1. VA Wound Conference 2nd Annual, Mobile, AL
Debridement/Wound bed preparation
Richard Bui, DPM, ABPM
Director, PAVE

2. Debridement/Wound bed preparation
Skin is an important organ whose diverse functions are not always appreciated.
Weighs 6-8lb and covers over 20 sq ft
The skin’s major functions are Protection, sensation, thermoregulation, excretion, metabolism, and communications.
Disruption of skin integrity due to traumatic injury and/or chemical injury, results in minimal tissue loss to complete tissue loss.
Tissue loss triggers a complex wound healing events and hemostasis is rapidly achieved to prevent invasion by pathogens and restore tissue function.

3. Phases of Wound Healing
Hours
Days
Weeks
Months
Hemostasis – Platelets
Remodeling – fibroblasts
Inflammation – Platelets, neurophils,macrophages
Proliferation – macrophages, fibroblasts, endothelial & epithelial cells ⧞

4. Hemostasis & Inflammation (hours to days)
Initiated with blood vessel disruption and the extravasation of the blood constituents
Rapidly activation of platelet aggregation and the coagulation cascadeformation of the fibrin molecule and hemostasis
Activation of complement occurs
Recruitment of macrophages and neutrophils
Platelets
Platelets are activated by collagen and thrombin,
Coagulation cascade
Production of fibrin
Activation of complement and other proteins
Stimulated by the Hageman factor
Neutrophils
Increase the permeability of undamaged vessels
Causing the leakage of plasma and proteins and the swelling associated with inflammation
Clear bacterial contamination consists of opsonization of bacteria by complement
Chemotactic factors, adhesion, wbc emigration
Macrophages
Dual roles of destruction of nonviable material and the stimulation of growth of new tissue
Phagocytosis of bacteria, spent neutrophils, and cell debris
Release prostaglandins, Leukotrienes, PDGF, bFGF, TFG beta and alpha, and other chemoattractants
Mast Cells
Degranulation mediated by both an immediate sensory nerve mediated response to injury and direct trauma
Release histamine, heparin, bFGF, IL4, TNFa, TGFb

5. Proliferative Phase (days to Weeks)
Both re-epithelialization and granulation tissue formation occur
Begins within 24 hours but not observable for the first 3 days eg. Lag phase
Granulation tissue formation begins in 3-5 days
Loss of neighboring cell stimulates the replication of epidermal cells (contact inhibition)
Macrophages stimulate fibroblast ingrowth, deposition of loose connective tissue, and angiogenesis

6. Re-epithelialization/Remodeling
Movement of keratinocytes from free edges, surrounding hair follicles and sweat glands, into the wound.
New cells adhere to the granulation tissue beneath and replicated cells migrate by a means of “leap frog or pouring over” of cells to reach the advancing wound edge.
Produce a provisional matrix consisting of fibrin, fibronectin, and type V collagen if the basement membrane is damaged.

7. Fibroplasia and contraction
Amplification of granulation tissue growth, networking
Contraction produces radial movement of intact skin around the wound toward the center
Also reduces the quantity of new tissue required to fill the wound
Remodeling (weeks to years)
Extracellular matrix and fibroblasts control each other until a stable matrix is formed
Increase tissue strength, reorganization, reinforcement.

8. Debridement/Wound bed preparation
Growth factors in the normal wound healing process
Angiogenic - stimulate the development of new transient blood vessels.
Chemotactic – attract various cell types to the wound bed
Mitogenic – stimulate cellular proliferation
Regulation – of the synthesis and degradation of the extracellular matrix
Influence – synthesis of cytokines and growth factors by neighbouring cells.
Wound bed preparation is not a new concept, but the concept to help practitioners focus on the causes of, and problem associated with, particularly with chronic wound.

9. Debridement/Wound bed preparation
Important growth factors
Angiogenesis growth factor (AGF)
Vital for the production of “transient” blood vessels
Epidermal growth factor (EFG)
Involved with angiogenesis
Important for the differentiation of keratinocytes before they proliferate, migrate, and clump together
Basic fibroblastic growth factor (BFGF)
Also promotes angiogenesis
Responsible for the induction and proliferation of epithelial and fibroblast cells
Transforming growth factor-beta (TGF-b2)
Is chemotactic, attracting macrophages, inducing the proliferation of procollagen as well as inhibiting the action of matrixmetalloproteases (MMPs)
Insulin-like growth factor (I-IGF)
Stimulates the production of energy required by the cells for replication, multiplication, and maturation.
Platelet derived growth factor (PDGF)
Active immune cells, fibroblasts, endothelial cells, angiogenesis, and collagen synthesis

