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380
C. Faure-Chazelles and S. Meaume
Their hemostatic capacity is also an interesting property [8]. In order to facilitate the removal of the dressing, saline or water may be used (Fig. 59.3). Alginates are contraindicated over dry wounds or during the epidermization stage. Sequential use of alginates during the debride­ment stage is recommended by numerous guide­lines [9].
59.2.3.2 Fiber Dressings
Hydrober technology was introduced in 1999 when launching the rst unwoven dressing com­posed of sodium CMC (Aquacel), a vertical and horizontal matrix containing regenerated cellu­lose. Other ber dressings containing CMC are now available and even other polymer-like poly­vinyl alcohol.
Those ber dressings are characterized by their high degree of hydrophilia combined with a large capacity for absorption. Looking at their composition, when they contains CMC they are similar to hydrocolloids as they jellify when in contact with exudates (Fig.59.4), but they have the capacity to retain moisture and bacteria inside the matrix (bacterial sequestration) [10]. The recently developed matrix enhances these prop­erties; thus, it is possible to cover the dressing with a secondary dressing, allowing some mois­ture (hydrocolloid, foams). Removal of all type of those new ber dressings is facilitated by hydration. Those dressings are suitable for rather exuding wound and allow painless dressing
removal which is very comfortable for patients with acute or chronic brinous wounds.
59.2.3.3 Polyacrylate Fibers Dressing forDebridement andCombined withNOSF toBoost Wound Healing Process
There is one unique dressing in this category. It consists of a gauze composed of polyacrylate bers and coated in a micro-adherent lipido­colloid layer (TLC-Contact). The mesh version does not contain lipido-colloid. Together with the hydro-debriding bers, polyacrylate bers jellify and adhere to brinous residues and microorgan­isms, absorb them and drain them in order to enhance their elimination: this mechanism favors autolytic debridement (Fig.59.5b). Resistance to traction is also observed. The clinical study EARTH, whose publication is in process, has conrmed advantage of these dressings in highly exudative, chronic wounds with non-inferiority to hydrobers with CMC [11] (Fig.59.5a).
The recently developed Urgostart Plus dress­ing contains NOSF (Nano-Oligosaccharide Factor) in addition to TLC bers which regulate metalloproteases which are in excess in chronic wounds and which have shown through several randomized controlled trials signicant efcacy in wound healing only chronic wounds [12, 13], and which is recommended to be used rst-line [14] in the local treatment of chronic wounds. Indeed, the NOSF acts as soon as the granulation tissue appears after the effect of the polyacrylate bers which helps in debridement allowing the wounds to heal more quickly. This dressing can be used from debridement to epithelialization of chronic moist wounds.
Fig. 59.4 Hydrober removal is easy thanks to the CMC gelication
59.2.3.4 Dressings andOsmotic
Pressure
Dressings Containing Salts
Salts with 20% NaCl were added to the initial composition of hydrogels to form a hyperosmotic dressing. This formulation is more adapted to the necrotic plaques, which are black, hard, and dry. The periwound has to be specically checked
ab
59 Dressings forNecrosed Skin
381
Fig. 59.5 (a) Polyacrylate ber dressing is a fast remover of undesired tissues over a brinous leg ulcer. (b) When saturated the polyacrylate dressing is mechanically resis-
when using these dressings with high risk of maceration and sometime uncomfort, that can prevent using protection with zinc paste.
Medical Honey Dressings
Sterile dressings are now available. They have physicochemical and microbiological properties that are comparable to the ancient description of honey when it was used empirically in ancient times [15]. Its high osmolarity favors wound exu­dation and mechanically induces the elimination of dead tissues and foreign bodies (including microorganisms). This mechanism induces a moist ambience that favors wound healing. This debridement is accompanied by an antibacterial effect on Gram-positive, Gram-negative, and Gram-resistant bacteria, whatever their presenta­tion, whether planktonic or biolm. Honey is either attached to the gauze or present as a paste.
tant enough to be removed as a whole, without leaving debris over the wound
this phase. The use of these debriding dressings does not prevent an active mechanical debride­ment at each dressing change.
59.4 How toChoose theDressing
This autolytic debridement is suitable for all types of wound, except for infected or heavily exudating wounds. It acts on the tissues in a selective manner. It is easy to use requiring no training before use, which makes them easily accessible to nurses. The cost is moderate com­pared with surgical debridement. Its main incon­venience is the slow process, but the absence of pain and bleeding, preventing microtrauma on the surface of the wound, is an advantage.

