Grabb and Smith's Plastic Surgery, 7th Edition [PDF]

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GRABB AND SMITH'S

PLASTIC SURGERY Seventh Edition

GRABB AND SMITH'S

PLASTIC SURGERY Seventh Edition

Editor-in-Chief Charles H. Thorne, MD Associate Professor of Plastic Surgery NYU Medical Center New York, New York

Editors Kevin C. Chung, MD, MS

Babak J. Mehrara, MD

Charles B. G. de Nancrede Professor of Surgery Section of Plastic Surgery, Department of Surgery Professor of Orthopaedic Surgery Assistant Dean for Faculty Affairs Associate Director of Global REACH University of Michigan Medical School Ann Arbor, Michigan

Associate Attending, Department of Surgery Memorial Sloan-Kettering Cancer Center Associate Professor of Surgery Weill Cornell University Medical Center New York, New York

J. Peter Rubin, MD

Division Head, Plastic Surgery Ann & Robert H. Lurie Children's Hospital of Chicago Professor of Plastic Surgery Northwestern University Feinberg School of Medicine Chicago, Illinois

UPMC Endowed Professor and Chair, Department of Plastic Surgery Professor of Bioengineering Director, Life After Weight Loss Body Contouring Program University of Pittsburgh and UPMC Pittsburgh, Pennsylvania

Geoffrey C. Gurtner, MD

ScoH l. Spear, MD

Professor, Department of Surgery Stanford University School of Medicine Stanford, California

Professor, Department of Plastic Surgery Georgetown University Medical Center Washington, District of Columbia

Arun K. Gosain, MD

• .. Wolters Kluwer II Lippincott Williams &Wilkins Health Philadelphia· Baltimo·re ·New York · Lo:ndon Buenos Aires · Hong Kong· Sydney· Tokyo

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p.;cm. Plastic surgery Preceded by Grabb and Smith's plastic surgery I editor-in-chief, Charles H. Thorne ... [et al.] ; editors Robert W. Beasley ... [et al.]. 6th ed. 2007. Includes bibliographical rekrences and index. ISBN 978-1-4511-0955-9 I. Thorne, Charles, 1952- editor of compilation. II. Chung, Kevin C., editor of compilation. III. Gosain, Arun, editor of compilation. IV. Guntner, Geoffrey C., editor of compilation. V. Mehrara, Babak Joseph, editor of compilation. VI. Title: Plastic surgery. [DNLM: 1. Reconstructive Surgical Procedures. 2. Cosmetic Techniques. 3. Surgery, Plastic. W0600] RD118 617.9'5-dc23 2013017779 Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication. Application of the information in a particular situation remains the professional responsibility of the practitioner. The authors, editors, and publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accordance with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new or infrequently employed drug. Some drugs and medical devices presented in the publication have Food and Drug Administration (FDA) clearance for limited use in restricted research settings. It is the responsibility of the health care provider to ascertain the FDA status of each drug or device planned for use in their clinical practice. To purchase additional copies of this book, call our customer service department at (800) 6383030 or fax orders to (301) 223-2320. International customers should call (301) 223-2300. Visit Lippincott Williams & Wilkins on the Internet: at LWW.com. Lippincott Williams & Wilkins customer service representatives are available from 8:30 am to 6 pm, EST.

To our patients who have inspired, humbled, frustrated,

and taught us, and without whom this book would have no reason to exist. --Charles H. Thorne, MD

David M. Adelman, MD, PhD

Scott P. Bartlett, MD

Assistant Profeuor Department of Plastic Surgery The University of Texas MD Anderson Cancer Center Houston, 'Thxas

ProkNo;Dep~mt~S~ery

Jamil Ahmad, MD Staff Plastic Surgeon The Plastic Surgery Clinic Mississauga, Ontario

AIS. Aly, MD Profeuor Ae&thet.ic & Plastic Surgery Institute Univeraity of California Irvine Orange, California

Perelman School of Medicine at the University of Pennsylvania Chief, Division of Plastic Surgery Children's Hospital of Philadelphia Philadelphia, PeMsylvaoia

Fritz E. Bart.n, Jr., MD ProkNo; Plastic Surgery Univeraity of Texas Soutlrwestun Medical Center Dallas, Texas

Nichalas Bastidas, MD Attmding Physician

North Shore-Uj Health System New York, New York

Katerina Anuli, MD, MRCS

Bruce S. Iauer, MD

CliDical Fellow Department of Plastic and Reconstructive Surgery Guy's and StThomas' NHS Trust London, United KiDgdom

CliDical Professor of Surgery, Plastic Surgery University ~Chicago, Pritzker School ~Medicine Chicago, Dlinois Chief, Division of Plastic and ~tructive Surgery North Shore University Health System Highland Park, Illinois

Mark W. Ashtan, MD Head, Rb::oD.Structive Plastic Surgery Royal Melbourne Hospital Victoria, Australia

Christapher E. Allinger, MD Profe.ooor, Department of Plastic Surgery Georgetown University Washington, District of Columbia

Kocli Azari, MD Associate Professor Department of Orthopaedic Surgery and Division of Plastic Surgery David Geffen School of Medicine at UCLA Los Angeles, California

Sl8phen B. Baker, MD, DDS Profe.ooor and Program Director Department of Plastic Surgery Georgetown University Hospibll Washington, District of Columbia Co-Director Craniofacial Anomalies Program INOVA Fairfax Hospital for Children Falls Church, Vuginia

Karim Bakri, MD Chief Resident Division of Plastic S~y Mayo Clinic Rochester, Minnesota

Michael S. leckenstein, MD Alabama Breast Surgery Center Binninglwn, Alabama

Keith M. Blechman, MD Chief R.esidmt Institute for Reconstructive Plastic Surgery New York University School of Medicine New York, New York

George C. Bahle Ill, DDS Implant & Proslhodontic Associates Oklahoma City, Oklahoma

James P. Bradley, MD ProkNo; Sarnat Chair Division of Plastic Surgery University of California, Los Angeles Los Angeles, California

Gerald lrandacher, MD Associate Professor Depattment ~Plastic and Reconstructive Surgery Johns Hopkins University School ~Medicine Baltimore, Maryland

Danald W. luck II, MD Division of Plastic & R«onstructive Surgery Nortlrwestun University Chicago, Dlinois

Contributing Authors

Louis P. Bucky, MD

Daniel J. Ceradini, MD

Clinical Professor Department of Surgery University of Pennsylvania School of Medicine Chief of Plastic Surgery Pennsylvania Hospital Philadelphia, Pennsylvania

Assistant Professor Department of Plastic Surgery New York University School of Medicine Chief of Plastic Surgery Manhattan Veterans Administration Hospital New York, New York

Due T. Bui, MD

Beniamin Chang, MD

Associate Professor of Surgery Department of Surgery Director, Reconstructive Breast Surgery Division of Plastic and Reconstructive Surgery Stony Brook School of Medicine Stony Brook, New York

Associate Professor of Clinical Surgery Division of Plastic Surgery The Perelman School of Medicine at the University of Pennsylvania Attending Surgeon Division of Plastic Surgery The Children's Hospital of Philadelphia Philadelphia, Pennsylvania

Renee M. Burke, MD Plastic Surgeon Department of Surgery Good Shepherd Hospital Barrington, Illinois Plastic Surgeon Chicago Aesthetic Surgery Institute Rosemont, lllinois

Mary C. Burns, OTR/1., CHT Assistant Professor Department of Surgery Southern Illinois University School of Medicine Certified Hand Therapist Division of Plastic Surgery Southern Dlinois University School of Medicine Hand Therapy Center Springfield, Illinois

Chartes E. Butler, MD Professor with Tenure Department of Plastic Surgery The University of Texas MD Anderson Cancer Center Houston, Texas

Dominick Cannavo, MD

James Chang, MD Professor, Departments of Surgery (Plastic Surgery) & Orthopaedic Surgery Stanford University Medical Center Chief, Division of Plastic & Reconstructive Surgery Stanford University Medical Center Palo Alto, California

Johnny T. Chang, MD, MSME Division of Plastic Surgery Brown Medical School Providence, Rhode Island

David W. Chang, MD Professor, Department of Plastic Surgery M.D. Anderson Cancer Center Houston, Texas

Harvey Chim, MBBS Chief Resident, Plastic Surgery Case School of Medicine Cleveland, Ohio

New York, New York

Manhew S.S. Choi, MD

Joseph N. Carey, MD

Associate Professor of Plastic Surgery Department of Plastic and Reconstructive Surgery Hanyang University College of Medicine Seoul, South Korea Chief, Department of Plastic and Reconstructive Surgery Hanyang University Guri Hospital Guri, Gyunggi-do, South Korea

Assistant Professor Division of Plastic Surgery University of Southern California Chief, Plastic Surgery LAC + USC Medical Center Los Angeles, California

Brian T. Carlsen, MD Assistant Professor Division of Plastic Surgery, Division of Hand Surgery Mayo Clinic Rochester, Minnesota

Grant W. Cartson, MD Professor of Surgery Emory University Wadley R. Glenn Professor of Surgery, Chief of the Division of Plastic Surgery Emory University Hospital Atlanta, Georgia

J. Guilherme Christiano, MD Assistant Professor Division of Plastic Surgery University of Rochester Rochester, New York

Kevin C. Chung, MD, MS Charles B. G. de Nancrede Professor of Surgery Section of Plastic Surgery, Department of Surgery Professor of Orthopaedic Surgery Assistant Dean for Faculty Affairs Associate Director of Global REACH University of Michigan Medical School Ann Arbor, Michigan

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Contributing Authors

Mark W. Clemens, MD

MaHhias B. Donelan, MD

~s~tantPro~sor

Chief, Plastic Surgery Department of Surgery Shriners Hospitals for Children-Boston ~sociate Clinical Professor of Surgery Harvard Combined Plastic Surgery Residency Training Program Harvard Medical School Boston, Massachusetts

Department of Plastic Surgery MD Anderson Cancer Center Houston, Texas

Mark A. Codner, MD ~s~tantPro~sor

Department of Plastic Surgery Emory University Atlanta, Georgia

Stephen H. Colbert, MD ~s~tantPro~sor

Department of Surgery University of Missouri Head, Hand & Microsurgery Division of Plastic Surgery University of Missouri Health Care Columbia, Missouri

Damon S. Cooney, MD, PhD ~s~tant Professor of Plastic and Reconstructive Surgery Johns Hopkins University School of Medicine Baltimore, Maryland

Peter G. Cordeiro, MD Chief, Plastic & Reconstructive Surgery Memorial Sloan-Kettering Cancer Center New York, New York

Russell J. CorleH, MD Jack Brockhoff Reconstructive Plastic Surgery Research Unit Department of Anatomy and Cell Biology University of Melbourne Melbourne, Australia

Catherine M. Curtin, MD Staff Physician Department of Surgery Palo Alto Veterans Hospital ~mtant Professor Division of Plastic Surgery Stanford University Palo Alto, California

Daniel Alexander Del Vecchio, MD, MBA ~sociate Clinical Staff Department of Surgery Massachusetts General Hospital Boston, Massachusetts

Christopher A. Derderian, MD ~mtant Professor Department of Plastic Surgery UT Southwestern Medical Center Pediatric and Craniofacial Surgery Children's Medical Center Dallas, Texas

Susan E. Downey, MD ~sociate Clinical Professor Department of Surgery (Plastic) II FIGURE 1.12. Importance of the pivot point. A skin flap rotated about a pivot point becomes shortx:r in effective length the farther it is rotated. Planning with a cloth pattern is helpful when designing sucha&ap.

t
alfentanil > remifentanil. Alexander14 has shown that decreased awareness (sedation) also markedly decreases the slope of ventilation in response to hypoxia following midazolam. Furthermore, the ventilatory response to C01 in a patient receiving midazolam is diminished to a greater extent and for longer duration in patiena with COPD.u Thus, individual titration to effect with careful monitoring is again the mainstay of sedative dosing. Amnesia, an additional component of sedation, is predominantly achieved through the use of beru:.odiazepines. It mast be appreciated though that aaually achieving amnesia is inconsistent. Specifically, in the absence of pain, little sedation is required to achieve amnesia. Pretreatment with a benzodiazepine, for example, S to 10 mg Valium, orally prior to OR entry should be considered. I£ benzodiazepines are administered after the patient feels pain, amnesia is not predic:table. Lastly, it is important to appreciate that while propofol and narcotics are not amnestic agena, they do synergize with benzodiazepines to help achieve this goal. In terms of monitoring the depth of anesthesia and there· fore awareness and amnesia, bifrontal referential ERG (BIS) has been used with variable success.1' The inconsistent results are likely a consequence of the muscle movement electromyogram artifact.

Oversedation A final consideration with respect to sedation is that of excess drug effect from a drug administration error, drug synergy, or a loss of offsetting noxious stimulus. In such a circumstance, the treatment approach is: 1. 2. 3. 4.

stimulate the patient and support the airway; administer supplemental oxygen; discontinue sedative drug administration; and lastly consider an intravenous drug antagonist if the excess effect is not attenuated or resolved by 1 to 3.

Toward that end, it is ideal to preferentially use sedative drugs with a short half-life or for which a specific antagonist is available. Narcotics can be antagonized with naloxone typically only requiring 20 to 40 J.lg (0.5 to 1 cc of 0.4 mg naloxone drawn up to a total volume of 10 cc). Benzodiazepines are antagonized with flumazenil typically requiring 0.1 to 0.3 mg (1 to 3 cc ofstandard concentration of 0.1 mglcc)P No facility where sedation is performed should be without these antagonists readily available. If only benzodiazepine has been administered, flumazenil should be utilized as naloxone would be of no benefit. If a patient has received both benzodiazepine

Chapter 11: Principle~ of Office Sedation for Co~mecic Surgery

and narcotic sedation, it is common to use naloxone first as the narcotic component is the more likely cause of the respiratory depression. Two other considerations are important. First;, when possible, titrate the antagonist to avoid a sympathetic surge from acute withdrawal. Second, if several rounds of antagonist do not have the desired effect; consider other diagnoses, for example, metabolic derangement or stroke.

Postoperative Nausea and Vomiting An important consideration with respect to any surgery is postoperative nausea and vomiting (PONV). This is particularly important in cosmetic surgery as PONV can detract from the perception of the overall experience, no matter how ideal the ou~me. Beyond the subjective implications, nausea and vomiting can also undermine the outcome, especially in procedures involving the head and neck. Specifically, during vomiting, as the intra-abdominal pressure is increased with a closed glottis, the intrathoracic pressure increases, thus impeding venous return. This may translate into oozing and more significantly the development of a wound hematoma. Vomiting is often accompanied by an increase in the blood pressure as well, which can further predispose to these complications. Prophylactic pretreatment is essential as preventing nausea is more easily accomplished and reliable than treating it. The use of low-dose intraoperative corticosteroids has become routine in plastic sw:gery and dexamethasone 10 mg has been shown to be efficacious in both preventing and treating PONV. The antiemetic mechanism of action is not well understood. It is thought that dexamethasone may antagonize prostaglandin or release endorphins that elevate mood, improve one's sense of well-being, and stimulate appetite. A useful multimodal algorithm also includes intraoperative administration of Ondansetron 4 to 8 mg IV along with the Decadron. Diabetes is a relative contraindication to Decadron as even this small amount of Decadron can play havoc with blood glucose control for 12 to 24 hours. A careful history should be taken preoperatively, and if a history of motion sickness is elicited, dimenhydrinate tablet po or a scopolamine patch applied preoperatively can also be very helpful.

