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Dermatology

American Manual
of Examination
in Medicine
(2CK)

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Dermatology

American Manual
of Examination
in Medicine
(2CK)
Authors

Dolores Mendoza

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

Index
01. Skin Layers ....................................................................................................... 1

02. Terminology. Elemental Cutaneous Lesions... 1


2.1. Clinical Lesions.......................................................................................................................... 1
2.2. Histological Lesions ........................................................................................................... 2

03. Allergic and Immune-mediated Diseases..............2


3.1.
3.2.
3.3.
3.4.
3.5.
3.6.
3.7.
3.8.

Hypersensibility Reactions ...................................................................................... 2


Atopic Dermatitis .................................................................................................................. 2
Contact Eczema ..................................................................................................................... 3
Seborrheic Dermatitis ................................................................................................... 3
Psoriasis ............................................................................................................................................... 3
Urticaria ............................................................................................................................................... 4
Toxicodermas ............................................................................................................................ 5
Multiform Erythema, Stevens-Johnson Syndrome
and Toxic Epidermal Necrolysis ........................................................................ 5
3.9. Erythema Nodosum .......................................................................................................... 6
3.10. Bullous Pemphigoid and Pemphigus Vulgaris ......................... 6

04. Infectious Diseases...................................................................................8


4.1.
4.2.
4.3.
4.4.
4.5.
4.6.
4.7.

Viral Infections ........................................................................................................................... 8


Bacterial Infections ......................................................................................................... 10
Fungal Infections .............................................................................................................. 12
Parasitic Infections........................................................................................................... 14
Ischemia .......................................................................................................................................... 15
Miscellaneous ......................................................................................................................... 15
Neoplasias.................................................................................................................................... 17

De rm ato l ogy

Skin
Chapter 01

Layers

There are three skin layers: epidermis, dermis and subcutaneous cellular tissue (Figure 1).

Superficial arteriovenous
plexus

Reticular layer

Epidermis

Dermis

Subcutaneous
tissue

Dermal Papillae

Sweat
gland

Sebaceous
(Oil) gland

Hair
follicle

Deep
arteriovenous
plexus

Figure 1. Microscopic structure of normal skin

Terminology.
Chapter 02

Elemental
Cutaneous Lesions

2.1. Clinical Lesions


Primary Clinical Lesions
Fluid-filled:
Vesicle: raised formation, less than 0.5 cm.
Blister: lesion equal or greater than 0.5 cm.
Phlyctena: large blister.
Pustule: vesicle of purulent content.
Cyst: encapsulated lesion of semi-solid or liquid content.
Of solid consistency:
Macule: a patch of skin that changed color, which is neither
raised nor depressed (non palpable).

When a macule is red in color, it is described as erythematous. If


it does not disappear after a diascopy, it is regarded as purpuric
(it translates the existence of extravasated blood).
In dierential diagnosis of purpuric lesions, senile purpura must
be taken into account, which consists in the presence of violaceous macules in areas exposed to trauma, as a consequence
of capillary fragility. Other cause for purpura is leukocytoclastic
vasculitis, which typically gives palpable purpuric papules, but
not nodules.
Papule: small, solid, circumscribed elevation of the skin, of less
than 1 cm, which resolves without leaving a scar. It is called
plaque if it is equal or greater than 1 cm. Unlike macule, both
are palpable.
Wheal: erythematous edematous plate of dermal origin and of
fleeting evolution (it disappears in less than 24 hours). It is characteristic of urticaria.
Nodule: circumscribed hypodermal lesion, identified by palpation. It may or may not be raised (it is palpable rather than visible). Nodules are typical lesions of panniculitis, like the erythema nodosum.
Tubercle: circumscribed, infiltrated and raised nodule that usually leaves a scar once it has resolved.
Gumma: granulomatous inflammation that softens and opens
gradually.

Secondary Clinical Lesions


Secondary clinical lesions, expected to disappear on their own:
Scales: plates in the stratum corneum, which come o by themselves.
Scab: secretion or exudate or dried blood over the skin.
Slough: black necrotic plate of tissue with demarcated borders.
Solutions of continuity:
Erosion: loss of epidermal substance that heals without leaving
a scar.
Ulcer: loss of epidermal and dermal substance that leaves a scar
after healing.
Excoriation: erosion secondary to scratching.
Fissure: crack that reaches high dermis as a result of hyperkeratosis.
Others:
Sclerosis: skin induration with elasticity loss, due to fibrosis and
dermal collagenization.
Scar: fibrous tissue that replaces normal skin.
Lichenification: thickening of the epidermis with accentuation of
skin folds, secondary to chronic scratching.
Intertrigo: cutaneous lesion located in skin folds.
Telangiectasia: arboriform erythematous macule secondary to
permanent dilation of cutaneous vessels.
Poikiloderma: hypopigmented and hyperpigmented areas
with atrophy and telangiectasias. Poikiloderma is unspecific
and it translates into the presence of chronic cutaneous damage.
As a summary, Figure 2 lists the main cutaneous elemental lesions commented on this item.

