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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5191_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Contents
- •2.1 Introduction
- •2.2 Dry Necrosis
- •3.2 Pathophysiology
- •3.3 Clinical Manifestations
- •2.3 Wet Necrosis
- •2.4 Debridement
- •2.4.2 Dissecting Haematomas
- •2.6 Conclusion
- •References
- •3.1 Introduction
- •References
- •4.1 Introduction
- •4.2.1 Conventional X-Rays
- •4.2.2 Duplex Ultrasonography
- •4.2.3 Computed Tomography (CT)
- •4.2.4 Magnetic Resonance Imaging (MRI)
- •4.2.5 Vascular Imaging
- •4.3 Treatment
- •4.3.1 AVM
- •References
- •5.1 Introduction
- •5.2 Imaging Methods
- •5.2.1 X-Ray Mammography
- •5.2.2 Ultrasound
- •5.2.3 Magnetic Resonance Imaging
- •5.3 Conclusion
- •References
- •6.1 Introduction
- •6.10 Revascularization Procedure
- •6.12 Nonoperative Treatment
- •6.13 Conclusion
- •References
- •7.1 Introduction
- •7.2 Metabolic Origin
- •7.3 Pathophysiology
- •7.4 Clinical Diagnosis
- •7.5 Vascular Explorations
- •7.6 Treatment
- •7.7 Conclusion
- •References
- •Reference
- •9.1 Introduction
- •9.4 Conclusion
- •References
- •10.4.1 Primary Necrosis
- •10.4.2 Secondary Necrosis
- •10.4.3 Tertiary Necrosis
- •References
- •11: Electrical Burns
- •11.1 Introduction
- •11.2 Tissue Injury
- •11.2.2 Muscle Injury
- •11.2.3 Myocardial Damage
- •11.2.4 Buccal Mucosa Damage
- •11.2.5 Nerve Damage
- •11.2.6 Deep Damage (Except Viscera)
- •11.2.7 Other Damages
- •11.3 Medical Management
- •11.3.1 Monitoring
- •11.4 Surgical Management
- •11.4.1 First Surgery
- •11.4.2 Second Look
- •11.5 Global Management
- •11.6 Prevention
- •11.7 Conclusion
- •References
- •12: Gunshot Wounds
- •12.1 Introduction
- •12.2 Etiopathogeny
- •12.3 Clinical Detailing
- •12.3.1.1 Cavity
- •12.3.1.2 Abrasion Ring (Marginal Abrasion, Contusion Ring)
- •12.3.1.4 Secondary Shock Wave
- •12.3.1.5 Skin Burn
- •12.3.1.6 Bullet Wipe
- •12.3.1.7 Smudging
- •12.3.1.8 Tattooing
- •12.3.1.9 Retained Foreign Materials
- •12.4.1 Save Life
- •12.5.1 Initial Dressing
- •12.5.2 Wound Surgery
- •12.6 Conclusion
- •References
- •13: Frostbite
- •13.1 Aetiology
- •13.3 Pathology
- •13.3.3 Long-Term Sequelae
- •13.4.1 History
- •13.4.2 Examination
- •13.5 Acute Frostbite Management
- •13.5.3 Pharmacological Support During Rewarming
- •13.6 Post-thaw Frostbite Care
- •14.3 Radiation Ulcers
- •14.4.1 Debridement
- •14.4.2.1 Surgical Treatment
- •14.4.2.2 Stem Cell Therapy
- •14.5 Case Reports
- •14.5.1 Case 1
- •14.5.2 Case 2
- •14.5.3 Case 3
- •14.5.4 Case 4
- •14.6 Conclusion
- •References
- •13.6.2 Physiotherapy Protocols
- •13.6.3 Surgery
- •13.7 Summary Points
- •References
- •14.1 Introduction
- •14.2 Ionizing Radiation
- •15.1 Introduction
- •15.2 Gastroschisis
- •15.3 Dissecting Hematoma
- •15.5 Diabetic Foot Abscesses
- •References
- •16.1 Introduction
- •16.3 Tele-Assistance
- •16.4 Technology
- •16.6 Conclusion
- •References
- •18.1 Introduction
- •18.2 Clinical Presentation
- •18.3 The Therapeutic Decision
- •18.3.1 Evolution
- •18.3.3 Surgical Intervention
- •18.3.4 Follow-Up
- •18.4 Conclusion
- •Bibliography
- •19.1 Introduction
- •19.2 Medications
- •19.2.1 Hydroxyurea
- •19.2.2 Anagrelide
- •19.2.3 Coumarins
