wounds and wound healing

1. WOUND AND WOUND
HEALING
Moderator: Dr. H.S.Jolly
Presentor: Dr. Azhar

2. Wound
• Wound is a break in the integrity of the skin or
tissues , often which may be associated with
disruption of structure and function.
• Etiology: - Trauma
- Radiation
- Infection
- Iatrogenic Etc

3. CLASSIFICATION OF
WOUNDS:

4. Classification of Surgical
Wounds
a. Clean wound
• Uninfected, no inflammation
• - Resp, GI, GU tracts not entered
• - Closed primarily
• Infective rate is less than 2%.

5. Clean wound
• eg: Herniorrhaphy, excisions.
• Surgeries of the brain, joints, heart, transplant.
• Thyroid, vascular, splenectomy

6. b. Clean contaminated wound
• Resp, GI, GU tracts entered, without significant
spillage or wounds which are mechanically drained.
• Appendicectomy, Bowel surgeries.
• Gallbladder, biliary and pancreatic surgeries.
• Infective rate is 10%.

7. c. Contaminated wound
• Acute abdominal conditions, Gross Spillage from GI
tract, Rectal surgery, penetrating wounds.
• Open fresh accidental wounds.
• Infective rate is 15-30%.

8. d. Dirty infected wound
• Old traumatic wounds, devitalized tissue
• - Existing infection or perforation
• - Organisms present BEFORE procedure
• Eg: Abscess drainage, Pyocele, Empyema
gallbladder, Faecal peritonitis, wound debridement,
positive cultures pre-op, perforated bowel.
• Infective rate is 40-70%.

9. Rank and Wakefield
Classification of wounds:

10. A. Tidy wound:
• They are wounds without any tissue loss like
surgical incisions and wounds caused by sharp
objects.
• Associated fractures are uncommon in tidy
wounds.
• Healing by primary intension.

11. A. Tidy wound:

12. B. Untidy Wound
• These are wounds resulting from crushing,
tearing avulsion, vascular injury or burns,
and contain devitalized tissue
• They are usually multiple and irregular
• Commonly associated with fractures
• Heals by second intention

13. Untidy wound

14. Untidy Wound

15. Other Types of Wound
• Bruising & contusion: mild type of hematoma.
• Clean Incised Wound
• Abrasion: Superficial damage to skin
• Penetrating wounds

16. Degloving Wound
• Degloving occurs when the skin and
subcutaneous fat are stripped by
avulsion from its underlying fascia,
leaving neurovascular structures, tendon
or bone exposed.
• A degloving injury may be open or
closed.

17. Degloving Hand Injury

18. Degloving Buttock Injury

19. Crush Injury
• Crush injury is one
where a part of the
body is being
squeezed/
compressed
between two high
force or pressure
systems.

20. Lacerated Wound
• Produced by the
tearing of soft body
tissue.
• This type of wound
is often irregular
and jagged.

21. Abrasion

22. Hematoma
• Abnormal collection of
blood outside a blood
vessel. It occurs
because the wall of a
blood vessel , artery,
vein, or capillary, has
been damaged and
blood has leaked into
tissues where it does
not belong.

23. WOUND HEALING

24. Wound Healing
• It is the Physiologic Response to tissue trauma.
• It is a complex method achieved by various
components like neutrophils, macrophages ,
lymphocytes, fibroblasts, & collagen in an organized
manner.

25. Types OF Wound Healing
1. Primary Healing.
2. Secondary Healing.
3. Tertiary Healing.

26. 1. Primary Healing(primary
intension):
• Occurs in clean incised
wound.
• More epithelial regeneration
than fibrosis.
• Wound heals rapidly
• Scar will be linear, smooth
and supple.

27. 2. Secondary Healing(Secondary
Intension)
• Occurs in wounds with extensive soft tissue loss.
• Heals slowly with fibrosis.
• Wide hypertrophied and contracted scar.
• Re-epithelialization from remaining dermal
elements or wound margins.

29. Tertiary Healing(Tertiary Intension or
Delayed Primary Closure)
• Initial wound
debridement and
control of local
infection
• Wound closed with
sutures or covered
with skin graft

30. Stages of Wound Healing
1. Stage of inflammation.
2. Stage of granulation tissue formation and organization .
3. Stage of epithelialization .
4. Stage of scar formation and resorption .
5. Stage of maturation.

31. Stages of Wound Healing

32. Phases of Wound Healing

33. Phases of Wound Healing
• Wound heals In 3 phases that partially
overlap:
1. Inflammatory Phase- Stop bleeding.
2. Proliferative phase- repair of wound.
3. Maturation Phase.

