The document discusses wound healing and classification, outlining the anatomy of the skin, various types of surgical wounds, and the phases of wound healing. It categorizes wounds based on factors like bacterial contamination, thickness, and rate of healing, and describes the healing process, including specific challenges and management strategies for chronic wounds. Additionally, it covers factors that impede wound healing and emphasizes the importance of appropriate antibiotic use in surgical prophylaxis.

1. Wound healing and classification
By. Emma. Olwa. Komagum.

2. Anatomy of Skin
• Epidermis:– composed of several thin layers:
stratum basale, stratum spinosum, stratum granulosum,
stratum lucidum, stratum corneum
The several thin layers of the epidermis contain the following:
a) melanocytes, which produce melanin, a pigment that
gives skin its color and protects it from the damaging
effects of ultraviolet radiation.
b) keratinocytes, which produce keratin, a water repellent
protein that gives the epidermis its tough, protective quality.

3. Anatomy cont’d
 Dermis:
– composed of a thick layer of skin that contains
collagen
and elastic fibers, nerve fibers, blood vessels, sweat and
sebaceous glands, and hair follicles.
• SubcutaneousTissue:
– composed of a fatty layer of skin that contains blood
vessels, nerves, lymph, and loose connective tissue
filled with fat cells

5. Classification of surgical wounds by:
 Risk of bacterial contamination
 Thickness of the wound
 Involvement of skin or other structures
 Time elapsing from trauma
 Morphology
 Rate of healing
 Rank & Wakefield classification

6. Classification of Wounds(bacterial
contamination)
Clean Wound:
Operative incisional wounds
2) Clean/Contaminated Wound:
uninfected wounds in which no inflammation is encountered but the
respiratory, GIT, genital, and/or urinary tract ve bn entered.
3) Contaminated Wound:
open, traumatic wounds or surgical wounds involving major break in
sterile technique that show evidence of inflammation.
4) Infected Wound:
old, traumatic wounds containing dead tissue and wounds with
evidence of a clinical infection (e.g., purulent drainage).

7. 2:Thickness of the wound
 Superficial – epidermis & papillary dermis
 Partial thickness – up to the reticular
dermis but hair follicles & sweat glands are
intact
 Full thickness - skin & subcutaneous tissue
 Deep wounds/ complicated wounds –
involving muscles, laceration of blood
vessels and nerves + wounds penetrating
into natural cavities or organs

8. 3. Involvement of skin or other
structures
 Simple wounds – one organ/ tissue
 Combined wounds – mixed tissue trauma

9. 4:Time elapsing from trauma
 Fresh wounds – up to 6hrs
 Old wounds - > 6hrs
 Remember this is a generalisation it
depends on the site i.e scalp wounds can
still be fresh 24hrs after injury

10. 5: Morphology
Open wounds Closed wounds
 Incised
 Abrasions
 Friction burns
 Laceration
 Avulsion
 Puncture wounds
 Penetrating wound
 Bite
 Crush
 Contusion
 Hematoma
 Ecchymoses
 Bruise

11. morphology
 Bruise/ Contusion; tissue bleeding with
discoloration
 Hematoma; locally collection of blood in
tissues
 Abrasion; shearing injury of skin
 Laceration; cut
 Avulsion; tearing away
 Crush; squeezed between 2 hard surfaces
 Puncture wounds and bites

12. 6: Rate of healing
 Acute
 Chronic (fail to heal within expected time
and despite proper wound care, by 3
months the wound has not healed)

13. 7: Rank & Wakefield classification
Tidy Un-tidy
 Inflicted by sharp objects
 No devitalised tissues
 Closed immediately
 Heal by primary intension
 Eg: surgical incisions,
lacerations from clean glass
or knife, abrasions
 Irregular skin damage with
skin loss
 External contamination
 Damage to underlying tss (bld
vss, nn, mm, #s)
 Shd not be closed
immediately
 Eg: crush injuries, avulsion
injuries with skin loss, burns,
infected wounds

14. Classification of Wounds Closure
 Healing by Primary Intention:
All Layers are closed. Heals in a minimum
amount of time, with no separation of the
wound edges, and with minimal scar formation.
 Delayed primary closure 3-5 day
• Healing by Secondary Intention:
Heal from the inside out. Healing is appropriate
in cases of infection, excessive trauma, tissue
loss, or imprecise approximation of tissue.