- •19.2.4 Heparin
- •19.2.5 Methotrexate
- •19.2.7 Hydralazine
- •19.2.8 Amezinium Methylsulfate
- •19.2.9 Diltiazem
- •19.2.10 Propylthiouracil
- •19.2.11 Nicorandil
- •19.2.12 Levamisole
- •19.2.13 Pentazocine
- •19.2.14 Tyrosine Kinase Inhibitors
- •19.3 Therapy
- •19.4 Conclusion
- •References
- •20: Toxic Syndromes
- •20.1.2 Skin Manifestation
- •20.1.2.1 Streptococcal Toxic Shock Syndrome
- •20.1.2.2 Skin Manifestation
- •20.2 Pathophysiology
- •20.3 Treatment
- •20.3.1 Antibiotic Therapy
- •20.3.2 Intravenous Immune Globulin
- •20.3.3 Surgical Therapy
- •References
- •21.1 Introduction
- •21.3 Dry Bite
- •21.4 First Aid
- •21.5 Antivenom Treatment
- •21.7 Surgical Treatment
- •21.9 Case Reports
- •21.9.1 Case 1
- •21.9.2 Case 2
- •21.9.3 Case 3
- •21.10 Conclusion
- •References
- •22.1.2 Habitat
- •22.1.3 Venomous Apparatus
- •22.2.1 General Ideas
- •22.2.2 Circumstances
- •22.2.3 Wound Location
- •22.2.4 Clinical Evidence
- •22.2.5 Diagnosis
- •22.2.7 Medical Complications
- •22.2.8 Treatment
- •22.2.9 Other Used Treatments
- •22.4 Clinical Cases
- •22.4.1 Case 1
- •22.4.2 Case 2
- •22.4.3 Case 3
- •References
- •23.1 Introduction
- •23.2 Case Examination
- •23.4 Conclusion
- •References
- •25.1 Introduction
- •25.2.1 Vasculitis
- •25.2.2 Neutrophilic Dermatoses
- •25.2.3 Venous Stasis
- •25.2.4 Arterial Disease
- •25.2.5 Corticosteroid Therapy
- •25.3.1 Systemic Lupus Erythematosus (SLE)
- •25.3.2 Systemic Sclerosis
- •25.3.3 Dermatomyositis
- •25.3.4 Sjögren’s Syndrome
- •25.3.5 Scleroderma
- •25.3.6 Behcet’s Syndrome
- •25.4.1 Systemic Approach
- •25.4.2 Topical Wound Treatment
- •25.4.3 Occlusive Dressings
- •References
- •26: Giant Cell Arteritis
- •26.1 Introduction/Physiopathology
- •26.2 Diagnosis
- •26.2.1 Medical Context
- •26.2.2 Semiology
- •26.2.4 Routine Evaluation
- •26.3 Treatment
- •26.4 Tocilizumab
- •26.5 Methotrexate
- •References
- •27: Hidradenitis Suppurativa
- •27.1 Introduction
- •27.2 Diagnosis
- •27.3 Pathophysiology
- •27.4 Treatment
- •27.5 Adjuvant Therapy
- •27.6 Conclusion
- •References
- •28: Martorell Hypertensive Ischemic Ulcer
- •28.1 Epidemiology
- •28.2 Etiopathogenesis
- •28.3 Clinical Diagnosis
- •28.4 Histopathology
- •28.6 Evolution
- •28.8 Other Treatments
- •28.9 Conclusion
- •References
- •29: Vasculitis
- •29.2 Pitfalls
- •29.4 Clinical Manifestations
- •References
- •30: Necrobiosis Lipoidica
- •30.1 Introduction
- •30.2 Epidemiology
- •30.5 Treatment
- •References
- •31: Purpura Fulminans
- •31.1 Introduction
- •31.2 Epidemiology
- •31.4 Pathogenesis
- •31.5 Clinical Presentation
- •31.5.1 Workup
- •31.5.2 Management
- •References
- •32.1 Physiopathology
- •32.2 Diagnosis
- •32.3 Treatment
- •33.1 Comorbidity
- •33.2 Exacerbation
- •33.3 Direct Cause
- •33.4 Treatment
- •References
- •34: Calciphylaxis
- •34.1 Introduction
- •34.2 Risk Factors
- •34.3 Clinical Manifestation
- •34.4 Pathophysiology
- •34.5 Diagnosis
- •34.6 Treatment
- •References
- •35: Livedo(id) Vasculitis
- •35.1 Introduction [1]
- •35.2 Histology [1]
- •35.3 Pathogenesis [1, 2]
- •35.4 Clinical Presentation
- •35.4.2 Location
- •35.5 Diagnosis [2, 3]
- •35.6 Treatment [6–11]
- •35.6.1 General Management
- •35.6.2 Therapeutic Modalities
- •35.6.3 Perspectives
