trauma wound healing medical education plastic surgery surgery African experience Nigerian surgery stages of wound healing phases of wound healing collagen storage disease

1. WOUND HEALING
DR ADESIYAKAN A.
Registrar BPSU

2. OUTLINE
• INTRODUCTION
• TYPES OF WOUND HEALING
• PHASES OF WOUND HEALING
• FACTORS AFFECTING WOUND HEALING
• COMPLICATIONS OF WOUND HEALING
• DISORDERS
• WOUND HEALING IN SPECIALIZED TISSUES
• WOUND CARE
• CONCLUSION

3. INTRODUCTION
• A wound is a discontinuity in the integrity of skin and soft
tissue often associated with disruption in structure and
function.
• Wound healing is a complex cascade of cellular and
biochemical processes that attempt to restore structure
and function following injury
• It is compulsory that a surgeon understands intricately, the
mechanisms involved in wound healing and identify
factors that could impact outcomes.

4. TYPES OF WOUND
HEALING
• Regeneration : this involves stem cell differentiation and
replacement of the original tissue
• Repair ; tissue do not return to normal architecture. Typically
results in the formation of scar tissue.
• This involves chemotaxis, phagocytosis, neocollagenesis,
collagen degradation and collagen remodeling with
angiogenesis, epithelization and glycosaminoglycan
synthesis
• culminating in replacement of normal skin structures with
fibroblastic mediated scar tissue.

5. PHASES OF WOUND
HEALING
• HEMOSTASIS AND INFLAMMATION
• PROLIFERATION
• MATURATION AND REMODELLING
• Overlap

6. • HEMOSTASIS - this process halts further hemorrhage,
precedes and initiates inflammation, it involves three
processes
• Vasoconstriction - neuroendocrine
• transection of the blood vessels and consequent exposure
of subendothelial collagen. Von willebrand factor ,alpha
and dense granules release
• Temporary plug - platelets exposure to sudendothelial
collagen
• Clot formation - intrinsic and extrinsic

8. INFLAMMATION
• Cellular migration to the wound occurs in an orderly predetermined
sequence ;
• Polymorphonuclear cells)PMNs are the first cells to migrate to the wound
site
• Occurs within 6hours and peaks within 24 - 48 hours
• margination, rolling, adhesion, transmigration and chemotaxis
• PMNs essentially - decontaminate wound by phagocytosis of bacteria and
debris
• Major source of cytokines and enzymes- TNF- alpha, collagenases
• The PMN population diminishes on day 3

9. INFLAMMATION(2)
• Macrophages peak on day 3 - 4
• Have a longer life span than PMNs and remain in the wound
till healing is complete
• Major function of macrophages include ;
• A) wound decontamination
• B) ingestion and processing of antigens for presentation
to T lymphocytes
• C) regulation of wound healing

11. INFLAMMATION(4)
• T-cells
• Role of T- cells not fully understood
• The amount of CD8 cytotoxic cells correlates inversely to
wound tensile strength
• The amount of CD4 helper cells have no correlation with
wound

12. PROLIFERATION
• Characterized by formation of granulation tissue - 4 -
• Principally two(2) cells predominate ;
• i) fibroblasts -
• ii) endothelial cells
• Processes involved include :
• Angiogenesis
• Collagen synthesis
• Epithelization

13. PROLIFERATION (2)
• Granulation tissue
• A fragile structure composed
an extracellular matrix of fibrin,
fibronectin,
glycosaminoglycans,
proliferating epithelial cells,
and fibroblasts mixed with
inflammatory macrophages
and lymphocytes

14. PROLIFERATION (3)
• A) Fibroblasts migrate into the wound environment from day 3 and peaks on
day 7
• Under the influence of several cytokines initially by platelets and
subsequently by macrophages and lymphocytes
• Proliferation; activation; synthesis
• Collagen synthesis, deposition, maturation and final remodeling determines
the tensile strength of a wound
• There are over 18 collagen types but type III is the predominant type in
granulation tissue
• Fibroblasts also synthesize glycosaminoglycans (chondroitin and dermatan)

16. PROLIFERATION(5)
• Endothelial cells proliferate extensively in response to various
cytokines
• Migrate from intact venues and arterioles close to the wound
• Migration, replication and new capillary formation is under the
influence of VEGF, TNF - alpha, TGF-B
• New vessels are formed and leaky; This is responsible for the
wet nature of new granulation tissue
• Fibroblasts also differentiate into myofibroblasts that align
perpendicularly to the axis of the wound and contract.
Apoptosis occurs once wound has closed