*

Postoperative Pain While the mainstay of pain management has always been narcotics, this class of drugs is not without side effects such as constipation and more importantly nausea and vomiting. The COX-2 inhibitors as nonsteroidal anti-inflammatory drugs decrease the mediators of pain and inflammation without affecting platelet function. Beginning these drugs preoperatively and continuing them for 3 days postoperatively can greatly decrease narcotic usage and the resultant narcoticrelated adverse side effects.

99

CONCLUSION A safe outcome from an office procedure performed under IV sedation is predicated on patient preparation, planning, and technique. Further, in the same way that understanding the operation helps the anesthesiologist optimize outc:om.e, Wlderstanding the sedation can afford the same benefit to the surgeon. While what we have written may seem unnecessarily detailed in some regards and superficial in others, our goal is to provide a conceptllal understanding of procedural sedation beyond a simple knowledge of drug dosage and effect.

References 1. Sun Tzu S. In: Griffith SB, eel Thtt Art of W.v. Oxford: Oxford Uni1'enity Preas; 1971. 2. Fleisher LA, Beclanan JA. Brown KA, eta!. ACCIAHA 2007 guidelin~ on periopetlltive cardio.aaculu evalwuion IUid care fur noDcardia.c surgery: ll report of the AmeriCIUI College of Cudiology/American Heart Association Task Force on Practice Guidelin£6. Cirt::wltuion. 2007;11 6(17):e418-e500. 3. DiW. AR. D'Souu S, Shulman MS. Brief rniew: coronuy drug-eluting stents~U~d JU~.estheaia... Qm J AnMsih. 2006;53:1230-1243. 4. I.e Man.ach Y, Ibanez B. Cristina M, et a!. Impact of perioperative mtin ther11.py on adverse postoperllli,.e ouii:OID.eS in pll.tients undergoing ,.ucular sutgery. Analhl18iolog)l. 2011;114:98-104. S. Kral JG. Surgic.al trutment of obe6ity. In: Bjomtorp P, ed. lnumtlliontll Tatboolt of Obe&#)l. Hoboken, NJ: John Wiley&: Sons Ltd; 2001. 6. Practice guidelines fur preoperative luting AJ~d the use of ph.armt!.cologic agents to reduce the risk of pulmonary aspiration: appliation to healthy patients undergoing eltttive procedUI.'t6. A report by the American Society of Anesthesiologists Task Force on Preoperative Fasting. Anuthesiolog'y. 1999;90:896-905.

7. Batie Aneathetic Monitoring,. SWicWds for (FHective july 1, 2011). www. aaahq.org.. A.c~ December 11,2012. 8. Papadoniloliuis A. Wi~ler ER, Olympic MA, et a!. Avoiding cawtrophic oompliclll:ions of stroke and du.th relilted to shoulder surgery in the sitting poeition. Arthroscopy. 2008;24(4):481-482. 9. Cte,.oitier C, Ziegler WH, Edcert M, et a!. Rcllltionship between plasma ooncentrlllion and effect of midazolilm after oral and intravenous admini.trlltion. Br J CJi# Phllmlll«)/. 1983;16!51S-61S. 10. Simulation of Propofol Phal'Dlllcokinetict. http:/hllm.uest.ufl.edu. A.cceased December 11,2012. 11. Bekker A. ~ufman B, Samir H, eta!. The use of dexmedetomidine infusion for awake aaniotomy. A-.th Alullg. 2001;92:1251-1253. 12. Joint Colllmitsion on A.ccrediw:ion of healthcare organiutions.: Sentinel Event Alert 29: pre'f'eD1iDg S'IU'gial j!Uie 24, 2003. www.joiD.toommission.org 13. McAieavy J, Way W, Altstatt A, et al The effect of PC01 on the depth of mesthesia. Anl!ltheomlo&'J. 1961;22{2):260-264. 14. Alexander CM, Gross JB. Sedative doses of midazolam depr~ hypoxic n11tilatory respoDMS in humans. ~th Antllg. 1988;67:377-382. 15. Gross JB, Zebrowski ME, Carel WD, eta!. Tune~ of ftlllilatory depreJsion afu!r thiopemal and midazolilm in normal subjects and in patimts with cllroni~ obsiZUCtive pulmonary disuse. AneJtheomlogy. 1983;58:540.5+4. 16. Glass PS, Bloom M, I20 em) (Chapter 20). They have some poten· tial to develop melanoma, although this risk is low except in the giant variety. Except for size, the overall appearance of congenital melanocytic nevi and acquired nevi is similar.2 Congenital nevi, however, may have dark, thick hair. Histologically, congenital nevi are distinguished by the pres· ence of nevomelanocytes in the epidermis and in the dermis as sheets, nests, cords, or single cells. 2 For treatment, see Chapter 20 (Figure 13.3). Blue Nevus. Blue nevi appear bluish because the nevus cells are deep in the dermis. These lesions are usually benign but the literature suggests they can be malignant. Clinically, blue nevi are solitary, nodular lesions with a smooth surface that tend to be blue or blue-gray. These lesions are generally treated conservatively unless there has been a change in their appearance or the patient requests excision for cosmetic reasons. The excision should include the subcutaneous component to ensure complete removal of deep dermal melonocytes. 3 Halo Nevus. When a melanocytic nevus is surrounded by a hypopigmented halo, it is termed a halo nevus. These lesions tend to occur on the torso in older children and teenagers. They are common, frequently multiple, usually acquired and asymptomatic. The central nevus tends to gradually disappear leaving a macular area of non-pigmented skin. This hypopigmented area may persist for years and may gradually return to a normal color. When biopsies are performed,

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Part II: Skin and Soft Tissue

·I

Epidem1is Papillae of dermis Dermis

ibi

Su bcutaneous fatty layer Sebaceous glands

FIGURE 13.1. Cr05HeC!ion view of skin.

there may be no trace of the originallesion.1 The treatment is expectant. avoiding sun exposure at the hypopigmented areas unless there are cosmetic concerns or the lesions have atypical features.

using the Q-switched ruby, neodymium:yttrium-aluminumgamet (Nd:YAG) or alexandrite lasers,4 or make up camouflage (Chapter 18).

Spitz Nevus. This is a common and usually acquired lesion

melanocytic nevi that have the clinical features of melanoma: asymmetry, border irregularity, color variability, and diameter greater than 6 mm (Chapter 14). When patients present with many atypical moles, they are at higher risk for melanoma. Patients who present with many atypical moles and a strong family history of malignant melanoma are at much higher risk for melanoma and must have at least annual full body examinations for their entire lives. It is difficult for even an experienced dermatologist to know

predominantly in children and young adults but can be found in older people as well. Spitz nevi are usually firm, domedshaped, reddish or dark brown nodules, frequently on the head and neck. They are compound nevus variations, which have distinctive histologic features that make the differentiation from malignant melanoma difficult.1 The treatment is surgical excision. There is controversy over whether an entity known as a malignant Spitz nevus exists or if these lesions are malignant melanomas. For these reasons, Spitz nevi require complete excision with histologic confirmation of clear margins.

Atypical Moles-Dysplastic Nevi. Dysplastic nevi are

Nevus of Ota. Nevi of Ota are hamartomatous melanocytic lesions that occur on the face in the distribution of the ophthalmic and maxillary division of the trigeminal nerve. They are much more common in women. The sclera is involved in two-thirds of cases.t The treatment consists of laser therapy,

FIGURE 13.2. Melanocytic: nevus.

FIGURE 13.3. Congenital melanoc:ytic: nevus.

Chapter 13: Dermatology for Plastic Sw:gcons 1-Skin Care and Benign Dermatologic Conditions

107

when to recommend excisional biopsy. The best indication for biopsy is a change in clinical appearance. The ideal surveillance involves total body photographs, which are compared annually with the patient's current condition in order to determine if any lesions have changed over time. The treatment is excisional biopsy. If step-sectioning of the entire specimen reveals melanoma, then further treatment is required (Chapter 14).

Solar Lentigo. Solar lentigines oa:ur on sun-exposed areas of the face, arms, and dorsum of hands, especially in lighter skinned white people with light eye color. These acquired lesions are pigmented macules that can be small or large, with a tendency to confluence and range in size from 0.2 to 2 em. They become more numerous with advancing age. Treatment is not required. A biopsy is taken to exclude melanoma from any lentigo that develops a highly irregular border, a localized increase in pigmentation, or localized thickening.z Bleaching agents like hydroquinone are not particularly effective. Topical tretinoin, microdermabrasion, or cryotherapy can be used.

Ephelides (Freckles). These are small, less than 3 mm, red or light brown macules that appear on sun-exposed areas predominantly in fair skinned people with red or blond hair, but can appear in darker skinned individuals as well. There is no increase in the number of melanocytes, but rather an increase in the amount of melanin in the skin. They are co.rwnon in childhood; however, they can be seen at any age. They are usually confined to the face, arms, and back. The number varies from a few spots on the face to hundreds of confluent macules on the face and arms. Treatment is not required, but sunscreen is recommended. Bleaching agents such as hydroquinone, peels, and intense pulsed light (IPL) can be used for cosmetic reasons.

Epidermal Lesions Seborrheic Keratosis. This is a common benign, usually pigmented, neoplasm in elderly people, arising from the basal layer of the epidermis and consisting of keratinocytes. The etiology is unknown, and factors like virus infection, genetics, and sun exposure can be related. Usually seborrheic keratoses are not photoinduced. These lesions occur in any body site (frequently in the face and upper trunk) and are usually asymptomatic or associated with itching. They are superficial verrucous plaques, smooth or rough, varying from 1 mm to several centimeters in size and varying from dirty yellow to dark brown. Histologically, they are characterized by hyperkeratosis, acanthosis, and papillomatosis. The classic description is of a "stuck-on," waxy appearance. Surgical excision or shave excision is appropriate if the patient complains of cosmetic appearance. Other treatment options include curettage, cryotherapy, or trichloroacetic acid (TCA). There are times when the lesion is atypical and an excisional biopsy is indicated for diagnostic purposes (Figure 13.4).

Keratoacanthoma. This is a common epithelial tumor related to sun exposure than may be better placed in the next chapter on malignant lesions. It is more co.rwnon in white phototypes and is usually found on the face or upper limbs. Classically, it presents as a solitary papule that develops a crater-like central, keratotic core;' The history is one of rapid growth over a few weeks. Spontaneous regression is said to occur, but most lesions are excised before it becomes clear if regression would have ever occurred. The histology is similar to squamous cell carcinoma and many consider it a low-grade squamous cell cancer. Surgical excision is usually the treatment of choice. Other potential treatment options are curettage, coagulation, and topical 5·fluorouraciL

Verrucous Nevus. These are congenital lesions that pres· ent as verrucous papules or plaques that are skin colored or brown. A linear configuration is common and it can be found in any body site. Malignant transformation is very rare. The treatment options due to cosmetic concerns are surgical excision, laser, electrodissection, dermabrasion, cryotherapy, TCA, or topical retinoic acid. Skin Tags (Acrochordon). Skin tags are composed of loose fibrous tissue and usually occur as multiple skin-colored or tan, filiform or smooth-surfaced papules that are 2 to 3 .rwn in diameter. These small, soft, pedunculated lesions are frequently located on the neck or major flexures. The simplest and most expeditious treatment is shave excision with scissors or a scalpel blade.

Premalignant Lesions Actinic Keratosis. Actinic keratoses may be the most common of the premalignant skin conditions. Caused by sun exposure in people with Fitzpatrick skin types I, n, and m, they are macules or papules with a scaly surface, generally between 1 mm and 2 em in diameter. Actinic keratoses occasionally evolve into squamous cell cancers and are therefore considered premalignant. These lesions frequently require biopsy to rule out a carcinoma. Multiple lesions are usually treated with S-fluorouracil or the immune stimulator imiquimod (Aldara) (Figure 13.5).

Leukoplakia. Leukoplakia is white intraoral plaque and is the most common precancerous lesion of the oral cavity. These lesions do not frequently become squamous cell cancer but must be followed and biopsied if they persist or undergo a change in appearance.

Cutaneous Hom. A cutaneous hom is different from a skin tag and is considered a premalignant lesion. They are usually yellowish brown protuberant "horns" and are found on the face and ears. Histologically, they are characterized by a compact proliferation of keratin. The treatment is surgical excision. Bowen's Disease. Bowen's disease is squamous carcinoma in situ of the skin. This tumor presents as a slowly growing, red lesion with a scaly surface and irregular borders. tnceration or bleeding may be a sign of invasive malignancy. The treatment of choice is surgical excision, but cryotherapy, curettage, cauterization, topical agents like S-fluorouracil, and topical photosensitizer can also be considered.

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Part II: Skin and Soft Tissue

and bleeding may occur at points of pressure. The treatment is surgical excision.

Cylindroma Cylindromas can be solitary or multiple. The multiple lesion type has a genetic component. They are classically found on the scalp as numerous small papules or large nodules with smooth surfaces. Sometimes they cover the entire scalp like a turban explaining the name tu1ban tumo1. They are usu· ally benign, but malignant development has been reported. Treatment options include surgical excision, electrosurgery, and carbon dioxide laser.

Clear Cell Hidradenoma

FIGURE U.S. Actinic keratosis.

HAIR FOLLICLE TUMORS Trichofolliculoma This is a rare hamartoma of the pilosebaceous follicle. They are typically solitary, small, raised nodules with two or three hairs, usually white, protruding together in a tuft. They frequently appear on the face and scalp. Malignant change is not typical but has been reported in a single case with perineural invasion.1 The treatment recommended is surgical excision.

Pilomauicoma, or Benign Calcifying Epithelioma of Malherbe A pilomatricoma is a hamartoma characterized by a firm, solitary nodule covered with intact but often discolored skin. The calcification makes the lesions particularly firm. They can occur on any body part but are most commonly found on the face and upper extremities. ln general, the lesions are O.S to S em in diameter. There is no malignant potential. The treatment is surgical excision.

Trichoepitheliomas Trichoepitheliomas are hamartomas of the hair follicle typically found in the center of the face. They tend to be small, skin-colored or slightly pink papules that are usually distributed symmetrically on the cheeks, eyelids, and the nasolabial region. Treatment is not required; excision may be contemplated for cosmetic reasons. Other options include electrodissection and curettage or cryotherapy. Recurrence is common.

ECCRINE TUMORS Syringomas This is a benign tumor that usually presents as firm, skin· colored to yellowish dermal papules on the lower eyelids, pre· dominantly in females. Syringomas can be sporadic or familial and are frequently associated with Down's syndrome. The treatment is punch or surgical excision for cosmetic reasons only. Electrodissection, curettage, and carbon dioxide laser can be considered.

Eccrine Poroma An eccrine poroma is a solitary, firm, skin-colored or erythem· atous papule, usually on the sole or palm in adults. Ulceration

Clear cell hidradenoma is an eccrine sweat gland tumor. It occurs as a slow growing usually solitary nodule. Classically, it is a firm nodule, 0.2 to S em in size. Some of these tumors discharge serous material, whereas others tend to ulcerate. Lesions may occur on any body part, but are most frequently found on the arms, thigh, and scalp. They can develop malignant tumors. The treatment is surgical excision.