- •References
- •36: Pyoderma Gangrenosum
- •36.1 Introduction
- •36.2 Etiopathogenesis
- •36.3 Clinical Detailing
- •36.4 Treatments
- •References
- •37: Cryoglobulinemia
- •37.1 Physiopathology
- •37.2 Diagnosis
- •37.3 Treatment
- •37.3.1 Systemic Treatment
- •37.3.2 Local Treatment
- •References
- •38: Hand Necrosis
- •38.1 Introduction
- •38.2 Vascularization
- •38.3 Mechanisms
- •38.4 Etiologies
- •38.6 Diagnosis
- •38.7 Management
- •References
- •39.1 Introduction
- •39.5 Conclusion
- •References
- •41.1 Introduction
- •41.2 Bacteria
- •41.3 Mycobacteria
- •41.4 Viruses
- •41.6 Yeast
- •41.7 Parasites
- •41.8 Pathological Mechanisms
- •References
- •42: Fusarium solani
- •References
- •43: Fournier Gangrene
- •43.2 Physiopathogenesis
- •43.3 Diagnosis
- •43.4 Treatment
- •43.5 Reconstruction
- •43.6 Conclusion
- •References
- •44: Infection Context: Necrotizing Fasciitis
- •44.1 Introduction
- •44.2 Epidemiology
- •44.3 Symptom
- •44.5.1 Physical Diagnosis
- •44.5.2 Laboratory Tests
- •44.6 Treatment
- •44.6.1 Medical Therapy
- •44.6.2 Surgical Therapy
- •References
- •46: Skin Necrosis Over Osteosynthetic Material
- •46.1 Introduction
- •46.2 Postoperative Skin Necrosis
- •46.2.1 Debridement
- •46.2.2 NPWTi
- •46.2.3 Hardware Removal
- •46.2.4 Soft Tissue Reconstruction
- •46.3 Delayed Skin Necrosis
- •46.4 Conclusion
- •References
- •47: Necrotic Complications After Skin Grafts
- •47.1 Introduction
- •47.2 Graft Survival
- •47.3.1 Recipient Site
- •47.3.3 Graft Shearing
- •47.3.4 Infection
- •47.3.5 Poor Systemic Conditions
- •47.3.6 Technical Errors
- •47.4 Graft Rescue
- •48: Arterial Leg Ulcers
- •48.1 Introduction
- •48.3 Clinical Findings
- •48.4 Diagnosis
- •48.5 Treatment
- •References
- •49.1 Introduction
- •49.1.1 Aesthetic Procedures
- •49.1.2 Filling Products
- •49.1.4.1 Ablative Lasers
- •49.1.4.2 Non-ablative Thermal Lasers
- •49.1.4.3 Vascular Lasers
- •49.1.4.4 Pigment Lasers
- •49.1.4.5 Radiofrequency
- •49.1.5 EBD
- •49.1.5.1 LEDs
- •49.1.5.2 High-Intensity Focused Ultrasound (HIFU)
- •49.1.5.3 Cryolipolysis
- •49.1.6 Peelings
- •49.1.6.1 Epidermal Peel
- •49.2 Complications
- •49.2.2 Scars
- •49.2.3 Infectious
- •49.3 Conclusion
- •References
- •50.1 Introduction
- •50.4 Clinical Indications
- •50.5 Conclusion
- •References
- •References
- •52: Skin Reconstruction Using Dermal Substitutes After Skin Necrosis
- •52.1 Introduction
- •References
- •53.1 Introduction
- •References
- •54.1 Introduction
- •54.3 Clinical Presentation
- •54.3.1 Detecting Early Change
- •54.3.2 Wet Necrosis
- •54.3.3 Dry Necrosis
- •54.4.1 Debridement
- •54.4.2 Vascular Intervention
- •54.4.3 Reconstruction Using Free Flaps
- •References
- •55: Exposed Necrotic Tendons
- •55.1 Introduction
- •55.3.1 Immobilization
- •55.3.2 Negative Pressure Wound Therapy
- •55.3.4 Flaps
- •55.4.1 Burns
- •55.4.2 Trauma
- •55.4.3 Miscellaneous
- •References
- •56.1 Introduction
- •56.2 Clinical Signs
- •56.4 Complementary Exams
- •56.5 Surgical Management
- •References
- •57.1 Introduction
- •57.3.1.2 Postoperative Management
- •57.3.1.3 Patient-Inherent Irreversible Causes
- •57.3.1.4 Vascular Disease
- •57.3.1.5 Systemic Disease
- •57.4.1 Repeat Free Flap Procedure
- •57.4.2 Non-microsurgical Therapy
