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BAB II

DISCUSSION
A. Definition of Wound Healing
A wound can be defined as the disturbance of the
skins normal structure and function and the soft tissue
beneath it (Taylor, 2015). Wound complications are major
contributors to both early and late postoperative morbidity
(Mizell, 2014). It can cause significant physical and
emotional distress to both patients and the treating
physician.

Most

surgeons

will

agree

that

wound

complications can be challenging to treat and everything


possible should be done to prevent it from happening.
Wounds are classified as clean-, clean-contaminated-, contaminated- or
dirty wounds. Clean wounds can be described as an incision into tissue,
other than hollow viscera, in which neither infection nor inflammation is
present followed by primary closure afterwards. Cleancontaminated
wounds result from intentional entry into the respiratory, gastro-intestinal,
genital or urinary tracts without remarkable contamination. Contaminated
wounds can be characterized by unintentional entry into a hollow viscus, a
major disruption in sterility, or encountering areas of nonpurulent
inflammation. Dirty wounds include old wounds with residual devitalised
tissue, perforated viscera or current clinical infection. Open wound is any
traumatic breach in continuity of skin and deep tissue. Contusion is a

closed wound and is an exception to the above definition. Classification of


wounds is important for medico-legal purpose as well as for management.
Wounds are classified mainly on the basis of mode of infliction and
causative agent as Closed wounds Contusion, closed fracture, etc (Tiwari,
2012). although wound are giving specific classification there are many
that have properties of several specific types. indeed are seldom any
classical wounds apart from those afflicted in the course of elective or
other surgical procedures (Knottenbelt, 2003).

B. Classification of Wound Healing


a. Graze / Abrasion Erosion
A graze is a superficial denuding of the epidermis with minimal
(capillary) bleeding and usually some serum plasma exudation, often
in pinpoint form at first. It arises from abrasion against a rough or hard
object such as a road surface.
Clinical management of graze involves application of soothing
ointments such as silver sulfadiazine (e.g. Flamazine smith and
nephew) to encourage rapid epithelialization and prevent infection.
Healing is usually complete, uncomplicated, uneventful, and rapid, and
usually there is no visible scar. Moist wound management methods
hasten recovery and reduce pain significantly.
b. Bruising
Bruising is the result of the bleeding and tissue destruction
within and under the intact skin, that causes damage to capillary beds

or larger blood vessels, bruising can occur in tissue adjacent to a


laceration or without any outward injury. It may be difficult to detect
skin bruising in horses because of the skin color and dense hair coat.
The extent of the bruise is variable, but where multiple significant
bruises arise from relatively trivial trauma than clotting parameters
should be checked.
Treatment is seldom required, but in some sites (such as eyelids
or penis) ice packs or possibly cold hosing can be used to reduce the
local inflammation and control swelling, and minimize further damage
to the skin. Healing is usually uneventful and with minimal scarring.
c. Hematoma
A hematomais the accumulation of a large volume of free blood
under the skin. Hematoma can be differentiated from edema or
inflammatory fluid by the finger press test. In the case of edema, a
finger pressed onto the swelling and then removed will leave and
indent that remains visible for some minutes. If the swelling is
inflammatory, there will probably be no pitting with pressure in the
case of hematoma the indentation will disappear immediately the
finger is removed.
Hematoma can be left to organize or can be drained according
to clinical preferences,direct pressure to the drained area is sometimes
helpful,but can also be difficult in some locations. A pressure stent
sutured over the site or a firm bandage,where this is feasible,may limit

extent and shorten recovery.


Healing may be problematical with slow organizing and
fibrosis, or continued bleeding or abscessation. The skin may crinkle at
the site, or there may be some functional problems if there is extensive
fibrosis. A scar may be visible as distorted skin, firmly bound down to
the underlying tissues. Organizing hematoma in some sites (e.g. penile
skin) can cause functional problems.
d. Contusions
Contusions are common they are in effect severe bruises with
some skin injury. A contusion is rarely a problem, except where it
involves structures other than skin. One the commonest sites for
contusions is the head (periorbital region) in horses that have severe
colic. The damage around the eyes involves bruising and superficial
grazing. Secondary effects include conjunctival edema

(with

protrusion). Contusions are usually managed by ac a combination of


ice packs and prophylactic antibiotics. Healing is usually uneventful
but some permanent scarring can occur
e. Puncture Wound
Puncture wound in the skin and hoof from sharp object (e.g.
nails, glass shards, or other foreign bodies) are common and
potentially very serious. Puncture wounds may easily be overlooked or
trivialized, as the size of the wound often belies the potential severity
of the injury, the skin defect is usually trivial by comparison to the

deeper damage, which can even be fatal if it affects a vital organ such
as the synovial structures of the foot or the cranium, or carries
(anaerobic) infection into the wound. This type of wound proves the
ideal anaerobic environment for clostridium tetaniorganisms to
flourish.
f. Incised Wound
An incised wound (including a surgical wound) has a sharp
defined margin and is caused bysharp metal or glass, flint, or
occasionally the leading edge of a shoe. The skin is cut cleanly with
minimal tearing and bruising of the wound margins. Injuries may
extend into other structures, e.g. tendons and synovial sheaths, these
are classified as complicated wound.
Some bleeding is common, although reflex vasospasm limits
instant blood loss. Thereafter, there may be considerable hemorrhage
may be controlled by pressure bandaging or clamping/ligation of
significant vessels. Treatment is straight forward primary closure by
suture, adhesive, or simply by dressings. In most cases, healing is
rapidly achieved. Scarring is usually obvious but of limited functional
importance.
g. Laceration
A laceration is a traumatic tearing of the skin in an uncontrolled
direction. Lacerated wounds are common, and multiple tears in the
skin may be accompanied by bruising. Hemorrhage is rarely a
problem.
Treatment of laceration is described in section. Healing is often
difficult especially on the limbs. The prognosis is less favorable than

