Decreasing Blood Transfusions in Premature Infants Through Quality Improvement.

BACKGROUND AND OBJECTIVES: Packed red blood cell transfusions (pRBCT) in preterm infants have been associated with significant morbidity. Although infants <26 weeks' gestational age typically require several pRBCT, preterm infants born between 26 and 34 weeks' gestational age may also require pRBCT during their hospitalization that are potentially preventable. We aimed to reduce pRBCT in this population by 20%. METHODS: This quality improvement project was conducted in the Duke University Hospital NICU between July 2018 and February 2023. Interventions included the implementation of evidence-based transfusion thresholds, supporting bone marrow erythropoiesis, and reducing laboratory specimen volumes by increasing capillary test panels. The rates per 1000 patient days for pRBCT (outcome measure), number of new patients initiated on erythropoietin (process measure), number of basic metabolic panels (process measure), and total capillary panels (process measure) were monitored during the project period. Statistical process control charts were used to observe trends over time. RESULTS: Among infants born between 26 0/7 and 34 6/7 weeks' gestational age, the rate of pRBCT decreased from an average of 23.8 to 12.7 transfusions per 1000 patient days, which is a 46.6% decrease. Increases in the use of erythropoietin and capillary panels were observed, along with a decrease in the use of basic metabolic panels. There was no change in mortality or the rate of necrotizing enterocolitis. Improvement was sustained for 24 months after implementation. CONCLUSIONS: pRBCT can be decreased in preterm infants born between 26 and 34 completed weeks' gestation through a combination of strategies utilizing quality improvement methodology.

Timely Delivery of Discharge Medications to Patients' Bedsides: A Patient-centered Quality Improvement Project.

INTRODUCTION: Patients who are unable to fill prescriptions after discharge are at risk of hospital readmission. Ensuring that patients have prescriptions in hand at the time of discharge is a critical component of a safe and effective discharge process. Using a "Meds to Beds" program, we aimed to increase the percentage of patients discharged from Holtz Children's Hospital with medications in hand from 49% to 80%, reduce turnaround time (TAT) from electronic prescription signature to bedside delivery from 4.9 hours (±2.6 hours) to 2 hours, and increase caregiver satisfaction. METHODS: We formed a multidisciplinary team and implemented 4 patient-centered interventions through iterative plan-do-study-act cycles. Statistical process control charts were used to understand the impact of the interventions over 10 months. Hospital length of stay and discharges before 2:00 pm were used as balancing measures. We measured caregiver satisfaction using a telephone survey administered by pediatric residents within 7 days after discharge. RESULTS: The mean percentage of patients discharged with medications in hand increased to 76%. TAT decreased to 3.5 hours (±1.8 hours). Length of stay did not significantly increase, whereas the percentage of patients discharged before 2:00 pm did. Caregivers of patients who had prescriptions delivered to their bedside reported high levels of satisfaction. CONCLUSIONS: Using a "Meds to Beds" program, we increased the percentage of patients discharged with medications in hand, decreased TAT with reduced variability, and achieved high levels of caregiver satisfaction. Importantly, there was a shift in the culture of the institution toward improved medication access for patients.

A phase II placebo-controlled study of tralokinumab in moderate-to-severe asthma.

Pre-clinical data demonstrate a pivotal role for interleukin (IL)-13 in the development and maintenance of asthma. This study assessed the effects of tralokinumab, an investigational human IL-13-neutralising immunoglobulin G4 monoclonal antibody, in adults with moderate-to-severe uncontrolled asthma despite controller therapies. 194 subjects were randomised to receive tralokinumab (150, 300 or 600 mg) or placebo subcutaneously every 2 weeks. Primary end-point was change from baseline in mean Asthma Control Questionnaire score (ACQ-6; ACQ mean of six individual item scores) at week 13 comparing placebo and combined tralokinumab dose groups. Secondary end-points included pre-bronchodilator lung function, rescue ß(2)-agonist use and safety. Numerical end-points are reported as mean±sd. At week 13, change from baseline in ACQ-6 was -0.76±1.04 for tralokinumab versus -0.61±0.90 for placebo (p=0.375). Increases from baseline in forced expiratory volume in 1 s (FEV(1)) were 0.21±0.38 L versus 0.06±0.48 L (p=0.072), with a dose-response observed across the tralokinumab doses tested. ß(2)-agonist use (puffs per day) was decreased for tralokinumab -0.68±1.45 versus placebo -0.10±1.49 (p=0.020). The increase in FEV(1) following tralokinumab treatment remained evident 12 weeks after the final dose. Safety profile was acceptable with no serious adverse events related to tralokinumab. No improvement in ACQ-6 was observed, although tralokinumab treatment was associated with improved lung function.

