This document provides a summary of wounds and wound healing. It begins with definitions of wounds and various classification systems for wounds based on factors like cleanliness, thickness, involvement of structures, time elapsed, and surgical context. It then discusses the stages and phases of wound healing, including inflammation, proliferation, remodeling and epithelialization. Various factors that can affect wound healing are outlined. Finally, it covers wound management principles and common problems like infection, dehiscence, hypertrophic scarring and keloids.

1. WOUNDS AND WOUND
HEALING
DR JITHIN M

2. WOUND : DEFINITION
• 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

3. CLASSIFICATION OF WOUNDS

4. I. RANK AND WAKEFIELD CLASSIFICATION
• a. Tidy wounds
• ► They are wounds like surgical incisions and wounds caused by sharp objects.
• ► It is incised, clean, healthy wound , without any tissue loss.
• ► Usually primary suturing is done. Healing is by primary intention.

6. b. Untidy wounds
They are due to:
- Crushing.
- Tearing.
- Avulsion.
- Devitalised injury.
- Vascular injury.
- Multiple irregular wounds.
- Burns.

7. • Fracture of the underlying bone may be present.
• Wound infection, delayed healing are common.
• Liberal excision of devitalised tissue and allowing to heal by secondary intention is
the management.
• Secondary suturing, skin graft or flap may be needed.

9. CLASSIFICATION BASED ON THICKNESS OF THE
WOUND

10. • ♦ Superficial wound : involving only epidermis and dermal papillae.
• ♦ Partial thickness wound with skin loss up to deep dermis with only deepest
part of the dermis, hair follicle shafts and sweat glands are left behind.
• ♦ Full thickness wound with loss of entire skin and subcutaneous tissue
causing spacing out of the skin edges.

11. • ♦ Deep wounds are the one extending deeper, across deep fascia into
muscles or deeper structures.
• ♦ Complicated wounds are one associated with injury to vessels or nerves.
• ♦ Penetrating wounds are one which penetrates into either natural cavities
or organs.

12. CLASSIFICATION BASED ON INVOLVEMENT OF
STRUCTURES
• ♦ Simple wounds are one involving only one organ or tissue.
• ♦ Combined wounds are one involving mixed tissues.

13. V. CLASSIFICATION BASED ON THE TIME ELAPSED
• ♦ Acute wound is up to 8 hours of trauma.
• ♦ Chronic wound is after 8 hours of trauma.

14. CLASSIFICATION OF SURGICAL WOUNDS
• a. Clean wound
• ► Herniorrhaphy.
• ► Excisions.
• ► Surgeries of the brain, joints, heart, transplant.
• ► Infective rate is less than 2%.

16. • b. Clean contaminated wound
► Appendicectomy.
► Bowel surgeries.
► Gallbladder, biliary and pancreatic surgeries.
► Infective rate is 10%.

18. • c. Contaminated wound
• ► Acute abdominal conditions.
• ► Open fresh accidental wounds.
• ► Infective rate is 15-30%.

20. • d. Dirty infected wound
• ► Abscess drainage.
• ► Pyocele.
• ► Empyema gallbladder.
• ► Faecal peritonitis.
• ► Infective rate is 40-70%.

22. WOUND HEALING

23. • Wound healing is complex method to achieve anatomical and functional
integrity of disrupted tissue by various components like neutrophils,
macrophages, lymphocytes, fibroblasts, collagen ; in an organised staged
pathways —
• haemostasis — > inflammation — > proliferation — > matrix
synthesis(collagen and proteoglycan ground substance) — > maturation — >
remodelling — > epithelialisation — > wound contraction (by myofibroblasts).

24. TYPES OF WOUND HEALING

25. PRIMARY HEALING (FIRST INTENTION)
• ♦ It occurs in a clean incised wound or surgical wound.
• Wound edges are approximated with sutures.
• There is more epithelial regeneration than fibrosis.
• Wound heals rapidly with complete closure.
• Scar will be linear and smooth.

26. HEALING BY ‘PRIMARY INTENTION’:
A CLEAN, SUTURED WOUND.

27. SECONDARY HEALING (SECOND INTENTION)
• ♦ It occurs in a wound with extensive soft tissue loss like in
• major trauma, burns and wound with sepsis.
• It heals slowly with fibrosis.
• It leads into a wide scar, often hypertrophied and contracted.
• It may lead into disability.
• Re-epithelialisation occurs from remaining dermal elements or wound
margins

28. AN OPEN WOUND:
HEALING BY SECONDARY INTENTION

29. HEALING BY THIRD INTENTION (TERTIARY WOUND HEALING
OR DELAYED PRIMARY CLOSURE)
• After wound debridement and control of local infection, wound is closed with
sutures or covered using skin graft.
• Primary contaminated or mixed tissue wounds heal by tertiary intention.