for incised wound because tissue necrosis and sloughing are frequent
complication.
h. Complicated Wound
Complicated wound are probably the commonest wound type
in equine practice. Injuries either involve other structures or are
complicated by factors that either preclude simple primary union, or
are likely to result in serious delays in healing. Comfortable foot and
half limb casts are usually tolerated very well, but full limb casts are
much more difficult.
C. Wound Healing Factors (S. Guo, 2010).
Multiple factors can lead to impaired wound healing. In general terms,
the factors that influence repair can be categorized into local and systemic.
Local factors are those that directly influence the characteristics of the wound
itself, while systemic factors are the overall health or disease state of the
individual that affect his orher ability to heal (Table 2). Many of these factors
are related, andthe systemic factors act through the local effects affecting
wound healing.
1. Local Factors That Influence Healing
a. Oxygenation
Oxygen is important for cell metabolism, especially energy
production by means of ATP, and is critical for nearly all woundhealing
processes. It prevents wounds from infection, induces angiogenesis,
increases

keratinocyte

differentiation,

migration,and

re-epitheli

alization, enhances fibroblast proliferation and collagen synthesis, and


promotes wound contraction. In addition, the level of superoxide

production (a key factor for oxidative killing pathogens) by


polymorphonuclear leukocytes is critically dependent on oxygen levels.
Due to vascular disruption and high oxygen consumption by
metabolically active cells, the microenvironment of the early wound is
depleted of oxygen and is quite hypoxic. Several systemic conditions,
including advancing age and diabetes, can create impaired vascular
flow, thus setting the stage for poor tissue oxygenation. In the context
of healing, this overlay of poor perfusion creates a hypoxic wound.
Chronic wounds are notably hypoxic; tissue oxygen tensions have been
measured transcutaneously in chronic wounds from 5 to 20 mmHg, in
contrast to control tissue values of 30 to 50 mm Hg. In wounds where
oxygenation is not restored, healing is impaired. Temporary hypoxia
after injury triggers wound healing, but prolonged or chronic hypoxia
delays wound healing. In acute wounds, hypoxia serves as a signal that
stimulates many aspects of the wound-healing process. Hypoxia can
induce cytokine and growth factor production from macrophages,
keratinocytes, and fibroblasts. Cytokines that are produced in response
to hypoxia include PDGF, TGF-, VEGF, tumor necrosis factor-
(TNF-), and endothelin-1, and are crucial promoters of cell
proliferation, migration and chemotaxis, and angiogenesis in wound
healing. In normally healing wounds, ROS such as hydrogen peroxide
(H2O2) and superoxide (O2) are thought to act as cellular messengers
to stimulate key processes associated with wound healing, including

cell motility, cytokine action (including PDGF signal transduction), and


angiogenesis. Both hypoxia and hyperoxia increase ROS production,
but an increased level of ROS transcends the beneficial effect and
causes additional tissue damage. In summary, the proper oxygen level is
crucial for optimum wound healing. Hypoxia stimulates wound healing
such as the release of growth factors and angiogenesis, while oxygen is
needed to sustain the healing process. One therapeutic option that can
sometimes overcome the influence of tissue hypoxia is hyperbaric
oxygen therapy. While HBOT can be an effective treatment for hypoxic
wounds, its availability is limited.
b. Infections
Once skin is injured, micro-organisms that are normally
sequestered at the skin surface obtain access to the underlying tissues.
The state of infection and replication status of the microorganisms
determine whether the wound is classified as having contamination,
colonization, local infection/critical colonization, and/or spreading
invasive infection. Contamination is the presence of non-replicating
organisms on a wound, while colonization is defined as the presence of
replicating microorganisms on the wound without tissue damage. Local
infection/ critical colonization is an intermediate stage, with
microorganism replication and the beginning of local tissue responses.
Invasive infection is defined as the presence of replicating organisms
within a wound with subsequent host injury. Inflammation is a normal

part of the wound-healing process, and is important to the removal of


contaminating

micro-organisms.

In

the

absence

of

effective

decontamination, however, inflammation may be prolonged, since


microbial clearance is incomplete. Both bacteria and endotoxins can
lead to the prolonged elevation of pro-inflammatory cytokines such as
interleukin-1 (IL-1) and TNF- and elongate the inflammatory phase. If
this continues, the wound may enter a chronic state and fail to heal.
This prolonged inflammation also leads to an increased level of matrix
metalloproteases (MMPs), a family of proteases that can degrade the
ECM. In tandem with the increased protease content, a decreased level
of the naturally occurring protease inhibitors occurs. This shift in
protease balance can cause growth factors that appears in chronic
wounds to be rapidly degraded. Similar to other infective processes, the
bacteria in infected wounds occur in the form of biofilms, which are
complex communities of aggregated bacteria embedded in a
selfsecreted extracellular polysaccharide matrix. Mature biofilms
develop protected microenvironments and are more resistant to
conventional antibiotic treatment. Staphylococcus aureus (S. aureus),
Pseudomonas

aeruginosa

(P.

aeruginosa),

and

-hemolytic

streptococci are common bacteria in infected and clinically noninfected wounds. P. aeruginosa and Staphylococcus appear to play an
important role in bacterial infection in wounds. Many chronic ulcers
probably do not heal because of the presence of biofilms containing P.

