Islets of Hope  care tips for persons with diabetes

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Articles disclaimer

Edited by Lahle Wolfe.

Orginial article can be found at

The two single most important things that you can do to prevent chronic wounds from developing from infection are:

1.  Keep your blood glucose levels in range -- high blood sugars increases your risk or infection, neuropathy, and circulatory problems.

2.  Check your feet daily and report any blisters, sores, or cuts that don't heal quickly to your doctor... immediately!

Information and Support

World Wide Wound - Resource and Information List

American Academy of Wound Management

Association for the Advancement of Wound Care

Pedsdermatlas, a dermatology digital image resource, enables health care professionals, parents, and patients to access high quality dermatology images on the World Wide Web. It is compiled, reviewed, scored and updated by physicians of the Johns Hopkins University. Currently more than 250 images are included in this fast growing collection of pediatric dermatology images.

Australian Wound Management Association Inc

European Tissue Repair Society

European Wound Management Association

Hyperbaric Medicine Unit of Aberdeen Royal Infirmary, Scotland provides hyperbaric oxygen therapy (HBO) for certain wounds and infections. The website contains useful information for patients about to undergo HBO therapy, including a virtual tour of the chamber.

Judy Waterlow Site.  Infomation on improving pressure ulcer care, prevention, and risk assessment, plus information on the Waterlow Scale and how to use it effectively.

Podiatry Online. Online resource for footcare.

MyFootShop - site dedicated to footcare and footcare products.

Pressure Sore Web Forum

Tissue Viability Society Includes patient information leaflets on Skin Care, Foot Care, Leg Ulcers, Wheelchairs, Discharge, and Complaints.

University of South Australia Wound Management Program.

Wound and Skin Care Links.   Dianne Brownson's 'wound and skin' links - other health care links too.

Wound Care Association of New South Wales  The association is now a multidisciplinary, non-profit organisation consisting of persons who are committed to developing and improving wound management through education, research, communication and networking. It is affiliated with the Australian Wound Management Association

Wound Care Institute

Wound Care Portal  Site run by Rand Feinstein (RN, PA-C, CWCN), intended to serve Wound Care Professionals by providing studies and a forum for the open discussion of wound care products, therapies, and related topics.

Wound Care Society

Wound Care Information Network

Wound Care Web Forum

Wound Healing Society

Wounds1 - woundcare related site covering diabetic foot ulcers, burns, scars and leg ulcers.

Wounds UK - specialist training, education, conferences, books and journals for healthcare professionals in the field of wound care and pressure care.

Wound Update - Wound Update provides a monthly literature awareness service for publications indexed on the Medline database as relevant to wound care. Every month all relevant new publications are categorised under the following two sections: CLINICAL STUDIES - Acute wounds, Chronic wounds, Burns, Infection; BASIC RESEARCH STUDIES - Wound Physiology, Treatment. The service is free to all wound care professionals.

Articles and Information

High-Tech Advances in Wound Care Yield New Promise from M.D. News - Dallas by Tina Cauller

Dr. Jeffrey Stone: Leading the Field in Hyperbaric Therapy from Wounds 1 by Erin K. Blakeley

Read about the latest advances in hyperbaric medicine in Hyperbaric Medicine Today

Wound Healing: Chronic Wounds; eMedicine


Alleva R, Nasole E, Di Donato F, Borghi B, Neuzil J, and Tomasetti M. 2005. α-Lipoic acid supplementation inhibits oxidative damage, accelerating chronic wound healing in patients undergoing hyperbaric oxygen therapy. Biochemical and Biophysical Research Communications, Volume 333, Issue 2, Pages 404-410.

Augustin M and Maier K. 2003. Psychosomatic aspects of chronic wounds. Dermatology and Psychosomatics, Volume 4, Pages 5-13. Available.

Brem H, Kirsner RS and Falanga V. 2004. Protocol for the successful treatment of venous ulcers. The American Journal of Surgery, Volume 188, Issue 1, Supplement 1, Pages 1-8.

Clark WM. 2005. Reperfusion Injury in Stroke. Available.

Mustoe T. 2005. Dermal ulcer healing: Advances in understanding. Presented at meeting: Tissue repair and ulcer/wound healing: molecular mechanisms, therapeutic targets and future directions. Paris, France, March 17-18, 2005. Available.


diabetes care tips                    
Wound Care for Diabetes

Mini Site Index
What is a Chronic Wound?
Types of Chronic Wounds
Contributing Factors
Treatment & Prevention of Infections

For more information, also see:
Diabetic Neuropathy
Foot Care

What is a Chronic Wound?

