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Hyponatremia — defined as serum sodium below 135 mEq/L — is the most common electrolyte disturbance in hospitalised patients and can be precipitated by psychotropic medications through the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Selective serotonin reuptake inhibitors (SSRIs) are a well-recognised cause, while second-generation antipsychotics such as quetiapine have been implicated less frequently. Cases involving the concurrent use of both drug classes in elderly patients with dementia are rarely reported.
We describe a 77-year-old man with advanced Alzheimer’s disease, type 2 diabetes, hypertension, chronic kidney disease, and multiple other comorbidities who developed severe hyponatremia (serum sodium 121 mmol/L) following concurrent treatment with sertraline 50 mg and quetiapine. He presented with worsening dyspnoea and an abrupt decline in cognition over two months, temporally associated with the reintroduction of quetiapine. Laboratory findings confirmed hypotonic hyponatremia with inappropriately concentrated urine, consistent with SIADH. Thyroid and adrenal function were normal. Cardiac evaluation revealed new-onset heart failure without an acute ischaemic event. After systematic exclusion of other aetiologies, psychotropic medications were identified as the probable cause. Management comprised discontinuation of both sertraline and quetiapine and fluid restriction to less than 1,000 mL per day, with close electrolyte monitoring.
This case underscores the importance of routine sodium monitoring in elderly patients with dementia initiated on serotonergic or antipsychotic therapy. Acute cognitive deterioration in this population should prompt evaluation for reversible metabolic causes, including drug-induced hyponatremia, before attributing decline to dementia progression. A multidisciplinary approach involving neurology, nephrology, and psychiatry is essential for accurate diagnosis and safe management.
Hyponatremia, defined as a serum sodium concentration below 135 mEq/L, represents the most common electrolyte abnormality encountered in clinical settings.
SSRIs are often prescribed for elderly patients for various conditions, such as mood changes or behavioural disturbances associated with dementia. Sertraline is one of the SSRIs frequently prescribed due to its efficacy, tolerability, and safety profile in elderly patients with comorbidities.
A 77-year-old male with a history of type 2 diabetes, hypertension, dyslipidaemia, a prior cerebrovascular accident without residual weakness, chronic kidney disease (baseline eGFR ~90–100), prostate cancer treated with radiotherapy, spine compression fracture, osteoporosis, and Alzheimer’s dementia. The patient was bedridden with a sacral bed sore, non-communicative, and dependent on oral feeding.
The patient’s cognitive decline had been noted over several years, with rapid worsening in the last year, 2024. He had been on memantine and rivastigmine for dementia. Sertraline 25 mg was initiated in July 2024 for apathy, and the dose was documented to be increased to 50 mg. Quetiapine was started in February 2024, then discontinued, and subsequently added as PRN for agitation in January 2025.
The patient presented to the emergency department on 13/04/2025 with a cough and dyspnoea as the main complaint. The family also reported worsening altered mental status, with an abrupt cognitive decline over the last two months, with the only recent change being restarting quetiapine in January 2025. The patient was admitted due to NSTEMI and new-onset heart failure and was treated accordingly.
Conscious but disoriented, confused, not responding or communicating (patient’s recent baseline). Vitals: BP 122/82 mmHg, HR 61 bpm, Temp 36.5 °C, RR 14/min, SpO
2 94% RA. Cardiovascular and respiratory exams were unremarkable except for mild bilateral lower limb edema. Chest CT: Mild left pleural effusion and atelectasis; no pulmonary embolism.
Serum Sodium: 121 mmol/L Serum Osmolality: 263 mOsm/kg Urine Osmolality: 317 mOsm/kg Urine Sodium: 44 mmol/L Creatinine: 53 μmol/L TSH: 2.87 mIU/L (normal) Cortisol: 847.80 nmol/L (normal) Troponin: 224.8 pg/mL (high), but no acute MI (no ischemic changes on ECG, echo EF >40%)
Neurology, nephrology, and psychiatry were consulted upon admission due to a low serum sodium of 121 mmol/L and muscle rigidity.
The neurology team report indicates that the sudden decline in cognition is likely attributable to hyponatremia induced by medication (quetiapine and sertraline), stress from the current active condition, NSTEMI, and the hospital stay, in addition to Alzheimer’s disease. The rigidity is currently most likely induced by quetiapine.
The nephrologist reviewed the patient’s laboratory results, noting that all serum sodium levels exhibited a decrease following the initiation of sertraline. High urine osmolality, along with elevated urine sodium levels, was documented. After ruling out other potential causes, it was concluded that the SIADH is most likely secondary to psychotropic medications.
Our psychiatry team, after reviewing the previous consults and assessing the patient’s current mental state, concluded that there is currently no urgency to continue sertraline and quetiapine, so sertraline and quetiapine should be discontinued.
Findings were consistent with SIADH: hypotonic hyponatremia with inappropriately concentrated urine, normal thyroid and adrenal function, and euvolemic status clinically.
Sertraline was tapered down and discontinued, and quetiapine was also discontinued. Fluid restriction to <1,000 mL/day. Close electrolyte monitoring was maintained throughout; electrolyte trends were reassessed at 48-hour intervals following discontinuation of both psychotropic agents and fluid restriction. Hypertonic saline was not required.
The syndrome of inappropriate antidiuretic hormone secretion (SIADH) refers to excessive release of antidiuretic hormone (ADH) or increased sensitivity of vasopressin receptors to ADH. Unlike normal ADH secretion, which ceases once fluid or cardiac status is corrected, ADH release in SIADH persists despite adequate hydration. SIADH is estimated to account for about one-third of all hyponatremia cases.
Individuals aged over 60 are at increased risk of developing hyponatremia.
Patients who develop SIADH secondary to psychotropic medications usually present with normal volume status but low serum osmolality (<285 mOsm/kg) and inappropriately concentrated urine (>100 mOsm/kg). Hyponatremia in such cases is often multifactorial, with long-term psychotropic users developing low sodium only when additional risk factors coexist. Drug-induced SIADH should be suspected when hyponatremia emerges within two to four weeks of starting a new psychotropic or after a major dose increase, particularly when other potential causes are excluded.
Antidepressants rank among the three most widely prescribed therapeutic drug classes in the United States.
When starting serotonergic and/or antipsychotic medication in the elderly, regular sodium monitoring and cognitive assessment are essential. Subtle changes in mental status should prompt evaluation for reversible metabolic causes such as hyponatremia to avoid misattribution to dementia progression. This case also highlights the importance of a multidisciplinary approach to reaching a diagnosis and management plan.
This article is a case report describing the clinical management of a single patient. As a case report, it does not constitute research on human subjects and formal ethical approval from an institutional review board (IRB) was not required under the applicable institutional and national guidelines. The case was managed in accordance with the ethical standards of King Abdulaziz Medical City, Ministry of the National Guard – Health Affairs, Jeddah, Saudi Arabia, and in compliance with the Declaration of Helsinki. Written informed consent for publication was obtained from the patient’s legal guardian prior to submission, as detailed in the Consent section below.
Written informed consent for publication of their clinical details and/or clinical images was obtained from the patient’s legal guardian.
This article is a case report. As a single patient case report, it does not generate datasets, statistical measures, graphs, figures, or extractable variables in the conventional sense, and therefore no underlying dataset is associated with this article. No means, standard deviations, or other aggregate measures were reported. No figures or graphs were included. There are no datasets to share. The clinical details described in this report cannot be made publicly available due to patient privacy and confidentiality requirements, even in de-identified form, as the combination of rare clinical characteristics could potentially identify the individual. Written informed consent for publication was obtained from the patient’s legal guardian.
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