wound and its healing processes

1. BY
baiyewunmi a.m

2. OUTLINE
Definition.
Classification.
Causes of wound.
Phases of Wound healing.
Management.
Factors affecting wound healing.
Complication of Wound healing.

3. DEFINITION
 A wound is a discontinuity in the epithelial
layer due to an application of an external
forces.
 Wound healing is the summation of a
number of processes which follow injury
including coagulation, inflammation,
matrix synthesis and deposition,
angiogenesis, fibroplasia, epithelialisation,
contraction, remodelling and scar
maturation.

4. CLASSIFICATION
 Contusion or bruise results from injury of the
tissues subjacent to the surface epithelia, for example
the subcutaneous or submucous tissues, and is usually
the result of blunt trauma. There is disruption of the
connective tissue with extravasation of blood, hence
the bruise or ecchymosis.
Open Wounds
 Mere loss of the superficial layers of the epithelium
is the simplest form of open wound. This is called an
Abrasion. Secondary bacterial invasion is the problem
in all open wounds; if this can be prevented, abrasions
become rapidly epithelialized from subjacent
germinating layer which in the case of the skin is
supplemented by the hair follicles and subcutaneous
glands.

5.  If the wound of entry is small as occurs when the
causative agent is a pointed instrument, a nail or
narrow bladed knife, a Puncture Wound results. On
the other hand, when the wound of entry is relatively
wider a Lacerated Wound is produced. These
wounds may be inflicted by a sharp instrument or
blunt force.
 Open wounds are sometimes described as
Penetrating or Perforating. In the former, the
wounds enter a body cavity such as the chest or
abdomen; in the latter, they entirely pass through an
organ or cavity and are characteristic of firearm
missile injuries.

6.  Occasionally portions of the body may be torn or
wrenched away. These Avulsion wounds, usually
irregular with jagged edges, occur in the scalp and the
extremities.
 The avulsion may be Complete where there is no
connection between the injured and its original site or
Partial where tenuous and strained strands of tissue
connect the tissue to the site. Complete avulsion
injuries are seldom attended by life
threatening haemorrhage.
 Based on How clean:
-Clean wound.
-Clean contaminated wound.
-Contaminated wound.
-Dirty wound.

7. Classification of operative wounds based
on degree of microbial contamination
Clean - Elective, not emergency, non-traumatic, primarily closed; no
acute inflammation; no break in technique; respiratory, ga strointestinal,
biliary and genitourinary tracts not entered.
Clean-contaminated- Urgent or emergency case that is otherwise
clean; elective opening of respiratory, gastrointestinal, biliary or
genitourinary tract with minimal spillage (e.g. appendectomy) not
encountering infected urine or bile; minor technique break.
Contaminated -Non-purulent inflammation; gross spillage from
gastrointestinal tract; entry into biliary or genitourinary tract in the
presence of infected bile or urine; major break in technique; penetrating
trauma <4 hours old; chronic open wounds to be grafted or covered.
Dirty Purulent inflammation (e.g. abscess); preoperative perforation of
respiratory, gastrointestinal, biliary or genitourinary tract; penetrating
trauma >4 hours old.

8. CAUSES OF TISSUE INJURY
 Mechanical Agents: Most are the result of some
mechanical injury sustained at work, in the home, on
the road or the result of assault. The wounds so
produced are of various types but generally they are
either closed, when they are described as contusions,
or open when the term lacerations is used.
 Chemical Agents: These are usually strong acids,
alkalis or other caustic and corrosive chemicals which
accidentally or as a result of assault come in contact
with tissues. Epithelial tissues take the brunt of this,
for example the cutaneous wounds from acid bums,
skin necrosis accompanying snake or insect bites; the
oesophageal stricture that follows swallowing
of caustics is another example of such tissue injury.

9.  Radiant Energy: Radiation in its various forms -
X-rays, radium, and other forms of atomic energy,
high voltage electricity, heat and intense cold -
produces extensive wounds notable for the degree of
tissue necrosis entailed; healing is necessarily delayed
in these wounds.
 Pathogenic Micro-organisms: Owing to the
natural capabilities of the integuments to resist
invasion, pathogenic organisms of themselves seldom
cause wounds; more often they are secondary invaders
of wounds produced by other primary agents.