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

Macule

Vesicle

Type II is mediated by IgM and IgG G. Cytotoxic. Hemolytic anemia.


Type I is mediated by immune complexes. Toxicodermas.
Type IV is mediated by T lymphocytes. (cellular) Contact dermatitis.

Wheal

Fissure

3.2. Atopic Dermatitis

Papule

Ulcer

Atopic dermatitis is an inflammatory disorder of the skin, with chronic


and recurring presentation, which aects 12 - 15% of children population. Atopic dermatitis manifests itself by dry skin and pruritus.
Patients have more risk of bacterial secondary infections (S. aureus) and
viral infections (simple herpes virus, SHV, or mollusca).

Nodule

Cyst

Figure 2. Cutaneous elemental lesions

2.2. Histological Lesions


The following are histological lesions of the skin:
Hyperkeratosis: increase in the stratum corneum (warts and psoriasis).
Hypergranulosis: granular layer thickening.
Acanthosis: thickening of the stratum spinosum.
Acantholysis: rupture of intercellular bridges of the stratum spinosum (typical of pemphigus).
Spongiosis: intercellular intraepidermal edema (characteristic of eczema).
Ballooning: intracellular edema (herpes).
Parakeratosis: presence of nuclei in the stratum corneum (typical
of psoriasis).
Dyskeratosis: abnormal keratinization of individual cells of the stratum spinosum (typical of Dariers disease).
Papillomatosis: lengthening of dermal papillae (psoriasis).

Allergic and
Chapter 03

There is a variety of triggering factors or factors that maintain eczema


outbreaks: aeroallergens (dust mites), bacterial antigens (S. aureus),
food (ovoalbumin), and psychological stress, among others.

Clinical Presentation
Clinical presentation is usually in the form of greasy, erythematous
and desquamative papules or plaques on the scalp (cradle cap in the
cases of newborns), central area of the face, sternal region, axilla and/
or groin. In newborns, this presentation can be generalized, causing
Leiners erythroderma desquamativum; in adults, it is likely to be related to blepharitis.
Dierential diagnosis includes atopic eczema in children, but dierential diagnosis in adults reveals subacute erythematous lupus or pink
pityriasis when the trunk is involved and inverted psoriasis when skin
folds are aected.

Remember
Letterer-Siwe disease can cause lesions similar to infantile seborrheic
dermatitis. However, unlike infantile seborrheic dermatitis, Letterer-Siwe
disease is associated with lymphadenopathies and hepatosplenomegaly.

Remember
Impetigo key words (yellowish scabs) should not be mistaken for seborrheic
dermatitis key words (yellowish scales).

Immune-mediated

Diagnosis

Diseases

Atopic dermatitis has a clinical diagnosis. Patients may present with eosinophilia and increase of IgE values.

Treatment

3.1. Hypersensibility Reactions


Type I is mediated by IgE. It is the most rapid. Anaphylaxis, asthma,
and urticaria.

It is essential for the patient to follow certain rules in his lifestyle. This
means the patient must avoid wearing perfumed products (like cologne
and cream), being exposed to extreme temperatures, the use of fabric
softeners and carpets or fluy toys (because of possible sensitization of
dust mites). Besides, the patient needs to wear 100% cotton clothing.

De rm ato l ogy

Precocious treatment is of the utmost importance.


Topic corticoids are the first line treatment.
It is worth to remember that prolonged use of topic corticoids can have
local and systemic secondary side eects.
The second line of treatment involves immunomodulators (tacrolimus
and pimecrolimus). These can be used in children older than 2 years of
age.
For acute outbreaks, oral corticoids are used in short cycles and not as
maintenance. To stop medication suddenly may cause a rebound eect.

3.3. Contact Eczema


The appearance of contact eczema is immunologically mediated (type
IV hypersensitivity) against foreign agents acquired by percutaneous
penetration. Contact eczema requires prior sensitization to allergen.
It is more common in adults than in children.

Diagnosis
Diagnosis is established with clinical records and epicutaneous tests of
contact. These tests are performed once lesions have been resolved, by
applying patches with allergens on healthy skin, leaving them in contact
with the skin during 48 hours. They are read after 48 and 96 hours. The
intensity of reaction is measured qualitatively: negative, weak positive
(erythema), strong positive (papules-vesicles) or extreme positive (blisters).

b. Seborrheic dermatitis in adult: erythematous desquamating papules or plates in fat areas of the facial region and scalp.

