WOUND HEALING: PRINCIPLES AND TECHNIQUES
April 28, 2005 Brian T Kunimoto, MD, FRCPC
INTRODUCTION Leg ulcers are very common. One Swedish study found that 4 to 5% of the population older than 80 sought help for ulcers. If one examines only active venous leg ulcers, the point prevalence ranges between 0.06 and 1%. This data probably underestimates the true prevalence of this disease since venous ulcers tend to be a recurrent problem over the years. One does not have to perform too many calculations to realize this is a very costly problem for patients and the health care system. It seems simple-minded to say that the first step in managing a leg ulcer is to make the diagnosis. I must emphasize the etiological approach to the management of leg ulcers. There are also some general principles in wound healing that are important to apply. Lastly, I will review the use of wound dressings. GENERAL PRINCIPLES Treat the whole patient Factors that affect the wound healing process: Systemic: A. Age B. Building blocks (anemia, hypoalbuminemia, carbohydrate metabolism, vitamins, trace metals). It is very important to treat these problems as they represent possible causes of non-healing in chronic wounds. C. Collagen disease (Ehlers-Danlos-rare) D. Drugs (prednisone >10mg/day) Routine blood work includes only a CBC/differential and an Prealbumin determination…..That’s all. At the Wound Healing Clinic, the Doppler Ankle-Brachial Index (ABI) and Systolic Toe Pressure are practically routine since many elderly patients have mixed disease. Routine bacterial swabs are to be discouraged (even abolished) (see later). Also do not underestimate the social / psychological implications of leg ulcers. There are many patients who find the resolution of their ulcers quite stressful. Their ulcer has, as a result of chronicity, become an integral part of life and it will be sometimes stressful to see it go. Do not overuse topical or systemic antibiotics I hope this is not a controversial statement. Unfortunately, many of us define an “infected” ulcer as one that has pathogenic bacteria growing on the surface. These contaminated and colonized wounds are not at all infected and the bacteria isolated have little or no effect on the wound healing process. The 3 Cs: “Contaminated”: Bacteria show no evidence of tissue invasion and are simply on the surface. No signs of clinical infection. No treatment. “Colonized” Histologically, bacteria have invaded normal tissue. No signs of clinical infection. No treatment necessary. Colonized wounds are divided into Simple and Complicated types. The simply colonized wounds have bacteria living in the tissues but are not detrimental to healing. Here, no treatment is required. In complicated colonization, the bacteria slow the healing process. Complicated colonization presents, clinically, with the following: New onset of wound pain
Wound Bed Deterioration such as the development of friable, dusky-coloured granulation tissue, loss of granulation tissue, and the appearance of a wound biofilm. Complicated colonization is managed by performing relentless debridement using an instrument such as a curette. Antimicrobial dressings such as Acticoat, Actisorb silver, Aquacel AG, or Iodosorb can be used as adjuncts. Topical or systemic antibiotics are of no value here. “Clinical infection” Bacteria are interfering with the wound healing process. Associated with clinical signs such as purulent drainage, surrounding swelling and spreading redness, loss of granulation tissue with replacement by yellow necrotic slough, cellulitis, severe pain, and occasionally systemic toxicity. Systemic antibiotic therapy is necessary. Avoid topical antibiotics. The only time to culture an ulcer is when you suspect there is clinical infection. The best culture technique involves a biopsy of the wound bed. If a swab is taken, it must be done properly. This means the wound is cleansed of debris using sterile saline. A culture swab is rubbed vigorously for 30 seconds being careful to sample well the edges of the ulcer. Do not sample the periulcer skin. If an anerobic infection is suspected, a tissue biopsy is needed transported in anerobic medium. Clinical infection is managed:
Type of Wound
Wound less than One Month (Think about gram positives) Wounds longer than One Month (Think about gram negatives and some anerobes)
Mild Infection Cellulitis < 2cm No systemic Toxicity Cephalexin 500mg PO QID for 2weeks
(Clindamycin 300mg PO TID if PCN allergic)
Severe Infection Cellulitis Extensive Systemic Toxicity Cloxacillin 2g IV Q6h for at least 2 weeks
(Clindamycin 600mg IV Q6h if PCN allergic)
Cephalexin 500mg PO QID plus Metronidazole 500mg PO BID for at least 2 weeks
(Cotrimoxazole if PCN allergic)
