1. Overview

There are several types of wounds which characteristically are much more difficult to heal than the acute traumatic wounds. The major reasons are the typical presence of impaired perfusion as seen, e.g. with venous hypertension or diabetes and an underlying disorder such as immobility as seen in the population with pressure ulcers.

Typically, these wounds begin healing by the normal acute healing process with the process simply being prolonged into months instead of weeks. There is also an increased risk of wound complications due to the underlying impediments to healing. These wounds are also at high risk for evolving into a chronic wound, which fit into the difficult to heal category are a diabetic, venous stasis and pressure ulcer.

Difficult to heal wounds:

• Diabetic Ulcer

• Venous Stasis Ulcer

• Pressure Ulcer

Each have distinct properties which make them difficult to heal. All of them share the characteristics of impaired perfusion and increased risk of infection, increased bacterial burden and inflammation.

Chronic wounds differ substantially from an acute wound.  The wound no longer follows the normal healing processes. The term “non-healing wound” is often used to describe the chronic wound. Characteristics are presented. However, the exact distinction between acute and chronic is still somewhat arbitrary and often based on the cause of the wound and physical status of the patient.

The time period most commonly used to define a chronic wound is usually 3 months of lack of healing. The most common chronic wounds are pressure ulcers, diabetic ulcers and venous stasis ulcers. The 3 categories account for 70% of chronic wounds. However, any acute wound, which fails to follow the normal healing process can become a chronic wound. It is important that criteria for determining when an acute wound becomes a chronic wound be met before calling a wound “chronic”. For example, a pressure ulcer characteristically heals slower than an acute surgical wound but a pressure ulcer can progressively heal by the normal healing process. It only becomes a chronic wound if there is failure of the normal healing process. Successful treatment of the chronic wound depends on a thorough understanding of the pathophysiologic mechanisms underlying the failure of the normal wound healing process.

2. Etiology

A number of etiologic factors have been identified which impede the normal healing process allowing a chronic wound to develop. Systemic factors such as malnutrition and chronic illness prevent the acute wound from healing due to inadequate protein synthesis needed for new tissue development. Other factors such as impaired perfusion, hypoxia, do not allow healing to occur because of inadequate oxygen. Other systemic factors such as infection, diabetes and corticosteroids directly impede healing.

The most common local factors which allow a chronic wound to develop are continued mechanical trauma to the wound and/or the use of wound care products toxic to the cells of the wound bed. Repeated loss of the new tissue synthesis will eventually lead to a chronically inflamed wound. 

3. Treatment of the Difficult to Heal and Chronic Wounds with Acticoat^TM

There is increasing evidence that nanocrystalline silver Acticoat^tm is very effective in the management of difficult to heal and chronic wounds.

The nanocrystalline silver is very effective at:

• Decreasing bacterial burden

• Controlling excess inflammation

• Deceasing

• Maintaining moist healing environment 

Chronic Wound

Management of Difficult to heal ulcers with a new silver dressing: A clinical evaluation. (Poster presentation, EWMA, Grenada, 2002) Romanelli M, et al (Dept Dermatology, University Hospital of Pisa, Italy)

The process of healing is an overlapping, interconnected process, where there is active interaction between the cellular components and the extra-cellular matrix. All play an active role in the process of healing and inflammation.

The slightest disruption to the proper functioning of any one of these overlapping chain-like processes may impede/delay healing resulting in a pathological/chronic wound.

The Use of Acticoat on an infected thigh stump (EVEAN Thiuszorg, Wondevrepleegkundige, Netherlands)

Infected ulcers on the anterior and posterior aspects of both legs.

Infected ulcers on the anterior and posterior aspects of both legs.

1. Treatment with Acticoat^tm
2. Acticoat^tm used in conjunction with a secondary dressing
3. Acticoat^tm and secondary dressing are under the compression dressing

After 64 days the ulcers had clearly improved with treatment.

4. Diabetic Ulcers

Incidence:

Approximately 15-20% of the estimated 16 million diabetics in the United States will be hospitalized for a foot complication, usually an ulcer, during the course of their disease. Progression of these ulcers are the leading cause of foot amputations.

