2. I dressed the wound; god healed Itâ
-Ambroise Pare, French Surgeon, 16th Century
3. LEARNING OBJECTIVES
ī§ WOUND
ī§ CLASSIFICATION OF WOUND
ī§ WOUND HEALING
ī§ CLASSIFICATION
ī§ PHASES AND STAGES
ī§ HEALING IN SPECIFIC TISSUE
ī§ FACTOR AFFECTING WOUND HEALING
ī§ MANAGEMENT OF WOUND
ī§ COMPLICATION OF WOUND
4. WOUND
ī§ Wound is a break in the integrity of skin or
tissue often ,which may be associated with
disruption of the structure and function.
ī§ Wound is an injury to the body that is usually
associated with damage to underlying
tissues.
ī§ Common causes are violence, accident or
surgery that typically involves laceration or
breaking of a membrane (as skin).
5. CLASSIFICATION OF WOUND
(Rank &Wakefield)
ī§ Two Types:
ī§ 1.TIDY-Incised,caused by sharp object,
no tissue loss,heal by primary intention.
ī§ 2.UNTIDY-Crushed,teared,devitalised,burn,
tissue loss,heal by secondary intention.
7. OTHER CLASSIFICATION
1.CLOSED WOUND
-Contusion or bruising
-Abrasion
-Haematoma
2.OPENED WOUND
-Incised
-Lacerated
-Penetrating
-Crushed or contused wound
8. ī§ Contusion:-Minor soft injury without break in skin
and there is discolouration of skin.
ī§ Abrasion:-Shearing of skin,surface rubbed off and
epidermis of skin scraped exposing dermis.Painful
as dermal nerve exposed.
ī§ Haematoma:-Collection of blood following injury.It
may be subcutaneous,intramuscular, subfascial and
intra articular.
ī§ Incised wound:-Caused by sharp object,neat and
clean scar,tidy
ī§ Lacerated wound:-Caused by blunt object like in
RTA or fall on stone.Edges are irregular and
ragged,devitalised tissue,untidy
9. ī§ Penetrating wound:Like stab injury of abdomen
.It look like small but may have been damage
internal organ.Depth is more than length.
ī§ Crushed wound:Caused by blunt trauma like
RTA,earthquakes,wall collapse.Dangerous as
they cause severe haemorrhge,death of tissue
and crushing blood vessel.More prone for gas
gangrene, tetanus,muscle ischemia, etc.
16. CRUSHED WOUND-caused by blunt traumadue to run over by
vehicle, wall collapse, earth quakes or industrial accidents.severe
haemorrhage,death of tissues and crushing of blood vessels
17. WOUND HEALING
Wound healing is a mechanism where by the
body attempts-
ī§ To restore the integrity and function of
injured part
ī§ To reform barrier to fluid loss and infection
ī§ Limit further entry of foreign organism and material
ī§ Re-establish normal blood and lymphaticâs patterns
18. CLASSIFICATION OF WOUND HEALING
1.By Primary intention:Occurs in clean incised
wound,edges opposed and minimal scar that is
clean,neat and thin.
2.By Secondary intention:Occurs in infected
wound,discharging pus and skin loss like in
major trauma,burn or sepsis.Wound left
open,increased inflammation and proliferation.
it heals by granulation,contraction and
epithelialisation.Poor,ugly and wide scar.
20. Wound Healing
Features Primary union
(First intention )
Secondary union
(Second intention )
1 ) Cleanliness Clean Unclean
2 )Infection Generally uninfected May be infected
3 )Margins Surgically clean Irregular
4 )Sutures Used Not used
5 ) Healing Scanty granulation tissue
at the incised gap and
along suture tracks
Exuberant granulation
tissue to fill the gap
6 )Outcome Neat linear scar Contracted irregular
wound
7 ) Complications Infrequent, epidermal
inclusion cyst formation
Suppuration, may require
debridement
21. PHASES OF WOUND HEALING
ī§ 1.Inflammatory phase
ī§ 2.Proliferative phase
ī§ 3.Remodelling phase(maturation phase)
ī§ All these 3 phase involve:
-stage of inflammation
-stage of granulation tissue formation and
organisation
-stage of epithelialisation
-stage of scar formation and resorption
-stage of maturation
22. ī§ Inflammatory phase/lag/substrate or exudative
phase:
Occasionally haemostatic phase is referred to
occur before inflammatory phase consisting of
formation of blood clot (vasoconstriction &
thrombus formation ) Inflammatory phase begin
immediately after wounding and last 2-3 days.
