Communication Training in Adult and Pediatric Critical Care Medicine. A Systematic Review.

Background: Interpersonal and communication skills are essential for physicians practicing in critical care settings. Accordingly, demonstration of these skills has been a core competency of the Accreditation Council for Graduate Medical Education since 2014. However, current practices regarding communication skills training in adult and pediatric critical care fellowships are not well described. Objective: To describe the current state of communication curricula and training methods in adult and pediatric critical care training programs as demonstrated by the published literature. Methods: We performed a systematic review of the published literature using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses checklist. Three authors reviewed a comprehensive set of databases and independently selected articles on the basis of a predefined set of inclusion and exclusion criteria. Data were independently extracted from the selected articles. Results: The 23 publications meeting inclusion criteria fell into the following study classifications: intervention (n = 15), cross-sectional survey (n = 5), and instrument validation (n = 3). Most interventional studies assessed short-term and self-reported outcomes (e.g., learner attitudes and perspectives) only. Fifteen of 22 publications represented pediatric subspecialty programs. Conclusion: Opportunities exist to evaluate the influence of communication training programs on important outcomes, including measured learner behavior and patient and family outcomes, and the durability of skill retention.

A Communications Bundle to Improve Satisfaction for Critically Ill Patients and Their Families: A Prospective, Cohort Pilot Study.

CONTEXT: Communication skills training with simulated patients is used by many academic centers, but how to translate skills learned in simulated settings to improve communication in real encounters has not been described. OBJECTIVES: We developed a communications bundle to facilitate skill transfer from simulation to real encounters and improve patient and/or family satisfaction with physician communication. We tested the feasibility of its use in our hospital's medical intensive care unit (MICU). METHODS: This prospective cohort 2-week feasibility study included patients admitted to the MICU with APACHE IV predicted mortality >30% and/or single organ failure. The communications bundle included simulation communication training for MICU physicians, scheduling a family meeting within 72 hours of MICU admission, standardized pre- and post-meeting team huddles with the aid of a mobile app to set an agenda, choose a communication goal, and get feedback, and documentation of meeting in the electronic medical record. The intervention group receiving the communications bundle was located in a geographically separate unit than the control group receiving standard of care from MICU physicians who had not received training in the communications bundle. Patient satisfaction surveys were given within 48 hours of the family meeting and scores compared between the two groups. We also compared trainee self-perceived communication preparation. RESULTS: The intervention group (N = 15) scored significantly higher on satisfaction than the control group (N = 16) (P = 0.018). Intervention group trainees reported improvement in self-perceived communication preparation. CONCLUSION: Use of the communications bundle proved feasible in the MICU and suggests association with improved patient satisfaction and trainee self-perception of communication preparedness.

Low Rate of Adverse Events Associated With Inpatient Parenteral Prostacyclins.

Parenteral prostacyclin is the most-effective therapy for patients with pulmonary arterial hypertension. Administration is complex, and administration errors are potentially life threatening. Hospital policies to minimize the risk to patients are necessary, but their effectiveness has not been well studied. We quantified the adverse event incident rate per at-risk patient day in a tertiary care hospital with an established parenteral prostacyclin policy. Patients on parenteral prostacyclin including new initiations from January 2003 to January 2013 were identified, encompassing 386 discrete admissions. Reports of adverse events were obtained from the inpatient risk feedback-reporting process and detailed chart review. Policy-divergent events were analyzed both categorically and by the degree of severity. Overall, 153 total policy-divergent events were identified. Data analysis indicated an incident rate of 45.9 per 1,000 patient days. In total, 21 of 153 potential errors reached the patient, translating to an incident rate of 6.3 per 1,000 patient days. Incident rate for "serious symptomatic" or "catastrophic" policy-divergent events was 3.3 per 1,000 patient days. Even with specific prostacyclin training and administration policy, there remains a small risk of adverse events in hospitalized pulmonary hypertension patients receiving parenteral prostacyclin.

Impact of a Simulation-Based Communication Workshop on Resident Preparedness for End-of-Life Communication in the Intensive Care Unit.

