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I dressed the wound; god healed It“
-Ambroise Pare, French Surgeon, 16th Century
CLASSIFICATION OF WOUND
PHASES AND STAGES
HEALING IN SPECIFIC TISSUE
FACTOR AFFECTING WOUND HEALING
MANAGEMENT OF WOUND
COMPLICATION OF WOUND
Wound is a break in the integrity of skin or
tissue often ,which may be associated with
disruption of the structure and function.
Wound is an injury to the body that is usually
associated with damage to underlying
Common causes are violence, accident or
surgery that typically involves laceration or
breaking of a membrane (as skin).
CLASSIFICATION OF WOUND
1.TIDY-Incised,caused by sharp object,
no tissue loss,heal by primary intention.
tissue loss,heal by secondary intention.
-Contusion or bruising
-Crushed or contused wound
Contusion:-Minor soft injury without break in skin
and there is discolouration of skin.
Abrasion:-Shearing of skin,surface rubbed off and
epidermis of skin scraped exposing dermis.Painful
as dermal nerve exposed.
Haematoma:-Collection of blood following injury.It
may be subcutaneous,intramuscular, subfascial and
Incised wound:-Caused by sharp object,neat and
Lacerated wound:-Caused by blunt object like in
RTA or fall on stone.Edges are irregular and
Penetrating wound:Like stab injury of abdomen
.It look like small but may have been damage
internal organ.Depth is more than length.
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.
CONTUSION-soft tissue injury without break in skin. collection of
ABRASION-epidermis is scraped, exposing dermis
HEMATOMA-collection of blood following injury or spontaneously
as in patients who have bleeding tendencies
INCISED WOUND-caused by sharp objects like knife,blade,glass
etc,have sharp edges
LACERATED WOUND-caused by blunt objects,like fall on hard
surface,road traffic accidents
PENETRATING WOUND-stab injuries, innocent injury with 1-2
cm cut, but internal organs might have been damaged
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
Wound healing is a mechanism where by the
To restore the integrity and function of
To reform barrier to fluid loss and infection
Limit further entry of foreign organism and material
Re-establish normal blood and lymphatic’s patterns
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.
3.ByTertiary intention:Wound initially left
open,edges later opposed when healing
Features Primary union
(First intention )
(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
tissue to fill the gap
6 )Outcome Neat linear scar Contracted irregular
7 ) Complications Infrequent, epidermal
inclusion cyst formation
Suppuration, may require
PHASES OF WOUND HEALING
3.Remodelling phase(maturation phase)
All these 3 phase involve:
-stage of inflammation
-stage of granulation tissue formation and
-stage of epithelialisation
-stage of scar formation and resorption
-stage of maturation
Inflammatory phase/lag/substrate or exudative
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.
Calor(heat),Dolor(pain) and loss of function.
Inflammatory Phase (cont…)
Damaged epithelial Blood platelets Macrophages
GROWTH FACTORS CYTOKINES ENZYMES
EGF TNF Prostaglandins Collagenase
Interleukin Histamine Elastase
Platelet factor I V
Platelets and local tissue release vasoactive amines like
&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
Macrophages regulate fibroblast activity by secreting FGF
which enhances angiogenesis
Beginning of Proliferative phase
Proliferative phase:Last from 3rd day to 3rd week.
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.
Production of collagen and ground
substance(proteoglycans help in binding
collagen fiber).from 5th day PMN cell decrease
and monocyte increase(specialised scavanger).
Start growth of new blood vessel as capillary
loop(angiogenesis) and re-epithelisation of
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
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.
80-90 % of final strength (in postop period ) is
achieved in 30 days.
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 .
Collagen production is not present after 42 days of wound healing.
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
B-Adhesive Glycoproteins (Glue)
C- Elastic Fibres (Elastic recoil)
D- Proteoglycans eg Dermatan & chondroitin sulphate
Healing in specific tissue
1. Bone:fracture of bone
Ist stage-stage of haematoma: From injury to blood
vessel to haematoma formation.
.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
IInd stage-Stage of granulation tissue:
Procallus formation(mass of tissue ,
Mineralisation of procallus
Fracture is mobile
Last up to 2-3week
IIIrd stag-stage of callus:Bony callus formed
,fracture clinically united.Last up to 4-12week.
