NORMAL WOUND HEALING CLINICAL IMPLICATIONS

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Presentation transcript:

NORMAL WOUND HEALING CLINICAL IMPLICATIONS 1. Meticulous hemostasis reduces inflammation & phagocytosis necessary to clear wound of blood 2. Atraumatic handling of tissues decreases load of necrotic or non-viable cells at the wound margin - use fine forceps or skin hooks to retract & assist

NORMAL WOUND HEALING CLINICAL IMPLICATIONS 3. Deep sutures are best placed in collagen laden structures that can hold tension (fascia & dermis) 4. Fat does not contain collagen and does not hold sutures 5. Epithelialization more rapid under moist conditions than dry (Winter & Scales, 1963)

NORMAL WOUND HEALING CLINICAL IMPLICATIONS 6. Traditional wet-to-dry dressing, if truly left to dry, simply produces desiccation & necrosis of surface layer of wound during epithelialization 7. Without dressings, superficial wound forms scab or crust = protective moisture barrier

NORMAL WOUND HEALING CLASSIFICATION OF WOUNDS Clean Clean-Contaminated Contaminated Dirty

NORMAL WOUND HEALING CLASSIFICATION OF WOUNDS CLEAN: Non-traumatic, uninfected operative wound Does not enter resp., GI, GU, or oral cavities No inflammation is encountered Closed primarily Not usually drained No break in aseptic technique occurs 75% of all surgical wounds fall into category

NORMAL WOUND HEALING CLASSIFICATION OF WOUNDS CLEAN-CONTAMINATED: Has usual normal flora No gross contamination Resp. and GI tract if no significant spillage GU or biliary tracts if no infected urine or bile Appendectomy Clean wounds with a MINOR break in aseptic technique

NORMAL WOUND HEALING CLASSIFICATION OF WOUNDS CONTAMINATED: Soft tissue lacerations, open fractures, penetrating wounds and other trauma Operations with gross spillage from GI tract GU and biliary tracts with infected urine or bile Operations with MAJOR break in aseptic technique. Eg emergency open cardiac massage

NORMAL WOUND HEALING CLASSIFICATION OF WOUNDS DIRTY: Wounds that are heavily contaminated Wounds that are clinically infected pre-op Abscess Perforated viscera Old traumatic wound with retained devitalized tissue or foreign body

NORMAL WOUND HEALING TYPES OF WOUND HEALING 1st Intention (Primary) Healing 2nd Intention (Secondary) Healing 3rd Intention (Tertiary) Healing = Delayed Primary Closure Partial Thickness Wounds

NORMAL WOUND HEALING TYPES OF WOUND HEALING 1st INTENTION (Primary) HEALING Wound closed within 24 hours Prior to formation of granulation tissue Fastest healing Generally best cosmetic result Treatment of choice for non-infected wound Time!! Infection Rate  Time since wounding “Golden Period” vs. individual evaluation

NORMAL WOUND HEALING TYPES OF WOUND HEALING 2nd INTENTION (Secondary) HEALING Open wound allowed to close by Contraction & Epithelialization Contraction by myofibroblasts Myofibroblasts disappear as contraction completed Direct correlation between number of myofibroblasts and extent of wound contraction

NORMAL WOUND HEALING TYPES OF WOUND HEALING 3rd INTENTION (Tertiary) HEALING = DELAYED PRIMARY CLOSURE Contaminated, left open to prevent infection Normal host defenses debride wound After 3-4 days, local phagocytes and inflammatory cells recruited and angiogenesis Wound edges approximated Collagen metabolism undisturbed Tensile strength develops as if primary closure

NORMAL WOUND HEALING TYPES OF WOUND HEALING PARTIAL THICKNESS WOUNDS Wounds involve epithelium and superficial dermis Heal mainly by epithelialization to cover exposed dermis Minimal collagen deposition Absence of wound contraction No or minimal scar formation

ABNORMAL WOUND HEALING

ABNORMAL WOUND HEALING ABNORMAL WOUND HEALING Excessive Wound Healing: Inadequate Wound Healing:

ABNORMAL WOUND HEALING ABNORMAL WOUND HEALING Excessive Wound Healing: Hypertrophic scar Keloid scar Inadequate Wound Healing: Widespread scar Chronic, unstable wound

