Vulnerability: the crossroads of frailty and delirium

Abstract

Frailty and delirium, although seemingly distinct syndromes, both result in significant negative health outcomes in older adults. Frailty and delirium may be different clinical expressions of a shared vulnerability to stress in older adults, and future research will determine whether this vulnerability is age related, pathological, genetic, environmental, or most likely, a combination of all of these factors. This article explores the clinical overlap of frailty and delirium, describes possible pathophysiological mechanisms linking the two, and proposes research opportunities to further knowledge of the interrelationships between these important geriatric syndromes. Frailty, a diminished ability to compensate for stressors, is generally viewed as a chronic condition, whereas delirium is an acute change in attention and cognition, but there is a developing literature on transitions in frailty status around acute events, as well as on delirium as a chronic, persistent condition. If frailty predisposes an individual to delirium, and delirium delays recovery from a stressor, then both syndromes may contribute to a downward spiral of declining function, increasing risk, and negative outcomes. In addition, frailty and delirium may have shared pathophysiology, such as inflammation, atherosclerosis, and chronic nutritional deficiencies, which will require further investigation. The fields of frailty and delirium are rapidly evolving, and future research may help to better define the interrelationship of these common and morbid geriatric syndromes. Because of the heterogeneous pathophysiology and presentation associated with frailty and delirium, typical of all geriatric syndromes, multicomponent prevention and treatment strategies are most likely to be effective and should be developed and tested.

Figure 1. Functional decline after a stressor

In patient A, the stressor results in a decline in function which does not cross the threshold of independent function. The patient is likely non-frail, because the functional level returns to the baseline, indicating that the patient was able to fully compensate to the stressor. In patient B, a similar stressor causes a decline in function which transiently results in dependence. While the patient subsequently recovers independence, it is at a lower level of functioning than prior to the stressor. The patient is likely frail because she does not return to her baseline level of function, indicating that she was unable to fully compensate to the stressor. This patient has a constricted functional reserve compared with the patient above. Note: Day-to-day functional variation is depicted by a sine wave.