slideshow presentation.

1. FATHIMA M SAHIR
2013 MBBS
ACME
WOUND HEALING AND ULCER
CLASSIFICATION

2. Contents
 Wound definition
 Classification of wounds
 Healing
 Types of wound healing
 Stages of wound healing
 Phases of wound healing
 Hard tissue healing
 Factors affecting wound healing
 Complication
 Management of wound

3.  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.
(SRB’s 4th Ed.)
• A cut or break in the continuity of any tissue, caused by injury
or operation.
(Bailey 23rd Ed.)

4. CLASSIFICATION OF WOUNDS
Rank and Wakefield classification
a) Tidy wounds
b) Untidy wounds

5. Tidy wound
 They are caused by sharp instruments &
contain no devitalised tissue.
 Eg:surgical incisions and cuts from glass
 Tendons,arteries, nerves may be cut
 Fractures are uncommon
a) Tidy incised wound on the finger.

6. Untidy wound
 They results from crushing, tearing, avulsion,
vascular injuries and contain devitalised
tissue.
 Tendons,arteries and nerves might be injured
in contnuity,but not divided.
 Managemnt is through wound excision to
create tidy wound and it then heals by second
intentation.
(b) Untidy avulsed wound on the hand.

7. Classification based on type of
wound
1.Bruising ,contusion & haematoma
2. Puncture wound & bites
3. Abrasion & friction burns
4. Laceration
5. Traction & avulsion
6. Crush

8. Bruise ,contution & haematoma
 A closed blunt injury may result in bruise.
 There is bleeding in to tissues and visible
discolouration.
 Bruise require no management
 Haematoma is formed when there is sufficent
bleeding to create a localised collection in the
tiisues
 A haematoma should be evacuated by open
surgery if its large or causing pressure effects.

9. Puncture wounds and bites
 Puncture wound is an open injury in which foreign
materials & organisms are likely to be carried deeply
in to underlying tissues.
 Deeper vital structures or organs may be injured, so
should be assesed:foreign body may be present in the
depth of the wound.
 Treatment is by wound irrigation,antibiotic treatment
and tetanus prophylaxis.
 Bites are particular type of puncture wound
associated with high incidence of infection,from mouth
organisms.
 There may be comb. Of deep laceration & crushing.
 All bites need careful wound excision to aviod deep
infection.
Dog bite in a child.

10. Abrasion and friction burns
 Abrasion is shearing injury in which skin surface
is rubbed off.
 Most are superficial and heal by epithelialisation
 In friction burns there will be an element of
thermal damage as well as abrasion
Abrasion

11. Laceration
 It is the result of contact with sharp objects.
 It has ragged edges with some part getting
devitalised:viabilty may be impaired.
 Wound excision, thorough warm saline wash and
suturing of wound layer by layer is required.
lacerated wound

12. Traction and avulsion
 Here,tissues are getting displaced from its normal
alignment and anatomical postion
 Occur when limbs are trapped in moving
machineries
 Degloving caused by shearing forces, rupturing
vasculature. And it can be open or closed and
localised or circumferntial
 After initial resuscitation,definitive treatment like
skin graft or nerve repair should be done.
Degloving hand injury.

13. Crush
 It’s a variant of blunt innjury and often
accompanied by compartment syndrome.
 Muscle will lose its viability ;loss of contractility
;turgid and will not bleed on cutting.
 Devitalised skin need to be removed ,de fatted
and replaced with full thickness graft.
 Compartment syndronme necesitate urgent
fasciotomy
 Muscle necrosis due to compartment syndrome
can lead to renal failure.
Fasciotomy of the lower leg.
Crush

14. Classification based on thickness of wound
a) Superficial wound –involoving epidermis and dermal
papillae.
b) Partial thickness wound- with skin loss upto deep
dermis.
c) Full thickness- loss of entire skin and subcutaneous
tissue
d) Deep wounds- extending across deep fascia into
muscles.
e) Complicated wounds-injuring nerve or vessels.
f) Penetrating wound- to cavities/orgns
Superficial
Partial thickness
Full thickness
Deep wound

15. Classification of surgical wounds
a) Clean wound- herniorrhaphy,excisions.
b) Clean contaminated wound-
appendicectomy,bowel Sx.
c) Contaminated wound-open fresh accidental
wounds,burst appendicitis.
d) Dirty infected wound-fecal peritonitis ,
empyema gallbladr.
Clean contaminated contaminated wound

16. Classification based on time elapsed
 Acute wounds –they progres through normal
phases of healing&shows signs of healing in<4
wks.
Eg:surgical/traumatic wounds.
Chronic wounds-they do not follow normal healing
process &no signs of healing in 4 wks.
Diabetes,venous /arterial disease,nutritional
deficiencies are the cause.

