SKIN TREATMENT

1. Illustrate/draw the anatomy of the skin; label the different layers correctly.

2. Describe each phase of healing.

Initial phase – Hemostasis

Following vasoconstriction, platelets adhere to damaged endothelium and discharge adenosine

diphosphate (ADP), promoting thrombocyte clumping, which dams the wound. This phase is initiated by
the release of numerous cytokines by platelets. Alpha granules liberate platelet-derived growth factor
(PDGF), platelet factor IV, and transforming growth factor beta (TGF-b), while vasoactive amines such
as histamine and serotonin are released from dense bodies found in thrombocytes. PDGF is chemotactic
for fibroblasts and, along with TGF-b, is a potent modulator of fibroblastic mitosis, leading to prolific
collagen fibril construction in later phases. Fibrinogen is cleaved into fibrin and the framework for
completion of the coagulation process is formed. Fibrin provides the structural support for cellular
constituents of inflammation. This process starts immediately after the insult and may continue for a few
days.

Second phase - Inflammation

Within the first 6-8 hours, the next phase of the healing process is underway, with polymorphonuclear
leukocytes (PMNs) engorging the wound. TGF-b facilitates PMN migration from surrounding blood
vessels where they extrude themselves from these vessels. These cells "cleanse" the wound, clearing it of
debris. The PMNs attain their maximal numbers in 24-48 hours and commence their departure by hour
72. Other chemotactic agents are released, including fibroblastic growth factor (FGF), transforming
growth factors (TGF-b and TGF-a), PDGF, and plasma-activated complements C3a and C5a
(anaphylactic toxins). They are sequestered by macrophages or interred within the scab or eschar.5

As the process continues, monocytes also exude from the vessels. These are termed macrophages. The
macrophages continue the cleansing process and manufacture various growth factors during days 3-4. The
macrophages orchestrate the multiplication of endothelial cells with the sprouting of new blood vessels,
the duplication of smooth muscle cells, and the creation of the milieu created by the fibroblast. Many
factors influencing the wound healing process are secreted by macrophages. These include TGFs,
cytokines and interleukin-1 (IL-1), tumor necrosis factor (TNF), and PDGF.

Third phase - Granulation

 This phase consists of different subphases. These subphases do not happen in discrete time frames but
constitute an overall and ongoing process. The subphases are "fibroplasia, matrix deposition, angiogenesis
and re-epithelialization".

In days 5-7, fibroblasts have migrated into the wound, laying down new collagen of the subtypes I and III.
Early in normal wound healing, type III collagen predominates but is later replaced by type I collagen.

Tropocollagen is the precursor of all collagen types and is transformed within the cell's rough
endoplasmic reticulum, where proline and lysine are hydroxylated. Disulfide bonds are established,
allowing 3 tropocollagen strands to form a triple left-handed triple helix, termed procollagen. As the
procollagen is secreted into the extracellular space, peptidases in the cell wall cleave terminal peptide
chains, creating true collagen fibrils.

The wound is suffused with GAGs and fibronectin produced by fibroblasts. These GAGs include heparan
sulfate, hyaluronic acid, chondroitin sulfate, and keratan sulfate. Proteoglycans are GAGs that are bonded
covalently to a protein core and contribute to matrix deposition.

Angiogenesis is the product of parent vessel offshoots. The formation of new vasculature requires
extracellular matrix and basement membrane degradation followed by migration, mitosis, and maturation
of endothelial cells. Basic FGF and vascular endothelial growth factor are believed to modulate
angiogenesis.

Re-epithelization occurs with the migration of cells from the periphery of the wound and adnexal
structures. This process commences with the spreading of cells within 24 hours. Division of peripheral
cells occurs in hours 48-72, resulting in a thin epithelial cell layer, which bridges the wound. Epidermal
growth factors are believed to play a key role in this aspect of wound healing.

This succession of subphases can last up to 4 weeks in the clean and uncontaminated wound.

Fourth phase - Remodeling

After the third week, the wound undergoes constant alterations, known as remodeling, which can last for
years after the initial injury occurred. Collagen is degraded and deposited in an equilibrium-producing
fashion, resulting in no change in the amount of collagen present in the wound. The collagen deposition in
normal wound healing reaches a peak by the third week after the wound is created. Contraction of the
wound is an ongoing process resulting in part from the proliferation of the specialized fibroblasts termed
myofibroblasts, which resemble contractile smooth muscle cells. Wound contraction occurs to a greater
extent with secondary healing than with primary healing. Maximal tensile strength of the wound is
achieved by the 12th week, and the ultimate resultant scar has only 80% of the tensile strength of the
original skin that it has replaced.

