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Types of wounds
i. Incised wound
ii. Lacerated wound
iii. Bruising and contusion
iv. Haematoma
v. Puncture wound
vi. Abrasion
vii.Crush injury
viii.Injuries to bone and joint (maybe open or
closed)
Types of wounds
ix.Injuries to nerve (either clean cut or crush)
x. Injuries to arteries and veins
xi. Penetrating wounds
xii. Degloving injury.
Healing
I Treat God Cures
• The ability to heal is inbuilt in our
physiology . We only help body to heal
itself and remove any obstacles in the
path of healing.
• There are no healing medicines / घाव
सूखनेकी दवा
TYPES OF WOUND HEALING
• Healing by first (Primary) intention -wounds with
opposed edges.
• Healing by second intention wounds with separated
edges
• By Third intention (tertiary intention)-delayed
primary
Wound initially left open
Edges later opposed when healing conditions
favourable
• Partial thickness wounds –Abrasions- heal by
epithelisation.
Healing by first intention (wounds with
opposed edges)
Healing of wound with following characteristics:
• Clean and uninfected
• Surgically incised
• Without much loss of cells and tissue
• Edges of wound are approximated by surgical
sutures.
• Wounds with opposed edges
• Primary union
• The incision causes
death of a limited number of epithelial cells and
connective tissue cells
disruption of epithelial basal membrane continuity
• The narrow incisional space immediately fills with
clotted blood containing fibrin and blood cells;
dehydration of the surface clot forms the well known
scab that covers the wound.
Healing by second intention
• Wounds with separated edges
• Secondary union
• When there is more extensive loss of cells and tissue
• Regeneration of parenchymal cells cannot
completely reconstitute the original architecture.
• Abundant granulation tissue grows in from the
margin to complete the repair.
Secondary healing VS primary healing
• Inflammatory reaction is more intense
• Much larger amounts of granulation tissue
are formed
• Wound contraction occurs in large surface
wounds
• Substantial scar formation and thinning of
the epidermis occurs
Difference between 1˚ & 2˚ union of
wound
FEATURES PRIMARY SECONDARY
CLEANLINESS CLEAN NOT CLEAN
INFECTION NOT INFECTED INFECTED
MARGINS SURGICALLY CLEAN IRREGULAR
SUTURES USED NOT USED
HEALING SMALL GRANULATION
TISSUE
LARGE GRANULATION
TISSUE
OUT COME LINEAR SCAR IRREGULAR WOUND
COMPLICATION NOT FREQUENT FREQUENT
Phases of Healing
• The inflammatory phase occurs
immediately following the injury and lasts
approximately 6 days.
• The fibroblastic (Proliferative) phase
occurs at the termination of the
inflammatory phase and can last up to 4
weeks.
• Scar maturation begins at the fourth week
and can last for years.
Wound Contraction
• Contraction of a wound across a joint can
cause contracture.
• Can be limited by skin grafts, full better
than split thickness.
• The earlier the graft the less contraction.
• Splints temporarily slow contraction.
Wound Infection: Local features
• Foul-smelling drainage
• spontaneously bleeding wound bed
• flimsy friable tissue
• increased levels of wound exudates
• increasing pain
• surrounding -
– cellulitis
– Crepitus
– necrosis,
– Fasciitis
– regional lymphadenopathy
Wound Infection: Local features
Osteomyelitis
• Fevers, malaise, chronic fatigue, and limited range
of motion of the affected extremity,
• patients often present with only a nonhealing
wound or a chronic draining sinus tract overlying
a bone or joint.
• Probe to bone test.
• Plain radiographs, CT scans, radionuclide bone
scans, and MRI
• Osteomyelitis is treated with surgical curettage
and appropriate systemic antibiotics.
Systemic Factors
• Malnutrition
• Cancer
• Old Age
• Diabetes- impaired neutrophil chemotaxis,
phagocytosis.
• Steroids and immunosuppression suppresses
macrophage migration, fibroblast proliferation,
collagen accumulation, and angiogenesis.
Reversed by Vitamin A 25,000 IU per day.
• Superstitions
Keloids and Hypertrophic
Scars
• Both from an overall increase in the
quantity of collagen synthesized.
• Recent evidence suggests that the
fibroblasts within keloids are different from
those within normal dermis in terms of their
responsiveness.
• No modality of treatment is predictably
effective for these lesions.
Wound Management
Local measures- “The golden hour”
• Haemostasis
• Anaesthesia
• Decontamination
• Repair and closure
• Delayed closure-
• Late presentation
• Heavy contamination
• Lot of dead and devitalized tissue.
Wound Management
• Local measures-
• Surgically debride nonvitalized tissue and
with appropriate irrigation
• Dressing changes require clean but not
necessarily sterile technique.
• Remove foreign bodies
• Pat the wound surface with soft moist
gauze; do not disrupt viable granulation
tissue.
Wound Management
Pressure sores
• Mobilise
• Appropriate turning and positioning
• Use of offloading support surface
• Appropriate wound care
• Appropriate management of incontinence
• Appropriate nutritional management
Wound Management
Diabetic foot ulcers
• Appropriate wound care
• Liberal debridement
• Maintain euglycemia with insulin.
• Antibiotics only if evidence of infection.
• Reperfusion.
Wound Management
Surgical Care
• Skin grafting
• Cadaveric allografting
• Application of bioengineered skin
substitutes
• Use of flap closures
Future and Controversies
• Human cell–conditioned media developed
in embryologiclike conditions
• transforming growth factor (TGF)–β3
• Hyperbaric oxygen has also been used to
promote healing.
• Agents such as platelet-rich plasma (PRP)
and erythropoietin (EPO
• Engineered tissue matrices
• Stem Cells
Take home messages
• Early closure of clean wounds.
• Delayed closure of dirty / infected wounds.
• Antibiotics are generally not indicated in
abrassions, contusions.
• For open wounds give three dosage of
antibiotic.
• Further antibiotics only if evidence of
infection.
• Spirit, Betadine,Savlon, Hydrogen peroxide
Sumag should not be applied on wounds.
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