skin sqtissue

Chapter 16: The Skin and Subcutaneous TissueINTRODUCTIONSkin

- largest human organ- protective barrier, environmental buffer- functions:1. creates a semipermeable barrier to chemical absorption2. prevents fluid loss3. protects against penetration of solar radiation4. rebuffs infectious agents5. dermal durability resists physical forces6. regulates body heat (body’s primary thermoregulatory organ)

ANATOMY AND PHYSIOLOGY OF THE SKIN- antomically: skin may be devided into 3 layers: epidermis, basement membrane, dermis

epidermis Basement membrane dermis-with very little ECM, the epidermis is composed primarily of specialized cells that perform vital functions

-between the epidermis and dermis-anchors these layers together-biologic functions:o tissue organizationo growth factor reservoiro support of cell monolayers

during tissue developmento semipermeable selective

barrier

-provides soft-tissue durability-primarily composed of a dense ECM that provides support for a complex network of nerves, vasculature, and adnexal structures

- Extracellular Matrix (ECM): a collection of fibrous proteins and associated glycoproteins embedded in a hydrated ground substance of glycosaminoglycans and proteoglycans; provides architectural framework that imparts mechanical support and viscoelasticity; can regulate the neighboring cells, including their ability to migrate, proliferate and survive injury

THE EPIDERMIS- composed primarily of keratinocytes- a dynamic, multilayered composite of maturing cells- (internal to external): stratum germinatum stratum spinosumstratum granulosumstratum

lucidumstratum corneum- basal cells: mitotically active, single cell layer of the least differentiated keratinocytes at the base of

epidermal structure; multiply leave the basal laminabegin differentiation and upward migration- spinous layer: keratinocytes are linked together by tonofibrils = keratin- entry into the granular layercells accumulate keratohyaline granules- horny layerkeratinocytes age, lose their intercellular connectionsshed- basal layer exitshedding=keratinocyte transit time = approx 40-56 days

- melanocytes and other cellular components w/n the skin deter absorption of harmful radiation- melanocytes: initially derived from precursor cells of the eural crestextend dendritic processes upward

into epidermal tissues from their position beneath the basal cell layer; 1 melanocyte : 35 keratinocytes; produce melanin from yrosine and cysteine- pigment is packaged into melanoomes w/n the melanocyte cell body transported into the epidermis

via dendritic processesapocopation (dendritic processes are sheared off)melanin is transferred to keratinocytes via phagocytosis

- Despite differences in skin tone, the density of melanocytes is constant among individuals. It is the rate of melanin production, transfer to keratinocytes, and melanosome degradation that determine the degree of skin pigmentation

- Genetically activated factors as well as ultraviolet (UV) radiation, hormones such as estrogen, adrenocorticotropic hormone, and melanocyte-stimulating hormone, increase melanin production.

- Cutamelanocytes – play a critical role in neutralizing the sun’s harmful rays- Exposure to UV lightdamageaffects the function of tumor suppressor genescell deathneoplastic

formation- majority of solar radiation that reaches the Earth is UVA (315 to 400 nm)- majority of skin damage is caused by UVB (240 to 315 nm)- UVB is the major factor in sunburn injury, and is a known risk factor in the development of melanoma.

Although UVB causes considerable DNA damage in the skin, UVA has only recently has been shown to damage DNA, proteins, and lipids.

- UV-related damage may be potentiated by ionizing radiation, viruses or chemical carcinogens- Keratins – maintains cellular integrity; intermediate filaments found w/n the spindle layer; provide flexible

scaffolding (to resist external stress); mitotically active ones mainly express keratins 5 and 14- Point mutations affecting these genes may result in blistering diseases, such as epidermolysis bullosa,

associated with spontaneous release of dermal-epidermal attachments.- In addition to its role in resisting radiation, toxin absorption, and deforming forces, the skin is a critically

immunoreactive barrier.- Following migration into epidermal structure from the bone marrow, Langerhans' cells act as the skin's

macrophages. This specialized cell type expresses class II major histocompatibility antigens, and has antigen-presenting capabilities.

- In addition to initiating rejection of foreign bodies, Langerhans' cells play a crucial role in immunosurveillance against viral infections and neoplasms of the skin.

THE DERMIS- mostly comprised of structural proteins, and to a smaller degree, cellular components.- Collagen: main functional protein within the dermis (70% of dermal dry weight); responsible for its

remarkable tensile strength.- Tropocollagen: a collagen precursor, consists of three polypeptide chains (hydroxyproline, hydroxylysine,

and glycine) wrapped in a helixcross- linked to one another = collagen fibers- skin: mostly composed of type I collagen - Fetal dermis contains mostly type III (reticulin fibers) collagen, but this only remains in the basement

membrane zone and perivascular regions during postnatal development.

Schwartz’s Principles of Surgery: CH16:

- Elastic fibers: highly branched proteins capable of stretching to twice their resting length.resist stretch forcesallow a return to baseline form after the skin responds to deforming stress

- Ground substance: consists of various polysaccharides and polypeptide (glycosaminoglycans) complexes; an amorphous material that occupies the remaining spaces.

- These glycosaminoglycans, secreted by fibroblasts, can hold up to 1000 times their own volume in water and constitute most of dermal volume.

- blood supply to the dermis = based on an intricate network of blood vessels which provide vascular inflow to superficial structures, as well as regulate body temperature. This is achieved with the help of vertical vascular channels that interconnect two horizontal plexuses, one within the papillary dermis, and the other at the dermal-subcutaneous junction.

- Glomus bodies: tortuous arteriovenous shunts that allow a substantial increase in superficial blood flow when stimulated to open.

- Cutaneous sensation is achieved via activation of a complicated plexus of dermal autonomic fibers synapsed to sweat glands, erector pili, and vasculature control points.

- These fibers also connect to corpuscular receptors relay information from the skin back to the central nervous system.

- Meissner's, Ruffini's, and Pacini's corpuscles transmit information on local pressure, vibration, and touch.- "unspecialized" free nerve endings report temperature, touch, pain, and itch sensations

CUTANEOUS ADNEXAL STRUCTURES- 3 main adnexal structures: eccrine glands, pilosebaceous units, apocrine glands

Eccrine glands Pilosabaceous units Apocrine glandsSweat producing Oil secreting sebaceous glands +

Eccrine + Apocrine GlandsPheromone producing glands

Located over the entire body but are concentrated on the palms, soles, axillae and forehead

Primarily found in the human axilae and anogenital region (these structures that predispose both regionsto suppurative hydroadenitis)

- Although pheromone-producing apocrine glands play a distinct role in lower mammalian life, these structures have not been shown to demonstrate significant activity in human populations.

