Medically ready for discharge: A multisite "point-in-time" assessment of hospitalized patients.

BACKGROUND: Time spent awaiting discharge after the acute need for hospitalization has resolved is an important potential contributor to hospital length of stay (LOS). OBJECTIVE: To measure the prevalence, impact, and context of patients who remain hospitalized for prolonged periods after completion of acute care needs. DESIGN, SETTING, AND PARTICIPANTS: We conducted a cross-sectional "point-in-time" survey at each of 15 academic US hospitals using a structured data collection tool with on-service acute care medicine attending physicians in fall 2022. MAIN OUTCOMES AND MEASURES: Primary outcomes were number and percentage of patients considered "medically ready for discharge" with emphasis on those who had experienced a "major barrier to discharge" (medically ready for discharge for ≥1 week). Estimated LOS attributable to major discharge barriers, contributory discharge needs, and associated hospital characteristics were measured. RESULTS: Of 1928 patients sampled, 35.0% (n = 674) were medically ready for discharge including 9.8% (n = 189) with major discharge barriers. Many patients with major discharge barriers (44.4%; 84/189) had spent a month or longer medically ready for discharge and commonly (84.1%; 159/189) required some form of skilled therapy or daily living support services for discharge. Higher proportions of patients experiencing major discharge barriers were found in public versus private, nonprofit hospitals (12.0% vs. 7.2%; p = .001) and county versus noncounty hospitals (14.5% vs. 8.8%; p = .002). CONCLUSIONS: Patients experience major discharge barriers in many US hospitals and spend prolonged time awaiting discharge, often for support needs that may be outside of clinician control.

Pregnant inflammatory bowel disease patients may require counselling regarding live vaccines in newborns.

Inflammatory bowel disease patients are prone to immunosuppression due to effects of their medications. Physicians are recommended to assess vaccination status and overall health in all patients, prior to initiation of immunosuppressive therapy. Immunosuppressant medications in women with inflammatory bowel disease are often continued during pregnancy, which can result in newborns having an increased risk of immunosuppression at birth. While medication-induced immunosuppression in infants is transient, parents should be counselled about delaying live vaccine administration in newborns until they are immune competent. A retrospective study was done over six months at an urban multispecialty medical center to assess whether physicians are counselling pregnant immunosuppressed inflammatory bowel disease patients regarding live vaccinations in their newborns. The study revealed that only 57% of patients had documented counselling in their charts. Further studies are necessary to determine physician counselling practices of pregnant women about live vaccines. It is critical that physicians and patients are aware of the risks of immunosuppression in pregnancy and the potential impact of live vaccines upon the newborn.

Reduced migration, altered matrix and enhanced TGFbeta1 signaling are signatures of mouse keratinocytes lacking Sdc1.

We have reported previously that syndecan-1 (Sdc1)-null mice show delayed re-epithelialization after skin and corneal wounding. Here, we show that primary keratinocytes obtained from Sdc1-null mice and grown for 3-5 days in culture are more proliferative, more adherent and migrate more slowly than wt keratinocytes. However, the migration rates of Sdc1-null keratinocytes can be restored to wild-type levels by replating Sdc1-null keratinocytes onto tissue culture plates coated with fibronectin and collagen I, laminin (LN)-332 or onto the matrices produced by wild-type cells. Migration rates can also be restored by treating Sdc1-null keratinocytes with antibodies that block alpha6 or alphav integrin function, or with TGFbeta1. Antagonizing either beta1 integrin function using a function-blocking antibody or TGFbeta1 using a neutralizing antibody reduced wild-type keratinocyte migration more than Sdc1-null keratinocyte migration. Cultures of Sdc1-null keratinocytes accumulated less collagen than wild-type cultures but their matrices contained the same amount of LN-332. The Sdc1-null keratinocytes expressed similar total amounts of eight different integrin subunits but showed increased surface expression of alphavbeta6, alphavbeta8, and alpha6beta4 integrins compared with wild-type keratinocytes. Whereas wild-type keratinocytes increased their surface expression of alpha2beta1, alphavbeta6, alphavbeta8, and alpha6beta4 after treatment with TGFbeta1, Sdc1-null keratinocytes did not. Additional data from a dual-reporter assay and quantification of phosphorylated Smad2 show that TGFbeta1 signaling is constitutively elevated in Sdc1-null keratinocytes. Thus, our results identify TGFbeta1 signaling and Sdc1 expression as important factors regulating integrin surface expression, activity and migration in keratinocyte and provide new insight into the functions regulated by Sdc1.