10. JJ Mendes 1,2 J Neves 3. Diabetic Foot Infections: Current Diagnosis and Treatment. The Journal of Diabetic Foot Complications.
2012; Volume 4, Issue 2, No. 1, Pages

11. Chronic Wound
are wounds that, following the orderly and timely repair process, fail to establish a sustained anatomic and functional result, for the period of 6 weeks or more.
high levels of MMPs and pro-inflammatory cytokines along with senescent cells, there is a low mitogenic activity that invariably results in chronicity.
JJ Mendes 1,2 J Neves 3. Diabetic Foot Infections: Current Diagnosis and Treatment. The Journal of Diabetic Foot Complications.
2012; Volume 4, Issue 2, No. 1, Pages

12. Phases of Abnormal wound healing
Chronic inflammation
Infection
Hyper-granulation
Slow granulation
Epiboly
Maceration
Dessication
Chronic proliferation
Mental and physical status*
Comorbidity*
Nutrition*
Supports*

13. Phases of Wound Healing
Hours
Days
Weeks
Months
Hemostasis – Platelets
Remodeling – fibroblasts
Inflammation – Platelets, neurophils,macrophages
Proliferation – macrophages, fibroblasts, endothelial & epithelial cells ⧞

14. Debridement/Wound bed preparation
All chronic wound are colonized with bacteria.
Do not incite an intense inflammatory response.
There is delayed healing through the inhibition of the growth of key cells in healing or by the presence of biofilm.
Biofilm, communities of bacteria, have high resistance to antibiotics and to the host immune system.
Evolved ways to communicate with each other through water channels and have a protective extracellular polysaccharide matrix covering, known as Quorum sensing.

15. Debridement/Wound bed preparation
Biofilm
Presents in 60% of chronic wound vs 6% of acute wound
2 methods
Tissue biopsy
Electron microscope, (wound swaps with microscopic exam is acceptable)

16. Bacterial load in chronic wounds
Can’t achieve sterility
Reduce bacterial density and pathogenicity
Impact of Host response to bacterial burden
Clinical infection is the presence of multiplying bacteria in body tissues that results in spreading cellular injury.
Heat, swelling, surrounding erythema and pain.

17. Chronic vs Acute wound
A: the initial chronic wound demonstrates a thick film on its surface.
B: Three days later, the film is still visible on the initial wound, but a new satellite wound shows no significant film.
C: Biofilm based wound care strageties were immediately used on the fresh satellite wound, and it quickly healed within two weeks.
D: The established wound (A) persisted for three additional weeks after the acute wound healed.

18. A: Acute wound shows the host’s extracellular matrix with occassional bacterial clusters dotted across the landscape
B: In wounds, bacteria multiply to form microcolonies that can develop into mature biofilm
C: Host defences and antibacterial agents have impaired affects on biofilm bacteria.

20. Debridement/Wound bed preparation
Biofilm: Percival et al 2012 advised
Failure to heal, despite the application of evidence based therapy
High levels of exudate and malodour
Sloughy, shiny, slimy wound bed
Persistent necrotic tissue
Unresponsive wound bed to antimicrobials
Polymicrobial microbiology

24. Wound bed preparation
Is the active creation of an optimal wound healing environment through planned interventions, essentially in order to maximize the benefits of chosen advanced materials.
This concept should not be viewed in isolation, but in the context of a systematic holistic assessment process.
Wound bed preparation is recognised as the management of wounds in order to accelerate endogenous healing or to facilitate the effectiveness of other clinical therapeutic measures.
Include the patient’s physical, psychological and social wellbeing, and consideration of the many factors that can delay the wound healing process, such as drug therapy, planned medical interventions, and patient’s nutritional state.
Addressing above may positively affect a patient’s perceived quality of life.

25. Patient Assessment Holistic patient care concept
The first step is to address systemic factors that impair healing
Controlling edema in patient with venous stasis ulcer,
Offloading footwear/cast in neuropathic ulcer,
Tight glycemic control in patients with diabetes
Infection must be addressed with antibiotics
Vascular status?
Respiratory status?
Include the patient’s physical, psychological and social wellbeing, and consideration of the many factors that can delay the wound healing process, such as drug therapy, planned medical interventions, and patient’s nutritional state.
Addressing above may positively affect a patient’s perceived quality of life.

26. Alvarsson A. Et al. A retrospective analysis of amputation rates in diabetic patients: can lower extremity amputations be further prevented? Cardiovascular Diabetology 2012.

27. Why Debridement
Debridement is important part of wound bed preparation.
A way to “introduce” not transform, an acute wound in a chronic wound.
Chronic wound tends to accumulate a necrotic burden of senescent cells, a corrupt ECM, and inflammatory enzymes.

