Case Presentation:

A 55‐year‐old female with history of hypertension, hypothyroidism, and osteopenia presented with altered mental status for 4 days. She was found to have confusion, anorexia, abdominal pain, and generalized weakness. Family members reported abuse of prescription medicines. Home medications: esomeprazole 40 mg/day, temazepam 15 mg at bedtime, prochlorperazine 10 mg tid, diazepam 5 mg bid, levolhyroxine 112 μg/day, trazodone 150 mg at bedtime, Premarin 0.625 mg/day. and calcium carbonate 1200 mg/day. Vitals on admission were BP 199/105, pulse 73, respiratory rate 14, temperature 97.7°F, and SaO2 97% on room air. She was drowsy, disoriented to time, and failed to spell “world” backward. She also had epigastric tenderness. Laboratories showed BUN 33, sodium 119 mEq/dL, chloride 73 mEq/dL, HCO3 36.6 mEq/dL, creatinine 1.2 mg/dL (baseline 0.6 mg/dL), calcium 20.5 mg/dL, albumin 4.1 mg/dL, phosphorous 4.1 mg/dL, magnesium 1.3 mg/dL (1.5–2.7 mg/dL), ionized calcium 2.3 mmol/L (0.89–1.21 mmol/L), lipase 509U/L. and amylase 540U/L. Initially, life‐threatening hypercalcemia was managed with normal saline. A dose of 90 mg of pamidronate was infused. However, after 8 hours, the calcium level remained elevated, and the patient's mental status had not improved. Hemodialysis was started, and her confusion, renal function and electrolyte abnormalities improved within 1 day. Further laboratory investigations showed a normal SPEP. PTH < 3 pg/mL (12–65 pg/mL). PTH related peptide < 0.3 pmol/L (0.0–1.5 pmol/L], vitamin D 25 hydroxy 48.4 ng/mL (32–100 ng/mL), random Cortisol 60.8 μg/dL (4.5–22.7 μg/dL), and TSH 0.07 mU/mL (0.47‐4.68 mU/mL). Chest x‐ray was normal. Based on the history medication abuse and the above lab results, the patient was diagnosed with MAS. Twenty‐four‐hour urine calcium excretion remained normal during outpatient follow‐up. No recurrent episodes of hypercalcemia have occurred within 1 year of follow‐up. Recenl mammogram had been normal.

Discussion:

MAS may present variably, from asymptomatic to life‐threatening hypercalcemia. Treatment usually consists of stopping calcium supplementation, IV hydration, furosemide. and IV bisphosphonate therapy. In our case, we implemented emergent hemodialysis because of the severity of our patient's symptoms, and The failure of standard therapy Based on our review of literature, no previous case of MAS has required emergent hemodialysis. We present this case to raise awareness of MAS as a cause of hypercalcemia in hospitalized patients.

Conclusions:

Milk alkali syndrome (MAS) is a triad of hypercalcemia, metabolic alkalosis, and renal insufficiency caused by the ingestion of calcium and absorbable alkali. With the recent emphasis on calcium therapy for the prevention of osteoporosis, MAS is now the third‐leading cause of hypercalcemia. The case we present required Treatment with hemodialysis.

Author Disclosure:

W. Yan, none; N. Traub, none; N. Shroff, none.