30. STAGES OF WOUND HEALING

31. • ♦ Stage of inflammation.
• ♦ Stage of granulation tissue formation and organisation. Here due to
fibroblastic activity synthesisation of collagen and ground substance occurs.
• ♦ Stage of epithelialisation.
• ♦ Stage of scar formation and resorption.
• ♦ Stage of maturation.

32. PHASES OF WOUND HEALING

33. INFLAMMATORY PHASE (LAG OR SUBSTRATE OR
EXUDATIVE PHASE)
• It begins immediately after wound healing. It lasts for 4-6 days.
• Features of inflammation are rubor, calor, tumour, dolor and loss of function.
• Macrophages secrete fibroblastic growth factor which enhances
angiogenesis.

34. CONTINUE
• ♦ Polymorphonuclear leukocytes (PMN leukocytes) appear after 48 hours
which secrete inflammatory mediators and bactericidal oxygen derived free
radicals.
• ♦ These cells also remove clots, foreign bodies and bacteria.

35. • ♦ Chemical factors involved in wound healing are:
• ► Growth factor — platelet derived, epidermal, transforming.
• ► Interleukin.
• ► Tumour necrosis factor.
• ► Prostaglandins.
• ► Collagenase.
• ► Elastase.

36. • Here haemostasis, coagulation and chemotaxis occurs.
• Coagulation begins in wound haematoma —> formation of platelet fibrin
thrombus —> release of cytokines, PDGF (platelet derived growth factor),
transforming growth factor p (TGF-P), platelet activating factor , fibrin ,
serotonin.

37. CONTINUE
• Chemotaxis causes neutrophil migration first, and then activation of
macrophages, lymphocytes , leading into phagocytosis, wound debridement,
matrix activation,angiogenesis.

38. • Chemotaxis factors are complement factors, interleukin- 1, TNF-alpha (tumour
necrosis factor-a) TGF-beta and platelet factor
• Activated macrophages produce free radicals and nitric oxide; release
cytokine to activate lymphocytes which release interferon and interleukin
(called as lymphokines). These actions are reduced in diabetes mellitus,
Cushing’s syndrome and immunosuppression increasing the rate of sepsis.

39. PROLIFERATIVE PHASE (COLLAGEN/FIBROBLASTIC
PHASE)
• ♦ It begins in 7 days and lasts for 6 weeks
• ♦ Collagen and glycosamines are produced by fibroblasts
• ♦ Hydroxyproline and hydroxylysine are synthesised by specific enzymes using
iron, alpha ketoglutarate and vitamin C.
• ♦ Tropocollagen is produced which aggregates to form collagen fibrils.
• ♦ 80-90% of their final strength (in postoperative wounds) is achieved in 30
days.

40. REMODELLING PHASE (MATURATION 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.

41. • Initially fibrin, fibronectin, proteoglycan deposition occurs; later collagen
protein develops to form scar.
• Normal dermal skin contains 80% type I (20% type III) collagen; granulation
tissue contains mainly type III collagen; scar contains both type I and III
collagen equally

42. FACTORS AFFECTING WOUND HEALING

43. LOCAL FACTORS
• Infection
• Presence of necrotic tissue and foreign body ,
• Poor blood supply
• Venous or lymph stasis
• Tissue tension
• Haematoma
• Large defect or poor apposition
• Recurrent trauma
• X-ray irradiated area

44. • Site of wound, e.g. wound over the joints and back has poor healing
• Underlying diseases like osteomyelitis and malignancy
• Mechanism and type of wound — incised/lacerated/crush/ avulsion
• Tissue hypoxia locally reduces macrophage and fibroblast activity

45. GENERAL FACTORS
• Age, obesity, smoking
• Malnutrition, zinc, copper, manganese , vitamin deficiency (Vit C,Vit A)
• Anaemia
• Malignancy
• Uraemia

46. • Jaundice
• Diabetes, metabolic diseases
• HIV and immunosuppressive diseases
• Steroids and cytotoxic drugs
• Neuropathies of different causes

47. MANAGEMENT OF WOUNDS
• a. Wound is inspected and classified as per the type of wounds.
• b. If it is in the vital area, then:
• ► The airway should be maintained.
• ► The bleeding, if present, should be controlled.
• ► Intravenous fluids are started.
• ► Oxygen, if required, may be given.
• ► Deeper communicating injuries and fractures, etc. should be looked for.

48. • c. If it is an incised wound then primary suturing is done after thorough
cleaning.
• d. If it is a lacerated wound then the wound is excised and primary suturing is
done.

49. • e. If it is a crushed or devitalised wound there will be oedema and tension in
the wound. So after wound debridement or wound excision by excising all
devitalised tissue, the oedema is allowed to subside for 2-6 days. Then
delayed primary suturing is done.

