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Wound Chronicity and Infection: Strategies for Prevention and Management

Practice Accelerator
February 27, 2018

Effective wound management and the prevention of infection for patients with wounds are not only key to wound improvement, but also to avoiding a slide into a state of chronicity. Unfortunately, many wounds that start out simple turn into chronic wounds because of the complications associated with comorbid conditions and secondary infection. Approximately 6.7 million patients in the United States are affected by chronic wounds, and the pervasiveness of these wounds and their connection to other chronic illnesses are underappreciated.

That said, estimates for treatment costs are in excess of $50 billion annually.1 When we examine the nation's health care costs as a whole, we find that currently 1% of the patients account for more than 20% of the total health care expenditure, and the top 5% account for nearly half. As the older segment of our population continues to increase, so does the incidence of chronic diseases such as diabetes and peripheral vascular disease. For example, the United States Census Bureau estimates that in 20 years the 65-year-old and older age group will account for 21% of the population. This will equate to peripheral vascular disease affecting approximately 8 million or 12% to 20% of persons age 65 and older.2 This does not include those people who are affected by venous insufficiency or trauma injuries. The prevalence of these and other comorbid conditions increases not only the risk of wounding, with the concomitant risk of developing a wound infection, but also the possibility that wounds will become chronic because of infection. Our purpose today is to discuss risk factors that cause wounds to become chronic and infection prevention strategies.

Factors Leading to Wound Chronicity and Infection

As we look at the patient as a whole, common medical conditions and disease states may affect wound repair and closure. For example, persons with diabetes often have slow-healing wounds. It is the lack of glycemic control that can lead to neuropathy and a lack of sensation, which in turn can cause repetitive trauma resulting in wounds. Peripheral vascular disease or coronary artery disease can result in decreased blood flow, and minor trauma to the lower extremities can lead to wounds and injuries in those areas.

The very nature of malignant cells and their actions may affect the body's ability to progress through the normal phases of wound healing. Now let's look at some common disease states that may impede healing and affect the body's ability to fight bacteria, as discussed in an article by Leaper, Assadian, and Edmiston.3 In diabetes mellitus the effects of hyperglycemia or uncontrolled glycemic levels alter white blood cell function and increase the risk for infection. Diabetes also affects multiple other body systems that all play a role in wound healing. One example is neuropathy that develops in response to the impact of diabetes on the nervous system.

The loss of protective sensation associated with neuropathy will impair the individual's ability to sense changes in the extremity and the wound, as well as lead to further trauma. Immune deficiencies affect the body's ability to proceed through the normal inflammatory phase of wound healing. Inflammation is the body's own defense through the white blood cells. Immune deficiencies affect not only inflammation, but the other phases of wound healing as well. Peripheral vascular disease, cardiopulmonary disease, and oxygen transport disorders can impede healing. This is especially true because a well-functioning vascular system is necessary to carry oxygen and nutrients to the tissues, actions that are essential to proper healing.

Cardiopulmonary and oxygen transport disorders impair wound healing because they interrupt oxygen delivery to the tissue, as well as carbon dioxide removal. Chronic obstructive pulmonary disease can affect oxygen transport if breathing is compromised. This condition results in altered oxygen and carbon dioxide flow rates. Dementia can play a role in the patient's ability to follow the plan of care. Based on the degree of dementia, patients may not be able to care for themselves at all.

Even with minor impairment, the information provided in a verbal conversation may not be well understood. If instructions for wound care cannot be understood, then the risk of infection rises as well because of the probability of poor technique in the provision of wound care. For individuals dealing with malignancies, sometimes the treatment has its own set of side effects that can affect multiple body systems. The immune, vascular, and neurological impacts of radiation and chemotherapy can play a role in wound healing. The list could go on and on. The point to remember is that the health status and disease state of a patient can not only affect healing, but also increase the risk of infection.

Understanding Wound Infection and Healing

For wounds to heal in a timely manner they must move appropriately through the phases of wound healing, which include the inflammatory, proliferative, and maturation phases. For most wounds this occurs in a few days to a couple of weeks. Wounds that show no sign of improvement within 30 days are deemed chronic and are contaminated with bacteria. The presence of bacteria can slow the healing process by prolonging the inflammatory phase of healing and, in addition to delaying wound repair, can also cause further damage. All chronic wounds are contaminated with microoganisms.

Low levels of bacteria can actually stimulate wounds to repair themselves. However, comorbidities such as diabetes and peripheral vascular disease can impair the body's ability to deal with bacterial overload effectively. When the organisms increase in the wound bed they can severely retard or prevent wound repair. Often these colonized wounds can go on to become infected.4 It is important to understand where the wound is in the phases of wound healing and what type of bacteria are present, as determined by a quantitative analysis of those bacteria. Wound contamination is the presence of non-replicating bacteria. The host controls the environment, and healing is not impaired by these bacteria. If wounds are not managed well, such as with ineffective wound bed preparation, bacteria will begin to replicate. If there is an increase in the number of bacteria, depending on the virulence of those bacteria, this process can begin to overwhelm the host.

