WOUND

DEFINITION, CLASSIFICATION AND

MANAGEMENT
TYPES OF WOUND HEALING
HEALING PROCESS
FACTORS AFFECTING HEALING
COMPLICATIONS
WOUNDS
 Wound: It is defined as the break in the
continuity of skin or the mucous
membrane or both which may or may not
be accompanied by a loss of tissue.

 Wound healing: It is the inherent property

of the damaged/injured tissue to come to
its original shape.

 Wound repair: It is the complete

restoration of the damaged tissue to its
normal shape which is done manually e.g.
skin grafting.
ETIOLOGY OF WOUND

 Mechanical stress: races etc. leading to

muscular rupture in race horses.
 Chemical agents: Acids, alkali etc.
 External violence: Fall, accidents etc.
 Thermal agents: Burns.
 Radiations
 Infective agents: Bacterial, viral etc.
 CLASSIFICATION OF WOUNDS
CLOSED AND OPEN WOUNDS
 Closed wounds:. Commonly known as Contusion,
a wound produced by blunt objects resulting in
damage to subcutaneous tissue without break in
the continuity of the skin. Depending upon the
severity the contusion can be:
 Ist degree contusion: Also known as ‘Bruise’
and is characterized by rupture of capillaries
of the skin and subcutaneous area.
 2nd degree contusion: It is characterized by
rupture of larger vessels with accumulation of
blood in subcutaneous area e.g. Haematoma.
 3rd degree contusion: There is tissue damage to
greater extent and gangrene may set in. The
internal organs may be injured and the
symptoms of shock are visible.
OPEN WOUND

 Incised wound Lacerated wound

 Punctured wound Penetrating wounds
 Perforating wounds Gunshot wounds
 Poisoned wounds Envenomed wound
Granulating wound
 Ulcerative wound

 Abrasions Avulsion
 Maggot wound
INCISED WOUND
A wound caused by sharp cutting
instruments e.g. knife, scalpel etc.
 The edges of the wounds are regular

 The wounds bleed freely with minimum

loss of tissue.
 The wounds tend to gape and the extent of
gapping depends upon the elasticity and
tension in the surrounding tissue.
 Healing is always by Ist intension which
is achieved after suturing.
LACERATED WOUND
 An open wound caused
by blunt objects.
 The edges of the wounds
are torn and uneven.
 There is typical tearing
of the tissue.
PUNCTURED WOUND
 A wound caused by
sharp pointed object.
 The wound normally
has a small opening.
 The wound is deep.

 There is more
chances of presence of
anaerobic infection
because of no oxygen
in deeper tissues.
PENETRATING WOUNDS
• These are deep wounds
which communicate to
cavities e.g. abdominal
wound, thoracic wound,
wounds of joint etc.

• Mostly caused by long

sharp pointed objects like
horn of cattle leading to
horn wounds of
abdomen/thorax etc.
PERFORATING WOUNDS

These are deep wound having

two openings, one at the
entrance and other at the exit
e.g. Perforating wounds of neck,
thigh etc.
 Envenomed wound:
 The wounds resulting from snake/dog/wasp/wild
animal bite.
 There is significant degree of tissue damage
depending upon the bite.
 Commonly known as ‘Bite wounds’. The snake
bites are penetrating type of wounds and are mostly
seen at the head, lips, tongue or extremities.
• Gunshot wounds:
 These are deep wounds caused by firearms.
 The point of entrance is very small but there is
extensive damage to the underlying tissue.
 The damage varies depending upon the kinetic energy
produced by the firearm.
 Granulating wound: A wound which shows
tendency to heal by formation of new healthy
granulation tissue.

 Proud Flesh: Also known as ‘keloid

tissue’. It is excessive granulation tissue of
unhealthy nature characterized as dark, red
or purple tissue with typical serous or sero-
sanginous discharge at the site of the wound.
A common condition of equines
ULCERATIVE WOUND

• A wound which does not show

tendency to heal.
• Decubitous ulcers or Pressure
sores
 Abrasions: These are the wound in which there is
loss only of the superficial layer (epidermis) of the
skin.

