WOUND HEALING

Rhona MacEachen
WVSUMC PGI
WOUND HEALING
•  Wound healing is a complex cellular and biochemical cascade that leads to restitution
of integrity and function.
•  Although individual tissues may have unique healing characteristics, all tissues heal by
similar mechanisms, and the process undergoes phases of inflammation, cellular
migration, proliferation, matrix deposition, and remodelling
•  Factors that impede normal healing include local, systemic, and technical conditions
that the surgeon must take into account.
•  Clinically, excess healing can be as significant a problem as impaired healing; genetic,
technical, and local factors play a major role.
•  Optimal outcome of acute wounds relies on complete evaluation of the patient and of
the wound and application of best practices and techniques
 3 PHASES OF WOUND HEALING
Hemostasis and Inflammation
•  Wounding promotes platelet aggregation,
degranulation, and activation of the coagulation
cascade
•  the fibrin clot serves as scaffolding for the migration
of neutrophils (PMNs) and macrophages into the
wound
•  PMNs peaking at 24 to 48 hours whose main function
is phagocytosis of bacteria and tissue debris and
release of cytokines
•  Macrophages peak by 48 to 96 hours post injury and
remain present until wound healing
Proliferative phase
•  spans days 4 through 12 and involves fibroblast and endothelial cells
•  PDGF is potent chemoattractant for fibroblast
•  Fibroblasts isolated from wounds synthesize more collagen, they proliferate less,
and they actively carry out matrix contraction
•  Lactate accumulates and regulates collagen synthesis (type I and III)
•  Endothelial cells also proliferate in this stage and participate in angiogenesis
•  Angiogenesis begins at ∼ 2 days continuous into proliferative and remodeling
stages
•  Granulation tissue begins to form and wound looks scarred
Maturation and Remodeling
•  Reorganization of previously synthesized collagen
•  extracellular matrix becomes acellular collagen-rich scar
•  Wound strength is determined by quality and quantity of
collagen, a pattern is followed:
•  fibronectin and collagen type III constitute the early matrix scaffolding
•  Glycosaminoglycans and proteoglycans represent the next significant
matrix
•  collagen type I is the final matrix
•  mechanical strength of the scar never achieves that of the
uninjured tissue
Epithelialization
•  Re-establishment of external barrier
•  proliferation and migration of epithelial cells adjacent
to the wound begins at day 1
•  seen as thickening of the epidermis at the wound
edge
•  Epithelium from the based enlarge, lose their
attachement to the dermis, and migrate towards the
surface and eventually keratinizes
•  This is completed in less than 48 hours
Wound contraction
•  For wounds that do not have surgically approximated edges, the area of the wound will
be decreased by this action (healing by secondary intention)

•  The myofibroblast has been postulated as being the major cell responsible for
contraction, and it differs from the normal fibroblast in that it possesses a cytoskeletal
structure

•  Fibroblasts placed in a collagen lattice in vitro actively move in the lattice and contract
it without expressing stress fibers. It is postulated that the movement of cells with
concomitant reorganization of the cytoskeleton is responsible for contraction
 Healing in Gastrointestinal Tract
•  begins with a surgical or
mechanical reapposition of the
bowel ends
•  Failure of healing results in
dehiscence, leaks, and fistulas,
which carry significant morbidity
and mortality.
•  Excessive healing results in stricture
formation and stenosis of the
lumen
•  Mesothelial (serosal) and mucosal
healing can occur without scarring
Healing in Bones
•  initial stage of hematoma formation consists of an accumulation of blood at the
fracture site. The next stage accomplishes the liquefaction and degradation of
nonviable products at the fracture site.

•  4 days following injury, soft callus tissue is deposited where neovascularization has
taken place and serves as an internal splint, preventing damage to the newly laid
blood vessels and achieving a fibrocartilaginous union. Characterized by the end
of pain and inflammatory signs

•  hard callus stage consists of mineralization of the soft callus and conversion to
bone.

