chapter 4 and 4a introduction to medicine and dermatology

8/2/2019 Chapter 4 and 4a Introduction to Medicine and Dermatology

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4 Medicine

C o n t e n t s

4.1 Dermatology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 240

by Bryan C. Markinson, DPM

4.2 Diabetes Mellitus and Wound Care . . . . . . . . . . . . 255

by Nabil Fahim, DPM and

Mark Mandato, DPM

4.3 Emergency Medicine in the Podiatric Office . . . . . 277

by Melvyn Grovit, DPM, MS, CMS

4.4 Podiatric Infectious Disease . . . . . . . . . . . . . . . . . 283

by Mark Kosinski, DPM

4.5 Internal Medicine . . . . . . . . . . . . . . . . . . . . . . . . 303

by Sushama Rich, MD

4.6 Neurology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343

by Lawrence Diamond, MD

4.7 Peripheral Vascular Disease . . . . . . . . . . . . . . . . . 357

by Arthur Steinhart, DPM

4.8 Pharmacology . . . . . . . . . . . . . . . . . . . . . . . . . . . 365

by Gus Constantouris, DPM

4.9 Rheumatology . . . . . . . . . . . . . . . . . . . . . . . . . . . 405

by Arthur Steinhart, DPM

Medicine 239


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4.1 Dermatology

Bryan C. Markinson, DPM

Introduction To The Review for Dermatology

During my fellowship training, my mentor, W. Clark Lambert, MD Ph.D., reminded me more than once that

there were some 3500 skin diseases. He would say, If every podiatrist would examine every patients skin up to the

tibial tuberosity, he or she would pretty much be certain to encounter the vast majority of them. Taking him at his

word, I am pretty certain that I have not yet encountered 3500 different diseases, but increasing just the anatomic

boundaries of my examination as he suggested has changed my practice greatly.

The depth of this chapter will not approach the magnitude of clinical volume that Dr. Lambert states exists on

the lower extremities. It is not designed for that task. However, it has been compiled with his admonition in mind.

This dermatology review is specifically designed to be a source of compact information on skin diseases. Since

many podiatric board questions are given in case format, knowledge of organ-specific disease processes must be

studied from a broad perspective. For example, while psoriasis may cause pitting nail changes, it is important to

know that it may be part of a larger clinical picture in a patient presenting with distal inter-phalangeal joint arthri-

tis. Similarly, a case presentation centered on a neurotrophic foot ulceration may require you to be able to identify

causes of neuropathy other than diabetes. So preparing for this examination requires knowledge of not only specific

skin lesions but their relationship to the general medical condition of the patient as well. Indeed, many of the skin

conditions discussed will overlap with your studies of internal medicine, infectious disease, diabetes, etc.

It is strongly urged that you use this review chapter along with a good color atlas of dermatology to view the

lesions. In addition, unfamiliar terminology should be reviewed with an appropriate text.

In an attempt to make the review comprehensive and at the same time quickly usable, I have listed the disease

entity by name in bold and followed with specific bulleted key points about the condition. You can think of these as

points to pass. I am confident that they should closely represent the information that would be required of you in

most cases. The diseases are not grouped in any specific fashion. Of course, no guarantee can be made as to the

absolute utility of this review chapter. In past years however, approximately 1,000 doctors of podiatric Medicine have

been presented this material in lecture format and we have received an overwhelmingly favorable response.Best wishes to you for success on your examinations.

Bryan C. Markinson, D.P.M.

240 The 2005 Podiatry Study Guide


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The Patient Examination

The Dermatological History

Chief complaint

Onset of symptoms

Factors that exacerbate or alleviate condition

Response to prior treatments Are lesions related to work environment?

Are lesions induced or worsened by sun exposure, cold, heat, dryness, or hydration?

Is skin disease associated with fever?

Has previously stable lesion changed in any way?

Examination of the Skin

Observation

Color

Topography

Gross abnormalities

Discharge Hair distribution

Palpation - nodules, elevation, hardness, hydration, etc.

TSAD METHOD

Type: Primary or secondary lesion

Shape: dome, flat-topped, polygonal, linear, annular, serpiginous

Arrangement: Annular, Linear, or serpiginous grouping

Distribution: Symmetrical, dermatomal, segmental, random, localized, generalized

In a podiatric medical evaluation, the skin of the entire lower leg and foot should be exposed.

The room should be well-lit.

With completely undressed patients, make every effort to preserve modesty.

Physical Diagnostic Tools

Magnifying lens: 2x-10x - helpful in examining pigment deposition and used to observe dilated nail fold cap-

illaries in connective tissue diseases

Mineral oil: Applying to certain lesions will highlight pattern of colors. Useful in enhancing pigment, nail

fold capillaries, and striae

Side lighting: Causes textural changes of the skin to cast shadows, thus making them more visible. Can be

done with a penlight beam aimed transversely over the lesion. This technique demonstrates elevations and

depressions, which are characteristic of certain lesions. Example: Elevation of purpura in vaculitis

Diascopy: The application of or pressing of flat transparent glass on the skin to blanch away redness. Allows

true color evaluation, as well as helping to differentiate between purpura and vessel inflammation

Woods lamp/light: Emits long-wavelength ultraviolet light (black light). The exam is done with room lights

off.

Uses for Woods lamp:

Assess amount and location of skin pigment

De-pigmented areas fluoresce bright white.

Hypo-pigmented areas become more visible but do not fluoresce brightly.

Hyper-pigmented areas appear darker than adjacent skin when pigment in epidermis.

Dermal pigmentation is not enhanced.

Medicine | Dermatology 241


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Erythrasma (corynebacterium) fluoresces coral red.

Tinea capitis (M. canis, M. audouini) fluoresces green. Rare on feet.

Gram stain for pathogenic bacteria

Take specimen (pus) and fix with methyl alcohol

Crystal violet stain

Grams iodine

Alcohol decolorizer

Alcoholic safranin

Fungal scraping or KOH mount

Direct examination of fungal hyphae

Use #15 blade to scrape leading edge of lesion

Apply KOH and heat without boiling to dissolve keratin

Observe for hyphae

Does not allow for species identification

Fungal culture

Saborauds agar or DTM (color indicator)

Useful for dermatophtyes and candida - scrapings of skin implanted on media

May take up to three weeks

For nail specimens, use most proximal, subungual debris

Tzanck smear

Used for diagnosis of herpes virus infections

Identifies multinucleated giant cells

Base of a vesicle is scraped and material is put on slide, air dried, and then heat fixed

Add Giemsa stain and allow to dry

Examine under microscope

Wound culture

Biopsy

Punch Shave

Excision

curettage

When to Biopsy

To establish a diagnosis

To remove a tumor and check its margins

Biopsy surgery

Definitive surgery

To assess the efficacy of a therapeutic procedure

To avoid unnecessary or debilitating treatments

Which Lesion Do I Biopsy?

Best lesions are well-developed.

Exception: Vesicular, bullous or pustular lesions are best biopsied in 24-48 hours

Multiple biopsies where lesions are present in various stages may save time

Areas of excoriation, rubbing, and application of medications should be avoided



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Skin Biopsy Methods

Punch

Shave

Scissors

Curettage

Incisional Elliptical (or fusiform) excisional

Other Biopsy Considerations

Do I have an idea of what the lesion is? For Example: Warts, seborrheic keratoses require different plan-

ning than lesions of scleroderma or melanocytic lesions try to anticipate the pathological defect.

A working differential is important as the kind, type, and depth of appropriate surgery will change!

A punch biopsy is inadequate for pathologic processes of fat such as morphea, panniculitis, erythema

nodosum, and scleroderma

A punch of less than 4 mm is inadequate for inflammatory conditions

Processes in the deep to lower dermis require scalpel incisional biopsy

Diseases

Psoriasis

Often symmetrical

Most commonly on extensor surfaces (knees, elbows, nails)

Presents as erythematous patches and plaques covered with white scales

Associated with the Auspitz sign tugging gently on scale results in bleeding

Associated with arthritis, classically sero-negative and exhibiting a predilection for the distal inter-phalangeal joints

Guttate Psoriasis

Guttate is Latin for drop-like. These lesions are therefore similar in color and texture but they are shaped

like drops or smaller circular lesions than in the classic form

Pustular Psoriasis

Characteristically presents as multiple, fresh,yellow pustules AND older, dry, brown macules on the palms and soles

Must be differentiated and is classically mis-diagnosed as vesicular tinea pedis

Psoriatic Nail Disease (Classic Changes)

Oil-drop staining

Pitting small depressions on the surface of the nail plate

Sub-ungual debris and hyperkeratosis

Transverse grooves

Looks clinically very similar to onychomycosis and may indeed coexist with onychomycosis



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Lichen Simplex Chronicus

Hallmark finding clinically is history of chronic rubbing and scratching

Accentuation of skin lines, known as lichenification, is very evident

Frequently on extremities and neck region, anal area, back of neck

Hyper-pigmentation and scaling very typical

Anterior ankle area very common podiatric presentation rubbing produced by opposite heel Rarely evident in an area where the patient cannot reach with hands

Excoriation may be present

An exaggerated form is known as prurigo nodularis

May be associated with certain personality type

Treatment directed at stopping the itch-scratch cycle

High-potency steroids usually required for symptomatic relief for lesions on the lower extremities

Atopic Dermatitis

Typically associated with history of allergies and/or hay fever in patient OR family members

Increased flexion creases in palms and soles

Dry skin

Circumoral pallor

Nail fold changes

Lesions commonly on dorsum of feet, antecubital fossa, popliteal fossa, neck, and face

Mycosis Fungoides

This is a form of cutaneous T-cell lymphoma (CTCL)

Presents with patch, plaque and tumor stages

Varying shades of red to violaceous

Systemic form with peripheral blood involvement is the Sezary syndrome

Scabies

Characteristic lesion is a burrow caused by the female of the mite Sarcoptes scabei Palms and soles, sides of toes, web spaces are common locations.

It is a mite infestation

Hallmark clinical sign is very intense pruritis

Lichen Planus

Typically present as violaceous polygonal papules

May coalesce into plaques.

Predilection for flexural surfaces, especially wrists and ankles

Pruritis may be prominent.

Classic destruction of nail matrix with ablation/deformity of nail plate is called pterygium



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Granuloma Annulare

Annular (circular) lesions with elevated periphery

Central areas of lesions exhibit clearing

Common on dorsum of foot

Usually self-limiting and requires no treatment unless there is severe itch.

This lesion is one of the palisading granulomas based on histologic changes. Other palisading granulomasare necrobiosis lipoidica, rheumatoid nodule, and nodules of rheumatic fever

Hand-Foot-and-Mouth Disease

Causative agent is Coxsackie A16 virus

Ulcerative lesions found in the mouth

Erythematous macules and papules with central gray round to oval vesicles on fingers, hands, toes, and feet

Resolves in 7-10 days

Secondary Syphilis

Called the great imitator as it resembles many other lesions

Clinical presentation is varied

Scaly erythematous plaques of palms and soles Macular-papular rash often described as salmon or ham colored

Should be in differential of many plantar dermatoses

Spirochete is causative organism

Warts (Verrucae)

Caused by the DNA containing human papilloma virus (HPV)

There are over 100 types of HPV, some are associated with malignancy

Four types of clinical lesions are vulgaris, plantaris, plana, and condyloma acuminatum

Clinically evident black dots within cauliflower-like keratosis and soft yellow centers are common clinical

descriptions

Black dots represent cutaneous hemorrhage from tips of dermal papillae Human papilloma virus, in addition to warts, also causes Bowenoid papulosis, verrucous carcinoma, and

epidermodysplaia verruciformis

Plantar Wart

Mostly under areas of pressure but do not have to be

Maybe solitary or grouped

Several solitary lesions may fuse forming a mosaic

Black dots prominent except in early lesions

Soft central clear to yellow core

Classically described as painful on lateral compression

Pinpoint bleeding noted on debridement represents papillomatosis where-in papillary dermis is actuallyabove the epidermis, causing transection of papillae and resulting bleeding



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Erysipelas

Caused by group A beta-hemolytic strep

Painful, well-defined lesion commonly on lower leg

Edematous

Raised margins

Cellulitis

Erythematous process

Warm to hot

Strep and staph most common organisms

Poorly defined borders

By definition, involves skin and subcutaneous tissues

Ecthyma

Painful indurated plaque

Group A beta strep

Becomes necrotic with crusting

Impetigo

Staph aureus and beta hemolytic strep are causes

Bullous and non-bullous forms exist.

Hallmark is honey colored crusts

Lesions clear centrally.

Furuncle

Infection of the hair follicle

On feet, commonly seen on hair bearing portions of the dorsal aspect

Commonly due to staph aureus

Develops into a painful erythematous nodule Several furuncles may coalesce into a carbuncle (boil)

Pitted Keratolysis

Typically occurs in the presence of hyperhidrosis

Very common on heels

Malodor may be prominent

Discrete plantar pits within macerated skin is hallmark feature

Diphtheroids are causative organisms.