 Avulsion: A wound in which there is actual loss of

the tissue e.g. avulsion of tooth/hoof etc.
AVULSION OF HOOF
MAGGOT WOUND (TRAUMATIC
MYIASIS)
 A wound infested with maggots. Also known as traumatic
myiasis.
 Primary myiasis: When the flies complete their life cycle in the
wound itself. The flies lay eggs on the wound; larvae burrow deep
in the tissues and enlarge the wound cavity; the tunnels are
formed; the maggots feed on the living tissue. e.g. Lucilia,
Calliphora, Phormia etc.
 Secondary myiasis: Only maggot stage is seen in the wound. The

maggots feed on the necrotic tissue and the exudates and don’t
burrow deep into the tissues. e.g. Chrysomia, Musca, Sarcophagi
etc.
MANAGEMENT OF MAGGOT
WOUND

Removal of maggots
Manually:
A combination of chloroform and turpentine oil
(1:1)
Negasunt powder (contains cumaphos COP 3%,
Proxopur 2% and sulfanilamide 5%),
Lorexane/maggocide cream (contains GBHC 0.1%,
proflavin hemi sulfate 0.1% and cetrimide 0.45%)
Phenyl

Once maggots are completely removed

treat the wound as an open wound
following the general principles of wound
management.
EFFECT OF NEGASUNT ON MAGGOT INFESTED MEDIAL
CANTHUS OF EYE

Maggot infested medial

canthus of eye in a bullock-
day1
•Note the presence of
maggots in the medial
canthus

Appearance of eye when the animal

was discharged
 EFFECT OF NEGASUNT IN THE MAGGOT INFESTED
PAW OF DOG

Maggot wound of paw-Day-1

Application of
Negasunt+Liquid
paraffin-Day-1

Wound after single

treatment-Day 2
SITES WHERE CONVENTIONAL MAGGOCIDAL
MEDICATIONS ARE IRRITANT AND NEGASUNT CAN BE
APPLIED WITHOUT ANY COMPLICATION

MAGGOT WOUND ON
PENIS OF DOG

MAGGOT WOUND ON
VULVA OF MARE
CLINICAL CLASSIFICATION OF THE
WOUND

 Aseptic wound: A wound created under aseptic conditions like

surgical wound.

 Contaminated wound: A wound infected with microbes, dirt, dust

etc. The microbes have entered the wound but don’t start
multiplying.

 Infected/septic wound: A wound in which the microbes have

started multiplying and there is production of
toxins/pus/exudate. A contaminated wound after a ‘lag period’ of
8-12 hours becomes an infected wound.
 Aseptic wound

Infected/septic wound

Contaminated wound
TREATMENT OF WOUNDS
ASEPTIC WOUND WHICH CAN BE SUTURED
 Tetanus in camel and horses.
 Arrest hemorrhage
 Clipping; shaving; scrubbing
 Irrigate the wound with NSS.
 Apply strong antiseptic (Povidone iodine 5%).
 Sprinkle antibiotic
 Suture the wound up to skin.
 Sealing with antiseptic
 antiseptic dressings of the wound on alternate
day or every 3-4 day till the sutures are
removed.
 Provide necessary rest.
 Use systemic antibiotics for 3-5 days. Use of fly
repellent
TREATMENT OF WOUNDS
ASEPTIC WOUND WHICH CAN’T BE SUTURED
A. Follow steps A, B, C and E as described earlier.
B. Irrigate the wound with any antiseptic
C. Do antiseptic dressing with antiseptic ointments
(BIPP or ZIPP) or antiseptic/antibiotic powders.
D. Apply the protective bandage, wherever possible.
E. Do antiseptic dressings of the wound on
alternate day or every 3-4 day
F. Provide necessary rest.
G. Use systemic antibiotics for 3-5 days.
H. Use of fly repellent creams
TREATMENT OF WOUNDS
Management of contaminated and septic
wounds
‘Principles of 4 D’s

 Disinfection:

 Debridement:

 Drainage

 Dressing
 MANAGEMENT OF PUNCTURED
WOUNDS
 Never sutured because of possible bacteria/foreign body.

 External opening must be enlarged to facilitate proper

drainage.

 Irrigation is always done with 0.5-2.00% H2O2 to provide

nascent oxygen to prevent anaerobic environment.

 Antiseptic dressing is always done with strong antiseptic

(Tr. Iodine) or antibiotics.