Diagnosis
Diagnosis of this condition is clinical.

Treatment
Treatment involves antifungals associated with topic corticoids. Seborrheic dermatitis on the scalp is usually linked to a keratolytic agent, like
the salicylic acid.

3.5. Psoriasis
Psoriasis is a chronic inflammatory disease of the skin that presents
with outbreaks. Psoriasis aects 1-2% of the population, and can appear at any age, with a maximum of incidence between 20 and 30 years
of age. There is a family history in a third of the patients.
Plates are the characteristic erythematous desquamating lesions, well
delimited, with a superficial thick and white-pearl scale.
The most frequent clinical form is vulgar psoriasis or psoriasis in plates.
Lesions are localized at extensor surfaces (elbows and knees) and the
scalp. The umbilical and the lumbosacral areas are often aected.
Nail involvement is frequent, and is most common with a pitting appearance. This form is little specific. The forms that combine hyperkeratosis and distal onycholysis are more specific. Oil spot is the most characteristic sign (Figure 3).

Treatment
Avoid contact with the allergen.
Treatment of acute eczema implies application of topic poultice (zinc
sulphate, sodium borate) and corticoids if lesions are limited, and system poultice if lesions are generalized.

3.4. Seborrheic Dermatitis


Seborrheic Dermatitis is a quite frequent disease. It aects 4 - 5% of the
population. Etiology of seborrheic dermatitis is unknown, although it
has been related to an abnormal immunological response to a fungus
called Pityrosporum ovale. Seborrheic dermatitis is more frequent and
intense when associated to neurological processes, alcoholism and immunodeficiencies.

Clinical Presentation
According to patients age:
a. Seborrheic dermatitis in infants. Yellowish scales on scalp, known
as cradle cab.

Figure 3. Generalized pustular psoriasis

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

3.6. Urticaria

Diagnosis
Diagnosis of this condition is generally clinical.
If there is no certainty, a biopsy must be done, which will reveal hyperkeratosis, acanthosis and parakeratosis.
There is an increase in polymorphonuclears (sterile abscesses) in the
stratum corneum, which are called Munro abscesses.

Treatment (Table 1)
For moderate severe forms of psoriasis that do not respond to classical systemic treatments (see table). They are monoclonal antibodies against proinflammatory substances that are high in patients with
psoriasis [alpha tumor necrosis factor (TNF), interleukin, IL, 12 and
23]. Some of them are infliximab, adalimumab, ustekinumab and
etanercept.
TREATMENT
Topic

Urticaria is an immunologic and inflammatory reaction of the skin


against diverse etiological factors. Independently of the cause, release
of histamine and other inflammatory mediators occurs, which cause vasodilation and increase in capillary permeability, producing an edema in
superficial dermis. Urticarias are divided in acute and chronic urticarias,
depending on whether outbreaks persist more or less than six weeks.
About 60% of acute urticarias are idiopathic. Chronic urticarias show a
higher percentage.
Urticarias of known origin are usually due to infections, drugs or food.

Clinical Presentation
Clinical presentation is characterized by the appearance of pruritic wheals
that last less than 24 hours and can be accompanied with angioedema.

USES

SIDE EFFECTS AND CONTRAINDICATIONS

Mild-moderate

Emollients (urea, glycerin)

Moisturizing

psoriasis

Keratolytics (salicylic acid)

Eliminate excess of scales

(< 25% body


surface)

Reductants (dithranol)

Hyperkeratotic plaques

Stain skin and clothing


Irritating
Acneiform eruptions

Corticoids

Stable psoriasis
in plates
The most used

Vitamin D analogues
(calcitriol, calcipotriol and
tacalcitol)

Stable psoriasis in plates

Irritating in face and skin folds


Hypercalcemia

Psoralens plus ultraviolet


light of the A wavelength
(PUVA)

Combinable with topics


and retinoids (RePUVA)

Cutaneous aging and carcinogenesis


Erythroderma and xerosis
Immunosuppression
Hepatitis by psoralens
Not in children, pregnancy, patients with hepatic or renal
insufficiency, photosensitivity or cutaneous precancerosis
Cataracts
It accumulates in the crystalline during 24 h (sunglasses)

Retinoids (acitretin)

Severe psoriasis,
pustular
or erythrodermic
It is not usually used
in women in fertile age
(see side effects)

Cutaneous dryness (the most frequent)