ī§ Features-Rubur(redness),Tumour(swelling),
Calor(heat),Dolor(pain) and loss of function.
24. Platelets and local tissue release vasoactive amines like
histamine,serotonin,prostaglandins.Vasoactive amines
&Growth factors attract inflammatory cells
Increase vascular permeability aiding inflammatory cell
Polymorphonuclear cell+macrophages ,PMN cells appears after
48hrs which secretes inflammatory mediators & bactericidal
oxygen derived free radicals
These cells remove devitalised tissue, microorganism, foreign
body
Macrophages regulate fibroblast activity by secreting FGF
which enhances angiogenesis
Beginning of Proliferative phase
25. ī§ Proliferative phase:Last from 3rd day to 3rd week.
ī§ As fibroblastic activity begin it give rise to
protocollagen which is converted into collagen
in presence of protocollagen hydroxylase by
hydroxylation require O2,vit-c and ferrous ions.
ī§ Production of collagen and ground
substance(proteoglycans help in binding
collagen fiber).from 5th day PMN cell decrease
and monocyte increase(specialised scavanger).
ī§ Start growth of new blood vessel as capillary
loop(angiogenesis) and re-epithelisation of
wound surface.
26. ī§ In early stage-Intense proliferation of fibroblast
and capillaries and granulation tissue formation
which is tissue in wound compromising newly laid
capillaries with fibroblast and ground substance
along with inflammatory cells.Epithelium of each
side continue to grow and eventually unites in the
upper dermis.
ī§ In late stage- There is increase tensile strength of
wound due to increase collagen,which is first
deposited in random fashion and consist of
type III collagen.
ī§ 80-90 % of final strength (in postop period ) is
achieved in 30 days.
27. ī§ Remodelling phase(maturation phase)(3week to 2
year):Begins during the fibroblastic phase.
Reorganisation of previously synthesized collagen.
Maturation of collagen (type-I replacing type-III
until 4:1 achieved).Balance between collagen
synthesis and collagenolysis.Realignment of
collagen fiber along line of tension and get cross
linked for giving further tensile strength to scar.
In latter decreased wound vascularity and wound
contraction due to fibroblast and myofibroblast
activity so redness of scar fades gradually.Scar may
be hypertophic at first but flatten out eventually due
to contraction of dermal collagen network and
increase breakdown of collagen .
28. Remodelling (Cont..)
Collagen production is not present after 42 days of wound healing.
ī§ Wound is strengthened by proliferation of Fibroblast
and myofibroblast which get structural support from
Extracellular matrix which has following components :
A- Collagen (Fibrous tissue,Bone, Cartilage,Valves,
Cornea etc ) Stimulated by GF. Defective collagen
synthesis leads to Fibrosis, Hypertrophic scar, Organ
dysfunction
B-Adhesive Glycoproteins (Glue)
C- Elastic Fibres (Elastic recoil)
D- Proteoglycans eg Dermatan & chondroitin sulphate
ī§
29. Healing in specific tissue
1. Bone:fracture of bone
Ist stage-stage of haematoma: From injury to blood
vessel to haematoma formation.
.osteoblast synthesis
.fracture end gap filled by blood
.blood clot act as frame work formed by fibrin
This stage last up to 7days.If gap exist, secondary
healing lead to malunion,delayed union and
nonunion.
30. ī§ IInd stage-Stage of granulation tissue:
Procallus formation(mass of tissue ,
disorganise tissue)
Mineralisation of procallus
Fracture is mobile
Last up to 2-3week
ī§ IIIrd stag-stage of callus:Bony callus formed
,fracture clinically united.Last up to 4-12week.
ī§ IVth stage:stage of remodelling of callus,done by
osteoclast.Out line of callus become dense and
sharply defined.It takes 1-4years
ī§ Vth stage:stage of modelling of endosteal
&periosteal,fracture site is indistinguishable.
31. 2.Cartilage:Injury lead to permanent defect due to
less blood supply.
In superficial injury healing power inadequate
®eneration is incomplete ,slow to heal result
persistent structural defect.
In deep injury healing is better as underlying bone
and soft tissue involvement(vascular).
32. 3.Tendon:Due to mobility of underlying bone or
muscle, damage ends usually separated.
Healing process is similar as other area of body.
Hypovascular tendon tends to heal with less
motion and more scar formation than tendon
with better blood supply.
33. 4.Nerve:Distal to wound ,wallerian degeneration
occur.Proximally the nerve suffer traumatic
degeneration as far as last node of Ranvier.
Regenerating nerve fiber attracted to their
receptors by neurotropism which is mediated by
growth factor,hormone and other extracellular
matrix trophins.Profuse growth of nerve fiber
which sprout from the cut proximal wound .