 Always use systemic antibiotics.

 TYPES OF CLINICAL WOUND HEALING
1. Ist intention (Primary Healing)
2. 2nd intention (Secondary healing)
3. Mixed intention
4. Delayed primary healing
IST INTENTION (PRIMARY HEALING)
 Mostly seen in wounds which are:
 Aseptic and fresh
 Free from hemorrhage
 Have minimum dead cells
 Have good blood supply to the wound edges
 The wound edges are in apposition with each other i.e. the
wounds are immobilized by suturing

 In such healing the

 narrow space is first filled with blood clot
 angioblasts and fibroblasts invade the clot
 healing is completed in 5-14 days
 negligible scar formation
 full function is restored.
2ND INTENTION (SECONDARY HEALING):
 Also known as healing by organization. Mostly
seen in wounds where:
 There is actual loss of tissue
 The wound edges are widely separated
 The healing starts from the base of the wound and the
gap is replaced by newly forming granulation tissue
 complete healing is seen in 6 weeks or more and there
is more scar formation
 full function may not be restored.
MIXED INTENTION HEALING

 When there is healing by both i.e. Ist and 2nd

intention.
 Such type of healing is seen in wounds which
have been sutured but sometimes, at places
the sutures are disrupted leading to gaping of
wound edges (called wound dehiscence).
 Mostly seen in patients suffering from jaundice.
DELAYED PRIMARY HEALING
 It is a type of healing which is achieved in such
wounds which can’t be sutured initially

 The wounds are allowed to heal by granulation till

epithelialization stage.
 At this stage the skin edges are separated from new
granulation tissue and sutured.

 The suturing is normally done 5-7 days after the

injury. Such type of healing, when achieved is
advantageous in 2 ways:
 The large wounds heal with minimum scar formation
 The wound healing is rapid
PROCESS OF WOUND HEALING ( STAGES)
 It is restoration of the function and structure of
the damaged tissues
 It involves the four stages

inflammatory
Debridement
proliferative
maturation
INFLAMMATORY STAGE
 Inflmmation is a protective tissue response
initiated by damage.
 This phase is characterized by increased vascular
permeability, chemotaxis of circulatory cells,
release of cytokines and growth factors, and cell
activation(macrophages,neutrophils,lymphocytes,
andfiroblasts).
 Vasoconstriction

 clot formation (activation of kinin and platelets

aggregation)
 vasodilation (influence by histamine from
platelets and mast cells)
 Duration of events 1-4 days
 White blood cells escapes into the cells and net
work of fibrin is formed
 Monocytes appears as increase no and becomes
dominent of up to 5th day
 Phygocytes

 New capillaries bud from the endothelial cells

DEBRIDEMENT STAGE
 Removal of dead and contaminated tissues and
cells
 Dead tissue acts as good medium for the growth
of micro organism
 Cellular or biological

neutrophill and monocytes

 Enzymatic debridement

streptokinase, streptodornase, trypsin

 Chemical debridement
copper sulphate
silver nitrate
 Surgical or mechanical debridement

when all above fail then surgical deb.

PROLIFERATIVE STAGE
 Fibroplasia
fiberoblast moves into the site of wound
collagen production
Granulation
it starts 3-5 days after the fibroplasia
 Epithelialization

the gap is filled with new tissues

chalone enzyme
 it fill up the gap and supply blood
velvety moist appearance (pink color)
 Wound contraction

wound contracts due to myofibroblast

depending upon the wound size it may take months,
weeks or days
 Process the proliferation follows by the process of
intact inhibition (mitosis stopped)
MATURATION STAGE
 Wound increases in strength
 Fiberoblast increases in no

 Collagen fiber are arranged along the pressure

line to strength
 This stage lost for weeks to months
FACTORS AFFECTING WOUND HEALING

Systemic factors:
1. Role of nutrients
2. Role of systemic diseases
3. Role of drugs/medicines used
4. Miscellaneous factors
 ROLE OF NUTRIENTS

Proteins:
 Deficiency- decreased fibroplasia
 Production of immature fibroblasts with
lower tensile strength.
Vitamins:

Deficiency of vitamins A and C

Decreased collagen synthesis,
improper epithelialization,
scanty blood vessels
and hence delayed healing.
ROLE OF SYSTEMIC DISEASES
Diabetes:
Diabetes - insulin deficiency - less energy-
decreased cell metabolism - healing delayed.

