Wound Healing

Presented by,
Dr. Srikant Patro

Senior Resident Surg. Oncology

The earliest accounts of wound healing date back to 2000B.C. Egyptians - infected & diseased / noninfected wounds. Eber papyrus, 1550B.C. honey, lint, grease Greeks - acute / chronic Galen(120-201A.D.) - moist environment to ensure adequate healing. Next major stride - discovery of antiseptics. The 1960s and 1970s - development of polymeric dressings Currently - use of, among others, inflammatory cytokines, growth factors and bioengineered tissue.

The injury alone has in all cases a tendency to produce the disposition & the means of cure. John Hunter

Repair

Remodelling
Re-epithelialization

Proliferation
Granulation tissue formation

Injury
Inflammation Clot formation

5ds

20-30ds

mos

Phase 1: Inflammation
Platelet plug Chemo-attraction
PMNs Monocytes Lymphocytes

INFLAMMATION
Following trauma Intrinsic and extrinsic pathways Exposure of type IV & type V collagen disturbs TxA2 /PGI2 balance Platelet aggregation Hemostasis by vessel contraction, serotonin, kinins, neural reflexes Acute inflammation follows these clotting, fibrinolytic and complement cascades

 Vascular permeability, diapedesis Controlled by expession of selectins, integrins, adhesion molecule changes(VCAM, ICAM) Influx of PMNs then Lymphocytes & Macrophages Release of NO, free radicals, PGs & cytokines(IL-1, IL-6, TNF-) & growth factors(PDGF, EGF, FGF, IGFI, IGF-II,TGF-,TGF-)

INFLAMMATION contd..

Phase 1: Inflammation

PDGF TGF IGF

EGF

Mediators of Inflammation
Platelets
PDGF IL-1, IL-6, TNF PMNs TGF 2,, Monocytes Fibroblasts
Maintain inflammation

FGF
Macrophages VEGF

Endothelial cell

Phase 2: Proliferation
Epithelial cells
Migrate to the sides of edges

Endothelial cells
Angiogenesis

Fibroblasts
ECM formation

Granulation tissue

Phase 2: Proliferation

EFG FGF

PDGF
IGF

TGF

Phase 3: Remodelling
Contracture of the wound Re-epithelization

Phase 3: Remodelling

Phase 3: Remodelling Phase 3: Remodelling

Wound Healing: Primary Union

Clean incision Line of closure fills with clotted blood Dehydration at surface creates scab

Wound Healing: Secondary Union

Large tissue defect More inflammation More granulation tissue Wound contraction - myofibroblasts

Wound Kinetics
1 week no change in the size of a wound 3 weeks almost 20% tensile strength A scar has only ~70% of strength of normal skin Healing time is logarithmically related to wound size

Which one of the wounds will heal faster?

All will heal in the same time under similar conditions

The rate of healing depends on the largest diameter of a circle contained within the wound

Normal Wound Healing

Proliferation Re-modelling

Inflammation

5ds

30ds

100ds

Impaired Wound Healing

Proliferation Re-modelling

Inflammation

5ds

30ds

100ds

Skin wounds . . .
Acute vs. chronic; likely to heal or not Chemotherapy agent extravasation Radiation damage Decubitus ulcers Malignant wounds

. . . Skin wounds
Associated with Pain Depression Anxiety Poorer interpersonal interactions

Key points
1. Pathophysiology 2. Assessment 3. Management

Skin symptoms
Organ system Highly innervated Visible Psychological, social, and spiritual Interdisciplinary care Symptom control

Chemotherapy extravasation: pathophysiology

Acute wound Products of inflammation
Redness Swelling Pain

Cell death
Necrosis, open wound

Radiation: pathophysiology
Radiation damage Acute wound Products of inflammation Cell death

Decubitus ulcers: pathophysiology

Pathophysiology
Ischemia

Fat is protective

Malignant wounds: pathophysiology

Disrupted physiology Products of inflammation Neovascularization
Bleeding

Necrosis
Anaerobic and fungal infections

Chemotherapy extravasation: assessment

Type of chemotherapy
Vesicant, eg, doxorubicin Irritant, eg, carmustine Non-irritants, eg, fluorouracil

Extent
Volume of extravasation, rate of flow and time Seconds, minutes, hours

Involved anatomy

Radiation: assessment
Radiation sensitizers
Topical agents Drugs, including chemotherapy

Dose and fractionation schedule

Expected course

Decubitus ulcers
Assessment
Risk factors

Prevention
Skin protection shear / tear / moisture Pressure reduction and pressure relief
Air/water mattress overlays Low-air-loss beds Air-fluidized beds Simple foam, Donuts----ineffective, discouraged.

Decubitus ulcers: staging

1. Non-blanchable erythema 2. Partial-thickness skin loss abrasion/shallow crater/blister 3. Full-thickness skin loss deep crater 4. Extensive necrosis exposing muscle or bone

Management
Acute versus chronic By wound type

Necrotic wound: management

Debridement - role of hyperbaric O2 Surgical Enzymes and gels Mechanical Pain control

Cleansing

 Contain damage

Chemotherapy extravasation: management

Stop infusion Neutralize Dexrazoxane.

Assess for surgical consultation Watch and wait

Radiation: management
Promote healing
Avoid cytotoxic agents Moist environment Treat infection Pain control

Decubitus ulcers: management

Goals: healing vs non-healing Healing
Debridement Dressings that promote healing

Non-healing
Pain control, comfort Prevent worsening

Decubitus ulcers: dressing

Moist, interactive environment Control infection 6 types of dressing[hypertonic/hypotonic]
Foams Alginates Hydrogels Hydrocolloids Thin films Cotton gauze

Malignant wounds: management

Healing vs non-healing Infections Odors Pain Exudate Bleeding

Odors
Topical and / or systemic antibiotics
Metronidazole Silver sulfadiazine

Kitty litter Activated charcoal Vinegar Burning candles

Golden Rules
Define the aetiology (Find the cause) Control factors affecting healing (those we know and can control) Select appropriate dressing or product Plan maintenance

Clich
Concentrate on the whole person not the hole in the person If the wound fails to heal, we haven't found the problem yet

Thank You