3. Definition
A complex integrated sequence of cellular and
biochemical responses directed toward restoring
tissue integrity and functional capacity following
injury.
Causes of tissue injury:
External: Trauma, chemical
Internal: Ischemia, Immune-mediated, microbial
4. Classification of wounds
According to the exposure to the outer environment
Open
Close
According to the level of risk sepsis
5. According to Exposure to External
Environment
Open
Incision
Avulsion
Laceration
Abrasion
Puncture/Penetration
Gunshot
Close
Contusion/Bruise
Hematoma
Strains
Sprains
Crush injury
6. According to the level of risk sepsis
Clean wound
Clean contaminated wounds
Contaminated wounds
Dirty wounds
7. Contusion
Commonly called a bruise
Usually caused by a blunt blow and the overlying skin
is unbroken
But the tissues and blood vessels below are damaged
Trapped red blood cells in tissue spaces become
deoxygenated and dark colored
Bruising can also develop after deeper tissues e.g bones
are damaged
Injury may only become apparent after a period as
blood tracks to the body surface
If the blood collects in a discrete pool within the
tissues it is described as a HEMATOMA
8. Strains
They are injuries to muscles, fascia or tendon caused
by stretching forces.
Patients complain of pain and stiffness and there may
be associated swelling
It is important to exclude other injuries e.g. fractures
Usually resolves with rest followed by progressive
mobilization
9. Sprains
This is an injury to the fibrous tissues surrounding a
joint
Usually as a result of excessive movement of the joint
A mild sprain may involve tearing of few fibres in a
ligament, while more serious cases may involve
hematoma formation
Severe cases may involve complete tearing and
disruption of a ligament
Patient presents with local heat, pain, swelling,
disability and discoloration over area.
10. Abrasion
Abrasion is a scrape or graze
Often caused by friction injuries e.g. fall from a bikes
It’s a superficial surface wound involving the epidermis
and part of the dermis
Its often very painful as dermal nociceptors are
exposed in the damaged dermis
Needs to be well cleaned to remove dirt sticking to
wound surface.
11. Avulsion
This involves wound where there is tissue loss,
preventing the closure of the wound edges
Can be caused by gouging or tearing of tissue
12. Laceration
Usually involves a wound made by blunt object
involving considerable force
Wound edges are usually split or torn with ragged
edges
After significant trauma there may be lacerations
involving internal organs e.g. kidney, liver, spleen
Causing serious hemorrhage requiring urgent surgical
attention
13. Incised wound
This is a cut caused by a sharp object
Usually appears neat and edges easily approximated to
allow primary healing to take place
May also involve deeper structures such as nerves,
blood vessels or tendons.
Should always be assessed for such deeper injuries and
treated as required
14. Puncture wounds
May be present and misleading as small wounds
Also described as penetrating wounds
They are made by pointed or sharp objects
The wound may be closed above areas of bacterial
contamination thus having potential for infection
If base of wound cannot be seen it should be surgically
assessed with urgency.
15. Clean wound
No septic area
No break in aseptic technique during management
Such wounds should never become infected
Have infection rates of less than 3%
16. Clean contaminated wounds
Operation enters a non infected area but may
encounter bacteria
Careful control of the area should result in minimal
spillage of organisms
E.g. surgery on the upper GIT or respiratory tract
Infection rates of less than 10%
17. Contaminated wounds
Gross spillage of organisms where there is infection
already present but without pus formation
Involves an open wound that has been exposed for less
than 4hrs
Sepsis frequently exceeds 30%
18. Dirty wounds
This involves wounds that have been infected and
exposed for over 4hrs
E.g. traumatic wounds, abscess.
19. Overview: Healing Process
Healing response depends primarily on
Type of tissue involved
Nature of tissue disruption and wound closure
20. Type of tissue involved
Categorized into:
Regeneration
Repair
21. Regeneration
This is the process whereby lost specialised tissue is
replaced by the proliferation of surrounding
undamaged specialised tissue.