17. WOUND HEALING
• Healing is the body’s response to injury in an attempt to
restore normal structure and function.
(SRB’s 5th Ed.)
• It’s a complex method to achieve anatomical &
functional integrity of disrupted tissues by neutrophils
,macrophages,fibroblasts,and collagen through the
summation of number of process that follows injury.
(Bailey 23rd Ed.)
• They include coagulation, inflammation, matrix
synthesis and deposition.
• Followedbyangiogenensis,fibroplasia,epitheliasation,co
ntaction,remodelling&scar maturation

19. The process of healing involves 2 distinct
processes:
A. REGENERATION
B. REPAIR
 Regeneration: Is when healing takes place by
proliferation of parenchymal cells and usually results
in complete restoration of the original tissues.
 The goal of all surgical procedures should be
regeneration which returns the tissues to their normal
microstructure and function.
 Repair: It is a healing outcome in which tissues do
not return to their normal architecture and function.

20. TYPES OF WOUND HEALING
 Healing by first intention (wounds with opposed
edges)
 Healing by secondary intention (wounds with
separated edges)

21. Healing by first intention (wounds with
apposed edges)
Healing of wound with following characteristics:
 Clean and uninfected
 Surgically incised
 Without much loss of cells and tissue & is with
apposed edges
 Edges of wound are approximated by surgical sutures.
 more epithelial regeneration than fibrosis.

22.  The incision causes
 death of a limited number of epithelial cells and
connective tissue cells
 disruption of epithelial basal membrane continuity
 The narrow incisional space immediately fills with
clotted blood containing fibrin and blood cells;
dehydration of the surface clot forms the well known
scab that covers the wound.

23. Within 24 hours
 Neutrophils appear at
margins of incision,
moving toward fibrin clot
 Epidermis at its cut edges
thickens as a result of
mitotic activity of basal
cells
• Within 24 to 48 hours,
spurs of epithelial cells
from the both edges
migrate and grow along
the cut margins of the
dermis, depositing BM
components as they
move. They fuse in the
midline beneath the
surface scab, thus
producing a continuous
but thin epithelial layer.

24. By day 3,
 Neutrophils replaced by macrophages
 Granulation tissue progressively invades incision space
• Collagen fibers are now
present in the margins of the
incision, but at first these are
vertically oriented.
• Epithelial cell proliferation
continues, thickening epidermal
covering layer

25. By day 5,
• Incisional space is filled with granulation tissue
• Neovascularisation is maximal
• Collagen fibrils become more abundant and begin to
bridge incision
• The epidermis recovers its normal thickness, and
differentiation of surface cells yields a mature
epidermal architecture with surface keratinization

26. During the second week
 Continued accumulation of collagen and
proliferation of fibroblasts
 Leukocytic infiltrate, edema, and increased
vascularity have largely disappeared.

27. By the end of the first month,
 Scar comprises a cellular connective tissue devoid of
inflammatory infiltrate, covered now by intact epidermis.
 Dermal appendages that have been destroyed in the line
of the incision are permanently lost.
 Tensile strength of the wound increases thereafter, but it
may take months for the wounded area to obtain its
maximal strength.

28. Healing by second intention
 Wounds with separated edges
 When there is more extensive loss of cells and
tissue
 Regeneration of parenchymal cells cannot
completely reconstitute the original
architecture.
o Angiogenesis and fibroblast proliferation result
in granulation tissue formation to complete
the repair and it contracts and allows
epithelialisation and scar formation.

29. Secondary healing differs from primary healing in several
respects:
Inflammatory reaction is more intense
Much larger amounts of granulation tissue are formed
Wound contraction occurs in large surface wounds
Substantial scar formation and thinning of the
epidermis occurs

30. Difference between 1˚ & 2˚ union
of wound
FEATURES PRIMARY SECONDARY
CLEANLINESS CLEAN NOT CLEAN
INFECTION NOT INFECTED INFECTED
MARGINS SURGICALLY CLEAN IRREGULAR
SUTURES USED NOT USED
HEALING SMALL GRANULATION
TISSUE
LARGE GRANULATION
TISSUE
OUT COME LINEAR SCAR IRREGULAR WOUND
COMPLICATION NOT FREQUENT FREQUENT

31. STAGES OF WOUND HEALING
1. Stage of inflammation.
2. Stage of granulation tissue formation and
organisation.
3. Stage of epithelialisation.
4. Stage of scar formation and resorption.
5. Stage of maturation.

