WOUND HEALING

Wound: A wound can be defined as the loss of continuity of the structure of the body
resulting from an injury.

ETIOLOGY:
Following are some of the common underlying causes or factors, which may interfere with
wound healing:
Trauma (initial or repetitive)

Scalds and burns both physical and chemical

Animal bites or insect stings

Pressure
Vascular compromise, arterial, venous or mixed
Immunodeficiency
Malignancy
Connective tissue disorders
Metabolic disease, including diabetes
Nutritional deficiencies
Psychosocial disorders
Adverse effects of medications
SYMPTOMS:
The symptoms resulting from wounds may be described as local, general, remote. Local
symptoms include haemorrhage, pain, gasping of the lips of the wound & the phenomena of
repair. General symptoms comprise those of febrile disturbance, & vary according to the
virulence of the infecting organism & the degree of injury to the tissues & the toxaemia.
Remote symptoms are observed in apart away from the wound.
Ex: Abcess formation in a dependent lymph gland; paralysis or loss of sensation to a
dependent part or neuritis extending along the course of a nerve involved in the wound.
HEALING OF A WOUND
Wound healing is the reestablishment of tissue continuity. Wound healing is a complex and

dynamic process with the wound environment changing with the changing health status of the
animal. The knowledge of the physiology of the normal wound healing trajectory through the
phases of hemostasis, inflammation, granulation and maturation provides a framework for an
understanding of the basic principles of wound healing. Through this understanding the
health care professional can develop the skills required to care for a wound and the body can
be assisted in the complex task of tissue repair.
The phases of wound healing are:
A. Hemostasis
B. Inflammation
C. Proliferation or Granulation
D. Remodeling or Maturation
A. Hemostasis:
Once the source of damage to a house has been removed and before work can
start, utility workers must come in and cap damaged gas or water lines. So too in
wound healing damaged blood vessels must be sealed. In wound healing the
platelet is the cell which acts as the utility worker sealing off the damaged blood
vessels. The blood vessels themselves constrict in response to injury but this
spasm ultimately relaxes. The platelets secrete vasoconstrictive substances to
aid in this process but their prime role is to form a stable clot sealing the
damaged vessel.
Under the influence of ADP (adenosine diphosphate) leaking from damaged
tissues the platelets aggregate and adhere to the exposed collagen3. They also
secrete factors which interact with and stimulate the intrinsic clotting cascade
through the production of thrombin, which in turn initiates the formation of fibrin
from fibrinogen. The fibrin mesh strengthens the platelet aggregate into a stable
hemostatic plug. Finally platelets also secrete cytokines such as platelet-derived
growth factor (PDGF), which is recognized as one of the first factors secreted in
initiating subsequent steps. Hemostasis occurs within minutes of the initial injury
unless there are underlying clotting disorders.
B. Inflammation Phase:
Clinically inflammation, the second stage of wound healing presents as
erythema, swelling and warmth often associated with pain, the classic rubor et

tumor cum calore et dolore. This stage usually lasts up to 4 days post injury. In
the wound healing analogy the first job to be done once the utilities are capped
is to clean up the debris. This is a job for non-skilled laborers. These non-skilled
laborers in a wound are the neutrophils or PMNs (polymorphonucleocytes). The
inflammatory response causes the blood vessels to become leaky releasing
plasma and PMNs into the surrounding tissue. The neutrophils phagocytize
debris and microorganisms and provide the first line of defense against infection.
They are aided by local mast cells. As fibrin is broken down as part of this cleanup the degradation products attract the next cell involved.
The task of rebuilding a house is complex and requires someone to direct this
activity or a contractor. The cell which acts as contractor in wound healing is
the macrophage. Macrophages are able to phagocytize bacteria and provide a
second line of defense. They also secrete a variety of chemotactic and growth
factors such as fibroblast growth factor (FGF), epidermal growth factor (EGF),
transforming growth factor beta (TGF-__ and interleukin-1 (IL-1) which appears to
direct the next stage5.
C. Proliferative Phase ( Proliferation, Granulation and Contraction):
The granulation stage starts approximately four days after wounding and usually
lasts until day 21 in acute wounds depending on the size of the wound. It is
characterized clinically by the presence of pebbled red tissue in the wound base
and involves replacement of dermal tissues and sometimes subdermal tissues in
deeper wounds as well as contraction of the wound. In the wound healing
analogy once the site has been cleared of debris, under the direction of the
contractor, the framers move in to build the framework of the new house. Subcontractors can now install new plumbing and wiring on the framework and
siders and roofers can finish the exterior of the house.
The framer cells are the fibroblasts which secrete the collagen framework on
which further dermal regeneration occurs. Specialized fibroblasts are responsible
for wound contraction. The plumber cells are the pericytes which regenerate
the outer layers of capillaries and the endothelial cells which produce the lining.
This process is called angiogenesis. The roofer and sider cells are the
keratinocytes which are responsible for epithelialization. In the final stage of
epithelializtion, contracture occurs as the keratinocytes differentiate to form the
protective outer layer or stratum corneum.

