The document provides an overview of wound classification and wound healing. It classifies wounds based on several factors such as cleanliness, thickness, involved structures, and time elapsed. There are different types of wound healing including primary intention, secondary intention, and tertiary intention. The stages of wound healing are inflammation, proliferation, remodeling. Factors affecting wound healing include infection, blood supply, nutrition, and underlying diseases. Wound management involves cleaning, debridement, closure techniques, and treatment of underlying injuries or issues. Complications of wound healing can include infection, dehiscence, hypertrophic scarring, and keloids.

1. WOUNDS ANDWOUND HEALING
Dr veeranath reddy
Assistantprofessor,
departmentofgeneral
surgery,

2. DEFINITION
• Awound is a break in the integrity of the skin or
tissues often, which may be
associated with disruption of the structure and
function

3. CLASSIFICATIONOF
WOUNDS

4. I. RANKANDWAKEFIELDCLASSIFICATION
b. Untidywounds
Theyare due to:
Crushing.
Tearing.
Avulsion.
Devitalised injury.
Vascularinjury.
Multiple irregularwounds.
Burns.
a.Tidy wounds
Theyare wounds like surgical
incisions and wounds causedby
sharpobjects.
It is incised, clean, healthy wound ,
without any tissue loss.
Usually primary suturing is done.
Healing is by primaryintention.

5. 2.CLASSIFICATIONBASEDON THICKNESSOFTHE
WOUND

6. Superficial wound :involving only epidermis and dermal
papillae.
Partial thickness wound: with skin lossup to deep dermis with
only deepest part of the dermis, hair follicle shafts and sweat glandsare
left behind.
Full thickness wound: with lossof entireskin and
subcutaneous tissue causingspacingout of the skinedges.

7. 3.CLASSIFICATIONBASEDON
INVOLVEMENTOFSTRUCTURES
♦Simple wounds are one involving only one organ
or tissue.
♦Combined wounds are one involving mixed
tissues.

8. 4.CLASSIFICATIONBASEDON THETIME ELAPSED
• Acute wound is up to 8 hours of
trauma.
• Chronic wound is after 8 hours of
trauma.

9. 5.CLASSIFICATIONOFSURGICAL
WOUNDS
• a. Cleanwound
• Herniorrhaphy.
• Excisions.
• Surgeriesof the brain, joints, heart, transplant.
• Infective rate is lessthan2%.

11. b. Cleancontaminated wound
Appendicectomy.
Bowelsurgeries.
Gallbladder, biliary and pancreatic
surgeries.
Infective rate is10%.

13. • c. Contaminated wound
• Acute abdominal
conditions.
• Open fresh accidental
wounds.
• Infective rate is15-30%.

15. • d. Dirty infectedwound
• Abscessdrainage.
• Pyocele.
• Empyemagallbladder.
• Faecalperitonitis.
• Infective rate is40-70%.

17. WOUNDHEALING

18. • Wound healing is complex method to achieveanatomical
and functional integrity of disrupted tissue by various
components like neutrophils, macrophages, lymphocytes,
fibroblasts, collagen. in an organised staged pathways.

19. TYPESOFWOUND HEALING

20. PRIMARYHEALING (FIRSTINTENTION)
• It occursin aclean incised wound orsurgical
wound.
• Wound edgesare approximated with sutures.
• There is more epithelial regeneration thanfibrosis.
• Wound healsrapidly with completeclosure.
• Scarwill be linear andsmooth.

21. HEALING BY‘PRIMARYINTENTION’: ACLEAN,
SUTURED WOUND.

22. SECONDARYHEALING (SECONDINTENTION)
• It occursin awound with extensive soft tissuelosslike in
• major trauma, burns and wound withsepsis.
• It healsslowly withfibrosis.
• It leads into awide scar,oftenhypertrophied and contracted.
• It may lead intodisability.
• Re-epithelialisation occursfrom remaining dermal elements or
wound margins

23. ANOPENWOUND:HEALINGBY
SECONDARYINTENTION

24. HEALINGBYTERTIARYINTENTIONORDELAYEDPRIMARY
CLOSURE
• After wound debridement and control of local infection,
wound is closed with sutures or covered using skingraft.
• Primary contaminated or mixed tissue wounds heal by tertiary
intention.

