Hospital-related allostatic overload, driven by stressors such as sleep disruption, poor nutrition, and mobility restriction, is proposed as a plausible pathophysiologic mechanism for posthospital syndrome.
Hospital-induced allostatic overload is proposed as a unifying pathophysiological mechanism for posthospital syndrome, suggesting that modifying the hospital environment to reduce stress could decrease post-discharge vulnerability.
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.
Goldwater et al. (Tue,) conducted a review in Posthospital syndrome. Hospital-related allostatic overload, driven by stressors such as sleep disruption, poor nutrition, and mobility restriction, is proposed as a plausible pathophysiologic mechanism for posthospital syndrome.