In the absence of chronic disease, dietary rickets may be adequately treated with daily doses of 1,200 to 1,600 IU of vitamin D2 (ergocalciferol) until healing occurs Alternatively, a single high IM dose to replenish stores may be administered as ergocalciferol 50,000 to 100,000 IU Serum phosphate usually returns to normal within to weeks, and radiographic improvement is generally apparent by weeks Once healing is complete, the child should continue to be treated with 400 IU/day to prevent recurrence If the initial serum calcium is borderline low or low, supplemental calcium should be initiated 48 hours before the institution of vitamin D, especially in the young child Otherwise, the initiation of therapy with vitamin D may cause a further decrease in serum calcium and elicit frank hypocalcemia This presentation may occur naturally if the vitamin D–deficient patient has relatively low serum calcium concentration and then has prolonged exposure to the sun This may lead to abrupt increases in vitamin D, ultimately leading to a rapid increase in bone recalcification (hungry bone syndrome) and severe hypocalcemia with possible seizures This syndrome is seasonally termed “spring fits.” Clinical Indications for Discharge or Admission Children with symptomatic hypocalcemia or with initial serum calcium of less than mg/dL on presentation warrant hospitalization and frequent calcium determinations Failure to respond to vitamin D treatment suggests that the child has a more complex cause of rickets, and consultation with a pediatric nephrologist or endocrinologist is recommended THYROID STORM Goals of Treatment After recognizing thyroid storm, the goals of emergency treatment are to control the metabolic rate and reduce cardiac workload CLINICAL PEARLS AND PITFALLS Thyroid storm is precipitated by intercurrent infection, trauma, or after subtotal thyroidectomy with an inadequately prepared patient The presence of high fever (often to 105.8°F [41°C]) is the primary distinguishing feature of thyroid storm from a simple hyperthyroid state A marked increase in cardiac workload may result in high-output heart failure and hypotension and pulmonary edema rather than classic hypertension Current Evidence In thyroid storm, thyroid hormone is suddenly released into the circulation, which results in the uncoupling of oxidative phosphorylation and/or increased lipolysis, both of which contribute to excessive thermogenesis Insensible fluid loss increases as a result of increased metabolism and sweating Tachycardia is caused by both the hyperthermia and the direct action of thyroid hormones on the cardiac conduction system Widened pulse pressure occurs as the result of increased cardiac contractility and decreased peripheral resistance The mortality rate in adults may be as high as 20%: similar data are not available for children