D. Remodeling or Maturation Phase:

Once the basic structure of the house is completed interior finishing may begin.
So too in wound repair the healing process involves remodeling the dermal
tissues to produce greater tensile strength. The principle cell involved in this
processis the fibroblast. Remodeling can take up to 2 years after wounding and
explains why apparently healed wounds can break down so dramatically and
quickly if attention is not paid to the initial causative factors.
Table: Phases of healing

Phase of Healing

Days Post Injury

Cells involved in

Hemostasis

Immediate

Phase
Platelets

Inflamation

Day 1-4

Neutrophils

Proliferation,

Day 4-21

Macrophases,

Granulation and

Lymphocytes,

contraction

Angiocytes,
Neurocytes,
Fibroblasts,
Keratinocytes

Remodelling

Day 21-2yrs

Fibrocytes

CHRONIC WOUND

In healthy animals with no underlying factors an acute wound should heal within three weeks
with remodeling occurring over the next year or so. If a wound does not follow the normal
trajectory it may become stuck in one of the stages and the wound becomes chronic. Chronic
wounds are thus defined as wounds, which have failed to proceed through an orderly and
timely process to produce anatomic and functional integrity, or proceeded through the repair
process without establishing a sustained anatomic and functional result. 6 Once a wound is
considered chronic it should trigger the wound care clinician to search for underlying causes,
which may not have been addressed. Better yet, an understanding of the causative factors
should lead us to be proactive in addressing these factors in at risk populations so that chronic
wounds are prevented.

COMPLICATIONS OF WOUND HEALING

Although most wound complications are not life-threatening, they involve prolonged
periods of animal discomfort and veterinary care, and increased costs to owners.
1.

Post operative Haemorrhage and Haematomas

Surgical incisions involve the disruption of blood vessels with an initial tissue

response of vasoconstriction.However, in the immediate postoperative period, vasodilation,

bleeding and haematoma formation can occur. Overt incisional haemorrhage is a burden in
patient management, but is usually a minor complication. Haematoma formation, however,
can predispose to wound infection, cause discomfort, and prevent healing of reconstructive
tissues (e.g. skin grafts) on to wound beds. Prevention of haemorrhage and subsequent
haematoma formation is more prudent than postoperative treatment. During surgery, using
appropriately sized ligatures or electrocautery can decrease haemorrhage. Minimizing the
amount of subcutaneous dissection will also prevent the accumulation of blood within a
defined space. Postoperatively, minor incisional oozing can be controlled with direct manual
pressure for 10-15 minutes. However, moderate to severe bleeding will require the
application of pressure bandages or surgical ligation of the offending vessels. Once
haematoma formation is evident, resolution may be accelerated by the application of warm
compresses on to the affected area for 10 minutes, three times a day. Dissipation of the
haematoma generally requires approximately 7 days.
2.

Seromas
Creation of dead space, either through trauma or by surgical dissection, can result in

the accumulation of sterile fluid within the subcutaneous space, a seroma. This fluid tends to
form in areas that have redundant, loosely attached skin (Figure 13.1) and are associated with
excessive motion (shoulder, axilla and dorsum). Other than the presence of fluid, seromas are
associated with few clinical signs. They are not painful, erythematous, oedematous or
associated with incisional dehiscence. In fact, seromas most often are a source of owner
anxiety, rather than patient discomfort. In some specialized reconstructive procedures, such as
skin grafting, seroma formation can be detrimental to the critical adherence of the tissue to
the wound bed. Seromas will also delay the ultimate healing of affected tissues.
Prevention of seroma formation is accomplished by practising gentle tissue handling
and eliminating dead space. Surgeries that involve extensive soft tissue dissection and
mobilization, such as regional mastectomies and skin flap transfers, will create large amounts

of dead space. Subcutaneous sutures, active or passive drains, and bandages are techniques
that can be used individually, or in combination, to decrease seroma formation. Although all
of these could be applied in clean surgical procedures, the use of buried suture material in
clean-contaminated cases should be avoided. In these situations, drains and bandages are
preferable. Open system drains (e.g. Penrose drains) should always be covered with bandages
to avoid ascending infection.
Seromas that occur after surgery usually do not require intervention. Attempts at
aspiration are futile and risk contaminating a sterile environment. Similarly, drain placement
often results in recurrence after drain removal and predisposes to iatrogenic infection.
Seromas do resolve spontaneously, but this process may require 2-3 weeks.
3.