Responds very well to systemic erythromycin

Topical erythromycin may also be used

Therapy directed towards hyperhidrosis is helpful



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Tinea Pedis

This disease should be known very well. It is a form of superficial fungal infection. Any aspect of it should be

considered fair game. In general, tinea pedis is classified into three general types: acute inflammatory, chronic or dry

scaly, and interdigital. Some texts discuss four types, dividing interdigital into dry and moist types. You should study

the fungal organisms as well.

Acute Inflammatory Tinea Pedis

Deep vesicles and bullae are present

Bullae are multi-locular

Typical location is in the long arch

May become eroded in severe cases

Trichophyton mentagrophytes, a dermatophyte, is most common organism

Drainage of the blisters provides some pruritis relief. Topical anti-fungals work rapidly

Topical steroid may be required in severe cases to control pruritis

Chronic or Dry-Scaly Tinea Pedis

Typically erythematous, dry, and scaly

Typically present in moccasin or sandal distribution Trichopyhton rubrum is most common organism

Often associated with concomitant onychomycosis

Interdigital Tinea Pedis/Tinea interdigitale

Fissuring and or scaling of toe web

Degree of maceration varies

May become super-infected with bacteria and become a cause of chronic cellulitis

Trichophyton mentagrophytes is common organism, but infection often mixed

When super-infected with pseudomonas, a green tinge overlying maceration may be present

May progress to gram-negative tinea pedis and ascending cellulitis requiring IV antibiotics

Onychomycosis: Recognized Types

Distal Subungual (most common)

White Superficial (common)

Proximal Subungual (uncommon)

Candida

Lateral nail fold

Distal Subungual Onychomycosis (DSO)

Primarily involves distal nail bed and hyponychium

Secondarily involves underside of nail plate

Results in a dermatitis that causes subungual hyperkeratosis and uplifting of nail plate Most commonly

caused by T. Rubrum

White Superficial Onychomycosis (WSO)

Primarily involves surface of nail plate.

Opaque, chalky, white islands are seen.

Nail plate becomes soft, rough, and crumbly.

T. Mentagrophytes most common causative agent



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Proximal Subungual Onychomycosis (PSO)

Same as distal subungual type but organisms infect via proximal nail fold

Most proximal portions of nail plate involved

White areas move distally as nail grows

Seen with greater frequency in HIV infection, may be considered by some as a marker for the disease

Candida Onychomycosis

Direct invasion by candida in chronic muco-cutaneous candidiasis

Opaque white strands

Pseudo-clubbing of distal digits

Distinct from candida paronychia

Lateral Nail Fold Onychomycosis

Essentially the same as DSO, except confined to medial or lateral nail fold

Most Common Organisms in Onychomycosis

Dermatophyte fungi - 91% - T. Rubrum, T. Mentagrophytes, E. Floccosum

Yeasts - 6% - Candida, other species Non - dermatophyte molds - 3% - Aspergillus, Scopulariopsis, Scytalidium, others

Summerbell RC et al. Mycoses 1989; 32:609-19.

Erythrasma

Caused by diphtheroid c. minutissimum

Affects intertriginous areas

Woods light examination reveals coral red fluorescence due to the porphyrin ring structure in the organism.

Round to oval patches with maceration and scaling interdigitally

Treatment with erythromycin orally or topically

Mycetoma A Deep Fungal Infection

Presents with draining sinuses

May progress to fungal osteomyelitis

Usually requires surgery and systemic anti-fungal therapy

Infection often occurs outside of United States



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Larva Migrans

Also called creeping eruption

Severe pruritis is common

Visible erythematous tract on the skin

Caused by the dog or cat hookworm, ancylostoma braziliense

May be eradicated with topical ethyl chloride to the caudal end or systemic thiabendazole

Diabetic Dermopathy

Round to oval brown lesions

Typically on the anterior aspect of the lower legs

Usually the lesions are atrophic

Clinically similar to post-inflammatory pigmentary changes

Necrobiosis Lipoidica

Yellow, indurated, atrophic, plaques on lower extremities

May ulcerate

Occurs 75% in women

Not always associated with diabetes 67% of patients affected are diabetic, but necrobiosis lipoidica is a rare complication of diabetes - .39%

One of the palisading granulomas

Bullous Diabeticorum or Diabetic Bullosa

Multiple bullae on feet and toes

Typically present with angular borders, which differentiate them from friction lesions, which are typically

rounded

Fluid in the bullae is sterile

Bullae seemingly appear without provocation

Leukocytoclastic Vasculitis (LVA)

Vessel inflammation causing bleeding into the skin resulting in a non-blanching erythema called purpura.

