Preliminary Analysis of a Modified Screening Tool to Increase the Frequency of Palliative Care Consults.

PURPOSE: Palliative care interventions have been shown to improve patient quality of life but the benefit may be less if interventions occur late in the patient's disease process. The objective of this study was to evaluate whether an objective screening tool could improve the frequency and timeliness of palliative care consultation. METHODS: Using a quasi-experimental design with 2 geographically separate medical intensive care units (MICUs), the control MICU continued existing consultation practice and the intervention MICU implemented a screening tool with each new admission. Any item checked on the screening tool triggered a palliative care consult within 24 hours of admission to the MICU. RESULTS: A total of 223 MICU admissions were evaluated: 156 patients in the control group and 67 patients in the intervention group. More consults were generated in the intervention group (22.39%) compared to the control group (7.05%; P < .001). The median time to consultation was lower in the intervention group compared to the control group (1 day vs 2 days; P < .01). CONCLUSION: Implementing a simple, objective screening tool increased palliative consultation rates and decreased median time to palliative consultation in our institution's MICU.

Aripiprazole-induced hypersensitivity pneumonitis.

Aripiprazole is an atypical antipsychotic agent commonly used in the management of schizophrenia. Aripiprazole has not been reported to have an association with interstitial lung disease. We describe a case of a 36-year-old woman who began to experience respiratory issues shortly after starting aripiprazole and presented to us 4 years later with progressive exertional shortness of breath. High-resolution CT of the chest showed a bilateral ground glass pattern. Video-assisted thoracoscopy with biopsy revealed alveolar septal thickening and an inflammatory infiltrate composed mainly of lymphocytes, suggestive of chronic hypersensitivity pneumonitis. After discontinuing aripiprazole and initiating prednisolone therapy, the patient's pulmonary symptoms improved. This case highlights that aripiprazole can cause hypersensitivity pneumonitis in susceptible individuals.

Predischarge bundle for patients with acute exacerbations of COPD to reduce readmissions and ED visits: a randomized controlled trial.

BACKGROUND: Hospital readmissions for acute exacerbations of COPD (AECOPDs) pose burdens to the health-care system and patients. A current gap in knowledge is whether a predischarge screening and educational tool administered to patients with COPD reduces readmissions and ED visits. METHODS: A single-center, randomized trial of admitted patients with AECOPDs was conducted at Henry Ford Hospital between February 2010 and April 2013. One hundred seventy-two patients were randomized to either the control (standard care) or the bundle group in which patients received smoking cessation counseling, screening for gastroesophageal reflux disease and depression or anxiety, standardized inhaler education, and a 48-h postdischarge telephone call. The primary end point was the difference in the composite risk of hospitalizations or ED visits for AECOPD between the two groups in the 30 days following discharge. A secondary end point was 90-day readmission rate. RESULTS: Of the 172 patients, 18 of 79 in the control group (22.78%) and 18 of 93 in the bundle group (19.35%) were readmitted within 30 days. The risk of ED visits or hospitalizations within 30 days was not different between the groups (risk difference, -3.43%; 95% CI, -15.68% to 8.82%; P = .58). Overall, the time to readmission in 30 and 90 days was similar between groups (log-rank test P = .71 and .88, respectively). CONCLUSIONS: A predischarge bundle intervention in AECOPD is not sufficient to reduce the 30-day risk of hospitalizations or ED visits. More resources may be needed to generate a measurable effect on readmission rates. TRIAL REGISTRY: ClinicalTrials.gov; No.: NCT02135744; URL: www.clinicaltrials.gov.

Aggregatibacter actinomycetemcomitans infection mimicking lung cancer: a case report.

Pulmonary infections can mimic a pulmonary neoplasm. Multiple organisms, including bacteria, viruses, and fungi, can present with similar clinical, radiographic, and surgical findings as neoplastic processes. Because treatment and the prognosis are completely different, an accurate diagnosis is crucial, and lung biopsy is usually required. Aggregatibacter actinomycetemcomitans is part of the normal oral flora and is a rare cause of invasive infection due to hematogenous dissemination or aspiration, particularly infective endocarditis. We present a case of A. actinomycetemcomitans and Actinomyces co-infection that presented as a mediastinal mass, with surgical findings similar to lung malignancy but with biopsy and culture showing an infectious origin. After antibiotic treatment, follow-up images showed resolution of the mass.

A welder with pneumosiderosis: a case report.

Pneumosiderosis or Welder's lung is an occupational lung disease which is usually seen after chronic exposure to iron dust. We present a case of a 64-year-old welder in whom the diagnosis of pneumosiderosis was made by lung biopsies. We also briefly review the literature regarding the disease, its prognosis and association with development of lung cancer. Avoidance of iron dust exposure and implementing prevention strategies in people at risk are the mainstay of therapy.

Monocytes recruited to the lungs of mice during immune inflammation ingest apoptotic cells poorly.

Apoptotic cells must be cleared to resolve inflammation, but few resident alveolar macrophages (AMo) from normal lungs ingest apoptotic cells. We examined how Mo ingestion of apoptotic cells is altered during immune inflammation induced by intratracheal challenge of primed C57BL/6 mice using sheep red blood cells. Resident AMo were labeled in situ before challenge using intravenous PKH26 to distinguish them from recruited monocytes. Using flow cytometry, we identified phagocytosis of fluorescently-labeled apoptotic thymocytes by alveolar mononuclear phagocytes in vitro and in vivo, and measured surface molecule expression. Intratracheal challenge induced rapid recruitment of monocytes, peaking at Day 3 and decreasing thereafter, whereas numbers of resident AMo did not change significantly. At all times, the percentage of phagocytes ingesting apoptotic thymocytes in vitro was greater among resident AMo (28-45%) than among recruited monocytes (9-19%), but was low in both cell types relative to ingestion of immunoglobulin-opsonized targets. There was also a nonsignificant trend toward lower ingestion by monocytes in vivo. MerTK, a receptor tyrosine kinase crucial for apoptotic cell phagocytosis, was expressed by resident AMo, but not by recruited monocytes. Relative to resident AMo, monocytes recruited to the alveolus ingest apoptotic cells meagerly, possibly due to absence of MerTK expression.

Resident murine alveolar and peritoneal macrophages differ in adhesion of apoptotic thymocytes.

Apoptotic cells must be cleared efficiently by macrophages (Mø) to prevent autoimmunity, yet their ingestion impairs Mø microbicidal function. The principal murine resident lung phagocyte, the alveolar Mø (AMø), is specifically deficient at apoptotic cell ingestion, both in vitro and in vivo, compared with resident peritoneal Mø (PMø). To further characterize this deficiency, we assayed static adhesion in vitro using apoptotic thymocytes and resident AMø and PMø from normal C57BL/6 mice. Adhesion of apoptotic thymocytes by both types of Mø was rapid, specific, and cold-sensitive. Antibody against the receptor tyrosine kinase MerTK (Tyro12) blocked phagocytosis but not adhesion in both types of Mø. Surfactant protein A increased adhesion and phagocytosis by AMø, but not to the levels seen using PMø. Adhesion was largely cation-independent for PMø and calcium-dependent for AMø. Adhesion was not inhibited in either Mø type by mAbs against beta1 or beta3 integrins or scavenger receptor I/II (CD204), but AMø adhesion was inhibited by specific mAbs against CD11c/CD18. Thus, resident murine tissue Mø from different tissues depend on qualitatively disparate receptor systems to bind apoptotic cells. The decreased capacity of murine AMø to ingest apoptotic cells is only partially explained by reduced initial adhesion.