Calcium, magnesium and phosphate disorders — viva

Opening (must-hit)

"This child has severe symptomatic hypocalcaemia with neuromuscular excitability, and the fact that it has not corrected after two adequate doses of calcium gluconate tells me the problem is magnesium. Hypomagnesaemia suppresses parathyroid hormone release and produces a functional hypoparathyroidism that no amount of calcium will fix, so my immediate next step is to check the magnesium and replace it with magnesium sulfate 25 to 50 mg per kilogram intravenously over 2 to 4 hours. I continue cardiac monitoring and I look for the cause of the magnesium loss — diuretics, proton pump inhibitors, a Gitelman picture, or an inherited tubulopathy." [1][7]

Examiner: "Why does low magnesium cause refractory hypocalcaemia?"

"Magnesium is required for parathyroid hormone release and for adenylate cyclase signalling in the target tissues, so a low magnesium produces a functional hypoparathyroidism. It also governs the ROMK potassium channel in the distal nephron, which is why hypomagnesaemia causes refractory hypokalaemia at the same time. Until magnesium is restored, the kidney keeps wasting potassium and the calcium will not be retained. This is why I check the magnesium early in any refractory hypocalcaemia and replace it before or alongside the calcium." [7][3]

Examiner: "How would you have given the calcium gluconate if she had presented fresh?"

"Intravenous 10 percent calcium gluconate at 0.5 to 1 mL per kilogram, to a maximum of about 20 mL, slowly over 5 to 10 minutes with continuous cardiac monitoring. I would choose calcium gluconate over calcium chloride peripherally because it is less vesicant if it extravasates, ensure a reliable intravenous line, and stop the infusion if the heart rate drops, because rapid calcium itself causes bradycardia and arrhythmia. I would also check the ionised calcium rather than relying on the total, and correct for albumin." [1][3]

Examiner: "Now pivot — a child with rickets. How do you separate vitamin D deficiency from X-linked hypophosphataemic?"

"The discriminator is the calcium and parathyroid hormone. Vitamin D deficiency lowers calcitriol, which lowers calcium and drives secondary hyperparathyroidism, so the phosphate falls too: low calcium, low phosphate, high parathyroid hormone, high alkaline phosphatase, low 25-hydroxyvitamin D. X-linked hypophosphataemic rickets is driven by excess fibroblast growth factor 23 from a PHEX mutation, which independently wastes phosphate and switches off calcitriol, so the calcium and parathyroid hormone stay normal while the phosphate falls and the alkaline phosphatase rises. Both produce rickets, so the alkaline phosphatase does not separate them; the calcium and parathyroid hormone do." [9][3]

Examiner: "Final corner — tumour lysis. Why does the calcium fall?"

"Tumour lysis releases a torrent of intracellular phosphate and potassium from lysed malignant cells, and the rising phosphate complexes the ionised calcium, driving it down even though total calcium may look near normal. The tetrad is hyperkalaemia, hyperphosphataemia, hypocalcaemia and hyperuricaemia, and they together produce acute kidney injury. I manage it with aggressive hydration and rasburicase for high-risk disease, and I withhold calcium unless the child is symptomatic, because adding calcium to a high phosphate risks metastatic calcification." [11]

Closing summary

"In summary: refractory hypocalcaemia is magnesium — check it and replace it before more calcium. Give calcium gluconate 0.5 to 1 mL per kilogram slowly with monitoring, gluconate peripherally. Separate the rickets by the calcium and parathyroid hormone. In tumour lysis the phosphate complexes the calcium, so hydrate and give rasburicase, and do not chase the calcium unless symptomatic." [1][7]