The document provides an overview of wounds, including their anatomy, classification, causes, healing process, and management. It discusses the different layers of skin, defines wounds and how they are classified based on factors like risk of contamination and depth. The four main phases of wound healing - haemostasis, inflammation, granulation, and remodeling - are summarized. Key aspects of wound management like cleaning, dressing selection, and treating underlying issues are also covered.
3. Anatomy of the 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.
4. 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.
• Subcutaneous Tissue:
– composed of a fatty layer of skin that contains blood
vessels, nerves, lymph, and loose connective tissue filled
with fat cells
5.
6. Definition;
A wound refers to the disruption in the
continuity of a tissue usually as a result of a
physical force.
For deep or visceral wounds, the term injury is
normally used, e.g. liver or splenic injuries
7. Classification of wounds depends on:
• 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
Classification
8. Classification of Wounds
1. (bacterial contamination)
1) 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).
9. 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
10. 3. Involvement of skin or other
structures
• Simple wounds – one organ/ tissue
• Combined wounds – mixed tissue trauma
11. 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
13. Morphology cont’d
• 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
14. 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)
15. 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
16. 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.
17. Causes of wounds
Being immobile-pressure sores
Burn injury
Trauma to the skin
Surgery – incisions made during operations
Underlying medical conditions such as diabetes or
some types of vascular disease
Specific types of infection such as Buruli ulcers
Tropic ulcers due to sensory loss e.g. leprosy
19. 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
20. 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.
21. 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.
22. 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
23. 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
24. 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
26. 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 )
27. 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
28. 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
29. 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,
30. Principles of Management
• Assessment
• Clean the wound
• Moist environment
• Bacterial load
• Prevent further injury
• Nutrition
• Rehabilitation
32. Treatment options
• Antibiotics
• Support stockings for varicose veins
• Treating other medical conditions, such as
anaemia and reviewing other treatments
• Surgery
– Wide excision
– Skin grafts
– Venous striping
33. Wound cleaning solutions
• Saline (0.9% NaCl+) is usually suitable
• Most other antiseptics are harmful to normal
tissue.
• Other antiseptics may be indicated for heavily
contaminated/infected wounds.
• Antiseptics are inactivated rapidly in presence
of pus/serum.
34. Wound cleaning solutions
• Recommended also are Chlorhexidine (aq
0.05% Unisept), Povidone-iodine (10% aq
solution (Betadine).
• Cetrimide is a detergent for cleaning and
can be used in presence of dirty.
• Acetic acid 5% or Oxygen are effective
against Pseudomonas aeruginosa.
• Hydrogen peroxide 3% can remove particles
of debris by its effervesces.
36. Properties of a good dressing
• Permit gaseous exchange to maintain PO2
and pH at required levels.
• Maintain high humidity: epithelization best
in moist environment.
• Maintain wound temperature close to body
core temperature for optimum mitosis and
phagocytosis.
37. Properties of a good dressing
• Enable removal of dead tissue and bacterial
chemicals, physical contaminants.
• Be impermeable to bacteria.
• Protect healing tissue from disruption by
physical forces.
• Be non adherent, no allergenic and free form
contaminants
38. Types of dressings
Conventional- gauze, cotton
Paraffin gauze
Polyurethane films (Opsite, Tegaderm)
Hydrocolloid dressings (Granuflex, Tegasorb)
Hydrogels dressings (Intrasite, Geliperm)
Osmotic Agents Dressings (Honey, Sugar)
Alginates from a sea weed (Kaltostat, Sorbsan)
Foams dressings (Lyofoam, Allevyn)