References

59.3 How toUse These Dressings
Hygiene should be respected during the dressing change. Whichever dressing is used, the protocol is important. The wound should be cleaned care­fully (with water and soap) and rinsed, and the periwound should be dried. The dressing should then be applied respecting the mode of use speci­ed by the manufacturer, and the frequency of the dressing change is usually every 1 or 2 days at
1. Winter GD.Effect of air drying and dressings on the surface of wounds. Nature. 1963;197:91–3.
2. James GA, Swogger E, Wolcott R, et al. Biolms in chronic wounds. Wound Repair Regen. 2008;16(1):37–44.
3. Vaneau M, Chaby G, Guillot B, Martel P, Senet P, Téot L, Chosidow O.Consensus panel recommenda­tions for chronic and acute dressings. Arch Dermatol. 2007;143(10):1291–4.
4. Chaby G, Senet P, Vaneau M, Martel P, Guillaume JC, Meaume S, Téot L, Debure C, Dompmartin A, Bachelet H, Carsin H, Matz V, Richard JL, Rochet
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JM, Sales-Aussias N, Zagnoli A, Denis C, Guillot B, Chosidow O. Dressings for acute and chronic wounds: a systematic review. Arch Dermatol. 2007;143(10):1297–304.
5. Hämmerle G, Strohal R. Efcacy and cost­effectiveness of octenidine wound gel in the treatment of chronic venous leg ulcers in comparison to modern wound dressings. Int Wound J. 2014;13:182. https://
doi.org/10.1111/iwj.12250.
6. Horrocks A. Prontosan wound irrigation and gel: management of chronic wounds. Br J Nurs. 2006;15(22):1222, 1224–8.
7. Humbert P, Faivre B, Véran Y, Debure C, Truchetet F, Bécherel PA, Plantin P, Kerihuel JC, Eming SA, Dissemond J, Weyandt G, Kaspar D, Smola H, Zöllner P, CLEANSITE study group. Protease-modulating polyacrylate-based hydrogel stimulates wound bed preparation in venous leg ulcers—a randomized controlled trial. J Eur Acad Dermatol Venereol. 2014;28(12):1742–50.
8. Sayag J, Meaume S, Bohbot S. Healing proper­ties of calcium alginate dressings. J Wound Care. 1996;5(8):357–62.
9. Belmin J, Meaume S, Rabus MT, Bohbot S.Sequential treatment with calcium alginate dressings and hydro­colloid dressings accelerates pressure ulcer heal­ing in older subjects: a multicenter randomized trial of sequential versus non sequential treatment with hydrocolloid dressing alone. J Am Geriatr Soc. 2002;5à(2):269–74.
10. Barnea Y, Amir A, Leshem D, Zaretski A, Weiss J, Shar R, Gur E.Clinical comparative study of Aquacel and parafn gauze dressing for split-skin donor site treatment. Ann Plast Surg. 2004;53(2):132–6.
11. Meaume S, Dissemond J, Addala A, Vanscheidt W, Stücker M, Goerge T, Perceau G, Chahim M, Wicks G, Perez J, Tacca O, Bohbot S.Evaluation of two brous wound dressings for the management of leg ulcers: results of a European randomised controlled trial (EARTH RCT). J Wound Care. 2014;23(3):105–16.
12. Meaume S, Truchetet F, Cambazard F, Lok C, Debure C, Dalac S, Lazareth I, Sigal ML, Sauvadet A, Bohbot S, Dompmartin A, CHALLENGE Study Group. A randomized, controlled, double-blind prospec­tive trial with a Lipido-Colloid Technology-Nano­OligoSaccharide Factor wound dressing in the local management of venous leg ulcers. Wound Repair Regen. 2012;20(4):500–11.
13. Edmonds M, Lázaro-Martínez JL, Alfayate-García JM, Martini J, Petit JM, Rayman G, Lobmann R, Uccioli L, Sauvadet A, Bohbot S, Kerihuel JC, Piaggesi A.Sucrose octasulfate dressing versus con­trol dressing in patients with neuroischaemic diabetic foot ulcers (explorer): an international, multicentre, double-blind, randomised, controlled trial. Lancet Diabetes Endocrinol. 2018;6(3):186–96.
14. Munter KC, Meaume S, Augustin M, Senet P, Kerihuel JC. The reality of routine practice: a pooled data analysis on chronic wounds treated with TLC-NOSF wound dressings. J Wound Care. 2017;26(suppl
2):4–15.
