C53-30 A Rare Case of Altered Mental Status Due to Milk-Alkali Syndrome

Abstract Milk-Alkali syndrome is characterized by a triad of clinical findings including hypercalcemia, metabolic alkalosis, and acute kidney injury due to calcium ingestion. Though rare, Milk-Alkali syndrome can cause severe altered mental status. We present a severe case of Milk-Alkali syndrome that resulted in coma and required mechanical ventilation. A 57-year-old female patient with a medical history of chronic alcohol use, hypertension, and gastric reflux presented with two days of lethargy and malaise. While initial assessment was limited as the patient was only oriented to self and agitated, the patient’s husband reported daily use of half a bottle of over-the-counter calcium carbonate due to persistent reflux from alcohol use. Her vital signs were notable for hypertension and tachycardia while laboratory workups revealed serum calcium 19.1 mg/dL, ionized calcium 1.83 mmol/L, bicarbonate 33 mmol/L, creatinine 2.15 mg/dL, and pH of 7.59. CT head, chest, abdomen, and pelvis were unremarkable. The patient’s mental status continued to worsen in the ED ultimately required intubation and medical intensive care unit admission. Additional workups showed suppressed PTH, normal PTHrP, normal vitamin D/calcitriol levels, and normal serum protein electrophoresis consistent with hypercalcemia from exogenous calcium intake. She was treated with aggressive volume resuscitation, calcitonin, and pamidronate with progressive improvement in mentation. She was extubated on hospital day 3 before discharged with strict instruction of calcium supplement cessation. At discharge, the patient’s serum calcium had normalized to 9.4 mg/dL. Once thought obsolete, Milk-Alkali syndrome is now the third leading cause of hypercalcemia behind malignancy and hyperparathyroidism in hospitalized patients due to readily available calcium supplements. While most patients are incidentally diagnosed and asymptomatic, severe presentations with altered mentation do occur promoted by a vicious cycle of hypovolemia, metabolic alkalosis, and increased renal calcium resorption. Cornerstones of management focus on volume resuscitation, early calcitonin to prevent bone calcium reabsorption, and subsequent bisphosphonate to maintain calcium reduction. This case report highlights the importance of early recognition, prompt initiation of treatment, and immediate cessation of offending agent in severe Milk-Alkali syndrome. This abstract is funded by: None