- Hair follicles are mitotically active germinal centers that produce hair, a cylinder of tightly packed cornified epithelial cells.

- The hairfollicle- Production of hair- Contains a reservoir of pluripotential stem cells critical in epidermal reproductivity- capable of near limitless expansion to replace lost or injured cells- restore epidermal continuity after wounding

- For example, in skin graft harvest, residual hair follicles supply new keratinocytes to regenerate the epidermis and restore skin integrity.

INJURIES TO THE SKIN AND SUBCUTANEOUS TISSUEA. TRAUMATIC INJURIES- possible causes: penetrating, blunt, shear force, bite, degloving injuries- clean lacerations may be closed primarily after irrigation, debridement, and careful evaluation- contaminated or infected wounds aloowed to heal by secondary intention or delayed primary closure- more complex wounds guiding principles are debridement of nonviable tissue and aggressive irrigation of

the wound- tangential abrasions approached similarly to second-degree burns- degloving injuries consider third degree or full thickness burns may be partially salvaged by placing it

back on the wound like a skin graft- replacement of clean, avulsed tissue can effectively provide wound coverage as a biologic dressing- areas of uncovered wound bed undergo delayed primary closure allowed to granulate in or undergo

definitive reconstruction- bite wounds 2% of all emergency room visits; small puncture wounds; impregnation of oral bacteria into

deep, contained tissue layers significant morbidity; most common organisms found in human bites: Viridans streptococci, Staphylococcus aureus, Eikenella corrodens, Haemophilus influenzae, and beta-lactamase-producing bacteria

- dog bites: most frequet animal related wound; canine jaw can exert over 450 pounds of pressure per square inch; often add a crushing element + penetrating injury + avulsion element; may contaminate tissues w both aerobic and anaerobic organisms; most commonly cultured bacteria: asteurella multocida, Staphylococcus species, alpha-hemolytic, streptococci, E. corrodens, Actinomyces, and Fusobacterium

- The bite wound, whether from human or animal, is a contaminated wound and should not be closed primarily. - Selected facial wounds may be closed primarily after very thorough cleansing and initiation of antibiotic

therapy. Although there remains a potential risk of serious infection, this risk may be low enough on the face to weigh in favor of the improved long- term wound appearance after primary closure.

- The great majority of bite wounds should be approached via drainage, copious irrigation, debridement of necrotic material, antibiotic therapy, extremity immobilization, and elevation.

- Digital infection(following puncture or bite wounds) often contain a variety of bacteria; rapid spread of infection is possible in the absence of antibiotic therapy

B. EXPOSURE TO CAUSTIC SUBSTANCES- acidic or alkali solutions

Acidic Alkali- determined by the concentration, duration of

contact, amount, and penetrability- deep tissue coagulative injury may result,

damaging nerves, blood vessels, tendons, and

- often used as household cleaning agents skin burns

- skin penetrationfat saponificationtissue


bone penetration tissue damage- initial tx: should include copious skin irrigation

for atleast 30mins w either saline or water dilutes active solution helps return the skin to normal pH

- to detoxify fluoride ions: topical quaternary ammonium compounds and topical calcium carbonate gel

- immediate irrigation of the affected area with continuous water flow (maintained for at least 2 hours, or until symptomatic relief is achieved)

- fluoride ions continue to injure underlying tissue until they are neutralized with calcium absorb the body’s calcium supply cardiac arrythmia

- liquifactive injury produced by alkali burnslonger more sustained period of injury

- intravenous fluid (IVF) extravasation leakage of injectable fluids into interstitial space chemical burn; occurs from underneath the skin surface; deep injury

extravasation = chemical toxicity, osmotic toxicity, pressure effects in a closed environment injury this displacement may be the result of IV catheter movement or vascular permeability most common substances associated with these injuries: cationic solutions (potassium ion, calcium

ion, bicarbonate), osmotically active chemicals (total parenteral nutrition, hypertonic dextrose solutions), antibiotics or cytotoxic drugs

most common site in the adult: dorsum of the hand = extensor tendon exposure tx: conservative management, icluding frequent dressing change and continued wound care (+) chemotherapy = 4.7% risk for developing extravasation (in children=58%) newborn babies=at risk due to fragility and small caliber of veins, poor ability to verbalize pain and the

frequent use of pressurized IVF pumps used in their care most common IVF extravasations causing necrosis in infants: high-concentration dextrose solutions,

calcium, bicarbonate, and parenteral nutrition in adults: most common: chemotherapeutic agents (doxorubicin (Adriamycin) and paclitaxel)

The direct toxic effects of doxorubicin causes cellular death that is perpetuated by release of doxorubicin-DNA complexes from dead cells. This cellular death prevents release of cytokines and growth factors=wound healing failure.

Following extravasation, edema, erythema, and induration usually are present. Injury to underlying nerves, muscles, tendons, and blood vessels must be taken into account. majority of such injuries are successfully managed through a conservative approach In the severe infusion injury, vigorous liposuction with a small cannula may be used to introduce saline flush

into the injured areaflush is then allowed to egress via the small liposuction wounds. (no benefit if >24hrs; beneficial in the acute setting)

Surgery should be limited to patients with necrotic tissue, pain, or damage of underlying structures

C. HYPER-AND-HYPOTHERMIC INJURY- skin exposed to extreme temperaturesignificant risk of hypo/hyperthermic injury- zone of coagulation: central area of injury; exposed to the most direct heat transfernecrosis- zone of stasis: surrounds the zone of coagulation; has marinal tissue perfusion and questionable viability- zone of hyperemia: outermost area; most similar to uninjured tissue and demonstrates blood flow due to

the body’s response to injury- hypothermic injury= (frostbite) results in the acute freezing of tissues and is the product of 2 factors: (a)

duration of exposure, (b) the temperature gradient at the skin surface- Severe hypothermia primarily exerts its damaging effect by causing direct cellular injury to blood vessel walls

and microvascular thrombosis. - the skin's tensile strength by 20% in a cold environment - tx protocol for frostbite rapid rewarming, close observation, elevation and splinting, daily hydrotherapy,

and serial debridements

D. PRESSURE INJURY- presure = pressure ulcer formation- pressure applied to overlying tissues cutaneous vascular flowischemia of local tissues- ≥1 hour of 60mmHg = histologically identifiable venous thrombosis, muscle degeneration, tissue necrosis- normal arteriole (32mmHg), capillary (20mmHg), venule pressures (12mmHg)- sitting can produce pressures as high as 300mmHg at the ischial tuberosities- sacral pressure (150mmHg) when lying on a standard hospital mattress- Patients unable to sense pain or shift their body weight (paraplegics or bedridden individuals) prolonged

elevated tissue pressures local necrosis- Because muscle tissue is more sensitive to ischemia than skin, necrosis usually extends to a deeper area

than that apparent on superficial inspection.- Tx:

- elements of pressure sore tx: relief of pressure, wound care, and systemic enhancement, such as optimization of nutrition.