Oedema
Early wound healing is associated with the process of inflammation. During this

process, vascular and lymphatic obstruction and the presence of cell- and plasmaderived
mediators result in the exudation of fluid into the interstitial subcutaneous space (oedema
formation). Traumatic wounds generally manifest more oedema than surgical wounds.
However, depending on the extent of dissection and the nature of the procedure, surgical
wounds can also appear oedematous in the first 3-4 days after surgery. Regional
mastectomies, for example, often result in marked peri-incisional oedema formation.
Large skin wounds of the distal limbs, which are managed with second intention
healing can also result in impaired lymphatic and venous drainage, and oedema formation.
Especially when wounds exceed 50% of the circumferential limb diameter, the tension
created by wound contracture creates a tourniquet effect and distal limb swelling.
Postoperative oedema can be treated using compression bandages. As loosening occurs, new
bandages need to be applied daily to maintain even pressure. The application of warm
compresses to the affected area 3-4 times daily promotes circulation and decreases oedema
formation. If oedema is confined to the limbs, active movement increases circulation and
promotes lymphatic and venous return.
4.

Wound Dehiscence
Dehiscence is defined as the breakdown of a surgically closed wound. Immediately

after closure, a problem incision may be erythematous, oedematous or painful. Often, a

serosanguineous discharge is associated with the wound edges. Generally, irrefutable
evidence of incisional breakdown becomes apparent at 3-5 days after surgery. Areas of nonviable necrotic tissue may also be evident at that time.
Wound dehiscence is rarely due to an intrinsic inability to heal; rather, problems

associated with surgical judgement or technique and the wound bed are incriminated.
Probably the most common reason for dehiscence after closure of a traumatic wound is
incomplete debridement of contaminated material and necrotic tissue. As all traumatic
wounds are contaminated, a thorough assessment of the cause and nature of the wound must
be performed initially.
5.

Infection
A break in the skin barrier, from either trauma or surgery, inevitably leads to bacterial

contamination. Postoperative infection has been documented to occur in approximately 5% of

all small animal surgical procedures and in 2.5% of clean surgeries (Vasseur, 1988). In most
patients, host defence systems will phagocytose microbes and prevent infection. However,
when bacterial numbers exceed a critical level (>106 organisms per gram of tissue), infection
will occur. Several factors, including local wound conditions, the type of bacteria involved
and the status of the patient, may dampen normal defence mechanisms and predispose to
infection. In traumatic wounds, the most common source of infection is the presence of nonviable tissue. Normally, after an incision or laceration, neutrophils migrate to the wound and
engulf and destroy microbes. Macrophage recruitment occurs later and enhances neutrophil
phagocytosis. Any local condition that prevents the ability of these cells to contact and kill
bacteria will potentiate infection. Haematoma or seroma formation will prevent the adherence
of neutrophils to the bacterial cell walls and may also serve as a substrate for microbial
growth. Implantation of foreign bodies, such as drains and sutures, will decrease the number
of bacteria necessary to cause an infection. Animals that are immunocompromised because of
pre-existing diseases (hyperadrenocorticism, diabetes mellitus, or neoplasia), or because of
exogenous medications (corticosteroids) are more susceptible to infections. Undeveloped or
senescent resistance processes may also affect the very young or old animal.
6.

Delayed and Incomplete wound development

Wounds that are left to heal by second intention can be complicated by delayed

healing and incomplete epithelialization. Skin defects over loose-skinned areas, such as the
thorax and abdomen, are generally not affected. However, wounds that encompass half the
circumference of the limbs or greater are at risk for these complications. As the size of a
defect increases, tension in the surrounding skin is created which overcomes the contraction
of myofibroblasts. Since the myofibroblasts cannot pull the wound edges together the net
effect is to delay and even stop wound contraction. Further healing can occur only by
epithelial migration over the wound bed. Epithelial migration begins at the wound edges and
moves centripetally. As the defect size increases, the regenerated epithelium becomes thinner

and complete coverage may not occur. In addition, scar epithelium is thinner and thus, more
prone to injur)- than normal skin. In cases where large wounds involving the limbs are likely
to result in prolonged and incomplete healing, reconstmctive procedures (skin flaps and
grafts) should be performed.
7.

Wound Contracture
Wound contracture, especially following second intention healing, can lead to loss or

altered function. The contracture of wounds situated over flexor surfaces may lead to
decreased range of joint motion and subsequent lameness. Defects involving any orifice (eye,
mouth and anus) can result in stenosis and functional deformity. Specialized reconstructive
procedures (e.g. Z plasties, advancement flaps) can be performed to restore normal function.