APOCRINE TUMORS Apocrine Cystadenoma This lesion results from a cystic dilatation of an apocrine secretory gland. It is generally a solitary, nodular lesion on the face that tends to be skin colored to bluish. The treatment is surgical excision.

Chondroid Syringoma This tumor is a firm intradermal nodule usually found on the head and neck that is composed of both sweat gland elements and cartilaginous elements.4 It is rare and there can be malignant degeneration. Surgical excision is recommended.

Syringocystadenoma Papilliferum These lesions are benign tumors, present at birth, usu· ally on the scalp and neck, that present as multiple trans· lucent or pigmented plaques or papules. The lesions can be verrucous with a central depression that oozes fluid. Treatment options include surgical excision and electrocoagulation.

SEBACEOUS TUMORS Sebaceous Nevus Sebaceous nevi are common tumors of childhood. Two· thirds are present at birth; the remaining one-third develop in infancy or early childhood. The lesions are usually soli· tary, oval to linear, yellowish in color, varying from O.S em to several centimeters, and frequently present on the scalp. Surgical excision is recommended before adoles· cence because of the potential for development of basal cell carcinoma (BCCA) and other malignant tumors. The rare nevus sebaceous of Jadassolm syndrome consists of the triad of a linear sebaceous nevus, convulsions, and mental retardation.

Sebaceous Epithelioma This lesion looks like a BCCA, but tends to be more yellowish because of the sebaceous cellular elements. It is most frequently located on the scalp and face. Treatment is recom· mended for cosmetic reasons only. Options include surgical excision, radiation, electrocoagulation, curettage, and carbon dioxide laser.

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Sebaceous Hyperplasia This is a small tumor composed of sebaceous glands that is commonly located on the forehead, cheeks, lower eyelids, or nose. lt begins as a pale yellow and slightly elevated papule and can become dome shaped, and sometimes umbilicated. Sebaceous hyperplasia does not have any relationship with solar expotro.te. Treatment options are electrodissection. curet· tage, cryosurgery, or surgical excision.

Rhinophyma Rhinophyma is a localized telangiectatic enlargement of the nose, most often in men. Histologically, it is characterized by sebaceous gland hyperplasia, fibrous infiltration, and lymphedema. Rhinophyma is considered a glandular form of acne rosacea. The reported incidence of occult cancer in the setting of rhinophyma varies from 15% to 30%. BCCA is the most common malignant neoplasm.2 Treatment options include dermabrasion or other form of deep resurfacing or surgical excision with reconstruction using a forehead flap (Figure 13.6}.

CYSTS Epidermal Cyst (or Sebaceous Cyst) This is the most common type of cyst and occurs because of proliferation of surface epidermal cells within the der· mis. Epidermal cysts are rare in children but common in adults. They are generally round, protruding, smoothsurfaced masses, varying in size from a few millimeters to several centimeters. Epidermal cysts grow slowly and are not symptomatic unless they become infected. Once infected, rupture is common. The only effective treatment is surgical excision. If infected, a course of antibiotics is recommended in an effort to prevent rupture and drainage so that excision can be accomplished. Staphylococcus aureus is the most common pathogen. The entire capsule must be removed to avoid recurrence. Genetic syndromes like Gorlin and Gardner may be associated with epidermal cysts.

Milium A milium (plural: milia) is a superficial, white epidermal cyst that appears immediately beneath the epidermis. They are most common on the eyelids and cheek and often appear along a healing upper blepharoplasty incision. The treatment is unroofing and removal of the central kernel with a #11 blade or needle, or light electrodissection.

Pilar Cyst A pilar cyst is similar to an epidermal (sebaceous) cyst and is a common scalp lesion containing keratin. The treatment of choice is surgical excision. Like epidermal cysts, if they present in an inflamed, infected state, they may require drainage. A course of antibiotics to "cool off" and shrink the lesion is worth an attempt, in hopes that the lesion can be excised.

SMOOTH MUSCLE TUMORS AND MESENCHYMAL TUMORS Leiomyomas Like leiomyomas elsewhere, these benign smooth muscle tumors present as solitary, firm, round, flesh-colored nodules, more commonly in the limbs, which are either subcutaneous, or in the deep dermis. The recommended treatment is surgical excision to eliminate what can be a tender lesion and rule out a malignant lesion.

FIGURE 13.6. Rhinophyma.

Pyogenic Granuloma This lesion is a common vascular nodule that exhibits rapid growth, not unlike a keratoacanthoma, but pyogenic granulomata are totally benign. They can appear at any age and vary in color from brown to bluish-black. They are com· pressible and do not pulsate, with a thin surface. Treatment options include curettage and surgical excision.

FIBROUS TUMORS Dermatofibroma This lesion is a myofibroblast proliferation, characterized by a firm, skin-colored or reddish brown sessile papule or nodule, more commonly in women. They vary in number from 1 to 10 and can be found anywhere on the extremities and trunk. They appear as 3- to 10-mm slightly raised, pink-brown, dome-shaped, sometimes scaly, hard growths that retract beneath the skin surface during attempts to compress and elevate them. They tend to remain stable for years as discrete solitary lesions. Treatment options include surgical excision for cosmetic reasons only, cryotherapy, or 600-nm pulsed dye laser (Figure 13.7).5

GENERALIZED DISORDERS Telangiectasias Telangiectasias are vascular malformations characterized by chronically dilated capiUaries or smaU venules. They are

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Pseudoxanthoma Elasti.cum This can be an autosomal dominant or recessive disorder causes calcification of elastic tissues and blood vessels arte· riosclerosis. Skin lesions generally appear as yellow papules or plaques and skin laxity. The most important aspect of treatment is to ensure that complications from vascular involvement are prevented or dealt promptly.1 Plastic surgical procedures can be performed to improve appearance.

Ehlers-Danlos This is a connective tissue disorder, characterized by skin and blood vessel fragility, hyperextensibility, and hyper· mobility. There are 11 subtypes.1 Patients must avoid pregnancy and trauma to soft tissues and be referred for genetic counseling.

Acne Rosacea FIGURE 13.7. Dennatofibroma.

small, red and linear and may appear like a spider or star design (Figure 13.8).

Xeroderma Pigmentosum This is an autosomal recessive disorder, characterized by damage to DNA repair. These patients have extreme sun sensitivity and develop many cutaneous malignancies. The lesions require surgical excision, but the outcome is usually poor.

Dystrophic Epidermolysis Bullosa This disorder is characb:rized by fragility and blistering after trauma to the skin. It can be autosomal recessive or domi· nant. lt does not have any specific treatment,. except to avoid trauma. The slightest friction or scrape may result in skin lesions that are also prone to infection.1"

Cutis Laxa This is a rare elastolysis disorder with lax skin and loss of elastic tissue. It can be autosomal dominant or recessive. The skin develops large redundant folds. Treatment consists of plastic surgical procedures such as facelift and blepharoplasty.

FIGURE 13.8. Telangiectasias.

This is a common chronic disorder of the face, usually in white skin characterized by flushing, erythema, and telangi· ectasias. Bouts of inflammation with swelling, papules, and pustules may occur. The goal is to avoid skin irritation and use sunscreen creams. Oral medications like tetracycline and isotretinoin (retin-A) can be effective. Topical treatment with metronidazole 1%, phototherapy, and makeup camouflage are also helpful.

Hidradenitis Suppurati.va This is a disorder of apocrine glands, more commonly in dark skin, and usually in the axilla, perineal regions, or beneath the breasts. The disease can be devastating with numerous, interconnecting comedones or subcutaneous pustules. Local care and antibiotics tend to keep the lesions somewhat quiescent but the only definitive treatment is surgical excision. The heavily contaminated wounds usually have to heal by second· ary intention, which is a slow, painful process.

Pyoderma Gangrenosum This is rare disorder, which is not infectious in origin, and presents as solitary or multiple, fragile papules that can progress to ulcers and necrosis. Treatment options include antibiotics, topical or systemic steroids, and immunosuppres· sant agents.

SKIN CARE Nonsurgical skin care plays a role in the preoperative and postoperative management in many aesthetic surgery prac· tices. Some plastic surgeons choose to provide services and treatments to complement surgical rejuvenation procedures. Topical treatments, soft tissue fillers, neurotoxins, skin tightening devices, chemical and laser peels, facial treatments, makeup consultations, lymphatic drainage massage (LDM), and a wide variety of other medical spa services have become integral components of many practices. Other plastic surgeons develop relationships with dermatology colleagues who pro· vide these treatments. The nonsurgical treatments mentioned above appeal to several groups of patients: 1. Younger patients who seek preventive measures to uslow" the aging process. 2. Patients who cannot afford or who do not have the time to recover from expensive and more extensive surgical procedures. 3. Patients who do not want surgical intervention and prefer procedures with reduced morbidity, rapid recovery, and a more rapid return to work.

Chapter 13: Dermatology for Plastic Sw:gcons 1-Skin Care and Benign Dermatologic Conditions

THE COMPLETE AESTHETIC PACKAGE In the senior author's practice, surgical and nonsurgical treatments are integrated in a comprehensive team approach. The "consulting team" includes the plastic surgeon, surgical nurse, medical aesthetician, and patient coordinator. The extended team of providers includes a massage therapist. micropigmentation artist. personal trainer, nutritionist. and others (Figure 13.9, Case 1). Admittedly, this form of practice does not appeal to all plastic surgeons who prefer to concenttatl: on surgical procedures or who perceive the benefit of cross-referral from other specialists who offer these modalities.

THE CONSULTATION AND EVALUATION The objectives of the consultation are to evaluate the patient and provide education and recommendations on the different nonsurgical and Nrgical alternatives including a discussion of risks, complications, and the financial implications of the various options. The evaluation, or aesthetic consultation, is performed by the plastic surgeon accompanied by the nurse and the aesthetician. A facial evaluation regarding skin type (dry, oily, or a combination), texture, thickness, photoaging damage, wrinkles, and age-related and gravitational changes is included in every patient. A skin care regimen may be recommended before or after the surgical procedure.

COMPREHENSIVE SKIN CARE PROGRAM A skin care program consists of cleansing, hydration, moisturizing, repair, protection, and prevention.

Cleansing Dirt, oil, grease, makeup, and microorganisms are removed from the sk.in in order to allow skin care renewal and cos· metic creams to be absorbed. Cleanser is prescribed according to the skin type and is applied in the morning and again at night. Application of cleanser is important at night because the lower pH increases microcirculation and allows greater absorption of the skin products.

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Hydration Water is required to maintain the smoothness of the skin. The simplest and most important way to maintain hydration is by drinking water. Moisturizers are a helpful adjunct by augmenting the barrier function of the epidermis. Moisturizers contain humectants, emollients, and occlusives. The emollients are lipids that hydrate the skin. The occlusives decrease transepidermal water loss. Humeaants enhance water absorption from the dermis into the epidermis, and in humid conditions they also help the stratum corneum to absorb water from the external environment.'

Repair To achieve repair, the formulations must reach the basal layer of the epidermis and the superficial dermis. The most effective are alpha-hydroxy acids (AHA) and topical tretinoin (retin-A). Glycolic acid (sugarcane), lactic acid (milk), malic acid (apple), citric acid (citrus fruits), and tartaric acid (grape) are examples of AHA. Glycolic and lactic acid are the most commonly used and are safe and effective. AHAs are indicated for dryness, rough texture, acne, rosacea, photodamage, melasma, and hyperpigmentation disorders. They can be found in different vehicles and concentrations, such us within moisturizers or in the form of peds. They can also be used in dark sk.in types. In the case of melasma and hyperpigmentation disorders, AHAs can be used in combination with bleaching agents. Tretinoin (retin-A) is a vitamin A derivative that, when used for the long term, is extremely effective in reversing sun damage. It promotes histologic changes such as increased epidermal and granular layer thickness, decreased melanin content. compaction of the stratum corneum, decreased cytologic atypia, increased collagen synthesis, an increase in collagenous anchoring fibrils, and an increase in the number of blood vessels. Tretinoin can be found in cream, gel, and liquid preparations. Available concentrations include 0.02%, 0.02S%, O.OS%, and 0.1 %. The clinical changes from long-term tretinoin use include smoother skin texture, reduced fine wrinkles, decreased sallowness, improved skin appearance, and a decrease in actinic keratoses. The treatment can cause irritation, and some patients find tretinoin difficult to tolerate. During the treat· ment sunscreen is mandatory. If patients undergo a facelift, the tretinoin can be restarted after 3 to 4 weeks.

FIGURE 13.,. Case 1-Complet:e aesthetic package. This S6-year~ld woman presented with significant tun damage and facial aging. The complete aesthetic package was perfonned. She had an aggressive skin cue treatme:Dt preoperatively, with intense pulsed light treatments to the face and Deck every 21 days, alternated with facial peels. She then underwent an endoscopic brow lift, bilateral ptosis repair, rhytidectomy with SMASectomy, and cenicoplasty. The lymphatic: drainage massage treatment wu started S days postoperatively and continued once a week for 3 weeks. She is shown 1 year postoperatively.

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Bleaching agents may be helpful in some patients, such as hydroquinone, kojic acid, azelaic acid, and also retinoic acid. Hydroquinone is used for reversible pigmentation of skin, usually at 4% concentration. It can be combined with other agents, such as prepeeling creams. The 1% kojic acid and 20% azelaic acid may be equally efkctive.1 All these topical agents can cause skin irritation and should applied first as a patch test.

Protection and Prevention Antioxidants and sunscreen are used to protect what has been achieved and prevent further damage. Antioxidants act to eliminate the free radicals caused by sunlight. The most popular are vitamins C (ascorbic acid) and E (tocopherol and tocotrienols), alpha-lipoic acid, soy isoflavones, tea extracts, grape seed extracts, niacinamide, and coenzyme Q 10. Vitamin C is a topical antioxidant agent that stimulates collagen synthesis, inhibits elastin synthesis, reduces pigmentation, improves epidermal barrier function, regenerates the oxidized forms of vitamin E. and has anti-inflammatory effects. Smoking cigarettes appears to deplete vitamin C from the skin. Vitamin E (tocopherol) is an antioxidant found in veg· etables, seeds, and meat. Vitamin E prevents lipid peroxi· dation and therefore protects the cellular membrane from free radicals. Vitamin E is a helpful ingredient in daytime moisturizers and sunscreen, because of its photoprotective properties and also as an anti-inflammatory agent. Alpha· lipoic acid is another strong antioxidant with anti-inflamma· tory proprieties. lt is stable and easily absorbed and should be applied every other day initially and then daily when the skin permits.7 lsoflavones work by raising hyaluronic acid production, increasing the thickness and collagen of the skin.7 Topical green tea and grape seed extracts are antioxidants with antiinflammatory action.7•1 Vitamin B improves protein produc· tion, decreases melanosome transfer, and reduces redness.7 Coenzyme Q10 is used to combat sun damage and therefore reduces wrinkles, reducing oxidation levels.7•8 Sunscreens are important to prob:ct the skin from ultravio· let light. The sun protection factor indicated on the container only indicates the extent to which that product blocks UVB. Since UVA causes wrinkles and skin cancer, it is also important to use a product that also blocks UVA. Unfortunately, UVA blocking agents are not as well developed as UVB blockers. At best; the current UVA blocking agents only partially block UVA. The only complete sun blocker is zinc oxide, but it is thick and greasy and not practical to cover all of one's exposed skin. Sunscreen should be applied daily, before makeup, and reapplied during the day (Figure 13.10, Case 2; Tables 13.1-13.3).