- Air flotation mattresses and gel seat cushions redistribute pressure = incidence of pressure ulcers= cost-effective in the care of px at high risk

- nutritional support services to facilitate proper dietary intake- Surgical management should include debridement of all necrotic tissue followed by thorough irrigation. - Shallow ulcers may be allowed to close by secondary intention, but deeper wounds with involvement of

the underlying bone require surgical debridement and coverage

E. RADIATION EXPOSURE- environmental elements: solar (UV) exposure, iatrogenic management, and industrial/occupational

applications- most common: solar or UV radiation- UV spectrum: UVA (400-315nm); UVB (315-290nm); UVC (290-200nm)- Ozone layer: absorbs UVC wavelengths <290nm, allowing only UVA and UVB to reach earth- UVB: acute sunburns; chronic skin damagemalignant degeneration, although it makes up less than 5% of

the solar UV radiation that hits the earth- Ionizing radiation: Mainstay in the tx of various malignancies; effectively blocks mitosis in rapidly dividing cell

types


- The extent of cellular damage is dependent on radiation dose, exposure period, and the cell type being treated

- Acute radiation changes: erythema and basal epithelial cellular death in the area of direct application- cellular repairpermanent hyperpigmentation is observed in healing areas- 4 to 6 months following radiation application, chronic radiation changes are characterized by a loss of

capillaries via thrombosis and fibrinoid necrosis of vessel walls.- Progressive fibrosis and hypovascularity ulceration when poor vascular inflow results in poor tissue

perfusion that progresses as the skin ages

INFECTIONS OF SKIN AND SUBCUTANEOUS TISSUE- cellulitis: heralded by erythema, warmth, tenderness and edema; superficial; spreading infection of the skin

and subcutaneous tissue- most common organisms as. W cellulitis: grp A streptococci and S. aureus- uncomplicated cellulitis tx: oral antibiotics on an out px basis

A. FOLLICULITIS, FURUNCLES, CARBUNCLES- Folliculitis: infection of the hair follicle

- causative organism: Staphylococcus, but gram negative organisms may case follicular inflammation as well

- tx: adequate hygiene- furuncle (boil): begins as folliculitisfluctuant nodule

- tx: soaking in warm water hastens liquefaction and hastens spontaneous rupture; often require incision and drainage before healing can be initiated

- carbuncle: more involved; deep seated infections that results in multiple draining cutaneous sinuses- tx: often require incision and drainage before healing can be initiated

B. NECROTIZING SOFT-TISSUE INFECTIONS- most common sites: external genitalia, perineum or abdominal wall (Fournier gangrene)- current classifications: based on (a) tissue plane affected ad extent of invasion (b) anatomic site (c)

causative pathogen(s)- deep soft tissue infections are classified as: (a) necrotizing fascilitis [represents a rapid, extensive infection

of the fascia deep to the adipose tissue] or (b) necrotizing myositis [involves the muscles but typically spreads to adjacent soft tissues]

- most common organisms (necrotizing soft tissue inf): gram-positive organisms: grp A streptococci, enterococci, coagulase-negative staphylococci, S. aureus, S. epidermidis, Clostridium species

- gram negative species (Escherichia coli, Enterobacter, Pseudomonas species, Proteus species, Serratia species,and bacteroides)

- polymicrobial infections are more common- clinical risk factors: DM, malnutrition, obesity, chronic alcoholism, periphera vascular disease, chronic

lymphocytic leukemia, steroid use, renal failure, cirrhosis, autoimmune deficiency syndrome - management: prompt recognitionbroad-spectrum IV antibioticsaggressive surgical

debridementintensive care unit support- debridement: must be extensive, include all skin, subcutaneous tissue, muscle until there is no further

evidence of infected tissue- initial resectionfrequent returns to the OR for additional debridementaggressive fluid replacement to

offset renal failure from ongoing sepsisC. HIDRADENITIS SUPPURATIVA- a defect of the terminal follicular epithelium- follicular defect = apocrine gland blockageobstructed infection abscess formation throughout affected

axillary, inguinal, and perianal regions spontaneous rupture of these localized collectionsfoul-smelling sinuses form and repeated infections create a wide area of inflamed, painful tissue

- Tx of acute infections: application of warm compresses, antibiotics, and open drainage - chronic hidradenitis: wide excision is required and closure may be achieved viaskin graft or local flap

placement

D. ACTINOMYCOSIS- a granulomatous suppurative bacterial disease caused by Actinomyces- In addition to Nocardia, Actinomadura, and Streptomyces, Actinomyces infections may produce deep

cutaneous infections that present as nodules and spread to form draining tracts within surrounding soft tissue.

- 40-60% of the actinomycotic infections occur within the face or head- Actinomycotic infection usually results following tooth extraction, odontogenic infection, or facial trauma- Accurate diagnosis depends on careful histologic analysis, and the presence of sulfur granules within purulent

specimen is pathognomonic.- Tx: Penicillin and sulfonamides; areas of deep-seated infection, abscess, or chronic scarring may require

surgical therapy

VIRAL INFECTIONS OF THE SKIN AND SUBCUTANEOUS TISSUEA. HUMAN PAPILLOMAVIRUS- Warts are epidermal growths resulting from human papillomavirus (HPV) infection. - common wart (verruca vulgaris): found on the fingers and toes and is rough and bulbous- Plantar warts (verruca plantaris): occur on the soles and palms, and may resemble a common callus- Flat warts (verruca plana) are slightly raised and flat; tends to appear on the face, legs, and hands- Venereal warts (condylomata acuminata): grow in the moist areas around the vulva, anus, and scrotum;

Histologic examination demonstrates hyperkeratosis (hypertrophy of the horny layer), acanthosis (hypertrophy of the spinous layer), and papillomatosis; one of the most common STDs; largely results from HPV 6 and 11

- Some warts (especially HPV types 5, 8, and 10) are associated with squamous cell cancers, therefore lesions that grow rapidly, atypically,or ulcerate should be biopsied.

