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Wounds are classified into two general categories: ‘
and 

× Acute wounds repair through an orderly process that results in anatomic and functional integrity.,
× Chronic wounds have failed to proceed through the orderly and timely process or have proceeded through
a repair process without establishing an anatomic or functional result.
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approximates the acutely disrupted tissue with sutures, staples, or tape. With time, the synthesis,
deposition, and cross-linking of collagen and other proteins provide the tissue with strength and integrity.
In ›› 
  
J approximation of the wound is delayed for several days after the wound has been
created. This is indicated to prevent infection in wounds in which there has been a significant bacterial
contamination, foreign bodies, or extensive tissue trauma.
  

   › 
›
Joccurs when the margins of the open wound move together by
a biologic process of contraction. Partial-thickness wounds heal by the process of epithelialization that occurs first
by migration and the mitosis of epithelial cells.
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Three distinct biologic mechanisms are involved in all healing processes. They include   ‘ ‘ J which is
the process by which keratinocytes migrate and divide to resurface the skin or mucosa. ‘   is the
mechanism whereby there is spontaneous closure of full-thickness skin wounds or constriction of tubular organs.
   
‘   is the process whereby fibroblasts are recruited to the site of injury and produce
a new connective tissue matrix.
Phases of Healing Under normal conditions, the phases of healing are divided into four specific events that actually
overlap and have complex interactions. There is not a ³lag phase´ in the healing process.
 

  Injury causes hemorrhage and damage from blood vessels and lymphatics. Vasoconstriction occurs
almost immediately. Vasoactive compounds initiate the process of diapedesis, the passage of intravascular cells
through the vessel walls into the extravascular space of the wound. Platelets derived from the hemorrhage form a
haemostatic clot and release clotting factors to produce fibrin, which is haemostatic. Fibrin forms a mesh for further
migration of inflammatory cells in fibroblasts. Platelets also produce essential cytokines that modulate the events of
wound healing.
  The inflammatory phase is characterized by the sequential migration of leukocytes into the wound.
Inflammatory cells regulate the connective tissue matrix by specific messengers. It is initiated as soon as the tissue
integrity is disrupted by injury. Platelet are the first cellular component that aggregates to the wound and as a result
of there degranulation ( platelet reaction) they release several cytokines E.G. PARACRINE GROWTH
FACTORS(PGDF) INSULINLIKE GROWTH FACTOR- 1( IGF- 1), EPIDERMAL GROWTH FACTOR ( EGF),
AND FIBROBLAST GROWTH FACTOR (FGF)(Bennett, 1993). Serotonis is also released which together with
histamine ( released by mast cells), induces a reversible, opening of the junctions between the endothelial cells,
alloeing the passage of neutrophls and monocytes (which become mcrophages) to site of injury. This cellular

 
  
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movement to the injury site is induced by cytokines secreted by platelets( chemotaxis) and b further chemotactic
cytokines secreted by macrophages themselves once at the site of injury. This includes transforming growth factor
Alfa (TGF Į) and TGF ȕ. Consequently an inflammatory exudates that contains RBCs neutrophil macrophages and
plasma proteins including coagulation cascade proteins and fibrin strands, fills the wound in hrs. Macrophages not
only scavenge but play central role in wound healing because there cytokine secretion.
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as the cells migrate to the site of injury the fibroblasts, epithelial cells and vascular endothelial
cell starts to proliferate and the cellularity of that area increases. The cytokines involved are- FGF-2, which
stimulates the angiogenesis, epithelial cells and fibroblast proliferation. The marginal basal cell of the wound starts
to migrate across the wound and within 48 hrs the entire wound is epithelised. In the depth of the wound the number
of inflammatory cells decreases with the increase in stromal cells e.g. endothelial cells, fibroblast cells which in turn
continue to secrete cytokines. Cellular proliferation continues to the formation of extracellular matrix proteins
including collagen and new capillaries (angiogenesis). This process may last for weeks.
0
 
 this phase is characterized by  
   During this phase, fibrous protein collagen is
synthesized and cross-linked, and there is deposition of collagen and other matrix proteins that provide the healed
wound with strength and integrity. Within 10 h after injury, there is evidence of increased wound collagen synthesis.
After 5±7 days, collagen synthesis peaks and then declines gradually. After this wound contraction occurs which is
seen in less in healing by primary intention and more pronounced I healing by secondary intention and is dye to the
myofibroblasts.
  
During this phase, acute and chronic inflammatory cells diminish, angiogenesis ceases, and fibroplasia
ends. The equilibrium between collagen synthesis and degradation is restored.
 
