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From the New NursingCenter

 

Options for Nonsurgical Debridement of Necrotic Wounds
Advances in Skin & Wound Care: The Journal for Prevention and Healing
March/April 2001 
Volume 14 Number 2
Page 96

Anu Singhal, BA , Ernane D. Reis, MD , Morris D. Kerstein, MD

PURPOSE
To offer an educational experience that will help to improve the participant's understanding of the various types of nonsurgical debridement.
 
TARGET AUDIENCE
This CME/CE activity is intended for physicians and nurses with an interest in the prevention, diagnosis, and treatment of chronic wounds.
 
LEARNING OBJECTIVES
At the conclusion of this activity, participants should be able to:
  1. Describe the role of debridement in wound healing.
  2. Identify the different types of nonsurgical debridement.
  3. Summarize the benefits and limitations of the different types of nonsurgical debridement.
  4. Identify wounds that should not be debrided.

The authors thank Gae O. Decker-Garrad for editorial assistance. Submitted November 16, 2000; accepted December 20, 2000.
ADV SKIN WOUND CARE 2001;14:96-103

Debridement is the removal of necrotic tissue, exudate, and metabolic waste from a wound. Accumulation of necrotic tissue results from a poor blood supply at the wound site or from increased interstitial pressure, a typical scenario in patients with pressure ulcers. Exudate usually results from infection. Staphylococcus aureus, for example, is known to produce a fibrin-rich biofilm that is resistant to the body's natural immune response to foreign bodies.1

The decision to debride a patient's wound represents an opportunity to improve the healing process. Despite scarce objective data, numerous agents and different types of interventions are used to remove debris from chronic wounds. Debridement may also be required to prepare the wound bed prior to application of some of the new biomaterials used to treat chronic wounds, such as cultured keratinocytes2 and a bioengineered human skin equivalent.3 As these modalities are used more extensively in clinical practice, selecting the appropriate debridement option will become more critical.

Several types of debridement are available, including mechanical, chemical, and autolytic.4 No standard protocol can be applied to all patients, however. Optimal wound management requires the selection of treatment options according to wound and patient characteristics and resources. This article will highlight the options available for nonsurgical wound debridement.

Role of Debridement

Debridement plays an essential role in the wound healing process. It reduces the bio-burden of the wound; controls and potentially prevents wound infection, especially in deteriorating wounds; and allows the practitioner to visualize the wound walls and base to assess viable tissue. If necrotic tissue is not removed, it not only can impede wound healing, but it can also result in protein loss (through large open wounds), osteomyelitis, generalized infection, septicemia, limb amputation, or even death.5

In an otherwise healthy person, the body's natural defenses will keep a wound debrided. Natural debridement, however, cannot keep pace with the accumulation of necrotic tissue in certain patients, such as those who are malnourished or have comorbidities, or in certain types of wounds, such as pressure ulcers. In those cases, the practitioner must intervene to prevent impaired wound healing.

Necrotic tissue (also called devitalized or dead tissue) has a characteristic moist, yellow, green, or gray appearance, although it may become thick, leathery black eschar if the wound dehydrates. Wound healing is impaired in the presence of necrotic tissue due to a lack of oxygen and nutrients. The accumulated dead tissue can also serve as a breeding ground for bacteria, and it may mask underlying buildup of fluid or abscesses.

Removing the necrotic tissue will restore circulation at the wound site. Adequate oxygen delivery to the wound is critical to healing. Wounds at sites of rich blood supply, such as the scalp, heal faster and are less prone to infection.6,7 Oxygen is required for energy-dependent metabolic processes, production of free radicals that kill bacteria, and proliferation of cells, such as fibroblasts and epithelial cells, which are crucial for wound healing.8-11 Bacterial overgrowth under hypoxic conditions may compete with the healing tissue for nutrients and produce exotoxins and endotoxins that could damage newly generated and mature cells.12

Contraction, initiated by migration of fibroblasts into the extracellular matrix, is a fundamental step in wound healing. Fibrils of collagen produced by fibroblasts are arranged as a mesh, laying the foundation for cells to grow and cover the wound.13 Although debridement is required for healing, it may destroy the framework necessary for healing if too much tissue is debrided.