aeruginosa, thus shielding the bacteria from the phagocytic activity of


invading polymorphonuclear neutrophils (PMNs). This mechanism may
explain the failure of antibiotics as a remedy for chronic wounds.
2. Systemic Factors That Influence Healing
a. Age
The elderly population (people over 60 years of age) is growing
faster than any other age group (and increased age is a major risk factor
for impaired wound healing. Many clinical and animal studies at the
cellular and molecular level have examined age-related changes and
delays in wound healing. It is commonly recognized that, in healthy
older adults, the effect of aging causes a temporal delay in wound
healing, but not an actual impairment in terms of the quality of healing.
Delayed wound healing in the aged is associated with an altered
inflammatory response, such as delayed T-cell infiltration into the
wound area with alterations in chemokine production and reduced
macrophage phagocytic capacity. Delayed re-epithelialization, collagen
synthesis, and angiogenesis have also been observed in aged mice as
compared with young mice. Overall, there are global differences in
wound healing between young and aged individuals. A review of the
age-related changes in healing capacity demonstrates that every phase
of healing undergoes characteristic age-related changes, including
enhanced platelet aggregation, increased secretion of inflammatory
mediators, delayed infiltration of macrophages and lymphocytes,
impaired macrophage function, decreased secretion of growth factors,

delayed re-epithelialization, delayed angiogenesis and collagen


deposition, reduced collagen turnover and remodeling, and decreased
wound strength. Several treatments to reduce the age-related
impairment of healing have been studied. Interestingly, exercise has
been reported to improve cutaneous wound healing in older adults as
well as aged mice, and the improvement is associated with decreased
levels of pro-inflammatory cytokines in the wound tissue. The
improved healing response may be due to an exercise-induced antiinflammatory response in the wound.
b. Sex Hormones in Aged Individuals
Sex hormones play a role in age-related wound-healing deficits.
Compared with aged females, aged males have been shown to have
delayed healing of acute wounds. A partial explanation for this is that
the female estrogens (estrone and 17-estradiol), male androgens
(testosterone and 5-dihydrotestosterone, DHT), and their steroid
precursor dehydroepiandrosterone (DHEA) appear to have significant
effects on the wound-healing. It was recently found that the differences
in gene expression between elderly male and young human wounds are
almost exclusively estrogen-regulated. Estrogen affects wound healing
by regulating a variety of genes associated with regeneration, matrix
production, protease inhibition, epidermal function, and the genes
primarily associated with inflammation. Studies indicate that estrogen

can improve the age-related impairment in healing in both men and


women, while androgens regulate cutaneous wound healing negatively.
c. Stress
Stress has a great impact on human health and social behavior.
Many diseasessuch as cardiovascular disease, cancer, compromised
wound healing, and diabetesare associated with stress. Numerous
studies have confirmed that stress-induced disruption of neuroendocrine
immune equilibrium is consequential to health. The pathophysiology of
stress results in the deregulation of the immune system, mediated
primarily through the hypothalamic-pituitaryadrenal (HPA) and
sympathetic-adrenal medullary axes or sympathetic. Studies in both
humans and animals have demonstrated that psychological stress causes
a substantial delay in wound healing. Caregivers of persons with
Alzheimers and

students

undergoing

academic

stress

during

examinations demonstrated delayed wound healing. The hypothalamicpituitary-adrenal and the sympathetic- adrenal medullary axes regulate
the release of pituitary and adrenal hormones. These hormones include
the adrenocorticotrophic hormones, cortisol and prolactin, and
catecholamines (epinephrine and norepinephrine). Stress up-regulates
glucocorticoids (GCs) and reduces the levels of the proinflammatory
cytokines IL-1, IL-6, and TNF- at the wound site. Stress also reduces
the expression of IL-1 and IL-8 at wound sitesboth chemoattractants
that are necessary for the initial inflammatory phase of wound healing.

Furthermore,

GCs

influence

immune

cells

by

suppressing

differentiation and proliferation, regulating gene transcription, and


reducing expression of cell adhesion molecules that are involved in
immune cell trafficking. The GC cortisol functions as an antiinflammatory agent and modulates the Th1-mediated immune
responses that are essential for the initial phase of healing. Thus,
psychological stress impairs normal cellmediated immunity at the
wound site, causing a significant delay in the healing process.

D. Management of Wound Injury


A. Wound Assessment
The assessment process assists in clinical decision making by
preventing undirected care and inappropriate treatment. Clinicians perform
a thorough assessment for all patients before determining the need for
special examinations and interventions. This process begins when the
patient is admitted to the agency or when referred for services.
Assessment involves gathering data from the patient history and
physical examination. The patient history determines which relevant
system reviews should be included in the physical examination. The
history and systems review determine whether the patient is a candidate
for services and the direction of the treatment plan. For nurses, the
assessment process provides the framework for planning comprehensive
wound care and for making referrals for physical therapy or other services.
For all providers, proper utilization management is mandatory in todays

healthcare environment. Utilization management, which is part of the


process of prospective management, is designed to ensure that only
medically necessary, reasonable, and appropriate services are provided.1
The interdisciplinary nature inherent in caring for a patient with a wound
requires clinicians to carefully determine candidacy for services before
initiating referral or treatment. For example, many practitioners believe
that a referral to physical therapy automatically confers candidacy for
wound care; however, not all patients are appropriately referred. The
physical therapist needs to review the case, make the appropriate
assessments, and determine candidacy and then advise the referring
provider of recommendations. Many patients with a wound have
comorbidities and coimpairments. For such patients, collaborative
interdisciplinary management is critical to prevent iatrogenic effects
caused by inappropriate selection of interventions or handling of a wound
and to reduce extrinsic and intrinsic complications.
Wound assessment involves evaluation of a composite of wound
characteristics, including location, shape, size, depth, edges, undermining
or pocketing and tunneling, necrotic tissue characteristics, characteristics
of drainage or exudate, drainage that contains dead cells and debris,
surrounding skin color, peripheral tissue edema and induration, and the
presence of granulation tissue and epithelialization (Sussman J. and Jensen
B., B, 2013)
B. Basic Wound Care
1. A Clean Wound