Because the bleeding is high in the skin, it is a palpable purpura

Lesions can ulcerate and form black eschars due to local ischemia

It may represent a drug reaction sulfonylureas are a well-known cause

May coexist with collagen vascular disease

LVA itself is merely a histologic description of this entity, which may occur in association with other diseases

Henoch Schonlein Purpura

This is an immune complex deposition disease

Commonly occurs in children accompanied by joint pain, hematuria, and abdominal pain

Histologically, it is LVA:



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Erythema Nodosum

Histologically, this disease is a septal panniculitis, or inflammatory reaction in the subcutaneous fat involving

the fibrous septae between fat cells

Large areas of tender, erythematous nodules on anterior legs; can break down

Represents a hypersensitivity response to strep infections, tuberculosis, deep mycoses, sarcoidosis, ulcerative

colitis, drugs (commonly oral contraceptives, laxatives) May be associated also with Chrohns disease and Bechets syndrome

Other infections: TB, Coccidiomycosis, Histoplasmosis, Yersinia, Leprosy

May be idiopathic up to 40% of cases

Nodular Vasculitis - Erythema Induratum (Bazins Disease)

Histologically, this disease is a lobular panniculitis, or inflammatory reaction in the subcutaneous fat involv-

ing the fat cell itself

Called Induratum or Bazins disease when associated with tuberculosis

Tender erythematous nodules that ulcerate and scar on the posterior calf area

Most clinicians will treat for tuberculosis even if patient tests negative

Livedo Reticularis

More of a reaction pattern than true disease

Presents as a fish net pattern of erythema on lower extremities

May accentuate on exposure to cold

Must be differentiated from cholesterol embolization

May herald the onset of systemic vasculitis or collagen vascular disease

Raynauds Phenomenon

Occurs on exposure to cold

Manifested by severe vasospasm

Characteristically presents with the tri-phasic color change of rubor-pallor-cyanosis

Many patient present with different areas of the feet in different phases of the color change Symptoms are coldness, numbness, pain, burning

Underlying causes should be ruled out such as collagen vascular disease, cryoprecipitants, internal malignancy

When no underlying cause is found, the condition is termed Raynauds disease

Keratoderma Blennorragicum (KDB)

Associated with Reiters Syndrome:

Diagnostic criteria: one month of arthritis in association with urethritis. Arthritis is in knees, ankles, and feet

Adjunctive findings: conjunctivitis, circinate balanitis and keratoderma blennorragicum

KDB - vesicles, papules, and macules early, becoming pustular, keratotic and crusted. Nail and mucous mem-

brane changes as well



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Pemphigus Vulgaris

A serious, acute or chronic, bullous, autoimmune disease of skin and mucous membranes

Can be fatal. Cell adhesion lost

Often starts orally, progresses to skin. Lesions are painful

Patients feel weakness, malaise; Weight loss due to inability to eat

Bullae rupture easily, are flaccid, and weeping and lead to erosion Exhibit Nikolsky sign pressure on bulla causes dissection of fluid and expansion of bulla

Hospitalization may be required

Steroids: 2-3mg/kg prednisone

Immunosuppressive therapy: Azathioprine, Methotrexate, Cyclophosphamide, Plasmapheresis, Gold

Bullous Pemphigoid

Autoimmune bullous eruption similar but less severe than pemphigus

Commonly occurs first on lower legs, as well as axillae, thighs, abdomen, forearms

Large oval or round bullae

Labs: Indirect immunofluorescence reveals anti-basement membrane IgG

Treatment: Systemic prednisone; May be combined with azathioprine

Mild cases may respond to topical treatment

Pyoderma Gangrenosum

Usually presents as deep-seated nodule or pustule, which breaks down to form a large ulcer with

serous/purulent/ hemmorhagic drainage

Weeping is extensive and continuous

Edges of lesion are raised, undermined, irregular and necrotic edges develop

Associated with inflammatory bowel (large and small) disease, arthritis, and internal malignancy

(hematopoietic myeloma, leukemia), diverticulitis, Bechets syndrome

Neurotrophic Ulceration (Mal perforans)

Typically on or under a bony prominence Vascularity typically good

Diabetes, leprosy, spinal syndromes, alcoholism, nutritional diseases, pernicious anemia are among the causes

of neuropathy

Rheumatoid Nodules

One of the palisading granulomas

Moveable firm nodules present in RA patients

May ulcerate

May become infected and discharge fluid

No treatment necessary unless symptomatic or infected

May rarely precede the onset of clinical arthritis



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Seborrheic Keratosis

Roughened, verrucous surface

Varying shades of brown, may be deeply pigmented

Slightly raised, stuck-on appearance

Very common on the lower legs, especially in elderly women

Called dermatosis papulosa nigra on the face of African-Americans Melanoma is in the differential diagnosis, as is basal and squamous cell carcinoma

