Wound healing pearls

1. +
Wound Healing Pearls

2. +
Objectives
Stages of wound healing
Factors affecting wound healing
Therapies

3. +
Defenition
Wound healing is a dynamic pathway
that optimally leads to restoration of
tissue integrity and function.

4. Wound Care

5. +
Why is this important?
 Mortality
 Morbitity
 Economics
 Dehisence
 Infection
 Delayed Healing

6. + Physiology
Haemostasis
Inflammatory
Proliferative
Remodeling
Wound contraction

7. Time Line of Wound Healing

8. +
Haemostasis (seconds to minutes)
Vasocostriction
Injury to endothelial cells
Clotting cascade activated
Formation of clot

9. +
Cytokines
 Depostion of extracellular matrix-TGF B
 Chemotaxis-PDGF
 Epithelisation-EGF, FGF
 Angiogenesis -VEGF
Janis and Harrison 2014

10. +
Inflammation (1 to 5 days)
IGF-1, TGFα, TGFß, PDGF (Platelets)
Attracts leucocytes and macrophages for
phagocytosis
Increased in blood flow (histamine,
serotonin and bradykinin)
Increased oxygen compensation and
lactic acid production

11. +
Proliferation (4 to 14 days)
Granulation tissue production
Angiogenesis
Collagen production
Epithelisation

12. +
Angiogenesis
Occurs within 2 to 3 days
Again driven by growth factors
PDGF,FGF, TNFα, TGFß
Metabolic factors

13. +
Remodelling
Immature collagen replaced by mature
collagen.
 Type III to Type I
 Woven bone to Laminar bone
Uninjured skin contains 10% Type III
Initial scar increases to 30% Type III

14. +
Remodeling (Day 8 to a Year)
Wound strength increases
3% at 1 week
20% at 3 weeks
80% at 3 weeks
Witte and Barbul 1997 (2)

15. +
Wound Contraction
Myofibroblasts
Secondary Intention
Contractures
Strictures

16. +
Strength of wounds


17. +Acute Wounds
History
 Symptoms
 Type of Force
 Contamination
 Event
 Potential for foreign body
 Function
 Non-accidental trauma
 Tetanus status
 Allergies
 Medications
 Comorbidities
 Previous scar formation

18. Universal Precautions
• Impermeable Gowns
• Goggles
• Masks
• Gloves
• Shoe Covers/boots
• Hair Cover

19. +
Wound Examination
 Location
 Size
 Shape
 Margins
 Depth
 Alignment with skin lines
 Neurological function
 Vascular function
 Tendon function
 Underlying structures
 Wound contamination
 Foreign bodies

20. +
Wound Consultation
Tarsal plate or
lacrimal duct
Open fracture or
joint space
Extensive facial
wounds
Associated with
amputation

21. +
Wound Consultation
Associated with loss
of function
Involves tendons,
nerves, or vessels
Involves significant
loss of epidermis
Any wound that you
are uncertain about.

22. +
Chronic Wound
A chronic wound occurs when some
factor causes the disruption of the
normal, controlled inflammatory phase
or the cellular proliferative phase.

23. +
Granulation tissue

24. +
Wound Bed Preparation
 Necrosis
 Slogh

25. +
Debridement Techniques
Surgical
Enzymactic
Mechanical
Larval

26. +
Larval Therapy
Achieve relatively rapid, atraumatic removal
of necrotic material.
May be used to remove slimy slough in
painful.
Aesthetics may be an issue

27. +
Enzymatic
 Collagenase
 Papainase –
 Grated green Paw-Paw

28. +
Mechanical
 Wet to Dry
 Saline soaked Gauze
 Hydrosurgery
 High power stream of water
 Cuts and aspirates soft tissue
 Spares delicate structures

29. Clinical Case
Surgical
Debridement
Restore perfusion

30. +
Aetiology
Intrinsic (Patient)
 Age
 Diabetes
 Hepatic Failure
 Renal Failure
 Medications
 Chemotherapy
 Steroids
 Anticoagulants
 NSAID
 Immunosuppresive
agents
 Tissue hypoxia
 Arterial
 Venous
 Nutrition
 Carbohydrates
 Proteins
 Vitamins
 C,E & A
 Trace Elements
 Zn, Fe, Cu & Mg

31. +
 Oxygen Tension is the important factor
 Arterial Partial pressure of oxygen not Hb%
 Vasoconstriction is damaging
 Nicotine
 Cold
 Fear
 Pain
 A1 antagonists
 B Anatagonists
 Hypovolaemia

32. +
Diabetes
 Formation of advanced glycosylation end products
 cell signaling pathways,
 gene expression
 which affect the ex- tracellular matrix,
 This manifests as a decreased inflammatory response,
decreased granulocyte response, and slower epithelialization.
 Neuropathy
 Vasculopathy.