Anaemia: Oxygen carrying capacity of the blood

decreased- hypoxia - collagen synthesis

Jaundice: Wound dehiscence is a common problem

Hemophilia: Deficiency of antihaemophilic factor (Factor

VIII) - difficult clotting - healing delayed.

Uraemia: High blood urea levels- protein degradation -

decreased number of fibroblasts - delayed
healing
 ROLE OF DRUGS/MEDICINES USED

Corticosteroids:
Excessive corticosteroid therapy –
decrease number of fibroblast,
decreased number of newly forming capillaries,
fragile capillaries –
wound healing delayed.

NSAIDs:
In excess- decreased granulation, decreased
tensile strength of newly forming tissue and
hence the healing will be delayed.
 MISCELLANEOUS SYSTEMIC FACTORS
 Age:
Wound healing is delayed in old patients because of decreased holding
power , decreased tensile strength of the newly forming tissue and
decreased fibroplasia

 Fat:
The wound healing is normally delayed in fatty patients because of
decreased holding power as well as decreased tensile strength of the
newly forming tissue and decreased fibroplasia

 Ambient temperature:
The wound healing is best when the ambient temperature is
approximately 30oC. At temperature 10-20oC the tensile strength of
newly forming tissue is decreased by 20% whereas at higher
temperature (>50oC) thermal injuries may occur and destroy the
newly forming tissue.
 LOCAL FACTORS
Vascularity: Normal blood - normal healing because of
proper nutrients, oxygen and phagocytes Avoid
tension during suturing
Trauma: Gentle handling - avoids excessive trauma.
Rough handling - decreased tensile strength,
prolonged healing period and more scar formation
Haematoma: Good seat for the proliferation of
infection - destroy the newly forming cells -
healing delayed.
Improper apposition of wound edges: Any gaping – no
primary healing
Infection/maggots: Presence of microorganisms or
maggots - continuously destroy the newly forming
tissue - healing delayed.
 LOCAL FACTORS
Foreign bodies:

Nerve injury:

Immobilization

Presence of neoplastic/dead tissue/proud flesh:

Presence of dead space: Anaerobic

environment - proliferation of microbes -
extensive destruction of newly forming
cells - healing delayed.
 COMPLICATIONS OF WOUND
Haemorrhage
Haemorrhage following injury may lead to anaemia (when
slight), haematoma (when closed) or shock and death (when
severe)
Always ensure proper haemostasis using different methods of
haemostasis (digital pressure, ligature etc.)
Wound dehiscence: Disruption of the suture line - ventral
abdominal and joint wounds.
Predisposing factors: Break in antiseptic procedure
 obesity; senility
 anaemia and jaundice
COMPLICATIONS OF WOUND

Traumatic neuralgia: Severe pain along the course

of nerve due to injury
Primary (pain ever since wound infliction)
Secondary (pain development after few days of wound
infliction due to infection).
Use anodyne preparations (systemic analgesics/NSAIDS
for 3-5 days with topical Iodoform).
The complication is more seen in horses.
COMPLICATIONS OF WOUND

Tetanus: More seen in camels and equines

Provide active immunization in these animals at
least 15-21 days before surgery using tetanus toxoid
(5-10 ml I/M)
In emergency surgery go for passive immunization
using ATS (Anti tetanus serum) @ 1500-3000 IU S/C.
Shock:
Due to excessive loss of fluid (haemorrhage),
massive infection or overdosing of general
anaesthesia
Prevent - preoperative corticosteroids and
intravenous fluids (before, during and after
 COMPLICATIONS OF WOUND

Haematoma and seroma: Accumulation of

blood/serum due to injury to blood vessels or
improper haemostasis

Proud Flesh: Excessive granulation tissue of

unhealthy nature
 COMPLICATIONS OF WOUND

Venous thrombosis: Injury to the medium sized vein

Dangerous when breaks – emboli- cause obstruction of
important vessels like coronary artery - death of the patient

Erysipelas: Mostly seen in horses, dogs and pigs due to

streptococcal infection of the wounds