The skin surrounding the wound looks relaively normal as in


Photo A. The skin is not tender to touch and not warm or swollen. If
the wound is acute the exposed flesh will look normal. If it is an older
wound, there may be a bed of granulation tissue (bright red tissue that
bleeds if you try to wipe it off) over the wound. There should be no
necrotic tissue overtop of the wound. There may be some
fibrinous/proteinaceous material (exudate, see below) on the woundbut it is not creamy, like pus. Systemic antibiotics are not required for
these wounds

.
A
2. An Infected Wound
In an infected wound, the surrounding skin is often red and warm
and swollen Photo B. There may be pus or other necrotic tissue on the
wound. In general, an infected wound is more painful than a clean
wound. Systemic antibiotics and debridement are required if the
wound is infected. It is important to distinguish between a clean wound
and an infected one so as to know when systemic antibiotics are
required. Just because someone has an open wound does not mean that
antibiotics are necessary. Antibiotics are only required if the wound is
infected.
3. Exudate
The material that naturally builds up on wounds. It is made up
of proteins, fluid, and cellular debris that gets to the wound from the

surrounding tissue as a result of the healing process. This is not pus.


(Nadine Bet al,2013).

C
a. Dressing materials
The best material for dressings is simple cotton gauze. You
only need enough to lightly cover the wound. Be sure to open the
gauze completely to

prevent unnecessary waste of supplies.

Remember, there is nothing sterile about an open wound. Bacteria will


always colonize the wound. Unless there is an important underlying
structure (a prosthetic joint), clean technique is usually sufficient.
b. Solutions
Various solutions are appropriate for wound care. These same
solutions can be used to cleanse the wounds at the time of dressing
change.
Solution
Povidone iodine

Preparation
Notes
Comes pre made in containers. Toxic to healthy
Best filluted for dressing: 1 used in diluted for

Saline

part povidine iodie to at least 3 only

few

days.

or 4 parts saline or sterile Then

change

to

water.
milder solution
Comes pre made, but easy to Safe anywhere on
make yourself. To 1 liter of the body
water add tsp salt. Boil the
solution for at least 60 seconds

and allow to cool. Store in a


closed, sterile container and
refrigerate if possible. Good
Sterile water

for several days.


Boil a liter of water for at least Safe anywhere on
60 seconds and allow to cool. the body
Store

in

closed,

sterile

container and refrigerate if


Dakins solution

posible. Good for few days.


Some pharmacles keep Dakins Better antibacterial
solution in stock, but it is easy agent than saline
to make. To 1 liter of saline so a little harsher
solution, add5-10 cc of liquid on normal tissue.
bleach . store in a closed sterile Do not use arround
container and refrigerate if the eyes. Makes
possible. If you are pharmacy wound smell better
carries Dakins solution. Its
bet used diluted. 1 part Dakins
solution mixed with 3-4 parts
saline

c. Antibiotik
Some wounds, for example a burn wound, are best treated with
a topical antibiotic ointment. The ointment keeps the wound moist and
helps decrease the pain associated with a wound that has dried out.

Also, the antibiotics can penetrate the wound and prevent infection
(Nadine Bet al, 2013)

COMPLICATIONS
A. Common Wound Complications
1. Haematoma and seroma
Wounds complicated by a collection of blood are known as
haematomas, whereas seromas are a collection of serum.Haematomas occur
more frequently than seromas and areusually from when haemostasis is not
achieved at the time ofsurgery or secondary to clotting defects (e.g.
anticoagulation). Both haematomas and seromas increase the risk of
infection by allowing bacteria access to the subcutaneous tissue following
disruption of the wound surface.
Patients usually present a few days post-operatively with painful or
painless swelling around the wound site, and/or drainage of fluid. Seromas
may present with drainage of straw-coloured fluid. If secondary infection is
present there might be local and/or systemic signs of sepsis, like fever,
erythema, cellulitis, pus draining from wound and leukocytosis. Diagnosis is
usually clinical but ultrasound and CT-scan might be of use.
Treatment usually depends on the size of the haematoma and seroma and
ranges from expectant management to surgical drainage. In the absence of

infection the wound may be closed primarily or left to heal by secondary


intention. Seromas may be managed with sterile aspiration.
Preventing these complications usually require proper surgical
technique, meticulous haemostasis and obliterating large potential dead
spaces. Prophylactic drain placementmay be indicated to prevent fluid
collection and infection, however randomised trials and meta-analysis found
that wound complications were not reduced by closed drainage of
subcutaneous tissue (Aardt V., MC and Mouton A., 2015)
2. Fascial dehiscence
Fascial separation is usually a product of suture or tissue failure
secondary to abdominal pressure. It can happen early or late following
surgery and include partial or complete fascial dehiscence. Early fascial
dehiscence, with or without evisceration, is regarded as an emergency
requiring surgical intervention, while late dehiscence manifest as incisional
hernias.
A retrospectivestudy performed in Greece identified a number of
risk factors associated with dehiscence. Factors associated with dehiscence
of the abdominal wound included advanced age (>65 years), emergency
procedures, malignancy, haemodynamic unstable patients, local and intraabdominal sepsis, low albumin, ascites, obesity and steroid usage. Gender,
anaemia, diabetes mellitus and lung disease were not shown to be
significantly associated with fascial dehiscence.
Fascial dehiscence is usually diagnosed clinically and occurs on
average around eight days post-operatively (4-14 days). Patients might report

a popping feeling followed by excessive drainage of serosanguinous fluid.


