Establishing an alternative accommodation for stable hospitalised antepartum patients: barriers and challenges.

BACKGROUND: Patients in remote communities who risk premature delivery require transfer to a tertiary care centre for obstetric and neonatal care. Following stabilisation, many patients are candidates for outpatient management but cannot be discharged to their home communities due to lack of neonatal intensive care unit (ICU) support. PROBLEM: Without outpatient accommodation proximal to neonatal ICU, these patients face prolonged hospitalisation-an expensive option with medical, social and psychological consequences. Therefore, we sought to establish an alternative accommodation for out-of-town stable antepartum patients. METHODS: Quality Improvement approaches were used to identify process strengths and opportunities for improvement on the antepartum ward in a tertiary care centre. Physician and patient surveys informed outpatient accommodation programme development by a multidisciplinary team. The intervention was implemented using a plan-do-study-act cycle. Barriers to patient discharge and enrolment in the programme were analysed by completing thematic and strengths-weaknesses-opportunities-threats (SWOT) analysis. RESULTS: Physicians broadly supported safe outpatient management, whereas patients were hesitant to leave the hospital even when physicians assured safety. Our alternative accommodation was pre-existing and cost-effective, however, we encountered significant barriers. The physical space limited family visits and social interaction, lacked desired amenities,and the programme proved inconvenient to patients. The thematic and SWOT analysis identified aspects of the intervention which can be optimised to develop future actionable strategies. CONCLUSION: The utilisation of acute care beds is costly for the healthcare system and must be allocated judiciously. Patient needs, experience and health system barriers need to be considered when establishing alternative outpatient accommodations and strategies for stable antepartum patients.

Towards an ethical policy for the prevention of fetal sex selection in Canada.

The troubling practice of fetal sex selection has historically been considered an Asian phenomenon. However, recent evidence shows that a similar situation is emerging in North America, albeit on a smaller scale. The Society of Obstetricians and Gynaecologists of Canada has firmly stated its opposition to sex selection for non-medical reasons, as well as to the use of any technology used solely for the purpose of determining fetal sex. However, because fetal sex may be disclosed to the parents at the time of ultrasound examination if they request this information, guidance for health care professionals to assist in discouraging fetal sex selection would be useful. Because no declaration of motives or reasons is required when a woman seeks a termination of pregnancy, we suggest that health care professionals need not disclose the sex of a fetus until it has reached a gestational age at which abortion for non-medical purposes would not be possible. This proposal would facilitate consistency between clinical practice and the values of Canadian citizens, the SOGC, the Canadian Medical Association, and other professional organizations, while still respecting current laws pertaining to disclosure of patient information and patients' rights to autonomous decision-making.

The phenotype and function of lung dendritic cells.

Dendritic cells (DCs) are central to the integration of innate and adaptive immunity. In contrast to B and T lymphocytes, DCs have retained many of the pattern recognition receptors and are thus uniquely able to sense stimuli such as tissue damage, necrosis, and bacterial and viral infection. Also, immature DCs respond to danger signals in the environment, which leads to their maturation, upon which DCs differentiate and acquire the ability to direct the development of the primary immune response. The ability of lung DCs to elicit specific CD4 and CD8 T lymphocyte responses have made them attractive targets for vaccine development strategies in the treatment and prevention of diseases such as allograft rejection responses, allergy, and asthma, as well as autoimmune disease and cancer.

Vaccinia virus infection induces dendritic cell maturation but inhibits antigen presentation by MHC class II.

Vaccinia virus (VV) infection is known to inhibit dendritic cells (DC) functions in vitro. Paradoxically, VV is also highly immunogenic and thus has been used as a vaccine. In the present study, we investigated the effects of an in vivo VV infection on DC function by focusing on early innate immunity. Our data indicated that DC are activated upon in vivo VV infection of mice. Splenic DC from VV-infected mice expressed elevated levels of MHC class I and co-stimulatory molecules on their cell surface and exhibited the enhanced potential to produce cytokines upon LPS stimulation. DC from VV-infected mice also expressed a high level of interferon-beta. However, a VV infection resulted in the down-regulation of MHC class II expression and the impairment of antigen presentation to CD4 T cells by DC. Thus, during the early stage of a VV infection, although DC are impaired in some of the critical antigen presentation functions, they can promote innate immune defenses against viral infection.

Pulmonary immunity to viral infection: adenovirus infection of lung dendritic cells renders T cells nonresponsive to interleukin-2.

Adenovirus (Ad) infection has been identified as predisposing hosts to the development of pulmonary disease through unknown mechanisms. Lung dendritic cells (DCs) are vital for initiating pulmonary immune responses; however, the effects of Ad infection on primary lung DC have not been studied. In contrast to the effects on bone marrow- and monocyte-derived DCs, the current study shows that Ad infection of murine BALB/c lung DCs in vitro and in vivo suppresses DC-induced T-cell proliferation. The effect of Ad on DCs was not due to a downregulation of major histocompatibility complex or costimulatory molecules. Analysis of the production of interleukin-12 (IL-12), alpha interferon (IFN-alpha), and IFN-gamma by the Ad-infected DCs shows no significant differences over noninfected control lung DCs. Ad-induced suppression was not due to a deficiency of IL-2 or other DC-secreted factors and was dependent on viral protein synthesis, as UV irradiation of Ad abrogated the suppressive effect. Results suggest that Ad-infected DCs induce T cells to be nonresponsive to IL-2 during primary coculture, as the addition of IL-2 in secondary cultures recovered T-cell proliferation. In vivo studies supported in vitro results showing that Ad infection resulted in lung T cells with decreased proliferative ability. This study demonstrates that Ad infection induces local immunoincompetence by altering DC-T-cell interactions.