The somatostatin analogue SOM230, compared with octreotide, induces differential effects in several metabolic pathways in acromegalic patients.

OBJECTIVE: Recently, our first clinical study with the novel multiligand somatostatin (SRIF) analogue SOM230 in acromegalic patients showed that SOM230, due to its beneficial inhibitory effects on GH levels compared with octreotide (OCT), might increase the number of patients that can be biochemically controlled. Since SRIF analogues are also known to interact with other metabolic pathways, IGF-I, IGFBP-1, glucose and insulin concentrations on the control day (CD) and on treatment days following a single s.c. injection SOM230 100 and 250 microg, were compared to those following OCT 100 microg. DESIGN AND PATIENTS: Randomized, cross-over, double-blinded proof-of-concept trial in 12 patients with active acromegaly. RESULTS: Free IGF-I levels were suppressed after 24 h by OCT, SOM230 250 and 100 microg, whereas at 48 h only both SOM230 dosages still induced these inhibitory effects. Circulating IGFBP-1 levels (AUC; 0830-1430 h) compared with CD, increased sharply after OCT (from 48 to 237 microg/l/h; P < 0.001 vs. CD), while SOM230 250 and 100 microg elicited a lower and dose-dependent effect (163 and 90 microg/l/h, respectively, P < 0.05 vs. CD and OCT). Neither insulin nor GH levels showed statistically significant correlation with IGFBP-1 levels either after SOM230 or OCT. An early rise in glucose levels 1 h postinjection with SOM230 250 microg compared with OCT and CD was observed 8.3 +/- 0.8, 4.4 +/- 0.5 and 4.9 +/- 0.4 mmol/l, respectively: P < 0.05). SOM230 250 microg (19 +/- 4 vs. 46 +/- 3 mU/l on CD: P < 0.05), although clearly less potent than OCT (5.4 +/- 0.4 mU/l: P < 0.01 vs. CD), inhibited insulin release. Since these corresponding absolute insulin levels cannot entirely explain this hyperglycaemic effect of SOM230, other mechanisms seem involved in this glucose rise. If SOM230 would influence glucose homeostasis in peripheral target tissues of insulin action, expression of SS-receptors (sst) seems a logical necessity. In normal human liver tissues, analysed by quantitative polymerase chain reaction (PCR), the average sst1 mRNA expression level appeared significantly higher compared with sst2 (n = 6, relative copy number 161 +/- 46 vs. 57 +/- 6; P < 0.05). Fat tissue expressed both sst1 and sst2 mRNA, whereas in muscle only sst2 mRNA was found. CONCLUSION: Both dosages of SOM230 inhibit free IGF-I in a more sustained fashion compared to OCT, implying longer duration of action. The superior action of OCT compared with SOM230 in stimulating IGFBP-1 levels, suggests direct regulation of IGFBP-1 by SRIF analogues via sst2. Finally, expression of only sst1 and sst2 in target tissues of insulin action, might point towards additional modulatory effects by SOM230 on glucose homeostasis.

A single-dose comparison of the acute effects between the new somatostatin analog SOM230 and octreotide in acromegalic patients.

Treatment with the somatostatin receptor (sst) subtype 2 predominant analogs octreotide and lanreotide induces clinical and biochemical cure in approximately 65% of acromegalic patients. GH-secreting pituitary adenomas, which are not controlled, also express sst(5). We compared the acute effects of octreotide and SOM230, a new somatostatin analog with high affinity for sst(1,2,3,5) on hormone release in acromegalic patients. In a single-dose, proof-of-concept study, 100 microg octreotide and 100 and 250 microg SOM230 were given s.c. to 12 patients with active acromegaly. Doses of 100 and 250 microg SOM230 dose-dependently suppressed GH levels from 2-8 h after administration (-38 +/- 7.7 vs. -61 +/- 6.7%, respectively; P < 0.01). A comparable suppression of GH levels by octreotide and 250 microg SOM230 was observed in eight patients (-65 +/- 7 vs. -72 +/- 7%, respectively). In three patients, the acute GH-lowering effect of 250 microg SOM230 was significantly superior to that of octreotide (-70 +/- 2 vs. -17 +/- 15%, respectively; P < 0.01). In one patient, the GH-lowering effect of octreotide was better than that of SOM230. Tolerability for SOM230 was good. Glucose levels were initially slightly elevated after octreotide and SOM230, compared with control day, whereas insulin levels were only significantly suppressed by octreotide. We conclude that SOM230 is an effective GH-lowering drug in acromegalic patients with the potential to increase the number of patients controlled during long-term medical treatment.