Hypertriglyceridemia
Hypercholesterolemia
Increase in transaminases
Diffuse alopecia
Vertebral hyperostosis, ligamentous calcifications
Teratogenicity: avoid pregnancy until 2 years after
finishing treatment!
Avoid in children and patients with hepatic or renal failure

Cyclosporine A

Inflammatory severe
psoriasis, resistant to
other treatments
Rapid action

Rebound effect
Nephrotoxicity
High blood pressure (HBP)
Epitheliomas and lymphomas
Hypertrichosis
Gingival hyperplasia
Hyperuricemia

Methotrexate

Severe psoriasis
resistant to other
treatments
Psoriatic arthropathy

Hepatotoxicity
Myelosuppression
Teratogenicity until 3 months after ending treatment
Photosensitivity

Systemic Moderatesevere psoriasis


(> 25% body
surface)

Table 1. Psoriasis treatment

Tachyphylaxis
Percutaneous absorption
Possible new outbreak after stopping medication
Avoid prolonged treatment

De rm ato l ogy

Vasculitis urticaria should be ruled out when lesions last more than 24 hours
and are accompanied with systemic clinical symptoms (i.e., arthralgias).

Treatment

3.8. Multiform Erythema,

Stevens-Johnson Syndrome
and Toxic Epidermal Necrolysis

Oral antihistamine therapy is the treatment of choice.


Systemic corticoids: for severe or refractory cases.
Adrenalin: for severe cases with anaphylaxis.

Multiform erythemas (ME) are of undetermined etiopathogenesis,


regarded as a cutaneous reaction against a diversity of stimuli. Their
histologies show similarities, what leads to consideration of a common
pathogenesis.

Clinical Presentation
3.7. Toxicodermas
Toxicodermas are quite variable cutaneous reactions that appear after
drug administration. They are one of the most frequent side eects of
drugs. The causative agents for many toxicodermas still remains unknown, either immunological or not, and clinical presentation does not
facilitate agent distinction.
Morbilliform exanthem is the most frequent. A morbilliform exanthem
is a generalized eruption formed by symmetric and confluent macules
and papules that usually start by the trunk.
They can appear one or two weeks after taking the drug.

Three dierent groups have been described, although many a time their
clinical symptoms overlap.
Erythema multiforme minor is the most frequent, with around 80%
of the cases. It usually precedes a symptomatic infection by simple
herpes virus (60%) or subclinical infection, about 15 days before.
Erythema multiforme minor manifests itself on extensor surfaces
at hands, elbows and feet, as a symmetric eruption of erythematous edematous lesions with target-shape, (herpes iris of Bateman
or rosette-patterned lesion), with a violaceous, sometimes bullous
center (Figure 5).
Mucosal aectation is rare, with small erosions in oral mucosa. Erythema multiforme minor tends to recurrence, with subsequent outbreaks
of herpetic lesions.

A morbilliform exanthem can be associated with fever, pruritus and eosinophilia.


The most frequent are non steroid anti-inflammatories, antibiotics (sulphamides and penicillins), antiepileptics, allopurinol, and N acetyl-cystene.

Diagnosis
Diagnosis is according to clinical presentation.

Treatment
Treatment implies withdrawal of potentially responsible drug. Topic or
systemic antihistamines and corticoids are given according to the extent
of symptoms (Figure 4).

Figure 5. Erythema multiforme minor. Herpes iris of Bateman


Erythema multiforme major or Stevens-Johnson syndrome is the
rarest. It normally has a prodromal period of until 14 days, with fever, cough, cephalea, arthralgias, and other symptoms. Subsequent
to the prodromal period, erythematous edematous plates appear,
which are more extensive, with a tendency to form blisters and
greater mucosal erosions (mouth, genitals, pharynx, larynx, and
conjunctive; Figure 6). Systemic symptoms are normal and do not
tend to recurrence.

Figure 4. Morbilliform exanthem due to amoxicillin

The most frequent etiological factors are drugs [sulphamides, non


steroid anti-inflammatory drugs (NSAIDs), anticonvulsants and antibiotics, in decreasing order). Infectious agents have been also involved, mainly mycoplasma pneumoniae.

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

3.9. Erythema Nodosum


Erythema nodosum is the most frequent panniculitis. Painful erythematous nodules occur mainly in the anterior side of legs, with a self-limiting course and predominantly aecting young women (Figure 7).

Figure 6. Exudative erythema multiforme major


Toxic epidermal necrolysis (TEN): many authors consider it the
most severe form of erythema multiforme major, arguing the same
pharmacological agents. A morbilliform rash appears which is rapidly confluent comprising almost the entire skin surface, with flaccid
blisters that leave wide areas of denuded skin. Involvement of several mucosae is constant.
Complications often occur (pneumonia, digestive hemorrhage, renal failure, and hemodynamic shock) with mortality rates close to
25%. In children, it must be performed a dierential diagnosis with
staphylococcal scalded skin syndrome, which does not aect mucosae.

