This text is not intended to cover each and every aspect relating to wounds presented in veterinary medicine. It is, however,
designed as a simplified handbook, which will assist members of the veterinary medical team in properly assessing patients
and their wounds. As you read the following pages, you will find a certain amount of repetition. This is necessary to reinforce
key issues and concepts as well as to insure that each section can stand alone as a total reference for that category of wound.
Healing process introduction
Before examining the management of wounds, it is important to review the fundamentals of wound healing.
Wound healing begins with insult to soft tissue, whether it be surgical or traumatic. This insult sets off a complex sequence
of cellular and molecular events, which ends in structural restoration. A fundamental understanding of this process is needed
by the veterinarian and technician to provide the necessary environment for normal healing to occur.
Ideally, the goal of wound healing is to fully restore the injured part to its pre-wound condition in a very short time. Unfortunately,
this is the exception and not the rule in most of the wounds we encounter. Most healing occurs as a result of epithelial regeneration
and fibroplasia. Generally, there is a good compromise between the minimal amount of fibrous tissue needed for structural
continuity and tensile strength, and that amount which is excessive and causes beds of granulation tissue, adhesions, strictures,
etc. The basic process of this fibroplasia as it relates to wound healing will now be reviewed.
The fibroplastic stage of wound healing occurs in three phases:
Immediately after insult to soft tissue occurs, whether surgical or traumatic, a state of acute inflammation develops. The
insult precipitates the inflammatory response by initiating release of chemical mediators. There are a number of different
substances that have been demonstrated or are believed to be important as mediators of inflammation. Some of the familiar
ones include histamine, bradykinin, complement, and lysosomal enzymes among others. 6 These mediators bring about the inflammatory response characterized by hemodynamic changes, permeability changes, and leukocytic
events. The three events are well underway by two hours. By 8-12 hours, the inflammation has produced an exudate consisting
of plasma proteins (especially fibrinigen), polymorpho-nuclear leukocytes, (PMNs), red blood cells, and macrophages. The fibrin
clots, and thereby forms an early but very weak bond between the edges of the wound. The numbers of PMNs increase rapidly
the first 24 hours but fragment over the next 48 hours. The macrophage population and activity increase between 24 and 72
hours and the cellular debris is phagocytized. Fibroblasts appear at the wound during the first 24 hours and become numerous
after 72 hours. In addition to the fibroblasts, newly formed collagen fibrils and numerous capillaries appear. there is a
significant increase in the number of fibroblasts at the wound between the third and fifth days. This increase of fibroblasts
signals the end of the first phase of healing and the beginning of the second phase.
The collagen phase begins on approximately the fifth day and extends to the fourteenth to sixteenth day. During this time
the fibroblasts are laying down collagen. The process of collagen deposition is not firmly understood. It is believed that
microfibrils are produced by fibroblasts and that the microfibrils serve as templates for the polymerization of tropocollagen
molecules. These molecules then bind themselves in a staggered fashion by cross linkages and chemical bonds in the ground
substance to form the collagen fibril. Further aggregation of collagen fibrils into larger fibers produces mature collagen.
At the beginning of the collagen phase, few collagen fibers are present to provide tensile strength. Also, at this time, absorbable
suture materials are beginning to weaken and problems can result if excess tension is applied to the wound. This is one reason
non-absorbable suture materials are indicated for most skin closures.
By the fifteenth day post-operatively, enough collagen has been laid down to provide approximately the same tensile strength
as normal skin. This fact leads to the recommendation of removing most sutures at about the fourteenth day post-operatively.
Once the collagen bed has been laid down, the process of maturation begins. Collagen fibers are turned over and remodeled
for weeks to months after the soft tissue insult. During this process, the collagen fibers become thicker and denser, the
number of fibroblasts decrease, the fibers develop a definite orientation related to normal tension on wound edges. The scar
formed becomes flatter, paler and softens somewhat. It may take months or years for the scar to fully mature.