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 PMN’s (polymorphonucleocytes). The

inflammatory response causes the blood vessels to become leaky releasing plasma and PMN’s

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 clean-up 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. Sub-contractors 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

Phase

Hemostasis Immediate Platelets

Inflamation Day 1-4 Neutrophils

Proliferation,

Granulation and

contraction

Day 4-21 Macrophases,

Lymphocytes,

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 non-

viable 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 non-

viable 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.