15. Vandamme L, Heyneman A, Hoeksema H, Verbelen J, Monstrey S.Honey in modern wound care: a system­atic review. Burns. 2013;39(8):1514–25.
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Surgical Debridement

SadanoriAkita
60

60.1 Introduction

Surgical debridement in acute and chronic wounds plays a crucial role in the wound healing process. Debridement is believed to accelerate wound healing and reduce the wound area by removing necrotic tissue, hyperkeratotic epider­mis, necrotic dermis, foreign debris, and bacterial pathogens, which all have inhibitory effects on wound healing [1]. Microarray analysis has shown marked cytoplasmic reduction and local­ization of the epidermal growth factor receptor (EGFR) in the epidermis, indicating that non­healing keratinocytes have a diminished capacity to respond to EGF. Additionally, broblasts derived from non-healing wounds demonstrate decreased migration [2]. This molecular analysis suggests that proper surgical debridement may be an effective solution to overcome these chal­lenges. However, the evidence and rationale for this technique should be further discussed for each specic pathologic condition, such as leg and diabetic foot ulcers.
Prior to surgical debridement, it is important to optimize the patient’s nutrition. If these criteria are not met, it may be best to delay wound clo­sure until conditions are more favorable for the
S. Akita (*) Department of Plastic Surgery, Tamaki-Aozora Hospital, Tokushima, Japan
Fukushima Medical University, Fukushima, Japan e-mail: akitas@hf.rim.or.jp
surgeon, physician, and patient. Debridement can be benecial for both acute and chronic wounds. If a wound is able to produce granulation tissue without bacterial overload, it is typically ready for subsequent skin grafting or ap coverage. For wounds that are unable to develop a granulation tissue bed, bioactive dressings or topical growth factors may be used.
60.2 Pathophysiology oftheUnderlying Diseases andConditions inSurgical Debridement
60.2.1 Burns
In the case of deep burns (third-degree burns, which penetrate all skin layers), surgical debride­ment of dead, eschar, and necrotic tissues is nearly always necessary. In general, surgical debridement continues until fresh tissue and bleeding are observed. This procedure may be performed in a multiplane fashion. After com­plete and thorough surgical debridement, skin coverage with a skin graft, ap, or bioengineered material such as an articial dermis is usually required. Skin grafting is the most commonly used method for skin coverage as it can cover larger post-surgical debrided wound beds and is easier to handle. Split-skin grafting is used for less vascular beds, as it has a lower metabolic demand compared to full-thickness grafts. These
© The Author(s) 2024 L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_60
383
384
S. Akita
areas with limited vascularity include the paratenon (tendon sheath), periosteum (bone envelope), and perineurium (neural envelope). Adequate debridement and skin coverage are par­ticularly crucial in pediatric burn cases (Fig.60.1).
In the case of deep dermal burns (second­degree burns, partial-thickness burns), surgical debridement is typically used in conjunction with skin grafting, but the debate continues. Some deep dermal burn wounds may heal within 2–3weeks, and aggressive surgical debridement
a
may not be necessary in such cases. However, the current standard techniques for determining burn depth and making treatment decisions are largely dependent on the subjective assessment of the clinician and can be inaccurate, even among experienced surgeons. A porcine contact deep dermal burn of 50cm2 in size, which takes more than 3weeks to heal through re-epithelialization by proliferation and migration of keratinocytes from the skin appendages in the deep dermis, is a model that can best demonstrate the impact of surgical interventions on burn healing [3].
b
Fig. 60.1 (a) A 9-month-old boy, extensive scald burn, debridement, and mesh skin grafting. (b) A 1.5years after surgery
a
60 Surgical Debridement
385
60.2.2 High-Energy Trauma Wound
As is often observed in the orthopedic specialty, high-energy open fractures often result in deep infections due to extensive damage and the pres­ence of necrotized tissue [4]. In a study compar­ing the use of negative pressure wound therapy (NPWT) and a control group, 5.4% of the NPWT group developed delayed deep infections, while 28% of the control group developed deep infec­tions. High-energy wounds are prone to infection due to both acute and delayed insufcient blood supply and extensive tissue damage.
Traumatic wounds can be caused by both blunt and penetrating injuries. Blunt trauma typi­cally results in a larger area of tissue damage and can include injuries such as crush, degloving, and avulsion. The extent of these wounds is not always clear and may change after aggressive debridement of non-vitalized tissue, bacterial control, and uid maintenance. In these cases, temporary coverage with articial dermis and
further assessment may improve proper healing (Fig.60.2).
