The Effects of Aging on Wound Healing

Wound healing is among the most complex processes that occur in the human body.  It involves many cell types, pathways, and systems working together efficiently to manage the task.  The physiological effects of advanced age paired with the co-morbidities that often accompany aging have been observed to impact every step of the wound healing process.  Non-healing wounds affect about 3 to 6 million people in the U.S.  Those aged 65 and older account for 85% of the non-healing wounds.  Costs incurred exceed $3 billion per year (Mathieu et al).

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Wound healing requires highly integrated and overlapping phases including hemostasis, inflammation, proliferation and remodeling to occur in proper sequence, at specific times, and continue for specific durations at an optimal intensity (Mathieu et al).  Any factor interfering with one or more phase in the process causes delayed, improper or impaired tissue repair (Guo & DiPietro).  Advanced age itself is considered a major risk factor for impaired wound healing.  In healthy adults, aging only causes a temporal delay in healing, so it is important to understand how age-related risk factors can further delay or derail the healing response.  The phases of wound healing and proliferative response can be decreased or delayed; remodeling can occur to a lesser degree; and collagen formation may be of a lessor quality.  (Gerstein et al, 1993).

Local Factors vs. Systematic Factors

Wound healing in older patients can be delayed by both local and systemic factors.

Local factors are characteristic of the wound itself and include wound desiccation, infection, maceration, necrosis and edema.

Systemic factors have no direct relation to the properties of the wound; rather involve body type, general health and disease state conditions that are common to the aging process and can be problematic to wound healing.  Systemic factors that commonly stall the healing process in aging persons include poor overall health, obesity, poor nutritional status, protein malnutrition, insufficient hydration, immunosuppression caused by chemo or other drug therapy, radiation therapy, chronic disease, vascular insufficiencies; and compromised immune, circulatory and respiratory systems, to name a few.   (Hess, 2011). The most common systematic factors that hinder wound healing are expanded upon below.

1. Poor Health

Poor overall health is, at times, reflected by body types known to have a negative effect on wound healing.  Obesity may result in poor blood supply to adipose tissue and protein malnutrition.  Emaciation, on the other hand, can lead to a lack of oxygen and poor nutritional stores.  Both states can interfere with healing.  Markers for malnutrition must be assessed and monitored as protein is needed for cell growth.

2. Obesity

Obesity is well-known to increase many diseases and health conditions including hyperglycemia and impaired wound healing.  Hyperglycemia can add to oxidative stress and is associated with impaired wound healing when damage from reactive oxygen species exceeds the antioxidant capacity (Vincent et al, 2004).  Obese individuals frequently incur additional wound healing complications including wound infections, dehiscence, hematoma and seroma formation, pressure ulcers, and venous ulcers.  These complications may result from hypoperfusion and ischemia that occur in subcutaneous adipose tissue.  Increased wound tension acts to increase tissue pressure, reducing microperfusion and the availability of oxygen to the wound (Wilson and Clark, 2004).  Further, adipose tissue secretes a large variety of bioactive substances, known as adipokines, that can have a profound impact on the immune and inflammatory response and negatively impact the healing process (Nieman et al, 1999).

3. Emaciation

Emaciation resulting from malnutrition, illness or debilitating disease, leads to specific nutrient deficiencies and is present in a large portion of the aging population.  This condition can have a profoundly negative effect on wound healing.  Proteins, carbohydrates and fats are the primary source of energy in the wound-healing process.  Glucose is used to create the cellular ATP providing energy for angiogenesis and deposition of new tissues (Shepard, 2003).  Protein deficiency can impair capillary formation, fibroblast proliferation, proteoglycan synthesis, collagen synthesis, and wound remodeling.  Protein deficiency also results in increased susceptibility to infection (Gogia, 1995).  Deficiencies in Vitamin C can have effects on tissue repair, leading to impaired wound healing.  Composite nutrition support to improve protein nutrition and hydration benefits both acute and chronic wound healing and may be required to assist the wound healing process (Arnold and Barbul, 2006).

4. Immunosuppression

Immunosuppression caused by chemo, radiation or drug therapy can interfere with clot formation, platelet function, inflammatory responses or cell proliferation and has the capacity to affect wound healing.  Glucocorticoid steroids, non-steroidal anti-inflammatory drugs and chemotherapeutic agents commonly have a significant impact on healing.