Introduction. Although residents frequently lead end-of-life (EOL) discussions in the intensive care unit (ICU), training in EOL care during residency has been required only recently, and few educational interventions target EOL communication in the ICU. This study evaluated a simulation-based intervention designed to improve resident EOL communication skills with families in the ICU. Methods. Thirty-four second-year internal medicine residents at a large urban teaching hospital participated in small group sessions with faculty trained in the "VitalTalk" method. A Likert-type scale questionnaire measured self-assessed preparedness before, immediately following, and approximately 9 months after intervention. Data were analyzed using Wilcoxon rank-sum analysis. Results. Self-assessed preparedness significantly improved for all categories surveyed (preintervention mean; postintervention mean; p value), including discussing bad news (3.3; 4.2; p < 0.01), conducting a family conference (3.1; 4.1; p < 0.01), discussing treatment options (3.2; 3.9; p < 0.01), discussing discontinuing ICU treatments (2.9; 3.5; p < 0.01), and expressing empathy (3.9; 4.5; p < 0.01). Improvement persisted at follow-up for all items except "expressing empathy." Residents rated the educational quality highly. Conclusion. This study provides evidence that brief simulation-based interventions can produce lasting improvements in residents' confidence to discuss EOL care with family members of patients in the ICU.

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.

Dedicated multidisciplinary ventilator bundle team and compliance with sedation vacation.

BACKGROUND: How compliance with a ventilator bundle is monitored varies from institution to institution. Some institutions rely on the primary intensive care unit team to review the bundle during their rounds; others rely on a separate team of health care personnel that may include representatives from disciplines such as nursing, respiratory therapy, and pharmacy. OBJECTIVES: To compare rates of compliance with ventilator bundle components between a dedicated ventilator bundle rounding team and the primary intensive care unit rounding team in a 68-bed medical intensive care unit. METHODS: A query of the medical intensive care unit's database was used to retrospectively determine rates of compliance with specific ventilator bundle components at a tertiary care hospital in an urban community for 1 year. RESULTS: Compared with the intensive care unit rounding team, the ventilator bundle rounding team had better compliance with sedation vacation (61.7% vs 54.0%, P < .001). Rates of compliance with spontaneous breathing trials and prophylaxis of peptic ulcer disease were similar in both study groups. CONCLUSIONS: A dedicated ventilator bundle rounding team improves compliance with sedation vacation, but not with spontaneous breathing trials and prophylaxis of peptic ulcer disease. In a large-volume tertiary center, a dedicated ventilator bundle rounding team may be more effective than the primary rounding team in achieving compliance with some bundle components.

Overexpression of sICAM-1 in the alveolar epithelial space results in an exaggerated inflammatory response and early death in Gram negative pneumonia.

BACKGROUND: A sizeable body of data demonstrates that membrane ICAM-1 (mICAM-1) plays a significant role in host defense in a site-specific fashion. On the pulmonary vascular endothelium, mICAM-1 is necessary for normal leukocyte recruitment during acute inflammation. On alveolar epithelial cells (AECs), we have shown previously that the presence of normal mICAM-1 is essential for optimal alveolar macrophage (AM) function. We have also shown that ICAM-1 is present in the alveolar space as a soluble protein that is likely produced through cleavage of mICAM-1. Soluble intercellular adhesion molecule-1 (sICAM-1) is abundantly present in the alveolar lining fluid of the normal lung and could be generated by proteolytic cleavage of mICAM-1, which is highly expressed on type I AECs. Although a growing body of data suggesting that intravascular sICAM-1 has functional effects, little is known about sICAM-1 in the alveolus. We hypothesized that sICAM-1 in the alveolar space modulates the innate immune response and alters the response to pulmonary infection. METHODS: Using the surfactant protein C (SPC) promoter, we developed a transgenic mouse (SPC-sICAM-1) that constitutively overexpresses sICAM-1 in the distal lung, and compared the responses of wild-type and SPC-sICAM-1 mice following intranasal inoculation with K. pneumoniae. RESULTS: SPC-sICAM-1 mice demonstrated increased mortality and increased systemic dissemination of organisms compared with wild-type mice. We also found that inflammatory responses were significantly increased in SPC-sICAM-1 mice compared with wild-type mice but there were no difference in lung CFU between groups. CONCLUSIONS: We conclude that alveolar sICAM-1 modulates pulmonary inflammation. Manipulating ICAM-1 interactions therapeutically may modulate the host response to Gram negative pulmonary infections.

Co-infection with pansensitive and multidrug-resistant strains of Mycobacterium tuberculosis.

We report a case of a 23-year-old HIV-negative man with multidrug-resistant Mycobacterium tuberculosis that became evident while he was being treated for M. tuberculosis that was sensitive to all first-line drugs. This case should alert clinicians to consider co-infection as a possible cause of recrudescent disease.

Disparate mechanisms of sICAM-1 production in the peripheral lung: contrast between alveolar epithelial cells and pulmonary microvascular endothelial cells.