- Buschke-Lewenstein tumor: extensive growths, facilitated by concomitant HIV infection; often multiple and


can grow large in size- Warts may be removed via application of chemicals, such as formalin, podophyllum, andphenol-nitric acid- Curettage with electrodesiccation also can be used for scattered lesions. - Tx of extensive areas of skin requires surgical excision under general anesthesia; adjuvant therapy with

interferon, isotretinoin, or autologous tumor vaccine to recurrence rates; immune response modifiers such as imiquimoid, to optimize long term eradication of HPV-induced anogenital lesions

- Because of the infectious etiology, recurrences are common, and repeated excisions are often necessary.

B. HUMAN IMMUNODEFICIENCY VIRUS- intrinsic wound-healing deficiencies and much lower resiliencechronic wounds- risk of postoperative soft-tissue complications directly with disease progression- cause for delayed wound healing is unknown but is thought to be secondary to: (a) decreasing T-cell CD4+

count, (b) opportunistic infection, (c) low serum albumin, and (d) poor nutrition- Overall, these effects are thought to result in poor collagen cross-linking and deposition producing a profound

compromise in wound healing

INFLAMMATORY DISEASES OF THE SKIN AND SUBCUTANEOUS SOFT TISSUEA. PYODERMA GANGRENOSUM- a relatively uncommon destructive cutaneous lesion- Clinically, a rapidly enlarging, necrotic lesion with undermined border and surrounding erythema characterize

this disease.- underlying systemic disease in 50% of cases- commonly associated with inflammatory bowel disease, rheumatoid arthritis, hematologic malignancy, and

monoclonal immunoglobulin A gammapathy.- Recognition of the underlying disease is of paramount importance. - Management of pyoderma gangrenosum ulcerations without correction of underlying systemic disorders =

complications - Tx: A majority of patients receive systemic steroids or cyclosporine; Although medical management alone

may slowly result in wound healing, many physicians advocate chemotherapy with aggressive wound care and skin graft coverage.

B. STAPHYLOCOCCAL SCALDED SKIN SYNDROME AND TOXIC EPIDERMAL NECROLYSIS- Staphylococcal scalded skin syndrome (SSSS) and toxic epidermal necrolysis (TEN) create a similar clinical

picture including skin erythema, bullae formation, and wide areas of tissue loss- SSSS: caused by an exotoxin produced during staphylococcal infection of the nasopharynx or middle ear- TEN: an immune response to certain drugs such as sulfonamides, phenytoin, barbiturates, and tetracycline- Dx: skin biopsyHistologic analysis of SSSS reveals a cleavage plane in the granular layer of the epidermis- TEN results in structural defects at the dermoepidermal junction and is similar to a second-degree burn- Tx: fluid and electrolyte replacement; wound care similar to burn therapy- > 30% of total body surface area involvement are classified as TEN- patients with < 10% of epidermal detachment are categorized as Stevens-Johnson syndrome- Stevens-Johnson syndrome, respiratory and alimentary tract epithelial sloughing intestinal malabsorption

and pulmonary failure- Patients with significant soft-tissue loss should be treated in burn units with specially trained staff and critical

equipment- Although corticosteroid therapy has not been efficacious, temporary coverage via cadaveric, porcine skin, or

semisynthetic biologic dressings (Biobrane) allows the underlying epidermis to regenerate spontaneously

BENIGN TUMORS OF THE SKIN AND SUBCUTANEOUS TISSUEA. CYSTS (EPIDERMAL, DERMOID, TRICHILEMMAL)

**cutaneous cysts: sometimes called “sebaceous cysts” because they appear to contain sebum-a misnomer and the substance is actually keratin

epidermal dermoid Trichilemmal (pilar)- most common type of

cutaneous cyst- may present as a single, firm

nodule anywhere on the body

- congenital lesions that result when epithelium is trapped during fetal midline closure

- eyebrow-most frequent site of presentation- common anywhere from the nasal tip to the

forehead

- second most common cutaneous cyst

- occur more often on the scalp of females

- ruptureintense, characteristic odor

- on clinical examination: subcutaneous, thin-walled nodule containing white, creamy material- histo: Cyst walls consist of an epidermal layer oriented with the basal layer superficial, and the more mature layer

deep (i.e., with the epidermis growing into the center of the cyst). The desquamated cells (keratin) collect in the center to form the cyst.

have a mature epidermis demonstrate squamous epithelium, eccrine Trichilemmal cyst walls do not


complete with granular layer. glands, and pilosebaceous units. In addition, these particular cysts may develop bone, tooth, or nerve tissue on occasion

contain a granular layer; however, these cysts contain a distinctive outer layer resemblingthe root sheath of a hair follicle (trichilemmoma)

Each of these cysts typically remain unnoticed and asymptomatic until they rupture, cause local inflammation, or become infected. Once infected, these cysts behave similar to abscesses, and incision and drainage is recommended. After resolution of inflammation, the cyst wall must be removed in its entirety or the cyst will recur.

B. KERATOSES (SEBORRHEIC, SOLAR)- arise in sun exposed areas of the body (face, forearms, back of hands)- most notable in the older age grps- leasions appear light brown or yellow and have a velvety greasy texture- premalignant lesions and a squamous cell carcinoma (SCC) may develop over time- sudden eruptions: may be associated w internal malignancies- bipsy and tx seldome required- histo: atypical-appearing keratinocytes and evidence of dermal solar damage- malignancies that do develop rarely metastisize- TOC: lesion reduction (applicaion of topical 5-fluorouracil surgical excision, electrodesiccation, and

dermabrasion)

C. NEVI (ACQUIRED AND CONGENITAL)- Depending on the location of nevus cells, acquired melanocytic nevi are classified as junctional, compound,

or dermal. (This classification does not represent different types of nevi, but rather different stages in nevus maturation.)

- nevus cells accumulate in the epidermis (junctional)As they mature, nevus cells migrate partially into the dermis (compound) finally rest completely within dermal tissues (dermal)Eventually most lesions undergo involution

- Congenital nevi are relatively rare, and may be found in less than 1% of neonates. - These lesions are larger and often contain hair. - Histologically, congenital and acquired nevi appear similar. - Giant congenital lesions (giant hairy nevi) most often occur in a swim trunk distribution, chest, or back- Not only are these lesions cosmetically unpleasant, but congenital nevi may develop into malignant

melanoma in 1 to 5% of cases- Total excision of the nevus is the treatment of choice; however, the lesion is often so large that

inadequate tissue for wound closure precludes complete resection. Instead, serial excisions with local tissue expansion/advancement are frequently required over several years

VASCULAR TUMORS OF THE SKIN AND SUBCUTANEOUS TISSUE- Hemangiomas: benign vascular neoplasms that present soon after birth

- They initially undergo rapid cellular proliferation over the first year of life, then undergo slow involution throughout childhood.