The replaced tissue is structurally and functionally
indistinguishable from the native tissue.
Example: Liver , Bone
22. Repair
The lost tissue is replaced by granulation tissue which
matures to form scar tissue.
The replacement tissue is coarse and has a lower
cellular content than the native tissue.
With the exception of bone and liver, tissue
disruption invariably results in repair rather than
regeneration.
23. Nature of tissue disruption and
wound closure
Quality of healing response is also influenced by the
nature of tissue disruption and circumstances
surrounding wound closure.
Categorized into:
Healing by First Intention
Healing by Second Intention
Healing by Third intention
24. First/Primary intention
This occurs when a clean laceration or surgical incision
is closed primarily with sutures/clips with the edges in
apposition.
Healing proceeds rapidly with no dehiscence and
minimal scar formation
Soundly united within 2weeks and dense scar tissue is
laid down within 1 month.
25.
26. Secondary Intention
Occurs when the wound edges are separated and the
gap between them cannot be bridged directly.
Commonly associated with avulsive injury, local
infection or inadequate closure of wound
Healing occurs slowly from bottom to the surface by a
protracted filling of the tissue defect with granulation
and connective tissue
Results in greater scar tissue formation
Scars shrink in time resulting in wound contracture.
27.
28. Third Intention
Occurs through a staged procedure that combines
secondary healing with delayed primary closure.
Avulsive or contaminated wound are repeatedly
debrided, along with antibiotic therapy and allowed to
granulate and heal by secondary intention for 5-7 days.
Once adequate granulation tissue has formed and risk
of infection minimal, the wound is then sutured close
to heal by primary intention.
31. Bleeding Phase
This is a relatively short lived phase
Normal time for bleeding to stop depends on nature of
injury and nature of tissue
E.g. Muscles bleeds longer with escape of blood into
the tissues while others e.g. ligament bleeds less (both
in volume and duration)
Average interval from injury to end of bleeding is
usually few hrs (approx. 6-8hrs)
32. However some tissues will continue to bleed for
significantly longer period although at a significantly
reduced rate
A crush type injury to a more vascular tissue e.g.
muscle could still be bleeding (minimally) 24hrs or
more post trauma
33. Inflammatory Phase
The inflammatory phase has a rapid onset (few hours)
and usually last 3-5days.
There are two essential elements to the inflammatory
events :
Vascular Events
Cellular Events
They occur in parallel and are significantly interlinked.
34. Vascular Events
Following bleeding there’s Vasoconstriction of injured
vasculature
Tissue trauma and local bleeding activate factor XII (
Hageman factor)
This initiates various effectors of the healing cascade
including the complement, plasminogen, kinin and
clotting systems.
Circulating platelets (thrombocytes) rapidly aggregate
at the injury site and adhere to each other and vascular
subendothelial collagen to form a primary haemostatic
plug.
35. Once hemostasis is secured the reactive
vasoconstriction is replaced by a more persistent
period of vasodilation which is mediated by histamine,
prostaglandins, kinins and leukotrienes.
There’s also increased vascular permeability allowing
blood plasma and other cellular mediators pass
through vessel wall by diapedesis and populate the
extravascular space.
Corresponding clinical manifestation includes
swelling, redness, heat and pain.
36. Cellular Events
The cytokines released provide chemotactic cues that
sequentially recruit the neutrophils and monocytes to site
of injury.
Neutrophils arrive at wound site within minutes of injury
and rapidly establish themselves as predominant cells.
Intracellular product release include free radicals,
cyclooxygenase products, lipooxygenase products, protease,
antiprotease, band2 protein
Proinflammatory cytokines released by perishing
neutropils including TNF- α and interleukins( IL-1a,IL-1b)
continue to stimulate the inflammatory response for
extended periods.
There’s deployment of moncytes to injury site as the levels
of neutrophils decline
37. Activated monocytes now macrophages continue with
the wound microdebridement initiated by
neutrophils
They secrete collagenases and elastases to breakdown
injured tissue and phagocytose bacteria and cell debris
(Scavengers).