28. Debridement
Is the removal of nonviable tissue, debris, and bacteria from the wound bed to encourage wound healing.
There is no definitive evidence that suggests that one method of debridement is superior to another.
Selection of this method should base on the needs of the patient, not the clinician.

29. Debridement/Wound bed preparation
Considerations
The state of the tissue to be debrided
Pain related to the wound involved
That exudate levels may increase in the short term, depending on the technique used
The presence of infection in the wound to be debrided and any potential consequences
The cost of the debridement method to be used,
The acceptability to the patient of the debridement method.

30. Debridement/Wound bed preparation
Effective wound bed preparation must
Removal of necrotic/fibrous tissue
Control of edema, if present
Achievement of a well-vascularized wound bed
Decrease bacterial burden or fungal organisms
Minimization of wound exudate
Correction of matrix abnormalities
PDGF, regranex (becaplermin) gel 0.01%
Diabetic neuropathic ulcers, ulcer extend into the subcut tissue or beyond with good blood supply.

31. Debridement/Wound bed preparation
Issue to consider
The classification of the wound: acute; mechanical; chronic; burn; or malignant
The framework to be used to assist with the data collection process
Specific information required from wound assessment process: number and location of wound; size and grade of the wound; nature of the wound bed and any wound fluid; any associated quality of life issues for the patient such as pain, related to the wound.
Any additional assessment techniques required to enhance the wound assessment process.

32. Debridement/Wound bed preparation
Issue to consider
Any associated problems on the skin surrounding the wound
Primary treatment objectives
Interventions required to achieve intended outcomes.
Documentation to be used for the reporting of wound assessment/management
If any photographic record is required of the wound being assessed
If the patient requires any additional information following your assessment or interventions for the ongoing management of the wound. (Collier 2002).

33. Debridement/Wound bed preparation
Mechanical*
Wet to dry, hydrotherapy, pulsed lavage
Enzymatic
Collagenase
Biosurgical*
Maggots
Autolytic
Ultrasonic*
Hydrosurgical*
Sharp/Surgical
*Recent advances in debridement

34. Mechanical Debridement
Wet to Dry
Application up to 3x a day
Associates with pain
Remains a common treatment in all health care settings.
Considerations
Larger wounds
Nonsurgical candidates
Nonselective
Painful
May macerate surrounding skin
Dry
Wet

35. Enzymatic Debridement
Safe, effective, and easy to use
Ideal option for patients who are not surgical candidates, patients in long-term care facility or at home
Avoid the use of nonselective enzymes on healthy tissue
Avoid solutions with metal ions, eg. Silver, zine oxide, mercury.
Papain-urea, is a cysteins protease, nonselective enzyme, derived from carica papaya.

36. Enzymatic Debridement
Collagenase
indicated for debriding chronic dermal ulcers and severely burned areas.
is the only enzymatic debrider approved by the FDA
Derived from clostridium histolyticum,
Up-regulates the migration of keratinocytes over the wound bed and stimulates granulation.
Has been shown to reduce scarring in partial thickness burn wounds.
Smith-nephew

37. Biosurgical Debridement Maggots
Uses larval therapy (over 400 years ago), by Maya Native Americans and Aboriginal tribes in Australia, during Renaissance,
First observed by Dr. Joseph Jones, a ranking Confederate medical officer during the American Civil War, but first documented therapeutic use of maggots in the United States by a second Confederate medical officer Dr. J.F. Zacharias: Maggots ... in a single day would clean a wound much better than any agents we had at our command ... I am sure I saved many lives by their use.
*Staphylococcus and Streptococcus species, P. aeruginosa and E. coli.

38. January 2004, FDA approved permission to produce and market maggots for use in humans or animals as a prescription-only medical device for the following indications
Non-healing necrotic skin and soft tissue wounds,
Pressure ulcers
Venous stasis ulcers
Neuropathic foot ulcers
Non-healing traumatic or post-surgical wounds

39. They secrete proteolytic enzymes while feeding on necrotic tissue, MOA
Debridement
Disinfection of the wound*
Stimulation of healing
Biofilm inhibition and eradication
Advances in wound debridement techniques
Biomonde.com

42. Autolytic Debridement
Endogenous enzymes present in wound fluid interact with moist dressing to soften and remove necrotic tissue.
Easy to perform, involves a moisture retentive topical dressing,
Autolytic debridement with hydrogel is more time and cost-effective than mechanical wet to dry dressings.
Contraindicated in infected wounds

43. Chemical Debridement Chemical Debridement Silver
Silver - restricted to wounds with proven infection or at high risk of infection
Restore, Acticoat, Actisorb,

44. Chemical Debridement Chemical Debridement Medihoney
Honey – by Osmosis process, used in diabetic with blood glucose levels are maintained.
Medihoney

45. Chemical Debridement Chemical Debridement
Povidine/Iodine – caution with renal impairment or thyroid disorders

46. Chemical Debridement Chemical Debridement
Sodium hypochlorite, hydrogen peroxide
Toxic to healthy granulation tissue
MSDS:
Very hazardous in case of skin contact (irritant), of eye contact (irritant), of ingestion, . Hazardous in case of skin contact, (corrosive), of eye contact (corrosive).

