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