Surgical exploration is indicated if clinically suspected. Seeing as complete
fascial dehiscence carries a mortality rate of up to ten percent, urgent
intervention is mandatory. Treatmententails careful wound exploration,
fascial edge debridement, mass closure with delayed absorbable sutures, with
or without skin closure. A large review which included four meta-analysis
concluded that the optimal technique to close a midline incision necessitate
closure of all layers except the skin as a single structure, in a simple
continuous fashion, with a delayed absorbable monofilament suture material
and the suture length four times that of the wound length (Aardt V., MC and
Mouton A., 2015).
3. Surgical site infection (SSI)
A wide spectrum of common endogenous bacteria produce wound
infections, including most gram positive cocci and aerobic and anaerobic
rods. Small numbers of bacteria are present in all surgical wounds,
however, bacterial growth is facilitated by decreased tissue oxygen and
excessive amounts of necrotic tissue. It requires between 100.000 to
1.000.000 bacteria per gram of tissue to produce an infection in surgical
wounds. The incidence of superficial skin infections is directly related to
the length of surgery. Every extra hour of operativetime result in a doubling
of the incidence of superficial skininfections. Infection complicates around
four percent of clean wounds. The first symptoms of wound infections
typically appear between five and ten days post-operative. Fever within the

first 48 hours usually results from atelectasis. Rare types of wound


infections caused by Clostridium species and acute -haemolytic
streptococci species are so virulent that they can produce toxicity within the
first two days. Woundinfections secondary to Clostridium species are
boggy, oedematous and has a discharge smelling like sweat. -haemolytic
streptococci infections appear swollen, red and the discharge is odourless.
In general wound infections present as an erythematous, indurated,
warm and painful incision area. Purulent fluid may drain from the wound
with local wound breakdown. Incisional abscesses may also be present.
More severe infections may manifest with systemic signs, ranging from fever
to septic shock. Although rare, necrotising fasciitis may occur in severe cases
and is a life-threatening condition requiring emergency surgical intervention
and support. These patients may present with excessive pain around the
surgical site. Subcutaneous tissue is usually very friable with pale,
devitalised fascia. The infection expands quickly in the subcutaneous spaces
and often tracks far beyond the superficial margins of the involved skin. The
disease carries a mortality of up to 50% and requires immediate surgical
intervention including wide debridement of all the necrotic tissue followed
by appropriate antibiotic administration.
Treatment generally depends on the extent of the infection.
Wounds complicated with cellulitis, without areas of fluctuation can
generally be treated with oral or parenteral antibiotics. Antibiotic cover
should usually be broad spectrum and include cover against grampositive
cocci from the skinand bacteria expected at the operation site. Antimicrobial

treatment should be tailored according to clinical response and microscopy,


culture and sensitivity resultsMore severe infections and wound abscesses
require surgical debridement with or without incision and drainage
Debridement is done using a scalpel and scissors and requires
removing all devitalised tissue that may impair healing and increase
infection risks. Due to the toxic effect of chemical agents like povidineiodine and hydrogen peroxide on fibroblasts, these agents are not
recommended. Saline is preferred for irrigation because it is isotonic and
does not halter wound healing.
Following debridement, wounds should be covered by dressings
that keep moisture and warmth, therefore holding tissue growth factors that
assist with re-epithelialisation and allowing autolytic debridement.In order
for wounds to heal by secondary intention, the best dressing to facilitate this
process will absorb exudates, resist water and microorganisms and does not
leave contaminants in the wound site after removal or damage granulation
tissue. According to the Centre for Disease Control guidelines, the following
preventative steps to limit surgical site infections are based on high quality
evidence from welldesigned trials: (1) Elective surgery should be avoided in
patients with current infections. (2) Optimal concentration of perioperative
antibiotics should be accomplished and prophylactic antibiotics continued
for a couple of hours following surgery. (3) If hair removal is indicated, it is
advised that it should be clipped and not shaved before commencing surgery
in the operating room.
Based on good quality evidence and expert consensus, the
following guidelines may also prevent SSI: (1) Optimal glucosecontrol in

diabetic patients peri-operatively. (2) Smoking or tobacco use cessation or


abstinence for a month before surgery. (3) Bathing or showering with an
antiseptic soap ahead of the operation. (4) Standards should be followed
regarding sterilising instruments, maintaining an aseptic operating theatre, as
well as appropriate air circulation. (5) Preventative measures from the
surgical team include, disallowing members with active infections, always
wearing sterile clothing and gloves, meticulous hand hygiene including short
fingernails, scrubbing with antiseptic agents for two to five minutes up to the
elbows and using sterile towels to dry afterwards. (6) Correct surgical
technique is crucial, and leaving sterile dressings on the surgical site for 24
to 48 hours may also prevent this complication (Aardt V., MC and Mouton
A., 2015).
B. Special Considerations
1. SSIs following lower segment caesarean section
Caesarean sections are one of the most frequently performed
procedures globally and steadily rising. It remains one of the main reasons
for SSI. SSIs following caesarean section, which includes all infections
occurring within 30 days following surgery, may be superficial, deep, or in
severe

cases

present

as

pelvic

and/or

abdominal

abscesses.

Endomyometritis can also be included as part of post-caesarean SSI.


