense thirst sometimes follows its administration. When accompanied by the ingestion of large quantities of liquid, thirst can lessen the effectiveness of the medication, as can chronic pain. Duration of Treatment. Out-patient follow-up. When discontinuing tolvaptan, a progressive reduction in dose is always preferable to abrupt withdrawal of the medication. In patients discharged on tolvaptan therapy, we recommend repeating S Na within a week, with new laboratory tests 2 to 4 weeks later, then monthly. In patients with chronic SIADH, in our experience, the tolvaptan dose can be progressively reduced once strict eunatremia is achieved. Hyponatremia is a very common disorder, yet it remains underdiagnosed, underappreciated, and often incorrectly managed. Concrete roadmaps for the treatment of hyponatremic patients are lacking. We have elaborated two complementary strategies to treat SIADH-induced hyponatremia in an attempt to increase awareness of its importance, simplify its therapy, and improve prognosis. In spite of the frequency and negative repercussions of hyponatremia, there is a paucity of evidence in the field of hyponatremia and its therapy. We are clearly in need of more research directed towards gathering evidence that can optimize therapy. We hope that the application of this protocol will simplify and help bring consistency to the treatment of SIADH-induced hyponatremia, thus reducing morbidity, and facilitating the accumulation of evidence. Isabelle Runkle has worked as a consultant for Otsuka and has given sessions sponsored by Otsuka, Amgen and Novartis. Carles Villabona has worked as a consultant for Otsuka and has given sessions sponsored by Novartis, Ipsen and Otsuka. Francesc Formiga has worked as a consultant for Otsuka and has given sessions sponsored by Otsuka. He has been a consultant for Otsuka and Astra Zeneca. Esteban Poch has worked as a consultant for Otsuka and has given sessions sponsored by Otsuka. Table 2. Classification of hyponatremia according to severity of clinical symptoms. Table 3. Probable duration of syndrome of inappropriate antidiuretic hormone secretion treatment as indicated by etiology. ISSN: Previous article Next article. July Pages More article options. DOI: Treatment of hyponatremia induced by the syndrome of Inappropriate antidiuretic hormone secretion: a multidisciplinary spanish algorithm. Download PDF. This item has received. Article information. Show more Show less. Palabras clave:. Conclusions: Two complementary strategies were elaborated to treat SIADH-induced hyponatremia in an attempt to increase awareness of its importance, simplify its therapy, and improve prognosis. Antidiuretic hormone. Full Text. Materials and Methods The algorithms were developed by a multidisciplinary group made up of 2 Endocrinologists, 2 Nephrologists, 2 Internists, and 1 Hospital Pharmacist. Hypertonic saline solution 1. Application of Algorithm 2 The aim of algorithm figure 2 is to achieve eunatremia in patients with SIADH-induced mild or moderate hyponatremia not posing as a medical emergency. Correction of hypokalemia If hypokalemia is present, Potassium Chloride supplements should be given, taking care NOT to administer potassium bicarbonate, or potassium supplements that result in the generation of bicarbonate, since the latter will increase renal sodium excretion, and can induce metabolic alkalosis Fluid Restriction Currently, fluid restriction is the cornerstone of treatment of SIADH-induced hyponatremia not requiring urgent intervention. Furosemide Therapy Furosemide can be useful as a short-term treatment for SIADH hyponatremia when the U Osm is sufficiently high, as it induces an increase in renal free water clearance. Tolvaptan Therapy We recommend the use of tolvaptan, the selective V2 receptor inhibitor 58 , in patients with SIADH who are not candidates for fluid restriction or furosemide. Conclusions Hyponatremia is a very common disorder, yet it remains underdiagnosed, underappreciated, and often incorrectly managed. Conflicts of interest Isabelle Runkle has worked as a consultant for Otsuka and has given sessions sponsored by Otsuka, Amgen and Novartis. A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone. Am J Med ; The syndrome of inappropriate secretion of antidiuretic syndrome. Nephrogenic syndrome of inappropriate antidiuresis. N Engl J Med ; Vasopressin function in the syndrome of inappropriate antidiuresis. Annu Rev Med ; Regulation of arginine vasopressin in the syndrome of inappropriate antidiuresis. Am J Med ;SS Mild chronic hyponatremia is associated with falls, unsteadiness, and attention deficits. Mild hyponatremia and risk of fracture in the ambulatory elderly. QJM ; Hyponatremia associated with large-bone fracture in elderly patients. Int Urol Nephrol ; Mild hyponatremia as