•  This may take up to 2 to 3 months and leads to complete bony union

Healing in cartilage and tendon
•  cartilage is very avascular and depends on diffusion for transmittal of
nutrients
•  injuries to cartilage may be associated with permanent defects

•  Tendons and ligaments can be subjected to a variety of injuries, such as

laceration, rupture, and contusion. Due to the mobility of the underlying
bone or muscles, the damaged ends usually separate.
•  Tenocytes, are metabolically very active and retain a large regenerative
potential, even in the absence of vascularity.
Healing in Nerve tissue
•  There are three types of nerve injuries:
•  neurapraxia or focal demyelination
•  Axonotmesis or interruption of axonal continuity but preservation of Schwann
cell basal lamina
•  neurotmesis or complete transection

•  nerve ends progress through a predictable pattern of changes involving three crucial
steps:
•  survival of axonal cell bodies
•  regeneration of axons that grow across transected nerve to reach the distal stump
•  Migration and connection of the regenerating nerve ends to the appropriate nerve
ends or organ targets
Fetal wound healing
•  No scar formation
•  Transition wound occurs in the third trimester where there is no scarring but
there is loss of ability to regenerate skin appendages

•  Factors that differ with adult healing

•  Wound environment- fetus in sterile fluid environment
•  Inflammation- immaturity of fetal immune system
•  Growth factors- lack of TGF-beta
•  Wound Matrix- excessive hyaluronic acid production
 Classification of Wounds
•  Wounds are classified into acute and
chronic

•  Acute wounds heal in a predictable

manner and time frame

•  Chronic wounds have not healed in three

months and have failed to proceed
through the orderly process of wound
healing
Factors that Affect Acute wound healing

•  Advanced age
•  Hypoxia, anemia, hypoperfusion
•  Steroids and chemotherapeutic Drugs
•  Metabolic disorders
•  Nutrition (Vit C, A, and zinc)
•  Infections
Chronic Wounds

•  Skin ulcers (malignant transformation to Marjolin’s ulcer)

•  Ischemia Arterial Ulcers
•  Venous Stasis Ulcers
•  Diabetic Wounds
•  Decubitus or Pressure ulcers
Excess Healing
•  Hypertrophic Scars( 4 weeks)- rise above the skin level but stay within the
confines of original wound and regress over time
•  Keloid(3 months to years)- rise above skin level and beyond the border of
the original wound and rarely regress spontaneously
Adhesions
•  form when the peritoneal surface is damaged due to surgery, thermal or ischemic
injury, inflammation, or foreign body reaction.

•  Surgical trauma is minimized within the peritoneum by careful tissue handling,

avoiding desiccation and ischemia, and spare use of cautery, laser, and retractors.
Fewer adhesions form with laparoscopic surgical techniques due to reduced tissue
trauma.
•  The second major advance in adhesion prevention has been the introduction of
barrier membranes and gels, which separate and create barriers between
damaged mesothelial surfaces, allowing for adhesion-free healing
Management of Acute Wounds
Local Care

•  Careful history, examination, and tetanus prophylaxis

•  Wound should be anesthetised and prepared with
antiseptic
•  Irrigation to visualize all areas of the wound and remove
foreign material is best accomplished with normal saline
•  Evacuate all hematomas
•  Dressing and suturing
Dressings

•  Absorbent dressings- excess fluid in wound can lead to bacterial growth

and maceration, absorbent dressings should not be soaked through
•  Nonadherent dressings- impregnated with paraffin, petroleum, or water-
soluble jelly, a secondary dressing must be placed on top
•  Occlusive and Semiocclusive dressings- these films dressings are
waterproof and impervious to microbes but permeable to water vapor
and oxygen
•  Hydrophilic and Hydrophobic Dressings
•  Hydrocolloid and Hydrogel Dressings- combine benefits of occlusion and
absorbency
•  Alginates- used when there is skin loss or in surgical wounds with medium
exudation, and full-thickness chronic wounds
•  Medicated dressings- with benzyl peroxide, zinc oxide, neomycin, and
bacitracin-zinc, increases epithelialization by 28%
•  Vacuum assisted closure- applied negative pressure to remove exudate
Skin Replacements
•  Conventional Skin grafts
•  Split patial thickness grafts contain parts of dermis and epidermis, full thickness
grafts retain the entire epidermis and dermis
•  Autologous grafts- from one site of the body to another
•  Allografts- from nonidentical donor
•  Xenografts- taken from another species
Sources

Schwartz, Seymour I.,Brunicardi, F. Charles., eds. Schwartz's Principles Of Surgery

Tenth Edition. New York : McGraw-Hill Medical, 2011. Print.