The concept of critical colonization was invented to describe the idea that bacteria may play a role in non-healing wounds that do not have any obvious signs and symptoms of infection. In reality, this concept likely describes the presence of a biofilm. When a wound is infected, it now has the presence of replicating bacteria that are invading the tissue whether superficially or through deep penetration. Again, the host response will show a local reaction or a systemic reaction.4

Infection Prevention Strategies in Patients with Wounds

Strategies for prevention of infection in wounds both acute and chronic begin with the principles of wound bed preparation. Appropriate cleansing, debridement practices, and choice of topical interventions are necessary components of effective wound bed preparation. When debris and foreign material are present in a wound bed, fewer organisms are required to produce an infection. Removal of these substances and of devascularized and necrotic material improves the host defense mechanisms.5

Wound cleansing with sterile saline, wound cleanser, or antimicrobial wound cleanser is performed to clean and remove debris and microorganisms physically from the wound bed. To be effective these solutions should be delivered at 8 to 15 psi, which is safe for delicate granulation tissue. Some wound cleansers also incorporate gentle surfactants to aid in loosening debris in the wound bed and making it easier to remove.4 If antimicrobial wound cleansers are used, then the components should be at a dilution and type that are not toxic to fibroblast activity.

If fibroblasts cannot function properly, granulation tissue cannot form, and thus wound closure is impeded or prevented. Some of the more common types of cleansing agents found to have a negative impact on fibroblast activity include povidone-iodine, chlorhexidine, alcohol, acetic acid, hydrogen peroxide, and sodium hypochlorite.5 Debridement is also a vital part of a wound bed preparation strategy. Any type of necrotic tissue such as eschar or slough must be debrided, and senescent or aberrant cells (that cannot be seen) may also be included in the debridement protocol. Any foreign material that inhibits healing, such as toxins, microbes, biofilms, bacteria, yeasts, or viruses, and also substances such as dressing residue, animal hair or dander, suture material, or any other types of debris, should be removed. There are multiple types of debridement, including sharp surgical debridement, conservative sharp debridement, and mechanical, enzymatic, biological, or autolytic debridement.

The method chosen will depend on the patient's specific needs, the clinical environment, and the availability of trained and authorized personnel to perform the debridement. There are times when it is contraindicated to debride stable, dry eschar. Before beginning any local wound care, all skin and wounds should be assessed; if they are found to have poor perfusion, referral for surgical and or medical assessment and treatment may be indicated. Stable dry eschar is also considered a biological dressing and is the most effective barrier to bacteria for most patients.4 Once a wound is debrided, multiple dressing formats can aid in inhibiting microbial proliferation, preventing infection, or treating local infection. Cadexomer iodine absorbs moisture and in so doing releases iodine in a controlled fashion that inhibits bacterial growth. Nanocrystalline silver is a slow-release silver preparation that has broad-spectrum antimicrobial activity and can be combined with dressing materials such as foams, hydrogels, alginates, collagens, and films.

New technologies are being developed that will aid in reducing the risk of and treating infection. However, because of increasing antimicrobial resistance, these agents should not be used for extended periods of time. Alternative technologies, such as dialkylcarbamoyl chloride (DACC)-based dressings, work by physically binding the bacteria versus killing bacteria. The dressing irreversibly binds bacteria at the wound surface, and these bacteria are removed when the dressing is changed.5 Once the bacterial burden has been reduced to acceptable levels, then dressings without antimicrobial properties should be implemented.6 In the event that a systemic infection has been identified and microbial levels are above those that can be managed with local wound interventions, systemic antimicrobial interventions should be implemented. This is especially necessary when fever, cellulitis extending at least 1cm beyond the wound margin, underlying deep structure infection, or systemic life-threatening infection is present.4


Wounds moving through the healing process appropriately will heal in a predicable amount of time and without complication. Any wound that has not shown significant improvement within 30 days is deemed chronic. Many factors not only affect the healing process, but also can predispose a wound to becoming chronic and to developing complications such as infection. To develop effective strategies in preventing wound infection we must understand and implement the principles of wound bed preparation. This includes identifying the etiology of the problem and then reviewing all the cofactors and comorbidities that may inhibit or delay the healing process or promote the development of infection. Prompt implementation of prevention and intervention strategies will lead the way to positive outcomes.


1. Healogics Wound Science Initiative. Wound care by the numbers: Medicare cost and utilization of patients with chronic wounds. Becker's Hospital Review. 2017. Available at:…. Accessed February 20, 2018.

2. Leaper D, Assadian O, Edmiston CE. Approach to chronic wound infections. Br J Dermatol. 2015;173(2):351-8. doi: 10.1111/bjd.13677.

3. Lipsky BA, Hoey C. Topical antimicrobial therapy for treating chronic wounds. Clin Infect Dis. 2016;49(10):1541-9. doi: 10.1086/644732.

4. Stotts NA. Wound infection: diagnosis and management. In: Bryant RA, Nix DP, eds. Acute and Chronic Wounds: Current Management Concepts. 5thed. St. Louis, MO: Elsevier; 2016:283-94.

5. Totty JP, Bua N, Smith GE, et al. Dialkylcarbamoyl chloride (DACC)–coated dressings in the management and prevention of wound infection: a systematic review. J Wound Care. 2017;26(3):107-14. doi: 10.12968/jowc.2017.26.3.107.

6. Barrett S. Wound-bed preparation: a vital step in the healing process. Br J Nurs. 2017;26(12):24-31. doi: 10.12968/bjon.2017.26.12.S24. 

The views and opinions expressed in this blog are solely those of the author, and do not represent the views of WoundSource, HMP Global, its affiliates, or subsidiary companies.