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Debridement of cutaneous ulcers: Medical and surgical aspects

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Debridement of Cutaneous Ulcers: Medical and Surgical Aspects JOSEPH A. WITKOWSKI, MD LAWRENCE CHARLES PARISH, MD D ebridement may be defined as the removal of devitalized or contaminated tissue and for- eign material from or adjacent to a traumatic or infected lesion. Many types of debride- ment exist, as shown in Table 1. Devitalized or contaminated tissue found in an ulcer consists of fibrinous material, nucleoproteins, collagen, and elastin. This potpourri has been referred to as debris, slough, and necrotic tissue. The presence of such a gimish interferes with the normal healing process. It impairs the wounds defenses which encourages the development of infection. The devitalized tissue acts as a culture medium promoting bacterial growth and also inhibits leukocyte phagocytosis of bacteria and subsequent kill.’ In addition necrotic material acts as a physical barrier to repair. Ulcers of all types, for example, decubitus* and vascular3 and metabolic4 leg ulcers, represent defects that may contain debris. High levels of bacteria and clinical infection are fre- quently associated with the presence of necrotic tissue in an ulcer. Following debridement, the number of bacteria is decreased, permitting the infection, when present, to subside. Removal of necrotic material also decreases the bacterial load which allows the host’s defenses to be more effective. Debridement is an essential component in the therapy of infected ulcers. If necrotic material is not re- moved, infection may persist despite even the use of sys- temically administered antimicrobial agents. Because the avascular necrotic tissue is not penetrated by these agents, the bacteria present are protected from the effects of both systemically and topically applied antimicrobials. The physical effects of necrotic material in an ulcer From the Department of Dermatology, School ofMedicine, University of Pennsylvania; the Pennsylvania College of Podiatric Medicine; and the De- partment of Dermatology, Jefferson Medical College of the ThomasIefferson University, Philadelphia, Pennsylvania. Address correspondence to: Joseph A. Witkowski, MD, 3501 Ryan Ave- nue, Philadelphia, PA 19136. include mechanical obstruction to wound contraction and a barrier to reepithelialization. Wound contraction is an important component of ulcer healing. Myelofibrob- lasts present in or around the ulcer are responsible for this effect. By contracting, these cells decrease the size of the ulcer, thus reducing the volume of tissue necessary for repair of the defect. The presence of a hard eschar also interferes with this natural process. Any necrotic debris impedes epithelialization. Epithelial cells require a moist environment in which to migrate. When necrotic tissue covers the ulcer surface, these cells must burrow beneath such material to reach the other side of the ulcer. In these circumstances, more energy is expended and the entire healing process is delayed. In some instances, necrotic material is not removed from an ulcer. For example, the black eschar attached to underlying bone is not treated. As long as bacterial growth beneath it is minimized, it serves as a temporary biologic dressing. The dry eschar should be excised if it is separated from the surrounding skin. Debridement should also be performed if fluctuation develops beneath it, or if the surrounding skin is erythematous, indurated, or tender, or if the patient is septic. Another exception to the general principle of removing all devitalized tissue from an ulcer is the presence of nerves or tendons. These specialized tissues perform im- portant functions, regardless of their viability.5 If these tissues can be rendered surgically clean, they should be left in the ulcer as they act as free grafts without living cells. During the healing process, cells invade these struc- tures.’ Types of Debridement Debridement may be selective or nonselective. Selective debridement removes only nonviable tissue, whereas nonselective debridement removes both viable and non- viable tissue. Selective methods include partial surgical debridement; autolytic, osmotic, chemical, enzymatic, 0 1992 by Elsevier Science Publishing Co., Inc. l 0738-082x/92/$5.00 585
Transcript
Page 1: Debridement of cutaneous ulcers: Medical and surgical aspects

Debridement of Cutaneous Ulcers: Medical and Surgical Aspects JOSEPH A. WITKOWSKI, MD LAWRENCE CHARLES PARISH, MD

D ebridement may be defined as the removal of devitalized or contaminated tissue and for- eign material from or adjacent to a traumatic or infected lesion. Many types of debride-

ment exist, as shown in Table 1. Devitalized or contaminated tissue found in an ulcer

consists of fibrinous material, nucleoproteins, collagen, and elastin. This potpourri has been referred to as debris, slough, and necrotic tissue. The presence of such a gimish interferes with the normal healing process. It impairs the wounds defenses which encourages the development of infection. The devitalized tissue acts as a culture medium promoting bacterial growth and also inhibits leukocyte phagocytosis of bacteria and subsequent kill.’ In addition necrotic material acts as a physical barrier to repair. Ulcers of all types, for example, decubitus* and vascular3 and metabolic4 leg ulcers, represent defects that may contain debris.

