TMI - The Mayer Institute: Primer in Wound Preparation by Rogers

Primer in Wound Preparation by Rogers (26 Sep, 2011)

Current Concepts In Wound Bed Preparation

Volume 24 - Issue 8 - August 2011
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Author(s):

Lee C. Rogers, DPM

Proper preparation of the wound bed is essential to priming the wound for effective healing. Accordingly, this author discusses key principles from the literature and shares insights from his clinical experience in employing debridement and adjunctive modalities to help facilitate better wound healing and eventual wound closure.

Wound bed preparation is a term that describes making the wound ready for closure by advanced means. If the wound is not properly prepared, even the most expensive products or devices are unlikely to produce a positive outcome. One does not usually perform wound bed preparation in a single visit. There is more of a process to prepare the wound to be closed. In addition to the wound itself, one must ensure the patient is prepared for wound closure.

Podiatric physicians must manage infection, ensure adequate vascularity and remove external pressure from the wound.¹ One can confirm the patient’s vascular status via noninvasive testing since pedal pulses alone are not a good indicator of sufficient perfusion. If there is vascular impairment, podiatrists should consider an appropriate referral for an intervention to improve circulation.

In regard to infection, patients with diabetes do not often mount systemic responses to infection. Therefore, clinicians must rely upon local signs. Is there erythema, purulent drainage or odor present? As infection is purely a clinical diagnosis, a culture cannot determine if the wound is infected. Cultures can only help to discern which bacteria are pathogens in that infection. Uninfected wounds should not be cultured.

One can mitigate external pressure either by surgical intervention or by using devices such as a total contact cast or removable cast walker.²

Completing the above process and creating a good wound healing environment is considered the standard of practice in most communities. One monitors the wound over four weeks. If the wound area does not reduce by at least 50 percent in that time period, the wound is unlikely to heal in 12 weeks and one should employ advanced therapies.³ There are many advanced therapies, ranging from skin grafts and flaps to bioengineered tissues, but they all require the wound to be adequately prepared.

A Closer Look At Key Factors That Can Affect Wound Healing

Wound bed preparation consists of far more than just a debridement and, in some cases, may take weeks to accomplish. The goal is to optimize the wound in order to promote healing with advanced means and remove the barriers to healing. Let us first consider the inherent factors that are detrimental to wound healing like bacteria, senescent cells and hyperkeratotic tissue.

Bacteria. A wound is a break in the dermal envelope. It is usually contaminated by bacteria and may even have a biofilm present. Just because a wound is colonized does not mean that it is infected. If the wound becomes critically colonized with bacteria, an infection may develop. Researchers suggest that bacterial loads between 10⁵ and 10⁶ per gram of tissue in the wound bed may cause infection.⁴

However, more virulent organisms may cause infection at lower concentrations. Biofilm itself is detrimental to wound healing and will hinder the process, but infection causes tissue destruction. Biofilm is difficult to treat. At this time, only thorough debridement has proven to be a definitive treatment.

Senescent cells. Cellular dysfunction is common in diabetic foot ulcers and other chronic ulcers. Somatic cells can only divide 50 times before their DNA telomeres have shortened and they can no longer replicate full copies of the DNA. At that point, there should be apoptosis or programmed cell death.

In some diabetic wound healing models, researchers have shown that the apoptotic mechanism is impaired. They note that these old (senescent) cells continue to live in the wound but do not replicate or produce growth factors.⁵ The senescent cells impair the ability of the wound to heal.

Hyperkeratotic tissue. This hardened tissue forms along the wound periphery and its formation is accelerated by pressure, either direct forces or shearing forces. Bearing weight on the hardened tissue causes subdermal tissue trauma and hemorrhage. Hyperkeratotic tissue acts as a barrier to epithelialization. This tissue can also undermine and collect fluid and debris, thus increasing the risk for infection.

