4/10/14 11:11 PMLangerhans cells

LCs, 2%–5% of epidermal cells, are a dendritic cell subset that originates from bone marrow precursors and populates the epidermis. They are the “professional” skin-specific APCs and ingest antigen locally in the skin. After antigen uptake, LCs migrate to the draining lymph node, where they mature to potent stimulators for antigen-specific T cells, expressing high levels of major histocompatibility complex molecules. (a) Section of immunostained skin shows Langerhans cells (yellow) abundant in hair follicles (F), where many microorganisms live, and throughout the epidermis (E). Keratin of the epidermis and follicles is stained green. (b) Langerhans cells among the other epidermal cells.(Reproduced, with permission, from Romani N et al. Acta Path Micro Immunol Scandinavica. 2003;111:725.)

Pastian Lines - Pastia's lines are pink or red lines seen in the body folds (especially elbows and axilla) during scarlet fever. Linear hyperpigmentation may persist after the rash fades

http://pedsinreview.aappublications.org/content/27/5/189/F2.expansion

What is a wound? It is a disruption or injury to the skin which may be caused by

trauma, surgical interventions, mechanical insult, systemic diseases/disorders

Layers of the Skin

Wound Healing – Types

PRIMARY INTENTION-wound edges approximated and secured-heal by epithelialization and connective tissue deposition-usually heal quickly-e.g. surgical sutures

SECONDARY INTENTION-wound edges not approximatedhealing occurs by formation of granulation tissue, epithelialization and contraction of wound edges (scar tissue formation)allowing wounds to heal without surgical closure-e.g. leg ulcer left to heal by scar tissue formation

TERTIARY INTENTION (Delayed Primary Closure)- surgical wound is left open for an extended period to minimize risk of infection-initially, wound is debrided then left open

-generally closed through surgical procedure

Three Phases of Wound Healing

Not mutually exclusive events, rather, they overlap

Hemostasis 0-3 hrs Initiates the healing process Epinephrine is released Clotting and vasoconstriction to reduce blood loss at site of injury Platelets aggregate, clot formation, hemorrhage arrested, limits

blood loss Clot acts as a provisional matrix, provides space in which cells can

migrate Platelets release growth factors and cytokines

Inflammatory Phase Main goal is debride wound, hemostasis Initial response after acute injury (0-5 days) May be present for longer periods in chronic wounds

Characterized by: Pain Edema Erythema Warmth

Inflammatory cells (platelets, neutrophils and macrophages) enter the wound

Phagocytosis is triggered – removal of harmful pathogens and celuular debris is initiated

Key nutrients: vitamin C, E, selenium, arginine, cysteine, methionine

Neutrophils- release cytokines which recruit fibroblast and epithelial cells-kill bacteria

Macrophages-Phagocytose and degrade foreign matter-Release extracellular enzymes to degrade necrotic tissue-Secrete growth factors and cytokines-Promote angiogenesis-Recruit fibroblasts

Proliferative Phase Overlaps with inflammatory phase Begins 3-5 days post injury and may continue up to 21 days Fibroblasts enter the wound, synthesize and deposite

o Extra cellular matrix(ECM)o Growth factors (cytokines, stored in platelets), e.g.

PlateletDerivedGF, EpidermalGF, KeratinocyteGF, FibroblastGFo Angiogenic factors

Granulation tissue + ECM fills in the wound deficit Angiogenesis forms new capillary growth Re-epithelialization occurs and new epithelial tissue covers the

deficit Myofibroblasts: contract the wound, pulling the edges together to

close the woundKey nutrients: vitamin A, C, thiamine, pantothenic acid, zinc, manganese

Implications: granulation tissue formation is the goal of this phase it is the active phase maintain moist wound healing

topical agents and antiseptics are known to be harmful to healing tissue

Maturation (remodeling) Phase Can start as early as 7 days and may last up to 2 years Fibroblasts leave the wound Collagen fibers, fibronectin and proteoglycan rearranged and

redistibuted Collagen is remodeled into a more organized matrix, degraded and

digested by other protease enzymes Granulation tissue matures into a scar The tensile strength of the newly formed scar increases

o potential strength is 70-80% of original tissue Key nutrients: vitamin A, C, zinc, copper, manganese

Implications: Still healing internally Increases risk of re-injury in the early phases of remodeling May be important to protect newly healed tissue from friction and

shear

SCAR FORMATION

10,000 collagen fibrils in one collagen fiber!

STALLED WOUNDS (CHRONIC WOUNDS)Interrupted inflammation:

*MMP = matrix degrading proteases

Lack of blood flow – perfusion/oxygenation essential to repair process (PAD, PVD, pressure, vasoconstiction, atherosclerosis, hypotension, hypothermia, anemia, COPD). Collagen fibril croslinking begins to fail as tissue oxygen pressure falls below 40 mmHg, O2 is required for hydroxylation of proline and lysine to synthesize mature collagen.

Nutrition – protein, magnesium, calcium, vitamin K are essential for collagen synthesis and development of normal tensile strength

Infection – prolongs inflammatory phase, delays collagen synthesis and epithelialization. Infection stimulates prostaglandin E2 and thromboxane, thrombosis and vasoconstriction, wound hypoxia. Infected wound may not have classical signs of infection, and may evade detection.

Medications – chemotherapeutic agents and anti-inflammatory medications compromise wound repair, antiseptics may be harmful to granulation tissue/inflammatory activity (e.g. acetic acid, betadine, sodium hypochlorite solution)

Stress – may contribute to delayed wound healing, elevate corticosteroid levels, compromise immune function

Aging – diminished inflammatory response Obesity – tissue is poorly oxygenated and vascularized Co-morbidities – siabetes, vascular and cardiac disease Immunosuppression – can retard wound healing and increase

susceptibility to infection Itch-scratch-itch cycle – cause irritation, pain, break in skin,

infection

INFECTED WOUND

NECROTIC TISSUE

-prevents the wound from healing-non-viable tissue-debridement offers opportunity to return a wound to an inflammatory state

ESCHARThe presence of an eschar implies tissue necrosis, infarction, deep burns, gangrene, or other ulcerating process. It is a circumscribed, adherent, hard, black crust on the surface of the skin that is moist initially, protein rich, and avascular.

ESCHAROTOMY

As edema fluid accumulates, ischemia may develop under any constricting eschar of an extremity, neck, chest, or trunk if the full-thickness burn is circumferential. Escharotomy incisions through the anesthetic eschar can save life and limb and can be performed in the emergency department or operating room.

Resourceshttp://www.woundcme.org/node/11006/course/11047/contenthttp://www.thewoundinstitute.com/ft/providers/accredited_courses.asp#intermediatehttp://www.thewoundinstitute.com/ft/providers/accredited_courses.asphttp://education.nhsinc.com/courselist.php#http://www.nature.com/jid/journal/v127/n5/fig_tab/5700715f1.htmlFitzpatrick’s Dermatology

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