Etiology

Characteristics

• Impaired perfusion leading to ischemia

• Foot neuropathy

• High risk of infection

• Full thickness wound usually surrounded by a rim of callous caused by compression of soft tissues against bony prominences: feet are most common

• Presence of diabetic neuropathy

• High risk of infection

Characteristics: 

The ulcer is usually full thickness, therefore extra-cellular matrix components are initially absent. The most common site is on the foot, especially over bony prominences and on the heel. The ulcers are typically full thickness and difficult to heal, often becoming chronic wounds. An adequate description of ulcer characteristics is necessary for selection of appropriate treatment. Description includes size, depth, appearance and location. In addition, it must be determined whether the ulcer is the result of neuropathy, ischemia or typically both. Gentle probing with a blunt sterile probe will detect the presence of an undermining ulcer and the presence of sinus tracts.

One classification system uses wound color as a marker of wound status:

Red wounds are usually the healthiest and need wound coverage for protection and to maintain moisture.

Yellow wounds indicate the presence of non-viable but moist tissue. Wounds need to be debrided to remove necrotic tissue and reduce the bacterial load. Frank infection does not need to be present to retard healing, simply an increased bacterial burden which overwhelms the wounds defenses.

Black wounds indicate dead, dehydrated tissue or eschar on the wound surface. The eschar needs to be removed to be able to assess the wound, prevent infection and promote healing.

Treatment:

The primary goal of treatment is to obtain wound closure. Treatment is multifaceted due to the complex nature of the wound. Relief of pressure on the ulcer is critical to the wound healing process. This endpoint often requires pressure relieving interventions. Total contact casting reapplied weekly is the optimum management of pressure off-loading. Treatment of any underlying ischemia is required. Distal vascular reconstruction may be required to restore pulsatile flow to the foot. When infection is present, appropriate aerobic and anaerobic antibiotic therapy is necessary. Adequate insulin availability to the wound is needed to stimulate healing. Also, blood sugar control is important for healing.

Debridement of all necrotic tissue and callous is also required. Debridement should be performed to bleeding tissue. Moist wound healing should then be initiated along with protection from external contamination. Nanocrystalline silver (Acticoat^TM) should improve healing by:

1. Decreasing bacteria
2. Decreasing inflammation
3. Providing a moist healing environment 

Treatment of Diabetic Ulcer

• Relief of pressure on the ulcer

• Correction of ischemia, if possible

• Debridement of necrotic tissue

• Control of bacterial burden and infection

• Maintain moist wound healing

• Adequate insulin therapy, control of blood glucose and increase anabolic activity

• Modulate excess inflammation

Evidence of Excessive Bacterial Content:

1. Increased wound drainage
2. Increase in very friable granulation tissue
3. Increasing pain, edema, peri-wound redness
4. Wound not healing despite appropriate optimum care

5. Experience with Acticoat^TM in treating Venous Stasis Ulcer

Definition & Etiology:

Venous stasis ulcer is a partial or full thickness wound on the lower extremities often over the malleolus caused by venous insufficiency, local stasis, edema and resulting ischemia. Venous ulcers occur when the superficial leg veins become dilated from inadequate valve function leading to stasis and venous hypertension.

There are several theories as to the etiology and the difficulty of healing:

1. Calf venous pump failure
2. Peri-capillary fibrin cuffs which impair oxygen diffusion to the wound
3. Macromolecules like fibrinogen leak into the dermis, due to venous hypertension, and trap Growth Factors and Matrix Proteins making them unavailable for the repair process.
4. Decrease in nutritive skin capillary blood flow
5. Combination of the above

Incidence:

Venous ulcers account for over 70% of chronic leg ulcers with the incidence increasing with age. The prevalence in the adult population either active or healed is about 1-2%.

Characteristics:

The classic presentation is an irregularly shaped wound with well defined borders surrounded by erythematous or hyper-pigmented skin. A yellow to white exudates is commonly observed. The lower leg is typically edematous. Varicosities are often present, and a dilated vein may be near the base of the ulcer. The surrounding skin change is known as lypodermatosclerosis. This process is caused by chronic changes in the soft tissue from edema and inflammation. The skin is often tender and can be mistaken for infection. 

Treatment:

The treatment goals for venous ulcers are first and foremost to decrease tissue edema with compression therapy, followed by healing of the ulcer, control of pain and prevention of recurrence, the latter by controlling edema. Local care to the ulcer includes optimizing the healing environment. Initiation of moist wound healing while minimizing infection risk, and environmental insults is the standard of care. Controlling excess inflammation and MMP would also be very advantageous for healing. As with any tissue ulcer, debridement of necrotic tissue along with control of exudates is necessary. A variety of hydrogels and alginates are used including a nanocrystalline silver alginate, in addition to the Acticoat^tm.

Case Study: