Wound Healing PDF

**WOUND HEALING**  **Definition of wound:** Any *break in the continuity of the skin* is called a wound. **Acute Vs Chronic Wounds:** - In Acute wounds, there is an orderly or linear progression from injury to coagulation, inflammation, cell or matrix proliferation, cell migration, and...

**WOUND HEALING**  **Definition of wound:** Any *break in the continuity of the skin* is called a wound. **Acute Vs Chronic Wounds:** - In Acute wounds, there is an orderly or linear progression from injury to coagulation, inflammation, cell or matrix proliferation, cell migration, and tissue remodelling. - Chronic wound - Non healing wound \> 6 weeks. All chronic wounds start as an acute wound. -- Lack of epithelization -- Absence of healthy granulation tissue -- Presence of necrotic tissue -- Recurrent wound breakdown **Phases of wound healing:** A diagram of a wound healing Description automatically generated **Wound Bed Preparation:** A nonhealing wound needs wound bed preparation to promote healing. "**TIME"** Tissue debridement, Infection/inflammation, Moisture balance and Epithelia edge tissue. **Tissue debridement** - Plays a key role in tissue preparation by removing nonviable tissue and pathogenic bacteria. - Techniques include surgical, enzymatic, biologic, mechanical and autolytic techniques. Newer tools include *low frequency ultrasound* and *hydro surgery devices* **"Closed" Occlusive Dressings:** - Moist Interactive Healing - Facilitates epithelization -- keratinocyte migration. Migration of keratinocytes is essential for resurfacing of the wound. - Low pH / oxygen tension -- Promotes fibroblast growth -- Promotes neovascularization - Chemical Occlusion: White soft paraffin, topical antibiotics, hydrogels-duoderm gels. - Wound Dressing: Film / wound contact layers, Alginate = haemostatic effect, Hydrocolloid (e.g. duoderm) **Infection and inflammation** - Inflammation is a physiological process in wound healing, but inappropriate inflammation can cause delayed healing. - Infection is a host response, as in cellulitis but bacteria can also delay healing through formation of *biofilm* (seen in 60% of chronic wounds). - Biofilms are colonies of microorganisms with a surrounding glycocalyx. Disruption of biofilms with debridement with or without antimicrobial agents, helps alleviate persistent inflammation. - The term antimicrobial includes disinfectants, antiseptics, and antibiotics. Antiseptics are nonspecific, broad spectrum with less risk of bacterial resistance while antibiotics work specifically on bacteria functions such as disputing cell wall function and develop resistance. As a result, topical antibiotics are not recommended for chronic wounds because of the risk of antibiotic resistance. **Antiseptics** 1. **Silver based** Microcrystalline silver Silver sulfadiazine cream Silver nitrate sticks - MOA: Silver ions bind to and destroy cell wall, interact with DNA thereby inhibiting cell division, interfere with enzymes that are critical to sustain cell growth. - Main advantage: Anti-inflammatory, antibacterial, antifungal, antiviral - Anti inflammatory effects: Supresses MMP-2 and TNF-a levels, induces apoptosis of inflammatory cells and kills microorganisms. - Main disadvantage: Silver toxicity, argyria with silver sulfasalazine; silver sulfadiazine + silver nitrate sticks may produce pseudo eschar/delay healing. - Ag resistant strains -- E coli, K pneumoniae, A. baumannii, Pseudomonas stutzeri 2. **Iodine Based -** Povidine-iodine 10% **Cadexomer iodine -** Sustained release of iodine, stimulates granulation tissue, effective against MRSA Inadine - Broad spectrum, good penetration to biofilm, proinflammatory - Toxic to granulation tissue in high concentration, risk of thyroid dysfunction, risk of contact dermatitis **Moisture imbalance** - Acute wound fluid promotes cell growth and is rich in cytokines and growth factors, while chronic wound fluid inhibits cell growth and contains high levels of proteases and proinflammatory cytokines. - Extra moisture can damage peri wound skin and lack of moisture can hinder keratinocyte migration. The major dressing types include hydrogels, hydrocolloids, alginates, foams etc. (For absorption of exudate-foams and alginates, for additional moisture-hydrogels) **Edge** - Assessment of non-advancing wound edges and proper use of therapies to advance the wound edge. **Signs of Infection:** **SUPERFICIAL** (Contamination, Colonization) \- Non-healing \- Unhealthy granulation tissue \- Exudate, size \- New areas of breakdown **DEEP** (Cellulitis, OM) \- Warmth, tenderness \- Pain \- Erythema \> 2 cm \- Probes to bone **Newer:** -- New synthetic sponges e.g.: polyurethane -- Carboxymethylcellulose (CMC) -- forms gel Advantages: Fluid Absorbency, fluid Retention, semi-Permeability, direction of wicking. **Compression Therapy:** "Gold standard"\ High compression (25 - 35 mmHg at the ankle) better than low compression\ Type of Compression:\ - Elastic vs Non elastic\ - 4 layer vs 2 layer\ - Stockings vs Bandage