Peter N. Johnson

Midodrine is an oral vasopressor option that allows for discontinuation of intravenous vasopressors for patients with cardiovascular conditions. It does not have a US Food and Drug Administration-labeled indication for use in children, and there is a paucity of literature in patients ≤6 years of age. This case series describes 2 infants with complex congenital heart diseases initiated on midodrine for augmentation of systolic (SBP) or diastolic blood pressure (DBP) to increase coronary perfusion. Case 1 was initiated on midodrine on hospital day 19 at a dose of 0.5 mg (0.17 mg/kg) enterally every 8 hours that was eventually increased to 1 mg (0.33 mg/kg) every 8 hours. Case 2 was initiated on midodrine on hospital day 15 at a dose of 2.5 mg (0.49 mg/kg) enterally every 8 hours, and this was decreased to 1.25 mg (0.25 mg/kg) every 8 hours due to high SBP. Both patients were discharged home on midodrine; other than the initially high SBP for Case 2, no other adverse drug events were noted. While midodrine was effective based on clinical response in these two infants, additional studies are needed due to the lack of safety and efficacy in children <6 years of age.

Background Cefotaxime shortage in 2015 led to increased ceftazidime use in the neonatal intensive care unit (NICU). Objective The purpose was to explore whether ceftazidime increases risk for development of resistant gram-negative organisms. Methods Retrospective evaluation of NICU patients with cultures positive for Escherichia coli, Pseudomonas aeruginosa, Klebsiella species, or Stenotrophomonas maltophilia between January1, 2015 and August 31, 2020. Isolates were excluded if obtained from same patient and source within 90 days or if patient ≤7 days of life or admitted from a referring hospital. Data collection included demographics and clinical parameters, and culture/susceptibility data. The primary objective was comparison of pathogens and clinical parameters in those with and without third-generation cephalosporin resistance. The secondary objectives included a comparison between those with and without ceftazidime exposure and identification of factors associated with resistance. Comparisons were made using χ 2 , Fisher exact tests, or Wilcoxon tests. A logistic regression was used to identify risk factors for resistance. Results Overall, 349 isolates, representing 215 patients, were included. The most common source was endotracheal (n = 192, 55.0%) and pathogens were E coli (31.8%) and P aeruginosa (29.2%). Overall, 12.3% (n = 43) were resistant and these were obtained after longer parenteral nutrition (PN), central line access, and antibiotic days versus susceptible isolates. Higher resistance was noted after ceftazidime exposure versus no exposure, 19.1% versus 6.6%. Each day of ceftazidime was associated with 13% greater odds of P aeruginosa resistance (adjusted odds ratio: 1.13 [95% confidence interval: 1.03-1.23]). Conclusion and Relevance Ceftazidime duration was associated with increased risk for P aeruginosa resistance. Additional studies are needed to confirm these findings.