NONSURGICAL lREATMENTS FOR SKIN QUALITY The most effective nonsurgical procedures are microderm· abrasion, dermabrasion, lPL, laser resurfacing, chemical peels, neurotoxins, and fillers. The procedures will be mentioned briefly because they are covered in depth in other chapters.

Microdermabrasion Microdermabrasion is a nonsurgical procedure that uses aluminum oxide (ALzO ) or sodium chloride (NaCl) crystals to exfoliate the skin. Topical anesthesia is not required and it is a safe and well-tolerated procedure. The treatment may be helpful for three to six sessions, every 2 weeks, before

FIGURE 13.10. Case 2-Sunsc:reen. This 70-year-old woman presented with a combination of sun damage and fac:ial aging. A complete aesthetic: package was performed, with sun protectors daily, avoidance of sun exposure and skin care treatment preoperatively, and microdermabrasion treatments. Surgically, she underwent an endoscopic brow lift, rhytidectomy with SMASec:tomy, and cervicoplatty. The lymphatic drainage massage was introduced during the first week postoperatively. She is shown 1 year postoperatively.

surgical procedures on the face. The best indications are oily skin, dilated pores, thick skin, mild acne scarring. melasma, and solar lentigines. Contraindications include severe acne rosacea, telangiectasias, uncontrolled diabetes, active acne, skin cancer, dermatitis, sunburned skin, oral isotretinoin. and blood thinners.

Dermabrasion Dermabrasion is the mechanical removal of epidermis and superficial dermis that will stimulate re-epithelialization. This can be performed with sandpaper, wire brush, or diamond fraise powered by a hand engine. The technique is performed under anesthesia in the operation room. Indications include wrinkles, facial scars, rhinophyma, syringoma, and epidermal nevus (Chapter 41).3

Intense Pulsed Light The IPL is a noninvasive system used for photorejuvenation (Chapter 18). It is a system that emits a broad spec· trum of non-coherent, polychromatic light in the range of 500 to 1,200 nm. These features allow great variability in adapting to different skin types and indications by varying the light spectrum, impulse length, impulse sequence, and fluence.7 Three to six sessions are recommended, every 2 to 3 weeks. The best indications are photoaging, telangiectasias, port wines stains, poikiloderma, red hypertrophic scars, hyper· trichosis, irregular pigmentation (lentigines, melasma, and ephelides), and postinflammatory hyperpigmentation. The contraindications are an abnormal response to sunlight, cur· rent treatment with oral tretinoin,. suspicious lesions, preg· nancy, conditions that affect wound healing, and blood thinners. Before treatment; the skin is cleansed and topical anesthetic applied for comfort. The skin can look like a sunburn and have some swelling from 2 to 48 hours after the procedure. The pigmented lesions appear much darker immediately after treatment. After a week, the skin starts to dear and microdermabrasion can be added to expedite this process (Figure 13.11, Case 3).

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Chapter 13: Dermatology for Plastic Sw:gcons 1-Skin Care and Benign Dermatologic Conditions

TABLE 13.1 FnzPATRICK CLASSIFICATION . • SKIN TYPE I

• SKIN COLOR/SUN EXPOSURE Highly 9ellsitive, never tans, always bums illld severely, fair skin

n m

Bums moderately, tans moderately, sun-seDsitive skiD

IV

Tans moderately and easily, burns minimally

V

Rarely bums, dark brown skin, sun-insensitive skin

Vl

Never bums, dark brown or blade skin, sun insensitive

Usually bums, tans mjnjmally, very SUD. 9ellsitive

TAILE 13.2 GLOGAU CLASSIFICATION . • PHOTOAGIN'G GROUP

• DEGREE OF SKIN WRINKLIN'G AND PHOTOAGING

I Mild (age 28-35 y)

MiDimal. wriDkles; no keratosis; requires little or no makeup

n Moderate

Rarely w:riokl.iiJg, mild scarring; sallow color with early keratosis; requires little makeup

(age 35-50 y)

m Advilllced Persistent wrinkling; discoloration with telilllgiectasias illld (age 5()-65 y) visible keratosis; wears makeup always ---------------------IV Severe

(age 6~75 y)

Wrinkl.iog: photoaging, gravitational, dynamic; actinic keratosis with or without skin cancer; wears makeup with poor coverage.

TAILE 13.3 SKIN CARE Cleansing Hydrate and moisturizers Protection (illltioxidilllts illld sun protectors)

Cleansing Hydrate and moisturizers Repair (alpha-hydroxy acids, topical tretinoin, bleaching agents)

Radiofrequency Radiofrequency is a nonsurgical treatment for skin rejuvenation. It causes a thermal injury to the dermis, stimulates the fibroblasts, increases collagen production. and provides some skin tightening. The indications are skin laxity in the face, neck, limbs, and abdomen. The best candidates are patients between 30 and 60 years and who have reasonably good skin quality and have no history of smoking. The response is variable.7

Lasers Lasers produce stimulation of fibroblasts and increase collagen deposition. They can be used for rejuvenation, hair removal, and treatment of vascular lesions. The most popular lasers for skin resurfacing are carbon dioxide and erbium:YAG, which, as described in Chapter 18, can be fractional or not (Chapters 18 and 41).

Chemical Peels Chemical peels can be superficial, medium, or deep depending on their penetration into the dermis where they result in improvement of collagen organization. A variety of chemical peels can be used, such as glycolic acid, TCA, beta-hydroxy acid, Jessner solution, and Croton

FIGURE 13.11. Case3-Intense pulsed light (IPL). This 65-yearolcl woman was conc:c:.med about her appearance aftu a c:utanwus faa:lift. An aggn:ssive skin care regimen of IPL treatments to the face and neck every 21 days was initiated and continued after Nrgety. An endoscopic brow lift, rhytidectomy with SMASec:tomy, and c:ervic:oplasty were performed. The lymphatic: drainage massage treatments were started S day• postoperatively and continued once a week for 3 weeks. She is shown 7 years postoperatively.

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oil. Each one has specific characteristics and indications (Chapter 41).

Neurotoxins Botulinum toxin is a temporary paralyzing agent that works by causing a chemical denervation at the neuromuscular junction providing temporary improvement in dynamic wrinkles. Patients should be informed that wrinkles that are present at rest will not be improved by bot:W.inum toxin. although they will not get deeper with animation (Chapter 43).

Fillers Fillers are designed to replace volume in dermis or subcutaneous tissue of the face. The most commonly used are hyaluronic acid (such as Juvederm and ~tylane), calcium hydroxyapatite (Radiesse), poly-lactic acid (Sculptra), and others mentioned in Chapter 42.

Lymphatic Drainage Massage LDM is a helpful tool that can be started before or after surgery. It is meant to deaease swelling, bruising, and recovery time. Preoperatively, LDM helps to remove stagnant fluids,

increase blood flow, and provide the psychological benefit of reducing stress/anxiety and focusing the patient on positive results. Postoperatively, the technique decreases inflammation, speeds up recovery time, reduces bruising, opens lymphatic channds, reduces the scar tissue buildup, and continues to reduce stress and tension.7

References 1. Bums T, Breatlmach S, Cox N, Griffiths C. Rook'3 T~:ctbook of Dm~S#tology. Malden, MA: Blackwell PublishiDg; 2004. 2. Mathes SJ, ed. Pltutic SNrgny. 2nd ed. Philadelphia, PA: Saunders Elsevier; 2006. 3. Wolff K, Goldsmith LA, Kat!: sr, GUcllrest BA, Paller AS, Lelfell DJ. fitzyurid:'1 Demt~~~ology in Ge'!U!'rtll M~Jid~. Columbus, OH: The ~Graw Hill Companies; 2008. 4. Thorne CH, Beasley EW, Aston SJ, Bartlett SP, Gunner GC, Spear SL, eds. Gt'Rbb Cl' Simth Pltutic S'"gt!'fY. 6th ed. Philadelphia, PA: Lippin~tt Williams & Wilkins; 2007. 5. Lee PH, Nehal KS. Disa lJ. llenigu and premalignant skin lesions. Pltut R~CQMtr Swg]. 2010;125(5):188-198. 6. Krait JN, Lynde CW. Moisturizers: what they are and a practical approach to prodll4't selection. SIUn ThtmJPy Lm. 2005;10(5):1-8. 7. Salt!: R, ed. Comsetic M~Jicine Cl' Mltbetic S'"gt!'fY. Str#tt!gia for Stu:ee/1$. St Lollis, MO: Qwillty Medical Publishing, In~.; 2009. 8. Bogdan Allem&DD I, Baumann L. Antioxidants used in skin care formulatioiD. Skin TberRP'Y Lm. 2008;13(7):5-8.

CHAPTER 14 • DERMATOLOGY FOR PLASTIC

SURGEONS II-CUTANEOUS MALIGNANCIES DANIEL J. CERADINI AND KEfiH M. BLECHMAN

INTRODUCTION Skin cancer is the most common form of cancer diagnosed in the United States, exceeding the combined incidence of breast, prostate, lung, and colon cancer cases annually. It is estimated that one in five Americans will be diagnosed with skin cancer during their lifetime.1 The incidence of cutaneous malignancies has increased dramatically over the past several deQldes. The most recent analysis of the incidence of non-melanoma skin cancer in the US population suggests that nearly 3.5 million new cases are diagnosed annually in 2 million patients.1 This figure has tripled from the estimated annual incidence of cutaneous malignancy from 1.9.94 and signi1ies a major public health problem that accounts for over 2 billion dollars in healthcare spending annually. The treatment of skin cancer comprises over 75% of all procedures performed by plastic surgeons in the United States.3

BASAL CELL CARCINOMA Epidemiology and Risk Factors The vast majority of skin cancer cases diagnosed in the United Stab:s are either basal cell carcinoma (BCC) or squamous cell carcinoma. BCC is by feu the most common cutaneous malignancy worldwide and accounts for nearly 80% of all skin cancers. There is marked worldwide geographic variability, most often affecting light-skinned populations in locations with the highest UV exposure. Although mortality is rare, locally aggressive BCC can result in significant patient morbidity. The predominant risk factor for BCC is intense sunlight and l.N exposure. Other risk factors include Fitzpatrick skin types 1-U, a family history of skin cancer, male sex, smoking, human papilloma virus (HPV), exposure to arsenic or hydrocarbons, previous radiation, and immunodeficiency resulting from either acquired immunodeficiency syndrome or systemic drugs required for transplant recipients. While most arise sporadically, BCC is also associated with several dinical syndromCSt including Bazex syndrome, Gorlin syndrome (basal c:ell nevus syndrome), and xeroderma pigmentosum. Constitutive acti· vation of the sonic hedgehog signaling pathway is thought to play a significant role in BCC pathogenesis.

or black macules, which can be easily confused with seborrheic keratosis or nodular malignant melanoma. Superficial BCC is the second most common tumor type. It appears as a demarcated multi-centric erythematous patch, frequently occurring on the trunk and extremities. The surface of this lesion is often scaly and ulcerated and can be misdiagnosed as a cutaneous fungal infection, discoid eczema, actinic keratosis, or psoriasis. Although there is frequently "normal" appearing skin between the tumor foci suggesting that each arises separately, this subtype exhibits a significant radial growth pattern and each focus is actually connected, likely arising from a single primary focus. Morpheaform. or sc:lerosing BCC is the most aggressive tumor type, usually found in the head and neck. It is the most difficult type to diagnose and manage due to its insidious onset and infiltrative growth characteristics. It frequently appears as a poorly defined flat indurated plaque that resembles a scar without a history of trauma. Histologically, this tumor exhibits numerous thin linear extensions that can reach into the deep dermis, making surgical resection difficult and recurrence frequent. Tissue biopsy definitively establishes the diagnosis and characterizes the histologic subtype. Additional workup is generally not required due to the very low rate of metastasis (5 mm. on high-risk sites of central face, ears, hands, feet >10 mm. on scalp, forehead, cheek, neck >20 mm. on tnwk, extremities Histologic characteristics MorpheafonnlsclerosiDg, infiltrative, or micronodular subtypes (BCC) Basosquamous differentiation Perineural invasioo

Cl..inical. features Recurrent tumors Previously irradiated site Poorly defined clinical borders Immunosuppression Site of chronic inflammation BCC, bual cell cucinoma.

Surgical Management The options for primary tumor eradication of BCC can be divided into destructive or surgicaVexcisional modalities. Destructive tteatment options are generally reserved for lowrisk basal cell tumors and use a variety of methods to destroy neoplastic tissue including electrosurgery, cryosurgery, topical 5-fluorouracil, topical irniquirnod, intralesional interkron, radiation, and photodynamic therapy. Notably, these modalities do not definitively ensure a margin clear of neoplasm. However, in selected low-risk cases, the overall success rate can be excellent. Surgical or excisional treatment of BCC can be used in low-risk and high-risk cases. Simple excisional biopsy of low-risk lesions in anatomically simple areas (trunk and extremities) can result in success rates over 95%.4 In order to achieve histologically negative margins, guidelines exist to assist the surgeon: for tumors 1 em a clinical margin of S to 10 mm is recommended.s In high-risk cases, especially on the face where obtaining adequate margins may result in significant deformity, direct excisional biopsy allows for histologic evaluation of the surgical margins to ensure that they are free of tumor to maximize the aesthetics of reconstruction. Mobs' micrographic: surgery is the most definitive modality and treatment of c:hoic:e in high-risk BCC of anatomic:ally complex areas on the face. High-risk tumors are serially excised and the entire margin of resection is examined histologically by the Mohs' surgeon. Presence of tumor at the margins is mapped, and further excision of affected areas is serially performed and examined until the margins are clear. Mobs' surgery achieves over 98% cure rate in primary tumors and over 95% in recurrent cases, although it is more expensive and time consuming to perform. The pri· mary advantage of Mohs' surgery is that it spares normal tissue and anatomic structures in complex areas while ensuring negative margins and excellent cure rates. Based on a recent

randomized clinical trial comparing Mobs' surgery to direct excision of BCC, Mohs' surgery resulted in better outcomes for treatment of recurrent basal cell tumors, while there were no significant statistical differences in the treatment of primaryBCC.' BCC generally carries a good prognosis as the tumors tend to grow slowly and metastasize very rarely, but can result in significant morbidity due to local invasion. One-third of recurrences occur in the first year following tn:atment, half in the second year, and two-thirds in the third year regardless of the treatment modality.7 Patients should be monitored every 6 months for the first year following treatment and annually thereafter.

