key: cord-0731105-su9aduif authors: Naaraayan, Ashutossh; Pant, Sushil; Jesmajian, Stephen title: Severe Hyponatremic Encephalopathy in a Patient With Covid-19 date: 2020-07-19 journal: Mayo Clin Proc DOI: 10.1016/j.mayocp.2020.06.033 sha: 0bbb736b34ed4af5756dff88bf77c8ed8620703b doc_id: 731105 cord_uid: su9aduif nan This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. The illness mainly manifests with fever and respiratory symptoms. We present the first reported case of life-threatening hyponatremia in a patient with Covid-19. A 56-year-old-female was brought to the hospital for sudden onset altered mental status. Patient was at work on the day of admission, when she had sore throat and within hours developed confusion and incoherent speech. Her only comorbidity was hypertension, being treated with hydrochlorothiazide for 3 years. She was taking no other medication or supplement. Vitals were stable with a blood pressure of 110/70 mmHg. On examination, she was obtunded and without focal neurological deficits. Laboratory testing showed serum sodium 115 milliequivalents per liter, potassium 3.2 milliequivalents per liter and magnesium 1.2 millimoles per liter. Serum osmolality was 247 milliosmoles per kilogram while urine osmolality was 670 milliosmoles per kilogram. Computed Tomography scan of the head and Chest X-ray showed no acute pathology. Urine toxicology was negative. She was clinically euvolemic, and diagnosed with acuteonset severe hyponatremia from an anti-diuretic hormone (ADH) dependent pathway. She was treated with 3%-hypertonic saline and desmopressin. Being at the epicenter of the Covid-19 pandemic, SARS-CoV-2 testing was performed and came back positive. Computed Tomography of the Chest revealed ground glass opacities bilaterally. Influenza testing, blood cultures and urinalysis were negative. Thyroid stimulating hormone level was normal and serum Cortisol appropriately elevated. Patient's serum sodium and mental status normalized over the next 4 days and she was advised to stop taking hydrochlorothiazide on discharge. She denied developing any respiratory symptoms on a telemedicine visit 10 days post discharge. Severe hyponatremia (<120 milliequivalents per liter) may present with manifestations of cerebral edema including obtundation, seizures, coma, respiratory arrest and death. Thiazides are known to cause severe hyponatremia that can simulate a Syndrome of Inappropriate Anti-Diuretic hormone-like picture associated with hypokalemia. The risk of thiazide induced hyponatremia is present as long as 10 years after initiation of therapy. 1 In patients on thiazides, severe hyponatremia could be precipitated by a lung infection, similar to our patient. 2 Pneumonia not only precipitates hyponatremia in patients on thiazides, but can cause it independently by an ADH-dependent pathway. Although classically described in legionella pneumonia, hyponatremia occurs with a variety of bacterial, viral, and fungal lung pathogens. 3 Mechanisms and risk factors of thiazide and pneumonia induced hyponatremia, and their interplay is shown in Figure 1 . 3, 4 Being the first-line antihypertensive agents, thiazides are widely prescribed. In 2012 in the United States alone, an estimated 30 million hypertensives were taking thiazides. 5 Approximately 30% of patients on thiazides develop hyponatremia. 1 Viral pneumonia via ADH-dependent pathways can facilitate the development of hyponatremia in patients on chronic thiazide therapy, as observed in our patient. Remarkably our patient had no respiratory manifestations from Covid-19 pneumonia. She rather presented with encephalopathy from hyponatremia, a consequence of viral pneumonia on chronic thiazide therapy. According to estimation models from the Imperial College of London, ~81% of the US population will be afflicted with Covid-19. This places the 30 million people on thiazides at risk for Covid-19 induced hyponatremia. 5 It is imperative that primary care physicians are aware of this mostly unrecognized effect of the current pandemic and are prepared to adjust accordingly. We recommend the cautious use of thiazide in the management of high blood pressure during the current Covid-19 pandemic. Closer monitoring of symptoms and laboratory values might be warranted. Ashutossh Naaraayan, MD FACP Sushil Pant, MD Stephen Jesmajian, MD FACP Montefiore New Rochelle Hospital New Rochelle, New York Risk of Thiazide-induced Hyponatremia in Patients with Hypertension Diuretic induced hyponatraemia in elderly hypertensive women Hospital-associated hyponatremia Thiazide-associated hyponatremia in the elderly: what the clinician needs to know Trends in Prescription Drug Use Among Adults in the United States From