IVth stage:stage of remodelling of callus,done by
osteoclast.Out line of callus become dense and
sharply defined.It takes 1-4years
Vth stage:stage of modelling of endosteal
&periosteal,fracture site is indistinguishable.
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).
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.
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
FACTOR AFFECTING WOUND HEALING
1. Age (older) - healing delayed
2. Obesity and weight loss
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.
5.Trace Metals- Zinc, Copper, Mg
7.Diabetic patient :delayed healing due to
microangiopathy , atherosclerosis and decrease
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)
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 WBC’s,
decreased fibroblast proliferation, decreased
woundcontraction, decreased protein synthesis
NSAIDs - decrease collagen synthesis by 45% even at
Tamoxifen(antiestrogen) delay healing
12.HIV and immunosuppresive disease
13.Peripheral vascular diseases
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
11.Type of wound
13.Faulty technique of wound closure
Investigate according to location and type of
Investigate to rule out cause of delayed healing
Hb gm%-to rule out anemia
Total leucocyte count-to rule out infection
Blood sugar-to rule out DM
Blood urea-to rule out uraemia
LFT-to rule out jaundice
Lipid profile and doppler study of arterial
pressure to rule out any ischemic aetiology
X-ray of dependent part to rule out is bony
pathology involve or fracture.
MANAGING THE WOUND
Examination of wound and classified it:
depth of wound
involvement of underlying structure
if vital area involve then -
airway maintained,bleeding controlled,IV FLUID
started,if require o2 given
Administration of tetnus prophylaxis
Administration of pain killer
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)
If exsessive bleeding is there, haemostasis
maintained by pressure pad and start I.V line.
If there is non-viable or devitalised tissue
debridement done until bleeding occur.
All hematoma present within wounds should be
carefully evacuated and bleeding sources
controlled with ligature or cautery.
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.
Approximation of superficial layer by
octyl-cyanoacrylate tissue glues and deeper layer
by absorble suture .
- incised wound-primary suturing
- lacerated wound-excison and primary
- crushed-delayed primary suturing after
- 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
suturing wound within few hour following
DONE IN-Incised wound,no infection and foreign
body,minimal injury to either side structure.
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.
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.
Suturing is avoided because of-gross
increase tissue tension
contamination with bacteria
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 .
If wound is associated with tension then
fasciotomy done to prevent compartment
Drain may be placed in area at risk of forming
Fascicular repair of nerve and vessel using 8/0 or
10/0 monofilament nylon
Tendon repair for acheiving mobilisation.
Removal of suture :4-5day of face and 7-10 day
of other skin ,failure to remove result
cosmetically inferior wound.
Antibiotics :used when obvious wound infection.
Systemic antibiotic used as topical antibiotic
frequently causes contact dermatitis.
Wound dressing:it provide ideal environment for
wound healing,comfortability,pain control,odour
control and prevent from viral and bacterial
contamination and further damage.
2type- primary:placed directly on wound and
provide absorption of fluid and prevent from
secondary:placed on primary dressing for
further protection .
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
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.
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
6.Absorbent material:Used within wound as hemostat
and include collagen,gelatin and oxidised cellulose.
7.Alginates(sorbsan,kaltostat):derived from brown
algae.Use –skin 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.
Complication of wound healing
2. Avoidable scar
3. Excess healing-keloid and Hypertrophic scar
4. Pigmentation of skin
5. Marjolin ulcer-occur due to scar tissue
7. Incisional hernia and wound dehiscence
INFECTED WOUND-when wound is red, swollen,
painful, it has discharging pus or smells bad
LIKE CLAW:Excessive scar tissue
that extend beyond the
boundaries of original incision or
Etiology is unknown usually
associated with elevated level of
growth factor ,deeply pigmented
skin and inherited tendencey.
Growth after 3month to year
xiphisternum,shoulder tip ,upper
Excess collagen and hyper
Itching present,margin slight tender,vascular,red
and erythematous.Burning sensation present.
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
Intralesional corticosteroid injection
Vit-E or palm oil massage
Excessive scar tissue does not
extend beyond the boundary
of original incision or wound
but rises above skin level.
Develop 4 week after trauma
Stocking ,armlet, elastic
Excision, if required skin
INCISIONAL HERNIA-bulge or protusion at or
near the area of surgical incision
CONTRACTURES-excessive contraction during wound