Hypocalcemia as an Independent Cause of Esophageal Dysphagia: A Case Report

Dysphagia, or difficulty swallowing, can result from esophageal motility disorders and is often linked to hypocalcemia. Calcium is essential for the proper function of pharyngeal and esophageal muscles, and low calcium levels can impair swallowing. Additionally, certain diuretics may worsen this by increasing calcium and magnesium loss, complicating the management of hypocalcemia. In this case, an 82-year-old male presented with a sudden onset of dysphagia, which had worsened over one week. He was intolerant to both solids and liquids and had a complex medical history, including non-erosive gastritis and previous benign adenoma surgery. Magnetic resonance imaging (MRI) of the brain ruled out acute stroke. On admission, he had severe hypocalcemia (serum calcium level of 1.19 mmol/L) and hypomagnesemia (serum magnesium level of 0.17 mmol/L). A mildly elevated parathyroid hormone (PTH) level of 7.5 pmol/L suggested a compensatory response. Despite intravenous (IV) calcium administration, his calcium levels showed only slight improvement. Hypomagnesemia contributed to resistance to calcium therapy, necessitating IV magnesium. His use of furosemide at a dose of 40 mg per day, a diuretic that increases renal calcium excretion, likely exacerbated both conditions. After two days of IV calcium and magnesium, his serum calcium normalized to 1.96 mmol/L, and magnesium improved to 0.84 mmol/L. Post-treatment, he showed marked improvement in dysphagia, regaining the ability to swallow both solids and liquids. The endoscopic examination of the upper gastrointestinal (GI) tract shows normal findings. The gastroesophageal junction and esophagus have healthy mucosa with no visible abnormalities such as lesions, strictures, or inflammation. The stomach appears normal, with smooth, intact mucosa and well-formed gastric folds. Some food debris is present but does not indicate any pathology. The resolution of symptoms with electrolyte correction confirmed that hypocalcemia was the primary cause of his dysphagia, which was challenging to manage due to hypomagnesemia. This case emphasizes the importance of considering electrolyte imbalances, particularly hypocalcemia, as potential reversible causes of severe dysphagia. The patient's improvement in swallowing function with calcium correction supports the hypothesis that these electrolyte disturbances significantly contributed to his symptoms. This case highlights the crucial role of calcium in esophageal motility and emphasizes the need to evaluate and correct electrolyte imbalances in acute dysphagia. This case also highlights the role of magnesium in overcoming resistance to calcium supplementation in cases of severe hypocalcemia. Further research could improve the understanding and management of similar cases.