Propylene glycol accumulated significantly in pediatric intensive care patients receiving continuous lorazepam infusion, and propylene glycol concentration correlated with the cumulative lorazepam dose the patient received. However, significant laboratory abnormalities due to propylene glycol accumulation were not observed.

Objectives To establish the steady-state pharmacokinetic profile of vancomycin in pediatric cardiology patients; determine an empiric vancomycin dose; and evaluate the correlation between fluid balance and volume of distribution (Vd), serum creatinine and clearance (CL), and daily dose of furosemide and Vd. Methods Retrospective pharmacokinetic evaluation in 36 pediatric cardiology, cardiac surgery, or cardiac transplant patients treated with vancomycin. The pharmacokinetic profile for vancomycin including elimination half-life (t1/2), elimination rate constant (ke), volume of distribution (Vd), and clearance (CL) was calculated for each patient. The relationship between fluid balance and Vd, serum creatinine and CL, and the total daily dose of furosemide and Vd was evaluated. Results The patient population had an average half-life of 5.9±1.2 hr and a Vd of 0.4±0.12 L/kg. A statistically significant correlation was noted between serum creatinine and CL (r2=0.19, P<0.01). Additionally, a statistically significant correlation exists between the total daily furosemide dose and the Vd (r2=0.31, P<0.01). A dose of 10 mg/kg/dose every 12 hrs was predicted to result in the greatest number of serum vancomycin concentrations within the reference range. Conclusions Routine monitoring of serum vancomycin concentrations is prudent for this population, and special consideration should be given to those with elevated serum creatinine and to those receiving large doses of furosemide.

The literature supports the use of erythromycin as a prokinetic agent. Many children with GER are adequately controlled with acid suppression alone; however, if use of a prokinetic agent is warranted, erythromycin in combination with acid suppression should be considered. Given the lack of prospective controlled studies demonstrating metoclopramide's efficacy and safety in the treatment of GER in children, metoclopramide should not be considered a treatment option.

Sickle cell disease affects 70,000 Americans who experience an average of 0.8 painful episodes each year. The pathophysiology of sickle cell pain is not completely understood. The disease is characterized by both acute and chronic pain syndromes. Patients with sickle cell pain often encounter barriers to receiving appropriate care, including lack of continuity of care and perceived opiate addiction. Studies describing pharmacotherapy for sickle cell pain have been primarily retrospective and uncontrolled. In analyzing the available literature regarding pathophysiology, assessment, and treatment of sickle cell pain, we found a need for increased practitioner education and intervention to improve the level of care provided to patients with this disease.

Sevelamer, a non-calcium-containing, non-aluminum-containing phosphate binder, is frequently prescribed for treatment in adults with hyperphosphatemia secondary to end-stage renal disease (ESRD). However, published information regarding sevelamer use in children younger than 11 years is lacking. We report the use of sevelamer as a phosphate binder in a 19-month-old girl with ESRD who was receiving calcium carbonate 1250 mg 3 times/day for hyperphosphatemia. The patient's initial serum phosphorus concentration was 8.6 mg/dl, and the calcium-phosphorus product was 75 mg(2)/dl(2). This was well above the level that places patients at risk for complications such as joint, vessel, and soft-tissue calcification. An aluminum-containing phosphate binder was not an option given the patient's renal disease and the concern for neurotoxicity. Sevelamer was considered, but a MEDLINE search revealed no pediatric dosing information. An initial dosage of 100 mg/kg/day divided every 8 hours was administered, as extrapolated from adult data, and then titrated to 130 mg/kg/day divided every 8 hours based on the patient's response. The child's dietary phosphorus intake remained constant throughout her hospital stay. During sevelamer therapy, her serum phosphorus concentration dropped as low as 5.2 mg/dl; at discharge it was 6.5 mg/dl, with a corresponding calcium-phosphorus product in the upper 50s. No adverse effects associated with sevelamer were observed. In the dosages we used, sevelamer resulted in an acceptable calcium-phosphorus product and returned the patient's serum phosphorus concentration to near normal. Sevelamer appears to be a viable option as a phosphate binder in children with ESRD.

Previously, investigators have measured endogenous digoxin-like immunoreactive substances (DLIS) in pediatric patients. Digoxin-like immunoreactive substances may cross-react with digoxin assays to produce false-positive digoxin concentrations; hence, the validity of digoxin concentrations in pediatric patients is questionable. The authors compared the presence and magnitude of apparent DLIS using the microparticle enzyme immunoassay (MEIA) AxSYM Digoxin II and the fluorescence polarization immunoassay (FPIA) TDx Digoxin II, in the serum of 80 pediatric patients who were hospitalized with normal serum creatinine but had not been administered digoxin. Patients ranged in age from 1 day to 16 years (mean age, 4.96 +/- 5.17 years). Serum creatinine and total bilirubin were 0.5 +/- 0.18 mg/dl and 1.3 +/- 0.17 mg/dl, respectively. Forty-eight percent of MEIA samples and 79% of FPIA samples had measurable DLIS values. Digoxin-like immunoreactive substance concentrations for the MEIA (0.07 +/- 0.09 ng/ml) and FPIA assays (0.1 +/- 0.1 ng/ml) were statistically different (p = 0.01); however, no sample had a DLIS value >0.38 ng/ml. A poor correlation was noted between patient age, serum creatinine, total bilirubin, and DLIS concentration. The MEIA and FPIA assays effectively minimized DLIS cross-reactivity making both technologies clinically acceptable for serum digoxin measurement in pediatric patients with normal serum creatinine and total bilirubin.

We report a case of ceftriaxone-induced immune hemolytic anemia in a 10-year-old with chronic active Epstein–Barr virus disease and hemophagocytic lymphohistiocytosis. After chemotherapy, she became febrile and received ceftriaxone. She rapidly developed respiratory failure and anemia. Her direct antiglobulin test was positive for IgG and C3. To confirm this was ceftriaxone-induced complement-mediated hemolysis, we adapted the complement hemolysis using human erythrocytes (CHUHE) assay by adding exogenous ceftriaxone to the patient’s serum which enhanced lysis of her erythrocytes. We confirmed that ceftriaxone initiated a classical complement pathway-mediated hemolysis by in vitro reversal with peptide inhibitor of complement C1 (PIC1).

OBJECTIVES Palivizumab is a monoclonal antibody approved for the prevention of serious lower respiratory tract infections caused by respiratory syncytial virus (RSV) in high-risk pediatric patients. While palivizumab is more effective if used correctly, compliance with the monthly dosing is suboptimal. We established a pharmacist-managed RSV prevention clinic in an effort to improve compliance. The primary objective of this study was to determine the impact of a pharmacist-managed RSV prevention clinic on palivizumab compliance. METHODS A chart review was performed. Patients who received palivizumab between September 2009 and April 2012 were identified. Compliance was determined as the number of patients who received eligible doses at 28- to 30-day intervals, consecutively. RESULTS One hundred seventy-two patients received at least 1 dose of palivizumab. An average of 92% of patients who received at least 1 dose subsequently received all doses of palivizumab during the RSV season. Of those, 88% received all eligible doses in consecutive 28-to 30-day intervals. CONCLUSION A pharmacist-managed RSV prevention clinic can assist physicians in the prevention of RSV by increasing compliance with palivizumab dosing.