34. Inflammatory phase (Lag or
Substrate or Exudative
Phase):
• Immediate to 2-5 days.
• Aim: to stop bleeding and to prevent further
injury.
• Characterized by :-

35. –Clotting cascade-haemostasis
–Platelets aggregation
–Vasoconstriction and vasodilatation
–Increased neutrophils
–Increased Macrophages

36. • Inflammatory Phase
• Vascular Cellular
Response Response
• Primary Secondary
Phase Phase

37. Vascular Response
• Primary Phase-
• Haemostasis
• Vasoconstriction
• Platelet Aggregation
• Degranulation
• Fibrotic clot
• Fibrinolysis

38. 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

39. Cellular Response
• Increased vascular permeability
• Margination
• Extravasation
• Migration of cellular mediators (neutrophils and
macrophages).

40. Growth Factors in Wound
Healing

43. Clotting cascade
• Injury to vascular tissue initiates the extrinsic
coagulation pathway.
• The resulting fibrin plug achieves hemostasis
and acts as a lattice for the aggregation of
platelets, the most common and “signature” cell
type of the early inflammatory phase.

44. Platelets aggregation
• Within minutes post-injury, platelets
(thrombocytes) aggregate at the injury site
to form a fibrin clot.
• This clot acts to control active bleeding
(hemostasis).

45. Vasoconstriction and
vasodilatation
• Immediately after a blood vessel is breached,
ruptured cell membranes release inflammatory
factors like thromboxanes and prostaglandins
that cause the vasoconstriction to prevent blood
loss and to collect inflammatory cells and
factors in the area .

46. Vasoconstriction and
vasodilatation
• This vasoconstriction lasts 5-10 minutes
and is followed by vasodilatation which
peaks at about 20 minutes post-wounding
• Vasodilatation is the result of factors
released by platelets and other cells.

47. Vasoconstriction and
vasodilatation……..
• The main factor involved in causing
vasodilation is histamine.
• Histamine also causes  vascular
permeability entry of inflammatory cells like
leukocytes into the wound site from the
bloodstream.

48. Increases polymorphonuclear
neutrophils
• Within an hour of wounding, PMNs arrive at the
wound site and become the predominant cells
in the wound for the first two days after the
Injury.
• These PMNs phagocytise debris and bacteria
and also kill bacteria by releasing free radicles.

49. Increased polymorphonuclear
neutrophils
• They also cleanse the wound by secreting
proteases that break down damaged
tissue
• PMNs usually undergo apoptosis once
they have completed their tasks and are
engulfed and degraded by macrophages.

50. Increased Macrophages
• Macrophages are essential to wound healing.
• They replace PMNs as the predominant cells in
the wound by two days after injury.
• Once they are in the wound site, monocytes
mature into macrophages

51. Increased Macrophages…..
• The macrophage's phagocytize bacteria and
damaged tissue.
• Macrophages secrete growth factors and other
cytokines that attract cells involved in the
proliferation stage of healing.

52. Proliferative phase
• It lasts about 3 weeks (or longer, depending on
the severity of the wound) .
• Aim: repair of wounded tissue.
• Characterized by
–Angiogenesis
–Fibroplasia and granulation tissue formation
–Epithelialization
–Wound contraction

53. Prolifarative Phase
• Fibroblasts deposit “ground substance”
composed mainly of glycosaminoglycans.
• Ground substance creases scaffold on which
collagen can be deposited and aggregated.

54. Angiogenesis
• Angiogenesis is the process of new blood
vessel formation and is necessary to support a
healing wound environment.
• New blood vessels are formed by vascular
endothelial cells.

55. Angiogenesis
• Endothelial cells are attracted to the
wound area chemotactically by angiogenic
factors released by platelets and
macrophages.
• Endothelial growth and proliferation is also
directly stimulated by hypoxia, and
presence of lactic acid in the wound .

56. Fibroplasia and granulation
tissue formation
• Fibroblasts begin accumulating in the wound
site 2-5 days after wounding and peaks at 1-2
weeks post-wounding .
• Fibroblasts then deposit ECM into the wound
bed, and later collagen and granulation tissue
formation.

57. Fibroplasia and granulation
tissue formation
• Granulation tissue consists of new blood
vessels, fibroblasts, inflammatory cells,
endothelial cells, myofibroblasts, and
extracellular matrix(ECM) .

58. Epithelialization
• Epithelial cells migrate across the granulation
tissue to form a barrier between the wound and
the environment .
• Epithelialization phase is usually complete
within 7-10 days.