SQUAMOUS CELL CARCINOMA Epidemiology and Risk Factors Cutaneous squamous cell carcinoma (cSCC) is the second most common skin cancer, accounting for 15% to 20% of all cases of skin cancer in the United States. Similar to BCC, there is marked geographic variability in the incidence of cSCC, with more patients affected in areas with increased sun exposure. Although primary tumors can be locally invasive, it is frequendy diagnosed in the early stages when it is a highly curable disease. Approximately 3,000 patients die from cSCC annually in the United States,8 and the incidence of more aggressive or advanced tumors is increasing. Chronic cumulative sun exposure is the prevalent risk factor for cSCC, and both UVA and UVB are implicated in tumor pathogenesis. This is significant because the sun protection factor in sunscreens only measures protection against UVB. The incidence of cSCC increases significantly with age, likely reflecting an increased cumulative exposure to sunlight. Other environmental risk factors for cSCC include a history of radiation, chronic inflamma· tion (as in Marjolin's ulcer), and exposure to arsenic and hydrocarbons. Chronic immunosuppression secondary to organ transplantation markedly increases the risk of cSCC up to 250 times the general population and is closely correlated to the type of transplant, immunosuppressive drug burden, and time since transplantation.M0 Host risk factors for cSCC include Fitzpatrick I-ll skin types, fair hair, previous history of non-melanoma skin cancer, and infection with HPV. Additionally, certain inherited disorders such as xeroderma pigmentosum, epidermolysis bullosa, and albinism confer a genetic susceptibility to developing cSCC. UV-induced mutations in the p53 tumor suppressor gene are thought to be the molecular mechanism of malignant transformation of keratinocytes.

Diagnosis and Staging The majority of cSCC is diagnosed on sun-exposed skin of the head and neck, dorsum of hands, lower arms, and legs. Unlike BCC, however, cSCC can arise from a premalignant actinic keratosis, identified as an area of erythematous, rough, scaly plaque that exhibits dysplastic growth and malignant potential. Up to 80% of cSCC tumors arise in association with a pree:Dsting actinic keratosis, although overall 1 em, rapid growth, ulceration, bleeding, and erythema.14 A cutaneous hom is a clinical variant of actinic keratosis that presents as a hyperkeratotic protuberance shaped like a cone extending above the plane of the skin. Approximately 15% of cutaneous horns actually contain cSCC,15 and excision is indicated. cSCC in situ, also referred to as Bowen's disease, frequently presents as a slowly growing, erythematous, scaly

Chapter 14: Dermatology for Plastic S1U'BeoD.8 R--Cutaneous Malignancies patch. It is most frequently diagnosed in older patients (>60 years} and can occur anywhere on the body including the mucosal surfaces. When cSCC in situ occurs on the mucocutaneous epithelium of the glans of the penis or labia majora, it is referred to as erythroplasia of Queyrat. It occurs most often in uncircumcised men and is thought to be associated with chronic irritation, infection with HPV, and immuno· suppression. It classically appears as a velvety red plaque on the glans of the penis. Progression to invasive cSCC occurs in up to 33% of cases over variable pe~ods of time. 1~ When cSCC in situ occurs in the oral or gemtal mucosa, 1t presents as adherent white patches clinically referred to as leu· koplakia. Notably, this must be differentiated from other causes of leukoplakia such as chronic irritation (usually from smoking), candidal infection, and HPV infection. This often requires a biopsy of suspicious lesions. Squ~ous ~ell carcinoma develops in 10% to 20% of all patients w1th leukoplakia. Keratoacanthoma is a rapidly growing nodule (over weeks to months) with a central ulceration or keratin plug that is found mainly in sun-exposed skin (Figure 14.2). Left untreated, it may spontaneously involute. Keratoacanthoma is felt to be a low-grade variant of cSCC, but is clinically ~~t to distinguish from high-grade invasive cSCC. Shave b1ops1es are not helpful in m.aldng this distinction; therefore, surgical excision is recommended. Invasive cSCC penetrates the basement ~emb~e to r~ch the dermis and either arises de novo or IS associated With actinic keratosis (Figure 14.3). Characteristic lesions are firm. raised, pink- or .flesh-colored papules with frequent keratini· zation, scaling, ulceration, or crusting on the surface. These most often represent well-differentiated tumor types. Poorly differentiated lesions are typically soft, granulomatous nodules with areas of hemorrhage, necrosis, and ulceration and lacking in keratinization. Invasive cSCC associated ~ith. actinic keratosis in sun-exposed areas has a low metastatic nsk and a favorable prognosis. De novo invasive cSCC, however, .is a high-risk variant typically occurring in immunocomprom1sed hosts or in areas of chronic irritation (such as burns) and has a metastatic rate as high as 14%.17

117

- - -- - - -..,

FIGURE 14.3. Invasive cutaneollll squamous cell cazcinoma.

Diagnosis of cSCC is made by tissue ~iopsy to distinguis!t it from other neoplasms or cutaneous 1nflammatory conditions. In addition to definitive tumor diagnosis, patients with cSCC should undergo clinical examination of the appropriate draining lymph node basins. Palpable nodes should be biopsied by fine needle aspiration. Routine i:magi.ng s~dies for cSCC is not indicated, but should be obtamed m patients that exhibit specific neurological symptoms or regional lymphadenopathy. . For the first time, the American Joint Comm1ttee on Cancer (AJCC) has introduced a completely separate staging system for cSCC, which was formerly incorporated into the "Carcinoma of the Skin" comprised of 80 different non· melanoma skin cancers. This new 1NM staging system uti· lizes a multidisciplinary evidence-based experience to more accurately describe the history and prognostic outcomes of cSCC (Tables 14.2 and 14.3).18 Due to the fact that most cSCC occurs in the head and neck, this system is meant to be consistent with the AJCC Head and Neck Staging system. The new cSCC staging system has several notable changes. The T staging (Tumor Characteristics) of the TNM system has been modified to eliminate the 5 em size criteria and invasion of extradermal structures criteria to define a T4 lesion. Instead, a new list of "high-risk" features has been added, which impacts the overall T staging. Of these features, tumor grade now also contributes to the overall stage groups. The N component (Regional LYJ:llph Nodes) of th~ ~~system has been totally revised to mcorporate data mdicatmg that overall survival deaeases with increased node size and number involved. While the majority of cSCC is diagnosed and cured in the early stages, the reported rate of re~onal me~stasis rangc:s from 0.5% to 10%. While there IS no consistent defimtion or stratification of what features of a primary tumor are considered "high risk" for regional spread, there are a number of tumor· and patient-specific characteristics that can be used to guide management. Tumor-specific features that are considered "high risk" include tumors located on the ears, lips, or within chronic wounds or scars, horizontal size >2 em, thickness of 2 to 6 mm (low risk) or >6 mm (high risk) poorly differentiated cell types, perineural invasion, and ~apidly growing or recurrent lesions.u Patients who are organ transplant recipients or who are diagnosed with chronic lymphocytic leukemia, smaU lymphocytic ~ym­ phoma, epidermolysis bullosa, or HIV/AIDS ~e more likely to exhibit more aggressive tumor types and disease progression (Table 14.1).

Surgical Treatment FIGURE 14.2. ~ratoacandtoma with clwu:teristic umbilicated center and keratin plug. If left untreated, it typically un~ergoes a period of rapid growth followed by spontaneous regresston ~ve.r seve~al months; however, it can p.rogres5 to squamous cell carcmoma wtth metastase&.

The surgical treatment options for cSCC are similar to those of BCC and are based on assessing the risk of local regional recurrence or distant metastasis. In seleaed low-risk cases, destructive treatment modalities can be used with excellent results. Direct surgical excision can be used for both low· risk and high-risk lesions. In order to increase the chance of

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TABLE 14.2 TNM STAGING CATEGORIES FOR CUTANEOUS SQUAMOUS CEll CARCINOMA • T CLASSIFICATION

• TUMORSIZB

1is

Carcinoma in situ

T1

Tumor S2 c:m in greatest dimension with 3 but 6 mm. and Evolution or change in the appearance of lesion over time. Using these criteria, the vast majority of

FIGURE 14.4. M:aligoant melanoma. Lesions Nspicious for melanoma demonstrate asymmetry, border irregularity, color variegation, diameter >6 mm, and evolution or change in the appearance. {Photos courtesy of Richard L. Shapiro, MD.)

119

melanomas are detected by clinical examination. It is important to note,. however, that a minority of lesions are atypical and can be nonpigmented (5%), resemble other types of cuta· neous malignancies (basal or squamous cell carcinoma), or be smaller than 6 mm in size. Melanoma can be classified into five clinical and histo· logic growth patterns, each of which has unique clinical characteristics: superficial spreading, nodular, lentigo maligna, acral lentiginous, and desmoplastic melanoma. With the exception of nodular melanoma, the remaining subtypes orig· inate from an in situ radial growth phase that does not have metastatic capability. The prognostic significance of growth pattern remains controversial, although there are some genetic factors identified within the subtypes that may have prognostic value. Superficial spreading melanoma presents as flat or slightly elevated lesion with variegate pigmenta· tion, most commonly occurring on the trunk in men and the legs in women, in patients aged 30 to SO years. As the name would imply, the growth pattern is typically supe.r:ficial and radial with scattered atypical melanocytes in the epidermis. It is the most common subtype in the Caucasian population and likely contributes significantly to the increasing incidence of melanoma over the past 30 years. Nodular melanoma is the second most common growth pattern, which often lacks the classic features commonly identified by the ABCDE melanoma screening tool. These lesions commonly present as a smooth, single colored (black or brown) elevated nodule or an ulcerated mass on examination, frequently affecting the legs or trunk. They are typically thicker and more advanced at the time of diagnosis, largely due to a relatively short or lack of radial growth phase. Overall, nodular melanomas account for most thick melanomas; however, the survival rate and prognosis is similar to that of the other clinical types when thickness and ulceration are taken into account. Both nodular and superficial spreading melanomas are associated with increased sun exposure in fair-skinned individuals. Lentigo maligna melanoma (Figure 14.5) is a slow growing lesion with radial spreading that typically arises in longstanding pigmented lesion on chronically sun-damaged anatomic sites (head and arms) in older patients. Hypopigmented lesions are also possible within this subtype. It occurs most often in fair-skinned older individuals, with an average age of diagnosis at 65 years, and is associated with solar elastosis of the surrounding skin. Aaallentiginous melanoma affects only 2% to 8% of Caucasians, but accounts for up to 36% of melanoma diagnosed in African Americans, making it the most common subtype within this demographic.V It commonly occurs on the palms of the hand, sole of the feet, or beneath the nail plate (subungual) and presents at a more advanced stage with an aggressive course compared with the other subtypes. Subungual variants commonly present as a longitudinal line of pigment extending the length of the nail plate, with the hallmark spread of the pigment to the prox· imal nail fold referred to as Hutchinson sign. Finally, desmoplastic melanoma is a relatively uncommon subtype that presents as an unremarkable plaque or nodule and can easily be misdiagnosed at an early stage. It affects older patients (although not as old as lentigo maligna melanoma) most com· monly in the head and neck and occurs in men twice as often as in women. Desmoplastic melanoma is frequently associated with nerve invasion and spread along fascial planes and tends to be thicker at the time of diagnosis. They are locally aggressive with a higher rate of local recurrence, but exhibit a low incidence of lymph node involvement. These clinical features more closely resemble a soft tissue sarcoma, suggesting that the underlying biology of desmoplastic melanoma may be unique compared with the other subtypes. Definitive biopsy remains a critical factor in both establishing the diagnosis and providing valuable information about staging and prognosis, as histologic characteristics of melanoma are powerful independent predictors of 5· and 10-year

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FIGURE 14.S. Lentigo maligna melanoma is a slowly progressive melanoma in situ that consists of malignant cells without invasive growth. (Photo courtesy of Richard L. Shapiro, MD.)

survival rates. A full thickness excisional biopsy with a 1 to 2 mm margin of normal tissue is the method of choice for suspicious lesions. In larger lesions locatl!d in areas where a completx! excision may be technically difficult or result in significant deformity (i.e., areas of the face), it may be necessary to perform an incisional biopsy or multiple punch biopsies. This should include the most raised area of the lesion. Shave biopsies should never be performed on lesions with a high clinical suspicion of melanoma as there is an unacceptably high rate of positive deep margins, which precludes accurate staging and treatment. All patients diagnosed with cutaneous melanoma undergo a thorough skin assessment and clinical evaluation of the relevant nodal basins. Further screening workup for newly diagnosed patients with invasive melanoma includes chest X-ray, complete blood count, liver function tests, and serum lactate dehydrogenase (LDH). Abnormal findings in the review of systems or these screening modalities should prompt further imaging studies such as computed tomography (CT) scanning or positron emission tomography (PET) scan. Patients with head and neck primary tumors are likely to benefit from CT or PET imaging to identify suspected nodal involvement. Further metastatic workup includes serum alkaline phosphatase, serum creatinine, body CT imaging, MRI of the brain, and bone scan. The AJCC recently updated the staging system for melanoma from the previous system described in 2001 (Tables 14.4 and 14.5).18 The widespread use ofsentinellymph node biopsy as well as a large collaborative effort among clinicians has allowed the AJCC to update the staging guidelines

using evidence-based data collected over the past decade. Using a population of 38,.918 melanoma patients, the 2009 AJCC Staging and Classification guidelines identified several new findings. Tumor thickness, mitotic rate, and ulceration were d:&e most significant prognostic factors associated with localized tumors. Furthermore, since mitotic rate is the second most powerful predictor of survival after tumor thickness, it was recommended that the mitotic rate replace Clark's level as a criterion for defining Tlb lesions. dark's level is no longer recommended for use in melanoma staging. TheN component (Regional Lymph Nodes) of the TNM classification system was modified to include the number of metastatic nodes, overall tumor burden, and ulceration of the primary lesion. The M component (Distant Metastasis) of the TNM classification system continues to be defined by the site of distant metastasis and elevation of serum LDH, which has been identified as an independent predictor of survival outcome in stage IV patients. Finally, all patients with microscopic nodal metasta· sis diagnosed by sentinel lymph node biopsy (including those identified by immunohistochemical staining) regardless of the overall tumor burden are classified as stage m, which gives a more accurate survival estimate for stage liB-IliA disease. The observed S- and 1 0-year survival rates by stage of patients diagnosed with melanoma are summarized in Table 14.6. However, prognostication in melanoma is a complex process and continues to evolve based on observations in clinical trials. Thus, factors not accounted for by the AJCC staging system, which are known to have an impact on prog· nosis (age, sex, anatomic location of the primary lesions, and number of distant metastases), contribute to the individual patient's long-term outlook. In an effort to develop a statistical model to predict survival outcome in localized melanoma using individual patient characteristics, the AJCC Melanoma Task Force released an Internet-based prognosis tool based on clinical data from >50,000 melanoma patients (http:/lwww. melanomaprognosis.org). 24 This tool was successfully validated on an independent data set and represents a valuable tool for clinicians to use to provide patients with real-time evidenced-based prognosis data based on their individual case characteristics.