- Histo:, composed of mitotically active endothelial cells surroundings several, confluent blood-filled spaces.

- Although these lesions may enlarge significantly in the first year of life, approximately 90% involute over time.

- Acute treatment is limited to hemangiomata that interfere with function, such as airway, vision, and feeding. In addition, lesions resulting in systemic problems, such as thrombocytopenia or high-output cardiac failure, should prompt resection.

- The growth of rapidly enlarging lesions also can be halted with systemic prednisone or interferon alpha-2a treatment use.

- In the absence of acute surgical indications or significant patient/parent concern, many lesions are allowed to spontaneously involute. However, hemangiomata that remain into adolescence or involute to leave an unsightly telangiectasia typically require surgical excision for optimal resolution

- Vascular malformations:A result of structural abnormalities formed during fetal developmentGrow in proportion to the body and never involuteHisto: they contain enlarged vascular spaces lined by nonproliferating endothelium

**arteriovenous malformations: high flow lesions that often present as subcutaneous masses associated with locally elevated temperature, dermal stain, thrill, and bruit. In addition, overlying ischemic ulcers, adjacent bone destruction, or local hypertrophy may occur

Very large malformations may cause cardiac enlargement and congestive heart failure. Complications of arteriovenous malformations, such as pain, hemorrhage, ulceration, cardiac effects,

or local tissue destruction, should prompt attempts at lesion destruction.Therapy consists of surgical resection. Even when complete lesion resection is not possible,

significant debulking may greatly diminish symptomatology. In addition, angiography with selective embolization just before surgery greatly facilitates operative

removal**capillary malformation (port-wine stain): a flat, dull-red lesion often located on the trigeminal nerve (cn5) distribution on the face, trunk or extremities

(+) presentation within the V1 or V2 facial regions possible link to Sturge-weber syndrome (leptominingeal angiomatosis, epilepsy, glaucoma); if midface (may signify Churg-strauss syndrome)

histo: composed of ecstatic capillaries lined by mature endotheliumtx: pulsed cye laser, cosmetics, surgical excision

**glomus tumor: uncommon, benign neoplasm of the extremity; <1.5% of all benign, soft tissue tumors; arise from dermal neuromyoarterial apparatus (glomus bodies)


most commonly affects the hand and presentation w/n the subungal region of the toe is raredx: traditionally delayedsx: severe pain, point tenderness, cold sensitivityappear as blue, subungual discolorations of 1-2mmTOC: tumor excision

A. SOFT-TISSUE TUMORS (ACROCHORDONS, DERMATOFIBROMAS, LIPOMAS)- lipomas: most common subcutaneous neoplasm

- found most frequently on the trunk but may appear anywhere- typically soft and fleshy on palpation- may grow to a large size and become deforming- histo: a lobulated tumor comosed of normal fat cells- benign with essentially no risk of malignant development- surgical excision is required for removal

- Acrochordons (skin tags) are fleshy, pedunculated masses located on the preauricular areas, axillae, trunk, and eyelids

- composed of hyperplastic epidermis over a fibrous connective tissue stalk- usually small, and are frequently treated via "tying off" or with resection in the clinic.

- Dermatofibromas are solitary, soft-tissue nodules usually approximating 1 to 2 cm in diameter, and are found primarily on the legs and flanks.

- Histologically, these lesions are composed of unencapsulated connective tissue whorls containing fibroblasts

- Although a majority of dermatofibromas can be diagnosed clinically, atypical presentation or course should prompt excisional biopsy to assess for malignancy.

- Although these tumors may be managed conservatively, operative removal is the treatment of choice.

B. NEURAL TUMORS (NEUROFIBROMAS, NEURILEMOMAS, GRANULAR CELL TUMORS)neurofibromas neurilemomas Granular cell tumors

- benign, cutaneous neural tumors- primarily arise from the nerve sheath- can be sporadic and solitary- majority are associated with

cafe au lait spots, Lisch nodules, and an autosomal dominant inheritance (von Recklinghausen's disease)

- firm, discrete nodules attached to a nerve.

- Histologically, proliferation of perineurial and endoneurial fibroblasts with Schwann cells embedded in collagen are noted

- solitary tumors arising from cells of the peripheral nerve sheath

- discrete nodules that may induce local or radiating pain along the distribution of the nerve.

- Microscopically, the tumor contains Schwann cells with nuclei packed in palisading rows.

- Surgical resection is the management option of choice.

- usually solitary lesions of the skin or, more commonly, the tongue

- consist of granular cells derived from Schwann cells that often infiltrate the surrounding striated muscle.

- Based on the severity of symptomatology, operative resection is the primary therapy of choice.

MALIGNANT TUMORS OF THE SKIN- Although malignancies arising from cells of the dermis or adnexal structures are relatively uncommon, the

skin is frequently subject to epidermal tumors, such as basal cell carcinoma (BCC), SCC, and melanoma.- Key factor perhaps of greatest significance - exposure to UV radiation = development of all skin cancer- those with risk/ risk factors:

persons with outdoor occupations those with fair complexions people living in regions receiving higher per capita sunlight albino individuals of dark-skinned races are prone to develop cutaneous neoplasms that are typically

rare in nonalbino members of the same group (This observation suggests that melanin, and its ability to limit UV radiation tissue penetration, plays a large role in carcinogenesis protection.)

Skin cancer development also has been strongly linked to chemical carcinogens such as tar, arsenic, and nitrogen mustard.

Radiation therapy directed at skin lesions increases the risk for local BCC and SCC. As an ongoing area of intense research interest, certain subtypes of HPV have been linked to SCC. Additionally, chronically irritated or nonhealing areas such as burn scars, sites of repeated bullous skin

sloughing, and decubitus ulcers present an elevated risk of developing SCC. Systemic immunologic dysfunction is also related to an increase in cutaneous malignancies. Immunosuppressed patients receiving chemotherapy those with advanced HIV/AIDS immunosuppressed transplant recipients have an increased incidence of BCC, SCC, and melanoma

A. BASAL CELL CARCINOMA- arising from the basal layer of the epidermis- most common type of skin cancer- divided into several subtypes: nodular, superficial spreading, micronodular, infiltrative, pigmented,

morpheaform- Nodulocystic or noduloulcerative type - 70% of BCC tumors

- Waxy and frequently cream colored, these lesions present with rolled, pearly borders surrounding a central ulcer.