Most wounds heal in an orderly set of stages and in a predictable amount of time; those that do not are called chronic wounds. Wounds that do not heal within three months are considered chronic. Chronic wounds seem to be detained in one or more of the phases of wound healing; for example, chronic wounds often remain in the inflammatory stage for too long . In acute wounds, there is a precise balance between production and degradation of molecules such as collagen; in chronic wounds this balance is lost and degradation plays too large a role.

Chronic wounds may never heal or may take years to do so. These wounds cause patients severe emotional and physical stress as well as creating a significant financial burden on patients and the whole healthcare system.

Acute and chronic wounds are at opposite ends of a spectrum of wound healing types that progress toward being healed at different rates.

Any wound, especially those on the feet where diabetic neuropathy may be present, should be of special concern to persons with diabetes.  Neuropathy destroys nerves so that a person may be unware that they have suffered an injury.  Since those with neuropathy may also have circulation problems, even a tuny cut or blistered, unattended, may lead to infection and a chronic wound that may not heal.  This may even result in amputation of part of the foot, entire foot, or even leg should gangrene result.

Chronic wounds mostly affect people over the age of 60. The incidence is 0.78% of the population and the prevalence ranges from 0.18 to 0.32%. As the population ages, and the number of diabetics is rapidly on the increase, the number of chronic wounds is expected to rise.  


Types of Chronic Wounds

The vast majority of chronic wounds can be classified into three categories: venous, diabetic, and pressure ulcers (Mustoe, 2004; Moreo, 2005) CW. A small number of wounds that do not fall into these categories may be due to causes such as radiation poisoning or ischemia (Mustoe, 2004).

Venous ulcers

Venous ulcers, which usually occur in the legs, exist in about 70% to 90% of chronic wounds (Snyder, 2005) and mostly affect the elderly. They are thought to be due to venous hypertension caused by improper function of valves that exist in the veins which exist to prevent backflow of blood. Ischemia results and, combined with reperfusion injury, causes the tissue damage that leads to the wounds.

Diabetic ulcers

Another major cause of chronic wounds, diabetes, is increasing in prevalence (Velander et al., 2004). Diabetics have a 15% higher risk for amputation than the general population (Snyder, 2005) due to chronic ulcers. Diabetes causes neuropathy, which inhibits the perception of pain (Snyder, 2005). Thus patients may not initially notice small wounds to legs and feet, and thus may fail to prevent infection and repeated injury (Moreo, 2005). Further, diabetes causes immune compromise (Snyder, 2005) and damage to small blood vessels, preventing adequate oxygenation of tissue, which can cause chronic wounds (Moreo, 2005). Pressure also plays a role in the formation of diabetic ulcers (Mustoe, 2004).

Pressure ulcers

Another leading type of chronic wounds is pressure ulcers (Supp and Boyce, 2005), which usually occur in people with conditions such as paralysis that inhibit movement on areas that press against bones such as the heels, shoulder blades, and sacrum (Thomas et al., 2005; Wilhelmi and Neumeister, 2005). Pressure ulcers are caused by ischemia that occurs when pressure on the tissue is greater than the pressure in capillaries, and thus restricts blood flow into the area (Supp and Boyce, 2005; Wilhelmi and Neumeister, 2005). Muscle tissue, which needs more oxygen and nutrients than skin does, shows the worst effects from prolonged pressure (Wilhelmi and Neumeister, 2005). As in other chronic ulcers, reperfusion injury damages tissue (Mustoe, 2004).


Contributing Factors

In addition to poor circulation, neuropathy, and difficulty moving, factors that contribute to chronic wounds include systemic illnesses, age, and repeated trauma (Yaple, 2005). Comorbid ailments that may contribute to the formation of chronic wounds include vasculitis (an inflammation of blood vessels), immune suppression, pyoderma gangrenosum, and diseases that cause ischemia (Snyder, 2005). Immune suppression can be caused by illnesses or medical drugs used over a long period, for example steroids (Snyder, 2005). Emotional stress can also negatively affect the healing of a wound, possibly by raising blood pressure and levels of cortisol, which lowers immunity (Augustin and Maier, 2003).