As mentioned before, there are many factors that increase the risk
of wound infection as with non-pregnant patients. Other factors specifically
to pregnancy include limited antenatal care, pregestational and gestational
diabetes, hypertensive conditions, higher orderpregnancies, emergency
caesarean sections, labour duration, prelabour rupture of membranes and

duration thereof, number of vaginal examinations and failure toadminister


prophylactic antibiotics, to name a few.
Preventing SSI following caesarean delivery should be directed
towards modifying specific risk factors. One such an important intervention
is administrating prophylactic antibiotics before performing a caesarean
section. Previously, antibiotic administration was delayed until after
clamping of the umbilical cord because of concerns that it may conceal
neonatal infections and cause bacterial resistance. However, this appears
not to be the case and there is high quality evidence that by giving
antibiotics earlier benefits the mother and does not harm the neonate.
The American Congress of Obstetricians and Gynecologists
(ACOG) recommends the first-line antibiotic that should be used as a
single dose within an hour of initiating surgery to be either a first
generation cephalosporin or ampicillin. Patients allergic to penicillin should
receive clindamycin and a aminoglycoside. A recent study from India found
the organisms most frequently associated with SSIs post-caesarean delivery
were

Acinetobacterspecies,

Staph.

Aureusand

coagulase

negative

Staphylococcus.
Operating room procedures that might contribute to reducing
infections include clipping instead of shaving hair immediately before
cutting, cleaning with chlorhexidine preperations, prophylactic antibiotics
before skin incision, removal of the placenta with traction and not
manually, closing subcutaneous tissue with a continuous suture if greater
than 2 cm and cleaning the vagina with povidoneiodine just before the
procedure (Aardt V., MC and Mouton A., 2015).

2. Vaginal cuff dehiscence/Evisceration


The overall incidence of dehiscence of the vaginal vault after
hysterectomy is reported to range between 0.24% and 0.39% and varies
depending on the route of hysterectomy. Total laparoscopic hysterectomy
carries the highest risk for cuff dehiscence and vaginal hysterectomy the
lowest risk. The average time it takes for this complication to occur varies
between 45 to 100 days after surgery, but may occur as late as 20 months.
Factors that increase the chance of dehiscence include sexual
intercourse, vault haematoma or abscess, smoking, postmenopausal state
and constant elevated intraabdominal pressure. The incidence of vaginal
cuff dehiscence may be reduced by administrating prophylactic antibiotics
and by treating post-operative vaginal infections in symptomatic patients.
Closing the vaginal vault with full thickness sutures, at least 10mm from
the resection margin, and avoiding diathermy usage may reduce vault
dehiscence. However, the type of suture material and technique used does
not appear to make a difference.
Vault dehiscence is diagnosed clinically and patients can present
with vaginal bleeding, discharge and/or pain. More severe presentations
include peritonitis, evisceration, bowel strangulation and septicaemia.
Treatment usually involves broad-spectrum antibiotics with surgical repair.
There is not sufficient evidence on the appropriate route to use for surgical
repair. Vaginal repair is probably best for small, uncomplicated dehiscence
whereas abdominal exploration and repair is mandatory for patients with
evisceration (Aardt V., MC and Mouton A., 2015).
3. The Obese Patient

Obesity is one of the most significant risk factors for wound


infections and disruption. In this group of patients, hyperglycaemia can
further contribute to complications. Adipose tissue is poorly vascularised
and causes suboptimal oxygenation leading to poor healing, collagen
synthesis and reepithelialisation.
Techniques to improve wound healing in obese patients can be
summarised as follows :
Chlorhexidine bath or shower the night prior to surgery
Women with BMI >35 should receive double the dosageof
prophylactic antibiotics Extending the dosing beyond surgery is not

helpful
Normothermia should be maintained during surgery
Subcutaneous tissue more than two centimetres shouldbe closed
Cover the wound with a sterile dressing between 24 to48 hours
Maintain euglycaemia
Excess oxygen administration during surgery andsubcutaneous
drains do not appear to improve outcome (Aardt V., MC and

Mouton A., 2015).


4. Wound complications in HIV-infected patients
There appears to be conflicting evidence regarding postoperative
morbidity and mortality among HIV-infected women. Factors that may
increase impaired wound healing, wound infections and post-operative
sepsis include immunodepletion manifested by a low CD4cell count,
malnutrition evident from a low albumin and/or a neutrophil count less than
500 cells. Allaran et al (2000) inAardt V., MC and Mouton A. (2015).
Found more post-operative complications and less favourableoutcomes six
months afterwards among patients with a CD4cell count below 200
cells/microliter. A pre-operative

viral

load

more

than

30

000

copies/milliliter and emergency surgery may also increase surgical


complications
Conclusion
Wound complications can be complicated and challengingto manage and
may cause significant distress for both the patients and the physician who cares
for them. Everything possible should me done to prevent post-operative wound
complications, but if they occur, early recognition andcorrect treatment is
imperative.

E. Clinical Manifestation (Alton, 2011).


A. Open Wounds
1. Abrasion
The top layer of skin is removed, with little or no blood loss.
Abrasions tend to be painful because the nerve endings often are abraded
along with the skin. Ground-in debris may be present. This type of wound
can be serious if it covers a large area or becomes embedded with foreign
matter. Other names for an abrasion are scrape, road rash, and rug burn.
2. Laceration
Cut skin with jagged, irregular edges. This type of wound is
usually caused by a forceful tearing away of skin tissue.
3. Incisions

Tend to have smooth edges and resemble a surgical or paper cut.


