Hyponatremia frequently occurs as an electrolyte disorder and causes several complications, including rhabdomyolysis [¹] Rhabdomyolysis is a clinical and biochemical condition that occurs when injured muscle tissue releases its proteins and electrolytes into the bloodstream, causing heart and kidney injury and permanent disability or even mortality [²]. Observational studies [³,⁴,⁵] have established hyponatremia as a risk factor for rhabdomyolysis in hospitalized patients, particularly in settings of rapid sodium correction, extreme physical exertion, or comorbid metabolic disturbances. However, existing literature mostly focuses on hospitalized patients with apparent risk factors, leaving gaps in understanding the condition’s presentation and management in non-hospitalized individuals. Although hyponatremia-induced rhabdomyolysis is uncommon, it represents a serious complication with significant renal morbidity. Our study presents a case report of hyponatremia-induced rhabdomyolysis with atypical presentation in a non-hospitalized patient with mild hyponatremia and no traditional triggers.

A 45-year-old male with a history of hypertension, hyperlipidemia, and an 8 cm right frontal porencephalic cyst communicating with the right lateral ventricle, colpocephaly, congenital left hemiparesis, paranoid schizophrenia, anxiety, depression, and psychogenic polydipsia experienced an episode of loss of consciousness. Witnesses reported that the patient often visited his favorite fast-food restaurants and requested large water refills to prolong his stay. Emergency medical services found him unresponsive on the floor of a fast-food restaurant for approximately two minutes.

At the Emergency Department (ED), his blood pressure measured 141/73 mmHg, his heart rate was 82 beats per minute, his temperature was 97.5°F, his respiratory rate was 18 breaths per minute, and his oxygen saturation was 95% on room air. Upon examination, the patient appeared lethargic but was awake, cooperative, and oriented to person, place, and time. He was normocephalic and atraumatic on physical exam. Trace bilateral lower extremity pitting edema was observed, but no signs of volume overload were present. Although he could follow commands, his level of alertness prevented a full neurological assessment.

Laboratory findings revealed hyponatremia (111 mmol/L), hypochloremia (77 mmol/L), hypomagnesemia (1.5 mg/dL), hypocalcemia (8.2 mg/dL), and normal serum glucose. Additional findings included mild leukocytosis (11.57 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\times$\end{document}× 10³/\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\mu$\end{document}μL) and an elevated venous lactate level (3.2 mmol/L). Serum creatine kinase (CK) levels were markedly elevated at 3571 U/L (, ).

The ED administered 2 liters of intravenous normal saline. A CT scan of the head showed no acute intracranial abnormalities, and chest imaging was unremarkable.

The patient was admitted to the intensive care unit (ICU) for close monitoring and gradual correction of sodium levels. Clinicians discontinued intravenous fluids, implemented fluid restriction, and corrected other electrolyte disturbances. A two-hour electroencephalogram (EEG) showed no seizure activity, and serum prolactin levels at admission (13 ng/mL; reference: 4.1–18.4 ng/mL) indicated no evidence of seizures. Over 36 hours, sodium levels were corrected to 143 mmol/L, and CK levels decreased to 124 U/L. The patient’s symptoms improved, and he remained seizure-free during his hospitalization. After stabilization, he was discharged with instructions for outpatient follow-up.

Psychogenic polydipsia manifests as a clinical disorder characterized by polyuria and polydipsia, which commonly affects psychiatric populations, particularly individuals with schizophrenia [⁶]. Although the exact mechanism by which psychogenic polydipsia leads to hyponatremia remains unclear, researchers attribute it to an increase in total body water relative to total body sodium content, which dilutes blood sodium levels [⁷].

Health practitioners frequently encounter hyponatremia in clinical practice but often fail to recognize its association with rhabdomyolysis. Malfunctioning of the sodium/calcium pump appears to drive the development of rhabdomyolysis in hyponatremic states by activating proteases and lipases that cause cell lysis [⁸]. While evidence linking low serum sodium levels to muscle breakdown continues to grow, a study involving animal models refuted a direct causal association between hyponatremia and rhabdomyolysis. Instead, factors such as genetic predispositions and convulsive states are well-established contributors [⁹]. Trimarchi et al. reviewed a case in 1999 involving acute excessive water ingestion and severe muscle pain in a patient on chronic hydrochlorothiazide therapy. The case demonstrated hyponatremia-induced rhabdomyolysis, emphasizing the importance of maintaining a high level of suspicion in patients presenting with acute muscle pain and hyponatremia. They recommended serial monitoring of muscle enzymes in such cases [¹⁰].

Several reports have identified hyponatremia as a trigger for rhabdomyolysis in patients using certain medications. For instance, myopathy has been documented with indapamide, a drug linked to hypokalemia and hyponatremia [¹¹]. Similarly, severe rhabdomyolysis and hyponatremia were reported in patients using bisacodyl and picosulphate for bowel preparation before colonoscopies [¹²]. Increased water intake during competitive sports often disrupts fluid and electrolyte balance, particularly sodium levels. Studies have shown that ultra-endurance athletes experience higher rates of rhabdomyolysis in hyponatremic states compared to non-hyponatremic counterparts. This was evident in an investigation of exercise-associated hyponatremia and rhabdomyolysis across seven races and disciplines [¹³].

Recurrent rhabdomyolysis has been observed in cases of psychogenic polydipsia-induced hyponatremia, underscoring the importance of monitoring muscle markers in patients with severe hyponatremia. Although our case does not confirm seizures as a cause of myopathy, further research is necessary to establish hyponatremia as the primary cause of rhabdomyolysis in the absence of other confounders.