Using Debridement And Adjunctive Modalities To Prepare The Wound Bed

The main goal of preparing the wound bed is to provide a healing surface, which would accept a graft. While wound bed preparation involves debridement, this is more than just debridement. It also includes consideration of the aforementioned factors such as bacteria, cell senescence and hyperkeratotic tissue. Debridement removes devitalized or contaminated material from within or surrounding the wound. Selective debridement stimulates the repair process. There are various methods of debridement including surgical (scalpel), hydrosurgical (Versajet, Smith and Nephew), biosurgical (maggots), enzymatic or mechanical (wet to dry dressings).⁶

I have heard the axiom that debridement converts a chronic wound into an acute wound. However, acute and chronic are specifically terms that describe time. One cannot take a chronic wound that has been open for four months and convert it into an acute wound present for one day. However, I believe debridement can put an acute injury into a chronic wound, which may provide growth factors and speed healing.

For the purposes of wound bed preparation, surgical or hydrosurgical debridement is preferred. It can occur at the same time as grafting or precede grafting by up to a week. Use a scalpel to remove the wound margins, saucerizing the tissue, and then use a curette or hydroscalpel to debride the wound bed. The goal is to obtain a bleeding granular wound. If you are preparing a wound in the operating room for grafting, ensure that bleeding is under control prior to applying the graft in order to avoid a hematoma. Hematoma between the wound bed and the graft is a leading cause of graft failure. One should avoid electric cautery, if possible, and employ pressure, epinephrine or thrombin if needed

If the wound is not completely granular, one should consider using either platelet-derived growth factor (PDGF, Regranex, Healthpoint Biotherapeutics) or negative pressure wound therapy (NPWT, VAC therapy, KCI) to make the wound granular and level with the surrounding tissue. The VAC therapy works well in combination with debridement to prepare the wound for grafting. VAC therapy can also assist in managing wound exudate. If one uses VAC therapy in the OR setting, ensure that bleeding is under control before applying NPWT.

Armstrong and Lavery studied 162 patients as part of a 16-week randomized clinical trial.⁷ As part of the study, 77 patients received NPWT while 85 received standard moist wound care. They found that VAC therapy had a faster rate of developing granulation tissue in comparison to standard moist wound therapy.

When choosing a biomaterial, foam is more effective than gauze at producing granulation tissue. Foam also compresses and contracts better than gauze, enhancing the wound’s ability to contract. Employing a silver impregnated foam can help manage bioburden.

When performing wound bed preparation a week prior to applying bioengineered tissue, one should perform an adequate debridement, saucerize the margins and promote a good wound healing environment with regular dressing changes until applying the tissue.

The first photo on page 1 shows two wounds on the lateral surface of a foot that are fibrotic but uninfected. We performed debridement with a scalpel and curette, which uncovered a healthy bleeding base (see the second photo on page 1). The use of bioengineered tissue prepared the wound for grafting. This preparation occurred in a single stage. One can apply a silver dressing to the wound to manage bacterial load and prevent infection until the application of bioengineered tissue.

Often, the wound requires a maintenance debridement at the time of grafting and during subsequent applications. Cardinal and colleagues retrospectively analyzed the results from two controlled, prospective, randomized trials of topical wound treatments on 366 venous leg ulcers and 310 diabetic foot ulcers over 12 weeks.⁸ The study results suggest that frequent debridement of diabetic foot and venous leg ulcers may increase wound healing rates. Maintenance debridements usually involve removing any obvious debris, fibrosis or hyperkeratotic margins.

In some cases, the purpose of bioengineered tissue application might be to aid wound bed preparation because the cellular therapy provides the wound with multiple growth factors.

Case Study: When There Is An Ankle Wound With Exposed Tendon

A 71-year-old male with diabetes presents to the clinic with a small, painful, undermining wound on the anterior ankle with an exposed extensor digitorum longus tendon. The wound was caused by direct trauma from a water sprinkler head. The tendon was visibly moving in the wound when the patient dorsiflexed and plantarflexed the ankle. This is problematic because bacteria has access to the tendon and can spread to adjacent compartments. The moving tendon also prevents granulation tissue from adhering.

