Milk-Alkali Syndrome: How Electronic Medical Record Open Notes Helped to Rule Out Cancer.

BACKGROUND Milk-alkali syndrome is caused by excessive consumption of calcium and absorbable alkali and typically presents as a triad of hypercalcemia, acute renal failure, and metabolic alkalosis. In the era of histamine receptor blockers and proton pump inhibitors, the incidence of milk-alkali syndrome has decreased. However, the disease has not been eliminated, due to existing calcium-containing therapies. Here, we present a case of severe milk-alkali syndrome with a challenging initial diagnosis. CASE REPORT We present the case of a 64-year-old man who came to the hospital with encephalopathy. Serologic evaluation revealed acute renal failure, severe hypercalcemia, and metabolic alkalosis. He underwent volume resuscitation, with the initiation of calcitonin. Despite our efforts, the patient developed anuria and proceeded to intermittent hemodialysis. His workup was unrevealing, including an appropriately suppressed parathyroid hormone level, low vitamin D, and normal serum protein electrophoresis and angiotensin converting enzyme levels. Considering his persistent encephalopathy, the team was unable to obtain information from the patient regarding his calcium intake. However, at home, the patient's significant other read his progress notes in the electronic medical record and reported that he consumed at least 1 bottle of calcium carbonate (Tums) every week. Once the encephalopathy resolved, the patient confirmed this information. CONCLUSIONS The search for malignancy in the setting of hypercalcemia was ceased because of the family's at-home electronic medical record use and reporting of Tums overuse. Milk-alkali syndrome, although a rarity, should not be forgotten as a cause of hypercalcemia.

Recent advances in the understanding of endothelial barrier function and fluid therapy.

Elucidation of the structural basis of endothelial barrier function and the study of transcapillary fluid exchange dynamics are areas of active research. There has been significant enhancement in our understanding of the ultrastructural basis of endothelial barrier function. The role of glycocalyx has received special attention. Experimental evidence has called for a revision in the classic Starling principle of transcapillary exchange. The glycocalyx model provides a potential structural mechanism for the revised Starling principle. This knowledge can provide the framework for understanding the volume expansion effect of fluid therapy and the physiological basis of fluid therapy.