This document discusses wound classification and the phases of wound healing. It defines a wound and classifies wounds based on etiology, Rank and Wakefield classification, and surgical wound classification. The three phases of wound healing are described as the inflammatory phase, proliferative phase, and maturation/remodeling phase. Key cellular and vascular responses are summarized for each phase. Factors affecting wound healing include local factors like infection and ischemia, and systemic factors like nutrition, diabetes, and medications.

1. Wound & Wound Healing

2. Definition of a wound :
ANY break in the integrity of the skin or
tissues which may be associated with
disruption of structure or function
 Etiology: - Trauma
- Radiation
- Infection
- Iatrogenic Etc

3. CLASSIFICATION OF WOUNDS

4. RANK & WAKEFIELD CLASSIFICATION
 Tidy Wounds
 Surgical incisions,
 wounds by sharp objects,
 keloid,
 Untidy Wounds
 Avulsion
 Crush injury
 Devitalised injury

5. BASED ON TYPE OF WOUND
 Bruising & contusion
 Haematoma
 Clean Incised Wound
 Lacerated Wound
 Abrasion
 Crush injury
 Penetrating wounds

6. CLASSIFICATION OF SURGICAL
WOUNDS
 Clean Wound
 Clean Contaminated Wound
 Contaminated Wound
 Dirty Infected Wound

7. CLEAN WOUND
 Clean wound is a nontraumatic, uninfected
operative wound in which neither the
respiratory, alimentary or genitourinary tracts
nor the oropharyngeal cavities are entered.
 Clean wounds are elective, primarily closed,
and undrained wounds.
 Infection rate is <2%

8. CLEAN CONTAMINATED WOUND
 Gastrointestinal, respiratory or genitor-
urinary tracts entered without significant
spillage or wounds which are mechanically
drained.
 Eg: appendicectomy, gallbladder, biliary,
pancreatic surgeries
 Infection rate <10%

9. CONTAMINATED WOUND
 Operative wound contaminated
 Fresh traumatic wound from clean source
 Gross spillage from the gastrointestinal tract
 When infected urine or bile is present
 Incision encountering acute non-purulent
inflammation.
 Eg: penetrating abdominal injury, enterotomy
 INFECTION RATE – 15 – 30%

10. DIRTY WOUND
 Traumatic wound from dirty source
 Fecal contamination
 Foreign body, Retained devitalized tissue
 Operative wound w/ acute bacterial
inflammation or perforated viscus
 Presence of pus
Eg: abscess drainage, pyocoele
INFECTION RATE : 40 – 70 %

11. WOUND HEALING

12. WHAT IS WOUND HEALING???
 Wound Healing Is the Physiologic
Response to Tissue Trauma
 It is related to tissue reconstitution which is
the process by which the body replenishes
cells that are being lost

13. TYPES OF WOUND HEALING
WOUNDHEALING
PRIMARY
SECONDARY
TERTIARY

14. PRIMARY HEALING
 Occurs in clean incised
wound
 More epithelial
regeneration than
fibrosis.
 Wound heals rapidly
 Scar will be linear,
smooth & supple.

15. SECONDARY HEALING
 Occurs in wounds
with extensive soft
tissue loss
 Heals slowly with
fibrosis
 Wide
hypertrophied and
contracted scar

16. TERTIARY / DELAYED PRIMARY
 Intial wound
debridement and
control of local
infection
 Wound closed with
sutures or covered
with skin graft

17. PHASES OF WOUND HEALING
Wound Heals In 3 Phases That Partially
Overlap:
 Inflammatory Phase
 Fibroplasia Phase
 Remodelling Phase

18. INFLAMMATORY PHASE

19. INFLAMMATORY PHASE
 (aka. lag phase or substrate phase) 0-48 hrs
INFLAMMATORY
PHASE
VASCULAR
RESPONSE
CELLULAR
RESPONSE

20. VASCULAR RESPONSE
PRIMARY PHASE –
Haemostasis
• Vasoconstriction
• Platelet Aggregation
And Degranulation
• Fibrinous Clot
• Fibrinolysis

21. VASCULAR RESPONSE
SECONDARY PHASE
 Venular Vasodilatation - 10 X Increase In
Blood Flow
 Increased Vascular Permeability - Aids In
Flow Of Chemical And Cellular Mediators
(PDGF) In Inflammation To Site Of Injury
 Lymphatic Obstruction Leads To Tissue
Edema

22. CELLULAR RESPONSE
Increased Vascular Permeability During
Inflammatory Phase Facilitates Margination,
Extravasation And Migration Of Cellular Mediators
(Pmn’s And Macrophages)
PMN’S
 Function Short Lived (0-48 Hours)
 Attacks Bacteria, Then Leaves
 Not Essential For Wound Healing Process

23. Macrophages
 Monocyte–derived
 Central Cell During Inflammatory Phase Of
Wound Repair
 Activated By Lymphokines, Immune Complexes
 Release Angiogenesis Factor
 Phagocytosis Of Wound Debris
 Essential For Wound Healing
CELLULAR RESPONSE

24. Factors Affecting Inflammatory Phase:
 Pus
Contains Both Proteolytic And Collagenolytic
Enzymes; Prolongs Inflammatory Phase And
Retards Epithelialization
 Necrotic Tissue, Foreign Body, Haematoma -
Prolongation Of Inflammatory Phase
 Steroids - Inhibit Macrophage Function

