RESUMEN
BACKGROUND: Clinical practice guidelines (CPGs) and associated order sets can help standardize patient care and lead to higher-value patient care. However, difficult access and poor usability of these order sets can result in lower use rates and reduce the CPGs' impact on clinical outcomes. At our institution, we identified multiple CPGs for general pediatrics admissions where the appropriate order set was used in <50% of eligible encounters, leading to decreased adoption of CPG recommendations. OBJECTIVE: We aimed to determine how integrating disease-specific order groups into a common general admission order set influences adoption of CPG-specific order bundles for patients meeting CPG inclusion criteria admitted to the general pediatrics service. METHODS: We integrated order bundles for asthma, heavy menstrual bleeding, musculoskeletal infection, migraine, and pneumonia into a common general pediatrics order set. We compared pre- and postimplementation order bundle use rates for eligible encounters at both an intervention and nonintervention site for integrated CPGs. We also assessed order bundle adoption for nonintegrated CPGs, including bronchiolitis, acute gastroenteritis, and croup. In a post hoc analysis of encounters without order bundle use, we compared the pre- and postintervention frequency of diagnostic uncertainty at the time of admission. RESULTS: CPG order bundle use rates for incorporated CPGs increased by +9.8% (from 629/856, 73.5% to 405/486, 83.3%) at the intervention site and by +5.1% (896/1351, 66.3% to 509/713, 71.4%) at the nonintervention site. Order bundle adoption for nonintegrated CPGs decreased from 84% (536/638) to 68.5% (148/216), driven primarily by decreases in bronchiolitis order bundle adoption in the setting of the COVID-19 pandemic. Diagnostic uncertainty was more common in admissions without CPG order bundle use after implementation (28/227, 12.3% vs 19/81, 23.4%). CONCLUSIONS: The integration of CPG-specific order bundles into a general admission order set improved overall CPG adoption. However, integrating only some CPGs may reduce adoption of order bundles for excluded CPGs. Diagnostic uncertainty at the time of admission is likely an underrecognized barrier to guideline adherence that is not addressed by an integrated admission order set.
RESUMEN
ACE inhibitors (ACEis) and angiotensin receptor blockers (ARBs) are standard-of-care treatments for hypertension and diabetes, common comorbidities among hospitalized patients with coronavirus disease 2019 (COVID-19). Their use in the setting of COVID-19 has been heavily debated due to potential interactions with ACE2, an enzyme that links the pro-inflammatory and anti-inflammatory arms of the renin angiotensin system, but also the entryway by which severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) invades cells. ACE2 expression is altered by age, hypertension, diabetes, and the virus itself. This study integrated available information about the renin angiotensin aldosterone system (RAAS) and effects of SARS-CoV-2 and its comorbidities on ACE2 into a mechanistic mathematical model and aimed to quantitatively predict effects of ACEi/ARBs on the RAAS pro-inflammatory/anti-inflammatory balance. RAAS blockade prior to SARS-CoV-2 infection is predicted to increase the mas-AT1 receptor occupancy ratio up to 20-fold, indicating that in patients already taking an ACEi/ARB before infection, the anti-inflammatory arm is already elevated while the pro-inflammatory arm is suppressed. Predicted pro-inflammatory shifts in the mas-AT1 ratio due to ACE2 downregulation by SARS-CoV-2 were small relative to anti-inflammatory shifts induced by ACEi/ARB. Predicted effects of changes in ACE2 expression with comorbidities of diabetes, hypertension, or aging on mas-AT1 occupancy ratio were also relatively small. Last, predicted changes in the angiotensin (Ang(1-7)) production rate with ACEi/ARB therapy, comorbidities, or infection were all small relative to exogenous Ang(1-7) infusion rates shown experimentally to protect against acute lung injury, suggesting that any changes in the ACE2-Ang(1-7)-mas arm may not be large enough to play a major role in COVID-19 pathophysiology.