25. STAGES OF WOUND
HEALING

26. 1.Stageof inflammation.
2.Stageof granulation tissue formation and organisation. Here due to
fibroblastic activity synthesisation of collagen and ground substance
occurs.
3.Stageof epithelialisation.
4.Stage of scar formation andresorption.
5.Stageof maturation.

27. INFLAMMATORYPHASE(LAGORSUBSTRATEOR
EXUDATIVEPHASE)
• 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 whichenhances
angiogenesis.

28. CONTINUE
• ♦Polymorphonuclear leukocytes (PMN leukocytes) appear after 48 hours
which secrete inflammatory mediators and bactericidal oxygen derivedfree
radicals.
• ♦Thesecells also remove clots, foreign bodies andbacteria.

29. • ♦Chemical factors involved in wound healingare:
• ► Growth factor —platelet derived, epidermal,transforming.
• ► Interleukin.
• ► Tumour necrosisfactor.
• ► Prostaglandins.
• ► Collagenase.
• ► Elastase.

30. • Here haemostasis, coagulation and chemotaxisoccurs.
• 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.

31. CONTINUE
• Chemotaxis causesneutrophil migration first, and then activation of
macrophages, lymphocytes , leading into phagocytosis, wounddebridement,
matrix activation,angiogenesis.

32. • Chemotaxis factors are complement factors, interleukin- 1, TNF-alpha(tumour
necrosis factor-a) TGF-betaand platelet factor
• Activated macrophages produce free radicals and nitric oxide; release
cytokine to activate lymphocytes which release interferon and interleukin
(called aslymphokines). Theseactions are reduced in diabetes mellitus,
Cushing’s syndrome and immunosuppression increasing the rate ofsepsis.

33. PROLIFERATIVEPHASE(COLLAGEN/FIBROBLASTIC
PHASE)
• ♦It begins in 7 daysand lasts for6 weeks
• ♦Collagen and glycosamines are produced by fibroblasts
• ♦Hydroxyproline and hydroxylysine are synthesised by specific enzymesusing
iron, alpha ketoglutarate and vitaminC.
• ♦Tropocollagen is produced which aggregates to form collagenfibrils.
• ♦80-90% of their final strength (in postoperative wounds) is achieved in 30
days.

34. REMODELLINGPHASE(MATURATIONPHASE)
• ♦It begins at 6 weeks and lasts for2 years.
• ♦There is maturation of collagen by cross-linking which is responsiblefor
tensile strength of thescar.
• ♦Collagen production is not present after 42 daysof woundhealing.

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

36. FACTORSAFFECTINGWOUNDHEALING

37. LOCALFACTORS
• Infection
• Presenceof necrotic tissue and foreign body,
• Poor blood supply
• Venousor lymph stasis
• Tissuetension
• Haematoma
• Largedefect or poor apposition
• Recurrent trauma
• X-ray irradiated area

38. • Site ofwound, e.g. wound over the joints and back haspoor healing
• Underlying diseaseslike osteomyelitis andmalignancy
• Mechanism and type of wound —incised/lacerated/crush/avulsion
• Tissuehypoxia locally reduces macrophage and fibroblast activity

39. GENERALFACTORS
• Age,obesity, smoking
• Malnutrition, zinc, copper, manganese, vitamin deficiency (Vit C,VitA)
• Anaemia
• Malignancy
• Uraemia

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

41. MANAGEMENTOFWOUNDS
• a. Wound is inspected and classified asper the type ofwounds.
• b. If it is in the vital area, then:
• ► Theairway should bemaintained.
• ► Thebleeding, if present, should becontrolled.
• ► Intravenous fluids arestarted.
• ► Oxygen,if required, may begiven.
• ► Deeper communicating injuriesand fractures, etc. should be looked for.

