Transcript Primary Healing

W
Burns
Dr AJ Fortin
Dermatology Week - Meds I
Wound Healing
Phases
• Factors affecting healing
• Technique for optimal healing
• Scars
•
- Hypertrophic
- Keloid
Types of Wound Healing
Primary Healing
• when a wound is closed within hours of its creation
• wound edges are reapproximated directly by using
sutures or staples
Delayed Primary Healing
• A contaminated wound is left open to prevent wound
infection
• The wound edges are approximated following a delay of
several days
Lawnmower injury
Types of Wound Healing
Secondary Healing
• an open full-thickness wound is allowed to close by both
wound contraction and epithelialization
• There is a direct correlation between the number of
myofibroblasts and the extent of wound contraction
Types of Wound Healing
Healing of Partial-Thickness Wounds
• Involve the epithelium and the superficial portion of
the dermis, heal mainly by epithelialization
• There is minimal collagen deposition and an absence
of wound contraction
Epithelialization
•
Epithelialization of an incisional wound
involves the migration of cells at the
wound edges over a distance of less
than 1 mm, from one side of the incision
to the other. Incisional wounds are
epithelialized within 24-48 hours after
injury.
Phases of Wound Healing
Rubor, Tumor,
Calor, Dolor
Maturation Phase
•
Remodeling begins approximately 21 days after injury,
when the net collagen content of the wound is stable.
•
During remodeling, collagen becomes more organized.
Collagenases and matrix metalloproteinases in the
wound assist removal of excess collagen while synthesis
of new collagen persists.
Contraction vs Contracture
•
Contraction must be distinguished from contracture
- a pathologic process of excessive contraction that limits motion of the
underlying tissues and is typically caused by the application of
excessive stress to the wound.
Factors Affecting Wound
Healing
Idiopathic manipulation:
•
tissue necrosis increases with
the severity of trauma, e.g..
rough tissue handling,
•
necrosis extends the period of
inflammation and retard healing.
Age:
•
Both tensile strength and wound
closure rates decreases with
age.
Mechanical stress:
•
Abnormal tension on the skin
can give rise to blanching and
subsequent necrosis.
Steroids:
•
Steroids interfere with
fibrogenesis, angiogenesis, and
wound contraction.
Smoking:
• Nicotine produces vasoconstriction
and limits distal perfusion.
Oxygenation/perfusion:
• Oxygen is important for collagen
synthesis, matrix deposition,
angiogenesis, and epithelialization.
Oxygen-derived free radicals:
• They may cause cellular injury by
1) degrading hyaluronic acid and
collagen; 2) destroying cell
membranes; 3) interfering with
important protein enzyme system.
Hydration:
• Amoistwoundwillhealfasterthan
the dry one.
Factors Affecting Wound
Healing
Infection:
• Wound infection occurs when the infective threshold
is >100,000 (105) organisms per gram of tissue.
• Bacterial infection promotes collagenolytic activity
Nutrition:
• Low serum protein level is associated with a
prolonged inflammatory phase and impaired
fibroplasia.
Denervation:
• Denervated skin is more prone to ulcerate than
normal skin because of high rates of collagenase
activity and lack of sensory protection.
Diabetes mellitus:
• Microcirculation impairment due to; stiffened RBC,
increased blood viscosity, susceptibility to
atherosclerosis, impaired phagocytosis, which along
with neuropathy and ischemia increase the risk of
infection.
Anti-inflammatory agents:
• NSAID (Aspirin and ibuprofen) have shown to
decrease collagen synthesis an average of 45% even
at ordinary therapeutic doses.
Chemotherapy:
• When chemotherapy is begun 10-14 days
postoperatively, little effect is noted on wound healing
over the long term despite a demonstrable early
decrease in wound healing.
Radiation therapy:
Vitamin C:
• Ascorbic acid is essential cofactor in the
synthesis of collagen.
Vitamin E:
Zinc:
• It is a common constituent of dozens of
enzymes in human tissues and is essential
for wound healing.
Vitamin A:
• Vitamin A stimulates collagen deposition
Growth factors:
• They are agents promoting cell proliferation
and induce the migration of the cells to the
injured area.
Nitric oxide:
• It’s suspected of playing a role in the early
phases of wound healing, possibly serving
as a modulatory/demodulatory second
messenger for several of the polypeptide
growth factors.
What Can We Do?
Optimal tissue handling technique
• Avoid pinching epidermis
• Debride unhealthy tissue
• Suturing technique
•
- Enter at 90º to skin
- Ensure skin edges align perfectly
- Appropriate tension
•
Protective dressing
- Keep clean
- Avoid shear, mechanical injury
- Keep moist but avoid excessive mois
•
Remove sutures at appropriate time
- 5-7 days for face
- 7-10 days elsewhere
Abnormal Scars
When an imbalance occurs between the
anabolic and catabolic phases of the
healing process, more collagen is
produced than is degraded, and the scar
grows in all directions.