High levels of bacteria and clinical infection are fre- quently associated with the presence of necrotic tissue in an ulcer. Following debridement, the number of bacteria is decreased, permitting the infection, when present, to subside. Removal of necrotic material also decreases the bacterial load which allows the host’s defenses to be more effective. Debridement is an essential component in the therapy of infected ulcers. If necrotic material is not re- moved, infection may persist despite even the use of sys- temically administered antimicrobial agents. Because the avascular necrotic tissue is not penetrated by these agents, the bacteria present are protected from the effects of both systemically and topically applied antimicrobials.

The physical effects of necrotic material in an ulcer

From the Department of Dermatology, School ofMedicine, University of Pennsylvania; the Pennsylvania College of Podiatric Medicine; and the De- partment of Dermatology, Jefferson Medical College of the ThomasIefferson University, Philadelphia, Pennsylvania.

Address correspondence to: Joseph A. Witkowski, MD, 3501 Ryan Ave- nue, Philadelphia, PA 19136.

include mechanical obstruction to wound contraction and a barrier to reepithelialization. Wound contraction is an important component of ulcer healing. Myelofibrob- lasts present in or around the ulcer are responsible for this effect. By contracting, these cells decrease the size of the ulcer, thus reducing the volume of tissue necessary for repair of the defect. The presence of a hard eschar also interferes with this natural process. Any necrotic debris impedes epithelialization. Epithelial cells require a moist environment in which to migrate. When necrotic tissue covers the ulcer surface, these cells must burrow beneath such material to reach the other side of the ulcer. In these circumstances, more energy is expended and the entire healing process is delayed.

In some instances, necrotic material is not removed from an ulcer. For example, the black eschar attached to underlying bone is not treated. As long as bacterial growth beneath it is minimized, it serves as a temporary biologic dressing. The dry eschar should be excised if it is separated from the surrounding skin. Debridement should also be performed if fluctuation develops beneath it, or if the surrounding skin is erythematous, indurated, or tender, or if the patient is septic.

Another exception to the general principle of removing all devitalized tissue from an ulcer is the presence of nerves or tendons. These specialized tissues perform im- portant functions, regardless of their viability.5 If these tissues can be rendered surgically clean, they should be left in the ulcer as they act as free grafts without living cells. During the healing process, cells invade these struc- tures.’

Types of Debridement

Debridement may be selective or nonselective. Selective debridement removes only nonviable tissue, whereas nonselective debridement removes both viable and non- viable tissue. Selective methods include partial surgical debridement; autolytic, osmotic, chemical, enzymatic,

0 1992 by Elsevier Science Publishing Co., Inc. l 0738-082x/92/$5.00 585

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586 WITKOWSKI AND PARISH

Table 1. Tuves of Debridement

Surgical Vaporization Mechanical Autolytic Osmotic Chemical Enzymatic Maggot therapy

and maggot debridement; and the use of a whirlpool or Hubbard tank. Nonselective methods include complete surgical debridement, mechanical abrasion, wet-to-dry dressings, and forceful irrigation.

As the amount of necrotic material decreases in an ulcer, the method of debridement must be changed from a nonselective to a more selective form. This is necessary to prevent removal of regenerating tissue, a process that would retard wound healing. All forms of debridement are discontinued when the ulcer is filled with healthy granulation tissue.

Surgical Debridement

Surgical debridement is defined as excision of devitalized tissue by sharp dissection. It may be total or partial. Total debridement implies removal of all devitalized tissue. The end result is a clean, healthy defect. A general anesthetic and use of an operating room are generally required. As bleeding may be extensive, provisions for establishing hemostasis and blood replacement are necessary. Tran- sient bacteremia also is often produced by total debride- ment, thus requiring the administration of systemic anti- biotics. The principal indication for total debridement is preparation of the ulcer for coverage with a graft or flap, where a sterile field is required. It is a nonselective form of debridement in that both necrotic and healthy tissue are often excised.