- superficial basal cell tumors - commonly occur on the trunk and form a red, scaling lesion, pigmented BCC lesions are tan to black in color

- Morpheaform BCC often appears as a flat, plaque-like lesion.- considered relatively aggressive and should prompt early excision.

- A rare form of BCC is the basosquamous type, which contains elements of both basal cell and squamous cell cancer.

- These lesions may metastasize similar to SCC, and should be treated aggressively.- BCCs are slow growing, and metastasis is extremely rare.- px often neglect these lesions for years and presentation with extensive local tissue destruction is common


- majority of small (less than 2 mm), nodular lesions may be treated via curettage, electrodesiccation, or laser vaporization.

***Although effective, these techniques destroy any potential tissue sample for confirmatory pathology diagnosis and tumor margin analysis.

- Surgical excision may be used to both effect complete tumor removal as well as allow proper laboratory evaluation.

- Basal cell tumors located at areas of great aesthetic value, such as the cheek, nose, or lip, may be best approached with Mohs' surgery.

- specialized dermatology surgeons: Mohs' surgery uses minimal tissue resection and immediate microscopic analysis to confirm appropriate resection.

- Large tumors, those that invade surrounding structures, and aggressive histologic types (morpheaform, infiltrative, and basosquamous) are best treated by surgical excision with 0.5-cm to 1-cm margins

B. SQUAMOUS CELL CARCINOMA*** Although basal cell carcinoma is the most common tumor involving the head and neck, squamous cell carcinoma (pictured here) occurs with high frequency on the nose, ears, and lower lip.

- arise from epidermal keratinocytes- less common than BCC- more devastating due to invasiveness and tendency to metastasize- Bowen’s disease – in situ SCC before local invasion- Erythroplasia of Queyrat – in situ SCC tumors specific to the penis- >4mm in thickness = tumor recurrence more prevalent- ≥10mm in diameter = lesions that metastasize- tumor location-also of great prognostic importance- Although SCC tumors in areas with cumulative solar damage are less aggressive, and respond well to local

excision, lesions arising in burn scars (Marjolin's ulcer), areas of chronic osteomyelitis, and areas of previous injury metastasize early

- Although small lesions can be treated with curettage and electrodesiccation, most surgeons recommend surgical excision.

- Lesions should be excised with a 1-cm margin, and histologic confirmation of tumor-free borders is mandatory.

- Tumors within areas of great aesthetic value, such as the cheek, nose, or lip, may be best approached with Mohs' surgery.

- Moh’s surgery: precise, specialized surgical technique; uses minimal tissue resection and immediate microscopic analysis to confirm appropriate resection yet limit removal of valuable anatomy

- Regional LN excision is indicated for clinically palpable nodes.- SCC lesions arising in chronic wounds are more aggressive and regional lymph node metastases are

observed more frequentlylymphadenectomy before development of palpable nodes (prophylactic LN dissection) is indicated

- Metastatic disease is a poor prognostic sign, and only 13% of patients typically survive 10 years

***MOH’S SURGERY FOR SCC AND BCC- basal and squamous cell lesions often present on sun-exposed portions of the body such as the head and

face. - Mohs' technique uses serial excision in small increments coupled with immediate microscopic analysis to

ensure tumor removal, yet limit resection of aesthetically valuable tissue.- One distinct advantage of Mohs' technique is that all specimen margins are evaluated. - In contrast, traditional histologic examination surveys selected portions on surgical margin. - The major benefit of Mohs' technique is the ability to remove a tumor with minimal sacrifice of uninvolved

tissue.- Useful for managing tumors of the eyelid, nose, or cheek, but one major drawback is procedure length. - Total lesion excision may require multiple attempts at resection, and many procedures may be carried out

over several days. - Recurrence and metastases rates are comparable to those of wide local excision

C. MALIGNANT MELANOMA- melanoma may arise from transformed melanocytes anywhere that these cells have migrated during normal

embryogenesis- nevi (freckles) – benign melanocytic neoplasms on the skin; dysplastic nevi contain a histologically

indentifiable focus of atypical melanocytes; intermediate stage between a benign nevus and a true malignant melanoma

- up to 14% of malignant melanomas occur in a familial pattern = family members = risk- melanocytemalignant phenotypetumor growth occurs radially in the epidermal planevertical growth

phase (cells develop different cell-curface antigens and their malignant bahavior becomes more aggressive- eye and anus are notable sites; >90% of melanomas are found on the skin- 4% of tumors are discovered as metastases w/o any identifiable primary site- 5-10% of melanomas are non pigmented- suspicious feats: any pigmented lesion with an irregular border, darkening coloration, ulceration, raised

surface; most critical to note recent changes in nevus appearance that may denote malignant transformation

- metastases do not occur until melanocytes form dermal nests- in order of decreasing frequency: 4 types of melanoma:

1. superficial spreading – most common type – 70% of melanomas – occur anywhere on the skin except hands and feet – typically flat and measure 1-2cm in diameter at diagnosis; before vertical extension, a prolonged radial growth is characteristic

2. nodular – 15-30% of melanomas – typically of darker coloration and often raised; noted for lack of radial growth; all are in the vertical growth phase at Dx; same prognosis as superficial spreading but considered to be more aggressive

3. lentigo maligna – 4-15% of melanomas; occurs most frequently on the neck, face, hands of the elderly; large at Dx but have the best prognosis because invasive growth occurs late; <5% are est. to evolve into melanoma


4. acral lentiginous – least common – 2-8% of melanomas in white populations – rare in dark skin; 29-72% of all melanomas in dark skinned people; palms, soles, subungual regions; most common on the great toe or thumb, subungual lesions appear as blue-black discolorations of the posterior nail fold***subungual melanoma – Hutchinson’s sign is diagnostic (presence of pigmentation in the proximal or lateral nail folds

- significant prognostic indicators:1. Independent of histologic type and depth of invasion, those with lesions of the extremities have a

better prognosis than patients with melanomas of the head, neck, or trunk (10-year survival rate of 82% for localized disease of the extremity compared to a 68% survival rate with a lesion of the face).

2. Lesion ulceration carries a worse prognosis. The 10-year survival rate for patients with local disease (stage I) and an ulcerated melanoma was 50% compared to 78% for the same stage lesion without ulceration.