Surgical Management Wide and Deep Excision. Surgical excision not only is critical for establishing the diagnosis but is also the definitive management of malignant melanoma. Historically, 5 em margins were advocated for local tumor excision based on observations that melanoma had a propensity to recur adjacent to the primary site. Over the past few decades, however, the guidelines for surgical margins have been redefined by sev· eral randomized prospective clinical trials25 -31 and are largely based on the thickness of the primary lesion (Table 14.7). In many cases, the primary tumor can be managed with a full thickness elliptical excision, down to the level of deep mus· cular fascia, with primary closure. Challenging anatomic sites include the ear, face, hands, and feet. Melanoma of the ear is generally treated by full thickness wedge excision and primary closure due to the proximity of the underlying car· tilage to the thin overlying skin. Primary lesions of the face can be particularly challenging, and every effort should be made to excise the primary lesion with recommended margins. However, narrower margins in anatomically complex areas for intermediate thickness lesions (1 to 4 mm) may be considered-there is a higher rate of local recurrence, but no significant impact on long-term survival.:u Invasive melanoma of the fingers and toes often requires amputation through the mid-phalanx proximal to the primary lesion (Figure 14.6). In subungual melanoma of the index, middle, ring, or little fingers, this requires amputation through the mid-portion of the middle phalanx; for the thumb, through the proximal phalanx. Likewise, for the great toe (most common site of

Chapter 14: Dermatology for Plastic S1U'BeoD.8 R--Cutaneous Malignancies

121

TABLE 14.4

TNM STAGING CATEGORIES FOR CUTANEOUS MELANOMA • T CLASSIFICATION

• 1HICKNESS (MM)

• ULCERATION STATUS

Tis

NA

NA

T1

Sl.OO

a: without ulceration ;wd lllltosis 11mm1

T2

a:~thoutulceration

1.01-2.00

b: ~th ulceration T3

2.01-4.00

T4

>4.00

a:~thoutulceration

b: ~th ulceration a:~thoutulceration

b: ~th ulceration • N CLASSIFICATION

• NO. OF METASTATIC NODES

• NODAL METASTATIC BURDEN

NO

0

NA

N1

1

a: MicrometaswiS" b: Macrometaswis•

N2

2-3

a: Miaometaswis-" b: Macrometaswis• c: In transit metastaseslsatellites without metastatic nodes

N3

• M CLASSIFICATION

4+ metastatic nodes, or matted nodes, or in traDsit metastases/satellites ~th metastatic nodes

• SITE.

• SERUM LDH

MO

No distant metastases

NA

Mla

Distant skin, subcutaneous, or nodal metastases

Normal

Mlb Mlc

Lung metastases

Normal

All other visceral metastases

Normal

Any distant metastasis

Elevated

NA, not applicable; LDH, lactate dehydrogenase. • Micrometast:ases are diagnosed after .!lltlltinellymph node biopsy or when nodal met.ast:uis exhibits gross extracapsular exte!Won. •Macrometutues are defined as clinically detectable nodal metast:a.ses. Reproduced from Edge SB, Byrd DR, Compton CC, et al., ed!l. A]CC Cma1- Staging MJmwl. 7th edn. New York, NY: Springer; 2010.

digital melanoma) and remaining toes, amputation through the mid-proximal phalanx is recommended. Palmar or plantar melanoma requires excision down to the palmar/plantar fascia with primary closure or local tissue rearrangement. Dorsal lesions on the hands/feet or web-space lesions require soft tissue resection down to the tendon or bone with skin grafting or local flap coverage.

Sentinel Lymph Node Biopsy. The sentinel lymph node is the first lymph node in the drainage basin to receive afferent lymphatic communication from the primary tumor site, prior to spread to the other nodes in this region. Based on observations that this functionally defined node was nearly universally involved when lymph node spread of melanoma was detected in lymphadenectomy specimens, it was postulated that selective sampling of this important "marker" could serve as an accurate predictor of involvement of the rest of the nodal basin. Supported by numerous prospective randomized clinical trials, the feasibility and accuracy of sentinel lymph node biopsy has been definitively established. Dne to

the growing experience and success of sentinel lymph node biopsy, it is standard of care for patients at high risk for nodal metastases. Most practitioners advocate sentinel lymph node biopsy in clinical stage 1/U melanoma with tumor thickness from 1.00 to 4.00 mm and clinically negative node basins (Table 14.7). Additionally, consideration can be given to patients with tumors between 0.76 and 1.00 mm with features such as ulceration, lymphovascular invasion, age 4.00 mm tumors and clinically negative nodes benefit from the prognostic information obtained from sentinel node sampling. Technical limitations to sentinel lymph node biopsy include a previous wide and deep excision with extensive reconstruction and local tissue rearrangement, anatomic sites where there are more than one drainage basin (i.e., scalp), or anatomic sites where the primary is very close to the sentinel node (i.e., overlying the parotid) and y-detl!ction is difficult. In patients with a previous wide and deep excision who underwent simple closure, sentinel lymph

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Pan 0:: Skin and Soft Tissue

TABLE 14.5

ANATOMIC STAGE/PROGNOSTIC GROUPS FOR CUTANEOUS MELANOMA • PATHOLOGIC STAGING

• CIJNICAL STAGlNG StageO

Tis

NO

MO

Stage 0

TlS

NO

MO

Stage lA

T1a

NO

MO

Stage lA

Tla

NO

MO

Stasem

T1b

NO

MO

Stagem

Tlb

NO

MO

na

NO

MO

na

NO

MO

Stage IIA

Tib

NO

MO

Stage IIA

Tib

NO

MO

T3a

NO

MO

T3a

NO

MO

T3b

NO

MO

T3b

NO

MO

Stageim

Stageim

T4a

NO

MO

T4a

NO

MO

Stage IIC

T4b

NO

MO

Stage IIC

T4b

NO

MO

Stagem

AnyT

~1

MO

Stage IDA

T14a

N1a

MO

T14a

N2a

MO

T14b

N1a

MO

T14b

N2a

MO

T14a

N1b

MO

T14a

N2b

MO

T14a

N2c

MO

T14b

N1b

MO

T14b

N2b

MO

T14b

N2c

MO

AnyT

N3

MO

AnyT

AnyN

M1

StageDIB

Stage me

AnyT

Stage IV

AnyN

Mt

Stage IV

Reproduced from Edge SB, Bynl DR, Compton CC, et al., eels. AJCC Cancn Smging Manwll. 7th edn. New York, NY: Springer; 2010.

node biopsy is a viable option and should be performed where indicated. The process of sentinel lymph node biopsy involves mapping the sentinel lymph node by two complementary techniques: preoperative lymphoscintigraphy and direct intra· operative visualization of draining lymphatic patterns using a blue dye. Typically on the morning of surgery, patients receive an injection of r-emitting radioactive colloid (commonly

technetium-.9.9m) around the primary tumor site, followed by serial images of the r-emission pattern. As the colloid enters the lymphatic channels surrounding the lesion, it travels to the first lymph node where it collects, forming a "hot spot" on the emission imaging (Figure 14.7). This identifies the anatomic l.oc:arion of the sentinel node, but gives no information as to whether it contains metastatic melanoma. This area is marked and the patient is sent to the operating suite with the images

TABLE 14.6

SURVIVAL RATES FOR CUTANEOUS MElANOMA BY STAGE • SY (%)

• tOY(%)

97

95

Stagem

92

86

Stage IIA

81

67

70

57

53

40

• STAGE Stage lA

Stage DB Stage DC

--

Stage IDA

78

59

StageDIB

59

43

Stage me

40

24

Stage IV

15

10

Data n:ttapolated from Edge SB, Byrd DR, Compton CC, et al., eels. AJCC c:-cn St~agmg ~. 7th edn. New York, NY: Springer; 2010.

Subungual melanoma

FIGURE 14.6. Typical level of amput11tion for a subungual melanoma..

Chapter 14: Dermatology for Plastic S1U'BeoD.8 R--Cutaneous Malignancies

123

TABLE 14.7 SURGICAL TREATMENT FOR CUTANEOUS MELANOMA

• TUMOR THICKNESS

• REGIONAL LYMPH NODB

• EXCISION MARGIN

TREAT.MENT

In situ

O.San

None

Less than 1.0 mm.

1an

None"

1.0to4.0mm

2cm.

Sentinel lymph node biopsy

Greater than 4.0 mm.

2to3an

Sentinel lymph node biopJt

"CoDSideration for sentiDelly:mph node biopsy can be given for tnmOts between 0.76 and 1.00 mm. with reatoft.S such as ulceration, lymphovascnlat invasion, age 2 em but SS em maximum tumor dimeDsion >5 em maximum tumor dimeDsion Primary tumor invades bone, muscle, fascia, or cartilage • NODAL METASTATIC BUIIDEN

No regional lymph node metastasis Nodes negative by clinical examiuatioll" (no pathologic node examination performed) Nodes negative by pathologic examination Metastases in regional lymph node(s)

Nl Nla Nlb

Maaometastasis•

N2

In transit metastasis4

• M CLASSIFICATION MO

Ml Mla

Mlb Mlc

Micromewwi~

• sm No distant metastasis Metastases beyond regional lymph nodes Metastases to skin, subcutaneous tissues, or distant lymph nodes Metastasis to lung Metastases to all other visceral sites

"CCinical detection of nodal diseaae may be ria inspection, palpation, and/or imaging. 'Mkromewtue~ are~ aft2r aentinel or elective lymp"hadenectomy. 'Macromewwes are defined as clinically detectable nodal metastases confirmed by therapeutic lymphadenectomy or needle biopay. "'n transit metastasia: a tumor distinct from the primary lesion and locaud either (1) between the primary leaion and the draining regional lymph noda or (2) distal ro the primary leaion.

Reproduced from Mtrkel cell carcinoma, Cbaptu 30, AJCC Cmcn St4gmg Mllmlal. New York, NY: Springer; ZOo.!'.

SEBACEOUS CARCINOMA

FIGURE 14.9. Dermatofibrosarcoma protuberans arising from a prior scar. (Photo cou.n:eoy of Richard L. Shapiro, MD.)

Sebaceous carcinoma (also refem:d to as sebaceous gland carcinoma, sebaceous cell carcinoma, or meibomian gland carcinoma) is a rare, aggressive neoplasm that originates from cells within the sebaceous glands. A majority a£ sebac:eous carc:ino-ma oc:au in the periocular region, oommoDly in the eyelid, and usually arise from the meibomian glands a£ the tarsus. These tumors may arise de novo, but some have been shown to originate from preexisting sebaceous lesions such as sebaceous nevus. Muir-Torre syndrome is an autosomal dominant skin condition characterized by sebaceous skin tumors (including sebaceous carcinoma) associated with internal malignancies such as gastrointestinal, gynecologic, or urologic tumors. The most common clinical presentation of sebaceous carc:inoma is a painless, round, subcutaneous nodule. However, due to their varied clinical and histologic appearance, sebaceous carcino-mas commonly mimic benign or less aggressive lesions, which may lead to a delay in diagnosis or inappropriate t.re.atment. Patients presenting with atypical or recurrent chalazion, eyelid thickening, or persistent blepharitis should prompt evaluation for sebaceous carcinoma. Older age and female sex are impor· tant risk factors for developing these tumors. Orbital imaging may be performed if there is extensive periocular involvement. Histologic diagnosis is confirmed by either incisional or excisional biopsy, which should include

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TABLE 14.9

ANATOMIC STAGE/PROGNOSTIC GROUPS FOR MERKEL CELL CARCINOMA • STAGB

• T

0

11s

IA

T1

IB

T1

IIA.

T2orT3 T2orT3 T4 AuyT AuyT AuyT

liB

nc IliA

IIIB IV

• N NO pNO c:NO pNO c:NO NO Nla NlborN2 AuyN

• M MO MO MO MO MO MO MO MO Ml

Reproduced from Merkd. cell carcinoma, ChaP= 30 AJCC Cmeer St4gmg ~- New York, NY: Springer; 2009.

full thickness skin, tarsus, and palpebral conjunctiva. The mainstay of treatment is Slll'gical, using wide local excision with S to 6 rwn margins or by Mobs' micrographic surgery. Tumor extension posteriorly may require orbital exenteration. Recurrence occurs in up to a third of cases and metastases arise in about 25% of patients. Radiation therapy is reserved for treatment of metastatic disease or for orbital involvement in patients who do not wish to undergo exenteration.

1. Am.etiaul. Cancer Society. Cuk:lff' FIICU 6' Piglll'll11 2010. Atlanta. GA: American CaJ1cer Society; 2010. 2. Rogeu HW. Wei11ttock MA. Harm AR. et al mcidence e.timate of nonmela110m11. skin C.t~.D.cer in the United States. 2006. Af'eh DtmNUol. 2010;146:283-287. 3. Americ.rulSocietyofP!atticSwgeollll.2008 R«omtfWaiveS~Proatllnw. Arli.Dgton Heights.IL.: American Society of Plastic Swgec>IIS; 2008. 4. Si1Te1'mll.ll. MK, Kopf AW. B.art RS, Grin CM. LeYmstein MS. Recunence rata of ueated bii.SII.l cell carci110mas. Part 3: sutgical excisioD.. J Demuuol SNrg Oneol. 1992;18:471-476. S. Wolf DJ. Zitelli JA. Surgical mugi11t for bual. cell carcinom~~.. Areh Dtlmf.fltOl. 1987;123:340-344. '· Mostetd K. Krehlt GA. Nieman FH. et Ill Swgical excision ..ersu.s Mohs• micrographic surgery for prim~~.ty 11.11d recuttent haul-cell carcinoma of the face: a proepective rll.lldomised controlled trial with S-yearti' follow-up. Uuu:# Onecl. 2008;9:1149-1156. 7. Rowe DB, Carroll RJ. Day CL Jr. Long-term~ mtea in preyiously Wlttell.ted (primllry) bual. cell carciiiOma.: implicatioiiS for patient follow-up. J DtlmUUOl SMrg Onecl. 1989;15:315-328. 8. jemal A, Siegel R. Xu J. Ward R. Cll.llcer ttatittics. 2010. CA Ctltnaf' J Clm. 2010;60:277-300. 9. jensen P. H.tmsell. s. Mlilller B. et Ill Skin CII.IICef in kidney and heart ttansp!ll.llt recipients ll.lld different long-term immunosuppressi...e therapy regimens. J AmAMJ ~ 1999;40:177-186. 10. Hartevelt MM. Ba'fillck JN. Kootte AM. Vermeer BJ. Vandenbrouclre JP. Incidence of akin cancer after renal transp!ll.lltation in The Netherlands. Tf'tlfl$p~. 1990;49:50'·509. 11. Glogau RG. The risk of progreaion to inYasi...e dise.ue. J Am At:~~d DtmN#Ol. 2000;42:23-24. 12. Mittelbro11.11 MA. Mullil1ll DL. ~Caro FA. Flowers FP. Frequency of pre-exitting actinic lceratotis in cut.t1.11e0ua squamous oell carcinom~~.. Int J Dl!l'ml4lol. 1998;37:6'77-681. 13. Crisc:ione VD, \VeillsttK:k MA. Naylor MF, et Ill A.:tinic bratoses: natural history and risk of malignant transformation in the Veterans Affairs Topical Tretinoin Chemoprevention Trial. Curar. 2009;115:2523-2530. 14. Quaedvlieg PJ, Tini E, 'Ihis!len MR, Krebls GA.~ keratosis: haw to diferentiate the good from the bad ones? EwJ Dmlf#tOI. 2006;16:335-339. 15. Yu RC, Pryce DW, Madiu:lane AW, Stewart T\V. A histopathological study of 6'43 cutlllleo\111 hol'IIS. Br J Dlmll4lal. 1991;124:449-452. 16. MicaH G, Inne50%

FT > 75%

1• closure wtth canthotomy and cantholyals, local tissue advanced with Tenzel semicircular flap, or sliding tarsoconjunctlval flap wHh skin graft

Sliding tarsoconjunctival flap wiltl skin graft

Composite graft with cheek advancement

H.f.f:llll

All: Routinely probe and intubate the lacrimal system

Cheek advancement flap

Hewes procedure

Hughes procedure

Medially based myocutaneous flap from upper lid

All: Lateral canthal support proc9dure

FIGURE 32.2. R.econsttuc:tive a.l3orithm based on recoD.SttUc:tive zones.

