Vitamin D is essential for calcium absorption and for maintaining bone health in the pediatric population. Vitamin D deficiency may develop from nutritional deficiencies, malabsorption, enzyme-inducing medications, and many other etiologies. It may present as hypocalcemia before bone demineralization at periods of increased growth velocity (infancy and adolescence) because the increased calcium demand of the body cannot be met. In children, inadequate concentrations of vitamin D may cause rickets and/or symptomatic hypocalcemia, such as seizures or tetany. In this review, we will discuss the pharmacology behind vitamin D supplementation, laboratory assessments of vitamin D status, current literature concerning vitamin D supplementation, and various supplementation options for the treatment of vitamin D deficiency in the pediatric population.

The Broselow tape is accurate for weight estimation in children < or =25 kg, but the Theron formula performs better with patients weighing >40 kg. The Broselow tape was not statistically superior to the Leffler formula in subjects weighing 25.1 to 40 kg. A separate cohort is needed to evaluate the validity of the alternative predictive formulae.

Common treatment options for deep vein thrombosis and venous thromboembolism in the pediatric population include unfractionated heparin, low molecular weight heparin, and warfarin. Other alternatives are bivalirudin, argatroban, and fondaparinux. Warfarin is the only approved oral option, but an oral agent without frequent monitoring would be optimal for pediatric patients. Thus, there is an increasing need for new anticoagulation options in this population. None of the current direct oral anticoagulants have FDA-approved indications and dosing in children. The two classes of DOACs and the drugs they are comprised of are factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) and direct thrombin inhibitor (dabigatran). Off-label usage of these agents is largely based on adult doses. By far, rivaroxaban and dabigatran have the most published data and ongoing trials in pediatric patients compared to edoxaban and apixaban. After evaluating the current literature available on these agents, it is, however, still too early to make any definitive recommendations on their usage in this special population.

Background. The pharmacokinetics of many medications change as we age, thus most would assume dosing strategies would adjust for these changes. The objective of this study is to evaluate the initial vancomycin dosing in three pediatric age groups based on measured serum trough concentrations. Methodology. This retrospective database review included patients aged from 1 month to 18 years old admitted to the Moses H. Cone Memorial Hospital. Patients had to have received vancomycin dosed at 15 mg/kg every 8 hours with an appropriately measured trough concentration. The primary outcome was to determine the percentage of patients in 3 pediatric age groups achieving therapeutic trough concentrations with the initial vancomycin dosing regimen. Results. Twenty-five patients were included in the study. None of the patients had therapeutic trough concentrations after receiving vancomycin 15 mg/kg every 8 hours. Only one patient had a supratherapeutic level, while all of the other patients had levels less than 10 mcg/mL. Conclusions. Vancomycin 15 mg/kg every 8 hours did not provide therapeutic serum trough concentrations for any pediatric age groups. Higher doses and/or more frequent dosing regimens need to be evaluated for each age group to determine the most appropriate strategies for producing therapeutic trough concentrations.