60.2.3 Pressure Injury
Pressure ulcers are a reection of a patient’s sys­temic health, including physical, nutritional, social, and psychological status. The complex pathophysiology of pressure injuries requires several stages of evolution. Firstly, sustained pressure or shear force is applied to the soft tissue between the body mass, bony process, and sur­face. This reduces capillary vessel ow and oxy­gen and nutrient transfer, leading to occlusion of blood vessels and lymphatic vessels and capillary thrombosis. The tissues become ischemic, caus­ing an increase in capillary permeability and uid accumulation in the third space (extravascular space). Pressure-related intact discolored areas of the skin are described as non-blanching erythema or suspected deep tissue injury. The prevalence of
Fig. 60.2 (a) A 67-year-old man, high-energy injury, open fractures of the ulna and radius, externally intact but later found thrombus-formed radial artery (right above) and severed ulnar artery after microanastomosis. (b)
External xation with thorough debridement and articial dermis (top), 10days later, some tissues are still necrotic and further debridement and ap reconstruction (middle), 2years after reconstruction (bottom)
386
S. Akita
b
Fig. 60.2 (continued)
suspected deep tissue injury is more frequent than deeper pressure ulcers such as stage III or IV and has increased more recently than any other stages of pressure ulcers [5]. Edematous tissues may result in necrosis, which is irreversible. Precise debridement is considered when necrosis of tissue has occurred. The deep surgical inter­vention may start with evaluating the necrosis of the tissue and how to effectively remove it from the healthy surrounding tissue (Fig.60.3).
60.2.4 Diabetic Foot Ulcer
The etiology of diabetic foot is a result of several combined factors, including peripheral vascular (arterial) disease, as well as sensory, motor, and autonomic neuropathy [6]. It is essential to evalu­ate the patient objectively for ischemia and
underlying deep tissue issues, such as bone infec­tions. Standard of care for the diabetic foot involves surgical debridement, proper wound dressings, and appropriate off-loading to promote moist wound healing. This can help to convert a chronic non-healing wound into an acute wound healing environment by removing senescent or non-vital cells, thereby improving the wound environment and enabling better local treatment response [7].
A biopsy of the edge of a non-healing chronic wound shows a hyperproliferative epidermis with hyper- and parakeratotic elements [2]. This is largely due to repetitive stress in the foot with sensory disturbances. Despite the activation of keratinocytes at the non-healing edge, wound healing is still impaired. Nuclear localization of β-catenin leads to downstream activation of c-Myc and the glucocorticoid pathway, resulting
60 Surgical Debridement
a
387
b
c
d
Fig. 60.3 A 92-year-old male, sacral pressure ulcer (a) Sacral pressure ulcer proved by a instrument. Wound opened fully. (b) 3-week negative pressure wound therapy provied an optimal wound bed with good granulation tissue (c) A perforator arterialized ap designed (d) Flap covered the defect and remained closed at 9 months post-operatively
388
73 years, male, hemodialysis, DM with ischemia
S. Akita
in the inhibition of keratinocyte migration [8]. Microarray analysis of non-healing ulcers reveals a reduction and cytoplasmic localization of EGFR, which decreases responsiveness to EGF.The broblasts at the edges of non-healing wounds display a clear pathogenic phenotype and slower migration [2]. Diabetic foot ulcers with ischemic conditions are often seen in hemo­dialysis would develop a rapid progression of necrosis and may result in major amputation (Fig.60.4).