In contrast, partial surgical debridement implies exci- sion only of devitalized tissue. Only necrotic tissue is removed, with both pain and bleeding being minimized. Because the mild bleeding that occurs can be controlled by pressure or application of a hemostatic agent, this form of debridement is performed at the bedside. Adequate visualization of the ulcer is essential to prevent accidental hemorrhage. Forceps, scalpel, or scissors are used. The procedure is often repeated in a piecemeal fashion on several consecutive days to remove all of the necrotic material.

Partial surgical debridement is frequently used in con- junction with some other form of debridement. It is a selective form of debridement as no healthy tissue is sacri- ficed. Partial surgical debridement is indicated in the

treatment of infected ulcers, in the promotion of healing by secondary intention, and in the preparation of the ulcer bed for autologous punch grafting.6 For the latter procedure, a completely sterile field is not required,

Vaporization

Vaporization is considered a form of surgical debride- ment. It may be partial or complete. The carbon dioxide laser is used most often for this purpose. Necrotic tissue and protruding bone, including necrotic bone, can be re- moved with minimal blood loss. A field 0.5 mm in diame- ter is treated when focused and a l-mm field when defo- cused. The end result is a relatively aseptic, bloodless field.7 Newer-vintage pulsed lasers can accomplish de- bridement without heat damage to underlying tissues.*

Mechanical Debridement

This form of debridement includes both selective and nonselective methods. The selective forms include whirl- pool bath and Hubbard tank. The nonselective forms are forceful irrigations, mechanical abrasion, and wet-to-dry dressings.

Hydrodebridement, as provided by a whirlpool bath or Hubbard tank, can remove loosened necrotic debris relatively painlessly when set at low agitation levels. In addition to cleaning the ulcer, hydrotherapy appears to have concomitant psychologic benefits. It also helps to resolve the induration surrounding the ulcer. By washing away some of the bacteria on the ulcer surface, the pro- cess reduces the bacterial load, thus helping to resolve infection. The whirlpool bath or Hubbard tank is espe- cially useful in the treatment of patients with multiple ulcers. On the negative side, hydrotherapy requires extra personnel for transporting the patient to and from the physical therapy department and for placing the patient in the apparatus. Whether hydrotherapy offers an ad- vantage over manual debridement is also debatable.

Hydrodebridement can also be accomplished by use of high-pressure irrigation, power spray, or the Water Pit. These modalities have the potential for treatment of ulcers with widely undermined edges. Their effectiveness is based on mechanical removal of surface contaminants and not on any pharmacologic effect of the irrigating solution.

Wet-to-dry dressing debridement is useful only when small amounts of necrotic tissue require removal from the ulcer. Coarse gauze having a wide mesh is wet with nor- mal saline and loosely packed into the ulcer. To be eff ec- tive, all of the recesses of the ulcer should be in contact with the gauze. The ulcer is then covered with a nonoc- elusive gauze dressing. After 6 to 8 hours, the relatively

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DEBRIDEMENT OF CUTANEOUS ULCERS

Table 2. Moisture-Retentive Dressings

Polymers (Films) Hydrocolloids

Bioclusive Blister Film Ensure-It Oproflex Op-Site Tegaderm Thin Film Wound Dressing Uniflex

Bard Intact Comfeel Ulcus Dressing DuoDERM DuoDERM CGF J & J Ulcer Dressing Restore CX Ultec

dry packing is removed, carrying with it loosened necrotic tissue. Dressings are replaced every 6 to 8 hours until the ulcer is clean. This form of debridement also reduces the bacterial load. It is, however, often traumatic to granula- tion tissue and newly formed epithelium. This procedure should be discontinued when the ulcer is clean; otherwise it will interfere with the healing process. Such debride- ment can be used only on ulcers where the dressing is able to dry out. For example, the packing in a sacral ulcer on which the patient is lying or in an ischial ulcer on which the patient is sitting may never dry out sufficiently to be effective.

Because removal of the dry packing is usually asso- ciated with some discomfort, a wet-to-moist technique has been advocated. In this method the gauze is not per- mitted to become completely dry before removal. The wet-to-moist technique is less effective in debriding ne- crotic tissue.