a risk factor for fractures: the Rotterdam Study. J Bone Miner Res ; Hyponatremia-induced osteoporosis. Hyponatremia: a prospective analysis of its epidemiology and the pathogenetic role of vasopressin. Ann Intern Med ; Mortality after hospitalization with mild, moderate, and severe hyponatremia. Impact of hospital-associated hyponatremia on selected outcomes. Arch Intern Med ; Mild hyponatremia carries a poor prognosis in community subjects. Hyponatremia, convulsions, respiratory arrest, and permanent brain damage after elective surgery in healthy women. Incidence and prevalence of hyponatremia. Age and gender as risk factors for hyponatremia and hypernatremia. Clin Chim Acta ; Lack of laboratory assessment of severe hyponatremia is associated with detrimental clinical outcomes in hospitalized patients. Int J Clin Pract ; Development of severe hyponatremia in hospitalized patients: treatment-related risk factors and inadequate management. Nephrol Dial Transplant ; The syndrome of inappropriate antidiuresis. Vasopressin receptor antagonists for the treatment of hyponatremia: systematic review and meta-analysis. Am J Kidney Dis ; Hyponatremia treatment guidelines Expert panel recommendations. Am J Med ;S1-S Ischemic and hypoxic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals. J Clin Invest ; Pulmonary complications of hyponatremic encephalopathy: noncardiogenic pulmonary edema and hypercapnic respiratory failure. Chest ; Chronic hyponatremic encephalopathy in postmenopausal women: association of therapies with morbidity and mortality. JAMA ; Hyponatremia with hypoxia: Effects on brain adaptation, perfusion, and histology in rodents. Kidney Int ; Influence of hypoxia and sex on hyponatremic encephalopathy. Predictors of outcome in hospitalized patients with severe hyponatremia. J Natl Med Assoc ; Rapid correction of severe hyponatremia with intravenous hypertonic saline solution. Treatment of hyponatremia. UpToDate Treatment of Hyponatremia. UpToDate edition 17, The treatment of hyponatremia. Sem Nephrol ; The pathophysiology and treatment of hyponatraemic encephalopathy: an update. Diagnosis and management of hyponatremia in acute illness. Curr Opin Crit Care ; Acute hyponatraemia and 'ecstasy': insights from a quantitative and integrative analysis. Defining conditions that lead to the retention of water: the importance of the arterial sodium concentration. DDAVP is effective in preventing and reversing inadvertent overcorrection of hyponatremia. Clin J Am Soc Nephrol ; Reversal of transtentorial herniation with hypertonic saline. Neurology ; Is the sodium level per se related to mortality in hospitalized patients with severe hyponatremia? Clin Nephrol ; Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction of hyponatremia. Medicine Baltimore ; A review of the causes of central pontine myelinolysis: Yet another apoptotic illness? Eur J Neurol ; J Neuropathol Exp Neurol ; Prevention of brain demyelination in rats after excessive correction of chronic hyponatremia by serum sodium lowering. Re-induction of hyponatremia after rapid overcorrection of hyponatremia reduces mortality in rats. Reinduction of hyponatremia improves survival in rats with myelinolysis-related neurologic symptoms. Therapeutic relowering of the serum sodium in a patient after excessive correction of hyponatremia. Reinduction of hyponatremia to treat central pontine myelinolysis. Diluting delirium. N Z Med J ;U Relowering of serum Na for osmotic demyelinating syndrome. Case reports in neurological medicine ; Osmotic demyelination syndrome and overly rapid correction of hyponatremia. Treatment of adrenal insufficiency in adults. J Appl Physiol ; Treatment of the syndrome of inappropriate secretion of antidiuretic hormone by urea. Oral urea for the treatment of chronic syndrome of inappropriate antidiuresis in children. J Pediatr ; Am J Med Sci ; Inappropriate secretion of antidiuretic hormone treated with furosemide. Treatment of the syndrome of inappropriate secretion of antidiuretic hormone by long loop diuretics. Nephron ; Efficacy and safety of oral tolvaptan therapy in patients with the syndrome of inappropriate antidiuretic hormone secretion. Eur J Endocrinol ; Vaptans are not the mainstay of treatment in hyponatremia: perhaps not yet. An initial dose of 7. Florence, Italy. May Nephrogenic syndrome of inappropriate antidiuresis in adults: High phenotypic variability in men and women from a large pedigree. J Am Soc Nephrol ; Subscribe to our newsletter. Print Send to a friend Export reference Mendeley Statistics. Recommended articles. Haemodialysis patients have worse postural balance with an Contrast-induced encephalopathy in patients with advanced This work is licensed under a Creative Commons Attribution 4. 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