Physiology of wound bealing

1. WOUND HEALING
FACILITATOR : DR. KILONZO
PRESENTER : DR. ZEYTUN
GROUP B MEMBERS
DR.JOSPHAT
DR. RUKIYA
DR. SARA
DR. ZEYTUN

2. DEFINITION
• Wound :A cut or a break in integrity of skin or tissue which maybe
associated with disruption of structure and function.
• Wound healing is a mechanism whereby the body attempts to
restore the integrity of the injured part.

3. CLASSIFICATION OF WOUND
• TYPE OF WOUND- Open and closed wounds
• CLOSED WOUND-
• 1.CONTUSIONS(bruise)-Caused by blunt trauma that damage the
tissue under the skin without breaking the skin. The injured area
becomes painful, swollen and discolored.
• 2.HAEMATOMA-It is collection of blood underneath the skin .If a
haematoma is small it can be aspirated by a wide bore needle
otherwise it is evacuated by a surgical incision under aseptic
precautions.

4. OPEN WOUNDS
• Injury with exposed underlying tissue/organ and open to the outside enviroment.
1.INCISED WOUNDS-These are produced by sharp acting objects as a razor or a knife. The
edges are clean cut and there is no much tissue destruction.
2.LACERATED WOUNDS -These are deeper cuts wounds caused by sharp objects e.g in RTA
or falling from a height . Wounds are irregular in shape and tissues are severely
traumatized and devascularised . They are usually contaminated and the risk of infection is
high.
Perforating wounds - e.g gunshot wounds ,with two openings,;exit and entrance.
3.PENETRATING WOUND-These are caused by penetration of a pointed objects as a knife.
The wound are deep and there is risk of injury to deep important structures.
4.ABRASIONS - It is scraping away of the superficial layers of skin due to friction with a
hard rough surface , it is painful due to exposure of sensitive nerve endings . requires
cleaning with an antiseptic and a non-adherent dressing.

5. RANK AND WAKEFIELD CLASSIFICATION
Tidy Untidy wounds
Incised Crushed or avulsed
Clean Contaminated
Healthy tissues Devitalised tissues
Seldom tissue loss Often tissue loss
E.g surgical incisions e.g RTA wounds
wounds caused by glass or knife
Healing by primary intention By secondary or tertiary healing

6. CLASSIFICATION OF SURGICAL WOUNDS.
1.CLEAN WOUND
It is an uninfected wound in which no inflammation is encountered and are
primarily closed. The respiratory, alimentary ,genital or urinary tracts are not
entered. No viscus entered and no break in aseptic technique. Infection rate
1-2%.
2.CLEAN-CONTAMINATED
Incision through which the respiratory, alimentary ,genitalourinary tract is
entered under careful control but with no contamination encountered.
Careful control of the area should result in minimal spillage of organisms e.g.
surgery on upper git, biliary tree or respiratory tract
Infection rates for this type of surgery is less than 10%.

7. • 3.CONTAMINATED
It is open , fresh, accidental wounds. Operations with major breaks in sterile
technique or gross spillage from the GIT tract and incisions in which acute
non purulent inflammation is encountered. There is an open wound that has
been exposed for less than 4 hours e.g. following major trauma .in this type
of wound ,sepsis frequently exceeds 30%.
4.DIRTY/INFECTED
Incision undertaken dring an operation in which the viscera are perforated or
when acute inflammation with pus is encountered during the operation (e.g
emergency surgery for fecal peritonitis) and for traumatic wounds whereby
treatment is delayed , and there is fecal contamination or devitalised tissue
present.

8. CLASSIFICATION BASED ON THICKNESS OF THE WOUND
A)Superficial - only involves the epidermis.
B)Partial thickness - deeper dermis,hair follicles and sweat glands are
left behind(epidermis +superficial dermis)
C)Full thickness - loss of skin and subcutaneous tissue
D)Deep wounds - deep fascia,muscles,deeper tissues are involved
E)penetrating wound - extend into organs,cavities
F)complex wounds-involves vessels,nerves

9. BASED ON DURATION
• Acute : wound whereby injury has occured within past 3-4 weeks.
• Chronic : Wounds persists beyond 4-6 weeks

10. • The process of healing involves 2 processes;
1.regeneration
2.repair
• REGENERATION-It is when healing takes place by proliferation of
parenchymal cells and usually results in complete restoration of the
original tissues
• REPAIR-It is a healing outcome in which tissues do not return to their
normal architecture and function.it results in the formation of scar
tissue

11. CLASSIFICATION OF WOUND HEALING
• HEALING BY PRIMARY INTENTION
Clean and uninfected wounds, surgically incised, with little tissue
loss.
Healing occurs quickly , rapid influx of wound healing
cells(macrophages , fibroblast etc. ), restoration of the gap by a small
amount of scar tissue .

