Low serum PTH levels also exclude primary hyperthyroidism. Phosphorus: low serum phosphorus levels due to low PTH. Creatinine and BUN: high levels can indicate severity of renal damage. Magnesium: serum magnesium levels are low as hypercalcemia inhibits mg^2+ reabsorption in the renal tubules. Vitamin D levels: low vitamin D levels are found. Normal vitamin D levels eliminate primary hypercalcemia. Electrocardiograms (ECG):
An ECG can also be used to diagnose MAS. The following findings related to hypercalcemia could appear on an ECG:
Short QT interval: most commonly seen as short OoT or OaT changes. Prolongation of PR and QRS intervals. Increased Amplitude of QRS complex. Osborn wave
Short ST segment.Radiology:
Chest x-rays can help exclude any malignancy or sarcoidosis when evaluating for hypercalcemia. Prevention
Increasing education in both people and clinicians surrounding milk-alkali syndrome can help prevent the disease. Over recent years, people have become more aware of the benefits of calcium and how to access it, leading to a consequential rise in cases of milk-alkali syndrome. It is crucial that people are educated by their healthcare provider(s) about how hypercalcemia can develop and the hallmark symptoms to monitor for. Often unknown to the person, calcium can come from many different dietary sources in addition to self- or prescribed-supplementation. Unfortunately, this can lead to the intake of amounts of calcium that exceeds recommended doses, causing harmful effects. Particularly in persons with any degree of renal disease, supplementation of calcium can more easily result in deadly hypercalcemia and alkalosis.
However, it is well known that MAS is usually associated with a triad of symptoms that include hypercalcemia, alkalosis, and acute kidney injury. In general, milk-alkali syndrome starts with excess calcium levels in the body (hypercalcemia), which causes the bodys pH to increase (become more alkaline) resulting in metabolic alkalosis and ultimately contributes to a decrease in renal function.Factors involved in the development of hypercalcemia include excess intestinal absorption of calcium, saturation of the bones buffering capacity for calcium, decreased renal excretion, and abnormal vitamin D metabolism. Underlying kidney disease is a risk factor for MAS, but even people with healthy kidneys can develop the syndrome.For a healthy individual, if calcium levels are high, the kidneys will decrease its production of calcitriol (active vitamin D) by reducing the hydroxylation of calcidiol (inactive vitamin D); lower calcitriol levels means a lower rate of calcium absorption in the small intestine, which eventually offsets the elevated calcium levels. However, excessive ingestion of calcium of more than 10-15 g per day has been reported to cause calcium levels too high for renal calcitriol suppression to control, resulting in net calcium absorption that ultimately causes hypercalcemia.Hypercalcemia affects the kidneys in multiple ways that altogether contributes to hypovolemia. Prolonged hypercalcemia can decrease glomerular filtration rate (GFR) via vasoconstriction, reduce creatinine clearance, and eventually cause renal insufficiency. Hypercalcemia also causes natriuresis by blocking the Na-K-Cl cotransporter (NKCC) in the medullary thick ascending limb of the loop of Henle, leading increased sodium excretion followed by water excretion that leads to hypovolemia.