When used appropriately, debridement encourages wound healing and avoids the potential problem of harming the wound. The following section discusses the various options for debridement.

(See Biodebridement Options )

Biodebridement Options

Sterile maggots are known to produce substances with antimicrobial properties. Some practitioners have applied the larvae of the blowfly (Phaenicia sericata) over necrotic and nonhealing wounds as a form of debridement therapy. Several reports on such treatment have supported its efficacy.1,2 Other laboratory experiments and clinical observation, however, indicate that larvae may not survive well in wounds containing residue of some hydrogel dressings.3

In addition, a mixture of endopeptidases and exopeptidases obtained from the digestive system of the Antarctic krill (a shrimp; Euphausia superba) has been shown to accomplish rapid breakdown of necrotic debris, fibrin, or blood crusts in vitro.4 No human studies have been reported to date.

Types of Debridement

Mechanical Debridement

Methods of mechanical debridement include the use of wet-to-dry dressings, whirlpool, and wound irrigation (pulsed lavage). Mechanical debridement, however, does not always discriminate between viable and nonviable tissue; newly formed epithelium can also be removed by these methods.14

Covering a wound with a moist gauze that dries and picks up debris when removed (wet-to-dry dressing) can be used to clean superficial debris from the wound.4,15 To apply a wet-to-dry dressing, follow these steps16:

  • Moisten the gauze with normal saline or another solution, then wring it out until it is slightly damp.
  • Fluff the gauze and apply it over the wound bed.
  • Remove the dressing when it is almost dry. The debris will adhere to the gauze when it is removed.

Because this method of mechanical debridement is nonselective and may be painful for the patient, it is not often used. Practitioners may instead use whirlpool or pulsed lavage. Whirlpool may be contraindicated in some patients, such as those who are incontinent, febrile, or have venous insufficiency.17 In addition, whirlpool may cause periwound maceration and increase the risk of cross-contamination.

Pulsed lavage allows practitioners to cleanse and debride a wound at variable irrigation pressures (pounds per square inch) according to the patient's condition.18 The pulsatile action may improve granulation tissue growth through effective debridement of the wound bed.17 Pulsed lavage treatment takes 15 to 30 minutes. Twice daily treatments should be considered if the wound has more than 50% necrotic tissue.17

Sharp debridement is sometimes considered a method of mechanical debridement. Surgical instruments (scalpel, forceps, scissors, or laser) are used to cut away dead tissue. Sharp debridement is imprecise, so viable tissue may also be cut away.5 It is usually indicated for urgent situationscellulitis and sepsisor for preparing the wound bed for flap reconstruction.4 Generally, sharp debridement is done only by physicians or other practitioners whose state licensing regulations (and institutional policies) allow them to perform the procedure.5

Chemical Debridement

Chemical debridement involves the topical use of enzymatic gels and solutions that can dissolve necrotic tissue from the wound. Various types of enzymes target specific components of dead tissue, such as fibrin and collagen.19 Enzymes that act on necrotic tissue are categorized as proteolytics, fibrinolytics, and collagenases. Given that these enzymes do not distinguish between viable and nonviable tissue, their application should be limited to the area of necrosis or slough.19

Chemical debridement is regarded as safe and effective, although the practitioner should keep in mind that the use of proteases as debriding agents has been associated with instances of bacteremia in burn patients.19 In general, chemical debridement is an ideal option for patients who cannot tolerate surgery or who are in long-term-care facilities where surgery is not an option. However, chemical debridement should not be used in place of surgical or mechanical debridement if the latter are indicated.4,14

Before the enzymatic agent is applied, the wound should be cleansed or flushed with normal saline solution. Eschar should be crosshatched to allow the enzymatic agent to penetrate to the necrotic tissue below the eschar.5 A topical antibiotic may have to be applied to prevent infection once the necrotic tissue separates from live tissue; check the package insert for the manufacturer's recommendation.5 The wound should be covered with a dressing after the enzymatic agent is applied to keep the wound moist and allow the enzymatic agent to work.5

(See Clinical Studies )

Clinical Studies

Literature on the use of chemical debriding agents is sparse. The following is a summary of the few studies that have been done.

