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I dressed the wound; god healed It“-Ambroise Pare, French Surgeon, 16th Century
WOUND CLASSIFICATION OF WOUND WOUND HEALING CLASSIFICATION 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 tissues.
Common causes are violence, accident or surgery that typically involves laceration or breaking of a membrane (as skin).
CLASSIFICATION OF WOUND(Rank &Wakefield)
Two Types: 1.TIDY-Incised,caused by sharp
object, no tissue loss,heal by primary intention.
2.UNTIDY-Crushed,teared,devitalised,burn, tissue loss,heal by secondary intention.
1.CLOSED WOUND -Contusion or bruising -Abrasion -Haematoma2.OPENED WOUND -Incised -Lacerated -Penetrating -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 intra articular.
Incised wound:-Caused by sharp object,neat and clean scar,tidy
Lacerated wound:-Caused by blunt object like in RTA or fall on stone.Edges are irregular and ragged,devitalised tissue,untidy
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 blood underneath
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 body attempts-
To restore the integrity and function of injured part
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 condition favourable.
Wound HealingFeatures 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
PHASES OF WOUND HEALING 1.Inflammatory phase 2.Proliferative phase 3.Remodelling phase(maturation phase) 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
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.
Features-Rubur(redness),Tumour(swelling), 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 histamine,serotonin,prostaglandins.Vasoactive amines &Growth factors attract inflammatory cells
Increase vascular permeability aiding inflammatory cellPolymorphonuclear cell+macrophages ,PMN cells appears after 48hrs which secretes inflammatory mediators & bactericidal oxygen derived free radicalsThese cells remove devitalised tissue, microorganism, foreign body
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 wound surface.
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.
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 dysfunction
B-Adhesive Glycoproteins (Glue) C- Elastic Fibres (Elastic recoil) D- Proteoglycans eg Dermatan & chondroitin
Healing in specific tissue1. Bone:fracture of boneIst 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 fibrinThis stage last up to 7days.If gap exist,
secondary healing lead to malunion,delayed union and nonunion.
IInd stage-Stage of granulation tissue: Procallus formation(mass of tissue
, disorganise 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 neuroma formation.
FACTOR AFFECTING WOUND HEALING GENERAL FACTOR:1. Age (older) - healing delayed2. Obesity and weight loss3. Smoking4. 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 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)
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 normal levels.
Tamoxifen(antiestrogen) delay healing11.Malignancy12.HIV and immunosuppresive disease13.Peripheral vascular diseases
LOCAL FACTOR:1. Local infection2. Presence of necrotic tissue and foreign
body3. Poor blood supply and perfusion4. Venous or lymph stasis5. Tissue tension6. Haematoma and dead space7. Large defect or poor opposition8. Recurrent trauma9. X-ray irradiated area10.Site of wound-eg.over joint and back
has poor healing
11.Type of wound 12.Hypoxia 13.Faulty technique of wound closure
INVESTIGATION Investigate according to location and type of
wound 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 Careful history 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
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 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.
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.
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 oedema increase tissue tension haematoma contamination with
SECONDARY SUTURINGSometimes 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 syndrome.
Drain may be placed in area at risk of forming fluid collection(craniotomy,intrathoracic, intraabdominal)
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 infection.
secondary:placed on primary dressing for further protection .
1. Absorbent-keep cotton or sponge2. 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.
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 –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
1. Infection2. Avoidable scar 3. Excess healing-keloid and
Hypertrophic scar4. Pigmentation of skin5. Marjolin ulcer-occur due to scar
tissue 6. Contractures7. Incisional hernia and wound
INFECTED WOUND-when wound is red, swollen, painful, it has discharging pus or smells bad
KELOID LIKE CLAW:Excessive scar tissue
that extend beyond the boundaries of original incision or wound.
Etiology is unknown usually associated with elevated level of growth factor ,deeply pigmented skin and inherited tendencey.
Growth after 3month to year Area involve
xiphisternum,shoulder tip ,upper back,ear lobe
Excess collagen and hyper vascularity
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 Topical retinods Vit-E or palm oil massage
HYPERTROPHIC SCAR 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 bandage(pressure garments)
Excision, if required skin grafting done
INCISIONAL HERNIA-bulge or protusion at or near the area of surgical incision
CONTRACTURES-excessive contraction during wound healing