Rickets and metabolic bone disease — branching viva

Opening: classify and treat

The candidate opens by recognising nutritional vitamin D deficiency rickets and reads the biochemistry as calcipenic: a low or low-normal calcium, a low phosphate, a high alkaline phosphatase, and a raised parathyroid hormone. The 25-hydroxyvitamin D of 22 nmol per litre confirms deficiency against the 50 nmol per litre sufficiency threshold. The candidate explains that the classification separates calcipenic from phosphopenic rickets, and that the calcium and parathyroid hormone are read before the vitamin D level because they redirect the work-up. ^{[1] [2]}

The treatment of nutritional rickets is cholecalciferol 2000 IU daily for three months, or a stoss dose of 100 000 to 300 000 IU, together with oral calcium at 30 to 50 mg per kilogram per day elemental. The candidate explains why calcium is given with the vitamin D and sets the monitoring targets: alkaline phosphatase falling within four to six weeks, biochemistry normalising within months, and radiographic healing within three to six months. ^{[1] [4]}

Branch 1: the hypocalcaemic seizing infant

The examiner pivots to a six-month-old exclusively breastfed infant of a veiled mother presenting in winter with a seizure and a calcium of 1.4. The candidate recognises symptomatic hypocalcaemia as an emergency and gives intravenous calcium gluconate slowly with cardiac monitoring, using calcium rather than standard anticonvulsants to terminate the seizure. The candidate checks and corrects magnesium and avoids alkalosis. ^{[3] [1]}

The examiner probes the order of the drugs. The candidate explains that calcium is given before or with the cholecalciferol, never vitamin D alone, because high-dose vitamin D accelerates mineralisation and can deepen the hypocalcaemia through hungry bone. The emergency sequence is calcium, then oral calcium with cholecalciferol, then monitoring. ^{[1] [4]}