Membrane-associated intercellular adhesion molecule-1 (mICAM-1; CD54) is constitutively expressed on the surface of type I alveolar epithelial cells (AEC). Soluble ICAM-1 (sICAM-1) may be produced by proteolytic cleavage of mICAM-1 or by alternative splicing of ICAM-1 mRNA. In contrast to inducible expression seen in most cell types, sICAM-1 is constitutively released by type I AEC and is present in normal alveolar lining fluid. Therefore, we compared the mechanism of sICAM-1 production in primary cultures of two closely juxtaposed cells in the alveolar wall, AEC and pulmonary microvascular endothelial cells (PVEC). AEC, but not PVEC, demonstrated high-level baseline expression of sICAM-1. Stimulation of AEC with TNFalpha or LPS resulted in minimal increase in AEC sICAM-1, whereas PVEC sICAM-1 was briskly induced in response to these signals. AEC sICAM-1 shedding was significantly reduced by treatment with a serine protease inhibitor, but not by cysteine, metalloprotease, or aspartic protease inhibitors. In contrast, none of these inhibitors effected sICAM-1 expression in PVEC. RT-PCR, followed by gel analysis of total RNA, suggests that alternatively spliced fragments are present in both cell types. However, a 16-mer oligopeptide corresponding to the juxtamembrane region of mICAM-1 completely abrogated sICAM-1 shedding in AEC but reduced stimulated PVEC sICAM-1 release by only 20%. Based on these data, we conclude that the predominant mechanism of sICAM-1 production likely differs in the two cell types from opposite sides of the alveolar wall.

GM-CSF and the impaired pulmonary innate immune response following hyperoxic stress.

We have previously demonstrated that mice exposed to sublethal hyperoxia (an atmosphere of >95% oxygen for 4 days, followed by return to room air) have significantly impaired pulmonary innate immune response. Alveolar macrophages (AM) from hyperoxia-exposed mice exhibit significantly diminished antimicrobial activity and markedly reduced production of inflammatory cytokines in response to stimulation with LPS compared with AM from control mice in normoxia. As a consequence of these defects, mice exposed to sublethal hyperoxia are more susceptible to lethal pneumonia with Klebsiella pneumoniae than control mice. Granulocyte/macrophage colony-stimulating factor (GM-CSF) is a growth factor produced by normal pulmonary alveolar epithelial cells that is critically involved in maintenance of normal AM function. We now report that sublethal hyperoxia in vivo leads to greatly reduced alveolar epithelial cell GM-CSF expression. Systemic treatment of mice with recombinant murine GM-CSF during hyperoxia exposure preserved AM function, as indicated by cell surface Toll-like receptor 4 expression and by inflammatory cytokine secretion following stimulation with LPS ex vivo. Treatment of hyperoxic mice with GM-CSF significantly reduced lung bacterial burden following intratracheal inoculation with K. pneumoniae, returning lung bacterial colony-forming units to the level of normoxic controls. These data point to a critical role for continuous GM-CSF activity in the lung in maintenance of normal AM function and demonstrate that lung injury due to hyperoxic stress results in significant impairment in pulmonary innate immunity through suppression of alveolar epithelial cell GM-CSF expression.

Shedding of soluble ICAM-1 into the alveolar space in murine models of acute lung injury.

Intercellular adhesion molecule-1 (ICAM-1; CD54) is an adhesion molecule constitutively expressed in abundance on the cell surface of type I alveolar epithelial cells (AEC) in the normal lung and is a critical participant in pulmonary innate immunity. At many sites, ICAM-1 is shed from the cell surface as a soluble molecule (sICAM-1). Limited information is available regarding the presence, source, or significance of sICAM-1 in the alveolar lining fluid of normal or injured lungs. We found sICAM-1 in the bronchoalveolar lavage (BAL) fluid of normal mice (386 +/- 50 ng/ml). Additionally, sICAM-1 was spontaneously released by murine AEC in primary culture as type II cells spread and assumed characteristics of type I cells. Shedding of sICAM-1 increased significantly at later points in culture (5-7 days) compared with earlier time points (3-5 days). In contrast, treatment of AEC with inflammatory cytokines had limited effect on sICAM-1 shedding. BAL sICAM-1 was evaluated in in vivo models of acute lung injury. In hyperoxic lung injury, a reversible process with a major component of leak across the alveolar wall, BAL fluid sICAM-1 only increased in parallel with increased alveolar protein. However, in lung injury due to FITC, there were increased levels of sICAM-1 in BAL that were independent of changes in BAL total protein concentration. We speculate that after lung injury, changes in sICAM-1 in BAL fluid are associated with progressive injury and may be a reflection of type I cell differentiation during reepithelialization of the injured lung.