32. PHASES OF WOUND HEALING
For soft tissue wound healing:
 1.Inflammatory phase
 2.Proliferative phase
 3.Maturation phase

33. Inflammatory phase
 The 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 ADP, which causes thrombocytic aggregates to fill
the wound. When bleeding stops, the platelets then release
several cytokines from their alpha granules. These are
PDGF, platelet factor IV and (TGFβ).
 These attract inflammatory cells such as
polymorphonuclear lymphocytes (PMN) and macrophages.
 Platelets and the local injured tissue release vasoactive
amines such as histamine, serotonin and PGs, which increase
vascular permeability, thereby aiding infiltration of these
inflammatory cells.
 Macrophages remove devitalised tissue and micro-organisms
while regulating fibroblast activity in the proliferative phase of
healing. The initial framework for structural support of cells is

34. Proliferative Phase
 It starts from day 3 lasts for 3-6 wks.
 Characterized by formation of granulation tissue
in the wound initially and then later tensile
strength of wound increases due to collagen type
3.
 Epithelial cells are active during this phage and
are responsible for initial wound closure.
 2 key cell types are present in this phase:
a) endothelial cells
b) fibroblasts

35.  Granulation tissue:
It is a fragile structure composed of an extracellular
matrix of fibronectin,collagen, glycosaminoglycans,
proliferating endothelial cells, neocapillaries and
fibroblasts mixed with inflammatory macrophages and
lymphocytes.

36. a)Endothelial cells: Angiogenesis
Formation of new blood vessels at the site of injury
takes place by proliferation of endothelial cells(GF) from
the margins of severed blood vessels.
And by action of TNF,TGF,PDGF released by
macrophages.

37. b)Fibroblasts: Fibroplasia
 They migrate into the wound site on the 3rd day
after injury and achieve their peak numbers by
approximately 7th day.
 This action is stimulated by combination of
cytokines produced initially by platelets and
subsequently by macrophages and
lymphocytes.
 As the number of macrophages declines and
fibroblasts population increases the wound
transforms from granulomatous tissue to
granulation tissue.
 Fibroblasts produces collagen (first detected in

38.  Fibroblasts produce type III collagen initially and as
the wound matures type I collagen is formed. As
wound healing progresses, the collagen fibers
become organized by cross-linking.
 A focused type of fibroblast known as a
myofibroblast plays a significant role in wound
contraction, particularly in incisional-type wounds.
 Myofibroblasts align themselves parallel with the
wound surface and then contract, drawing the
wound edges together.
 These cells are eliminated by apoptosis after

39. Maturation Phase
• Characterised by maturation of collagen type 1
replacing collagen type 3.
• There is reallignemt of collagen fibres along the lines
of tension, decreased wound vascularity &wound
contraction due to fibroblast and myofibroblast activity

40.  Scar strength is:
 3% in 1 week
 20% in 3 weeks
 80% in 12 weeks
The phases of healing. (a) Early inflammatory phase with
platelet-enriched blood clot and dilated vessels. (b) Late inflammatory
phase with increased vascularity and increase in polymorphonuclear
lymphocytes (PMN) and lymphocytes (round cells). (c) Proliferative
phase with capillary buds and fibroblasts. (d) Mature contracted scar.

41. NORMAL HEALING IN SPECIFIC
TISSUES
 Bone
 The phases are same, but periosteal and endosteal
proliferation
leads to callus formation, 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

42.  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 neurotropism, which is mediated by
growth factors,hormones and other extracellular
matrix trophins. Nerve regeneration is
characterised 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.

43. FACTORS AFFECTING WOUND
HEALING:
1) Site of the wound
2) Structures involoved
3) Mechanism of wounding: inscisin ,crush,crush avulsion
4) Contamination
5) Loss of tissues
6) Systemic fcators
Malnutrition or vitamin and mineral deficiencies
Disease (e.g. diabetes mellitus)
Medications (e.g. steroids)
Immune deficiencies [e.g. chemotherapy, acquired
immunodeficiency syndrome (AIDS)]
Smoking

44. MANAGEMENT OF WOUNDS
 1.WOUND CLEANING
 To optimise healing envt.,by removing devitalised
tissues,exudates /crusts.
 Gentle irrigation with warm sterile isotonic NS
 2.SPECIFIC MANAGEMENT
 Inspect and classify wound
 Control bleeding,start Intravenous fluids,O2
 Inscised wound –primary suturing
 lacerated wound-wound excisd &primary suture
 Crushed injury –delayed primary suturing
 Deep devitalised –secondary suturing
 Wound with tension-fasciotomy
 Antiobiotics,fluid,blood transfusion,TT

45. COMPLICATION
 1.Deficient scar formation:
a) Wound dehiscence
b) Ulceration
 2.Excessive formation of the repair components:
a) Aberrations of growth: -hypertrophic scar
-keloid
 b)Excessive amount of granulation tissue formation:
Exuberant proliferation of fibroblasts and other
connective tissue elements: Desmoids or Aggressive
fibromatoses
 3. Formation of contractures

47. Ulcer
 An ulcer is a break in the contnuity of covering
epithelium,
either skin /mucous membrane due to molecular
death.
(SRB’s 5th ED.)
 An ulcer is a discontinuity of an epithelial surface.
It is characterised by progressive destruction of
the surface epithelium and a base which may be
necrotic granulating or malignant
(Bailey 23rd ED.)