They also release growth factors and cytokines (TGF-
α, TGF-β, PDGF, IGF,TNF-α and IL-1)
Regulate local tissue remodelling by proteolytic
enzymes (e.g. matrix metalloproteases and
collagenases), inducing formation of extracellular
matrix , modulating angiogenesis and fibroplasia.
40. Proliferative Phase
Starts as early as the 3rd day - 3 weeks post injury.
It is stimulated by cytokines and growth factors
secreted earlier
There’s initial deposition of granulation tissue which
matures to form scar tissue
The processes involved are fibroplasia, angiogenesis
and reepithelialization
Fibroblasts and endothelial cells migrate into the
wounded area from adjacent areas and proliferate
within the 1st few days after tissue damage
41. The damaged capillaries bud and grow forming
anastomoses re-establishing blood flow, providing
oxygen and nutrients while removing metabolic and
repair waste products.
Fibroblasts initially produce type III collagen which
becomes type I collagen as the repair matures (during
remodeling)
They also produce fibronectin and proteoglycans
which are essential components of the ground
substance.
42. New epithelium form at the surface of the dermal
wound to seal off the denuded wound surface
There’s proliferation of epidermal cells above the
basement membrane
Reepithelialization is facilitated by the shrinking of
the connective tissue to draw the wound margins
together.
Myofibroblasts derived from activated fibroblasts are
reponsible for wound contraction and early repair
strength, therefore reduce the size of the final scar.
43. Remodeling Phase
This primarily involves the collagen and its associated
extracellular matrix.
A proportion of the original fine Type III collagen is
reabsorbed and replaced with Type I collagen with
more cross links and greater tensile strength.
Homeostasis of scar collagen and ECM is regulated by
serine proteases and matrix metalloproteinases
(MMP’s) under the control of regulatory cytokines
Old fibrous tissue is removed and new scar tissue is
laid down
Final remodeling may continue for months and
possibly over a year beyond obvious healing of the
damage
45. Nerve
Neurones do not divide and are not capable of mitosis
after injury
Any functional recovery which occurs after death of
CNS neurones is only as a result of reorganisation of
surviving nerve cells to reestablish neural connections.
In peripheral nervous system axons may slowly regrow
but this doesn’t occur in most of the CNS.
This explains why transverse spinal cord injuries cause
permanent paralysis
47. Neuropraxia
This is the mildest form of nerve injury
A transient interruption of nerve conduction without
loss of axonal continuity
The continuity of the epineural sheath and axons is
maintained and morphorlogic alterations are minor.
Recovery is spontaneous and takes about 3 - 4 weeks
48. Axonotmesis
There’s physical disruption of one or more axons
without injury to stromal tissue
The individual axons and their myelin sheath are
severed but the investing schwann cells and
connective tissue elements remain intact.
Morphologic changes manifest as degeneration of the
axoplasm and associated structures distal to the site of
injury
Recovery of functional deficit depends on degree of
damage
49.
50. Neurotmesis
This is complete transection of nerve trunk with loss
of normal architecture
Spontaneous recovery is rare
Response to injured nerve in the first 12- 48hrs include
wallerian degeneration (the part of the axon separated
from the neuron’s cell body degenerates distal to the
injury)
Within 78hrs injured axons start breaking up and are
phagocytosed by adjacent schwann cells and
macrophages
51. After clearance of axonal debris, schwann cells
outgrowths attempts to connect the proximal stump
with distal nerve stump
Schwann cells proliferate to form a band(Bungers
band) which accepts the regenerating axonal sprouts
from the proximal stump
Schwann cells also secrete numerous neutrophic
factors that coordinate cellular repair and cell adhesion
molecules (CAM) that direct axonal growth
52. Regeneration rate is approx. 1mm/d and may require
6-18 months depending on length of nerve and site of
lesion
To repair severed peripheral nerves, epineural suture
repair using fine (9-0/10-0) monofilament nylon is the
accepted criterion standard.