Figure 7. Erythema nodosum


They heal without leaving a scar within a period of four to six weeks.
Erythema nodosum may be accompanied with fever, deterioration of
the general state and arthralgias.
Patients with erythema nodosum may have a false positive VDRL.

Etiology
Remember
Diseases that have the Nikolsky sign are TEN, staphylococcal scalded skin
syndrome (SSSS) and pemphigus. In TEN, the whole epidermis comes off
(bad prognosis), while in SSSS, epidermal detachment occurs at the granular
layer.

Histopathology

Diagnosis

It must be highlighted the eacement of dermoepidermal junction by a


lymphohistiocytic infiltrate and vacuolar degeneration of the baseline layer with necrotic keratinocytes. In TEN, keratinocytes necrosis is massive.

Erythema nodosum requires a deep biopsy to reveal septal panniculitis


without vasculitis.

Treatment
In ME minor, only symptomatic treatment is prescribed, with topic
corticoids and oral antihistamines. Treatment for herpes simplex virus
(HSV) infection is useful, to prevent ME lesions if patient is in the initial
stage of the viral infection.
ME major requires treatment of the underlying infection or withdrawal
of implied drug and support measures. The use of oral steroids according to the patients general state is under discussion.
A patient with TEN requires to be admitted at the burn treatment room,
with monitoring of hematocrit, hydroelectrolytic balance, and antibiotic
prophylaxis and support measures. It is controversial the use of systemic corticoids, immunoglobulins and/or cyclosporine.

This condition is thought to be an immunological response triggered by


multiple and dierent stimuli: bacterial, fungal and viral infections, systemic diseases (sarcoidosis, inflammatory intestinal disease, Behcets
syndrome), neoplasias (lymphomas and leukemias), and drugs (oral
contraceptives, sulphamides, bromides, and iodines).

Complementary tests can be performed to rule out systemic involvement,


for example, chest X-ray, Mantoux, and antistreptolysin O antibody (ASLO).

Treatment
Treatment entails eliminating underlying cause if found, then rest and
anti-inflammatories.

3.10. Bullous Pemphigoid

and Pemphigus Vulgaris


See Table 2 and Figures 8, 9, 10 and 11.

De rm ato l ogy

GENERALLY

PEMPHIGUS VULGARIS
Clinical presentation

40-50 years of age


They usually affect mucosae
No pruritus
Flaccid blister
Nikolsky

Elderly
Sometimes mucosae
With pruritus
Tense blister
No Nikolsky

DERMATITIS

HERPES GESTATIONIS

IDIOPATHIC

Pregnant women
No mucosae
With pruritus
Herpetiform
No Nikolsky

HERPETIFORMIS

15-35 years of age


No mucosae
With pruritus
Herpetiform
No Nikolsky

Direct immunofluorescence (DIF) IgG

IgG

IgG

IgA

Histology

INTRAepidermal blister
There is acantholysis

SUBepidermal blister
There are eosinophils

SUBepidermal blister
There are eosinophils

SUBepidermal blister
Neutrophils in dermis

Treatment

Corticoids
Corticoids at high doses,
immunosuppressants, rituximab
and immunoglobulins

Corticoids

Diet +/- dapsone

Remember

Mortality rate 10%

Relapse if new
pregnancy

Associated to enteropathy
by gluten! 90%

The most frequent

Table 2. Autoimmune blistering diseases

Intercellular
substance ac.

Lucid
layer

Thick
layer

Lineal
storage
in lucid
layer

Basal
sublayer

Granular
storage
in papillary
dermis

Anti-Collagen Ac.

Pemphigus

Pemphigoid bullous
Herpes gestationis

Acquired blistering
epidermolysis

Dermatitis
herpetiformis

Figure 10. Pemphigus vulgaris with oral mucosa involvement with


erosions

Figure 8. Key points for histological diagnosis


of autoimmune blistering diseases

Figure 9. Pemphigus vulgaris

Figure 11. Pemphigoid bullous. Tense blisters. No sign of Nikolsky

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

Infectious Diseases
Chapter 04

4.1. Viral Infections


Simple Herpes
Infection by Simple Herpes Virus
There are two types of simple herpes (Figure 12):
Type I is responsible for most extragenital herpes and 20% of the
genital herpes.
Type II causes genital herpes and a small percentage of extragenital
herpes.