Excessive scar tissue is classified either
as a keloid or a hypertrophic scar.
Abnormal Scars
•
Hypertrophic scars are elevated over
the skin surface but limited to the
initial boundaries of the injury, tends to
regress spontaneously, and are
generally responsive to treatment.
Abnormal Scars
•
A keloid is an overgrowth of dense
fibrous tissue that extends beyond
the borders of the original wound,
does not usually regress
spontaneously, and tends to recur
after excision.
•
May be tender, painful, or pruritic or
they may cause a burning sensation.
•
Keloids tend to be present on the face
(with cheek and earlobes
predominating), upper extremities,
chest, presternal area.
Abnormal ScarsTreatments:
Prevention
• Silicone gel sheets
• compression therapy
• intralesional corticosteroid injections
• Cryosurgery
• Excision
• radiation therapy
• laser therapy
• interferon therapy
• imiquimod 5% cream
•
Burns
Diagnosis & Prognosis
Inhalational injury
• Burn size (TBSA)
• Depth or Degree
•
(history & mechanism of injury)
Location
• Circumferential
• Age
• Associated injuries
• Comorbidities
•
Prognostic Indicators
Depth of injury
• Age
• TBSA
• Inhalation
•
Age (y)
Percentage of TBSA w 50%
mortality
0-14y
98%
15-44
72%
45-64
51%
>65
25%
Inhalational Injury
Contributes heavily to morbidity and
mortality in burned patients
• Injuries
•
- Carbon monoxide intoxication (smoke
inhalation)
- Upper airway injury
- Pulmonary inhalational injury (steam)
- Circumferential chest scar
Risk factor is enclosed, smoke-filled
space. ie. airplane cockpit
Escharotomy
Fluid Resuscitation
Massive fluid shifts (edema) lead to
intravascular hypovolemia
•
Goal of resuscitation is to maintain
circulation to all tissue
•
Choice of Fluids and Rates
•
•
Parkland Formula
4 cc/ kg/ %TBSA burn / 1st 24 hours
- 1/2 over 1st 8 hours
- 1/2 over 2nd 16 hours
Percent Total
Body Surface Area
Traditional and current CLASSIFICAION of burns.
Nomenclatu Traditional Depth
re
Clinical
findings
Superficial
First degree
Epidermis
Erythema,
painful, no
blisters
Partial
thickness
(superficial)
Partial
thickness
(deep)
Second
degree
Superficial
Dermis
(papillary)
Deep dermis
(reticular)
Blisters w clear
fluid, painful
Full thickness
3rd-4th
degree
Dermis +\underlying
tissues
Hard leatherlike
eschar, purple
fluid, insensate
Second
degree
Whiter, less
pain, diff to tell
from full thick.
Estimation of Burn Depth
Superficial
Erythematous
May Form
blisters
Very painful,
hypersensitive
Blanch w
pressure
Wet and pink
Estimation of Burn Depth
Superficial
Partial Thickness
Erythematous
May Form
blisters
Very painful,
hypersensitive
Blanch w
pressure
Wet and pink
May blister
Discomfort rather than
pain
Less sensitive to touch
but sensate
Cap refill slow or absent
Dry and whitish
Estimation of Burn Depth
Superficial
Partial Thickness
Full thickness
Erythematous
May Form
blisters
Very painful,
hypersensitive
Blanch w
pressure
Wet and pink
May blister
Discomfort rather than
pain
Less sensitive to touch
but sensate
Cap refill slow or absent
Dry and whitish
Dry white
Leathery
Rarely blanches
Coagulated vessels
may be visible
Estimation of Burn Size
The Rule of
Nines
Children
Indications for Transfer
to a Burn Unit
•
Large burn
•
- 2° and 3° burn >20% TBSA
• >10% if <10 or >50y old
•
- inhalational injury
•
Deep burn
Sensitive areas
- Face
– Hands
- Feet
- Genitalia
– Perineum
–
Overlying major joints
Difficult to assess injury
- Significant electric injury
- Significant chemical injury
- 3° burn >5% TBSA
•
Respiratory compromise
•
Significant comorbidities
- DM, CVD, PVD etc.
