Clinical Approach to Chronic Wound Management in Older Adults

Wahila Alam MD; Jonathan Hasson MD, MBA; May Reed MD


J Am Geriatr Soc. 2021;69(8):2327-2334. 

In This Article

Pathophysiology of Wound Healing

There are four stages of wound healing; hemostasis, inflammation, granulation, and maturation (Figure 1A). The cascade of events begins with clot formation followed by the release of growth factors, chemotaxis, angiogenesis, collagen formation, and epithelialization. Understanding the mechanism and pathophysiology of these stages underlies the foundation for strategies to optimize wound healing. Most wounds heal in 4–6 weeks when they follow a timely reparative process, but ongoing remodeling processes can continue over several months resulting in either maturation or scar formation.

Figure 1.

Wound care in older adults. (A) Stages of wound healing showing. (A1) hemostasis, where platelets form a clot and release growth factors (1–3 h); (A2) inflammatory phase with neutrophils and macrophages entering wound site to clear dead tissue (1–3 days); (A3) proliferative phase which consists of formation of capillaries and collagen framework by fibroblasts to form granulation tissue (3–21 days); (A4) epithelialization, which is an essential step between granulation and maturation indication wound closure; (A5) maturation, which is the final phase where collagen reorganizes, matures and remodels. (B) NPIAP stages of pressure injury. (B1) Stage 1 pressure injury showing non-blanchable erythema of intact skin; (B2) Stage 2 pressure injury showing partial thickness skin loss with exposed dermis; (B3) Stage 3 pressure injury showing full thickness skin loss; (B4) Stage 4 pressure injury showing full thickness skin loss and tissue; (B5) Unstageable pressure injury showing obscured full thickness skin and tissue loss; (B6) Deep tissue pressure injury showing persistent non-blanchable deep red, maroon, or purple discoloration. (C) Vascular and neuropathic wounds. (C1) Venous ulcer with associated venous stasis dermatitis (web source able to use for educational purposes); (C2) Arterial insufficiency ulcer with gangrene of 5th toe and part of foot; (C3) full thickness arterial insufficiency ulcer on ankle showing characteristic punched out wound with smooth edges; (C4) arterial ulcer on great toe; (C5) Malum perforans ulcer.
Source: (B) Used with permission from the National Pressure Injury Advisory Panel (NPIAP). Copyright 2020 NPIAP. (C) Used with permission from Jonathan Hasson, MD C2 and C4. Unknown web source C1, C2, and C3

Wounds become chronic if they fail to follow a timely reparative process. The exact mechanisms are unknown; however, hypoxia, bacterial colonization, altered cellular responses, and defects in ECM can all contribute to delayed wound healing.[12] Wounds typically arrest during the inflammatory or granulation stages.

The microenvironment of a normal wound is characterized by an abundance of growth factors, well-organized ECM, regulation of proteases (such as matrix metalloproteases [MMPs], tissue inhibitors of metalloproteases [TIMPs], and other modulators of enzyme activity), and a responsive cell population. This is followed by recruitment of endothelial progenitor cells, timely angiogenesis, and proliferation as well as apoptosis of fibroblasts. Normal wounds are also low in bacterial burden.

Chronic wounds, on the other hand, remain in an inflammatory phase, characterized by low levels of growth factors, unregulated protease activity, and high bacterial burden. There is a failure of ECM formation and cell migration, likely due to the absence of functional receptors and progenitor cells. A lack of angiogenesis results in deficient delivery of oxygen and nutrients, further contributing to poor healing.[13]