The patient went to the operating room for a wide debridement and I removed all undermining tissue. The patient was admitted to the hospital

We started the patient on a VAC Ulta, a new product by KCI that instills a fluid into the wound. In this case, I infused one-quarter strength Dakin’s solution for the anti-infective and anti-inflammatory properties. With the VAC Ulta, one can tightly control the infusion/suction rate. I set this to instill 50 mL of Dakin’s solution, hold for five minutes, then resume suction and repeat the process every two hours.

After three days, the wound appeared to improve but the tendon was still exposed. The patient went back to the OR, where we performed debridement with a Versajet. I placed Integra (Integra Life Sciences) on the wound and used traditional VAC therapy with the Granufoam Bridge Dressing as a bolster. The patient wore a total contact cast (TCC-EZ, MedEfficiency) to keep the tendon from moving under the graft. I changed the TCC-EZ and VAC therapy twice per week. After two weeks of treatment, the wound became granular and the tendon was covered.

The aforementioned process describes wound bed preparation. I debrided the margins with a scalpel and performed light debridement of the wound bed with a Versajet. A split thickness skin graft was harvested from the anterolateral ipsilateral thigh at a thickness of 0.020 inches. I meshed this at 1:1.5 ratio, placed it on the wound and stapled it in place. I used a Mepitel silicone dressing (Molnlycke) as an interface. I placed VAC therapy on the graft as a bolster dressing and set this to -125 mmHg continuous pressure for five days.

After VAC therapy removal, I covered the wound with Mepilex Ag (Molnlycke) at that point. The graft interstices healed in about 10 days. I covered the donor site with a Mepilex Border (Molnlycke) and changed it as needed. The wound healed uneventfully.

Final Words

Proper preparation of the wound bed is vital to graft or tissue success. Wound bed preparation is much more than just a debridement and takes into account factors that impede wound healing.

By creating a recipient wound bed that is well vascularized, free from infection and granular with even sloping margins, we can increase the chance of graft take and facilitate more reliable wound healing.

Dr. Rogers is the Associate Director of the Amputation Prevention Center at Valley Presbyterian Hospital in Los Angeles

1. Rogers LC, Bevilacqua NJ. Organized programs to reduce lower-extremity amputations. J Am Podiatr Med Assoc. 2010;100(2):101-104.
2. Armstrong DG, Boulton AJ. Pressure offloading and “advanced” wound healing: isn’t it finally time for an arranged marriage? Int J Low Extrem Wounds. 2004; 3(4):184-187.
3. Snyder RJ, Kirsner RS, Warriner RA, Lavery LA, Hanft JR, Sheehan P. Consensus recommendations on advancing the standard of care for treating neuropathic foot ulcers in patients with diabetes. Ostomy Wound Manage. 2010; 56(4 Suppl):S1-24.
4. Sen RK, Murthy N, Gill SS, Nagi ON. Bacterial load in tissues and its predictive value for infection in open fractures. J Orthop Surg. 2000; 8(2):1-5.
5. Rogers LC, Bevilacqua NJ, Armstrong DG. The use of marrow-derived stem cells to accelerate healing in chronic wounds. Int Wound J. 2008; 51(1):20-25.
6. Attinger CE, Bulan E, Blume PA. Surgical debridement: the key to successful wound healing and reconstruction. Clin Podiatr Med Surg. 2000; 17(4):599-630.
7. Armstrong DG, Lavery LA. Negative pressure wound therapy after partial diabetic foot amputation: a multicentre, randomised controlled trial. Lancet. 2005; 366:1704-1710.
8. Cardinal M, Eisenbud DE, Armstrong DG, et al. Serial surgical debridement: a retrospective study on clinical outcomes in chronic lower extremity wounds. Wound Rep Regen. 2009; 17(3):306-311.