Other local flaps

OR Skin graft wtth FTSG

354

Part IV: Head and Neck

width of the flap should match the width of the upper eyelid defect, and vertical full-thickness incisions are made to the inferior fornix at this width. The flap is advanced posterior to the remaining lid margin and s~red into the upper eyelid defect with a multilayer closure. The conjunctiva can be separated from the musculocutaneous flap, and a cartilage graft can be placed for added support as this flap typically has little or no tarsus within it.2 The flap is divided at approximately 6 weeks with 2 mm excess vertical height. This allows for the removal of 1 to 2 mm of musculocutaneous tissue and anterior rotation of a conjunctival flap, which in tum provides a lid margin with a mucous membrane lining instead of keratinized epithelium. The lower eyelid often requires revision. The disadvantages of this repair include (1) a two-stage reconstruction with obstructed vision between stages, (2) disturbance to the lower eyelid that may require future revision and/or lid-tightening procedures, and (3) lack of lashes in the reconstructed segment. The Tenzel semicircular flap is a regional flap that provides tissue for both the anterior and posterior lamellae. 8 A superiorly based semicircular flap of up to 6 em in diameter is designed and advanced medially. A canthotomy is required; and once advanced, the flap must be secured to the lateral orbital wall to provide support and help recreate the natural convexity of the upper eyelid. The conjunctiva is also undermined and advanced to provide the lining of the flap. This flap is ideally suited for those defects that encompass 40% to 60% of the upper eyelid.2 For large defects (those greater than 75%), the Mustarde lower lid switch flap is an option.9 A large full-thickness portion of the lower eyelid is rotated based on the marginal vessels to fill the upper eyelid defect. This flap is typically delayed up to 6 weeks before pedicle division and inset. This flap provides a composite reconstruction of the upper eyelid and, therefore, the possibility for adequate protection of the globe. The disadvantage is that it sacrifices a significant portion of the lower eyelid that must then be reconstructed with cheek advancement and posterior lamella grafts. Other options for large upper eyelid defects that involve other surrounding zones include a forehead flap, a Fricke flap, or a glabellar flap (see section "Zone 3: Medial Canthal Reconstruction"). The Fricke flap borrows lower forehead tissue as a laterally based unipedicled flap, which can be transposed to reconstruct either an upper or lower eyelid defect.

Zone 2: Lower Eyelid Reconstruction Lower eyelid defects are more common than defects in other zones because of the higher incidence of lower eyelid skin cancer (Chapter 14). The lower eyelid is anatomically analogous to the upper eyelid, that is, where the capsulopalpebral fascia is homologous to the levator aponeurosis and the inferior tarsal muscle is homologous to Mueller•s muscle. The main difference is that the lower eyelid is shorter and the tarsal plate is 4 mm in vertical height compared with 10 mm in the upper eyelid. Although lower eyelid position is extremely important in protecting the globe and preventing dryness, it plays a relatively passive role when compared with the upper lid. Reconstruction of the lower eyelid can be approached algorithmically. Similar to the upper eyelid, lower eyelid defects are treated based on size and on which layer is missing. For superficial defects involving up to 20% of lower lid length, primary closure is usually possible in older patients; younger eyelids have less laxity. As the wound approaches 50%, closure with local tissue advancement is required and, in many cases, a lateral canthotomy is required. A tension-free repair is necessary or lid malposition will result. There are aesthetic benefits to using the normal lid margin when local tissue advancement is utilized in comparison to reconstructive options that reconstruct the lid margin with other tissues.

For superficial defects greater than 50% of lid length with a healthy wound bed, a full-thickness skin graft is a good option. Alternative options are local myocutaneous flaps, including the unipedicled Fricke flap and the bipedicled Tripier flap. The Tripier flap is a bipedicled flap from the upper eyelid transposed to reconstruct lower eyelid defects. This flap includes preseptal orbicularis oculi muscle. The Fricke flap is similar but is a unipedicled flap and is adequate for defects that extend to the mid-lower eyelid or just beyond. The bipedicled option is better utilized in larger defects. Both flaps incorporate more soft tissue than a full-thickness skin graft and, thus, provide for a thicker reconstruction that may require revisional debulking. Small full-thickness lower lid defects are closed primarily. Care is taken to align and repair the tarsal plate. As in partial-thickness defects, a lateral inferior cantholysis may be required to prevent tension. To avoid dog-ear formation at the inferior aspect of the closure, the incision should be slanted laterally or a Burow's triangle can be removed. Once defects are greater than a few millimeters, they are best divided into those that involve 75% of the lower eyelid. Full-thickness defects that are 50% or less of the lower eyelid can be approached with the inferiorly based Tenzel semicircular flap. 8 The semicircular incision extends superiorly and laterally with a diameter of 3 to 6 em depending on the defect size and tissue laxity. Dissection is in a submuscular plane, and the inferior ramus of the lateral canthal tendon is divided to allow medial rotational advancement. In larger defects, there may be a paucity of support laterally since the tarsus is advanced medially. In these cases, the flap can be supplemented with a laterally based periosteal flap, concha] cartilage, or septal cartilage. The flap can also be supported with sutures to the lateral orbital periosteum. For defects larger than 50%, the anterior and posterior lamellae are typically reconstructed separately. For lateral full-thickness defects involving 50 to 75% of the lower eyelid margin, the posterior lamella can be addressed with the Hewes procedure.10 A laterally based upper eyelid tarsoconjunctival flap is pedicled on the superior tarsal artery and transposed to the lower eyelid. The anterior lamella can then be reconstructed with a skin graft or a second upper eyelid flap such as the Tripier flap. When defects of this size are centrally located, the Hewes procedure may not provide enough length for transposition; and a tarsoconjunctival graft is an alternative option. When the posterior lamella is reconstructed with a nonvascularized graft, the anterior lamella must incorporate well-vascularized tissue. Options include a myocutaneous flap from the upper eyelid or vertical myocutaneous flap from the lower eyelid and cheek.2 The vertically based myocutaneous flap is developed just as a skin muscle flap is elevated in a lower blepharoplasty. On vertical advancement, triangles of redundant tissue are removed. An alternative method for reconstruction of the posterior lamella is the Hughes tarsoconjunctival flap procedure6 from the upper lid which is best for defects greater than 50%, including total lower eyelid reconstructions. The flap is developed starting 4 mm above the upper eyelid margin to avoid compromising upper eyelid integrity and consists of a segment of tarsus and conjunctiva. The width is designed to match the missing posterior lamella segment of the lower eyelid and advanced into the lower eyelid defect. The advanced tarsal segment is secured to the remaining lower eyelid tarsal borders, canthal tendons, or periosteum depending on what remains. This vascularized flap is then covered with a full-thickness skin graft or a myocutaneous flap obscuring vision for several weeks. Separation of the Hughes flap can be performed at 3 to 6 weeks. At this stage, care is taken to allow both Muller's muscle and the levator to retract to their native positions to preserve upper eyelid function. In addition, in the lower eyelid the conjunctiva is rolled over the recreated lid margin to prevent irritation from corneal contact with keratinized skin.

Chapter 32: Rec.onmuc:tion of the Eyelicb, Correction of PtoJ:is, and Caathoplasty The alternative for defects greater than 75% is the Mustarde flap. 11 The traditional Mustarde approach includes a large rotational cheek flap advanced to reoonstruct the anterior lamella and a nasal chondromucosal graft to reoonstruct the posterior lamella. As highlighted earlier, alternatives are available for posterior lamella grafts. The flap is designed to extend superiorly toward the brow so that closure will result in upward tension on the lower lid. Once elevated and advanced, the flap is secured either to the medial canthus or to medial orbital periosteum. The flap is sutured to the periosteum laterally at a point above the lateral canthus.

Zone 3: Medial Canthal Reconstruction The medial canthal region is anatomically complex and requires attention to the lacrimal system. When defects of both the upper and lower eyelids encroach on the medial canthus, one must address the canalicular system via intubation with a silicone tube. Once the lacrimal system is protected, attention is directed to the supporting structures of the medial canthus. If the medial retinaculum is detached from the bone, it must be .reattached via the posterior reflection on the lacrimal crest posterior to the lacrimal sac. This location of fixation serves the dual function of avoiding damage to the lacrimal system and maintaining the natural curve of the lower eyelid directly apposed to the globe. When a medial canthal tendon deficiency is present, a fascial graft can be incorporated into the repair. Methods for fixation include sutures to the periosteum, drill hole fixation, bone anchors, and in cases of bone deficiency, transnasal wires or to a gap spanning plate. The skin defect is addressed in a number of ways. In the appropriately selected patient, healing by secondary intention is an acceptable method in the medial canthus. This method may result in epiphora, epicanthal folds, and medial ectropion. As in other periorbital defects, a .full-thickness skin graft is also a valid option, but contraction may yield an unsightly result. A medially based upper eyelid myocutaneous flap, based on the infratrochlear vessels, can be rotated to cover relatively small defects. Unique to the medial canthus is the glabellar flap, which is a modified rhomboid flap or a V-Y flap that provides for immediate closure of large medial canthal defects.5 Cutaneous coverage in this region by any method frequently results in cicatricial epicanthal folds requiring revision.

Zone 4: Lateral Canthal Reconstruction The crucial element of zone 4 is the fixation provided by the lateral canthal tendon, which almost always requires attention in zone 4 reconstructions and a large number of other periorbital reconstructions. When the tendon is present but lax, a simple canthopexy is performed. When the lateral canthus is disrupted but present, a canthoplasty is performed. In both situations, the goal is to overcorrect the tissue laxity as recurrent laxity is expected.s When no lateral canthus remains, alternative reconstructive methods must be employed. If sufficient upper and lower tarsal plates are present, then lateral advancement is possible. The tarsal plates can be secured to the lateral orbital periosteum at the level of Whitnall's tubercle. If needed, a tarsal strip can be fashioned to help with lateral fixation (see section "Lower Eyelid Malposition"). If no orbital perios· teum is present, then drill holes are made; and in situations of bone deficiency, a bone spanning plate is used.l.S If there is no preexisting eyelid laxity, then a tarsal strip may not be sufficient; in these situations, crossing periosteal flaps can be elevated from the lateral orbital rim. When larger defects of the upper or lower eyelid tarsal plates are present, then the reconstructive technique utilized for posterior lamella reconstruction is incorporated into the lateral can· thal reconstruction. The skin defect is approached either with a local flap or a full-thickness skin graft. Local flap options include an

355

inferiorly based cheek flap, two small semicircular flaps, or a superiorly based rotational flap. Rhomboid transposition flaps can also be used. The goal is to create an acute angle with a lateral canthus slightly higher than its corresponding medial canthus (Chapter 46).

Zone 5: Periocular Defects Reconstruction Zone 5 defects include the periocular areas that are contiguous with zones 1 through 4. Often a zoneS defect occurs in conjunction with defects in other zones, and, in these situations, the principles discussed above are modified to allow reconstruction from the remaining available tissue. When an isolated zone S defect occurs, the other zones are often still affected. For instance, cheek rec.onstruaion will often result in lower lid malposition, even if the lower lid is normal if insufficient attention is paid to lower lid and/or canthal support.

CO:MPLICATIONS Complications occur more commonly in large reconstructions, specifically when the defect is greater than SO% in zone 1 or 2 and when the defect is greater than 4 em in zones 3, 4, and S. AU medial canthal reconstructions are fraught with higher complication rates. Inadequate lateral canthal support also results in higher complication rates. 5 Early complications include corneal abrasion, chemosis (which can often be limited by a Frost stitch or temporary tarsorrhaphy), hematoma, and/or flap/graft failure. Late complications include corneal exposure, canthal laxity. lid malposition, abnormal lacrimal drainage, and an unsatisfactory cosmetic result.

ADJUNCTIVE PROCEDURES Periorbital anatomy is a critical component of appearance. Therefore, a thorough understanding of secondary procedures to optimize the aesthetic outcome is paramount. Contour defects often occur following periorbital reconstruction. These defects can be related to fat atrophy and/or adhesions between the various layers. As in other areas, fat grafting is a validated periorbital adjunctive procedure (Chapter 44). In both the medial and lateral canthal zones. epicanthal folds can develop following reconstructive efforts. These are addressed with a single Z-plasty, double Z-plasties, or a Mustarde "jumping man" flap.l1 In addition, a larger transposition Z..plasty and canthal tendon repositioning are required for vertical displacement of either the medial or lateral canthus.

LOWER EYELID MALPOSmON Lower eyelid position is dictated by the balance of intrinsic and extrinsic forces. When in equilibrium, the lower eyelid is positioned approximately 1 mm above the lower limbus firmly in contact with the globe. Imbalance in these forces results in lower lid malposition, producing scleral show and potentially ectropion (eversion of the lid) or entropion (inver· sion of the lid). Age produces involutional changes, and scarring from trauma or surgical intervention produces cicatricial changes, both of which affect the balance of forces resulting in lid malposition. Age-related instability in the lower eyelid is caused by progressive laxity in the tarsoligamentous sling. Ectropion may result from orbicularis oculi atrophy, and entropion may result from orbicularis oculi hypertrophy. The approach is similar between the two conditions with the focus on tightening of the tarsoligamentous sling with various types of canthopexy or canthoplasty. In contrast, cicatricial ectropion or entropion is typically caused by scarring in one of the lower eyelid layers resulting in a tissue deficiency and is treated by tissue replacement.2

356

Pan IV: Head and Neck

film breakup test. In addition, any signs of corneal irritation are documented. t.l

Preoperative Evaluation As in all periorbital procedures, a standard eye examination is important. Specific to lower lid malposition, evaluation focuses on the important regional anatomy, including the canthal position, the lower lid position, the extent of eversion or inversion, anterior distraction and snap tests to asses tone and laxity, and the malar Npport. The snap test is performed by pulling the lower eyelid down and away from the globe, holding it there for a kw seconds, and grading its propensity to ret:um to the initial position. A normal lid returns to a normal anatomic position immediately, and an abnormal examination is any deviation away from this. The relationship between malar support and the globe has been described by Jelks in terms of a positive or negative vector and is discussed in terms of cosmetic surgery in Chapter 46. If the comea projects past the inkrior orbital rim, then a negative vector exists. A negative vector is a known risk factor for lower eyelid malposition in periorbital surgery.u The adequacy of globe lubrication via 1Ur production is evaluated with the Schirmer test and the 1Ur

Surgical Approaches Lower eyelid malposition can be addressed with a number of corrective procedures.14 A proc:edure addressing the lateral c:anthus is always required. Cases of c:katricial abnormality require addition of tissue and cases of lid laxity require removal of the tissue. In cicatricial ectropion, the anterior lamella can be reconstructed with a skin graft or local flap as described in the eydid reconstruction section. In cicatricial entropion, the posterior lamella can be reconstructed with a palatal mucosal graft. There are also complex forms of ectropion and entropion involving multiple layers that require a combination of procedures including a cartilage spacer graft.2

Canthopexy. In a standard aanthopexy (Figure 32.3), the canthal tendon is not divided or shortened but is resecared in a new position. Only mild lower lid laxity can be treated in this fashion. Canthopexy is attractive because it involves

A Eyelid droop due to lateral canlhal tendon attenuation

Line of division of lateral rellnaculum

for common canthoplasty

B Common canlhal tendon Is retracted laterally and superiorly then anchored to periosteum

Closeup of common canthopexy

C Effect of completed repair

FIGURE 32.3. Canthopexy. The auuhopexy is a common procedure WJed in adjunct to other periorbital procedures. Reproduced from Spinelli HM. Eyelid malposition& 1D: Spinelli HM, ed. Atlas ofAesthetic Eyelid and Pt:riocu/4r Surgery. Philadelphia, PA: Ebevier; 2004:47, with permission.