3. incidence of ulceration = thickness, from 12.5% in melanomas less than 0.75 mm to 72.5% in melanomas greater than 4.0 mm.

4. tumors ulcerate as the result of increased angiogenesis.5. Gender is also a substantial prognostic indicator. 6. females have an improved survival compared to males; Women tend to acquire melanomas in more

favorable anatomic sites, and these lesions are less likely to contain ulceration. After correcting for thickness, age, and location, females continue to have a higher survival rate than men (10-year survival rate of 80% for women vs. 61% for men with stage I disease).

- most current staging system (American Joint Committee on Cancer or AJCC) – best method of interpreting clinical info in regard to prognosis of disease:

evidence of tumor in regional LNs=poor prognostic sign associated w a precipitous drop in survival at 15-yr follow up

based on the TNM tumor staging system=this finding advances and classification from stage I or II to stage III distant metastasis=worst prognostic sign (stage IV disease)

Historically, the vertical thickness of the primary tumor (Breslow thickness) and the anatomic depth of invasion (Clark level) have represented the dominant factors in the T classification.

The T classification of lesions comes from the original observation by Clark that prognosis is directly related to the level of invasion of the skin by the melanoma.

Whereas Clark used the histologic level [I, superficial to basement membrane (in situ); II, papillary dermis; III, papillary/reticular dermal junction; IV, reticular dermis; and V, subcutaneous fat], Breslow modified the approach to obtain a more reproducible measure of invasion by the use of an ocular micrometer.

The lesions were measured from the granular layer of the epidermis or the base of the ulcer to the greatest depth of the tumor (I, 0.75 mm or less; II, 0.76 to 1.5 mm; III, 1.51 to 4.0 mm; IV, 4.0 mm or more).

- Dx of melanoma typically requires excisional biopsy: 1mm margin of normal skin is taken if the wound can be closed primarily; if removal of the entire lesion is too large a defectincisional bipsy of a representative partsubsequent wide excision of the bipsy site may be done


- Tx of melanoma may range from simple excision to more complex lymphadenectomy or immunotherapy

- surgical excision is the management of choice: Lesions 1 mm or less in thickness can be treated with a 1-cm margin. For lesions 1 mm to 4 mm thick, a 2-cm margin is recommended. Lesions of greater than 4 mm may be treated with 3-cm margins.The surrounding tissue should be removed down to the fascia to remove all lymphatic channels. If the deep fascia is not involved by the tumor, removing it does not affect recurrence or survival rates, so the fascia is left intact.

- With lesions deeper than 4 mm, it is highly likely that the tumor cells already have spread to the regional LNs and distant sites. Removal of the melanomatous LNs has no effect on survival. Most of these patients die of metastatic disease before developing problems in regional nodes.

- Others:1. prophylactic dissection – intermediate thickness tumors (T2 and T3, 1-4.0mm); no clinical evidence of

metastasis or nodal disease - survival but still controversial2. sentinel lymphadenectomy – for malignant melanoma3. complete LN dissection – micrometastasis is identified in the removed node by frozen section

examination4. regional nodal dissection – microscopically or clinically positive LNs; groin LNs removeddeep iliac

nodes must be removed + superficial inguinal nodes to avoid recurrence of disease5. axillary dissections – nodes medial to the pectoralis minor muscle must also be resected6. superficial parotidectomy + modified neck dissection – for lesions on the face, anterior scalp, and ear

- Once melanoma has spread to a distant site, median survival is 7 to 8 months and the 5- year survival rate is less than 5%.

- Solitary lesions in the brain, GI tract, or skin that are symptomatic should be excised when possible.


- cure is extremely rare, degree of palliation can be high and asymptomatic survival prolonged.- in-transit disease (local disease in lymphatics) develops in 5 to 8% of melanoma patients with a high-risk

primary melanoma (>1.5mm).- Hyperthermic regional perfusion with a chemotherapeutic agent (e.g., melphalan) is presently the treatment

of choice. - The goal of regional perfusion therapy is to increase the dosage of the chemotherapeutic agent to maximize

tumor response while limiting systemic toxic effects.- Melphalan generally is heated to an elevated temperature [up to 41.5Â°C, (106.7Â°F)] and perfused for 60 to

90 minutes. Although difficult to perform and associated with complications (neutropenia, amputation, death), it does produce a high response rate (greater than 50%).

- The introduction of tumor necrosis factor alpha or interferon-with melphalan results in the regression of more than 90% of cutaneous in-transit metastases.

- High-dose-per-fraction radiation produces a better response rate than low-dose large-fraction therapy.- As the treatment of choice for patients with symptomatic multiple brain metastases, radiation therapy

produced measurable improvement in tumor size, symptomatology, or performance status in 70% of treated patients.

- Interferon alfa-2b is the only Food and Drug Administration approved adjuvant treatment for AJCC stages IIB/III melanoma. Side effects were common and frequently severe; the majority of the patients required modification of the initial dosage and 24% discontinued treatment.

- Melanoma cells contain a number of distinctly different cell-surface antigens, and monoclonal antibodies have been raised against these antigens.

- These antibodies have been used alone or linked to a radioisotope or cytotoxic agent in an effort to selectively kill tumor cells.

- Gangliosides are carbohydrate antigens found on the surface of melanomas as well as many other tumors.

ADDITIONAL MALIGNANCIES OF THE SKINA. MERKEL CELL CARCINOMA (PRIMARY NEUROENDOCRINE CARCINOMA OF THE SKIN)- actually of neuroepithelial differentiation- associated with a synchronous or metasynchronous SCC 25% of the time- aggressive- tx: wide local resection with 3cm margins - local recurrence rates; distant metastases (1/3 of px)prophylactic regional LN dissection and adjuvant

radiation therapy- overall prognosis is worse than for malignant melanoma

B. KAPOSI’S SARCOMA- KS: appears as rubbery bluish nodules that occur primarily on the extremities but may appear anywhere on

the skin and viscera- Usually multifocal rather than metastatic.- Histo: lesions are composed of capillaries lined by atypical endothelial cells- Early lesions may resemble hemangiomas, while older lesions contain more spindle cells and resemble

sarcomas.- Classically, KS is seen in people of Eastern Europe or sub-Saharan Africa. - locally aggressive but undergo periods of remission- (+) AIDS or with immunosuppression from chemotherapy - occurs primarily in male homosexuals and not in

IV drug abusers or hemophiliacs. In this form of the disease, the lesions spread rapidly to the nodesGI and respiratory tract often are involved.