Clindamycin 600mg IV Q6h plus Ciprofloxacin 400mg IV Q12h for at least 2 weeks
(Avoid the use of Levofloxacin – not potent enough and may predispose to resistance)
Do not use antiseptics For the healable wound there is never a need to use such antiseptics such as: Sodium hypochlorite (Dakin’s solution) Would you drop household bleach in your eye? Povidone iodine (great for disinfecting the skin pre-op but no good for wounds) Acetic acid (traditional remedy for pseudomonas infection) Hydrogen peroxide (it just causes fizzing and leaves bacteria alone while killing fibroblasts. The fizzing indicates failure of the antiseptic!) Chlorhexidine (Hibitane) Tissue culture work has indicated these agents actually kill fibroblasts. Clinical studies show that wounds treated with these have lower tensile strength and are slower to heal. When you think about it there really is never an instance when one of these agents should be used instead of normal saline. Do not be afraid to debride If there is slough or eschar and you are not dealing with an ischemic ulcer, sharp debridement using a curette is indicated. Slough and eschar provide a haven for bacteria as a result of the foreign body effect and may be a potential source of later clinical infection. Also they constitute what is known as the “wound burden” which stands in the way of healing. Dying cells produce substances that slow proliferation. The eschar itself provides a physical barrier for keratinocytes
to migrate over the wound as they must try to burrow underneath and the dry environment is not conducive to epithelialization. Wound Biofilms inhibit and even stop healing completely. They need to be removed usually by physical means (curettage etc). If a wound biofilm is thought to exist, management includes relentless debridement and the use of antimicrobial dressings such as Acticoat, Actisorb silver, Aquacel AG, and Iodosorb. A good trick is to have the patient apply EMLA (Astra) for about 3 hours under occlusion prior to debridement.
ETIOLOGICAL APPROACH There are only a few causes of leg ulcers that would be considered to be common. The rest are quite uncommon and are seen only occasionally. Venous leg ulcers: 80% Arterial ulcers: 5-10% Neuropathic (diabetic): 5% Pressure ulcers: <5% Thus if you consider only venous, arterial, and diabetic ulcers, about 95% of all ulcers are covered. Less common ones include infections, pyoderma gangrenosum, vasculitis, and neoplasia (eg SCC or BCC). I have seen two BCCs referred to my clinic as venous leg ulcers! Venous leg ulcers Compress, compress, compress. If you do not compress a venous ulcer, it will not heal. Types of compression to consider include: Short stretch bandages: Comprilan (Beiersdorf-Jobst) Inexpensive, self-applied, washable, and is the best system to use in order to reduce edema. In this regard, it is better than long-stretch systems for initial reduction of edema. This may be tried for the first few weeks of therapy Long stretch bandages: Surepress (Convatec) Inexpensive, self-applied, washable. May be used for the entire treatment course to healing. The bandage has little indicators printed on them that facilitate the application of correct tension to obtain proper compression. Profore (Smith & Nephew) Relatively expensive bandage system that is able to achieve the highest compression pressures and is reported to be able to maintain them for longer times. Trained personnel must apply this. Cannot be used if the ABI is <0.8 Use Profore Lite if the ABI is less than 0.8 but more than 0.6 Duke Boot This is a combination of traditional zinc-oxide paste bandage and compression provided by Coban (3M). Like Profore, this may be left on for up to a week. Also, it cannot be used if the ABI is <0.6 Stockings: Elastic compression stockings may be used to treat small ulcers. They are most useful in the prevention of
recurrent ulceration. They are absolutely essential to wear after the ulcer has healed. Only knee high stockings are required. Request 30 – 40 mm Hg compression. Since they are not worn at night, they may be used in patients with mixed arterial / venous disease. Diabetic ulcers Ulcers that affect the foot in diabetics often have more than one cause. Neuropathy is the commonest cause and should be suspected when the ulcer has a prominent callus at the margin and the patient presents with numbness. Arterial insufficiency also occurs frequently in this group and should always be ruled out by requesting Systolic Toe Pressure measurements at the local vascular laboratory (if the pressure is less than 60 mm Hg, healing is doubtful without vascular reconstruction). Do not depend on an Ankle-Brachial Index as it is unreliable in diabetics due to calcification of the arteries. Treatment is simple for neuropathy. If