Surgical wounds can be classified based on cleanliness from clean to dirty. Wound healing involves three phases - inflammatory, proliferative, and remodeling. The inflammatory phase begins immediately after injury and involves hemostasis and inflammation. The proliferative phase lasts 2-3 weeks and involves granulation tissue formation, angiogenesis, and collagen deposition. During the remodeling phase, collagen matures and wound strength increases. Factors like nutrition, infection, and underlying illness can influence wound healing. Different tissues like bone, nerve, and tendon heal through similar phases but with tissue-specific processes like callus formation or nerve regeneration. Wound closure techniques include primary intention, secondary intention, and tertiary intention.

1. Surgical wound and wound
healing

2. Wound Definition
A wound is a break in the integrity of the skin or tissues often,
which may be associated with disruption of the structure and
function.

3. 1. Rank and Wakefield classification

4. II. Classification of surgical wounds
a. Clean wou nd(2%)
Herniorrhaphy.
Excisions.
Surgeries of the brain, joints, heart, transplant.
b. Clean contaminated wound (10%)
Appendicectomy.
Bowel surgeries, gastrojejunostomy.
Gallbladder, biliary and pancreatic surgeries.

5. c. Contaminated wound (15–30%)
Acute abdominal conditions.
Open fresh accidental wounds.
d. Dirty infected wound (40–70%)
Abscess drainage.
Pyocele.
Empyema gallbladder.
Faecal peritonitis.

6. Classification based on the type of the wound
1. Clean incised wound: It is a tidy, simple, clean cut wound with
• linear cut edges; usually due to a sharp object like blade, glass
• piece or knife. It is treated by primary suturing.

7. Lacerated wound:
It has ragged edges with some part of the tissues getting devitalized;
viability of the tissues may be impaired;
depth of the injury and tissue damage should be carefully assessed.
Proper adequate wound excision,.

8. Bruise or contusion:
 It is due to blow or blunt force to the skin and tissues underneath
wherein blood vessels or capillaries are damaged underneath.
There is skin discoloration without breaking of the skin; broken
vessels cause seepage of blood underneath; minor soft tissue injury
crushes small vessels without breaking the skin accumulating trapped
blood underneath.
 It is more on the skin over the bones; lax area like face, scrotum,
eyes; vascular areas; children, old aged, fair skin people.

9. Haematoma:
 It is a localized collection of blood after blunt trauma or after surgery.
Collected fluid blood in few minutes to hours gets clotted; later
eventually it gets liquefied and shows discoloured fluid.
Large haematoma needs drainage under general or regional
anaesthesia.
 Small haematoma usually gets absorbed (like scalp haematoma).

11. Abrasion:
 It is superficial injury (scratch/graze/pressure/ contact) and is due to
shearing of the skin where the surface is rubbed off.
This tangential force causes loss of epidermis exposing dermal
vessels and nerves leading into profuse painful oozing.
Abrasion heals by epithelialization.

12. Traction and avulsion injuries:
 These are complex injuries with tissues getting displaced from its
normal anatomical position and alignment.
Degloving
occurs when the skin and subcutaneous fat are stripped by avulsion
from the underlying fascia, leaving neurovascular structures, tendon or
bone exposed.

14. 1. Definition.
 Wound healing is a mechanism whereby the body attempts
to restore the integrity of the injured part.

15. NORMAL WOUND HEALING
This is variously described as taking place in three or four phases, the
most commonly agreed being:
1 . Hemostatic and inflammatory phase;
2 . Proliferative phase;
3 . Remodelling phase (maturing phase).

16. 1 . Hemostasis and inflammatory phase
Begins immediately after wounding and lasts 2–3 days.
 Bleeding is followed by vasoconstriction and thrombus
formation to limit blood loss.
Platelets stick to the damaged endothelial lining of vessels,
releasing adenosine diphosphate (ADP), which causes
thrombocytic aggregates to fill the wound.

17. 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
leukocytes (PMN) and macrophages

18. 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.
Macrophages remove devitalised tissue and microorganisms
while regulating fibroblast activity in the proliferative phase of
healing.
The initial framework for structural support of cells is provided
by fibrin produced by fibrinogen.