Autolytic Debridement

Autolysis is defined as the spontaneous disintegration of tissues or cells by the action of their own autogenous enzymes or by the body’s own serum. It is a natural pro- cess that is potentiated by keeping the lesion moist. Al- though all dressings that keep an ulcer moist encourage autolytic debridement, moisture-retentive dressings such as films and hydrocolloids have proven to be most effec- tive (Table 2).

The precise mechanism of autolytic debridement is not known: tissue hydration, fibrinolysis, and enzymes present in the ulcer appear to play a prominent role (Table 3). With exposure to air, the base of an ulcer becomes dry. The tissue assumes a yellowish gray color and appears necrotic. Much of this tissue, however, can be revitalized by hydration in wound fluid. Moisture-retentive dress- ings salvage this tissue that might otherwise be destroyed by drying.

Of the many dressings available only one of the hy- drocolloid dressings, DuoDERM, has fibrinolytic activity. This has been demonstrated by the failure of a clot to

form on ulcers treated with DuoDERM9 and by the disso- lution of fibrin clots in both in vitro and in vivo experi- merits.‘‘’ This fibrinolytic activity aids in the removal of necrotic debris as a large component is fibrin.” Polymor- phonuclear leukocytes and macrophages present in ulcer fluid and bacteria supply the enzymes for the remaining component of autolytic debridement.

All of the moisture-retentive dressings are able to facili- tate accumulation of these cells on the surface of an ulcer. On their injury or death, leukocytes release lysosomal granules into the ulcer fluid. Enzymes derived from the granules are capable of degrading substrates such as pro- teins, mucopolysaccharides, glycoproteins, glycolipids, DNA, and RNA.12 Some of these enzymes are more active at an acid pH. Because wound fluid accumulating be- neath a hydrocolloid dressing is more acetic than that accumulating under a film dressing, greater activity might be expected with the hydrocolloids.13 Bacteria are found on the surface of ulcers until the final reepithelialization occurs, even in the absence of clinical infection.14 These organisms also contain enzymes as evidenced by the com- mercially available products for debridement derived from bacteria. It seems likely that the enzymes elaborated by these microorganisms also play a role in autolytic de- bridement of ulcers covered by moisture-retentive dress- ings.

Wound fluid is essential for autolysis. Water is neces- sary for the migration of leukocytes as well as for activa- tion of enzymes. Autolysis begins between 72 and 96 hours after occlusion. The amount of necrotic debris, the thickness of the eschar, and the size and location of the ulcer determine how long it will take for complete de- bridement. As necrotic tissue is cleaned away, the ulcer may increase in size and depth. This is an expected phe- nomenon and is not an adverse reaction. Although auto- lytic debridement takes longer than surgical debride- ment, it is generally both painless and selective.

The use of autolytic debridement is an appropriate choice for noninfected exudating ulcers with a small to moderate amount of necrotic debris. Thick eschars must be crosshatched with a scalpel to permit wound fluid to permeate the necrotic material. Because moisture-reten- tive dressings will not adhere to dermatitic skin, the skin surrounding the ulcer should be normal. The skin should also be free of grease and hair. After the ulcer is cleansed

Table 3. Autolytic Debridement: Mechanism ofAction

Tissue hydration Fibrinolysis Enzymes

Lysozomes Bacterial products

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588 WITKOWSKI AND PARISH

Table 4. Osmotic Debriding Agents

Karaya gum powder

Magnesium sulfate paste

Granulated sugar

Honey

Dextranomer beads

Graft copolymer starch

Hydrocolloid powders Calcium a&ate

with normal saline, the surrounding skin is blotted dry and then the moisture-retentive dressing is applied. Be- cause of the accumulation of wound fluid, dressings may require changing every 24 hours during the early phase of treatment. Film dressings may have to be changed more frequently because they do not control wound fluid. An alternative approach when using a film is to aspirate aseptically the wound fluid with a syringe and large-bore needle. Hydrocolloid dressings must be changed when wound fluid leaks from beneath the edge of the dressing or the dressing is displaced. In highly secreting ulcers, the concomitant use of a hydrocolloid powder or paste placed in the ulcer can prolong the life of the dressing.

When using moisture-retentive dressings on ulcers containing necrotic material, one must be alert to the pos- sibility of infection. A sudden increase in the amount of wound fluid, a change in odor or color of the exudate, periulcer erythema, induration or pain, and fever, being clinical indicators of infection, suggest the need for bacte- riologic studies. The use of a moisture-retentive dressing should then be temporarily suspended until the infection is cleared.