The amount of bleeding depends on the depth, the location, and the size of
the wound.
4. Punctures
Usually deep, narrow wounds in the skin and underlying organs
such as a stab wound from a nail or a knife. The entrance is usually small,
and the risk of infection is high. The object causing the injury may remain
impaled in the wound.

5. Avulsion
Piece of skin is torn loose and is hanging from the body or
completely removed. This type of wound can bleed heavily. If the flap is
still attached, lay it flat and realign it into its normal position. Avulsions
most often involve ears, fingers, and hands.
6. Amputation
Involves the cutting or tearing off of a body part, such as a finger,
toe, hand, foot, arm, or leg.
B. Closed Wounds
1. Bruises and contusions occur when blood collects under the skin in the
injured area. The victim will experience pain and swelling (immediately or
within 24 to 48 hours). As blood accumulates, a black-and-blue mark may
appear.
2. A hematoma is a clot of blood under the skin. There may be a lump or
bluish discoloration.

3. Crush injuries are caused by extreme forces, which can injure vital organs
and bones without breaking open the skin. Crush injuries may indicate an
underlying problem such as a fracture. Signs and symptoms include
discoloration, swelling, pain, and loss of use.
F. Types of Wound Healing
1. Primaryintention healing
Wound healing by primary intention is typical for noncomplicated
surgical wounds. Wound edges are approximated and kept together with
sutures or staples and healing occurs by wound epithelialisation and
connective tissue deposition. These wounds usually heal quickly provided
there is no infection.

2.

Se
co
nd
ar
y-

intention healing

Wound healing by secondary intention is typical for chronic


wounds such as venous leg ulcers. The wound is left open and healing
occurs by granulation tissue formation, contraction of the wound edges
and subsequently epithelialisation. These wounds show delayed healing
due to the volume of connective tissue required to fill the defect. Since
there is no epidermal barrier,
The risk of an infection is significantly higher in these wounds.

Tertiary-intention healing

Wound healing by tertiary intention (delayed primary closure) is sometimes


necessary in abdominal incisions (e.g. abdominoplasty) to lower the risk of
infection. After leaving the wound open for several days, which allows formation
of granulation tissue, the wound edges are then stitched together in a second
procedure (Gupta S et al, 2015).

G. Phase of Wound Healing (Reinke and Sorg, 2012).


1. Inflammatory
The inflammatory phase of the wound healing cas-cade gets
activated during the hemostasis and coagula-tion phase and can roughly be
divided into an early phase with neutrophil recruitment and a late phase
with the ap-pearance and transformation of monocytes . Due to the
response of the activated complement pathway, de-granulated platelets and
by-products of bacterial degra-dation, neutrophils are recruited to the site
of the skin injury and are present for 25 days unless the wound gets
infected. The work of the neutrophils is crucial within the first days after
injury because their ability in phagocyto-sis and protease secretion kills
local bacteria and helps to degrade necrotic tissue. Furthermore, they act as
che-moattractants for other cells that are involved in the in-flammatory

phase.

Fig. 1.Inflammatory phase after a cutane-ous cut; hemostasis and invasion of inf lammatory cells.

Neutrophils release mediators such as TNF- !, IL-1 "and IL-6,


which amplify the inflammatory response and stimulate VEGF and IL-8
for an adequate repair response. Furthermore, they start their debridement
by releasing highly active antimicrobial substances (cationic peptides and
eicosanoids) and proteinases (elastase, cathepsin G, proteinase 3 and a
urokinase-type plasminogen activa-tor) [5]. In vitro studies further showed
that neutrophils could change the phenotype and cytokine profile expression of macrophages, which leads to an innate immune response during
healing .
Approximately 3 days after injury macrophages enter the zone of
injury and support the ongoing process by performing phagocytosis of
pathogens and cell debris as well as by the secretion of growth factors,

che-mokines and cytokines. Apart from their actual support in wound


healing, these molecules keep the healing pro-cess intact, as some of them
are able to activate the next phase of wound healing (proliferative phase).
The in-flammatory response to injury is essential for supplying growth
factor and cytokine signals that are responsible for cell and tissue
movements, which are crucial for the subsequent repair mechanisms in
adult mammalians. There is evidence that the amount of inflammation
determines the extent of scar formation. The lack of in-trauterine
inflammation is mentioned as evidence for the theory of scarless wound
healing in fetuses .
Macrophages have many functions including host de-fense, the
promotion and resolution of inflammation, the removal of apoptotic cells
and the support of cell prolif-eration and tissue restoration following
injury. Be-side their immunological functions as antigen-present-ing cells
and phagocytes during wound repair, macro-phages supposedly play an
integral role in a successful healing response through the synthesis of
numerous po-tent growth factors such as TGF- ", TGF- !, basic FGF,
PDGF and VEGF, which promote cell proliferation and the synthesis of
extracellular matrix (ECM) molecules by resident skin cells.
2. Proliferasi
A. Reepithelialization/Resurfacing
In the phase of proliferation (approx. 310 days after
wounding) the main focus of the healing process lies in covering the
wound surface, the formation of granulation tissue and restoring the
vascular network. Therefore, next to the immigration of local
fibroblasts along the fi-brin network and the beginning of
reepithelialization from the wound edges, neovascularization and
angiogen-esis get activated by capillary sprouting . Un-der the control
of regulating cytokines like IFN and TGF- , the synthesis of collagen,
fibronectin and other basic substances needed for wound healing by
fibroblasts represents the basis for the new matrix of connective tis-sue,