15. Phases of wound healing
1) Haemostasis by: vasoconstriction, platelet plug,
clot
2) Inflammation involving cellular and vascular
events ; histamine, bradykinin, serotonin,
complement, interleukin
Cells
Platelets; release PDGF,TGF,Von Willebrands factor,
serotonin, elastase, collagenase, thrombokinase
Neutrophils 30sec-2min, macrophages ( 3-5 )
days

16. Cells of wound healing cont’d
 Lymphocytes; release stimulating and
inhibitory factors to neutrophils and
macrophages and colony stimulating factor
 Epithelial cells From; wound edges, hair
follicles, sweat and sebaceous. Closure is
complete in 72hrs in sutured wounds.
 Keratinocytes produce GM CSF,TGF,VEGF,
fibroblast growth factor, IL 1,3,6. IL 1
stimulates fibroblast proliferation, collagen
1&3

17. 3) Granulation tissues formation
 Starts about 4-21 days after wounding.Tissue
contains; fibrin, fibronectin, collagen, GAGs,
microphages, blood vessels
 Fibroplasia; starts 24hrs myofibroblasts secret
GAGs, elastin and collagen and contribute to wound
contraction. Proliferation of fibroblasts is by thrombin,
serotonin, IL 1
 Angiogenesis; starts from capillary loops of blood
vessels adjacent to the wound by FGF and fibronectin.
Hypoxia initially plays a role later much Oxygen is
needed for neovasculisation complete in 7/7.Takes 12-
16/7 in burns.

18. Re-epithelialisation
 Re-construction of epithelium- Cells
at the free edge migrate across matrix and
become stationary then those behind migrate
( leap-frog). Cessation of migration generates a
basement with laminin v collagen iv deposition.
Bacteria delay process by release of proteolytic
enzymes.
 Contraction; this occurs 8-10/7 after injury.
Full thickness freeze injuries don’t contract.

19. 4) Remodeling/maturation
Starts from the 3rd wk - 9-12 months.This is
where collagen III is converted to collagen I, and
the tensile strength continues to increase up to
80% of normal tissue
Extracellular matrix has GAGs, proteoglycans,
glycoptns, collagen, fibronectin, laminins
Synthesis of collagen is intracellular
extracellular (amino/ carboxy-propeptidase )
then cross linkages which if abn give abn healing.
Fibroblasts play a role in collagen organization

20. Fetal wound healing
 No scar formation till early 3rd
trimester
 High hyaluronic acid and rapid deposition
of collagen is responsible for no scar
formation.
 The growth factor profile is reduced in the
fetus with low PDGF and high Epidermal
GF giving high rate of wound healing.
 Higher type III collagen has also been
attributed to lack of scar in fetus

21. Scar tissue and abnormalities
(weaker, brittle, abn contraction, kelloids, hypertrophy)
Hypertrophic scar kelloid
 Begin after surgery
 Limited boundary
 Size commensurate with
injury
 Predilection flexor surfaces
 Improve with surgery
 Usually subside with time
 Collagen I:III decreased
 May take months to begin
 Overgrow their boundary
 Minor injury may cause
large lesion
 Predilection ear lobes
 Worsened with surgery
 Progressive
 Collagen I >>III than
normal

22. Factors that affect wound healing
local systemic
 Poor blood supply
 Infection
 Foreign body
 Radiotherapy
 Corticosteroids
 Trauma
 hematoma
 Peripheral vascular disease
 Malnutrition macro & micro
 Chemotherapy & irradiation
 DM, RA, jaundice, uremia
 Aging, obesity, mental status,
shock, smoking
 Anticoagulants,
corticosteroids,
immunosuppresion