50. • f. If it is a deep devitalised wound , after wound debridement it is allowed to
granulate completely. Later , if the wound is small secondary suturing is done.
If the wound is large a split skin graft (Thiersch graft) is used to cover the
defect.
• g. In a wound with tension, fasciotomy is done so as to prevent the
development of compartment syndrome

51. • h. Vascular or nerve injuries are dealt with accordingly.
• Vessels are sutured with 6-zero polypropylene nonabsorbable suture
material.
• If the nerves are having clean cut wounds it can be sutured primarily with
polypropylene 6-zero or 7-zero suture material.

52. • i. Internal injuries (intracranial by craniotomy, intrathoracic by intercostal tube
drainage, intra-abdominal by laparotomy) has to be dealt with accordingly.
• Fractured bone is also identified and properly dealt with.

53. • j . Antibiotics, fluid and electrolyte balance, blood transfusion, tetanus toxoid
(0.5 ml intramuscular to deltoid muscle), or antitetanus globulin (ATG)
injection.

54. PRINCIPLES OF WOUND SUTURING
• ❖ Primary suturing should not be done if there is oedema/
infection/devitalised tissues/haematoma
• ❖ Always associated injuries to deeper structures like vessels/ nerves or
tendons should be looked for before closure of the wound
• ❖ Wound should be widened by extending the incision whenever needed to
have proper evaluation of the deeper structures

55. • ❖ Proper cleaning, asepsis, wound excision/debridement
• ❖ Any foreign body in the wound should be removed
• ❖ Skin closure if it is possible without tension
• ❖ Skin cover by graft/flap — immediate or delayed
• ❖ Untidy wound should be made tidy and clean before suturing

56. • ❖ Proper aseptic precautions should be undertaken
• ❖ Antibiotics/analgesics are needed
• ❖ Sutured wound should be inspected in 48 hours
• ❖ Sutures are removed after 7 days

57. PROBLEMS WITH WOUND HEALING
• ♦ Wound infection is common in devitalized deep difficult wounds.
• Diabetes, immunosuppression, cytotoxic drugs, anaemia, malnutrition,
malignancy increases the chances of wound infection.

58. • ♦ Wound dehiscence is common in all above said adverse factors.
• Wound suddenly gives away with pain causing copious serosanguineous
discharge
• It needs emergency closure of the abdominal wound using specialized
sutures or retention sutures.

59. • ♦ Deeper wound will cause specified problems like paraesthesia, ischaemia,
paralysis, etc.

60. EXCESSIVE HEALING
• Hypertrophic Scars
• Keloids

61. HYPERTROPHIC SCARS
• ♦ Occurs anywhere in the body.
• ♦ Not genetically predisposed. Not familial.
• ♦ Growth usually limits up to 6 months.
• ♦ It is limited to the scar tissue only. It will not extend to normal skin.

62. • ♦ It is pale brown in colour, not painful, nontender.
• ♦ Often self-limiting also. It responds very well for steroid injection.
• ♦ Recurrence is uncommon.
• ♦ It is common in wounds crossing tension lines, deep dermal burns, wounds
healed by secondary intention

63. • Complications :
• ♦ Often this scar breaks repeatedly and causes infection, pain.
• ♦ After repeated breakdown it may turn into Marjolin’s ulcer.

64. • Treatment :
• It is controlled by pressure garments or often revision excision of scar and
closure, if required with skin graft.

65. HYPERTROPHIC SCARS

66. KELOIDS
♦ Keloid is common in blacks. Common in females.
♦ Genetically predisposed. Often familial. Very rare in Cauca-
sians.
♦ There is defect in maturation and stabilization of collagen
fibrils. Normal collagen bundles are absent

67. • Keloid continues to grow even after 6 months, may be for many years.
• It extends into adjacent normal skin.
• It is brownish black/ pinkish black (due to vascularity) in colour, painful,
tender and sometimes hyperaesthetic; spreads and causes itching.
• Keloid may be associated with Ehlers-Danlos syndrome or scleroderma.

68. • ♦ When keloid occurs following an unnoticed trauma without scar formation
is called as spontaneous keloid , commonly seen in Negroes.
• ♦ Some keloids occasionally become nonprogressive after initial growth.
• ♦ Pathologically keloid contains proliferating immature fibroblasts,
proliferating immature blood vessels and type III thick collagen stroma

69. • Treatment :
• a. Steroid injection — intrakeloidal triamcinolone , is injected at regular
intervals, may be once in 7-10 days, of 6-8 injections.
• b. Steroid injection — excision — steroid injection.
• c. Methotrexate and vitamin A therapy into the keloid.

70. • d. Silicone gel sheeting; topical retinoids.
• e. Laser therapy.
• f. Vitamin E/palm oil massage.
• g. Intralesional excision retaining the scar margin may prevent recurrence. It is
ideal and better than just excision.
• h. Excision and irradiation or irradiation alone.
• i. Excision and skin grafting may be done.

72. THANK YOU