Chapter 32: Rec.onmuc:tion of the Eyelicb, Correction of PtoJ:is, and Caathoplasty minimal tissue disruption, can be performed from either a transcutaneous or transconjunctival approach, is relatively easy to perfol'D1, and does not risk deforming the normal acute angle of the lateral canthal region like the canthoplasty.

Canth.oplasty. Candtoplasty involves division o£ the lateral canthus with reconstitution and repositioning and is more oompl.a and versatile than canthopexy. When repositioning the canthal tendon, it should be reinserted on the inside of the lateral orbital rim to maintain lower eyelid contact with the globe. As mentioned in Chapter 46, the more prominent the globe, the higher the canthus is placed. The canthoplasty can

A

357

be combined with a lid-shortening procedure for laxity. The degree of lower lid excision is determined by pulling the lower eydid laterally to the lateral orbital rim. The new tarsal border is then s~ inside the lateral orbital rim. In some sitllations, specifically in cases of involutional entropion, redraping of the orbicularis oculi muscle is important for successful correction.1

Tarsal Strip Canthoplasty. The tarsal strip canthoplasty (Figure 32.4) is similar in design to the combined procedures described above but incorporates a canthoplasty with a lidshortening procedure. The redundant lower eyelid tissue is not completely excised but instead a strip of tarsus is denuded of

Lateral canthotorny

B

Dllllslon of lowar crus and wide

lateral lysis

c

D

Suture loe&tion of strip to interllfll

periosteum of lateral orbital rim

F Commissuropluty

E 'THm exoess skin and/or orbicularis muscle FIGUKB 32.4. The latx:ral tar&al strip procedure provides for a great deal of veraatility in repo&itiolliDi the lawai canthu&. Reproduced fr()DI Spinelli HM. Eyelid malpositions.ID: SpiDelli HM, ed. Atlal ofAesthetic Eyelid and Periocu/4r Surgery. Philadelphia, PA: Elsevier; 2004:39, with permission.

358

Pan IV: Head and Neck

skin and is used tD recreate the inferior component of the lateral canthal tendon. An approximately 3 mm wide segment of tarsus (depending on shortening required) is cirCUlllferentially stripped of all tissues, including the skin. lashes, conjunctiva, and capsulopalpebral attachments. This strip is then advanced and secured inside the lateral orbital rim. Redundant superficial tissue is excised, and care is taken to appropriately align the gray line of the upper and lower eyelids. This validated powerful tool has produced long-term satisfactory results, but has the potential disadvantages of distorting the punctual position of the inner canthus and creating a discrepancy be~n the upper and lower eyelids.:Z.14

UPPER EYELID PTOSIS Blepharoptosis, or ptosis, is an upper eyelid malposition in which the upper eyelid falls below its normal level of 1 to 2 mm below the upper limbus. Upper eyelid ptosis is caused by a number of anatomic problems involving the levator palpebrae superioris muscle or its aponeurosis and/or Muller's muscle. In addition to recognition of the anatomic problem, the etiology is relevant. Ptosis can be congenital or acquired. Congenital cases have poor levator function.

Evaluation and Examination Initial examination is focused on the levator palpebrae superioris muscle and the levator aponeurosis. The levator function, or excursion, is measured by immobilizing the brow and monitoring the upper eyelid movement from downward gaze to upward gaze. The difference between levels of the upper lid margin in each position is recorded. Normal excursion is 12 mm with an acceptable range of 10 to 15 mm. Fair function is 6 to 9 mm and poor function is S mm or less. Levator dehiscence is typically from a thinning and stretching of the levatDr aponeurosis, allowing dehiscence from the tarsal plate and ptosis. In many cases, the connections to the dermis are not attenuated, which results in an increasingly elevated supratarsal fold as the ptosis worsens. Levator dehiscence is an acquired involutional problem in older adults but can occur in trauma as weU. As in the other areas of periorbital surgery, standard ophthalmologic examination is important. Specific to the upper eyelid ptosis, important clinical information includes a standard history to elicit systemic disorders that could cause eyelid ptosis. There should be a low threshold for a formal neurological examination, especially when there are other signs of a neuromuscular process, such as myasthenia gravis. Regionally, pseudoptosis can present as an inferiorly displaced upper eyelid that is not actllally related to the eyelid retractors but instead to a separate orbital issue. This is seen in enoph· thalmos, brow ptosis, orbital tumors, and dermatochalasia.

The goal o£ ptosis surgery it to restore the upper eyelid to its correct position while creating as 1ittk lid stiffness and lagophthalmos as possible. In an effort to avoid compromit· ing proteaion of vision, a preoperative examination should verify an intact Bell's phenomenon and the protective capacity of both eyelids.

Surgery The surgical approach to ptosis typically involves levator manipulation (Table 32.1). Regardless of the chosen procedure, some technical points are worth emphasizing. Epinephrine can stimulate Muller's muscle and produce a 1 to 2 mm elevation of the upper lid and must be accounted for during final eyelid adjustments. When assessing upper eyelid position, the lights should be dimmed as bright lights cause squinting. If available, transparent corneal shields are used to allow for visualization of the pupil.

Levator Repair or Resection with Advancement. The levator repair or advancement procedure is the versatile procedure used for upper eyelid ptosis and is applicable to a wide range of severity. As long as greater than 5 mm of levator excursion exists, this procedure is an option. A standard upper blepharoplasty incision is used, allowing for concurrent removal of redundant skin and orbicularis oculi muscle. The septum is opened and preaponeurotic fat is retracted exposing the leva· tor aponeurosis. If intact, the aponeurosis is incised near the tarsal border; and the levator is elevated of£ of Muller's muscle. The levator is advanced over the tarsal border to simulate the levator advancement. In general, 1 mm of levator advancement gives a 1 mm coiTC(;1]on of ptosis, but results vary based on the degree of levator function and can be difficult to standardize. An awake patient can cooperate to help guide the appropriate amount of advancement. If this technique is utilized, a temporary suture is placed at the presumed level of advancement, the patient is repositioned to a sitting position, the overhead lights are pointed away from the patient, and the patient is asked to look up and down. Once the appropriate advancement is determined, the aponeurosis is secured to the tarsal border and excess is excised.3 An alternative technique involves placement of a double-ann suture 2 to 3 mm below the superior border of the tarsal plate at the pupil midline brought out at the mus· culoaponeurotic junction. A surgeon knot is then tightened until the upper and lower eyelids are gapped; and a spring back test, similar to that utilized for evaluating lower eyelid laxity, is employed to set final tension.1 A levator plication can alternatively be performed with a similar approach. In this technique, the levator aponeuro· sis is exposed but not divided or elevated and vertical plication sutures are placed to tighten the levator aponeurosis. lt requires less dissection than the levator advancement but can result in a bulge from redundant tissue.

TAILE 32.1 PTOSIS ALGORITHM: BASED ON THE EXTENT OF LEVATOR EXCURSION AND THE DEGREE OF PTOSIS THE APPROPRIATE PROCEDURE CAN BE SYSTEMATICALLY DETERMINED • UPPBR BYELID PTOSIS

. PTOSIS

Z

~

~ ~

Good (1Q-1S mm)

Mild (2-3 mm)

Moderate (3-5 mm)

Severe (>5 mm)

Levator advancement

Levator advancement

Levator advancement

Levator plication

Levator plication

Tarsal conjunctival mullerectomy Fair {6-9 mm) Levator advancement Levator advancement Levator advancement ----~----~------------------------------------------------------------------------Poor ( 4, NIMF > 9, and PCSEF < 20%) are also prone to rippling. These situations should be identified preoperatively. No type of breast implant can compensate for inadequate tissue coverage, and deformities that occur are largely uncorrectable. Surgeons should consider refusing to augment breasts when such tissue problems are significant. The role of tissue coverage in preventing rippling cannot be overstated. Therefore, the priority at primary augmentation is to maximize coverage and avoid tissue damage.

FIGURE 53.15. Same patient after using a higher cohesive implant. Underfill rippling is eliminated, but traction rippling creates lines of tension. Just as with underfill rippling, thicker tissue coverage and betu:r skin elasticity redua:.s its appearance.

FIGURE 53.17. But the implant is just one component of her deformity; parenchymal atrophy, thinned skin, redundant skin, and a chest

wall concavity will preclude her from n-er having attractive breasts.

Chapter 53: Augmentation Mammaplasty: Principles, Techniques, Implant Choices, and Complications

571

Asymmetry Breast asyrwnetry is normal but if it is not documented pre· operatively it may later be attributed to the surgery. 'Threedimensional breast photo analysis has revealed that 72% of patients have significant nipple asyrwnetry and 94% have significant breast-mound asyrwnetry.' These should be demon· strated to the patient preoperatively and the patient should be made specifically aware that her breasts will not match. Attempts to treat underlying asymmetries require trading one asymmetry for another. When trying to equalize breasts of different volumes, the larger breast would receive the smaller implant and the smaller breast would le(;Cive a larger implant. The smaller breast would appear more full and the larger breast less full. These choices can be appropriate but should be made only after careful consideration. The use of different size implants to aeate more volume symmetry frequently aeates a $hape Wliwnatch 1hat is more noticeable than the si2:e mismatch. The same planned N:IMF distance should be used on both sides, even if one nipple is higher. This assures breasts of more similar fill distribution, which is more aesthetically desirable than I.MFs at the same height. Patients must be aware preoperatively that this is intentional and implants placed in this manner are not malpositioned.

Permanent Tissue Damage Thin, weakened, stretched, and damaged tissues are responsible for the occurrence, severity, and difficulty in correaion of many of the common reasons for reoperation. The same minor malposition or capsular contracture which would not be vis· ible under thick tissue and tight skin can be quite visible under damaged tissue. Rippling is rarely an issue with good tissue coverage but becomes one when tissue is thinned. Finally, any problem that requires correction is more problematic to cor· rect when tissues are thinner or weaker (Figures 53.18-53.27). Both the surgical act of dissecting a pocket for a breast implant and the longstanding presence of an implant can cause atrophy of breast tissue. Prudent implant selection and exacting surgical technique can help preserve tissue integrity and minimize long-term parenchymal atrophy. Longstanding pressure against tissue causes remodeling: bras cause acromial grooving, orthodontics move teeth, and tissue expanders stretch and thin skin. A breast implant that stretches the

FIGURE 53.18. Two years after augmentation with high-profile implants. In addition to the inferior malposition, the pressure of the implants remodeled the rib cage. This reduces projection, makes an e:xplantation option highly defo1'1I1iD3, and increases the future likelihood of unde.dill ripplinl (see ..Ripplinl" section) because this forces redundancy of the ann:rior surfac:e of the implant.

FIGURE 53.19. Thinning of skin, parenchymal atrophy, and rib cage c:oncav:ity are all present in this patient. There is always a question of the extent to which this was preexisting, an iDev:itabllity of time, or an e:ffc:ct of the implant. Notice how her tissue changes e:xacdy correspond to the position of her implant.

breast envelope as much as would lactation can be anticipated to permanently stretch and alter breast tissue. Highly projecting implants place more pressure per area than a wider implant of the same volume. If width is held constant, highly projecting implants can be nearly twice the volume and weight, thereby placing substantially greater pressure on the rib cage as well as the soft tissue. This causes parenchymal atrophy, thinning of subcutaneous tissues, thinning and stretching of skin, loss of skin elasticity, rib cage deformation, and loss of sensation. In any case, if an implant of the proper volume is selected for a given breast, a high-profile implant would be excessively narrow for the breast and thereby create an imbalanced fill. If a high-profile implant is chosen of the proper base width for the breast, the volume is almost inevita· bly too great for the breast. These tissue changes can result in rippling, skin stretch requiring mastopexy, and bizarre animation deformities. Such problems are often not correctable, and attempts to mask them with highly cohesive implants, an acellular dermal matrix, and fat injections all result in imperfect corrections which are expensive and pose their own risks and drawbacks. On the other hand, extremely damaged tissue can almost rule out explantation alone as an option because of the severe deformity that results (and explantation should always be considered in recalcitrant post-augmentation complications). Preoperative decisions should make soft tissue cover· age a priority and surgical technique should strive to protect it. When the pinch of tissue overlying the IMF is less than S mm, consideration should be given to not dividing the origins of the pectoralis major muscle along the medial IMF. If the muscle is going to be divided along the IMF, it should only be released to the junction of the IMF and the lateral sternal border, but not even one interspace above that. To do so permanently thins tissue along the sternum, which can cause uncom:S em in greatest dimension Tumor of any size with direct extension to chest wall or skin only T4a Extension to chest wall T4b Edema (including peau d'orange) or ulceration of the skin of the breast or satellite skin nodules confined to the same breast T4c Both T4a and T4b T4d Inflammatory carcinoma

Rqponall~ph~(N)

NX

NO NO(i+) N1

N1mi N1a N1b N1c N2

RegiODallymph nodes cannot be assessed (e.g., were previously removed) No regiODallymph node metastasis Malignant cells in lymph nodes not greater than 0.2 nun Micrometastases or metastases in one to three axillary lymph nodes and/or internal mammary nodes with metastases detected by SLN biopsy Micrometastases only, >0.2 em but none greater than 2.0 mm. Metastasis in ODe to three axillary lymph nodes, at least ODe metastasis greater than 2.0 nun Metastasis in intemal mammary nodes detected by SIN biopsy Metastasis in ODe to three axillary lymph nodes and in intemal mammary lymph nodes detected by SIN biopsy Metastasis in four to nine axillary lymph nodes or clinically den:cted, internal mammary lymph nodes in the absence of axillary lymph node metastases Metastases in 10 or more axillary lymph nodes or infraclavicular lymph nodes

N3 Distant metutuis (M) MX

MO M1

Distant metastasis cannot be assessed No distant metastasis Distant metastasis, including metastasis to ipsilateral supraclavicular lymph nodes

balloon catheter. This allows radiation to be delivered locally the tissue at highest risk of recurrence. Randomized trials comparing APBI with standard external beam radiation have yet to mature but the early results appear promising. to

Oncoplastic Surgery Onc::oplasti.c surgery combines the oncological principles of tumor extirpation with plastic surgical te