48. Etiology
 Traumatic causes
 Mechanical
 Physical – electrical, radiation etc
 Chemical
 Vascular insufficiency
 Arterial
 Venous
 Neoplastic conditions
 SCC
 BCC
 KS
 Malignant melanoma etc

49.  Metabolic diseases
 diabetes mellitus
 Malnutrition
 Beriberi
 Tropical ulcer
 Inflammatory processes
 cellulitis
 Infective processes
 TB
 Syphilis
 Fungal infections Neurogenic causes
 Bed sores
 Perforating ulcers
 Cord Lesions
 Peripheral Neuropathies
 Other causes
 Bazin ulcer
 Martorell’s (hypertensive ulcer

50. Parts of an ulcer
 Margin-Junction between normal epithelium
&ulcer
 Edge-Area between margin &floor of ulcer
 Floor-Exposed surface of ulcer.
 Base-On which ulcer rests.

51. CLASSIFICATION
 1.Clinical classification
 2.Pathological classification
 3.Wagner’s classification

52. 1.Clinical classification
 A)Spreading ulcer
 B)Healing ulcer
 C)Callous ulcer

53. A.Spreading ulcer
 Surrounding skin is inflamed
 Floor is covered by slough
 No evidence of granulation tissue
 Purulent discharge

54. B.Healing ulcer
 Surrounding skin not inflamed
 Floor covered with granulation tissue
 Edges show bluish outline of the growing
epithelium
 Slight serous discharge

55. C.Callous ulcer
 Pale granulation tissue in the floor
 Considerable induration at the base, edge and
surrounding skin
 Show no tendency towards healing

56. 2.Pathological classification
 A)Specific ulcers
 B)Non-specific ulcers
 C)Malignant ulcers

57. A)Specific ulcers
 These include:-
 Infective ulcers e.g. syphilitic ulcers, Tuberculous
ulcer, fungal ulcers, Buruli ulcer (a neglected
tropical disease caused by infection with
Mycobacterium ulcerans)
Syphilitic

58. B)Non-specific ulcers
 These include:-
 Traumatic ulcers-mech,physi,chemical
 Arterial ulcers -atheroscleosis
 Venous ulcers e.g. Varicose ulcer
 Neurogenic ulcers (trophic ulcer) -bedsore
 Ulcers associated with malnutrition-tropical
Arterial ulcers
 Ulcers associated with other diseases e.g. Anemia, Avitaminosis,
Gout, Rheumatoid arthritis,diabetes
 Miscellaneous ulcer
Venous ulcer trophic ulcer

59. C)Malignant ulcers
 These include:-
 Squamous cell carcinoma –ulcer bleeds on
touch,vascular,induration is felt,rolled out edge,floor
contain unhealthygranulation tissue,necrotic content
 Basal cell carcinoma ( rodent ulcer)-raised and
beaded edge,floor is pigmented ,erodes in deeper
planes(face,tibia)
 Malignant melanoma-rapid spread,arise from
melanocyes(in mucosa,gelitalia,eye)
Malignant melanoma

60. 3.Wagner’s Classification
 Grade 0- Preulcerative/Healed
 Grade 1- Superficial
 Grade 2- Deeper to subcutaneous
 Grade 3- Abscess formation
 Grade 4- Gangrene of part of tissue
 Grade 5- Gangrene of entire limb

61. PATHOPHYSIOLOGY
 The natural history of an ulcer consists of three
phases:-
 Extension phase-ulcer floor is covered with
slough,purulent discharge &inflammed edge
&margin
 Transition phase-floor shows separted slough,
healthy granulation tissue, serous discharge.
 Repair phase –fibrosis, collagen diposition, scar
formation occurs

62. Investigation
 Study of discharge
 Wedge biopsy
 Xray
 FNAC of lymph nodes
 Hb,ESR,CBC,Serum protein

63. Management
 Identify the cause and treat
 Correction of anaemia,deficiencies
 Blood transfusion if neede
 Control pain and infection
 Ulcer debridement,cleaning &dressing,
 Topical for infected ulcers (Ag sulfadiazine)
 Maggot debridement therapy.

64. Thank you