Quality improvement project demonstrating a sustained increase in the assessment and sampling of ascites for hospitalised patients with cirrhosis.

Objective: Using quality improvement techniques, we aimed to improve the rate of assessment and sampling of ascitic fluid for the purpose of diagnosing spontaneous bacterial peritonitis in patients with cirrhosis admitted to the hospitalist service of our institution. Design/methods: Based on stakeholder needs assessment, we implemented interventions targeting provider knowledge, procedure workflows and clinical decision support. We analysed key metrics during preintervention (September-December 2020), intervention roll-out (January-April 2021), postintervention (May-September 2021) and sustainability (September-December 2022) periods for admissions of patients with cirrhosis to our hospitalist service at Maine Medical Center, a 700-bed tertiary-care academic hospital in Portland, Maine, USA. Results: Among patients with cirrhosis admitted to our service, documentation of assessment for paracentesis increased from a preintervention baseline of 60.1% to 93.5% (p<0.005) postintervention. For patients with ascites potentially amenable to paracentesis, diagnostic paracentesis rate increased from 59.7% to 93% (p<0.005), with the rate of paracentesis within 24 hours increasing from 52.6% to 77.2% (p=0.01). These improvements persisted during our sustainability period. Complication rate was low (1.2%) across all study periods. Conclusion: Our quality improvement project led to a sustained improvement in the identification of patients with cirrhosis needing diagnostic paracentesis and an increased procedure completion rate. This improvement strategy serves as a model for needed work toward closing a national performance gap for patients with cirrhosis.

Integrative genomic and proteomic analyses identify targets for Lkb1-deficient metastatic lung tumors.

In mice, Lkb1 deletion and activation of Kras(G12D) results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and metastatic de novo lung cancers with integrated genomic and proteomic profiles, and have identified gene and phosphoprotein signatures associated with Lkb1 loss and progression to invasive and metastatic lung tumors. These studies revealed that SRC is activated in Lkb1-deficient primary and metastatic lung tumors, and that the combined inhibition of SRC, PI3K, and MEK1/2 resulted in synergistic tumor regression. These studies demonstrate that integrated genomic and proteomic analyses can be used to identify signaling pathways that may be targeted for treatment.