In absence of surgical reapproximation of the nerve
stumps, proliferating schwann cells and outgrowing
axonal sprouts may align randomly within the fibrin
clot forming a disorganised mass called a neuroma
53.
54. Bone
Similar to that of soft tissue healing except that it also
involves calcification of connective tissue matrix.
Heals by regeneration instead of repair
Indirect healing: Fractured bone restores itself
spontaneously through sequential tissue formation
and differentiation
Direct healing: The displaced bone segments are
surgically manipulated into an acceptable alignment
and rigidly stabilized through the use of internal
fixation devices.
55. Stages of fracture healing
Tissue destruction and Hematoma formation
Inflammation and cellular proliferation
Stage of callus formation
Stage of consolidation
Stage of remodeling
56. Tissue destruction and Hematoma
formation
Hemorrhage from torn
vessels in harvesian
canals, marrow and
periosteum
Formation of a mass of
clotted blood
(hematoma) at the
fracture site
Site becomes swollen,
painful and inflamed
57. Inflammation and cellular
proliferation
Within 8hrs inflammatory reaction starts
PMN leukocytes and subsequently macrophages move
to fracture site and scavenge debris
Proliferation and differentiation of mesenchymal stem
cells which begin to rapidly produce a soft fracture
callus
Secretion of TGF- β, PDGF and various BMP(bone
morphogenetic protein) factors
58. Callus formation
Granulation tissue ( soft
callus) forms a few days
after fracture
Inflammation triggers cell
division and growth of new
blood vessels
Among the new cells,
chondrocytes secrete
collagen and proteoglycans
creating fibrocartilage that
forms the soft callus
59. Stage of Consolidation
Bony callus begins 3-4
weeks after injury and
continues until firm
union is formed 2-3
months later.
New bone trabeculae
appear in the
fibrocartilagenous callus
Fibrocartilaginous callus
converts into bony
(hard) callus
60. Stage of remodeling
Remodeling restores the
original shape and
internal architecture of
the fractured bone
Carried out by juxtaposed
osteoclasts and osteoblasts
called Basic Multicellular
Unit (BMU)
61. Stage of remodeling
Osteoclast at the leading edge of the BMU excavate
bone through proteolytic digestion
While active osteoblast move in, secreting layers of
osteoid slowly refilling the cavity.
Afterwards the osteoid begin to mineralize when its
about 6 μm thick.
Over time mechanically strong ,highly organized
cortical bone replaces the weaker disorganized woven
bone
62. Extraction wound
Healing of an extraction socket is a specialized
example of healing by 2nd intention
Blood fills extraction site immediately after tooth
removal from socket
Intrinsic and extrinsic pathways are activated
Fibrin meshwork formed seals the torn blood vessels
and reduces the extraction wound
63. Organization of the clot begins within the 1st 24 -
48hrs
Migration of inflammatory cells
There's accumulation osteoclast along the alveolar
crest for crestal resorption
Formation of new blood vessels in the remnants of
periodontal ligament
In the 2nd week trabeculae of osteoid slowly extend
into clot from alveolus
64. By the 3rd week extraction socket if filled with
granulation tissue with poorly calcified bone at the
wound perimeter
The surface of the wound is completely
reepithelialized with minimal or no scar formation
Active bone remodeling by deposition and resorption
continues for several weeks
Radiographic evidence of bone formation becomes
apparent about 6-8 weeks following extraction
65. Sequence of soft tissue repair
Initial examination Involves evaluation and stabilizing the
trauma patient.