3. How does each layer participate in healing?

INFLAMMATORY STAGE:
Epithelialisation by Epidermis. Epithelial cells (keratinocytes) migrate across the wound bed from the
wound edge. Re-epithelization begins hours after injury by the migration and proliferation of epithelial
cells to the wound. While migrating inward from the margin of the wound, they lay down basement
membrane proteins in a zipper-like fashion. About one day later, the wound margin undergoes
proliferation of epidermal cells. Continuous microscopical examination, reveal that the edge of the
epidermis starts to move toward the center of the wound within a few minutes after the wound is made.
The epidermal layer advances over the coagulum, moving equally from all sides toward the center of the
 wound. If the edge of the wound is irregular, the advancing layer is correspondingly irregular in outline.
Over large wounds the advancing epidermis thins out until it may be only one or two cells in thickness.
Subcutaneous tissue facilitates wound perfusion, granulation, contraction, epithelialization, and total
healing. The subcutaneous tissues make an important contribution to 2nd intention cutaneous healing.
Extensive debridement of subcutaneous tissue may delay wound healing.
PROLIFERATIVE STAGE
About four days after injury, macrophages, fibroblasts, and blood vessels from the Dermis invade the
stroma to form granulation tissue. Macrophages stimulate fibroplasia and angiogenesis by releasing
growth factors, fibroblasts provide structural support by synthesizing extracellular matrix, and blood
vessels transport nutrients to the site. Two weeks after injury, fibroblasts undergo a phenotypic alteration
into myofibroblasts and migrate to the wound bed, where they begin to contract the wound. Also the
deficient epidermis surrounding the wound is built up, by cell proliferation, to the normal thickness of the
layer. In wounds made entirely through the skin the dermis is slow in closing, but the epidermis closes as
usual, subsequently thickening until it is much thicker than the normal epidermis. Sometimes the
thickness of the layer over a healed wound may he equal to the combined thickness of the normal
epidermis and the dermis. When transplantations are made, the small gaps that necessarily exist between
host skin and graft are closed by epidermis which grows in to fill the deficiency as if to maintain a
smooth surface to the body. As the dermis is built up, the epidermis returns to its usual thickness.
MATURATION STAGE
During this stage, the epidermis regenerates by undergoing reduction of transient hypertrophy, while the
provisional matrix is replaced by a dermal matrix of collagen and later by a low cellularity scar.
Degradation of the collagen matrix is mediated by matrix metalloproteinases, which are secreted by the
epidermal cells, fibroblasts, endothelial cells, and macrophages. Eventually, the wound is replaced by a
new functional tissue.
During the migration of the epidermal cells, their space relationships are continually changing. Further,
the epidernial cells closest to the edge of the wound or graft move faster than those successively farther
from the wound or graft. In the initial advance of cells in covering the wound, the cells closest to the edge
of the wound travel a greater distance than cells successively farther from the edge. Continuous
microscopic observations made on living epidermis at the edge of a wound support in every detail the
suggestion.
Dermal Wound Healing: May involve the complete epidermis, dermis and subcutaneous tissues. Bone
and muscle may also be involved. Referred to as Full Thickness Wounds. Heals by scar formation.

4. Give one intrinsic factor , one extrinsic factor and one iatrogenic factor that contribute to abnormal
wound healing. Explain how it makes wound healing abnormal.

Intrinsic factor : Age. There are age and sun-induced changes in the structure and function of the skin
resulting in thinner, less elastic tissue that bruises easily, and ageing results in dysfunctional molecular
mechanisms that affect the ability to repair damaged cells and tissues.

Extrinsic factor : poor Nutrition. Carbohydrates, protein and amino acids, fatty acids, minerals and
vitamins are required for normal wound healing.

Iatrogenic factor: Poor wound care. If tissue is constantly in contact with pathogens which, under the
proper conditions, are able to proliferate to create pathological conditions and where many different types
of pathogens may be involved.
5. Give one wound assessment tool and monitoring system. Discuss its indication and how it is used
(method).