5. Age-Related Diseases

Chronic, age-related diseases and medical conditions common in the elderly, such as cardiovascular disease, diabetes and those effecting blood flow can be detrimental to wound healing by stalling the healing process.  The resulting tissue oxygenation restriction and stress -induced disruption of neuroendocrine immune equilibrium is consequential to wound healing and to health.  Hyperglycemia can also add to oxidative stress associated with impaired wound healing when damage from reactive oxygen species exceeds the antioxidant capacity (Vincent et al, 2004).

6. Diabetes

Diabetic individuals are prone to have difficulty healing wounds.  In addition to hypoxia, dysfunction in fibroblasts and epidermal cells, impaired angiogenesis and neovascularization, high levels of metalloproteases (MMPs), formation of advanced glycation end-products (AGEs), decreased host immune resistance and neuropathy can occur with diabetes.

High levels of MMPs are a feature of diabetic foot ulcers and MMP levels in chronic wound fluid are almost 60 times higher than those in acute wounds.   Increased protease activity supports tissue destruction and inhibits normal repair processes (Woo et al, 2007).  Chronic, non-healing diabetic foot ulcers (DFUs) are estimated to occur in 15% of people with diabetes.  DFUs are a serious complication and precede 84% of all diabetes-related lower leg amputations (Brem and Tomic-Canic, 2007).

7. Vascular Insufficiency

Vascular insufficiency leading to decreased blood supply and restricted tissue oxygenation can result in arterial, diabetic, pressure and venous ulcers affecting the lower extremities.  The proper oxygen level is crucial for sustaining the wound healing process (Bishop 2008).  This underlying condition can also lead to a hypoxic wound, negatively impacting the wound healing response.   Chronic, non-healing wounds are always accompanied by hypoxia according to Tandara and Mustoe (2004).

When treating patients of advanced age, a multidisciplinary approach to wound healing drives the best results.  If you are seeing a delay in healing, identify patients in who are suffering from other local and systemic factors.  Work with other specialists to provide continuity of care to patients in high-risk categories and provide high-quality wound care products that have demonstrated a history of positive wound care outcomes.

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References

  • Arnold M, Barbul A. (2006).  The obese surgical patient:  a susceptible host for infection.  Surg Infect (Larchmt) 7:473-480 (Pub Med).
  • Bishop A, (2008).  Role of oxygen in wound healing. J Wound Care 17:399-402 (Pub Med).
  • Brem H, Tomic-Canic M. (2007).  Cellular and molecular basis of wound healing in diabetes.  J Clin Invest 117:1219-1222 (Pub Med).
  • Gerstein AD, Phillips TJ, Rogers GS, Gilchrest BA. (1993).  Wound Healing and Aging.  Dermatol Clin. Oct;11(4)L749-57.Gogia PP, (1995).  Physiology of Wound Healing.  IN:  Clinical wound management.  Gogia PP, editor.  Thorofare, NJ:  Slack Incorporated, pp8-12.
  • Guo S, DiPietro LA (2010).  Factors affecting wound healing.  Jrnl Dental Rsch. 89 (3):219-29.
  • Hess, CT, (2011) Checklist for Factors Affecting Wound Healing.  Advances in Skin & Wound Care (24) 4:192.
  • Mathieu, D, Linke J-C, Wattel F. (2006).  Non-healing wounds.  In:  Handbook on hyperbaric medicine, Mathieu DE, editor.  Netherlands:  Springer, pp. 401-427.
  • Nieman DC, Henson DA, Nehlsen-Cannarella SL, Ekkens M, Utter AC, Butterworth DE, et al, (1999).  Influence of obesity on immune function. J Am Diet Assoc 99:294-299.  (Pub Med).
  • Shepard AA. (2003).  Nutrition for optimum wound healing.  Nurs Stand 18:55-58 (Pub Med).

    Tandara AA, Mustoe TA. (2004).  Oxygen in wound healing – more than a nutrient.  World J Surg 28:294-300 (Pub Med).

  • Vincent AM, Russell JW, Low P, Feldman EL. (2004).  Oxidative stress in the pathogenesis of diabetic neuropathy.  Endocr Rev 24:612-628 (Pub Med).
  • Wilson JA, Clark JJ. (2004).  Obesity:  impediment to postsurgical wound healing.  Adv Skin Wound Care 17:426-435 (Pub Med).
  • Woo K, Ayello EA, Sibbald RG.  (2007).  The edge effect:  current therapeutic options to advance the wound edge.  Adv Skin Wound Care 20:99-117 (Pub Med).

     

     

     

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