Dr. Anand Jagannath presents a Human Dx unknown to Reza and U of C residents – Drs. Alec and Austin Rezigh.
Dr. Alec Rezigh
Alec Rezigh is a third-year internal medicine resident at The University of Colorado. He is originally from Houston, TX and received his undergraduate degree at the University of Texas at Austin. He then went back to Houston for medical school at the University of Texas at Houston (McGovern) Medical School. In his free time, he loves all things basketball, traveling with his wife, and napping on the couch with his dog. Following completion of his training, he will return to Houston to be an academic hospitalist. He wishes to thank Dr. Juan Lessing for his amazing mentorship and inspiring his interest in clinical reasoning – and introducing him to Rabih and Reza!
Dr. Austin Rezigh
Austin Rezigh is a third-year internal medicine, primary care track resident at the University of Colorado. He completed medical school at UT Southwestern and is excited to pursue a career in academic general internal medicine. In his free time, he enjoys trying new cuisines, exercising, and spending time with his fur-niece, Kensie.
Dr. Anand Jagannath
Dr. Anand Jagannath is a clinician-educator at the University of California, San Diego (UCSD) and hospitalist at the VA San Diego. He completed medical school at the Tufts University School of Medicine and internal medicine residency and chief residency at Albert Einstein College of Medicine/Montefiore Medical Center. At UCSD, Anand’s interests include bedside team rounding, teaching clinical reasoning to medical students and residents, learning from his learners, and promoting a safe and inclusive learning environment. He is also a Section Editor for adult medicine cases at the Human Diagnosis Project. When he’s not getting excited about medicine, you’ll probably find Anand cooking food, watching shows about food on Netflix, running, or playing basketball or his violin.
Human Dx Case Summary
A 66-year-old man with alcohol use disorder and chronic NSAID use presented with one day of abdominal pain and nausea. Laboratory analysis was notable for hypercalcemia to 16 mg/dL (with low parathyroid hormone and vitamin-D levels), metabolic alkalosis, and an acute kidney injury. The patient disclosed that he had recently consumed large amounts of calcium carbonate for his abdominal pain, and he was diagnosed with the milk alkali syndrome. His serum calcium normalized after receiving intravenous fluids and withholding further calcium supplementation.
The milk alkali syndrome, the third most common cause of hospital admission for hypercalcemia, develops from excess consumption of calcium supplements (e.g., calcium carbonate). Patients classically present with hypercalcemia, metabolic alkalosis, and renal insufficiency. The metabolic alkalosis is thought to be due to hypercalcemia-induced nephrogenic diabetes insipidus, while renal insufficiency develops as a result of calcium-induced renal tubular damage and vasoconstriction of the renal afferent arteriole. Treatment includes intravenous fluid resuscitation and cessation of calcium supplementation.