Changing the Care Paradigm for Patients: Advanced Illness Beds Care Model.

BACKGROUND: Over 90 million Americans suffer from advanced illness (AI) and spend their last days of life in critical care units receiving costly, unwanted, aggressive medical care. OBJECTIVE: Evaluate the impact of a specialized care model in medical/surgical units for hospitalized geriatric patients and patients with complex care requirements where designated AI beds align care with patient's wishes/goals, minimize aggressive interventions, and influence efficient resource utilization. DESIGN: US based multi-facility retrospective, longitudinal descriptive study of screened positive AI patients in AI Beds (N = 1,237) from 3 facilities from 2015 to 2017. RESULTS: Patient outcomes included 60% referrals to AI beds from ICU, a decrease of 39-49% in average ICU LOS, a 23% reduction of AI bed patient expirations, 9.0% referrals to hospice, and projected cost savings of $4,361.66/patient, US dollars. CONCLUSION: Allocating AI beds to deliver care to AI patients resulted in a decreased cost of care by reducing overall hospital LOS, mortality, and efficient use of both critical care and hospital resources.

Accentuated T helper type 2 airway response after allergen challenge in cyclooxygenase-1-/- but not cyclooxygenase-2-/- mice.

Acute pharmacologic inhibition of cyclooxygenase (COX)-1 or -2 during allergen sensitization and exposure leads to enhanced T helper type 2 (Th2) airway responses. COX-1 and -2 play functionally distinct roles in lymphocyte development, and consequently, genetic deficiency of either enzyme, as opposed to acute pharmacologic inhibition, may modulate Th2-mediated allergic airway disease differently. An ovalbumin-induced mouse model of allergic airway disease was used. The immunophenotype of bronchoalveolar lavage lymphocytes was assessed by flow cytometry, bronchoalveolar lavage cytokines, and chemokines were measured by enzyme-linked immunosorbent assay, adhesion molecule expression was assessed by immunoblotting in combination with immunohistochemistry, and bronchoconstriction was assessed by whole body plethysmography. The airways of COX-1-/- mice contained increased numbers of CD4+ and CD8+ T cells, exaggerated levels of the Th2 cytokines interleukin-4, -5, and -13, and increased levels of eotaxin and thymus- and activation-regulated chemokine. Allergen-induced bronchoconstriction was also increased in COX-1-/- mice. Vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 levels were increased in lungs of both COX-1-/- and COX-2-/- mice relative to wild type. These data suggest that genetic deficiency of COX-1 but not COX-2 modulates T cell recruitment, Th2 cytokine secretion, and lung function in the allergic airway.