Figure 13. Herpetic gingivostomatitis


Eczema herpeticum or Kaposi varicelliform eruption: dissemination of herpetic infection on pre-existing dermatosis (above all,
atopic dermatitis).
Neonatal herpes is due to intrapartum contagion of HSV-II, with
neurological involvement, general deterioration and skin vesicles or
ulcers.
Other clinical forms are herpes gladiatorum, herpetic whitlow and
keratoconjunctivitis.

Diagnosis
Diagnosis of this condition is mainly clinical. Virological culture is the
most reliable method of confirmation. The extent of a smear of the lesions (Tzanck cytodiagnosis) allows visualization of multinucleated cells,
and intranuclear inclusions, which become evident through histological
study.

Treatment
Figure 12. Herpes simplex
Contagion is produced by direct contact, though the carrier may be asymptomatic. After primary infection, virus remains silent in the sensitive portion of cranial or spinal ganglia. Immunosuppressed patients
endure the greatest severity of this condition.

Clinical Presentation
Extragenital simple herpes: recurring orofacial herpes simplex is
the most frequent. Most primary infections are asymptomatic. Only
5% manifest themselves in the form of herpetic gingivostomatitis, a
profile characterized by oral ulcers with cervical adenopathy and affectation of the patients general state (Figure 13). During relapses,
clinical symptoms are milder, with cluster vesicles on an erythematous base. Some factors facilitate relapses: trauma, sunlight, cold,
stress, fever, and the menstrual cycle.
Genital simple herpes is the most common cause of genital ulcers
after trauma. Primary infection is usually symptomatic and occurs
between 3 to 14 days after sexual contact. It causes clustered ulcers
in the balanopreputial sulcus or in the prepuce with painful inguinal
adenopathy. Relapses are less severe than primary infection and occur more frequently when genital herpes is due to HSV type II.

Mild forms do not need treatment. Treatment is required in the following cases:
Primary infection.
Severe or frequent relapses if they aect life quality.
Complications, like erythema multiforme and eczema herpeticum.
Drug of choice is oral acyclovir and its derivatives (valacyclovir, famciclovir). Topic antivirals have not proven useful, favoring maceration of
lesions, and thus, over infection. It is not infrequent that topic antivirals
cause allergic contact dermatitis due to hypersensitivity.

Varicella-Zoster Virus
A primary infection gives way to varicella (see Pediatrics section). After
varicella, the virus remains latent in the sensitive portion of the neural
ganglia and when relapse occurs, it leads to zoster herpes.
Varicella: the following symptoms appear after 15 days of incubation:
fever, cephalea, pruritus and polymorphic lesions in dierent stages:
macules, papules, vesicles (Figure 14), ulcers and scabs (starry sky
appearance). Mucosal (ulcers) and scalp involvement is characteristic.
Manipulation can leave scars. Bacterial over infection of lesions is the
most usual complication. About 20% of adults suer from varicella

De rm ato l ogy

pneumonia radiologically demonstrable, but clinical symptomatology is


only present in around 4% of the cases.

Ophthalmic involvement can result in severe keratitis and requires urgent referral to an ophthalmologist. Suspicion should exist on patients
that present herpetic lesions on the tip of the nose) (Hutchinsons sign).
Disseminated zoster herpes: several dermatomes are aected bilaterally. Ramsay-Hunt syndrome is characteristic in the immunosuppressed.

Remember
Affectation of the nose tip makes it necessary for ophthalmological
examination because the nose tip is innervated by the same nerve that
innervates the cornea (first branch of the trigeminal nerve).

Treatment
Varicella without complications is treated symptomatically. Antivirals
are reserved for severe or complicated forms. There is a commercialized vaccine of live virus, whose indications are still under discussion.
Figure 14. Typical vesicles in patients with varicella

Zoster herpes: thoracic zoster herpes is the most usual. It seldom occurs more than once throughout a persons lifetime.
It is characterized by vesicles on pre-existing erythema, with
metameric distribution and lateral extension. The most common complication is post herpetic neuralgia, more frequent in
advanced age. Carbamazepine or tricyclic antidepressants (Figure 15).

Zoster herpes must be treated with antivirals when detected during the
first 48-72 hours and aecting patients with:
Immunosuppression.
Age above 55.
Special clinical forms previously cited.
Drugs to be used are oral acyclovir and its derivatives (valacyclovir and
famciclovir). They accelerate the cure of lesions and decrease the intensity of post herpetic neuralgia. Patients with renal failure need a dose
adjustment, as acyclovir is nephrotoxic. These patients are administered brivudine in a single daily dose.