- •References
- •59.1 Introduction
- •59.2.1 Hydrating Dressings
- •59.2.1.1 Hydrogels
- •59.2.1.2 Hydrogel-Like Devices
- •59.2.2.1 Irrigo-Absorbents
- •59.2.2.2 Hydrocolloids
- •59.2.3 Absorbent Dressings
- •59.2.3.1 Alginates
- •59.2.3.2 Fiber Dressings
- •Dressings Containing Salts
- •Medical Honey Dressings
- •References
- •60: Surgical Debridement
- •60.1 Introduction
- •60.2.1 Burns
- •60.2.2 High-Energy Trauma Wound
- •60.2.3 Pressure Injury
- •60.2.4 Diabetic Foot Ulcer
- •60.2.5 Leg Ulcer
- •References
- •61.1 Introduction
- •61.4 Clinical Indications Outside Burns
- •61.4.1 Arterial Leg Ulcer
- •61.4.3 Diabetic Foot Ulcer
- •61.5.1 Malignant Wound
- •61.5.2 Radionecrosis
- •61.8 Conclusion
- •References
- •62: Honey Debridement
- •62.1 Introduction
- •62.2 Antibacterial Properties
- •62.3 Debridement
- •62.4 Tissue Growth
- •62.5 Deodorizing
- •62.7 Contraindications
- •62.8 Conclusion
- •References
- •63.1 Introduction
- •63.3 Clinical Indications
- •References
- •References
- •65.1 Introduction
- •65.2.1 General Aspects
- •65.2.2 Predisposing Factors
- •65.2.3 Laboratory Examinations
- •65.2.4 Diagnosis
- •65.3.3 Epidemiology
- •65.3.5 Care
- •65.3.6 Physiology of Extravasation
- •65.3.9 Dangerous Substances
- •65.3.10 Treatments
- •65.4.1 Introduction
- •65.4.2 Care
- •References
- •66: Neonatal Pressure Ulcer
- •66.1 Introduction
- •66.2 Risk Assessment Scales
- •66.3.1 Topic Treatment
- •66.3.2 Surgical Treatment
- •66.4.1 The Nose
- •66.5 Conclusion
- •References
- •67.1 Introduction
- •67.2.1 Progeroid Syndromes
- •67.2.2 Vascular Anomalies
- •67.2.3 Metabolic Disorders
- •67.2.5 Harlequin Ichthyosis
- •67.2.6 Olmsted Syndrome
- •67.2.8 Other Genetic Diseases
- •References
- •68.1.1 Physiopathology
- •68.1.2 Clinical Presentation
- •68.1.3 Diagnosis
- •68.1.4 Treatment
- •68.2 Ulcerated Congenital Hemangiomas
- •68.2.1 Physiopathology
- •68.2.2 Clinical Presentation
- •68.2.3 Diagnosis
- •68.2.4 Treatment
- •68.3 Arteriovenous Malformations
- •68.3.1 Physiopathology
- •68.3.2 Clinical Presentation
- •68.3.3 Diagnosis
- •68.3.4 Treatment
- •References
- •70.1 Background
- •70.2 Etiology/Pathophysiology
- •70.3 Presentation
- •70.5 Prevention
- •70.6 Treatment
- •References
- •71.1 Pathophysiology
- •71.2 Epidemiology
- •71.3 Clinical Signs
- •71.5 Complications
- •71.6 Additional Examinations
- •71.7.1 Medical Management
- •71.7.2 Surgical Management
- •71.7.3 Healing
- •71.8 Prevention
- •71.9 Conclusion
- •References
- •72: Introduction
- •References
- •References
- •74.1 Introduction
- •74.3 Conclusion
- •References
- •75.1 Introduction
- •75.2.1 Autolytic Debridement
- •75.2.2 Enzymatic Debridement
- •75.2.3 Mechanical Debridement
- •75.2.4 Biological Debridement
- •References
- •76.1 Introduction
- •76.4 Who Can Debride?
- •76.6 Assess
- •76.7 Pain Relief
- •76.10 Conclusions
- •References
- •77.1 Introduction
- •77.4 Regulations
- •77.5 Conclusion
- •References
- •78: Distance Skin Necrosis Management
- •78.1 Introduction
- •78.2 Who Is Concerned?
- •78.2.1 The Patients
- •78.2.2 Local or First-Line Caregivers
- •78.2.3 The Experts
- •78.4 When? How? ‘OR’ What?
- •78.5 Conclusion
- •References
- •Index

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