12. • HEALING BY SECONDARY INTENTION
Wounds that heal by secondary intention have the following characteristics
1.wounds with separate edges
2.secondary union
3.there is more extensive loss of cells and tissue
4.regeneration of parenchymal cells cannot completely constitute the
original architecture
5.abundant granulation tissue grows in from the margin to complete the
repair
• Wounds that cannot be stitched causes large amount of tissue loss are left to heal
naturally. Wound left open. More common for wounds with a rounder edge ,
cover uneven surfaces or are on surfaces where movement makes stitches or
other closure methods impossible.
• . Heals by granulation, contraction and epithelialisation Increased inflammation
and proliferation resulting to a poor scar .

13. • HEALING BY TERTIARY INTENTION
• Also referred to as delayed primary closure.
• When there is a need to delay the wound closing process incase of
infected wounds etc.
• The inflammatory and proliferative phases of healing have become
well advanced when closure of the wound is carried out.
• Less satisfactory scar than after healing by primary intention.

15. Stages Of Wound Healing
• Wound healing is a continuous , dynamic process with distinct and overlapping
phases.it occurs as a cellular response to tissue injury and involves activation of
keratinocytes, fibroblast, endothelial cells , macrophages and platelets
• Acute wounds transition through the stages of wound healing in a linear pathway
with clear start and end points
• Chronic wounds are arrested in one of these stages , usually the inflammatory
stage and cannot progress further.
• Classified into 3 or 4 phases
• 1.haemostasis
• 2.inflammatory phase
• 3.proliferative phase
• 4.remodeling or maturation phase

16. Despite the difference in amount of time taken and scar tissue produced. The sequence
of events in primary and secondary intention is similar.

17. HAEMOSTASIS
• The initial injury results in an outflow of blood and lymphatic
fluid. Both the intrinsic and extrinsic clotting mechanisms are
activated. Following vasoconstriction, platelets adhere to
damaged endothelium and discharge adenosine diphosphate
(ADP), promoting thrombocyte clumping, which dams the
wound. With the short-lived vasoconstriction complete, the
vessels dilate allowing the influx of more thrombocytes and
other blood cells.

18. • When bleeding stops, the platelets then release several cytokines
from their alpha granules. These are platelet derived growth factor
(PDGF) , platelet factor IV and transforming growth factor beta
(TGFβ). These attract inflammatory cells such as polymorphonuclear
lymphocytes (PMN) and macrophages.
• Platelets and the local injured tissue release vasoactive amines such
as histamine , serotonin and prostaglandins, which increase vascular
permeability , thereby aiding infiltration of these inflammatory cells..

19. INFLAMMATORY PHASE
• Starts within the first 6-8 hours and lasts 2-3 days.
• TGF-β facilitates PMN migration from surrounding blood vessels, where
they extrude themselves from these vessels. These cells cleanse the
wound, clearing it of debris. The PMNs attain their maximal numbers in 24-
48 hours and commence their departure by hour 72 . Other chemotactic
agents are released, including FGF, TGF-β and TGF-α, PDGF, and
plasma-activated complements C3a and C5a (anaphylactic toxins) .
• As the process continues, macrophages also exude from the vessels. The
macrophages continue the cleansing process and manufacture various
growth factors during days 3-4. The macrophages orchestrate the
multiplication of endothelial cells with the sprouting of new blood
vessels , the duplication of smooth muscle cells, and regulate
fibroblast activity in the proliferative phase. Many factors influencing
the wound healing process are secreted by macrophages. These include
TGFs, cytokines and interleukin 1 (IL-1) , tumor necrosis factor (TNF), and
PDGF.

20. PROLIFERATIVE/PROLIFERATIVE PHASE
• The proliferative phase lasts from the third day to the third week consisting
mainly of fibroblast activity with the production of collagen and ground
substance (glycosaminoglycans and proteoglycans), angioneogenesis and the re-
epithelialisation of the wound surface.
• Fibroblasts require vitamin C to produce collagen. The wound tissue formed in
the early part of this phase is called granulation tissue. In the latter part of this
phase, there is an increase in the tensile strength of the wound due to increased
collagen, which is at first deposited in a random fashion and consists of type III
collagen but is later replaced by type 1 collagen .

