ABSTRACT
BACKGROUND: Diagnostic delays in the pediatric emergency department (ED) can lead to unnecessary interventions and prolonged ED length of stay (LOS), especially in patients with diabetes mellitus evaluated for diabetic ketoacidosis (DKA). At our institution, baseline DKA determination time (arrival to diagnosis) was 86 minutes, and 61% of patients did not meet DKA criteria. Subsequently, intravenous (IV) placement occurred in 85% of patients without DKA. We aimed to use point-of-care (POC) testing to reduce DKA determination time from 86 to 30 minutes and to reduce IV placements in patients without DKA from 85% to 20% over 18 months. METHODS: Four key interventions (POC tests, order panels, provider guidelines, and nursing guidelines) were tested by using plan-do-study-act cycles. DKA determination time was our primary outcome, and secondary outcomes included the percentage of patients receiving IV placement and ED LOS. Process measures included the rate of use of POC testing and order panels. All measures were analyzed on statistical process control charts. RESULTS: Between January 2015 and July 2018, 783 patients with diabetes mellitus were evaluated for DKA. After all 4 interventions, DKA determination time decreased from 86 to 26 minutes (P < .001). In patients without DKA, IV placement decreased from 85% to 36% (P < .001). ED LOS decreased from 206 to 186 minutes (P = .009) in patients discharged from the hospital after DKA evaluation. POC testing and order panel use increased from 0% to 98% and 90%, respectively. CONCLUSIONS: Using quality-improvement methodology, we achieved a meaningful reduction in DKA determination time, the percentage of IV placements, and ED LOS.
Subject(s)
Diabetic Ketoacidosis/diagnosis , Diabetic Ketoacidosis/therapy , Emergency Service, Hospital/organization & administration , Point-of-Care Testing , Quality Improvement , Time-to-Treatment , Adolescent , Blood Glucose/analysis , Child , Child, Preschool , Delayed Diagnosis/prevention & control , Diabetes Mellitus, Type 1/complications , Female , Fluid Therapy , Guidelines as Topic , Hospitals, Pediatric , Humans , Hypoglycemic Agents/therapeutic use , Infant , Insulin/therapeutic use , Length of Stay , Male , Patient Care Team , Wisconsin , Young AdultABSTRACT
While pituitary adenylate cyclase activating polypeptide (PACAP) signaling in the hypothalamic ventromedial nuclei (VMN) has been shown to regulate feeding, a challenge in unmasking a role for this peptide in obesity is that excess feeding can involve numerous mechanisms including homeostatic (hunger) and hedonic-related (palatability) drives. In these studies, we first isolated distinct feeding drives by developing a novel model of binge behavior in which homeostatic-driven feeding was temporally separated from feeding driven by food palatability. We found that stimulation of the VMN, achieved by local microinjections of AMPA, decreased standard chow consumption in food-restricted rats (e.g., homeostatic feeding); surprisingly, this manipulation failed to alter palatable food consumption in satiated rats (e.g., hedonic feeding). In contrast, inhibition of the nucleus accumbens (NAc), through local microinjections of GABA receptor agonists baclofen and muscimol, decreased hedonic feeding without altering homeostatic feeding. PACAP microinjections produced the site-specific changes in synaptic transmission needed to decrease feeding via VMN or NAc circuitry. PACAP into the NAc mimicked the actions of GABA agonists by reducing hedonic feeding without altering homeostatic feeding. In contrast, PACAP into the VMN mimicked the actions of AMPA by decreasing homeostatic feeding without affecting hedonic feeding. Slice electrophysiology recordings verified PACAP excitation of VMN neurons and inhibition of NAc neurons. These data suggest that the VMN and NAc regulate distinct circuits giving rise to unique feeding drives, but that both can be regulated by the neuropeptide PACAP to potentially curb excessive eating stemming from either drive.