Rufinamide is a triazole derivative with broad-spectrum antiepileptic effects that is unrelated to any antiepileptic drug currently on the market. The European Commission and the US FDA approved rufinamide in 2007 and 2008, respectively, for adjunctive treatment of seizures associated with Lennox-Gastaut syndrome in children 4 years of age or older and adults. The mechanism of action of rufinamide is not completely understood but it is believed to prolong the inactive state of sodium channels, therefore limiting excessive firing of sodium-dependent action potentials. Rufinamide is well absorbed when taken with food, with an absolute bioavailability between 70% and 85%. The elimination half-life of the drug is around 6-10 hours, with a time to maximum plasma concentration (C(max)) of approximately 4-6 hours. The C(max) at a dosage of 10 mg/kg/day and 30 mg/kg/day is 4.01 μg/mL and 8.68 μg/mL, respectively, and the area under the plasma concentration-time curve from time 0 to 12 hours was 37.8 ± 47 μg · h/mL and 89.3 ± 58 μg · h/mL, respectively. Rufinamide exerts non-linear pharmacokinetics with increasing doses. The volume of distribution in children is similar to that in adults (0.8-1.2 L/kg) and the drug binds rather poorly to plasma protein (26.2-34.8%). Rufinamide is mainly metabolized by carboxylesterases to an inactive metabolite (CGP 47292), and the majority of the metabolites are excreted in the urine (91%). No dosage adjustment is required in patients with renal dysfunction. Rufinamide does not affect the plasma concentration of other antiepileptics, but phenytoin, phenobarbital, valproate, and primidone affect the clearance of rufinamide. In a clinical study of 138 patients averaging 12 years of age, rufinamide used as an adjunctive therapy (with an initial dosage of 10 mg/kg/day up to a target dosage of 45 mg/kg/day) in patients with Lennox-Gastaut syndrome reduced the median total seizure frequency by 32.7% versus 11.7% in the placebo group (p = 0.0015). Similar reduction in total seizure frequency was maintained in the extension phase of this study. In other studies, rufinamide also seemed to provide improvement in both partial seizures and refractory epilepsy, but further studies need to validate this observation and to identify its clinical significance. Rufinamide is usually started orally at 10 mg/kg/day, titrating up by 10 mg/kg/day every 2 days to a target dosage of 45 mg/kg/day divided twice daily (maximum dosage of 3200 mg/day). Dosing of rufinamide has not been established in patients <4 years of age. Rufinamide is available as 100, 200, and 400 mg tablets in Europe, and 200 and 400 mg tablets in the US; a suspension of 40 mg/mL can be prepared extemporaneously. Rufinamide is well tolerated, with the most common adverse effects being dizziness, fatigue, nausea, vomiting, diplopia, and somnolence. From the current data, rufinamide serves as an adjunctive therapy in the management of Lennox-Gastaut syndrome. Further studies need to evaluate its efficacy as a first-line agent in the management ...

Kawasaki disease is an autoimmune disease found predominantly in children under the age of 5 years. Its incidence is higher in those who live in Asian countries or are of Asian descent. Kawasaki disease is characterized as an acute inflammation of the vasculature bed affecting mainly the skin, eyes, lymph nodes, and mucosal layers. Although the disease is usually self-limiting, patients may develop cardiac abnormalities that can lead to death. The exact cause of the disease is unknown; however, researchers hypothesize that an infectious agent is responsible for causing Kawasaki disease. Initial treatment options with intravenous immune globulin and aspirin are sufficient to cure most patients who acquire this disease. Unfortunately, in up to one-quarter of patients, the disease will be refractory to initial therapy and will require further management with corticosteroid, immunomodulatory, or cytotoxic agents. The lack of randomized, controlled trials makes treatment of refractory disease difficult to manage. Until larger randomized, controlled trials are published to give more guidance on therapy for this stage of disease, clinicians should use the data available from observational studies and case reports in conjunction with their clinical expertise to make treatment decisions.

Anticoagulation therapy for internal jugular vein thrombosis associated with Lemierre's syndrome remains a controversy. In the absence of any contraindication or presumed risk, anticoagulation therapy should be considered in high risk patients.

OBJECTIVES Accurate determination of ideal body weight (IBW) in pediatric patients is important for the proper dosing of many medications and the classification of nutritional status. There is no consensus on the best method to calculate IBW. The purpose of this study is to evaluate and compare 7 different methods used to calculate IBW in the pediatric population. METHODS This was a retrospective observational study. All subjects were pediatric inpatients at a 536-bed community teaching hospital between January 1, 2016, and June 30, 2017. Subjects were divided into 2 cohorts: cohort 1 was aged 12 months and 0 day to 35 months and 30 days, and cohort 2 was aged 36 months and 0 day to 17 years and 364 days. The McLaren method was used as the reference to compare with 6 other methods: Moore method, Devine method, American Dietetic Association (ADA) method, body mass index (BMI) method, Traub equation, and simplified Traub equation. RESULTS For cohort 1 (n = 347), the Moore method was not statistically different from the McLaren method with a mean difference of −0.07 kg (95% CI: −0.14 to 0.01, p = 0.07). For cohort 2 (n = 1095), the BMI method was not statistically different from the McLaren method with a mean difference of 0.17 kg (95% CI: −0.07 to 0.40, p = 0.17). CONCLUSIONS In both cohorts, the majority of methods used to calculate IBW in pediatric patients leads to statistically different results when compared with the McLaren method. For certain methods, these differences become pronounced at high and low height percentiles and in older age groups.