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

43. • e. If it is acrushed or devitalised wound there will be oedema and tension in
the wound. Soafter wound debridement or wound excision by excising all
devitalised tissue, the oedema is allowed to subside for 2-6 days.Then
delayed primary suturing isdone.

44. • f. If it is adeep devitalised wound , after wound debridement it is allowed to
granulate completely. Later , ifthe wound is small secondary suturing is done.
If the wound is large asplit skin graft (Thiersch graft) is used to cover the
defect.
• g. In awound with tension, fasciotomy is done soasto preventthe
development of compartmentsyndrome

45. • h. Vascular or nerve injuries are dealt withaccordingly.
• Vesselsare sutured with 6-zero polypropylene nonabsorbablesuture
material.
• If the nerves are having clean cut wounds it can be sutured primarily with
polypropylene 6-zero or 7-zero suturematerial.

46. • i. Internal injuries (intracranial by craniotomy, intrathoracic by intercostal tube
drainage, intra-abdominal by laparotomy) hasto be dealt withaccordingly.
• Fractured bone is also identified and properly dealtwith.

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

48. PRINCIPLESOFWOUNDSUTURING
• ❖ 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 deeperstructures

49. • ❖ Proper cleaning, asepsis,woundexcision/debridement
• ❖Any foreign body in the wound should be removed
• ❖ Skinclosure if it is possible without tension
• ❖ Skincover by graft/flap —immediate ordelayed
• ❖Untidy wound should be made tidy and clean before suturing

50. • ❖ Proper aseptic precautions should beundertaken
• ❖ Antibiotics/analgesics areneeded
• ❖ Sutured wound should be inspected in48 hours
• ❖ Sutures are removed after 7days

51. PROBLEMSWITHWOUNDHEALING
• ♦Wound infection is common in devitalized deep difficultwounds.
• Diabetes, immunosuppression, cytotoxic drugs, anaemia,malnutrition,
malignancy increases the chancesof woundinfection.

52. • ♦Wound dehiscence is common in all above said adversefactors.
• Wound suddenly gives away with pain causing copiousserosanguineous
discharge
• It needs emergency closure ofthe abdominal wound using specialized
sutures or retention sutures.

53. • ♦Deeper wound will causespecified problems like paraesthesia,ischaemia,
paralysis, etc.

54. EXCESSIVEHEALING
• Hypertrophic Scars
• Keloids

55. HYPERTROPHICSCARS
• ♦Occursanywhere in the body.
• ♦Not genetically predisposed. Notfamilial.
• ♦Growth usually limits up to6 months.
• ♦It is limited to the scar tissue only. It will not extend to normal skin.

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

57. • Complications:
• ♦Often this scarbreaks repeatedly and causesinfection, pain.
• ♦After repeated breakdown it may turn into Marjolin’s ulcer.

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

59. HYPERTROPHICSCARS

60. KELOIDS
♦Keloid is common in blacks. Common infemales.
♦Genetically predisposed. Often familial. Very rare inCauca-
sians.
♦There is defect in maturation and stabilization ofcollagen
fibrils. Normal collagen bundles areabsent

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

62. • ♦When keloid occurs following an unnoticed trauma without scarformation
is called asspontaneous keloid , commonly seenin Negroes.
• ♦Somekeloids occasionally become nonprogressive after initial growth.
• ♦Pathologically keloid contains proliferating immature fibroblasts,
proliferating immature blood vesselsand type III thickcollagen stroma

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

64. • d. Silicone gel sheeting; topicalretinoids.
• e. Lasertherapy.
• f. Vitamin E/palm oilmassage.
• g. Intralesional excision retaining the scar margin may prevent recurrence. It is
ideal and better than justexcision.
• h. Excision and irradiation or irradiationalone.
• i. Excision and skin grafting may bedone.

66. THANKYOU