Airway, Breathing and Circulation
General neurologic assessment
Glasgow Coma Scale
Thorough Head and neck examination along with general
systemic review to determine extent of associated injuries
Clinical examination and radiographs are used to diagnose
suspected fractures
66. Control bleeding/Haemostasis
Pressure dressing
Clamping/Ligation/Electrocautery of vessels
Suturing the soft tissue
Immunization of patient
Administration of 0.5mL tetanus toxoid booster dose
(immunized 5yrs prior injury)
1500 IU of tetanus immunoglobulins + booster dose
(non- immunized patients)
67. Under G.A or L.A
Administration of 2% lidocaine with 1:100,000
adrenaline
Avoid injecting directly into the wound where
important landmarks could be distorted
Regional nerve blocks are beneficial in minimizing the
amount of L.A given
68. Thorough debridement and copious irrigation with
normal saline and antiseptic solution
Aimed at minimizing bacteria wound flora and
preventing foreign bodies from being trapped beneath
the sutured skin.
Conservative excision of non-vital tissue
Devitalized tissue potentiates infection and inhibits
phagocytosis
Persistent infection leads to release of inflammatory
cytokines from monocytes and macrophages which
delays wound healing.
69. Closure of wound
Suturing
Applying adhesives
Stapling
Wound closure using sutures is preferable for facial
lacerations due to aesthetic considerations.
Layered closure is neccessary for deep lacerations and
eliminates dead space beneath the wound
Deep layers should be re-approximated with 3-0/ 4-0
buried resorbable sutures
Superficial skin can be closed with 5-0/6-0 sutures
Skin edges should be handled with care and apposed
accurately with no overlapping
Allow slight eversion of wound margins
70. Skin sutures should be removed 4 - 6days after
placement
Should have gained 3-7% tensile strength
At 7-10 days following suture removal collagen has
begun to cross-link
Tolerate controlled motion with little risk of
distruption
The wound continue to contract due to collagen and
fibroblast maturation and can continue to remodel up
to a year following injury
But never regains greater than 80% strength of intact
skin.
72. Vascular supply
Tissue perfusion play fundamental roles in wound healing
Impaired local circulation hinders delivery of nutrients ,
oxygen and antibodies to wound.
Areas with good vascularity e.g. scalp and face heal well
whereas those with poor blood supply e.g. pretibial skin
heal poorly
Oxygen is necessary for:
hydroxylation of proline and lysine,
polymerization and cross linking of procollagen strands,
collagen transport,
fibroblast and endothelial cell replication
Effective leukocyte killing
Angiogenesis and many more
73. Infection
Failure to follow aseptic technique is a frequent reason
for introducing virulent microorganisms into wound
Transformation of contaminated wounds into infected
wounds is also aided through excessive tissue trauma,
remnant necrotic tissue, foreign bodies (e.g. hair) or
compromised host defencies.
It also results in larger and more prolonged
inflammatory reaction predisposing also to excess scar
tissue formation
74. Most important factor in minimizing the risk of
infection is meticulous surgical technique including
Thorough debridement
Adequate hemostasis
Elimination of dead space
Post operative emphasis on keeping wound site clean
and protecting it from trauma
75. Wound tension
Tensions across a healing wound serves to separate the
wound edges, impairs the blood supply to the area and
predisposes to wound healing complications
Care should thus be taken when planning incisions
Where there are large gaps between wound edges and
primary apposition might not be appropriate or
possible
Such defects may be bridged using skin grafts or tissue
flaps
Better cosmetic results are obtained when incisions
follow natural skin creases on face, transversely at
joints and longitudinally on long parts of the limbs.