11. PHASES OF WOUND HEALING
1. Traumatic Inflammation: Immediately after
the infliction of a deep incised wound, the edges
become sealed together first with platelet clot and
then fibrin clot. The adjacent capillaries constrict and
are plugged with clot, but within a few hours they
dilate following release of vasodilators such as
serotonin, histamine, bradykinin and prostaglandins.
 The platelets release also:
• Growth factors, PDGF, TGF-B, IGF-l, adhesive
glycoproteins-fibronectin, thromboplastin, laminin.
• Serotonin which increases vascular permeability.
Other chemoattractants and lysosomes containing
hydrolases and proteases.

12.  The aggregation and activation of platelets and
release of chemotactic factors are initiated and
promoted by exposure of blood to fibrillar collagen of
injured tissues.
 Following the vasodilation and increased
permeability of the vascular endothelium, plasma,
plasma proteins, C5a and C3a are poured into the
wound site causing the turgid wound.
 Neutrophils, activated by the platelets, and later
monocytes migrate through the capillary wall and
enter the wound site too. The response is similar in
principle to that seen in the early stages of bacterial
inflammation.

13.  The body temperature is raised usually to
37.5-38.50C .The process probably serves to
raise the metabolic rate of the wound
preparatory to its repair.
 It also brings together the materials
necessary for the subsequent stages of repair,
i.e. plasma, fibrin, polymorphonuclear
leucocytes.
 The ground substance of the connective
tissue undergoes depolymerization and

14. 2. Destructive Phase (Demolition): This
immediately follows the inflammatory phase
and is concerned with removal of dead and
dying tissues from the wound.
 The neutrophils and monocytes migrate
into the wound, kill any bacteria around and
ingest dead bacteria and tissues.
 Monocytes convert to macrophages but
some macrophages are local in origin.
 The macrophages secrete b-FGF, other
growth factors and other cytokines.

15.  The first two phases described represent
the lag period in wound healing during which
the wound has no tensile strength.
 Preparation phase would be more
appropriate, for the foundations for repair are
being laid down at this time.
 The period varies from 4-6 days and is
rather constant . It is prolonged by the
development of bacterial inflammation.

16. 3. Proliferation Phase: This is the stage of
granulation tissue formation. As congestion of
the wound subsides collagen formation
becomes evident.
 The growth factors, secreted by the
macrophages, platelets and fibroblasts,
activate local endothelial cells, fibroblasts and
epithelia1 cells to start the process of repair.
 The endothelial cells divide and migrate to
form a new capillary network in the wound.

17.  The fibroblasts from cells surrounding the
wound are also activated and migrate into the
Wound.
 The endothelial cells and fibroblasts use
fibronectin, hyaluronic acid, laminin and
other glucosaminoglycans in the extracellular
space in the wound as the scaffolding matrix.
 Fibroblasts now deposit collagen on the
fibronectin and GAC scaffolding. Matrix
degradation is blocked; synthesis of proteases
is decreased but synthesis of protease
inhibitors is increased at the same time.

18.  The ground substance now shows striking
metachromasia indicating depolymerization and
increasing quantities of mucopolysaccharides.
 The process whereby capillary loops, fibroblasts
and collagen replace the initial fibrin clot is known
as Organisation.
 At first, the collagen fibrils are fine
(Tropocolagens) and few in relation to the cells but
as healing proceeds, the Fibre cell ratio increases
until in the adult scar tissue only a few elongated
fibroblasts are visible.

19. 4. Maturation Phase: The peak of fibroplasia
is soon followed by gradual shrinkage and
maturation of connective tissue in the wound.
The scar, which up to this time has remained
elevated and congested, over a period of weeks
or months thins out and flattens and becomes
progressively less conspicuous.
 Histologically the blood vessels gradually
disappear (Endarteritis obliterans).

20. Types of Wound closure
The 3 categories of wound closure are primary,
secondary, and tertiary.
Primary healing involves closure of a wound within
hours of its creation.
Secondary healing involves no formal wound closure;
the wound closes spontaneously by contraction and
reepithelialization.
Tertiary wound closure, also known as delayed primary
closure, involves initial debridement of the wound for
an extended period and then formal closure with
suturing or by another mechanism.

21. MANAGEMENT OF WOUND
1. Debridement: All dead and dying tissues
are removed as well as all foreign material
because these encourage infection. This may
entail prior irrigation or scrubbing of the
wound with soapy antiseptic to remove
ingrained grit.
In crush injuries, it is not always possible to
determine the viability of affected tissue and
over- enthusiastic debridement may lead to
undue tissue loss.