the pressure overlying the ulcer is relieved, the ulcer will heal easily. This may require the assistance of your local podiatrist who may be able to redistribute pressures within the shoe away from the ulcer using padding. Sometimes, total contact casting is necessary. Be aware of the Charcot joint. This is the situation where neuropathy causes articular degeneration. Acutely, it may present with erythema, swelling, and some pain, resembling cellulitis, gout, or acute osteomyelitis. Even x-rays and later bone scans are unable to distinguish neuropathic arthropathy from osteomyelitis. Suspect diabetic Charcot joint destruction if the patient seems to complain of less pain than is expected when one looks at the x-ray films. Arterial ulcers Because of the age of most of the patients suffering from venous ulcers, combined disease is not uncommon. As compression therapy is indicated for these patients, arterial disease must be ruled out. I do not rely on clinical acumen alone as studies have shown that patients may have significant arterial disease without showing signs. It is important to get the patient evaluated by the local vascular laboratory with Ankle-Brachial Index and Systolic Toe Pressure determinations. If there is significant arterial compromise (ABI less than 0.6 or STP less than 60), do not hesitate to refer to the vascular surgeon for consultation early, not late after you have been beating the patient’s head against the wall for 3 months. DRESSINGS Believe it or not, the last thing to consider in wound management is the selection of a dressing. I will review different clinical situations and will suggest which class of dressing would be appropriate. Exudative (wet) ulcers: Consider xerodressings. These dressings dry the wound and are the most efficient at absorbing exudate. Examples of xerodressings include: Normal saline compresses Allevyn foam dressings (Smith & Nephew) Calcium alginates such as Kaltostat (Convatec) Mesalt (Sancella) Often xerodressings are required early in the treatment of venous leg ulcers as exudation may be quite prominent over the first month of compressive therapy. Xerodressings are especially good for infected ulcers as they provide no occlusive effect. The Calcium Alginates are very good for infected ulcers. Shallow ulcers with good granulation tissue and erosions: These ulcers have little depth and generally are not too exudative. Often the base of the wound is at or near the surrounding level of skin and reepithelialization is imminent. A good example of this kind of wound is the donor site of a split-thickness skin graft. Another example is the deeper ulcer that has now filled in with granulation tissue. Consider three classes of dressings: Hydrogels:
Intrasite gel (Smith & Nephew) DuoDERM hydroactive gel (Convatec) Aquacel (Convatec) Hydrogels must be changed daily and must not be used on infected wounds. They have a cooling effect which may relieve pain. Polyurethane Film Dressings: Op-site (Smith & Nephew) Tegaderm (3M) Biocclusive (J & J) These dressings may be left on for more than a few days or until the dressing develops a fluid bubble. They are not appropriate for infected, or heavily exudative wounds. Hydrocolloid Dressings: DuoDERM (Convatec) Comfeel Ulcus (Smith & Nephew) Restore (Hollister) These dressings are probably the most versatile wound coverings. They have the ability to absorb moderate amounts of exudate, autolytically debride slough, and provide the moist wound healing environment needed for healing the chronic wound. They cannot be used on infected ulcers and are contraindicated for diabetic wounds, and ischemic ulcers. Ulcers with poor granulation tissue These ulcers require a dressing that will stimulate granulation tissue. Hydrocolloid dressings do well in this regard. They create a relatively hypoxic wound environment at the wound surface resulting in a very strong stimulus for the formation of new blood vessels. These dressings work very well with the compression bandage systems mentioned above. Deep undermined ulcers These are usually pressure sores. Although Hydrogels are good for keeping the base of the wound clean and well hydrated, the treatment of choice for these ulcers is actually surgical. For especially deep undermined ulcers with large cavities, osteomyelitis must be investigated. Clinically Infected ulcers The infected ulcer should not be treated with any occlusive dressing such as a Hydrocolloid, or Polyurethane Film. Since Hydrogels can support bacterial growth, they should not be used as well. Xerodressings and Calcium Alginates are well suited for treating clinically infected ulcers. Remember that the first line of treatment of clinically infected ulcers is to use the appropriate systemic antibiotic.