Jean Paulene W.

Rivera
September 19, 2016
2D
BASIC SURGERY SGD
WOUND HEALING
Case #1
A 45 years old male patient came to your clinic complaining of a 5cm
lacerated wound to his right elbow after being hit by bamboo stick two
hours prior to consult. Full range of motion on right elbow, no
paresthesia noted. As the attending physician, your immediate plan
was to give anti-tetanus vaccination.
1. What is the management of acute wounds?

Treatment of acute wounds depends upon its location and severity.

General wound care may include the following:

Controlling the bleeding Identify the source of bleeding

and applying pressure (if applicable) to make it stop.

Cleansing the wound General soap and water may be

used on minor acute wounds. Saline solutions may be used on
larger, deeper or more complex wounds.

Debridement If necessary, clear the wound of any debris, dirt

or objects. A health care professional may remove dead tissue
from the wound.

Dressing and/or closing the wound Some wounds may

require a health care professional to apply staples, skin
adhesive, sterile strips or stitches to bring the wound edges
together to close. Wounds may be left open to air or covered
with dressings depending upon their location and severity.

Antibiotics and other medicines In some cases,

antibiotics may be prescribed to thwart off infection. This is
typical in wounds with a high risk of developing infection, as in
those contaminated with debris. Medications for pain, swelling
and other wound specific treatments (such as a tetanus shot)
may also be recommended.

2. Discuss the phases of wound healing.

The 3 phases of wound healing are:
1. Hemostasis and Inflammation
2. Proliferation
3. Maturation and Remodeling
HEMOSTASIS

Hemostasis - precedes and initiates inflammation with the

ensuing release of chemotactic factors from the wound site.

Wounds, which disrupt tissue integrity, would lead to collagen

synthesis.

In early phase of wound healing:

o PMNs release proteases such as collagenases, which
participate in matrix and ground sub- stance degradation
(these cells do not appear to play a role in collagen
deposition or acquisition of mechanical wound strength;
neutrophils delay epithelial closure of wounds)

Macrophages are the second population of inflammatory cells

that invades the wound; they participate in wound dbridement
via phagocytosis and contribute to microbial stasis via oxygen
radical and nitric oxide synthesis
o Most pivotal function: activation and recruitment of other

cells via mediators: cytokines and growth factors, as well

as directly by cell-cell interaction and intercellular adhesion
molecules (ICAM).
o Regulate cell proliferation, matrix synthesis, and
angiogenesis through the following mediators: TGF-,
vascular endothelial growth factor (VEGF), insulin-like
growth factor (IGF), epithelial growth factor (EGF)
o Regulate angiogenesis
remodeling

and

matrix

deposition

and

T
lymphocytes
comprise
another
population
of
inflammatory/immune cells that routinely invades the wound;
peak at about 1 week post-injury and truly bridge the transition
from the inflammatory to the proliferative phase of healing.
o Their role in wound healing is not fully defined. Hypothesis
is that T lymphocytes play an active role in the modulation
of the wound environment.
o Lymphocytes also exert a down regulating effect on
fibroblast collagen synthesis by cell-associated interferon
(IFN)-, TNF-, and IL-1.

PROLIFERATION

th
Second phase of wound healing and spans from the 4
th
to 12 day
Tissue continuity is re-established
Fibroblasts and endothelial cells last cell population to
invade the wound
PDGF strongest chemotactic factor for fibroblasts
(mediated by cytokines and growth factors) to carry out
their function of matrix synthesis and remodeling
Wound fibroblasts synthesize more collagen than
non- wound fibroblast, by proliferating less and
actively carrying out matrix contraction
Lactate a potent regulator of collagen synthesis through a
mechanism involving adenosine diphosphate (ADP)ribosylation
Endothelial cells participate in angiogenesis
o Migrate from intact venules to close wound

o Migration, replication and new capillary tubule

formation is via:
TNF-
TGF-
VEGF
MATURATION AND REMODELING

Begins during the fibroblastic phase

Characterized by a reorganization of previously synthesized
collagen
Matrix metalloproteinase (MMP) breaks down collagen
Net wound collagen balance between collagenolysis and
collagen synthesis
Pattern for the deposition of matrix in the wound:
Early matrix scaffolding fibronectin and
collagen type III
Middle
matrix
scaffoldingGAGs
and
proteoglycans
Final matrixcollagen type I

After weeks of injury, collagen amount in the wounds

reaches a plateau but tensile strength increases

Fibril formation and cross-linking result from:

Decreased collagen solubility

Increased strength

Increased resistant to enzymatic degradation

Fibrillin a glycoprotein secreted by fibroblast, essential for

the formation of elastic fibers in connective tissue

Scar remodeling continues for 6-12 months post injury

resulting in a mature, avascular and acellular scar

Mechanical strength of the scar never achieves that of

uninjured tissue

3. What are the factors that affect wound healing?

Advanced Age
Delayed and impaired wound healing (1.9 days)