19. PMNs
 are the first infiltrating cells to enter the wound site, peaking at 24
to 48 hours.
Functions:
 Primary role is phagocytosis of bacteria and tissue debris.
Major source of cytokines early during inflammation, especially
TNF-α3
TNF-α3: angiogenesis and collagen synthesis.
Release proteases (collagenases), which participate in matrix
and ground substance degradation in the early phase of wound
healing.
not appear to play a role in collagen deposition or acquisition of
mechanical wound strength

20. Macrophages,
participate in wound débridement via phagocytosis
The macrophage’s most pivotal function is activation and recruitment
of other cells via mediators such as cytokines and growth factors.
By releasing such mediators as TGF-β, vascular endothelial growth
factor (VEGF), insulin-like growth factor (IGF), epithelial growth
factor (EGF), and lactate, macrophages regulate cell proliferation,
matrix synthesis, and angiogenesis.
 Macrophages also play a significant role in regulating angiogenesis
and matrix deposition and remodeling

21. Clinicaly in inflammatory phase patient present with
1. rubor (redness),
2. Tumor (swelling),
3. calor (heat)
4. dolor (pain).

22. 2. 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),
the growth of new blood vessels as capillary loops (angioneogenesis)
 the re-epithelialization of the wound surface.

23. 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.
This proliferative phase with its increase of collagen deposition is
associated with wound contraction, which can considerably reduce the
surface area of a wound over the first 3 weeks of healing.

24. 3. The remodelling phase
Characterized 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.
This maturation of collagen leads to increased tensile strength in the
wound which is maximal at the 12th week post injury and represents
approximately 80% of the uninjured skin strength.

25. Factors influencing healing of a wound
Site of the wound
Structures involved
 Mechanism of wounding
Incision Crush
Crush avulsion
Contamination (foreign bodies/bacteria)a
Loss of tissue
Other local factors
Vascular insufficiency (arterial or venous)
Previous radiation
Pressure

26. ● Systemic factors
Malnutrition or vitamin and mineral deficiencies
Disease (e.g. diabetes mellitus)
Medications (e.g. steroids)
Immune deficiencies (e.g. chemotherapy, AIDS)
Smoking

27. Bone
The phases are as above,
but periosteal and endosteal proliferation leads to the formation of callus, which is
immature bone consisting of osteoid (mineralised by hydroxyapatite and laid down
by osteoblasts).
In the remodelling phase, cortical structure and the medullary cavity are restored.
If fracture ends are accurately opposed and rigidly fixed, callus formation is minimal
and primary healing occurs.
 If a gap exists, then secondary healing may lead to delayed union, non-union or
malunion.

28. Nerve
Distal to the wound, Wallerian degeneration occurs.
Proximally, the nerve suffers traumatic degeneration as far as the last
node of Ranvier.
The regenerating nerve fibres are attracted to their receptors by
neurotrophism, which is mediated by growth factors, hormones and
other extracellular matrix trophins.
Nerve regeneration is characterized by profuse growth of new nerve
fibres which sprout from the cut proximal end.
Overgrowth of these, coupled with poor approximation, may lead to
neuroma formation.

29. Tendon
Repair follows the normal pattern of wound healing,
There are two main mechanisms whereby nutrients, cells and new
vessels reach the severed tendon.
 These are intrinsic, which consists of vincular blood flow and
synovial diffusion,
And extrinsic, which depends on the formation of fibrous
adhesions between the tendon and the tendon sheath.

30. The random nature of the initial collagen produced means that the
tendon lacks tensile strength for the first 3–6 weeks.
Active mobilisation prevents adhesions limiting range of motion, but
the tendon must be protected by splintage in order to avoid rupture of
the repair.

31. Classification of wound closure and healing
● Primary intention
• Wound edges opposed
• Normal healing
• Minimal scar

32. Secondary intention
• Wound left open
• Heals by granulation, contraction and epithelialisation
• Increased inflammation and proliferation
• Poor scar

33. Tertiary intention (also called delayed primary intention)
• Wound initially left open
• Edges later opposed when healing conditions favourable