Overgrowth with poor approximation lead to
neuroma formation.
34. FACTOR AFFECTING WOUND HEALING
ī§ GENERAL FACTOR:
1. Age (older) - healing delayed
2. Obesity and weight loss
3. Smoking
4. Malnutriton=vit-c and zinc deficency delay wound
healing as vit-c is cofactor for hydroxylation and
zinc is cofactor for collagen synthesis, protein
depletion prolongs inflammatory phase, Copper -
extracellular cofactor, required for collagen
crosslinking,Magnesium -cofactor in glycolization
Vit-A increase inflammatory response in membrane
so deficiency delay wound healing. Vit E does not
increase wound healing, in absence of steroids may
reactivate disease for which steroids are given, it
decreases collagen synthesis and inhibits wound healing.
35. 5.Trace Metals- Zinc, Copper, Mg
6 .Anemia
7.Diabetic patient :delayed healing due to
microangiopathy , atherosclerosis and decrease
phagocytic activity
8.Jaundice and uraemic patient :healing delayed due to
fibroblastic repair delayed
9.Colonisation (gram-ve bact) and translocation in
GI tract(failure of gut-associated with lymphoid
tissue and villous atrophy)
36. 10.Drug-Steroids(early given delay, after healing no
effect) inhibit macrophage function, decrease
inflammatory response and its inhibitory effects
reversed by VitA .
Anti neoplastic agent -
(cyclophosphamide,methotrexate) decreased WBCâs,
decreased fibroblast proliferation, decreased
woundcontraction, decreased protein synthesis
NSAIDs - decrease collagen synthesis by 45% even at
normal levels.
Tamoxifen(antiestrogen) delay healing
11.Malignancy
12.HIV and immunosuppresive disease
13.Peripheral vascular diseases
37. ī§ LOCAL FACTOR:
1. Local infection
2. Presence of necrotic tissue and foreign body
3. Poor blood supply and perfusion
4. Venous or lymph stasis
5. Tissue tension
6. Haematoma and dead space
7. Large defect or poor opposition
8. Recurrent trauma
9. X-ray irradiated area
10. Site of wound-eg.over joint and back has poor
healing
38. 11.Type of wound
12.Hypoxia
13.Faulty technique of wound closure
39. INVESTIGATION
ī§ Investigate according to location and type of
wound
ī§ Investigate to rule out cause of delayed healing
ī§ Hb gm%-to rule out anemia
ī§ Total leucocyte count-to rule out infection
ī§ Blood sugar-to rule out DM
ī§ Blood urea-to rule out uraemia
ī§ LFT-to rule out jaundice
ī§ Lipid profile and doppler study of arterial
pressure to rule out any ischemic aetiology
ī§ X-ray of dependent part to rule out is bony
pathology involve or fracture.
40. MANAGING THE WOUND
ī§ Careful history
ī§ Examination of wound and classified it:
depth of wound
involvement of underlying structure
configuration
nonviable tissue
if vital area involve then -
airway maintained,bleeding controlled,IV FLUID
started,if require o2 given
41. ī§Administration of tetnus prophylaxis
ī§Administration of pain killer
ī§With normal saline clean the wound and remove the
foreign material.(Iodine,hydrogen peroxide and
organically based antibacterial not used as they impair
wound healing due to injury to neutrophil and
macrophage at wound site)
42. ī§ If exsessive bleeding is there, haemostasis
maintained by pressure pad and start I.V line.
ī§ If there is non-viable or devitalised tissue
debridement done until bleeding occur.
ī§ All hematoma present within wounds should be
carefully evacuated and bleeding sources
controlled with ligature or cautery.
ī§ Having ensured hemostasis and adequate
debridement and removal of foreign
body,irregular wound edge should be debride in
order to provide fresh edge for reapproximation.
43. ī§ Approximation of superficial layer by
nonabsorable suture,staples,monofilament,
octyl-cyanoacrylate tissue glues and deeper layer
by absorble suture .
- incised wound-primary suturing
- lacerated wound-excison and primary
suturing.
- crushed-delayed primary suturing after
debridement
- deep devitalised tissue-after debridement and
granulation if it is small then secondary suturing,if
it is large then split skin grafting done.
- in significant tissue loss require tissue mass for
closure.
44. ī§ Primary suturing:
suturing wound within few hour following
injury(ideal 6hr).
DONE IN-Incised wound,no infection and foreign
body,minimal injury to either side structure.