23. Healing defects
 Chronic wounds; the wound remains same size
despite care up to 3 months with no signs of
epithelialisation.
 The factors that delay healing can be local or
systemic and these ve to be addressed. DM or
venous insufficiency that cannot be alleviated may
pose difficulty in mgt.
 Chronic wounds show high turnover pathology
( rapid cell proliferation and death or growth
factor composition alteration like high TGF β3 no
β1 in DM )

24. DM ulcers
 Caused by pressure over bonny
prominences in neuropathy.
 There are rigid RBCs with micro-thrombi
compromising micro-circulation.
 Glycosylated Hb has increased affinity for
O2 reducing delivery to tissues
 Abnormal matrix proteins are synthesized
in DM
 Angiopathy in DM impaires wound healing

25. impaired healing
 Venous ulcers; valvular incompetence is implicated with
edema  tissue ischemia and are subject to reperfusion injury
plus abn growth factor composition in the matrix  chronicity.
Pressure stockings can abate the process.
 Pressure ulcers; tissue ischemia due to pressure. Patients
with spinal cord injury ve abn leukocyte response.
 Rheumatoid arthritis
 osteogenesis imperfecta ( collagen 1 gene mutation )
 Ehlers-Danlos syndrome ( amino-protease deficiency )
 Epidermolysis bullosa ( high synthesis of
metalloproteinases )
 Marfan’s syndrome

26. About management
 Clean wounds-surgical toilet+suturing+abx
 Dirty wounds/old -debridement+toilet+abx+tt
delayed closure
 Gun shot wounds and human bites, animal bites
managed as very contaminated wounds
 Burns managed as per protocol
 Full thickness wounds may need grafting
 Chronic wounds- manage underlying cause plus
wound care(DM, venous stripping,
 Read more on mgt

27. END

28. Risk Factors for SWI
 Patient-related factors:
 – Age > 60, sex (female), weight (obesity)
 – Presence of remote infections
 – Underlying disease states
 – Diabetes, Congestive heart failure (CHF)
 – Liver disease, renal failure
 – Duration of preoperative stay hospitalization
 – > 72 hours, ICU stay
 – Immuno-suppression
 – ASA (American Society of Anesthesiologists) physical
status (3,4, or 5)

29. SWI
 Surgery-related factors:
 – Type of procedure, site of surgery, emergent
surgery
 – Duration of surgery (>60- 120 min)
 – Previous surgery
 – Timing of antibiotic administration
 – Placement of foreign body
 – Hip/knee replacement, heart valve insertion,
shunt insertion
 – Hypotension, hypoxia, dehydration, hypothermia

30. SWI
 Surgery related factors:
 – Patient preparation
 – Shaving the operating site
 – Preparation of operating site
 – Draping the patient
 – Surgeon preparation
 – Hand washing
 – Skin antiseptics
 – Gloving

31. SWI
 Wound-related factors:
 – Magnitude of tissue trauma and
devitalization
 – Blood loss, hematoma
 – Wound classification
 – Potential bacterial contamination
 – Presence of drains, packs, drapes
 – Ischemia
 – Wound leakage

32. ANTIBIOTICS
 Characteristics of an optimal antibiotic for
 surgical prophylaxis:
 – Effective against suspected pathogens
 – Does not induce bacterial resistance
 – Effective tissue penetration
 – Minimal toxicity
 – Minimal side effects
 – Long half-life
 – Cost effective

33.  Appropriate antibiotic use for prevention
of SWI includes the following:
 – Appropriate timing of administered agents and
repeated dosing based on length of
 procedure and antibiotic half-life Consider re-
dosing if procedure > 4 hours
 – Appropriate selection based on procedure
performed
 – Appropriate duration to avoid infection and
decrease potential for development of resistance