Osmotic Debridement

Karaya gum powder, magnesium sulfate paste, granu- lated sugar, and honey have been used to debride ulcers for many years (Table 4). These agents are considered effective for cleaning ulcers, even those that are dry and heavily contaminated. They are capable of debriding moderate to large amounts of necrotic debris. Infection is thought to be suppressed because moisture necessary for bacterial growth is decreased in the ulcer. The bacteria are sucked dry by osmosis. l5 The formation of good granula- tion tissue is enhanced by all of these agents possibly because of the extra flow of nutrients into the ulcer. Sugar and magnesium sulfate are thought to cause excessive granulation tissue formation, possibly because of their more powerful osmotic effect.16 Although no long-term studies are available to support these claims, personal experience with magnesium sulfate as an adjunctive method to partial surgical debridement has been most

salutary. Sugar and honey have caused candidal infection when diluted on the skin surface.”

After cleansing with normal saline, karaya gum powder or granulated sugar is loosely packed into the ulcer. Honey or magnesium sulfate paste (dried magne- sium sulfate 38.0%, phenol 0.5%, and anhydrous glyc- erol 61.5% [Lowthian P. 1986. Personal communication] is poured into the ulcer and spread over the base and sides to ensure that all surfaces are in contact with the prepara- tion. The ulcers are then covered with dry gauze dress- ings. Because magnesium sulfate paste can irritate normal skin, the ulcer is rimmed with zinc oxide paste before the dressing is applied. These osmotic agents must be re- newed every 8 hours to prevent overdilution by exudate.

Osmotic agents that have become available more re- cently include dextranomer beads, graft copolymer starch, hydrocolloid powders, pastes, and calcium algin- ate dressings. These preparations can be used only in exudating ulcers. They absorb exudate to form a gel that continues to absorb exudate, dead cells, and bacteria. The moist environment created liquefies small amounts of necrotic debris, thus cleansing and debriding the ulcer.i8

Dextranomer is used either in granular form or as a paste, graft copolymer starch is used as a gel, and hydro- colloid is used as a powder or paste. After cleansing with normal saline, at least a one-quarter-inch-thick layer of either preparation is placed on the ulcer bed. The ulcer is then covered with a dry dressing. Repeat applications are made every 8 hours or more frequently if the top dressing becomes moist. Dextranomer turns a grayish color when it is fully saturated. The spent material is removed by wiping with a moistened gauze pad or by lavaging with normal saline in a 50-mL syringe. This agent has been shown to be superior to Santyl and sugar.19

Calcium alginate is available as a nonwoven fibrous mat or as a short twisted rope. The mat is placed directly over the ulcer, whereas the rope may be loosely packed into the ulcer. Both preparations are kept in position with a gauze pad. Absorbed exudate transforms the fiber overlying the ulcer into a gel that is easily removed with saline. The frequency of dressing changes is determined by the amount of exudate produced by the ulcer. It should be changed when the overdressing becomes moist. Ini- tially a daily change may be necessary. Less frequent changes are required as the ulcer heals.

Chemical Debridement

Topically applied 5-fluorouracil has been effective in re- moving the black eschar when it is tightly adherent to the surrounding skin (Koelsch R. 198 1. Personal communica- tion). Five percent fluorouracil cream is applied liberally to the margins of the eschar. After it is rimmed with zinc

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Table 5. Enzymatic Debriding Agents

Name Enzume Form Substrate

Elase

Gram&x

Panafil Santyl

Travase

Fibrinolysin-desoxyribonuclease

Trysin

Papain Collagenase

Sutilains

Lyophilized powder/ointment

Aerosol

Ointment Ointment

Ointment

Fibrin and nuclear debris

Eschar and other necrotic material

Nonviable protein Native and denatured

collagen Necrotic tissue

oxide paste to protect the surrounding skin, the entire lesion is covered with an occlusive polyvinylidine film. Treatments are repeated every 8 hours. After 7 to 10 days, a clean separation usually occurs and the necrotic tissue can be excised.20

Enzymatic Debridement

Enzymatic debridement is defined as the removal of devi- talized tissue by application of a nontoxic and nonirritat- ing enzyme that is capable of lysing fibrin, denatured collagen, and elastin but does not destroy normal tissue.