47. Ultrasonic Debridement
Misonix SonicOne O.R. System
ultrasonic surgical debridement system
allows for surgical debridement layer by layer from superficial to deep while protecting underlying viable tissues.
Utilizing low frequency, high intensity ultrasound, vibrate at 22.5 kHz
precise vibration creates mechanical energy that is transferred to tissue, causing molecules to oscillate

48. Ultrasonic Debridement
destruction of bacteria and biofilm occurs due to the ultrasonics phenomenon of transient cavitation, the gas-filled bubbles undergo rapid expansion followed by collapse.
Post-treatment a log5 reduction in bacterial count
reduced blood loss when compared to standard excision methods
have a 90% take of split thickness skin graft.

49. Misonix SonicOne O.R. System

50. Case 1
Mr. S.
63y/o male, Diabetes, diabetic neuropathy, Loss of use both LE, htn, hx of DFU, leg ulcer,
Injury to right foot x 3 wks,
Initial treatment
Cadexomer ointment
Surgical
Mistronic
Dermapure Graft
NPWT – SNAP wound vac
Leg cast

54. 24 weeks

55. Sharp/Surgical Debridement
Is considered the “gold standard”
Should be the first choice for wounds demonstrating signs of advancing cellulitis or sepsis
Painful, anesthesia often required
Excellent judgement must be used when performing sharp debridement
Must able to differentiate where and what to cut, line of demarcation-based on the pathology of the abnormal keratinocytes at the wound edges.

56. Case 2
57y/o male, Dm, Dm neuropathy, s/p TMA left foot, OM, noncompliance with treatment

57. Excision,
Ostectomy cuboid bone
Dermapure graft
Negative pressure,
Nonweightbearing

58. @ 6 weeks
@ 11 weeks

59. Hydrosurgery Reduced bacterial burden Preserves viable tissue
Removes unwanted necrosis and debris
Improved graft and synthetic dressing results 
Improved excision of contoured areas, web spaces and facial structures
Minimized peripheral tissue damage 
Smith-nephew
Source: Smith-Nephew.com

60. Surgical Debridement Case 3, D1788
58y/o M, PVD, chronic alcoholic, tobacco dependence, and malnourished.
Presents with traumatic leg/foot injury after intoxication of alcohol,

61. Versajet
Apligraf
Modified Jones compression
Nonweightbearing
Protein supplement

65. Robert G. Frykberg, DPM, MPH, et al. DIABETIC FOOT DISORDERS:
A CLINICAL PRACTICE GUIDELINE (2006 revision). The journal of foot and ankle surgery.

66. Thank You

67. References:
Anderson, I. Debridement methods in wound care. Nursing Standard
Alvarsson A. Et al. A retrospective analysis of amputation rates in diabetic patients: can lower extremity amputations be further prevented? Cardiovascular Diabetology 2012.
Ayello, E. A. et al. TIME heals all wounds. Nursing, also 9/2016.
Chamanga, E.T., et al. Chronic wound bed preparation using a cleansing solution. British Journal of Nursing
Baranoski, S., Ayello, E. A. Wound care essentials: Practice principles. 2nd edition. Lippincott Williams and Wilkins.
Collier, M. Wound bed preparation: theory to practice. Nursing Standard
Gwynne, B., Newton, M. An overview of the common methods of wound debridement. British Journal of Nursing.
Gordon, K.A., et al. The role of surgical debridement in healing of diabetic foot ulcers. Jan/Feb 2012.
Panuncialman, J., Falanga, V. The science of wound bed preparation. Clinics in Plastic surgery
Kim, P.J., Steinburg, J.S. Wound Care: Biofilm and its impact on the latest treatment Modalities for ulcerations of the diabetic foot. Seminars in Vascular Surgery
Rodeheaver, G.T. Pressure ulcer debridement and cleansing: A review of current literature. Ostomy/wound management, 1999.
Sherman, R.A. Mechanism of Maggot-induced wound healing: what do we know, and where do we go from here. Evidence Based Complementary and Alternative medicine
Sherman, R.A. Maggot Therapy takes us back to the future of wound care: New and improved maggot therapy for the 21st century. Journal of Diabetes science and technology
Wolcott, R.D., Rhoads, D.D. A study of biofilm-based wound management in subjects with critical limb ischemia. Journal of wound care