25. PROLIFERATIVE PHASE

26. PROLIFERATIVE PHASE
(Aka. Fibroplasia Phase) Day 2 To ~ 6 Weeks
CLINICAL SIGNS:
 Disappearance Of Inflammatory Signs,
 Reduction Of Swelling,
 Reduction Of Wound Size (Contraction),
 Itching

27. KEY-ELEMENTS:
 Net Collagen Synthesis,
 Increase In Wound Tensile Strength,
 Scar Formation
PROLIFERATIVE PHASE

28. PROLIFERATIVE PHASE
EPITHELIALISATION
WOUND CONTRACTION
C COLLAGEN DEPOSITION

29. EPITHELIALIZATION
 Is A Requirement For Orderly Progression
Into The Proliferative Phase. It Starts In The
Inflammatory Phase.
 It Requires De-differentiation, Mitosis,
Migration And Then Re-differentiation By
Basal Cells Of Epidermis
PROLIFERATIVE PHASE

30. WOUND CONTRACTION
 “wounds heal from side to side but contract
from end to end”
 Thought to be mediated by myofibroblast -
can produce collagen but also contains
smooth muscle filaments.
 Highest rate of contraction from days 10-21
PROLIFERATIVE PHASE

31. Wound Contraction
 Begins approximately 4-5 days after
wounding.
 Represents centripetal movement of the
wound edge towards the center of the
wound.
 Maximal contraction occurs for 12-15
days, although it will continue longer if
wound remains open.

32. Wound Contraction
 The wound edges move toward each other at an
average rate of 0.6 to .75 mm/day
 Wound contraction depends on laxity of tissues,
so a buttocks wound will contract faster than a
wound on the scalp or pretibial area.
 Wound shape also a factor, square is faster than
circular.

33. Wound Contraction
 Contraction of a wound across a joint can cause
contracture.
 Can be limited by skin grafts, full better than split
thickness.
 The earlier the graft the less contraction.
 Splints temporarily slow contraction.

34. COLLAGEN DEPOSITION
 Prior to collagen deposition fibroblasts deposit
“ground substance” composed mainly of
glycosaminoglycans.
 Function of ground substance is to create
scaffold onto which collagen can be deposited,
aggregated, and oriented in appropriate fashion
PROLIFERATIVE PHASE

35.  Starting at day 3 or 4 collagen is deposited,
net collagen deposition is positive until day
21.
 It reaches a maximum at 60 days post-
injury (80% of tensile strength of normal
skin)
PROLIFERATIVE PHASE

36. MATURATION &
REMODELLING

37. MATURATION AND RE-
MODELLING PHASE
 3 Weeks To 1-2 Years
 Type III Collagen Is Replaced By Type I Collagen,
Creation Of More Stable Bonds Between Fibers -
Decreases The Amount Of Collagen Required To
Maintain Wound Integrity
 Duration Of Phase Dependent Upon Patient Age
(Decreased Age - Increased Duration), Racial
Differences, Type Of Wound, Body Location And
Duration Of Inflammatory Phase

42. Incised wound
 Caused by sharp cutting instruments.
 Minimum loss to tissue tends to gap (the
extent of gaping depends upon elasticity
and tension).
 Edges are regular.
 Bleeds freely and painful.
 Heals by primary intension healing.

44. Lacerated wound
 Caused by tearing of
tissues,
 Wounds have irregular
jagged borders
 Loss of tissue is limited
to skin and s/c tissue.

46. DEGLOVING/AVULSION
INJURY
 Occurs when skin &
subcutaneous tissue
are stripped from
underlying fascia
leaving
neurovascular
structures, tendons,
bone exposed.

47. What is the type of wound according to Rank & Wakefield classification?

48. FACTORS AFFECTING
WOUND HEALING

49. FACTORS
WOUND
HEALING
LOCAL
SYSTEMIC

50. LOCAL FACTORS
 Infection & haematoma
 Presence of necrotic tissues and foreign
body
 Poor blood supply
 Venous or lymph stasis
 Tissue tension
 Large defect or poor apposition

51. LOCAL FACTORS
 H/O IRRADIATION
 Underlying diseases lie malignancy /
osteomyelitis
 Tissue hypoxia

52. GENERAL/SYSTEMIC FACTORS
 Age
 Obesity, smoking
 Malnutrition
 Vitamin deficiency
 Anaemia, uremia, jaundice
 Diabetes
 Steroids & cytotoxic drugs

53. MANAGING ACUTE WOUND
 HAEMOSTASIS
 CLEANSING
 EXPLORATION AND DIAGNOSIS
 DEBRIDEMENT
 REPAIR OF STRUCTURES
 REPLACEMENT OF LOST TISSUES

54.  SKIN COVER IF REQUIRED
 SKIN CLOSURE WITHOUT TENSION
 ALL THE ABOVE WITH CAREFUL
TISSUE HANDLING

55. WHEN DOES A WOUND BECOME
CHRONIC?
 In healthy individuals with no underlying factors
an acute wound should heal within three weeks
with remodeling occurring over the next year or
so.
 If a wound does not follow the normal trajectory
it may become stuck in one of the stages and the
wound becomes chronic.


56.  Chronic wounds are thus defined as wounds,
which have “failed to proceed through an
orderly and timely process to produce anatomic
and functional integrity, without establishing a
sustained anatomic and functional result.