Effects of Aging on Inflammation and Hemostasis through the Continuum of Critical Illness

Abstract

Older age has long been associated with altered inflammation and hemostasis regulation. Emerging evidence suggests that age-related differences in inflammation and hemostasis abnormalities may play a role in the development of and long-term outcomes after critical illness. A better understanding of underlying mechanisms may provide new possibilities for therapeutic interventions. In this review, we will examine how age-related differences in inflammatory and coagulation responses are affected through the continuum of healthy state, before infection occurs, to severe sepsis and recovery.

Keywords: Aging; Coagulation; Infection; Inflammation; Sepsis.

Figure 1. Age-stratified risk of severe sepsis and mortality rates from a prospective cohort study of adults hospitalized with community-acquired pneumonia

90-day mortality measured from day of hospital admission. 1-year post-discharge mortality measured from day of hospital discharge. All rates increased significantly across age groups (P<0.001).

Figure 2. Conceptual model showing the relationship between inflammation/hemostasis abnormalities throughout the continuum of critical illness and aging

Aging is associated with a baseline increase in inflammation and hemostasis abnormalities (dark black line). Three potential outcomes are shown following sepsis. Younger adults have a lower incidence and mortality with and are expected to return to baseline inflammatory and hemostasis levels after infection (A). In older adults, a higher baseline inflammation/hemostasis burden increases the risk of sepsis and higher mortality (B). Even among older survivors of sepsis, processes that down-regulate inflammation after infection may be dysregulated, leading to a higher inflammation/hemostasis burden post-infection and worse long-term outcomes, including repeat infection and exacerbation of chronic conditions (C).