ī§ Wound excision and primary suturing of skin
indicated when wound edge are jagged ,
contamination of wound by organism or foreign
body,tissue are crushed or devitalised then wound
is explored ,remove foreign body, wound irrigated
with saline ,convert lacerated wound into incised
then suturing done.
45. ī§ Wound excision and delayed primary suturing
done in lacerated wound with major crush injury
so in such situation excision of dead tissue ,
irrigation of wound by antiseptic agent,dressing
done and after 4-6 day wound re-examined if no
infection then suturing done.
ī§ Suturing is avoided because of-gross
oedema
increase tissue tension
haematoma
contamination with bacteria
46. SECONDARY SUTURING
Sometimes after operations sutures may give way
because of severe infection with persistent
discharge of pus
IN SUCH SITUATIONS
7-14 Days later, after controlling infection,skin is
free from the edge of the wound from granulation
tissue and skin is approximated .This is called
secondary suturing .
47. ī§ If wound is associated with tension then
fasciotomy done to prevent compartment
syndrome.
ī§ Drain may be placed in area at risk of forming
fluid collection(craniotomy,intrathoracic,
intraabdominal)
ī§ Fascicular repair of nerve and vessel using 8/0 or
10/0 monofilament nylon
ī§ Tendon repair for acheiving mobilisation.
ī§ Removal of suture :4-5day of face and 7-10 day
of other skin ,failure to remove result
cosmetically inferior wound.
48. ī§ Antibiotics :used when obvious wound infection.
Systemic antibiotic used as topical antibiotic
frequently causes contact dermatitis.
ī§ Wound dressing:it provide ideal environment for
wound healing,comfortability,pain control,odour
control and prevent from viral and bacterial
contamination and further damage.
ī§ 2type- primary:placed directly on wound and
provide absorption of fluid and prevent from
infection.
secondary:placed on primary dressing for
further protection .
49. 1. Absorbent-keep cotton or sponge
2. Non adherent dressing-paraffin,petroleumjelly,jelonet
they maintain moist environment and allow exudate
to pass through them.Secondary dressing must be
kept
3. Semipermiable films(tegaderm)-Useful in superficial
wound and dressing around catheter
sites.Impermiable to bacteria and fluid but permeable
to air and water vapour.
4. Hydrogel(actiform cool,sterigel)transluscent,jelly like
having soothing,cooling and analgesic effect.They are
able to donate water to wound surface to maintain
moist environment.useful in superficial and deep
wound,sinus and cavity.useful in burn treatment.
50. 5.Hydrocolloid(tegasorb)-adhere to dry or moist site and
allow patient to bathe.useful in shallow or cavity
wound especially in difficult area such as sacrum and
heels.
6.Absorbent material:Used within wound as hemostat
and include collagen,gelatin and oxidised cellulose.
7.Alginates(sorbsan,kaltostat):derived from brown
algae.Use âskin loss,open surgical wound with medium
exudation and full-thickness chronic wound
8.Medicated dressing: Used as drug delivery
system.Agent delivered in dressing include benzoyal
peroxide,zinc oxide,neomycin and bacitracin-zinc.They
shown increase epithelisation by 28%.Used depends
upon amount of wound drainage.
51. Complication of wound healing
1. Infection
2. Avoidable scar
3. Excess healing-keloid and Hypertrophic scar
4. Pigmentation of skin
5. Marjolin ulcer-occur due to scar tissue
6. Contractures
7. Incisional hernia and wound dehiscence
53. KELOID
ī§ LIKE CLAW:Excessive scar tissue
that extend beyond the
boundaries of original incision or
wound.
ī§ Etiology is unknown usually
associated with elevated level of
growth factor ,deeply pigmented
skin and inherited tendencey.
ī§ Growth after 3month to year
ī§ Area involve
xiphisternum,shoulder tip ,upper
back,ear lobe
ī§ Excess collagen and hyper
vascularity
54. ī§ Itching present,margin slight tender,vascular,red
and erythematous.Burning sensation present.
ī§ Treatment:Excision alone of keloids is subject to
high recurrence rate 45 to 100%.Fewer recurrence
when surgical excision combined with other
modalities such as-application
of silicone sheet
use of radiation or pressure
ī§ Intralesional corticosteroid injection
ī§ Topical retinods
ī§ Vit-E or palm oil massage
55. HYPERTROPHIC SCAR
ī§ Excessive scar tissue does not
extend beyond the boundary
of original incision or wound
but rises above skin level.
ī§ Develop 4 week after trauma
ī§ Stocking ,armlet, elastic
bandage(pressure garments)
ī§ Excision, if required skin
grafting done