1David Geffen School of Medicine at UCLA, Divisions of Cardiology and Geriatric Medicine, University of California, Los Angeles, California; 2Clover Health, Jersey City, New Jersey; 3Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York, New York; 4Section of Cardiovascular Medicine, Yale School of Medicine and the Department of Health Policy and Management, Yale School of Public Health, Center for Outcomes Research and Evaluation, Yale-New Haven Hospital, New Haven, Connecticut.
Disclosures
Dr. Dharmarajan is Chief Scientific Officer for Clover Health, a Medicare Preferred Provider Organization. Drs. Dharmarajan and Krumholz work under contract with the Centers for Medicare & Medicaid Services to develop and maintain performance measures that are publicly reported. Dr. Krumholz is a recipient of research grants, through Yale, from Medtronic and Johnson & Johnson (Janssen) to develop methods of clinical trial data sharing and from Medtronic and the Food and Drug Administration to develop methods for postmarket surveillance of medical devices; chairs a cardiac scientific advisory board for UnitedHealth; is a participant/participant representative of the IBM Watson Health Life Sciences Board; is a member of the Advisory Board for Element Science and the Physician Advisory Board for Aetna; and is the founder of Hugo, a personal health information platform.
After discharge from the hospital, patients face a transient period of generalized susceptibility to disease as well as an elevated risk for adverse events, including hospital readmission and death. The term posthospital syndrome (PHS) has been used to describe this time of enhanced vulnerability. Based on data from bench to bedside, this narrative review examines the hypothesis that hospital-related allostatic overload is a plausible etiology of PHS. Resulting from extended exposure to stress, allostatic overload is a maladaptive state driven by overuse and dysregulation of the hypothalamic-pituitary-adrenal axis and the autonomic nervous system that ultimately generates pathophysiologic consequences to multiple organ systems. Markers of allostatic overload, including elevated levels of cortisol, catecholamines, and inflammatory markers, have been associated with adverse outcomes after hospital discharge. Based on the evidence, we suggest a possible mechanism for postdischarge vulnerability, encourage critical contemplation of traditional hospital environments, and suggest interventions that might improve outcomes.