What appears to be a chronic wound may also be a malignancy; for example, cancerous tissue can grow until blood cannot reach the cells, and the tissue becomes an ulcer (Trent, 2003). Cancer, especially squamous cell carcinoma, may also form as the result of chronic wounds (Brem et al., 2004), probably due to repetitive tissue damage that stimulates rapid cell proliferation (Trent, 2003).

Another factor that may contribute to chronic wounds is old age (Mustoe, 2004). The skin of older people is more easily damaged, and older cells do not proliferate as fast and may not have an adequate stress response in terms of gene upregulation of stress-related proteins (Mustoe, 2004). In older cells, stress response genes are overexpressed when the cell is not stressed, but when it is, the expression of these proteins is not upregulated by as much as in younger cells (Mustoe, 2004).

Comorbid factors that can lead to ischemia are especially likely to contribute to chronic wounds and include chronic fibrosis, atherosclerosis (Mustoe, 2004), edema (Moreo, 2005), sickle cell disease, and arterial insufficiency-related illnesses

Repeated physical trauma plays a role in chronic wound formation by continually initiating the inflammatory cascade. The trauma may occur by accident, for example when a leg is repeatedly bumped against a wheelchair rest, or it may be due to intentional acts. Heroin users who lose venous access may resort to 'skin popping', or injecting the drug subcutaneously, which is highly damaging to tissue and frequently leads to chronic ulcers (Williams and Southern, 2005). Children who are repeatedly seen for a wound that does not heal are sometimes found to be victims of a parent with Munchausen syndrome by proxy, a disease in which the abuser may repeatedly inflict harm on the child in order to receive attention (Vennemann et al., 2005).  



Chronic wounds may affect only the epidermis and dermis, or they may affect tissues all the way to the fascia (Crovetti et al., 2004). They may be formed originally by the same things that cause acute ones, such as surgery or accidental trauma (Moreo, 2005), or they may form as the result of systemic infection, vascular, immune, or nerve insufficiency, or comorbidities such as neoplasias or metabolic disorders (Crovetti et al., 2004). The reason a wound becomes chronic is that the body’s ability to deal with the damage is overwhelmed by factors such as repeated trauma, continued pressure, ischemia, or illness (Crovetti et al., 2004; Moreo, 2005).

Though much progress has been accomplished in the study of chronic wounds lately, advances in the study of their healing have lagged behind expectations. This is partly due to the fact that animal studies are difficult because animals do not get chronic wounds, since they usually have loose skin that quickly contracts, and they normally do not get old enough or have contributing diseases such as neuropathy or chronic debilitating illnesses (Mustoe, 2004). Nonetheless, current researchers now understand some of the major factors that lead to chronic wounds, among which are ischemia, reperfusion injury, and bacterial colonization (Mustoe, 2004).


Ischemia is an important factor in the formation and persistence of wounds, especially when it occurs repetitively (as it usually does) or when combined with a patient’s old age (Mustoe, 2004). Ischemia causes tissue to become inflamed and cells to release factors that attract neutrophils such as interleukins (Clark, 2005), chemokines, leukotrienes, and complement factors (Mustoe, 2004).

While they fight pathogens, neutrophils also release inflammatory cytokines and enzymes that damage cells (Mustoe, 2004; Snyder, 2005). One of their important jobs is to produce ROS to kill bacteria, for which they use an enzyme called myeloperoxidase (Mustoe, 2004). The enzymes and ROS produced by neutrophils and other leukocytes damage cells and prevent cell proliferation and wound closure by damaging DNA, lipids, proteins (Alleva et al., 2005), the ECM, and cytokines that speed healing (Mustoe, 2004). Neutrophils remain in chronic wounds for longer than they do in acute wounds, and contribute to the fact that chronic wounds have higher levels of inflammatory cytokines and ROS (Schönfelder et al., 2005; Taylor et al., 2005). Since wound fluid from chronic wounds has an excess of proteases and ROS, the fluid itself can inhibit healing by inhibiting cell growth and breaking down growth factors and proteins in the ECM (Snyder, 2005).

Bacterial colonization

Since more oxygen in the wound environment allows white blood cells to produce ROS to kill bacteria, patients with inadequate tissue oxygenation, for example those who suffered hypothermia during surgery, are at higher risk for infection (Mustoe, 2004). The host’s immune response to the presence of bacteria prolongs inflammation, delays healing, and damages tissue (Mustoe, 2004). Infection can lead not only to chronic wounds but also to gangrene, loss of the infected limb, and death of the patient (Dow, 2001).

