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Hypernatremia induced by low-dose Tolvaptan in a Patient with refractory heart failure: A case report

RATIONALE: Tolvaptan (TLV) is a selective vasopressin type 2 receptor antagonist, which has an active effect on patients with congestive heart failure especially combined with hyponatremia. Increasingly, evidence has demonstrated that low-dose tolvaptan can dramatically relieve patients’ dyspnea and...

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Detalles Bibliográficos
Autores principales: Li, Tian, Li, Gui-Shuang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer Health 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6635281/
https://www.ncbi.nlm.nih.gov/pubmed/31277136
http://dx.doi.org/10.1097/MD.0000000000016229
Descripción
Sumario:RATIONALE: Tolvaptan (TLV) is a selective vasopressin type 2 receptor antagonist, which has an active effect on patients with congestive heart failure especially combined with hyponatremia. Increasingly, evidence has demonstrated that low-dose tolvaptan can dramatically relieve patients’ dyspnea and the dose would not cause severe electrolyte abnormalities. Even hypernatremia is a major adverse effect of tolvaptan, treatment with tolvaptan shows good security and is well-tolerated. Few cases have reported that patients who developed severe hypernatremia induced by low-dose Tolvaptan. PATIENT CONCERNS: A 68-year-old man was admitted to our hospital with dyspea and general fatigue. He was diagnosed with acute decompensated heart failure due to ischemic cardiomyopathy. In order to improve fluid retention and relieve his dyspnea, low-dose TLV (7.5 mg qd) was performed. After the 3-day treatment using TLV, we observed that he became delirious and his limbs shook uncontrollably. High serum sodium 173 mmol/L was noted compared to the results of the first examination (137 mmol/L). After intensive rescue, serum sodium was restored to normal (135 mol/L). Later, when the patient refused continuous renal replacement therapy (CRRT), we tried again to use a lower dose of TLV to improve diuretic resistance. Two days later, Serum sodium rose again (162 mmol/L). DIAGNOSES: During the course of therapy, we did not strictly require the patient to control the fluid intake. No other medication could cause elevation of serum sodium. Therefore, we suspected a high sensitivity to the side effect of TLV. INTERVENTION: Stop the use of TLV and encourage the patient to drink plenty of water. Gastric tube was inserted orally to increase the intake of fresh water. OUTCOMES: His serum sodium decreased gradually and his psychiatric symptom recovered. During this period, Overall condition of the patient was stable. After being discharged from the hospital, the patient eventually died of cardiac arrest due to critically ill heart failure. LESSONS: Hypernatremia is a severe side effect of TLV. For critical patients, TLV should be used at a low dose and electrolyte should be detected in time.