A recent study used a literature-based computer model for decision analysis to compare 4 debridement alternatives for the management of a pressure ulcer.1 The chance of a clean wound at 2 weeks was estimated at 70% for collagenase, 57% for fibrinolysin, 50% for autolysis, and 30% for wet-to-dry dressings. Collagenase treatment was also associated with the lowest cost. These results, however, have not been validated through a randomized, prospective study.

In another study of collagenase, a 70% reduction in the area of necrotic tissue was noted after 1 week of topical application of collagenase.2 The proteolytic combination of fibrinolysin and DNase was reported to have reduced the relative area of the wound to 56%.2

Fibrinolysin/DNase was tested in a double-blind, randomized, prospective study of 84 patients with chronic ulcers of the lower extremity. No long-term clinical benefit was noted when compared with a placebo ointment.3

In another study, a papain/urea combination was more effective in reducing necrotic tissue than collagenase.4 The overall response to papain/urea was 4.1 times greater than to collagenase.

A double-blind, controlled trial showed that using a hydrogel dressing alone was as cost-effective as using a hydrogel dressing and streptokinase/streptodornase to treat Stage IV pressure ulcers.5 In a small, single-blind study, a solution of streptokinase/streptodornase in saline was slightly more effective than saline alone in cleansing leg ulcers.6 In a single-blind, randomized trial of 28 patients with pressure ulcers, streptokinase/streptodornase was slightly less effective in removing necrotic tissue than zinc oxide (43% vs 50%).7

The enzymatic agents used for chemical debridement are capable of producing chemical disruptions in the structure of proteins. Typically used products include the following:

  • Collagenase. Collagenase breaks down collagen, a major and rigid component of devitalized tissue. Collagen provides the framework to hold necrotic cells to the soft tissue bed. Therefore, when collagen dissolves, necrotic tissue detaches and granulation can occur, providing the surface needed for proper epithelialization. Collagenase is manufactured as a hydrophobic ointment containing the bacteria collagenase, Clostridiopeptidase A, and other proteases, all derived from cultures of Clostridium histolyticum. 20 The ointment is active in a pH range of 6 to 8.14 In the United States, the collagenase ointment SANTYL (Smith & Nephew, Inc, Largo, FL) is commonly used in practice. In other parts of the world, the product is known as Iruxol or Novuxol.
  • Papain/urea combination. Papain is a proteolytic enzyme and urea is a chemical that denatures nonviable protein.14 Denaturing by urea renders proteins more susceptible to the enzymatic action of papain. This hydrophilic, nonenzymatic agentavailable commercially as Accuzyme (Healthpoint, Ltd, Fort Worth, TX)is derived from papaya and is active in a pH range of 3 to 12.14
  • Fibrinolysin. The proteolytic enzyme fibrinolysin targets fibrin. Fibrin-degradation products stimulate macrophages to release growth factors into the wound bed.21 Derived from bovine plasma, fibrinolysin is usually prepared in combination with deoxyribonuclease (DNase) and is applied twice daily. Using a fibrinolysin/DNase debridement product, however, may impair healing because the enzymes digest fibrinan early matrix protein essential for wound healing. In addition, DNase digests DNA, another necessary intracellular component of dividing fibroblasts needed for healing. One of the fibrinolysin/DNase products used in practice is Elase (Jouveinal, France); it is no longer available commercially in the United States.
  • Streptokinase/streptodornase. A proteolytic preparation, streptokinase/streptodornase also is no longer available in the United States. It is, however, still marketed outside of this country as Varidase (Wyeth, Princeton, NJ).22 Streptokinaseused commonly for hydrolyzing blood clotsis fibrinolytic and activates the transformation of inactive plasminogen into the active enzyme plasmin. Streptodornase liquefies a major constituent protein of pus called deoxyribonucleoprotein23; however, this enzyme combination does not break down collagen, which is abundant in necrotic tissue.

Autolytic Debridement

Autolytic debridement promotes detachment of necrotic tissue in a wound by the action of endogenous enzymes. Moisture is essential for autolytic debridement: In a moist environment, phagocytic cells and proteolytic enzymes in a wound clear the dead tissue by liquefaction.14,19 Macrophages can then digest this soluble tissue.

