Course Overview
Course Overview
Wounds are classified in several ways according
to incidence, cause, status, and others. Several
factors are associated with impaired wound
healing, including ongoing disease and
malnutrition. This course will present a
background on wounds, the healing process,
treatment options, and guidelines.
Learning Objectives
Upon completion of this Journal Club the
participant will be able to:
1. List four barriers to wound healing
2. Describe two ways chronic wounds are
categorized
3. Describe two advanced
treatment treatment options for
chronic wounds
The Learning Objectives for this course are
fairly straightforward.
1. There are four main barriers to wound
healing which we will explore in this
course. They can prevent wounds from healing,
cause them to heal more slowly, and cause more
discomfort to the patient. All, if present, will
cause more health care dollars to be spent.
2. There are several classifications of wounds,
including pressure injuries, venous stasis
ulcers, and diabetic ulcers.
Each of these types of wounds is further
sub-classified according to severity and phase.
In the case of diabetic foot ulcers, multiple
sub-classifications are used to assist in
determining an appropriate course for assessment
and treatment. Patient assessment factors
include the wound and patient background
information to remove or reduce the causal or
aggravating factors. The wound is then
classified and documented.
3. Wound care plans are tailored to the patient
according to their systemic barriers to wound
healing and local wound factors. If healing does
not occur as expected, additional assessment is
conducted and additional therapeutic options can
be considered. This course will outline
definitions and descriptions of chronic wound
characteristics, systemic and local factors that
contribute to non-healing, and selected
therapeutic options to promote healing. A
summary algorithm for chronic wound care will be
presented as well.
So let’s get started…
Background Information
Stage/Time |
Characteristics |
Description |
Hemostasis
0-3 hours |
Bleeding is minimized, clots are formed |
Platelet cells release epinephrine to
constrict peripheral vessels and reduce
bleeding into soft tissues, platelet
cells assist blood clotting and release
cytokines that orchestrate the
inflammatory stage and platelet-derived
growth factor for later stages |
Inflammatory
0-3 days |
Swelling and heat, prevention of
infection |
Immediately after hemostasis stage,
leukocytes and macrophages are attracted
to destroy bacteria and clear cellular
debris from devitalized tissues;
cytokines, chemo-attractants, and
enzymes are released to initiate healing
process and contract the wound |
Proliferative
3-21 days |
Granulation, angiogenesis, and epithelialization
|
Macrophages, neutrophils, fibroblasts,
immature collagen (deposited by
fibroblasts), blood vessels, and
extracellular ground substance form red,
shiny, “beefy” granulation tissues to
fill the cavity; epithelial cells
migrate from wound margins and
divide/cover wound; contraction is
signaled; the proliferative stage
requires adequate vascularization and
epithelialization cannot occur over
necrotic tissues |
Maturation
21 days - 1.5 years |
Contraction and improved tensile
strength of tissues |
Fibroblasts, matrix metalloproteinases (MMPs),
growth factors are involved in collagen
fibers reorganization over time to
improve tensile strength to 80% of
uninjured tissues |
Wounds can be categorized as acute or chronic.
Acute wounds have a predictable pathway to healing
characterized by four phases, including
hemostasis, inflammatory reaction,
proliferation, and maturation.
Chronic wounds differ from acute wounds primarily because they
stall in the inflammatory phase of the healing
process.
Let’s look at the Normal Healing Process. The
acute wound follows a predictable and timely
process of healing within a short period of time
and with limited care. In this case the function
of tissues is generally well-sustained after the
healing process. This slide shows the four
stages to wound healing. The first stage,
hemostasis, prevents continued bleeding and allows the
subsequent processes to start. Platelets are key
cells in this stage which mediate clotting. The
next stage involves inflammatory processes. Leukocytes and macrophages are
featured during this stage to destroy bacteria
and clean the wound of cellular debris. The
third stage, proliferation, is characterized by growth factor stimulation of
epithelialization angiogenesis granulation tissue formation, and collagen deposition. The
wound environment, including the newly formed
extracellular matrix and fluids, stimulates
healing in acute wounds, the wound is responsive
to healing signals. The fourth and final stage
is maturation.
During this stage the wound and healed tissue
contract to result in smaller amounts of scarred
tissue. The tensile strength of the healed
tissues is up to 80% of the tensile strength of
uninjured tissue. However, this tissue is never
fully restored to its full tensile strength.