Clinical Pearls & Morning Reports

Posted by Carla Rothaus

Published December 16, 2020


How is severe, asymptomatic hypocalcemia that is associated with vitamin D deficiency managed?

Childhood causes of vitamin D deficiency include obesity, malabsorption, and low sun exposure, as well as decreased nutritional intake. Read the NEJM Case Records of the Massachusetts General Hospital here.

Clinical Pearls

Q: Is nutritional rickets rare in high-income countries?

A: Nutritional rickets is often thought of as a historical relic — the discovery of vitamin D and the implementation of supplementation and food-fortification strategies in the early 20th century sharply decreased the prevalence of what had been a common disease, particularly in urban centers. However, the incidence of vitamin D deficiency appears to be rising in high-income countries, and the prevalence is persistently high in low- and middle-income countries.

Q: What are some of the risk factors for nutritional rickets?

A: In a 2015 case-finding survey of Canadian pediatricians, risk factors for nutritional rickets included demographic characteristics (recent immigration), physiological features (skin melanin content, food allergies, feeding challenges associated with prematurity, developmental delay, and maternal vitamin D deficiency), and aspects of diet (lack of vitamin D supplementation and dietary restrictions) and behavior (lack of sun exposure).

Morning Report Questions

Q: How is severe, asymptomatic hypocalcemia that is associated with vitamin D deficiency managed?

A: Patients who have profound hypocalcemia that is complicated by severe symptoms (seizure or tetany) receive intravenous calcium to rapidly restore normocalcemia. Unfortunately, there is limited evidence from randomized, controlled trials to guide subsequent repletion of vitamin D stores. In 2016, an international panel developed recommendations for the prevention and management of nutritional rickets. The panel recommended a daily dosing strategy to minimize the risk of hypercalcemia but also recognized that a single high dose may be more feasible in some circumstances and thus offered dosing recommendations for this strategy, as well. Vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol) have similar efficacy when given in daily doses; some evidence suggests that vitamin D3 has better efficacy than vitamin D2 when given in a single dose. In addition, adequate calcium intake, through dietary calcium or supplementation, is necessary to support bone remineralization. Adequate calcium provision is also necessary to prevent hungry bone syndrome, a condition in which there is paradoxical worsening of hypocalcemia after initiation of vitamin D therapy. This condition is thought to be due to rapid bone-mineral uptake by the demineralized skeleton, and management may require very high doses of calcium, as well as occasional therapeutic doses of calcitriol (1,25-dihydroxyvitamin D), the active form of vitamin D.

Q: How quickly do the radiographic changes of nutritional rickets improve with adequate treatment?

A: The response to treatment can be monitored by obtaining blood levels of calcium, phosphate, 25-hydroxyvitamin D, parathyroid hormone, and alkaline phosphatase and the urinary calcium:creatinine ratio approximately 4 weeks after the initiation of treatment and at monthly intervals until resolution of laboratory abnormalities. In most children with nutritional rickets, laboratory values will typically normalize and radiographs will show substantial healing after 3 months of adequate treatment, although some patients may require continued treatment.

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