More Is Not Always Better: A Case Report of Excess Calcium Carbonate Ingestion Causing Milk-Alkali Syndrome

Abstract

CASE DESCRIPTION: A 54-year-old female with a medical history significant for CKD stage 4 and alcohol use disorder presented to the Emergency Department with altered mental status. Labs were significant for hyponatremia, hypokalemia, hypochloremia, hypercalcemia, metabolic alkalosis, and Cr 9.3. Lorazepam was given due to concern for alcohol withdrawal. Ultimately, her symptoms were discovered to be due to excessive ingestion of calcium carbonate (aka: Tums), and she was diagnosed with milk-alkali syndrome (MAS). Pt was treated with IV KCl and normal saline, and her labs and mental status normalized over the subsequent 48 hours. | CLINICAL SIGNIFICANCE: MAS is constituted by metabolic alkalosis, acute kidney injury, and hypercalcemia. It is a result of a large intake of calcium and absorbable alkali. The syndrome was first recognized in the early twentieth century, and it essentially disappeared when histamine blockers began being used to treat peptic ulcers in the 1980s. Recently, the syndrome is becoming more common with the increased use of calcium-carbonate in antacids and osteoporosis prevention medications. MAS is the third most common cause of hypercalcemia, after malignancy and hyperparathyroidism. Management involves holding calcium and vitamin D supplements and administering aggressive intravenous hydration. Bisphosphonates and dialysis may be useful in severe cases. Prognosis of MAS is typically good as the condition is reversible. | CONCLUSION: The prevalence of MAS is increasing due to the wide availability of calcium-containing supplements and antacids. In order to counteract this, increased awareness amongst at risk patient populations, such as the elderly and those with renal disease, is vital. Furthermore, increased awareness amongst healthcare professionals may help prevent complications that can arise from untreated MAS.