Like ischemia, bacterial colonization and infection damage tissue by causing a greater number of neutrophils to enter the wound site (Mustoe, 2004; Snyder, 2005). In patients with chronic wounds, bacteria with resistances to antibiotics may have time to develop (Halcón and Milkus, 2004). In addition, patients that carry drug resistant bacterial strains such as methicillin-resistant Staphylococcus aureus (MRSA) have more chronic wounds (Halcón and Milkus, 2004).

Growth factors and proteolytic enzymes

Chronic wounds also differ in makeup from acute wounds in that their levels of proteolytic enzymes such as elastase (Edwards et al., 2004; Schönfelder et al., 2005; Snyder, 2005) and matrix metalloproteinases (MMPs) are higher, while their concentrations of growth factors such as PDGF and KGF are lower (Crovetti et al., 2004; Schönfelder et al., 2005; Snyder, 2005).

Since growth factors (GFs) are imperative in timely wound healing, inadequate GF levels may be an important factor in chronic wound formation (Crovetti et al., 2004). In chronic wounds, the formation and release of growth factors may be prevented, the factors may be sequestered and unable to perform their metabolic roles, or degraded in excess by cellular or bacterial proteases (Crovetti et al., 2004).

Chronic wounds such as diabetic and venous ulcers are also caused by a failure of fibroblasts to produce adequate ECM proteins and by keratinocytes to epithelialize the wound (Foy et al., 2004). Fibroblast gene expression is different in chronic wounds than in acute wounds (Foy et al., 2004).

Though all wounds require a certain level of elastase and proteases for proper healing, too high a concentration is damaging (Edwards et al., 2004). Leukocytes in the wound area release elastase (Edwards et al., 2004; Schönfelder et al., 2005), which increases inflammation, destroys tissue, proteoglycans, and collagen (Kanda and Watanabe, 2005), and damages growth factors, fibronectin, and factors that inhibit proteases (Edwards et al., 2004). The activity of elastase is increased by albumin, which is the most abundant protein found in chronic wounds (Edwards et al., 2004). However, chronic wounds with inadequate albumin are especially unlikely to heal, so regulating the wound's levels of that protein may in the future prove helpful in healing chronic wounds (Edwards et al., 2004).

Excess matrix metalloproteinases, which are released by leukocytes, may also cause wounds to become chronic (Stanley et al., 2005). MMPs break down ECM molecules (Stanley et al., 2005), growth factors, and protease inhibitors, and thus increase degradation while reducing construction, throwing the delicate compromise between production and degradation out of balance (Lai et al., 2004; Schönfelder et al., 2005).  



Though treatment of the different chronic wound types varies slightly (Gottrup, 2004), appropriate treatment seeks to address the problems at the root of chronic wounds, including ischemia, bacterial load, and imbalance of proteases (Mustoe, 2004). Various methods exist to ameliorate these problems, including antibiotic and antibacterial use, debridement, irrigation, vacuum-assisted closure, warming (Mustoe, 2004), oxygenation, moist wound healing, removing mechanical stress (Moreo, 2005), and adding cells or other materials to secrete or enhance levels of healing factors (Velander et al., 2004).

Preventing and Treating Infection

To lower the bacterial count in wounds, therapists may use topical antibiotics, which kill bacteria and can also help by keeping the wound environment moist (Patel et al., 2000; Brem et al., 2004), which is important for speeding the healing of chronic wounds (Taylor et al., 2005; Thomas et al., 2005). Some researchers have experimented with the use of tea tree oil, an antibacterial agent which also has anti-inflammatory effects (Halcón and Milkus, 2004). Disinfectants are contraindicated because they damage tissues and delay wound contraction (Patel et al., 2000). Further, they are rendered ineffective by organic matter in wounds like blood and exudate and are thus not useful in open wounds (Patel et al., 2000).

A greater amount of exudate and necrotic tissue in a wound increases likelihood of infection by serving as a medium for bacterial growth away from the host’s defenses (Mustoe, 2004). Since bacteria thrive on dead tissue, wounds are often surgically debrided to remove the devitalized tissue (Brem et al., 2004; Mustoe, 2004; Snyder, 2005). Debridement and drainage of wound fluid are an especially important part of the treatment for diabetic ulcers, which may create the need for amputation if infection gets out of control (Gottrup, 2004). Mechanical removal of bacteria and devitalized tissue is also the idea behind wound irrigation, which is accomplished using pulsed lavage (Mustoe, 2004).