21. CT
• These processes are mediated by a host of cytokines and
growth factors. The interleukins strongly influence the
inflammatory process. Vascular endothelial growth factor
(VEGF) and other factors enhance blood vessel formation, and
some have multiple roles such as fibroblast growth factor
(FGF)–2, which affects not only the process of angiogenesis but
also that of reepithelialization.
• PDGF is chemotactic for fibroblasts and, along with TGF-β, is a
potent modulator of fibroblastic mitosis , leading to prolific
collagen fibril construction in later phases. Fibrinogen is cleaved
into fibrin, and the framework for completion of the coagulation
process is formed and initial framework for structural support of
cells .

22. • Angiogenesis is the product of parent vessel offshoots. The
formation of new vasculature requires extracellular matrix and
basement membrane degradation followed by migration,
mitosis, and maturation of endothelial cells. Basic FGF and
vascular endothelial growth factor are believed to modulate
angiogenesis.
• Re-epithelization occurs with the migration of cells from the
periphery of the wound and adnexal structures. This process
commences with the spreading of cells within 24 hours. Division
of peripheral cells occurs in hours 48-72, resulting in a thin
epithelial cell layer, which bridges the wound. Epidermal growth
factors are believed to play a key role in this aspect of wound
healing.

23. REMODELING/MATURATION PHASE
• After the third week, the wound undergoes constant alterations,
known as remodeling, which can last for years after the initial injury
occurred.
characterised by maturation of collagen (type I replacing type III until a
ratio of 4:1 is achieved). There is a realignment of collagen fibres along the
lines of tension, decreased wound vascularity and wound contraction due
to fibroblast and myofibroblast activity.
• Contraction of the wound is an ongoing process resulting in part
from the proliferation of the specialized fibroblasts(myofibroblasts),
which resemble contractile smooth muscle cells. Wound contraction
occurs to a greater extent with secondary healing than with primary
healing. Maximal tensile strength of the wound is achieved by the
12th week, and the ultimate resultant scar has only 80% of the
tensile strength of the original skin that it has replaced.

24. FACTORS AFFECTING WOUND HEALING
SYSTEMIC FACTORS
• 1. Age –the increased incidence of comorbidity may contribute to impaired wound healing.
Non collagenous protein accumulation at wounded sites is decreased with aging which may
impair the mechanical properties of scarring in elderly.
• 2.Nutritional state- protein is the main building block in wound healing, protein deficiency leads
to diminished synthesis of collagen and ground substance. Vitamin c deficiency is responsible for
lack of maturation of protocollagen .Vitamin A deficiency leads to deficient epithelialization.
Calcium,zinc,copper an manganese also affect wound healing.
• 3.Therapeutic agents –steroids , chemotherapeutic agents and immunosuppressive drugs inhibit
wound healing
Steroids inhibit the inflammatory phase of wound healing(angiogenesis, neutrophil and
macrophage migration and fibroblast proliferation) and the release of lysosomal enzymes
Chemotherapeutic drugs inhibit early cell proliferation and wound DNA and protein
synthesis.
• 4.Systemic diseases -several diseases are known to impair wound healing via a number of
mechanisms e.g. Diabetes results in reduced inflammation, angiogenesis and collagen
synthesis.

25. • 5.Smoking -substances in tobacco smoke nicotine, carbon monoxide, hydrogen
cyanide have been identified to have negative impact on healing.
• 6.Malnutrition -energy,carbohydrate,fat ,vitamin,protein and mineral metabolism
can affect wound healing.glucose is a major source that provides energy for
angiogenesis and deposition of new tissues.It also affects immune system which
increases susceptibility of infections.

26. LOCAL FACTORS
• 1.Vascularity -a good blood supply e.g in the face,scalp leads to nice healing while a
poor blood supply delays wound healing
• 2.Irradiation -impairs wound contraction and granulation tissue formation as it causes
ischemia.
• 3.Tension -any increased tension in the wound will lead to ischemia and impaired
healing. Sutures under tension, haematoma and infection increase the tension inside the
wound.
• 4.Foreign bodies – İncreases risk of infection,prolongs inflammatory processpredisposes
excess scar formation
• 5.Infection -it delays healing as fibroblasts compete with bacteria for oxygen and
nutrition. Bacteria secrete collagenolytic enzymes which destroy collagen fibres.
• 6. Poor technique - surgical technique affect blood supply to the area. proper extension
to prevent retraction pressure, careful hemostasis ,proper suture material selection and
proper suturing technique are important for proper wound healing,poor wound dressing

27. Principles of wound management
• The primary goal of wound management is to
1.Aid natural body process
2.produce optimal functional and cosmetic result
• Good history of the events surrounding the injury.
• Examination of the wound - depth and configuration of the wound,
presence of non-viable tissue, presence of foreign body and other
contaminants .
• Antibiotic administration and tetanus prophylaxis may be needed and
planning timing and type of wound repair should take place.

