Acute Milk-Alkali Syndrome After Calcium Supplementation Post-Thyroidectomy
Poster #: 050
Session/Time: A
Author:
Zi Guo, MS
Mentor:
Amanda Brooke Hooper, MD
Research Type: Case Report
Abstract
INTRODUCTION:
Milk-alkali syndrome (MAS) is characterized by the triad of hypercalcemia, metabolic alkalosis, and acute kidney injury, historically linked to the "Sippy regimen" for peptic ulcer disease. The incidence declined with the advent of modern ulcer therapies but has re-emerged due to widespread calcium and vitamin D supplementation. We present a case of acute MAS precipitated by postoperative calcium/vitamin D therapy following thyroidectomy, highlighting the importance of monitoring calcium levels in the postoperative setting.
CASE INFORMATION:
A 35-year-old woman underwent total thyroidectomy, thymectomy, and median sternotomy for removal of a substernal goiter. The right superior parathyroid gland, devascularized during surgery, was autotransplanted into the left sternocleidomastoid. She was discharged on levothyroxine, calcitriol, calcium acetate, and calcium-vitamin D due to postoperative hypocalcemia. Ten days later, she developed nausea, vomiting, malaise, diarrhea, cold intolerance, and 10 lb weight loss. Outpatient labs showed calcium 17.0 mg/dL (ionized 7.4 mg/dL), prompting ED transfer. Vitals: afebrile, BP 112/72 mm Hg, HR 107 bpm. Physical exam was unremarkable except for well-healed surgical scars. Labs showed metabolic alkalosis (CO₂ 36 mmol/L), creatinine 2.3 mg/dL (baseline 0.7), BUN 23 mg/dL, suppressed PTH (<1 pg/mL), and elevated phosphorus (5.1 mg/dL). Chest radiograph was normal. She received IV normal saline boluses followed by maintenance fluids, with calcium supplements discontinued. Over several days, calcium and creatinine levels normalized with fluid resuscitation. A headache during hospitalization resolved with symptomatic therapy. She was discharged with outpatient endocrinology follow-up.
DISCUSSION:
While primary hyperparathyroidism and malignancy account for most hypercalcemia cases, suppressed PTH and negative malignancy evaluation directed attention to medication-induced causes. This patient's high calcium/vitamin D intake and calcium acetate ingestion created the conditions for MAS. Pathophysiology involves excessive calcium intake overwhelming homeostatic suppression, vitamin D-enhanced absorption, and renal vasoconstriction leading to reduced glomerular filtration. Contraction alkalosis from hypovolemia further enhances calcium reabsorption, perpetuating the cycle. This case illustrates the acute "toxemic" phase of MAS, which occurs within weeks of initiating excessive supplementation. Literature emphasizes that MAS is preventable with careful dosing and monitoring of calcium therapy, especially in patients with altered parathyroid function postoperatively.
CONCLUSION:
MAS should be considered in postoperative patients receiving calcium and vitamin D who present with hypercalcemia, metabolic alkalosis, and renal impairment. Prompt recognition and withdrawal of supplementation, coupled with aggressive hydration, are effective. Post-thyroidectomy protocols should include close monitoring of calcium levels to prevent this complication.
Milk-alkali syndrome (MAS) is characterized by the triad of hypercalcemia, metabolic alkalosis, and acute kidney injury, historically linked to the "Sippy regimen" for peptic ulcer disease. The incidence declined with the advent of modern ulcer therapies but has re-emerged due to widespread calcium and vitamin D supplementation. We present a case of acute MAS precipitated by postoperative calcium/vitamin D therapy following thyroidectomy, highlighting the importance of monitoring calcium levels in the postoperative setting.
CASE INFORMATION:
A 35-year-old woman underwent total thyroidectomy, thymectomy, and median sternotomy for removal of a substernal goiter. The right superior parathyroid gland, devascularized during surgery, was autotransplanted into the left sternocleidomastoid. She was discharged on levothyroxine, calcitriol, calcium acetate, and calcium-vitamin D due to postoperative hypocalcemia. Ten days later, she developed nausea, vomiting, malaise, diarrhea, cold intolerance, and 10 lb weight loss. Outpatient labs showed calcium 17.0 mg/dL (ionized 7.4 mg/dL), prompting ED transfer. Vitals: afebrile, BP 112/72 mm Hg, HR 107 bpm. Physical exam was unremarkable except for well-healed surgical scars. Labs showed metabolic alkalosis (CO₂ 36 mmol/L), creatinine 2.3 mg/dL (baseline 0.7), BUN 23 mg/dL, suppressed PTH (<1 pg/mL), and elevated phosphorus (5.1 mg/dL). Chest radiograph was normal. She received IV normal saline boluses followed by maintenance fluids, with calcium supplements discontinued. Over several days, calcium and creatinine levels normalized with fluid resuscitation. A headache during hospitalization resolved with symptomatic therapy. She was discharged with outpatient endocrinology follow-up.
DISCUSSION:
While primary hyperparathyroidism and malignancy account for most hypercalcemia cases, suppressed PTH and negative malignancy evaluation directed attention to medication-induced causes. This patient's high calcium/vitamin D intake and calcium acetate ingestion created the conditions for MAS. Pathophysiology involves excessive calcium intake overwhelming homeostatic suppression, vitamin D-enhanced absorption, and renal vasoconstriction leading to reduced glomerular filtration. Contraction alkalosis from hypovolemia further enhances calcium reabsorption, perpetuating the cycle. This case illustrates the acute "toxemic" phase of MAS, which occurs within weeks of initiating excessive supplementation. Literature emphasizes that MAS is preventable with careful dosing and monitoring of calcium therapy, especially in patients with altered parathyroid function postoperatively.
CONCLUSION:
MAS should be considered in postoperative patients receiving calcium and vitamin D who present with hypercalcemia, metabolic alkalosis, and renal impairment. Prompt recognition and withdrawal of supplementation, coupled with aggressive hydration, are effective. Post-thyroidectomy protocols should include close monitoring of calcium levels to prevent this complication.