Negative-pressure wound therapy (NPWT) is a treatment that improves ischemic tissues and removes wound fluid used by bacteria (Mustoe, 2004; Moreo, 2005). This therapy, also known as vacuum-assisted closure, reduces swelling in tissues, which brings more blood and nutrients to the area, as does the negative pressure itself (Moreo, 2005; Mustoe, 2004; Snyder, 2005). The treatment also decompresses tissues and alters the shape of cells, causes them to express different mRNAs and to proliferate and produce ECM molecules (Moreo, 2005; Snyder, 2005).

Treating Ischemia and Hypoxia

Blood vessels constrict in tissue that becomes cold and dilate in warm tissue, altering blood flow to the area. Thus keeping the tissues warm is probably necessary to fight both infection and ischemia (Thomas et al., 2005). Some healthcare professionals use ‘radiant bandages’ to keep the area warm, and care must be taken during surgery to prevent hypothermia, which increases rates of post-surgical infection (Mustoe, 2004).

Underlying ischemia may also be treated surgically by arterial revascularization, for example in diabetic ulcers, and patients with venous ulcers may undergo surgery to correct vein dysfunction (Gottrup, 2004).

Diabetics that are not candidates for surgery (and others) may also have their tissue oxygenation increased by Hyperbaric Oxygen Therapy, or HBOT, which can compensate for limitations of blood supply and correct hypoxia (Gottrup, 2004; Alleva et al., 2005; Snyder, 2005). In addition to killing bacteria, higher oxygen content in tissues speeds growth factor production, fibroblast growth, and angiogenesis and (Alleva et al., 2005; Snyder, 2005). Unfortunately, increased oxygen levels also means increased production of ROS (Alleva et al., 2005). Antioxidants, molecules that can lose an electron to free radicals without themselves becoming radicals, can lower levels of oxidants in the body and have been used with some success in wound healing (Schönfelder et al., 2005).

Growth Factors and Hormones

Since chronic wounds underexpress growth factors necessary for healing tissue, chronic wound healing may be speeded by replacing or stimulating those factors (Crovetti et al., 2004) and by preventing the excessive formation of proteases like elastase that break them down (Edwards et al., 2004; Schönfelder et al., 2005).

One way to increase growth factor concentrations in wounds is to apply the growth factors directly, though this takes many repetitions and requires large amounts of the factors (Schönfelder et al., 2005). Another way is to spread onto the wound a gel of the patient’s own blood platelets, which then secrete growth factors such as VEGF, IGF 1–2, PDGF, TGF-β, and EGF (Crovetti et al., 2004; Yaple, 2005). Other treatments include implanting cultured keratinocytes into the wound to reepithelialize it (Brem et al., 2004; Velander et al., 2004) and culturing and implanting fibroblasts into wounds (Brem et al., 2004). Some patients are treated with artificial skin substitutes (Brem et al., 2004; Supp and Boyce, 2005) that have fibroblasts and keratinocytes in a matrix of collagen to replicate skin and release growth factors (Ehrlich, 2004).

In other cases, skin from cadavers is grafted onto wounds (Supp and Boyce, 2005), providing a cover to keep out bacteria and preventing the buildup of too much granulation tissue, which can lead to excessive scarring (Ehrlich, 2004). Though the allograft (skin transplanted from a member of the same species) is replaced by granulation tissue and is not actually incorporated into the healing wound, it encourages cellular proliferation and provides a structure for epithelial cells to crawl across (Snyder, 2005). On the most difficult chronic wounds, allografts may not work, requiring skin grafts from elsewhere on the patient, which can cause pain and further stress on the patient’s system (Taylor et al., 2005).

Collagen dressings are another way to provide the matrix for cellular proliferation and migration, while also keeping the wound moist and absorbing exudate (Schönfelder et al., 2005).

Since levels of protease inhibitors are lowered in chronic wounds, some researchers are seeking ways to heal tissues by replacing these inhibitors in them (Lai et al., 2004). Secretory leukocyte protease inhibitor (SLPI), which inhibits not only proteases but also inflammation and microorganisms like viruses, bacteria, and fungi, may prove to be an effective treatment (Lai et al., 2004).

Research into hormones and wound healing has shown estrogen to speed wound healing in elderly humans and in animals that have had their ovaries removed, possibly by preventing excess neutrophils from entering the wound and releasing elastase (Kanda and Watanabe, 2005). Thus the use of estrogen is a future possibility for treating chronic wounds.

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