Polytrauma
• Special social/emotional
circumstances
•
Operative Treatment
Excision of deep partial thickness and
full thickness burns with immediate skin
grafting
•
Improves survival, decreases hospital
stay, fewer metabolic complications
•
Skin Grafting
•
Tools:
- Harvesting
•
Knife
• Dermatome
- Application
•
Mesher
• Bolster
• Splinting
• VAC
Skin Graft Harvesting
Split Thickness
vs
Full Thickness
Split-Thickness
Skin Graft Harvesting
Split-Thickness
Skin Graft Harvesting
Split-Thickness
Skin Graft Harvesting
Split-Thickness
Skin Graft Harvesting
Graft Healing
•
Imbibition (0 - 2 d)
- Graft held in place by fibrin
•
Neovascularization (2 - 3d)
- New blood vessel ingrowth
•
Proliferation (3d - 4 m)
- New collagen bridges across the wound
bed
•
Maturation (1 - 2 y)
- Revision of collagen
Full-Thickness
Skin Graft Harvesting
•
Technique:
- Template
- Harvest & De-fat
- Apply & Bolster
Full Thickness Skin Graft
•
Advantage:
- Less contraction
- Better colour match
- Lower maintenance donor sit
•
Disadvantage:
- Poorer take (thickness)
- Available only for small defects
Special Burns
ELECTRICAL BURNS
High voltage >1000 volts
Low voltage <1000 volts
2 types of injury:
Arc injury: thermal
injury that occurs when
patient is to close to
electric source when
the current arcs
superficial burns to
exposed skin
usually face, hands and
forearms
Entry
Exit
Electrical Burns
Current flow injury:
current flows through the body
entrance and exit wounds
damage more extensive than surface
wounds indicate
often associates injuries
damage depends on:
1. cross sectional diameter of the
body part that current flows through …
damage to tissue greatest in the limbs
less in the torso
2. resistance to current
Electrical Injury
Cardiac arrhythmias are common in low voltage household injuries
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Associated fractures secondary to falls/muscle contracture
Muscle damage may be severe & worsen
•
Compartment syndrome develops
- Fasciotomies to prevent necrosis
•
Myoglobin
- Acute renal failure -- 50% mortality
- Alkalinize urine, high urine output
Electrical Injury
•
•
LIP & Oral Commissure
4% of burn injuries in children
- Biting electrical cord/ sucking on wall socket
•
Bleeding (labial artery)
•
Scar contractures
- Microstomia
- Asymmetry
- Splinting
Special Burns
CHEMICAL BURNS
Alkalis & Acids:
cause damage by breaking down tissue proteins
Treatment: remove contaminated clothes
COPIOUS IRRIGATION
with extensive injuries monitor for
metabolic disturbance: ABG’s, lytes
renal & liver function
after lavage/debridement treatment of the wound
is no different from thermal burns
Use of specific neutralizing agents debated
most common hydrofluoric acid- calcium chloride/gluconate
Chemical Burns
Factors affecting severity of burn
Concentration of chemical
• Duration of skin contact
• Manner of skin contact (occlusive garment)
• Prior condition of skin
• Lipid solubility of chemical
• Inherent toxicity of compound
•
Chronic Leg Ulcers
•
Venous Stasis
- 70%
•
Peripheral Vascular Disease (ischemia)
- 10%
•
Peripheral Neuropathy (diabetes etc)
•
Trauma
- Biopsy chronic wounds to rule out malignancy (marjolin’s ulcer)
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•
Leg Ulcers
Arterial Insufficiency
- Feet and legs often feel cold
- Whitish or bluish, and shiny
- Ulcer is dry, ‘punched out’
- Distal location
- Painful
- Inadequate blood flow
•
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Venous Insufficiency
- Feet and legs are
swollen
- Surrounding skin is
brownish, dry, scaley
- Medial malleolus
- Ulcer is weepy
- Painless
- Inadequate drainage
Neuropathic
- Feet are insensate
- Dry, callused skin
- Often sinus tract & deep abscess
-Ulcer over pressure point
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Venous Stasis
•
Incompetent valves
- Pericapillary fibrin deposition
- Barrier to O2 diffusion
- White cell plugging of capillary loops
- Lipodermosclerosis
•
Clinical Signs:
- Edematous, hyperpigmented
- Varicosities/ thrombophlebitis
- Ulcerations often around ankles/lower legs Hemosiderin
Staining
& Edema
Venous Stasis
•
Treatment:
- Bedrest, leg elevation
- Compression garments
•
Up to 7 in 10 venous ulcers heal within 12 weeks if
treated with compression bandaging Nutrition
- Debride devitalized tissue
- Dressings
- Ligation of incompetent perforating veins
- Resistant ulcers may need complete excision &
reconstruction/coverage (skin grafting)
Vasculopaths
Beware the comorbidities
•
- Diabetes
- Coronary artery disease
- AAA
– Smoking
- Pulmonary disease
- Anticoagulation
•
Contraindication for
compression therapy!
•
50% of patients with
arterial insufficiency
also have chronic
venous stasis