Topical dressings are used to encourage autolytic debridement. Hydrogel and hydrocolloid dressings, for example, promote autolysis of necrotic tissue by hyperhydration. However, care must be taken in using these dressings; maceration of surrounding skin is a possible adverse effect.12 In addition, dead space in a deep wound should be loosely filled with dressing materials to prevent walling off an area that could become an abscess.5

The following dressings are commonly used for autolytic debridement:

  • Hydrocolloids. These dressingsavailable as wafers, powders, and pastesare composed of gelatin, pectin, and carboxymethylcellulose.24 Hydrocolloids are usually impermeable to oxygen, water, and water vapor.19,24 These dressings are changed approximately every 3 days.19
  • Hydrogels. Available as sheets or gels,24 hydrogels are water-based dressings.24 They are cross-linked polymer dressings that maintain humidity in the wound while absorbing excessive moisture.12,19 They have the ability to cool the wound by 5F, which provides a soothing effect on the wound surface.19,24 However, hydrogels must be changed frequently and can cause maceration.
  • Foam dressings. These sheets and fillers are made from hydrophilic polyurethane foam, a sponge-like polymer.19,24 They are used on wounds with moderate to heavy exudate. Foam dressings create a moist environment and provide thermal insulation to the wound. Their occlusive properties promote autolysis of the wound.24 These dressings are changed every 3 to 7 days.
  • Alginates. Available as pads, ropes, and ribbons, alginates are natural derivatives of seaweed, composed of polysaccharide nonwoven fibers.19,24 Their principle ingredient is alginic acid.19 These dressings are usually applied when the wound has moderate to heavy exudate: They are capable of absorbing up to 20 times their weight in exudate, forming a gel as they absorb the exudate.19 Alginates have hemostatic properties and may result in a brownish-green viscous residue in the wound bed.12 One distinctive feature of alginates is that, unlike woven and nonwoven gauzes, they do not inhibit wound contraction.24 Alginates are changed every 12 hours to 3 days, depending on the amount of exudate.
  • Transparent film dressings. These dressings can be used on superficial wounds with limited production of exudate; they are not appropriate over cavities.5,12 Transparent films have an adhesive membrane and are waterproof. They provide a barrier to bacterial contamination and are permeable to water vapor and oxygen.24 This type of dressing is also used as a secondary dressing for nonadhesive alginates, gauzes, and foams. Transparent films are changed every 3 to 7 days.

    (See Patient Parameters )

Patient Parameters

Before debridement is considered, a complete history and physical examination should be done, including current medications and psychosocial and smoking history. The etiology and history of the wound should be determined, along with previous regimens and plans of care.

Patient values should also be considered before determining whether to debride. Some patients may be distressed by the thought of losing body tissue, even if the tissue is necrotic and should be removed. Patients also may choose to avoid the discomfort associated with sharp debridement. Clinicians must honor patients' wishes and goals.

Conclusion

The presence of necrotic tissue in a wound has known deleterious effects, including sepsis and delayed healing. Debridement is, therefore, an essential adjunct in treatment of nonhealing wounds, pressure ulcers, and acute wounds containing foreign material or devascularized areas. Sharp debridement remains the fastest and most effective means of removing necrotic tissue, although it may not be appropriate for all patients or in all health care settings. Nonsurgical methods of debridement can be used instead. A number of products appear promising in accelerating wound healing by gentle and selective chemical or autolytic debridement; however, most of these products have not yet been subjected to sufficient clinical evaluation.

A fine line exists between beneficial and harmful debridement. The types of debridement discussed in this article can be used in combination, according to changes in the patient's wound and the practitioner's clinical judgment, to augment wound repair. Sound treatment decisions, dedicated health care providers, and a compliant patient remain the ideal combination for optimal healing. Attention to the patient's general condition and use of the appropriate form of debridement for the situation cannot be overemphasized.