Pressure Ulcer Scale for Healing (PUSH) Tool 3.0

It observes and measures the pressure ulcer, categorizing the ulcer with respect to surface area, exudate,
and type of wound tissue. A sub-score is recorded for each of the ulcer characteristics, and the sub-scores
are added to obtain a total score. A comparison of the total scores measured over time provides an
indication of the improvement or deterioration of the pressure ulcer healing.

Length  0 1 2 3 4 5 Sub-score
Width
0 cm2 <0.3 cm2 0.3-0.6 0.7-1.0 cm2 1.1-2.0 cm2 2.1-3.0
cm2 cm2

6 7 8 9 10

3.1-4.0 4.1-8.0 8.1-12.0 12.1-24.0 >24.0

cm2 cm2 cm2 cm2 cm2

Exudate 0 1 2 3 Sub-score
Amount
None Light Moderate Heavy

Tissue 0 1 2 3 4 Sub-score
Type
Closed Epithelial Granulatio Slough Necrotic
n

Total Score

6. Give one type of dressing, one type of debridement and one type of skin grafting. Discuss when and
how it is done.

Synthetic wound dressings - Hydrocolloids: used in wounds with light to heavy exudate, sloughing or
granulating wounds.

Mechanical Debridement - A nonselective, physical method of removing necrotic tissue and debris from
a wound using mechanical force, is generally easy to perform and is more rapid than autolytic and
enzymatic debridement.

Wet-to-dry dressings are the simplest method of mechanical debridement. Wet gauze dressings are placed
onto the wound bed and allowed to dry, trapping the necrotic debris within the gauze. Upon removal of
the dressing, embedded necrotic tissue and debris are mechanically separated from the wound bed.[73]
 Pressurized irrigation involves applying streams of water, delivered at either high or low pressure, to
wash away bacteria, foreign matter, and necrotic tissue from the wound.

Split-thickness grafts - consists of sheets of superficial and some deep layers of skin. The grafts removed
from the donor sites may be up to 4 inches wide and 10 to 12 inches long. The grafts are then placed at
the recipient site. Once the graft is in place, the area may be covered with a compression dressing or the
area maybe left exposed. Split-thickness grafts are used for non-weight-bearing parts of the body.

7. Given a 21 year-old patient with healing major burns in the face, neck and anterior upper arms,
two weeks post-burn injury, what would be your home instructions to the patient and
family/caregivers on the following:

a. TYPE AND METHOD OF DRESSING

 Creams, lotions and hydrogels = Sorbolene with 10% glycerine. Provides moisture to skin
surrounding the burn and to the newly healed burn.
 Topical silicone gel.

b. PROPER POSITIONING
Anterior neck: Neck in midline with 10-15 degrees of extension. Towel roll under shoulder. Not to use a
pillow for positioning the neck or the head.

Shoulders: 90 degrees abduction with 15-20 degrees horizontal adduction and slight external rotation.
Monitoring radial pulse and reposition the arm frequently to avoid compression of the brachial plexus
which may lead to a neuropathy, and look for sensory (tingling, numbness) or motor (weakness,
paralysis) deficits. Positioning the shoulder in abduction with slight horizontal adduction is to avoid
brachial plexus injury.

Elbow in full extension with the forearm in neutral and slight supination. Avoiding locking the elbow in
extension.

c. USE OF PHYSICAL AGENTS

 Gradient pressure chin strap.

 Gradient elastic compression for the arms.
 Gradient pressure stockings temporarily used for 1-2 weeks since most possibly patient may still
have orthostatic hypertension

d. SPLINTING
Face: Transparent Face Mask (UVEX) or the Silicone Elastomer Face Mask, for they prevent/ correct
scar hypertrophy and is cosmetically appealing.

Neck: Anterior hard neck conformer.

Nose Splints: Nasal obturators like the “mustache nostril splint”.

Ear Splints: Internal; ear obturator. External; “oyster” splint.