Molluscum Contagiosum
Dome shaped pink papules with central umbilication (Figure 16). Molluscum contagiosum is typical of children that go to swimming pools. It
is also present in the genital zone after sexual contact and in immunosuppressed patients. It is caused by Poxvirus.

Figure 15. Zoster herpes

Special Clinical Forms


Special clinical forms are as follow:
Ramsay-Hunt syndrome: aectation of geniculate ganglion of the
facial nerve.
It produces vesicles in the outer ear, external auditory canal and
pharynx, homolateral facial paralysis, deafness and vertigo.

Figure 16. Molluscum contagiosum

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

Lesions are asymptomatic.

Diagnosis
Diagnosis is clinical. Histology reveals characteristic inclusion bodies.

Treatment
Lesions can resolve spontaneously.
Curettage, cryotherapy or local trichloroacetic acid are eective methods to destroy lesions.

Warts

Figure 18. Condyloma accuminata

Human papillomavirus can cause verruca vulgaris, palmoplantar and


flat warts and condyloma accuminata. Human papillomavirus is the
most frequent sexual transmitted disease.
Some subtypes of this virus (16, 18) are of high risk and can cause epidermoid carcinomas.

4.2. Bacterial Infections


Impetigo

Direct contact is the mechanism of contagion.

Diagnosis
Diagnosis of this condition is clinical.

Impetigo is a very contagious superficial infection, without systemic repercussion and normally mixed etiology, by Gram positive cocci (streptococci and staphylococci). Classically, the most frequent accepted
cause was Streptococcus pyogenes. However, at present Staphylococcus
aureus stands out as the predominant cause.

Staining with acetic acid can help visualize mucosal lesions.

Treatment
Genital warts are treated with cryotherapy, podophyllotoxin, trichloroacetic acid, imiquimod and 5-fluorouracil.

The most typical form is impetigo contagiosa (Figure 19), characterized by honey-colored (meliceric) scabs, which normally appear on
the face and other exposed areas. It is typical of children. Although
infrequent, poststreptococcal glomerulonephritis is a dreadful complication.

Cervical lesions should be monitored, by cytology and biopsy whenever


necessary, to rule out cervical cancer (Figures 17 and 18).

Figure 19. Impetigo contagiosa


On the contrary, rheumatic fever shows no relation to cutaneous streptococcal infections, but only with pharyngeal infections.

Figure 17. Warts in HIV patient

10

There are other less habitual forms, called bullous impetigo, exclusively
of staphylococcal origin. Clinical presentation involves the presence of
blisters and erosions on the aected skin, as a consequence of the epidermolytic toxins that these bacteria contain. Impetigo is treated with
topical mupirocin, penicillin or oral fusidic acid.

De rm ato l ogy

Cellulitis

Treatment

Cellulitis is an infection that aects deep dermis and subcutaneous cellular tissues, normally caused by streptococci (Streptococcus pyogenes
or of group A).

Treatment entails precocious surgical debridement. It is a surgical emergency. In addition to surgery, broad-spectrum antibiotherapy will be
needed.

Community methicillin-resistant S. aureus (CMRSA) is a triggering agent


that is becoming more and more frequent.
Most common risk factors are diabetes, chronic venous insuciency
and immunosuppression.

Folliculitis
Folliculitis is an infection and inflammation of one or several follicles
caused mainly by staphylococci.

Clinical Presentation
Clinical Presentation
Folliculitis shows pustules with follicular distribution.
Cellulitis presents with erythematous plaques that are ill-defined, painful and hot. It is usually accompanied with fever and chills.

Diagnosis
Diagnosis is clinical. If there is an open door, a culture of this area may
help see the source germ and resistance to antibiotics.
It is important to rule out abscesses, osteomyelitis and necrotizing fasciitis.
If bacteremia is suspected, blood cultures need to be performed.

When the infection is deeper, it is called furuncle.


If several furuncles are infected, a fluctuating erythematous plaque forms,
containing several points of suppuration. This plaque is labeled as anthrax.
Diabetic and immunosuppressed patients are at higher risk.

Characteristics of Folliculitis
1. Hot tub or swimming pool folliculitis: caused by Pseudomonas aeruginosa.
2. HIV associated pruritic folliculitis or eosinophilic folliculitis.

Treatment
Treatment
Treatment implies oral antibiotics for 7-10 days to cover Gram positive
cocci. They are intravenously administered in case of lack of response
to oral treatment, involvement of hands or periorbital zone, diabetes or
extremes of age.

Necrotizing Fasciitis
Necrotizing fasciitis is a deep infection up to muscular fascia that produces very intense pain and subsequent anesthesia.
In 10% of the cases, cellulitis is due to an infection by S. pyogenes. In the
remaining cases, it occurs by a polymicrobial infection caused by aerobes
and anaerobes, including S. aureus, E. coli and Clostridium perfringens.