Hydrober 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
forDebridement
andCombined withNOSF
toBoost 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
conrmed advantage of these dressings in highly
exudative, chronic wounds with non-inferiority
to hydrobers 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 signicant efcacy
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 Hydrober removal is easy thanks to the CMC
gelication
59.2.3.4 Dressings andOsmotic
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 specically checked

ab
59 Dressings forNecrosed 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 biolm. 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 toChoose theDressing
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 toUse 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 specied 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. Biolms
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

382
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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. Efcacy 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,
Shar R, Gur E.Clinical comparative study of Aquacel
and parafn 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.
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Surgical Debridement
SadanoriAkita
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 specic 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 benecial 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
oftheUnderlying Diseases
andConditions inSurgical
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 articial 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
2–3weeks, 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 50cm2 in size, which takes more
than 3weeks 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 1.5years 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 insufcient 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 articial dermis and
further assessment may improve proper healing
(Fig.60.2).
60.2.3 Pressure Injury
Pressure ulcers are a reection 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 articial
dermis (top), 10days later, some tissues are still necrotic
and further debridement and ap reconstruction (middle),
2years 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 conrmed that this process is exacerbated in patients with chronic venous insufciency (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 inammatory 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 oftheSurgical
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 supercial 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
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Repair Regen. 2009;17:306–11.
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
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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.
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Lachenbruch C, Meyer S.The demographics of sus-
pected deep tissue injury in the United States: an
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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
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