60.2.5 Leg Ulcer
Although venous ulcers are always linked to venous hypertension during ambulation, the exact mechanism connecting the pathological hemodynamics in venous circulation to the for­mation of necrotic lesions in the skin remains unknown. It appears that the underlying causes
First at outpatient clinic
are more complex than previously anticipated. Numerous experiments have shown that tissue injury in venous ulcer patients is caused by leu­kocytes. These cells become trapped in the microcirculation of the legs when they are in a dependent position. Subsequently, several authors have conrmed that this process is exac­erbated in patients with chronic venous insuf­ciency (CVI). It is believed that the increased trapping of leukocytes in patients with CVI is due to an increase in the expression of adhesion mol­ecules in the capillaries of the papillary dermis. In patients with CVI, leukocytes enter the micro­vascular regions affected by venous hyperten­sion. As the distance between leukocyte adhesion molecules and endothelial adhesion molecules is less than 1 μm, the rst step in the leukocyte– endothelial interaction is the displacement of leu­kocytes toward the endothelium by erythrocytes. This process occurs predominantly in postcapil­lary venules. When circulating leukocytes
3 weeks after first visit
4 moths after first visit
and 2 months after major amputation
Fig. 60.4 A 73-year-old male, neuro-ischemic diabetic foot ulcer and necrosis resulted in a major amputation
60 Surgical Debridement
389
encounter the endothelium, they may start to form weak, rolling adhesive interactions medi­ated by L-selectin and P-selectin glycoprotein ligand-1 (PSGL-1) on leukocytes and P-selectin and E-selectin on endothelial cells. Hypertension in postcapillary venules has been shown to increase leukocyte rolling and adhesion. Rolling leukocytes can then develop into stationary adhe­sion, which is dependent on the interaction between adhesion molecules CD11/CD18 on leu­kocytes and intercellular adhesion molecule-1 (ICAM-1) on endothelial cells. Once the leuko­cytes are rmly adhered to the vascular wall, they can migrate into the extravascular space, become activated, and trigger an inammatory process in the skin and surrounding tissues. VCAM-1 is another adhesion molecule that plays a role in the process of leukocyte adhesion to the endothe­lium, and its expression is heightened in patients with CVI [9].
60.3 Choice oftheSurgical Debridement
Wound bed preparation through sharp and mechanical debridement using surgical instru­ments is the most essential step in managing wound healing. This method effectively and selectively reduces the bio-burden of a wound. Elimination of necrotic tissue, which serves as a breeding ground for bacteria competing for the same nutrients and oxygen needed for wound healing, is crucial for promoting normal tissue healing. If the boundary between healthy and devitalized skin is not clear, consider tangential excision, starting from the center of the necrotic skin, until scattered bleeding is seen in the der­mis. However, bleeding is not necessarily an indicator for debridement of subcutaneous tissue as fat tissue has less vascularity compared to skin. The debridement should continue until the shimmering yellowish fat tissue level is reached. Hemostasis can be achieved through clamping or compression, and scattered bleeding can be con­trolled through electrocautery. If bleeding from larger diameter vessels is observed, ligation should be attempted.
Fascia that is not vascularized should be removed with caution to avoid damaging the neu­rovascular bundles in the supercial area. Muscles, tendons, cartilage, and bones can be resected if there is no visible blood supply. In the case of deep tissue injury in pressure ulcers, sharp penetration to the muscle and deeper tissue level can be useful in determining the extent of the wound.
Surgical equipment includes scalpel blades, pickups, electrocautery, scissors, curettes, ron­geurs, elevators, chisels, osteotomes, saws, rasps, burrs, the Harmonic scalpel, Cavitron ultrasonic surgical aspirator (CUSA®), water-jet (hydro­jet) system (Versajet II), radio-frequency energy system (Coblation® technology), low-frequency ultrasound debriding device (SonicVac), and more. Further information will be covered in Part VI.

References

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Driver V, Attinger C, Phillip T, Harding K.Serial sur-
gical debridement: a retrospective study on clinical
outcomes in chronic lower extremity wounds. Wound
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2. Brem H, Stojadinovic O, Diergelmann RF, Entero
H, Lee B, Pastar I, Golinko M, Rosenberg H, Tomic-
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3. Wang XQ, Kempf M, Liu PY, Cuttle L, Chang
HE, Kravchuk O, Mill J, Phillips GE, Kimble
RM. Conservative surgical debridement as a burn
treatment: supporting evidence from a porcine model.
Wound Repair Regen. 2008;16:774–83.
4. Stannard JP, Volgas DA, Stewart R, McGwin G Jr,
Alonso JE. Negative pressure wound therapy after
severe open fractures: a prospective randomized study.
J Orthop Trauma. 2009;23:552–7.
5. VanGilder C, MacFarlene GD, Harrison P,
Lachenbruch C, Meyer S.The demographics of sus-
pected deep tissue injury in the United States: an
analysis of the international pressure ulcer preva-
lence survey 2006–2009. Adv Skin Wound Care.
2010;23:254–61.
6. Edwards J, Stapley S. Debridement of dia-
betic foot ulcers. Cochrane Database Syst Rev.
2010;1:CD003556.
7. Everett E, Nestoras Mathioudakis N. Update on
management of diabetic foot ulcers. Ann N Y Acad