 Noncollagenous protein accumulation at wounded

sites is decreased with aging, impairing
mechanical properties of scarring
Hypoxia, Anemia and Hypoperfusion
o Collagen synthesis requires oxygen as a cofactor,
specifically for the hydroxylation steps
o Mild to moderate normovolemic anemia does
not appear to adversely affect wound oxygen
tension and collagen synthesis unless hematocrit
falls between 15%
Steroids and Chemotherapeutic Drugs
o Reduce collagen synthesis and wound strength
o Steroids inhibit the inflammatory phase of
wound healing and release of lysosomal enzyme,
epithelialization, contraction and contribute to
increase rates of wound infection
o Chemotherapeutic antimetabolite drugs inhibit
early cell proliferation and wound DNA and protein
synthesis
Metabolic Disorders
o Diabetes Mellitus
affects wound healing by:increased
rates of wound infection and failure
reduce inflammation, angiogenesis and
collagen synthesis

defects in granulocyte function, capillary

growth and fibroblast proliferation

Type 1 diabetics decrease wound collagen

accumulation, independent of degree of
glycemic control

Type 2 diabetics no effect on collagen

accretion

o Uremia
Decreased wound collagen synthesis and
breaking strength
o Obesity
have higher risk for wound dehiscence,
surgical site infections, incisional hernias,

seromas, hematoma and fat necrosis

Nutrition
o Induction of energy-deficient states that by
providing only 50% of normal caloric requirement
leads to:

Decreased granulation tissue formation

Matrix protein deposition

Malnutrition correlates clinically with enhanced

rate of wound
complications and increased
wound failure post-operation, reflecting:

Impaired healing response

Reduced cell mediated immunity

Reduced phagocytosis

Reduced intracellular killing of bacteria by

macrophages and neutrophils

Arginine most active in terms of enhancing

wound fibroplasias. In healthy individuals,
arginine supplementation enhanced collagen and
protein deposition at the wound site

Vitamin C - deficiency (Scurvy) leads to failure in

collagen synthesis and cross linking, Increase in
severe wound infection.

Vitamin A
o Increases
inflammatory
increase
the
lability
membranes.

response
and
of
lysosomal

o Increase collagen production and epidermal

growth factor receptors.
o Restores wound healing properties impaired
by
diabetes,
tumor
formation,
cyclophosphamide and radiation

o Trace elements - cofactor or part of an enzyme

that is essential for homeostasis and wound
healing
o Zinc deficiency leads to

Decreased fibroblast proliferation

Decreased collagen synthesis

Impaired overall wound strength

Delayed epithelialization

Infection
o Lead to disfiguring, unsightly or delayed closures

Case #2
A 60 years old female, diabetic patient was referred to you due to a
non-healing wound at the left plantar area. On physical examination a
4x4cm, erythematous, swollen lesion with foul smelling yellowish
discharge was noted on her plantar area.
1. What is the management of chronic wounds?
Assess the entire patient
Characterize the wound - (1) size and depth of involvement
and the extent of undermining, (2) the appearance of the
wound surfaceis it necrotic or viable, (3) amount and
characteristic(s) of wound exudate, and (4) status of the
periwound tissues (eg, pigmented, scarred, atrophic,
cellulitic).
Ensure adequate oxygenation
Ensure adequate nutrition
Treat underlying infection
Remove foreign bodies
Manage pain
Ischemial Arterial Ulcers - revascularization or re-establish
blood adequate blood supply progress to healing

 Venous Stasis Ulcers - treatment is compression therapy,

via rigid or flexible means. Most common is rigid: zinc
oxide-impregnated, non- elastic bandage.
Diabetic Wounds - treatment should address the possible
presence of Osteomyelitis and employ antibiotics that
achieve adequate levels both in soft tissue and bone
Decubitus or Pressure Ulcers - treatment comprises
debridement of all necrotic tissue, maintenance of a
favourable moist wound environment that will facilitate:
Healing , relief of pressure and addressing host issues:
nutritional, metabolic and circulatory status
Peritoneal Scarring - Major strategies for adhesion
prevention or reduction: (1) Trauma is minimized within
the peritoneum by careful tissue handling, avoiding
desiccation and ischemia, and spare use of cautery, laser
and retractors (2) Introduction of barrier membranes and
gels which separate and create barriers between
damaged mesothelial surfaces, allowing for adhesion-free
healing
2. Discuss the factors for the development of chronic wounds.
Repeated trauma
Poor perfusion or oxygenation
Excessive inflammation
Unresponsiveness to normal regulatory signals
Failure of norma lgrowth factor synthesis
Over expressed protease activity or failure of antiprotease mechanism