- AIDS-related KS is associated with concurrent infection with a herpes-like virus.- Tx for all types of KS consists of radiation to the lesions. Combination chemotherapy is effective in controlling

the disease, although most patients develop an opportunistic infection during or shortly after treatment. - Surgical treatment is reserved for lesions that interfere with vital functions, such as bowel obstruction or

airway compromise

C. EXTRAMAMMARY PAGET’S DISEASE- histologically similar to the mammary type- a cutaneous lesion that appears as a pruritic red patch that does not resolve- biopsy: demonstrates classic Paget’s cells- paget’s disease – thought to be a cutaneous extension of an underlying adenocarcinoma, although an

associated tumor cant always be demonstrated

D. ANGIOSARCOMA- may arise spontaneously- mostly on scalp, face, neck- usually appear as a bruise that spontaneously bleeds or enlarges w/o trauma- Stewart-Treves syndrome – tumors may also arise in areas of prior radiation therapy/in the setting of chronic

lymphedema of the arm (such as mastectomy)- Tumor consists of anaplastic endothelial cells surrounding vascular channels- Tx: total excision (occasional cure); for palliation: chemotherapy and radiation therapy- Prognosis: usually poor; 5-yr survival rates = <20%

E. DERMATOFIBROSARCOMA PROTUBERANS- DFSP: accounts for 1 to 2% of all soft-tissue sarcomas, occurs most frequently in persons aged 20 to 50

years, and is more common in males.- most common presenting location is on the trunk (50 to 60%), although the proximal extremities (20 to 30%

of cases), as well as head and neck also are frequently affected (10 to 15%).- often appears as a pink, nodular lesion that may ulcerate and become infected- Histo: the lesions contain atypical spindle cells, probably of fibroblast origin, located around a core of

collagen tissue - Despite what appears to be complete lesion excision, local recurrence remains frequent and mortality

associated with metastasis relatively high.- minimum resection margin needed to achieve local control remains undefined- Local recurrence rates = 50% (after simple excision), and 20% (wide local excision with 3-cm margins)


- Most authorities seem to advocate a three-dimensional margin of 2 to 3 cm with resection of skin, subcutaneous tissue, and the underlying investing fascia.

- The periosteum and a portion of the bone may also need to be resected to achieve negative deep surgical margins.

- wide macroscopic resectionconformation of negative microscopic - considered to be a radiosensitive tumor, and radiotherapy following wide local excision local control rates

approximating 95% at 10 years- Imatinib, a selective inhibitor of platelet-derived growth factor (PDGF) -chain alpha and PDGF receptor beta

protein-tyrosine kinase activity, alters the biologic effects of deregulated PDGF receptor signaling. - Clinical trials have shown activity against localized and metastatic DFSP containing the t(17:22) translocation,

suggesting that targeting the PDGF receptors may become a new therapeutic option for DFSP.

F. FIBROSARCOMA- hard, irregular masses found in the subcutaneous fat- fibroblasts appear markedy anaplastic w disorganized growth- if not excised metastasis- 5 yr survival rate after excision = 60%

G. LIPOSARCOMA- arise in the deep muscle planes (and rarely from the subcutaneous tissue)- occur most commonly on the thigh- enlarging lipoma: excised and inspected to distinguish it from liposarcoma- TOC: wide excision (radiation therapy reserved for metastatic disease)

SYNDROMIC SKIN MALIGNANCIES1. basal cell (Gorlin’s) syndrome- linked with BCC- an autosomal dominant disorder characterized by the growth of hundresds of BCCs during young adulthood- palmar and plantar pits – common physical findings; represent foci of noplasms- tx: excision of aggressive and symptomatic lesions2. nevus sebaceous of Jadassohn- linked with BCC- a lesion containing several cutaneous tissue elements that develop during childhood- associated w a variety of neoplasms of the epidermis as well3. skin diseases that cause chronic wounds (epidermolysis bullosus and lupus erythematosus

- associated with incidence of SCC4. epidermodysplasia verruciformis- associated with infection with HPV- a rare autosomal recessive disease- large verrucous lesions develop early in life- often progress to invasive SCC in middle age5. xeroderma pigmentosum- associated with a defect in cellular repair of DNA damage- an autosomal recessive disease- inability of the skin to correct DNA damage from UV radiation = px prone to cutaneous malignancies6. familial dysplastic nevus syndrome- an autosomal dominant disorder- px develops multiple dysplastic nevi- almost 100% incidence of melanoma- tx: close surveillance and frequent biopsy of all suspicious lesions

**SCCs are most frequent**dysplastic nevi – considered precursor to melanoma**colon cancer can be arrested w total proctocolectomy

FUTURE DEVELOPMENTS IN SKIN SURGERY- autologous skin grafts – best method to cover skin defects- tissue expansion w subcutaneous balloon implants – produces new epidermis and mobilization via expansion

= wound coverage- engineered skin replacements- in clinical use: several dermal replacements based on synthetic materials or cadaveric sources- bovine-collagen and shark-proteoglycan based dermis (Integra) for burns; prosthetic dermis, available in

ready-to-use form, can cover large surface areas- Vascularization of this dermis takes 2 - 3 weeks, and final epidermal coverage of the wound requires a thin

skin graft. The final result is functionally and aesthetically good but cost - Cadaveric dermis, with all of the cellular elements removed - not antigenic and is not rejected by the

recipient patient. This human dermal matrix is commercially-available (AlloDerm) and functions much like Integra, with similar limitations of engraftment and cost.

- Both forms of dermal replacements are more frequently used in delayed reconstruction of burn patients than in the acute setting

CONCLUSION “Anatomically, the epidermal, basement membrane, and dermal layers of the skin each play a vital role in maintaining dermal/epidermal integrity. Multiple, complex mechanisms within these soft tissues protect us from injury as well as relay external information along a vast neural network. In addition to penetrating trauma, the environment offers a host of potentially injurious elements such as caustic substances, extreme temperatures, prolonged or excessive pressure, and radiation. Infections ranging from simple bacterial to necrotizing, life-threatening disease may also affect the skin and subcutaneous tissues. Perhaps of greatest public concern, a multitude of benign and malignant tumors threaten to disrupt, disfigure, and invade normal skin structure. Although the risks associated with many of these lesions are great, a broad variety of medical and surgical management options currently exist. Although contemporary medicine may not have an optimal answer for each threat the skin may face, continued research, advances in our understanding, and technical improvements in the field promise to enhance our ability to replace and protect the skin well into the future.”


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