w burns dr aj fortin dermatology week - meds i. wound healing phases factors affecting 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 Infection: Healing • 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 Scars-Treatments:

• Prevention • Silicone gel sheets • compression therapy • intralesional corticosteroid injections

• Cryosurgery • Excision • radiation therapy • laser therapy • interferon therapy • imiquimod 5% cream

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)

0-14y

Percentage of TBSA w 50% mortality

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 Clinicalre findingsSuperficial

Partial thickness (superficial) Partial thickness (deep)

Full thickness

First degree

Second degree

Second degree

3rd-4th degree

Epidermis

Superficial Dermis (papillary) Deep dermis (reticular)

Dermis +\-underlying tissues

Erythema, painful, no blisters

Blisters w clear fluid, painful

Whiter, less pain, diff to tell from full thick.

Hard leatherlike eschar, purple fluid, insensate

Estimation of Burn Depth

Superficial

Erythematous

May Form blisters

Very painful, hypersensitive

Blanch w pressure

Wet and pink


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


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

• Deep burn - 3° burn >5% TBSA

• Sensitive areas - Face – Hands - Feet - Genitalia – Perineum

– Overlying major joints

• Respiratory compromise - inhalational injury

• Difficult to assess injury - Significant electric injury - Significant chemical injury

• 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

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

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 Burns

Electrical Injury Cardiac arrhythmias are common in low voltage household injuries

QuickTime™ and a decompressor

are needed to see this picture.

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)





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

Neuropathic - Feet are insensate - Dry, callused skin

• Venous Insufficiency - Feet and legs are

swollen

- Surrounding skin is brownish, dry, scaley

- Medial malleolus

- Ulcer is weepy

- Painless

- Inadequate drainage



- Often sinus tract & deep abscess -Ulcer over pressure point

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 co-morbidities

- Diabetes

- Coronary artery disease

- AAA

– Smoking

- Pulmonary disease

- Anticoagulation

• Contraindication for compression therapy!

• 50% of patients with arterial insufficiency also have chronic venous stasis

w burns dr aj fortin dermatology week - meds i. wound healing phases factors affecting healing...

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