Frailty screening and a frailty pathway decrease length of stay, loss of independence, and 30-day readmission rates in frail geriatric trauma and emergency general surgery patients.

BACKGROUND: Frail geriatric trauma and emergency general surgery (TEGS) patients have longer lengths of stay (LOS), more readmissions, and higher rates of postdischarge institutionalization than their nonfrail counterparts. Despite calls to action by national trauma coalitions, there are few published reports of prospective interventions. The objective of this quality improvement project was to first develop a frailty screening program, and, then, if frail, implement a novel frailty pathway to reduce LOS, 30-day readmissions, and loss of independence. METHODS: This was a before-after study of a prospective cohort of all geriatric (≥65-years-old) patients admitted to the TEGS service from October 2016 to October 2017. All patients were screened for frailty for 3 months (preintervention) to obtain baseline outcomes. Subsequently, frail patients were entered into our frailty pathway (postintervention). Nonparametric statistical tests were used to assess significant differences in continuous variables; χ and Fisher exact tests were used for categorical variables, where appropriate. Both process and outcome measures were evaluated. RESULTS: Of 239 geriatric TEGS patients screened, 70 (29.3%) were frail. All TEGS geriatric patients were screened within 24 hours of admission. Following frailty pathway implementation, median LOS for frail patients decreased from 9 to 6 days (p = 0.4), readmissions decreased from 36.4% to 10.2% (p = 0.04), and loss of independence decreased by 40%, (100% vs 60%; p = 0.01). Outcomes for nonfrail geriatric patients did not differ between cohorts. CONCLUSIONS: Screening for frailty followed by implementing a frailty pathway decreased LOS, loss of independence, and 30-day readmission rates for frail geriatric TEGS patients at a single urban academic institution. The pathway required no additional resources; rather, we shifted focus toward frail patients without negatively affecting outcomes in nonfrail geriatric TEGS patients. Implementation of this pathway with larger patient cohorts and in varied settings is needed to confirm a causal relationship between our intervention and improved outcomes. LEVEL OF EVIDENCE: Therapeutic study, level IV.

Clostridium difficile recurrence is characterized by pro-inflammatory peripheral blood mononuclear cell (PBMC) phenotype.

Clostridium difficile infection (CDI) is a prevalent nosocomial and increasingly community-acquired problem. Little is known about the productive cellular response in patients. We used flow cytometry to define inflammatory (Th1 and Th17) and regulatory [Foxp3(+) T-regulatory (Treg)] cells present in circulating peripheral blood mononuclear cells (PBMC) from CDI patients. We consented 67 inpatients that tested either positive or negative for CDI and 16 healthy controls and compared their PBMC phenotypes. PBMC were collected, isolated, and stained for CD3, CD8 and either IL17 (Th17), IFN-γ (Th1) or Foxp3 (Treg) and analysed using flow cytometry. Twenty thousand events were collected in the lymphocyte gate (gate 1) and T-cell phenotypes were defined. CDI patients who clear the primary initial infection have greater numbers of non-CD3 PBMC. CDI patients who develop recurrence of CDI have a greater percentage of CD3(+)CD8(+), CD3(+)CD4(+)Foxp3 and fewer low granular CD3(-)Foxp3(+) PBMC. These patients have greater numbers of IFN-γ-producing lymphocytes, as well as PBMC phenotypes represented by increased IFN-γ- and IL17-co-expressing CD4(+)CD3(+). This initial pro-inflammatory phenotype decreases with repeated recurrence, demonstrating importance of timing of sample collection and history of symptoms. Patients with a history of recurrence had increased Foxp3(+)CD3(+)CD4(+) and IL17(+)CD3(+)CD4(+) populations. Hence, CDI recurrence is hallmarked by greater numbers of circulating CD3(+) lymphocytes skewed towards a Th1/Th17 inflammatory population as well as possible immune plasticity (Th17/Treg).