17. PROLIFERATION(6)
• Epithelialization -
• Involves formation of an epithelial seal on the surface of
granulation tissue. It begins the edge of the wound
• where the basal and supra basal prickle cells rapidly
undergo mitosis
• Migration stops a result of contact inhibition of the
epithelial cells from the opposing edge
• Wound healing by primary intention -21 to 28 hours

18. MATURATION PHASE
• Begins day 5 - 7
• Involves conversion of granulation tissue to fibrous
connective tissue and decreased parallelism of collagen to
the plane of the wound
• Balance between collagenolysis and collagen synthesis
• Replacement of type I collagen to type III collagen
• This coincides with the formation of epithelial seal

20. MATURATION
• Tensile strength increases after the lag phase
• 3% - 1 week
• 20% - 3 weeks
• 80% - 12 weeks

22. FACTORS
LOCAL SYSTEMIC
INFECTION AGE
FOREIGN BODY OBESITY
NECROTIC TISSUE MALNUTRITION( ZINC,COPPER)
REPEATED TRAUMA ANEMIA
RADIATION MALIGNANCY
POOR BLOOD SUPPLY JAUNDICE
VENOUS/ LYMPH STASIS DIABETES
TISSUE TENSION IMMUNOSUPPRESSION
HEMATOMA STEROIDS
LARGE DEFECT CYTOTOXIC DRUGS
SITE
UNDERLYING DISEASE

23. COMPLICATIONS
• A) Deficient scar formation
• I) wound dehiscence
• ii) ulceration
• B) excessive formation of repair elements
• Aberration of growth -hypertrophic scar
• - keloid
• C) contractures and adhesions
• D) malignant change

24. COMPLICATIONS

25. DISORDERS
DISEASE DEFICIENCY
MARFANS FBN1
EHLERS DANLOS TYPE III
OSTEOGENESIS IMPERFECTA TYPE 1 COLLAGEN
EPIDERMOLYSIS BULLOSA COL7A
ACRODERMATITIS
ENTEROPATHICA
ZINC

26. SPECIALIZED
TISSUES
• BONE -
• TENDONS
• CARTILAGE
• NERVES
• GASTOINTESTINAL TRACT
• FETUS

27. SPECIALIZED
TISSUES

28. SPECIALIZED
TISSUES
• TENDONS and LIGAMENTS
• Subject to lacerations, rupture and contusion. Due to hyper
mobility the wound edges are rarely primarily apposed
• Consists of bundles of collagen fibers arranged in parallel,
interspersed with tenocytes
• Extrinsic(sheath fibroblasts) or intrinsic (tenocytes) controversy
• Proliferation of epitendinous cells that migrate into the defect,
forming a “callus”equivalent. Tenocytes and fibroblasts invade
the callus producing further collagen

29. SPECIALIZED
TISSUES
• Cartilage - consists of chondrocytes, extracellular matrix,
proteoglycans, collagen and water
• Avascular - major blood supply comes from the fragile
perichondrium
• Superficial injuries generate very little inflammatory
reaction
• Deeper injuries generate hemorrhage and provides a more
robust inflammatory process

30. SPECIALIZED
TISSUES
• NERVES
• Neuropraxia, axontemesis , neurotemesis
• Neural healing evolves three crucial steps
• I) survival of axonal cell bodies
• ii) regeneration of axons that grow across transected stumps
distal stump
• iii)migration and connection of the regenerating nerve ends to
the appropriate nerve ends or organ targets

31. SPECIALIZED
TISSUES
• FETAL TISSUES
• - nil scaring
• Wound environment and reduced inflammation

32. WOUND CARE

33. WOUND CARE
• SKIN SUBSTITUTES
• FLAPS AND GRAFTS
• VACCUM ASSISTED CLOSURE

34. FUTURE TRENDS
• Laser techniques and non- laser techniques
• Hyperbaric oxygen with human cell- conditioned media
developed in embryologiclike conditions

35. CONCLUSION
• Every surgeon, especially plastic surgeons require an in-
depth understanding of the pathophysiology of wound
healing and factors that modulate outcome so as to
proper care in the best way possible.

36. references
• Schwartz textbook of surgery
• Medscape review of current trends in wound healing
• Oloruntoba et al vol 12 ACSJ 22,2007
• Principles of surgery ;baja