33. +
Steroids
 Direct inhibitory effect on macrophages, leukocytes,
and fibroblasts, decreased collagen deposition,
 impaired angiogenesis,
 delayed epithelialization,
 decreased wound contraction,
 increased infection
 Vitamin A 25000U/ day X 8 –
 Improves epithelisation and collagen production
84

34. +
Steroids
Patients on chronic steroids have thin dermis that
avulses easily, resulting in large wounds from minor
abrasions

35. +
Aetiology
Extrinsic factors
 Smoking
 Radiation
 Cancer
 Foreign Bodies
 Trauma
 Wound infection

36. +
Chronic Wounds
 Venous
 Diabetes
 Arterial
 Haemoglobinopathies

37. +
Evidence Based Medicine
 Therapy for acute and chronic wounds, is more tradition and art
than evidence-based for a given therapy.

38. +
Wound Dressings
 Protection
 Prevent heat and water loss
 Warm and moist environment
 Reduce oedema
 Nonadherent
 Absorb exudate
 Aesthetically attractive

39. +
Wound Dressings
 Nonadherent
 Absorbitive
 Occlusive (Biologic & Nonbiologic)
 Creams/Ointments/Solutions
 Vacuum Assisted Closure

40. +
Wound Dressings
NonAdherent
Sofratulle
Adaptic
Fucidintulle
Xeroform

41. +
Wound Dressings
Absorbitive
Gauze
Foams

42. +
Wound Dressings
Occlusive
Biologic
Homograft
Xenograft
Amnion

43. +
Wound Dressing
Non Biologic
Films (Opsite / Tegaderm)
Hydrocolloids (Duoderm)
Alginates
Hydrogels

44. +
Wound Dressing
Growth Factors
Platelet Derived Growth Factor
Ketanserin- serotonin receptor anatagonist
Sucralfate-binds growth factors

45. +
Wound Dressing
Vacuum Assisted Closure
 Negative Pressure Therapy
Revolutionized wound care
Promotes granulation tissue formation
Reduces oedema
Pulls out exudate
Pulls wounds together

46. +
Hyperbaric oxygen
100% Oxygen delivered at greater than 2
atmospheres.
Increases neutrophil bactericidal capacity
Destroys anaerobic organisms
Fibroblasic activity increased
Promotes angiogenesis

47. +
Topical Antiseptics
 Hypochlorite solution(Eusol)
 Toxic to fibroblasts
 Broad spectrum antimicrobial
 Hydrogen Peroxide
 Anerobic organism
 haemostasis
 Poviodone-Iodine
 broad spectrum antimicrobial
 Inhibits fibroblasts

48. +
Topical Antiseptics
Silvadine
Acetic Acid
Pseudomonas

49. +
Overhealing
 Contractures
 Hypertrophic Scars
 Keloids

50. Contracture

51. +
Splints

52. Scar Management

53. Keloid

54. +
Scar management
Keloids
Adjuvant therapy is a must.
Superficial radiotherapy.
Triamcinolone acetate.
Pressure therapy.

55. +
References
 O'Toole E.A., Goel M., Woodley D.T., Hydrogen peroxide inhibits human keratinocyte
migration. Dermatol Surg (1996) 22 : pp 525-529.
 Margolis D.M., Berlin J.A., Strom B.L., Risk factors associated with the failure of venous
leg ulcer to heal. Arch Dermatol (1999) 135 : pp 920-926.
 Phillips T.J., Machado F., Trout R., Prognostic indicators for venous ulcers: analysis of a
randomized, double blind, placebo controlled study. J Am Acad Dermatol (2000) 43 : pp
627-630.
 Wei Li, et al Wound Healing- Prespectives.- Dermatol Clin - 01-APR-2005; 23(2): 181-92
 Zamboni W. et al. Hyperbaric Oxygen and Wound Healing. Plastic Surgey Clincs (2003) 30
67-75
 Burns J, Mancoll J and Phillips L. Impairments in Wound Healing.Plastic Surgey Clincs
(2003) 30 47-56.
 Lionelli g and Lawrence T. Surgical Clinics of North America (2003) 83 617-638
 Apractical Guide to Wound Healing. J Janis et al. Plast. Reconstr. Surg. 125: 230e, 2010.