(See When not to debride )

When Not To Debride

Not all ulcers require debridement. It may be advantageous to leave eschar in place rather than to remove it and create an open wound. For example, eschar on stable heel ulcers may be left in place.1 Stable means that (1) eschar is firmly adherent to the surrounding tissue, (2) there is no inflammation, (3) there is no drainage from beneath the eschar, and (4) eschar does not feel soft or boggy on palpation. A stable heel ulcer may not progress and may even heal, depending on the patient's arterial blood supply. A heel ulcer that has drainage from beneath the eschar, has soft tissue inflammation surrounding the ulcer, or feels soft and boggy on palpation should be debrided.

Arterial insufficiency may be a contraindication to sharp debridement. If there is decreased arterial flow, there may not be enough blood to heal the wound created by debridement.

Anu Singhal, BA, is a medical student at The Mount Sinai School of Medicine, New York, NY

Ernane D. Reis, MD is an assistant Professor in the Department of Surgery at The Mount Sinai Medical Center, New York, NY

Morris D. Kerstein, MD is a professor and vice-chairman in the Department of Surgery at The Mount Sinai Medical Center, New York, NY

The authors have disclosed that they have no significant relationships with or financial interests in any commercial companies that pertain to this educational activity.

References

  1. Nemoto K, Hirota K, Ono T, et al. Effect of Varidase (streptokinase) on biofilm formed by Staphylococcus aureus. Chemotherapy 2000;46:111-5.
  2. Horch RE, Bannasch H, Kopp J, Anree C, Stark GB.Single-cell suspensions of cultured human keratinocytes in fibrin-glue reconstitute the epidermis. Cell Transplant 1998;7:309-17.
  3. Eaglstein WH, Falanga V. Chronic wounds. Wound healing. Surg Clin North Am 1997;77:689-98.
  4. Cervo FA, Cruz AC, Posillico JA. Pressure ulcers. Analysis of guidelines for treatment and management. Geriatrics 2000;55(3):55-60.
  5. Sieggreen MY, Maklebust J. Debridement: choices and challenges. Adv Wound Care 1997;10(2):32-71.
  6. Carlson EV, Kemp MG, Shott S. Predicting the risk of pressure ulcers in critically ill patients. Am J Crit Care 1999;8:262-9.
  7. Hunt TK, Hopf HW. Wound healing and wound infection, what surgeons and anesthesiologists can do. Surg Clin North Am 1997;77:587-604.
  8. Lawrence WT. Clinical management of nonhealing wounds. In: Cohen IK, Diegelmann FR, Lindblad WJ, editors. Wound Healing Biochemical & Clinical Aspects. Philadelphia, PA: WB Saunders Co; 1992:541-61.
  9. Hunt TK, Hussain Z. Wound microenvironment. In: Cohen IK, Diegelmann FR, Lindblad WJ, eds. Wound Healing Biochemical & Clinical Aspects. Philadelphia, PA: WB Saunders Co; 1992:274-81.
  10. Erlichman RJ, Seckel BR, Bryan DJ, Moschella CJ. Common complications of wound healing. Prevention and management. Surg Clin North Am 1991;71:1323-51.
  11. Forsling E. Comparison of saline and streptokinase-streptodornase in the treatment of leg ulcers. Eur J Clin Pharmacol 1988;33:637-8.
  12. Degreef HJ. How to heal a wound fast. Dermatologic therapy. Dermatol Clin North Am 1998;16:365-74.
  13. Miller EJ, Gay S. Collagen stricture and function. In: Cohen IK, Diegelmann RF, Lindblad WJ, editors. Wound Healing: Biochemical and Clinical Aspects. Philadelphia, PA: WB Saunders Co; 1992:130-51.
  14. Alvarez OM, Fernandez-Obregon A, Rogers RS, Bergamo L, Masso J, Black M. Chemical debridement of pressure ulcers: a prospective, randomized comparative trial of collagenase and papain/urea formulations. Wounds 2000;12(2):15-25.
  15. Mosher BA, Cuddigan J, Thomas DR, Boudreau DM. Outcomes of 4 methods of debridement using a decision analysis methodology. Adv Wound Care 1999;12:81-8.
  16. Hess CT. Clinical Guide: Wound Care. Springhouse, PA: Springhouse Corporation; 2000. p 42-3.
  17. Loehne HB. Pulsatile lavage with concurrent suction. In: Sussman C, Bates-Jensen BM, editors. Wound Care: A Collaborative Practice Manual for Physical Therapists and Nurses. Gaithersburg, MD: Aspen Publishers, Inc; 1998. p 389-403.
  18. Scott RG, Loehne HB. 5 questionsand answersabout pulsed lavage. Adv Skin Wound Care 2000;13:133-4.
  19. Maklebust J. Using wound care products to promote a healing environment. Crit Care Nurs Clin North Am 1996;8:141-58.
  20. Mekkes JR, Zeegelaar JE, Westerhof W. Quantitative and objective evaluation of wound debriding properties of collagenase and fibrinolysin/desoxyribonuclease in a necrotic ulcer animal model. Arch Dermatol Res 1998;290:152-7.
  21. Tallon RW. Wound care dressings. Nurs Manage 1996;27(10):68-70.
  22. Persson M, Bilgrav K, Jensen L, Gottrup F. Enzymatic wound cleaning and absorbable sutures. An experimental study on Varidase and Dexon sutures. Eur Surg Res 1986;18:122-8.
  23. Baxter CR. Immunologic reactions in chronic wounds. Am J Surg 1994;167(1A):12S-14S.
  24. Krasner D. Dressing decisions for the twenty-first century: on the cusp of a paradigm shift. In: Krasner D, Kane D, editors. Chronic Wound Care. 2nd ed. Wayne, PA: Health Management Publications; 1997:139-51