    
Healing of clean surgical approximated incision (first intention) involves an orchestrated sequence of events, as
follows-
1. 0 hrs: the incision is filled by clot
2. 3 to 24 hrs: neutrophil from the margin infiltrate the clot. Mitosis begins to appear in epithelial basal cells;
epithelial closures take place by 24 to 48 hrs.
3. Day3: neutrophil are replaced by macrophages. Granulation tissue begins to appear.
4. Day 5: the incision space is filled with granulation tissue neovascularisation is maximal, collagen fibrils
begin to appear and epithelial proliferation is now maximal
5. Week 2: there is proliferation of fibroblast and continued collagen accumulation to produce a scar.
Collagen deposited early in granulation tissue is type 3, which is then replaced by adult type 1 collagen.
Collagen fibers account in large part of wound strength. Inflammation and newly formed vessels have
largely disappeared.
6. Month 2: scar now consist of connective tissue devoid of inflammation and covered by intact epidermis.

 
     

 
  
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Healing by secondary intention occurs when there is extensive loss of tissue, such as infection, ulceration
abscess and large wounds. In these situations the regeneration of parenchymal cells alone notant restore the
original architechture. Abundant granulation tissue grows in from the margins to fill the defects but at the same
time the wound contracts; that is the defect is markedly reduced from its original size. Myofibroblast contribute
to wound contraction.
Secondary healing differs from primary wound healing in different aspect like:
1. Large tissue defect intrinsically have a greater volume of necrotic debris, exudates, and fibrin that must be
removed. Constantly the inflammatory reaction is more intense with greater potential for secondary,
inflammation- mediated, and injury.
2. Much larger amount of granulation tissue is formed. Larger defects accrue a greater volume of granulation
tissue to fill in the gaps in the stromal architechture and provide the underlying network for the regrowth of
tissue epithelium. A greater volume of granulation tissue generally results for greater amount of scar tissue.
3. Secondary wound healing exhibits the phenomenon of wound contraction. Within 6 weeks large skin
defects can be reduced to 5% to 10% of their original size. This is due to the Myofibroblast- modified
fibroblast exhibiting many of the ultrstructural and functional features of contractile smooth muscles.

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Wound strength at the end of the first week is about 10% of normal; it is largely dependent upon surgical
suturing and tissue adhesion. The progressive recovery of tensile strength is about 70% to 80% in about 3rd
month( which may persist for life,) is associated first with increased collagen synthesis exceeding collagen
degradation and subsequently with the cross- linking and increased fiber size of the collagen fiber.

   

 

A number of systemic and local factors modify the severity of inflammatory response and the quality of repair.
The systemic influences are following:-
× Nutritional status of the host( protein and vitamin C intake)
× Metabolic status( diabetes delays the wound healing)
× Circulatory status or the adequacy of blood supply.
× Hormone, concurrent glucocorticoid therapy, which hinders the inflammatory- reparative process.
× Anticancer chemotherapy
× Ionizing radiation
× Àaundice
× Age
× Uraemia alcoholism
The local factors that affect wound healing are:
× Infection that can delay healing
× Mechanical factors e.g. motion that are directly affecting the wound ± can delay wound healing.

 
  
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× Foreign bodies that impede wound healing.
× Size, location and type o the wound.
× Shock, anaemia, compartmental syndrome, ischemia.
× Smoking malignancy.

The etiology of wound healing can e remembered by the mnemonics device DIDN¶T HEAL as follows
× D = Diabetes: long term effects of diabetes impair wound healing by diminishing sensation and arterial
flow. In addition every acute loss of diabetic controle can affect wound healing bu causing diminished
cardiac output. Poor peripheral perfusion and impaired polymorphoneuclear leukocyte phagocytosis.
× I = Infection: infection potentiate collagen lysis. Bacterial contamination is a necessary condition but is not
sufficient for wound infection. A susceptible host and wound environment is also required. Foreign bodies
including sutures potentiate wound infection.
× D = Drugs: steroids and antimetabolite impede proliferation of fibroblast and collagen synthesis.
× N = Nutritional problems: protein calorie malnutrition and deficiency of vitamins A C and zincimpair
normal wound healing mechanism.
× T = tissue necrosis: resulting from local or systemic ischemia or radiation injury impairs wound healing.
Wounds in characteristically well perfused areas , such as head & neck , may heal surprisingly well despite
unfavorable circumstances. Conversely even a minor wound in the foot which has a borderline blood
supply may mark tha onset of long term nonhealing ulcers. Hypoxia and excessive tension on the wound
edges also interfare with wound healing because of local oxygen deficits.
× H = Hypoxia: inadequate tissue oxygenation due to local vasoconstriction resulting from sympathetic
overactivity may occur because of blood volume deficits, unrevealed pain, or hypothermia, especially
involving the distal extent of extremities.
× A= another wound: competition between several healing areas for the substrates required for wound
healing areas impaires wound haling in all sites.
× L= Low temperature: the relatively low tissue temperature in the distal aspect of the upper and lower
extremities ( a reduction of 1-1.5 deegree centigrade from normal body temperature may slow wound
healing at those sites.