A variety of enzyme preparations are available for this purpose (Table 5). All have been shown to be effective in degrading necrotic tissue, fibrinous accumulations, puru- lent exudate, and clotted blood in vitro; however, their ability to accomplish these goals in a clinical setting is controversial. Some of the enzyme formalations can irri- tate normal tissue; others may even cause systemic reac- tions. These preparations should be used only for short periods to minimize adverse reactions.

Because avascular material and enzymatic digestion products provide a medium for bacterial proliferation, the ulcer should be carefully monitored for clinical evidence of infection. Topical enzyme treatment of burns has been associated with the development of sepsis,21 but now in ulcer therapy, use of enzymes with closed dressing tech- nique increases the possibility of this complication. At best, the utility of these compounds is adjunctive and not essential for the management of ulcers.

Collagenase is derived from the formation of Clostrid- ium histolyticum. It degrades both denatured and unden- atured collagen. Because of the latter effect it is claimed that the preparation produces better debridement by act- ing on collagen fibers that anchor necrotic material to the base of the ulcer. Optimal activity occurs between pH 6.0 and 8.0. The enzyme is inactive above and below these levels and at a temperature above 56°C. It is also inacti- vated by detergents, including benzalkonium chloride, antiseptics (hexachlorophene, nitrofurazone, tincture of iodine), and heavy metals (thimerosal, silver nitrate, and aluminum acetate). Dermatitis of the periulcer skin which

occasionally occurs can be prevented by rimming the ulcer with zinc oxide paste.

The enzyme is applied once daily or more frequently if the dressing becomes soiled. Prior to application, the ulcer should be cleaned with hydrogen peroxide, sodium hypochlorite, or normal saline. A thick dry eschar must be cross hatched with a scalpel before application of the ointment for lysis to occur.

Good results were obtained in all of 10 patients in a double-blind study of dermal ulcers and decubitus ulcers.22

Combined fibrinolysin and desoxyribonuclease is derived from bovine plasmin (Fibrinolysin) and from bo- vine pancreatic desoxyribonuclease. Fibrinolysin de- grades fibrin in necrotic debris, whereas desoxyribonu- clease acts directly on DNA derived from dead tissue cells and leukocyte nuclei. It hydrolyzes the polymer into smaller units, thereby reducing the viscosity of exudates. The preparation is available as a lyophilized powder for solution and as an ointment. The powder is dissolved in saline and must be freshly prepared before use as most of the activity of the solution is lost in 24 hours even with refrigeration. The ointment is stable at room temperature. Dermatitis of the periulcer skin may occur in patients sensitive to mercury present as a preservative in the oint- ment formulation. Allergic reactions may also occur in patients sensitive to bovine products.

After the ulcer is cleansed, the ointment is applied and covered with petrolatum gauze or other nonadherent dressing. Following reconstitution with saline the solu- tion may be applied topically as a liquid, spray, or wet dressing. Dressing changes should be performed two or three times daily. The enzymes will not affect a thick dry eschar, which must be excised surgically.

The solution form of the enzymes was statistically sig- nificantly more effective in debridement and in enhanc- ing granulation tissue than saline in chronic venous stasis ulcersz3

Sutilains is elaborated by Bacillus subtilis. The enzyme is most effective within a pH range of 6.0 to 6.8 at body temperature. It is virtually inactive on viable tissue. In vitro, detergents such as benzalkonium chloride and an-

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tiseptics such as hexachlorophene, iodine, silver nitrate, and nitrofurazone may render the substrate indifferent to the action of the enzyme. Compounds containing metal- lic ions such as thimerosal interfere directly with enzyme activity to a slight degree. The ointment should be kept refrigerated because it is not stable at room temperature. Adverse reactions consist of mild transient pain, paresthe- sias, dermatitis, and bleeding. Pain and burning can be controlled by administration of a mild analgesic. Derma- titis can be prevented by rimming the ulcer with zinc oxide paste. Bleeding may require discontinuation of ther- apy. The refrigeration requirement is a great disadvan- tage in both the hospital and home setting.

After the ulcer is cleansed with saline, the ointment is applied over the necrotic tissue extending beyond the area to be debrided. The ulcer is covered with a moist dressing or a moisture-retentive dressing as a wet environ- ment is necessary for enzymatic activity. Crosshatching a dry eschar hastens the debridement with sutilains. Treat- ment should be repeated three to four times daily. The ulcer should be carefully monitored for possible infection when sutilains is used in conjunction with moisture-re- tentive dressings.