28. • Irrigation to visualize all areas of the wound and removal of foreign material is best achieved with
normal saline.
• High pressure wound irrigation is more effective in achieving complete debridement of foreign
material and nonviable tissue.
• The use of antiseptic solutions such as povidone-iodine and hydrogen peroxide on wounds is
discouraged multiple studies have shown them to be effective at controlling the growth of
microorganisms in wounds when used at low concentrations, however at high concentrations
they are cytotoxic and may actually hinder the healing process . they are useful for cleansing the
skin around the wound.
• After the wound has been explored ,irrigated and debrided, the area surrounding the wound
should be cleaned . irregular or uneven wound edges should be debrided in order to provide a
fresh edge for re-approximation.
• Initial sutures that realign the edges of these different tissue types will speed and greatly enhance
the aesthetic outcome of wound repair.
• The smallest suture required to hold the various layers of wound in approximation should be
selected in order to minimize suture related inflammation.

29. • In areas with significant superficial tissue loss ,split thickness skin grafting may be
required.This will speed the formation of an intact epithelial barrier to fluid loss
and infection
• After closing deep tissue and replacing significant tissue deficits, skin edges
should be reapproximated for cosmesis and to aid in rapid wound healing.
• Skin edges may be quickly re approximated with stainless steel staples or non
absorbable monofilament sutures.
• Failure to remove sutures or staples by 7 to 10 days after repair may result in
cosmetically inferior wound.
• When wound cosmesis is important ,placement of buried dermal sutures using
absorbable braider sutures can be considered.

30. • Dressing
• The main purpose of wound dressing is to provide the ideal environment for wound
healing.
• The dressing should facilitate the major changes taking place during healing process to
produce an optimally healed wound.
• Covering a wound with a dressing mimics the barrier role of epithelium and prevents
further damage.In addition, application of compression provides hemostasis and limits
edema.
• Characteristics of an ideal dressing include; creates a moist , clean ,warm environment.
• Provides hydration if dry or dessicated , removes excess exudate, prevents dessication
and is non-traumatic, provides protection to periwound area , allows for gaseous
exchange, impermeable to microorganism, free of toxic or irritant particles, does not
release particles or fibers, can conform to wound shape, minimal pain during application
and removal , easy to use and cost effective.

31. COMPLICATIONS OF WOUND HEALING
• WOUND DEHISCENCE – it is total breakdown of all the layers of the surgical repair of a wound.it
can be cause by suture breakage , knot slippage, cutting and excess tension on the suture line, it
can also occur in patients with poor nutrition and infection.
• Treatment : 1.Antibiotics if an infection is present
• 2. changing wound dressing often to prevent infection, open wound to air will speed
up healing , prevent infection and allow growth of new tissue from below.
• 3. surgery for 1 or more of the following; remove damaged ,infected and or dead tissue
,put new sutures in the wound, place a piece of mesh to help close the wound
• INFECTION - it is the most common cause of delayed wound healing . microbial contamination of
wound can progress to colonization , to localized infection through to systemic infection , multi-
organ dysfunction.
• Sources of contamination can be patient themselves or operating room and personnel.
• The clinical presentation of infected wounds include fever , erythema , edema , increased pain
and change in drainage to purulent nature.
• If systemic oral antibiotics will be given; if localized to the wound area it can be treated with
topical antibiotics; drainage or debridement may be necessary to remove slough and devitalized
tissue

32. HYPERTROPHIC SCAR- Excess collagen scar tissue formation , almost an over healing of a wound
.This scar is raised above the surface but it remains within the confines of the wound. Usually
occurs within 4-8 weeks following wound infecion, wound infecion , wound closure with excess
tension or other traumatic skin injury. within months it may regress .
• KELOID FORMATION- there is over activity of the healing process leading to excessive scar tissue
which is raised above the surface and extends beyond the confines of the original wound . It
continues to enlarge after 6 months upto several years .
• CONTRACTURES - this is pathologic shortening of scar tissue resulting in deformities if the scar
overlies a joint. It occurs commonly with delayed healing wounds.it can cause marked limitation
of movement if the scar is across a joint.
• INCISIONAL HERNIA – it is breakdown of deeper layers of a wound in which the skin layer remains
intact with protrusion of underlying structures through the deeper defect.

33. REFERENCES
• SRB’S Manual of surgery , Sri Ram Bhatt , 4th edition .
•
• Bailey and love’s short practice of surgery , 23rd edition
• Skin wound healing. Medscape reference