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J Hosp Med. 2018 May 30;13(5). doi: 10.12788/jhm.2986.

Is Posthospital Syndrome a Result of Hospitalization-Induced Allostatic Overload?

Author information

1
David Geffen School of Medicine at UCLA, Divisions of Cardiology and Geriatric Medicine, University of California, Los Angeles, California, USA.
2
Clover Health, Jersey City, New Jersey, USA.
3
Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York, New York, USA.
4
Section 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, USA. harlan.krumholz@yale.edu.

Abstract

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 hospitalrelated 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.

PMID:
29813141
DOI:
10.12788/jhm.2986

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