ABNORMAL WOUND HEALING HYPERTROPHIC SCAR Histologically similar to keloid scars Overabundance of dermal collagen Respect the boundaries of the original wound Do not extend into unwounded skin Less genetic predisposition But do occur more frequently in Asian & Black populations

ABNORMAL WOUND HEALING HYPERTROPHIC SCAR Often in upper torso & across flexor surfaces Usually develop in first month after wound Often subside gradually on own

ABNORMAL WOUND HEALING HYPERTROPHIC SCAR TREATMENT OPTIONS: Observation - may improve with time Pressure garments Topical silicone sheeting Re-excision and closure (esp if wound was second intention or complicated by infection)

ABNORMAL WOUND HEALING KELOIDS “Cheloide” - Alibert in 1816 True keloids uncommon Etiology unknown Histologically, overabundance of collagen: absolute number of fibroblasts not increased Collagen production outpaces collagenase

Increased in Blacks: 6:1 to 19:1 Female > Male (min.) KELOIDS Incidence Increased in Blacks: 6:1 to 19:1 Female > Male (min.) Mostly 10-30 years old (but any age) Commonest on ears, face, chest Family history - autosomal dominant

IgG levels increased - ? Autoimmune KELOIDS Etiology IgG levels increased - ? Autoimmune Aberration of melanocyte-stimulating hormone secretions Sebum-antigen

Various abnormalities, significance unclear: KELOIDS Biochemistry Various abnormalities, significance unclear:  TISSUE WATER  CALCIUM  ACID PHOSPHATASE  G-6-P  ALANINE TRANSAMINASE  PROLINE HYDROXYLASE  COLLAGENASE  RATIO CLLAGEN TYPE III:TYPE I

Histologically identical Epithelium KELOIDS Histology Histologically identical Epithelium thin and flattened rete pegs and dermal papillae absent appendages decreased or absent Dermis elastic fibers absent abnormally broad, swollen eosinophils interlacing, glassy appearing collagen

Poorly circumscribed, dense connective tissue in dermis KELOIDS Pathology Poorly circumscribed, dense connective tissue in dermis Skin of eyelids, areola, & penis - very thin, highly modified dermal layers: No Keloid Only one authentic case of sarcomatous degeneration

Difficult because cause unknown KELOIDS Treatment Difficult because cause unknown Some improvement with excision followed by intralesional steroid injection Unresponsive cases, excision follwed by short course radiotherapy has been successful Resulting scar unpredictable and potentially worse

ABNORMAL WOUND HEALING KELOIDS PEARL: Keloids exceed original boundaries of wound and continue producing collagen in pseudotumour fashion. (Distinguishes from hypertrophic scars)

NORMAL WOUND HEALING FACTORS AFFECTING WOUND HEALING Anatomic Site: fastest in areas of greatest blood supply (face and neck) Weight: fat most vulnerable tissue to trauma due to poor blood supply Age: delayed healing, less wound strength Oxygen: wound PO2, hyperbaric O2 Infection: local or systemic

NORMAL WOUND HEALING FACTORS AFFECTING WOUND HEALING Medication: Chemotherapy, steroids Local Factors: Wound tension, foreign body, dead or devitalized tissue Nutritional Status: Protein, zinc, vitamins Nature of Wound: Contusion, abrasion, laceration Chronic Disease: Diabetes, cirrhosis

NORMAL WOUND HEALING FACTORS AFFECTING WOUND HEALING Smoking: Nicotine induced vasoconstriction, Toxins, Metalloproteinase stim’n Radiation therapy: Stasis and vessel occlusion Hydration: moist wound heals faster Growth Factors : Endogenous or exogenous - stimulate wound healing - area of active research - no magic bullet to date

NORMAL WOUND HEALING WOUND CLOSURE

NORMAL WOUND HEALING IDEAL SCAR 1. Accurate alignment of sharply incised tissue, parallel to natural line of resting skin tension. 2. Closure of wound without tension on epidermis & without underlying dead space 3. Primary healing without complications (eg. infection or dehiscence) 4. Patient’s genetic makeup - scar history 5. Wound location on body

WOUND HEALING SUTURE MATERIALS Absorbable Non-absorbable