serving for the closure of tissue gaps and the restora-tion of the
mechanical strength of the wound. Subse-quently, the synthesis of
collagen increases throughout the wound, while the proliferation of
fibroblasts declines successively, adjusting a balance between synthesis
and degradation of the ECM.
The reepithelialization process is ensured by local keratinocytes at the wound edges and by epithelial stem cells from hair
follicles or sweat glands. This process is activated by signaling
pathways of epithelial and nonepithelial cells at the wound edges,
which release a myriad of different cytokines and growth factors, e.g.
EGF, KGF, IGF-1, and NGF. Furthermore, the aboli-tion of the contact
inhibition and physical tension at des-mosomes and hemidesmosomes
produces lipid media-tors and activates membrane-associated kinases
(SRCkinases) resulting in an increased permeability of the membranes
for ions, e.g. calcium. This displays an initiat-ing signal to the cells at
the wound edges with a retraction and reorganization of their
intracellular tonofilaments in the direction of migration. By the
enzymatic loosening of the intercellular desmosomes via collagenase
and elas-tase, activated keratinocytes migrate along the preformed
fibrin blood clot in the higher layers of the granulation tissue. This
process is called the shuffling of keratino-cytes and describes the
ability of these cells to mi-grate competitively along a chemotactic
gradient estab-lished by mediators such as IL-1, and over a fibronectinrich matrix into the center of the wound.
B. Neovascularization/Angiogenesis
The restoration of the vascular system of the skin is a complex
cascade of cellular, humoral and molecular events in the wound bed to
reconnect to the nutritive per-fusion. Initiators are growth factors, e.g.
VEGF, PDGF, bFGF and the serine protease thrombin. The first step in
new vessel formation is the binding of growth factors to their receptors
on the endothelial cells of existing vessels, thereby activating

intracellular signaling cascades. The activated endothelial cells secrete


proteolytic enzymes which dissolve the basal lamina. Thus, the
endothelial cells are now able to proliferate and migrate into the wound,
a process also known as sprouting. The endothe-lial cells orientate
themselves

at

superficial

adhesion

mol-ecules,

e.g.

integrin.

Furthermore, they release matrix metalloproteinases at the front of proliferation, lysing the surrounding tissue for the ongoing endothelial
proliferation. The newly built sprouts form small tubular canals which
interconnect to others form-ing a vessel loop. Thereafter, the new
vessels differentiate into arteries and venules and mature by a further
stabili-zation of their vessel wall via the recruitment of pericytes and
smooth muscle cells. Finally, the initial blood flow completes the
angiogenic process. Within full dermal thickness wounds the
neovascularization process follows a distinct pattern in time and shape.
At the beginning the vessels form an inner ring of circularly arranged
vessels at the wound margin followed by outer radially arranged vessels
supplying the inner ones. Because the design of the vessels is similar to
the sun, this has also been called sola cutis se reficientis. As the
wound closure pro-ceeds, the inner vascular ring shrinks, resulting in
the complete disappearance of the vessel ring. The radially arranged
vessels, however, interconnect with each other in time, forming a new
dermal vascular network.

Fig. 2.Proliferative phase; organization of the thrombus, secretion of growth factors, synthesis of
collagen III and the beginning of angiogenesis.

C. Granulation Tissue Formation


The last step in the proliferation phase is the develop-ment of
the acut granulation tissue. At the same time the remodeling phase is
already

initiated.

As

tran-sitional

tissue

it

replaces

the

fibrin-/fibronectin-based provisional wound matrix and might produce a


scar by maturation. Furthermore, it is charac-terized by a high density
of fibroblasts, granulocytes, macrophages, capillaries and loosely
organized collagen bundles. Due to this high amount of cellular compounds it is called granulation tissue. Also, as the angio-genesis is not
completely finished yet, this tissue is highly vascular. As a result it
appears with a classic redness and might be traumatized easily.
However, the dominating cell in this phase is the fibroblast, which
fulfils different functions such as the production of collagen and ECM
substances (i.e. fibronectin, glycosaminoglycans, proteo glycans and
hyaluronic acid). The formation of the ECM represents another
important step as it provides a scaffold for cell adhesion and critically
regulates and organizes the growth, movement and differentiation of the
cells within it. The fibroblast is, therefore, the precur-sor of the

provisional wound matrix on and in which the respective cell migration


and organization takes place. At the end of this phase the number of
maturing fi-broblasts is reduced by myofibroblast differentiation and
terminated by consecutive apoptosis.
3. Remodelling
Remodeling is the last phase of wound healing and oc-curs from day 21
to up to 1 year after injury. The forma-tion of granulation tissue stops through
apoptosis of the cells. A mature wound is, therefore, characterized as avascular
as well as acellular. During the maturation of the wound the components of the
ECM undergo cer-tain changes. Collagen III, which was produced in the
proliferative phase, is now replaced by the stronger col-lagen I. This type of
collagen is oriented in small parallel bundles and is, therefore, different from
the bas-ket-weave collagen in healthy dermis. Later on the myofibroblasts
cause wound contractions by their mul-tiple attachment to collagen and help to
decrease the sur-face of the developing scar Furthermore, the angiogenic
processes diminish, the wound blood flow de-clines, and the acute wound
metabolic activity slows down and finally stops. Contrary to fetal wound
healing, there are certain skin components that will never fully recover after
wound clo-sure. Subepidermal appendages such as hair follicles or sweat
glands have no potential to heal or grow back after serious injury. The
epidermis of the resultant scar differs from uninjured skin after wound healing
due to the lack of rete pegs that are normally anchored into the underly-ing
connective tissue matrix and are responsible for the tight connection of the
epidermis to the dermis.

Fig. 3.Remodeling phase; regenerative processes fade and are followed by reorganization of the
connective tissue and con-tractile response.