22. 2. Strict Asepsis:- Surgical technique should
observe strict asepsis. Gowns, caps and efficient masks
must be used as for all major surgical procedures with
the usual skin preparation and draping. The surgeon
should strive to maintain his usual routine so as to
prevent breaks in technique.
3. Wound closure:- Is undertaken only when
complete. Debridement is assured and the wound
reasonably clean.
The individual components or layers of tissues should
be apposed as accurately as possible to each other,
epithelium to epithelium and mesothelial structures in
similar fashion.

23. 4. Gentleness in the handling of tissues is ideal for
it reduces tissue trauma, bruising, exudation, and
hence minimizes infection thus promoting early
healing.
Wherever possible, smaller haemostats should be
employed so as to reduce the amount of tissue crushed
while clamping vessels and sharp dissection should be
preferred to blunt dissection except where safety
demands otherwise.

24. 5. Blood loss should be kept to a minimum by
prompt haemostatic control and any deficit should be
made up adequately by blood transfusion.
6. General Management of the Patient:
Immobilization and elevation of the injured part are
essential for they promote venous and lymphatic
drainage and thus prevent congestion and pain.
 In extensive wounds, a period of total body rest by
reducing the metabolic requirements promotes more
speedy recovery.
 Prophylaxis against tetanus by active or passive
immunization should be instituted, and where
significant wound contamination is suspected,
adequate doses of a broad spectrum bactericidal
antibiotic should be exhibited.

25. FACTORS AFFECTING WOUND HEALING
1.Advanced Age:
Most surgeons believe that aging produces
intrinsic physiologic changes that result in
delayed or impaired wound healing.
 Clinical experience with elderly patients
tends to support this belief.
 Studies of hospitalized surgical patients
show a direct correlation between older age and
poor wound healing outcomes such as
dehiscence and incisional hernia.

26. 2.Severe Constitutional Disease: It has
been observed that patients with diabetes mellitus,
chronic nephritis, congestive cardiac failure,
chronic liver
disease and syphilitic lesions heal less readily.
 Cancer patients in general heal their wounds
poorly; this may arise from progressive nutritional
deprivation but direct influences from the
neoplastic process have not been adequately
analysed.
 There is experimental evidence that
hyperglycaemia in diabetics impairs synthesis of
procollagen and collagen, fibroblast proliferation
and capillary ingrowth.

27. 3.Nutritional Factors
 Ascorbic Acid – Wounds of patient deficient in
this vitamin heal poorly. Early experimentalists had
long shown that reticulin and collagen are poorly
formed in the healing wounds of scorbutic animals.
More modem studies on the biosynthesis of collagen
in these wounds have confirmed this and indicated.
That the scanty deposits of collagen and reticulin
correlate with Reduced levels of hydroxyproline but
are associated with large
quantities of proline. within a day of treatment with
Vit. C, the prolinelhydroxyproline ratio is found to
alter from an excess of 30 to 7 indicating that collagen
precursors are readily available in the wound.

28. 4. Trace Elements Deficiencies: Zinc deficiency,
uncommon except in children in the Middle East, is
known to retard wound healing by preventing cellular
mitosis.
 Zinc is a necessary component of several DNA
and RNA polymerases and transferases essential for
cell proliferation.
 Severely stressed patients such as those with
extensive burns and individuals undergoing major
operations may become deficient and need zinc
supplementation.
 This needs to be cautiously done as excessive zinc
levels may hinder macrophage and phagocytosis and
impair wound healing.

29. 5. Hormones: In general, wound healing seems to be
very little influenced by physiological levels of
hormonal secretion or hormone deficiency.
 Very large doses of cortisone given to experimental
animals for some days before wounding on the other
hand delay healing by inhibiting fibroplasia.
 One view is that the hormone probably acts by
preventing capiIlary dilatation and permeability –
a manifestation of its anti-inflammatory effect.
 This would prevent the development of capillary
budding and of healthy well-vascularized granulation
tissue.
 ACTH has similar effect on wound healing.