Epithelioma Cuniculatum or Squamous Carcinoma

Plantar foot is common location for this variant

May be mistaken for large verruca

A cheesy discharge can be expressed from crypts within the lesion representing degenerated keratin

Malodorous

Requires surgical excision

May metastasize

Basal Cell Carcinoma

The most common of all malignancies in humans Very rarely metastasizes slow growing

Most frequent in men over 50 years old

Rare on feet but does occur

Classically described as an ulcer surrounded by a pearly or waxy border

Telangiectases are a hallmark finding

Dysplastic Nevus (Atypical Mole)

Precursor lesion of melanoma

1992 NIH consensus panel on proper terminology since 1992 replaced the term dysplastic nevus with

atypical mole

Histologically it is termed nevus with architectural disorder Characteristically, these lesions share similar characteristics of melanoma

May run in families as the FAMM Familial Atypical Mole and Melanoma Syndrome

The presence of atypical moles significantly increases the chances that one may get a melanoma in their

lifetime

Junctional Nevus

Dark brown macules representing a collection of nests of melanocytes at the dermo-epidermal junction

Color uniform throughout

Benign process

Lesion should be observed for change in size, texture, color uniformity, border regularity



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Blue Nevus

Presents as well-defined, blue-black papule

Common on dorsum of hands and feet

Represents a melanocytic process deep in the dermis, causing different refraction of light clinically evident as

blue color

Benign, but does exist in a particularly virulent malignant form

Superficial Spreading Melanoma

Most common type of melanoma

Grows slowly, usually within a pre-existing benign melanocytic process

Nodular Melanoma

Next most common type

Often said not to have a radial growth phase that it starts out in the vertical growth phase

Poorer prognosis as depth tends to be deeper

Acral Lentiginous Melanoma

Most common type in African-Americans Commonly affecting the soles, palms and toes, particularly the nail unit

Can cause melanonychia, which is pigment in the nail plate

Leakage of pigment proximally away from nail fold is called Hutchinsons sign and should be considered very

foreboding

Must be differentiated from normal pigmented linear bands in nails of African-Americans

Often diagnosed at later stages and therefore has a poor prognosis

Nail matrix biopsy is diagnostic

Lentigo Maligna Melanoma

Least frequent type

Develops from lentigo maligna, the in-situ form of lentigo maligna melanoma Known to stay in radial growth phase for up to 40 years

Most common on face and upper extremities

Common Features of All Melanomas

Usually greater than 6 mm. in greatest diameter before clinically evident as melanoma

Lesions are asymmetrical you cannot bisect the lesion anywhere to make two mirror images

Varied degree of pigmentation throughout the lesion with varying shades of tan to brown to black in early

lesions; red, white, and blue in later lesions

Irregular borders

Elevation or enlargement



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General Principles Regarding Management of Melanoma

Excisional biopsy when possible is always preferred

Incisional biopsy for large lesions is very much acceptable

Shave or curettage biopsies are never appropriate

Ulcerated lesions have a much poorer prognosis

For biopsy surgery, only small margin of normal skin is required For definitive surgery, marginal tissue excision determined by depth from pathology report. In general, start

with 3 cm margin, adding 1 cm more for each millimeter of depth

Excision surgery should be oriented parallel to direction of lymphatic drainage

Pigmented bands in nails must be biopsied at the matrix level

Prognostic Indicators for Melanoma

Clarks Levels of Invasion

Clarks Levels of Invasion is a method of prognosticating based on visualization of tumor at certain depths.

Level 3 and beyond is considered the point where significant risk of metastases begins. Described as Levels 1-5 as

follows:

1. Confined to epidermis in situ2. Extends beyond epidermis 1 mm into the papillary dermis

3. Extends to the junction of the papillary and reticular dermis

4. Extends into the reticular dermis

5. Extends into the subcutaneous fat

Breslows Tumor Thickness (Depth)

Breslows tumor thickness (depth) is a method of prognosticating based on actual depth in millimeters of

extension into the skin starting at the granular layer using a measuring device in the eyepiece of the microscope

called an ocular micrometer. Thought to be more reliable and reproducible than Clarks levels. .76 mm is the break-

point after which the risk of metastasis rises sharply.


chapter 4 and 4a introduction to medicine and dermatology

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