Mounth Splints: Micro-stomia Prevention Appliance (MPA)

Axilla/Shoulder: Airplane Splints: custom made; SCOI

Elbow: Static extension splint.

e. THERAPEUTIC EXERCISES
 Active-assisted ROM exercises for the neck and both upper extremities at every joint in every
plane to prevent skin contractures, maintain joint integrity, prevent muscle atrophy, and prevent
edema.
 Wrist curls/flexion and reverse curls/extensions using 5 pound dumbbell on 20 repetitions X 1-2
sets everyday.
 Supine single leg raises.
 Walking on even and uneven surfaces, stair climbing and descending, and stationary bicycle if
possible, as aerobic exercises.
 To avoid aggressive passive stretching which could result in tissue/wound damage,
bleeding and skin graft loss.
 Firm, slow massage of evolving hypertrophic areas done several times each day as after
application of bland skin emollients.
 Retrograde massage to reduce extremity edema or massaging the distal portions of the healing
wound.
 Exercises incorporate feeding, self-grooming and dressing, increasing patient participation to
achieve independent care and responsibility and asform of resistive exercise.
 To always watch for bleeding, lightheadedness, cellulites, excessive pain and edema. May need to
wait a few more days if any of the above are noted.

f. NUTRITION

A regular diet taken by mouth is the most physiologic and that is the ideal method of providing adequate
nutrition. If this is not possible, nasogastric or nasoenteric tube feedings is used where continuous drip-
feeding is preferable to bolus tube feedings.

Protein: 20-25% of total daily calories as protein, translates to 2.5-4.0 gm/kg

Fat: There is evidence supporting the use of 10-15% total overall calories from fat in burn patients. This
helps improve immunity and increase survival rates.

Carbohydrates: 60-65% of calories as carbohydrate. When providing parenteral nutrition, the following
limit is established: 5mg carbohydrate/kg/min (Example) 70kg x 5mg x 1440min/day = 504gm Carb/day
(2016 Kcal) 1000mg/gm

Fluid Maintenance: 1cc/kcal intake/day

One Multivitamin daily; 500 mg Ascorbic Acid 1-2 times per day , 220 mg zinc sulfate daily,

10,000 IU Vitamin A daily.

Other instructions:

 Tolerate food likes and dislikes; give him as much control as possible in food selection and choice of
the order in which they eat their food.
 Allow the patient some autonomy in food selection.
 Record bowel movement. Use stool softeners as needed.
 Permit the patient to take extra time to eat their food.
 Keep reminding him in case he loses attention about nutrition that food is essential for optimal wound
healing.
8. What are the highest and lowest level of evidences for intervention, prognosis and diagnosis?
Discuss why are they considered highest and lowest forms of evidences?

LEVEL 1A

Level Therapy/Prevention, Aetiology/Harm = 1a SR (with homogeneity*) of RCTs

Prognosis = SR (with homogeneity*) of inception cohort studies; CDR† validated in different populations

Diagnosis = SR (with homogeneity*) of Level 1 diagnostic studies; CDR† with 1b studies from different
clinical centres

* Homogeneity here means a systematic review that is free of worrisome variations (heterogeneity) in the
directions and degrees of results between individual studies. Not all systematic reviews with statistically
significant heterogeneity need be worrisome, and not all worrisome heterogeneity need be statistically
significant. As noted above, studies displaying worrisome heterogeneity should be tagged with a "-" at the
end of their designated level.

† Clinical Decision Rule. (These are algorithms or scoring systems that lead to a prognostic estimation or
a diagnostic category.)

Level 1A is considered as highest form of evidence for it contain definitive, excellent evidence of support.
Its applicability is always acceptable, safe, definitely useful, proven in both efficacy & effectiveness, and
must be used in the intended manner for proper clinical indications. For they are definitely recommended
where one or more Level 1 studies are present (with rare exceptions). Its study results consistently
positive and compelling in its level of evidence. The design from its component of study has highly
appropriate sample or model, randomized, proper controls and has outstanding accuracy, precision, and
data collection in its class of methods being from randomized clinical trials or meta-analyses of multiple
clinical trials with substantial treatment effects.

LEVEL 5

Level Therapy/Prevention, Aetiology/Harm = Expert opinion without explicit critical appraisal, or based
on physiology, bench research or "first principles"

Prognosis = Expert opinion without explicit critical appraisal, or based on physiology, bench research or
"first principles"

Diagnosis = Expert opinion without explicit critical appraisal, or based on physiology, bench research or
"first principles"

Level 5 is considered as lowest form of evidence for it is considered only as a rational conjecture or
common sense, common practices accepted before evidence-based guidelines and the component of its
study and rating in its design & methods is anecdotal, and may have no controls. Are off target end-points
or not defensible in its class with insufficient data or measures. And are unacceptable, not useful clinically
and may even be harmful where some of its studies may suggest or confirm harm.