Effective results were obtained in 80% of patients in a double-blind study comparing sutilains with a placebo ointment. Burns responded quickly, decubitus ulcers re- quired longer treatment, and the response of peripheral vascular ulcers was less predictable.24

Papain is derived from the fruit, carica papaya. The enzyme digests only nonviable protein material. Papain is active over a wide pH range, 3 to 12. It is inactivated by salts of heavy metals and hydrogen peroxide. Urea is present in the formulation to exposed sulfhydryl groups, which activate papain, and to denature nonviable pro- tein. Chlorophyll-copper complex is included to reduce odor and to suppress inflammation. The papain (white) preparation does not contain the chlorophyll-copper complex.

After the ulcer is cleansed with saline, the ointment is applied directly to the necrotic material and the ulcer is covered with a dry gauze dressing. Applications are re- peated twice daily. A transient burning sensation occurs on application of the ointment in a small number of pa- tients. This can be alleviated by prior administration of a mild analgesic. Occasionally the ulcer fluid containing the enzyme causes irritation of the perilesional skin. More frequent dressing changes or rimming the ulcer with zinc oxide paste will control this problem. Rare skin sensitivity to the ointment occurs.

Uncontrolled clinical trials demonstrated efficacy in a variety of cutaneous ulcers.

Trypsin contains crystallized trypsin derived from an extract of ox pancreas. The enzyme has proteolytic activ-

ity. It is said to be effective over a wide pH range. Balsam of Peru is present in the formulation, allegedly for its stimulating effect on indolent ulcers and for its antibac- terial effect. The castor oil is included to reduce desicca- tion and to aid in pain reduction.

After it is cleansed with normal saline, the lesion is sprayed with the enzyme preparation. The treated site may be left open or covered with a wet dressing. Twice- daily applications are recommended.

No proven efficacy has been demonstrated and the preparation may cause contact dermatitis,

Maggot Debridement

Maggots have always been found in neglected wounds. If one’s initial repugnance is overcome and the maggots are permitted to remain in the wound, healthy granulation tissue and a clean ulcer will be produced. This observa- tion led to the use of maggots in the treatment of difficult surgical infections during the 1930s. Although more ag- gressive surgical debridement and antibiotic therapy have replaced maggot treatment, there may still be an occasional need for this alternative form of debridement when traditional treatment fails.

A variety of theories have been proposed to explain how maggots achieve their beneficial effects: (1) The pres- ence of maggots causes increased production of wound fluid, which washes the ulcer. (2) The continuous move- ment of the maggots mechanically stimulates the forma- tion of granulation tissue. (3) The maggots consume the necrotic material; bacteria are ingested and destroyed.25 (4) Larval secretions liquefy necrotic material,26 kill bacte- ria,27 and increase the alkalinity of the wound. (5) Allan- toin, ammonium ion, and calcium carbonate are se- creted into the wound.

Two hundred to six hundred maggots are placed in the ulcer. To localize the organisms, restrictive dressings are placed around the wound. After 3 to 4 days the maggots are removed and destroyed, and the treatment is repeated if necessary. Mild sedation or an antipruritic agent may be necessary to alleviate the intense pruritus caused by mag- gots crawling on normal skin.29

Conclusion

Removal of necrotic material is an essential component of ulcer therapy. This can be accomplished by a variety of methods. Some forms of debridement are selective wher- eas others are nonselective; some are painful whereas others are painless. The choice is determined by the pres- ence of infection, the amount of necrotic debris, the pres- ence of wound fluid, the condition of the periulcer skin, and the goal of therapy.

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Drug Names

dextronomer: Debrisan

graft copolymer starch: Bard Absorptive Dressing

hydrocolloid powders: ComFeel Ulcus Powder, Duo- DERM Granules

hydrocolloid pastes: ComFeel Paste, DuoDERM Paste

calcium alginate pads: Kaltostat, Sorbsan

calcium alginate rope: Kaltostat

polyvinylidine film: Saran Wrap

5% 5-fluorouracil cream: 5% Efudex Cream

collagenase: Santyl, Biozyme-C

fibrinolysin - desoxyribonuclease: Elase

sutilains: Travase

papain: Panafil

trypsin: Granulex

References

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

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