76. Previous irradiation
Therapeutic radiation produces collateral damage in
adjacent tissue and reduces its capacity for
regeneration and repair
Clinical and histologic features may not be apparent
for weeks, months or even years
Cellular and molecular responses are immediate
Areas that have undergone radiotherapy suffer from
patchy vasculitis, impairing their blood supply and
their healing potential
Damage to skin stem cells results in poor
reeiptheliasation
77. Poor technique
Care should be taken when making incison to create a
clean precise cut
Gentle handling of tissues is important
Rough handling and damaging tissues can result in
tissue edge necrosis, predisposing to poor healing and
infection
Careful hemostasis allows good visualisation and
reduces tissue bruising and hematoma formation
Choice of appropriate suture material and suture
removal at correct time is mportant and helps prevent
scarring associated with the sutures themselves
78. Nutritional deficiencies
Vitamin A is involved in epithelialisation and collagen
production
Vitamin C is important in the production and
modification of collagen
Zinc acts as an enzyme cofactor and has a role in cell
proliferation deficiency may be seen in patients on
long term parenteral nutrition
Protein is the main building block in wound healing
Protein amino acids are essential for collagen
production
A malnourished, hypoproteinaemic patient has
impaired inflammatory and immune responses
79. Systemic diseases
Several diseases are known to impair wound healing
e.g. diabetes, uremia and jaundice
Diabetes: tissue hyperglycemia affects wound healing
by affecting the immune system including neutrophil
and lymphocyte function, chemotaxis and
phagocytosis
Uncontrolled blood glucose also hinders red blood cell
permeability and impairs blood flow through blood
vessels at wound surface
80. Impaired hemoglobin release of oxygen results in
oxygen and nutrient deficiency at wound site
Wound ishaemia and impaired recruitment of cells
renders the wound vulnerable to infection
Uremia: can interfere with wound healing by slowing
granulation tissue formation and inducing the
synthesis of poor quality collagen.
81. Therapeutic agents
Steroids prolonged use inhibit macrophage function
and decrease inflammatory response
Diminish prolyl hydroxylase and lysyl oxidase activity,
depressing fibroplasia and collagen formation.
Epithelialization and wound contraction are also
impaired
Inactivate complement
Leads to T and B cell dysfunction
Decrease leukocyte bactericidal activity
82. Anti-neoplastic agents
Decrease WBC’s, decrease fibroblast proliferation,
decrease wound contraction, decrease protein
synthesis
Colchicine decrease collagen precursors, decrease
collagen secretion , increase activity of collagenases
Penicillamine is a calcium chelator ( calcium is
required for collagen x-linking)
NSAIDS: decrease collagen synthesis
83. Age
Wound healing is faster in young and protracted in
elderly
Decline in healing results from gradual reduction of
tissue metabolism as one ages which is also due to
decreased circulatory efficiency
This results in delayed onset of healing, protraction of
phases, and an inability to reach same level of healing
There’s also decreased tensile strength and wound
closure rate
84. Smoking
Smoking causes decreased tissue oxygenation due
peripheral vasoconstriction
It also increases carboxyhemoglobin, platelet
aggregation and blood viscosity
It also decreases collagen deposition
86. Dehiscence
Partial or Total breakdown of the layers of a surgically
repaired wound
Most instances result from tissue failure rather than
improper suturing techniques
Dehisced wound may be closed again or left to heal by
secondary intention depending on the extent of
disruption and surgeons clinical assessment
87. Incisional hernia
Dehiscence of deeper layers of a wound in which the
skin layer remains intact
There’s protrusion of underlying structures through
the deeper defect
Particularly important for abdominal wounds where
viscera such as small intestine can herniate with risks
of irreducibility, obstruction and strangulation
88. Proliferative scaring
Two common forms
Keloids
Hypertrophic scars
Keloids are overgrowth of dense fibrous tissue that
usually develops after healing of skin injury.
The tissue extends beyond the borders of the original
wound
Does not usually regress spontaneously and tends to
recur after excision.
89. This is in contrast with hypertrophic scars which typically
do not expand beyond the boundaries of the initial injury
May undergo partial spontaneous resolution
Standard treatment
Corticosteroid injections
Occlusive dressings
Compression dressings
Excisional Surgery
Radiation
Freezing (Cryosurgery)
Laser therapy
Interferon therapy
90.
91. Contractures
Can occur in any wound but more frequently in
wounds that experience delay healing, burns and those
which incision crosses langer”s lines
Contraction of a scar across a joint can result in
marked limitation of movement
It is thus important to avoid vertical incisions across a
joint
Surgical treatment of scar contracture can include skin
grafting, local flap or wound z-plasty.
92. Conclusion
Tissue healing is a complex and dynamic system which
enables effective repair of damaged tissue.
Appropriate surgical technique has the capacity to
influence the process in a positive way.