30. LOCAL FACTORS
1. Blood Supply: Trivial wounds on the ischaemic
legs of atherosclerotic patients heal very slowly.
 In contrast, wounds in vascular areas heal very
quickly; sutures may be safely removed from scalp and
facial wounds after three days in the knowledge that
healing is already well advanced.
 Venous ulcers also heal poorly because of
impairment of the local circulation.
2. Residual Infection: Invasion of a healing wound
by pathogenic bacteria is invariably followed by a delay
in Methionine healing. The tissue destruction may be
great and healing delayed for weeks.

31. 3. Immobilization and Trauma: Inadequate
immobilization may lead to separation of wound edges
with subsequent infection. Repeated movement has the
effect of disrupting the newly regenerate capillaries and
collagen laid down during the phase of fibroplasia.
One of the most frequent causes of Delayed healing of
an abdominal wound is the development of a persistent
cough early in the post-operative period.
4. Foreign bodies: Any kind of foreign material
retained in the wound will delay healing if infection is
present. The wound remains unhealed until the foreign
body, usually stitch is extruded or removed.

32. 5. Surgical Technique: If wound edges are not
correctly opposed, a dead space forms which soon
becomes filled with tissue fluid or blood and
subsequently replaced by granulation tissue. Healing is
then in effect by secondary intention.
 Rough handling of tissues and excessive trauma
also delay healing not only because of increased
tendency to infection but also from production of
much tissue necrosis.
 Excessive tension in the wound from unduly tight
sutures applied in an effort to close a gaping wound has
the effect of delaying the healing of the wound.

33. 6.Oxygen: It has become evident that oxygen is
the most important wound nutrient.
 Its delivery to the healing wound is impaired
by a number of local factors such as tissue
trauma and tight suturing techniques.
 More serious problems arise when wound
capillary perfusion is impaired by systemic
disorders as occurs in shock.

34. Complications of Wound Healing
1. Infection: This enters via the primary wound and interferes
with the healing process. Discharge is profuse
Tissue death occurs and sloughs accumulate. Only when this is
shed would adequate granulation tissue form. In effect infection
converts healing by primary to healing by secondary intention.
2. Keloid formation: This is due to excessive fibroblastic
activity with marked granulation tissue formation resulting in a
markedly raised scar. The exact cause is unknown.
Negroes or dark skinned people are predisposed to this and
there may be a genetic basis. Age is important, the condition
occurring more often in younger people. The neck is a frequent
site for such lesions.

35. 3. Hyperpigmentation: It frequently occurs at sites of
chronic scars. Deposition of degradation products of
haemoglobin probably contributes but the exact cause
is uncertain.
4. Implantation cysts: These are the result of
epithelial elements penetrating the wound and
proliferating in situ to form epidermoid cysts. Such may
occur along stitch tracts.
5. Neoplasia: The intense cellular proliferation and
migration that characterizes healing tissues is
reminiscent of embryonic activity or the uncontrolled
growth of a neoplasm. In a healing wound, the
embryonic status is temporary, a resting state is soon
induced presumably by contact inhibition and remodel-
ling ensues.

36. 6. Weak scars: They are more Likely to follow healing
by secondary intention. If put under stress, the scar
stretches and incisional hernia results.
7. Cicatrization: Continued thickening and
shortening of collagen may on occasion produce
contractures which later embarrass function.
The deformity so produced is frequently gross with
untoward effects on function e.g. distortion of limbs, or
stricture formation in important organs – oesophagus,
intestine, and urethra.

37. Suture materials and wound healing
 The ideal suture material has the following
features:
 It is completely inert, its presence exciting little or
no reaction in the tissues of the wound.
 It does not affect the tensile strength of the wound.
 It maintains its tensile strength indefinitely.
 It does not harbour micro-organisms.
 the suture material should disappear as soon
as its function is accomplished.
 The material entirely satisfying these conditions is
still to be found, but the modem synthetic sutures
increasingly approach this ideal.

38.  There are two types of sutures:-
1. Absorbable, e.g. catgut which is absorbed by the
tissues and
2. Non-absorbable, e.g. nylon which remains in the
wound for prolonged periods.
 There are several gauge sizes of suture material
but the finest are preferred as they cause least tissue
reaction.
 Monofilament sutures are also better than
multifilament or twisted ones as they do not harbour
bacteria and do not exert a capillary or wick-like
action.

39. REFERENCES
 Textbook of surgery; badoe
 www.Wikipedia.org
 Medscape
 uptodate

40. THANK YOU