59. Epithelialization
• Basal keratinocytes from the wound edges
and dermal appendages such as hair
follicles, sweat glands and sebacious
glands are the main cells responsible for
the epithelialization phase of wound
healing.

60. Wound contraction
• “wounds heal from side to side but contract
from end to end”.
• Contraction is a key phase of wound healing.
• If contraction continues for too long, it can lead
to disfigurement and loss of function .

61. Wound contraction
• Myofibroblasts, which are similar to
smooth muscle cells, are responsible for
contraction.
• Highest rate of contraction from days 10-
21.

62. 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.

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

64. Maturation and Remodeling
phase
• The maturation phase of tissue repair begin
when the levels of collagen production and
degradation equalize .
• The maturation phase can last for a year or
longer, depending on the size of the wound
and whether it was initially closed or left open.

65. Maturation and Remodeling
phase
• It begins at 6 weeks and lasts for 2 years.
• There is maturation of collagen by cross-linking
which is responsible for tensile strength of the
scar.
• Collagen production is not present after 42
days of wound healing.

66. Maturation and Remodeling
phase
• Initially fibrin, fibronectin, proteoglycan
deposition occurs; later collagen protein
develops to form scar. Normal dermal skin
contains 80% type I & 20% type III collagen but
granulation tissue contains mainly type III
collagen; scar contains both type I and III
collagen equally.

67. Maturation and Remodeling
phase
• Basic essential components of collagen
are proline and lysine. Hydroxylation of
lysine and later glycosylation of this
hydroxylysine decides the collagen
molecule type.

68. Maturation and Remodeling
phase
• Hydroxylation of both proline and lysine are
essential steps of collagen synthesis requires
vit-C, iron , & alpha ketogluteric acid.
• Scar strength is 3% in 1 week, 20% in 3 weeks ,
80% in 12 weeks.

69. Extra cellular matrix and cell
matrix interactions
Functions :
1. Turgor to the soft tissue
2. Rigidity to the bone
3. Supplies a substratum for the cell division
4. Regulates growth, movement, and
differentiation of the cells living within it.

70. ECM consists of 3 components :
1. Collagen
2. Adhesive glycoproteins : fibronectin,
integrins , laminin.
3. Proteoglycans.

71. Factors Affecting Wound
Healing
1. Local Factors
2. General factors

72. Local Factors
• Infections & presence of necrotic tissue
and foreign body.
• Poor blood supply.
• Venous & lymph stasis.
• Tissue tension.

73. Local Factors
• Large defects or poor apposition .
• Recurrent trauma.
• X-ray irradiation

74. General Factors
• Age, Obesity , Smoking.
• Malnutrition, Zn, Cu, Mn, and Vit-A & C
deficiency.
• Anemia.
• Pregnancy

75. General Factors
• Uremia , Jaundice , Diabetes Mellitus.
• Immunodeficiensies

76. Abnormal Wound Healing
1. Keloid.
2. Hypertrophic scar.

77. Keloid
• Defect in maturation and stabilization of
collagen fibrils, normal collagen bundles are
absent here.
• They are brownish black to pinkish black in
color due to vascularity .
• Painful, tender, hyperaesthetic (sometimes),
spreads and cause itching.

78. Keloid

79. Keloid
• Common in black females.
• Genetically predisposed (familial).
• Associated with scleroderma and Ehler-
Danlos syndrome.
• Contains : proliferating fibroblasts and
immature blood vessels, type 3 thick collagen

80. Keloid
• Spontaneous Keloid: Keloid following an
unnoticed trauma without scar formation,
seen in Negroes.
• Site : MC- sternum followed by upper arm,
chest wall and lower neck.
• DD: Hypertrophic scar

81. Treatment
• Intralesional triamcinolone injection.
• Steroid injection----excision----steroid
injection.
• Silicon gel sheeting, topical retinoids.
• Intralesional excision retaining the scar
margins may prevent recurrence. It is ideal
and better than just excision.

82. Hypertrophic Scar
• It is a cutaneous
condition
characterized by
deposits of excessive
amounts of collagen
which gives rise to a
raised scar, but not
to the degree
observed with
keloids.

83. Hypertrophic Scar
• It can occurs anywhere in body.
•
• Not genetically predisposed.
• Not extends to normal skin.
• Good response to steroids.
• Usually seen children (M=F).
• Color is pale brown .
• Not painful, non-tender.

84. Treatment
• Steroids
• Pressure garments
• Revision excision of scar and closure, if
required skin graft
• Complication- Infection, Marjolin’s Ulcer.

85. Thank You For
Guidance