References WhenNot To Debride

1. Bergstrom N, Bennett MA, Carlson CE, et al. Treatment of Pressure Ulcers. Clinical Practice Guideline, No. 15. AHCPR Publication No. 95-0652. Rockville, MD: Agency for Health Care Policy and Research; December 1994.

From Sieggreen MY, Maklebust J. Debridement: choices and challenges. Adv Wound Care 1997;10(2):32-7.

References Patient Parameters

From Sieggreen MY, Maklebust J. Debridement: choices and challenges. Adv Wound Care 1997;10(2):32-7.

References Clinical Studies

1. Mosher BA, Cuddigan J, Thomas DR, Boudreau DM. Outcomes of 4 methods of debridement using a decision analysis methodology. Adv Wound Care 1999;12:81-8.

2. Mekkes JR, Zeegelaar JE, Westerhof W. Quantitative and objective evaluation of wound debriding properties of collagenase and fibrinolysin/desoxyribonuclease in a necrotic ulcer animal model. Arch Dermatol Res 1998;290:152-7.

3. Falabella AF, Carson P, Eaglstein WH, Falanga V. The safety and efficacy of a proteolytic ointment in the treatment of chronic ulcers of the lower extremity. J Am Acad Dermatol 1998;39(5 Pt 1):737-40.

4. Alvarez OM, Fernandez-Obregon A, Rogers RS, Bergamo L, Masso J, Black M. Chemical debridement of pressure ulcers: a prospective, randomized comparative trial of collagenase and papain/urea formulations. Wounds 2000;12(2):15-25.

5. Martin SJ, Corrado OJ, Kay EA. Enzymatic debridement for necrotic wounds. J Wound Care 1996;5:310-1.

6. Forsling E. Comparison of saline and streptokinase-streptodornase in the treatment of leg ulcers. Eur J Clin Pharmacol 1988;33:637-8.

7. Agren MS, Stromberg HE. Topical treatment of pressure ulcers. A randomized comparative trial of Varidase and zinc oxide. Scand J Plast Reconstr Surg 1985;19:97-100.

References Biodebridement Options

1. Thomas S, Andrews A, Jones M. The use of larval therapy in wound management. J Wound Care 1998;7:521-4.

2. Namias N, Varela JE, Varas RP, Quintana O, Ward CG. Biodebridement: a case report of maggot therapy for limb salvage after fourth-degree burns. J Burn Care Rehabil 2000;21:254-7.

3. Thomas S, Andrews A. The effect of hydrogel dressings on maggot development. J Wound Care 1999;8:75-7.

4. Hellgren L, Mohr V, Vincent J. Proteases of Antarctic krilla new system for effective enzymatic debridement of necrotic ulcerations. Experientia 1986;42:403-4.