Introduction

Discharge communication is critical for the continuity of patient care. However, discharge summaries are often not available in time for follow-up visits, and the content is inconsistent. We aimed to decrease the average time to discharge summary completion by 25%, reduce deficiencies (information errors) by 50%, and increase discharge summary template use to >80% in 6 months.

Methods

A pediatric interprofessional team used quality improvement methods to identify barriers and implement interventions, including discharge summary completion time expectation, electronic health record discharge summary template changes addressing gaps, and training. Notable changes to the template included embedded writing tips to guide writers and specific template choices for common diagnoses to standardize content. The primary outcome measure was the mean discharge summary completion time. Secondary measures were the percentage of discharge summaries with deficiencies and the rate of template use.

Results

After interventions, the mean discharge summary completion time decreased by 70% (from 71.5 to 21.8 hours). Discharge summary deficiencies decreased 44% (from 4.5% to 2.5%), and template use increased from 62% to 97%.

Conclusion

Quality improvement methods and a newly designed electronic health record-discharge summary template were used to dramatically improve discharge summary timeliness and standardize content to streamline continuity of care.

Food insecurity is associated with worse health, education, and socioeconomic status. In 2015, United States Department of Agriculture (USDA) reported 3 million households with children were food insecure. The USDA defines food insecurity as "the limited or uncertain availability of nutritionally adequate and safe foods." A recent American Academy of Pediatrics policy statement advised food insecurity screening for children. While this is embraced by primary care, locally we identified a gap in screening by subspecialty practice and aimed to address this in one pediatric subspecialty clinic within a busy tertiary referral center.

We report five fetuses and a child from three families who shared a phenotype comprising cerebral ventriculomegaly and echogenic kidneys with histopathological findings of congenital nephrosis. The presenting features were greatly elevated maternal serum alpha-fetoprotein (MSAFP) or amniotic fluid alpha-fetoprotein (AFAFP) levels or abnormalities visualized on ultrasound scan during the second trimester of pregnancy. Exome sequencing revealed deleterious sequence variants in Crumbs, Drosophila, Homolog of, 2 (CRB2) consistent with autosomal-recessive inheritance. Two fetuses with cerebral ventriculomegaly and renal microcysts were compound heterozygotes for p.Asn800Lys and p.Trp759Ter, one fetus with renal microcysts was a compound heterozygote for p.Glu643Ala and p.Asn800Lys, and one child with cerebral ventriculomegaly, periventricular heterotopias, echogenic kidneys, and renal failure was homozygous for p.Arg633Trp in CRB2. Examination of the kidneys in one fetus showed tubular cysts at the corticomedullary junction and diffuse effacement of the epithelial foot processes and microvillous transformation of the renal podocytes, findings that were similar to those reported in congenital nephrotic syndrome, Finnish type, that is caused by mutations in nephrin (NPHS1). Loss of function for crb2b and nphs1 in Danio rerio were previously shown to result in loss of the slit diaphragms of the podocytes, leading to the hypothesis that nephrosis develops from an inability to develop a functional glomerular barrier. We conclude that the phenotype associated with CRB2 mutations is pleiotropic and that the condition is an important consideration in the evaluation of high MSAFP/AFAFP where a renal cause is suspected.