In mild cases, treatment of choice comprises antiseptics and topic antibiotics.


In more severe cases, treatment of choice requires oral antibiotics.
Large sized lesions must be drained and a microbiological culture must be
performed to rule out methicillin-resistant Staphylococcus aureus MRSA.

Acne Vulgaris
Acne is an inflammatory disease of the pilosebaceous follicle, as a consequence of an alteration in follicular keratinization. It aects adolescents and young adults.

There may be prior history of trauma or surgery.

Clinical Presentation
Clinical presentation involves pain of sudden onset and edema on the
aected zone. Pain may progress to anesthesia. There appears subsequent erythema that progresses rapidly into necrosis.
Characteristic clinical signs are tissue necrosis, blisters, intense pain
and gas production.

Diagnosis
Diagnosis is clinical and requires image testing, X-rays or a computed
tomography CT.
A biopsy of the border of the lesion helps achieve diagnosis.

Etiology is multifactorial: alteration of keratinization of follicular infundibulum, quantitative and qualitative alteration of sebum production in
the sebaceous gland, and alterations of bacterial microflora (increase in
quantity of P. acnes).
Aggravating factors are stress, androgenic oral contraceptives, and the
use of cosmetic products that are not oil-free.

Clinical Presentation
A comedo is the initial lesion, which can be closed (whitehead) or open
(blackhead) and it evolves into inflammatory lesions that listed in ascending order of severity are papules, pustules, nodules and cysts.
Lesions progress and leave scars. Scars can be increased if lesions are
manipulated.

11

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

Diagnosis is clinical.

especially aects young patients (15 - 45 years of age), but it is rare


in childhood and advanced age. Versicolor pityriasis relates to heat,
humidity and sebaceous hypersecretion. It is characterized by the appearance of hyperchromic or hypochromic macules that desquamate
on scratching (nail sign) if infection is active. Macules usually appear on
the center thoracic region and on the back, that is to say, on seborrheic
zones. Relapses are habitual despite treatment.

Treatment

Diagnosis

Comedonal acne is treated with topic retinoids and benzoyl peroxide.


Inflammatory acne treatment requires benzoyl peroxide combined
with topic antibiotics (erythromycin and clindamycin). Systemic
antibiotic treatment with oral tetracyclines will be prescribed if response to topic antibiotic treatment fails.
Severe nodular cystic acne treatment involves the use of isotretinoin (13-cis-retinoic acid). It is a derivative of vitamin A. Isotretinoin
produces atrophy in the sebaceous gland and regulates keratinization. The most frequent side eect is cutaneous and mucosal xerosis. Triglycerides, cholesterol and transaminases should be monitored, as their values may increase.
It can be associated with depression.
It is teratogenic, so pregnancy should be avoided during treatment
and until a month after treatment.

Diagnosis is normally clinical. To that purpose, the following serve as


support:
Woods lamp emits yellow-orange fluorescence.
Potassium hydroxide (KOH) test: filaments and round elements can
be observed (spaghetti and meatball appearance; Figure 20).

Dierent lesions habitually combine simultaneously, so acne becomes


polymorphic. It is located in sebaceous areas: face, back, shoulders and
the center thoracic region.

Diagnosis

Treatment
Treatment is performed with topical azoles. Oral administration applies
for extensive cases or immunosuppressed patients. Dierential diagnosis includes pink pityriasis and eczemas (Figure 21).

Pilonidal Cysts
Pilonidal cysts are abscesses in the sacrococcygeal region.
This type of cysts has predominance in men between 20 and 40 years
of age. It is believed that repeated trauma on the aected area favors
their appearance.

Clinical Presentation
Pilonidal cysts present with an indurated lesion that is fluctuating, hot,
painful, but non-adherent to deep planes in the sacrococcygeal region.
Pilonidal cysts may or may not be associated to cellulitis and purulent drainage.

Diagnosis
Diagnosis is clinical and anal or perirectal abscesses should be dismissed.

Treatment
Treatment implies an incision and surgical drainage.
On some occasions, a general surgery is required.

4.3. Fungal Infections


Pityriasis Versicolor
Versicolor pityriasis is caused by commensal yeast called Pityrosporum
ovale, which transforms into its pathogen form (Malassezia furfur). It

12

Figure 20. Versicolor pityriasis. Histological cut

De rm ato l ogy

Treatment
Oral Candidiasis: fluconazole or nystatin.
Candidiasis of the skin (intertrigo): apply topical antifungal medication
and keep zone clean and dry.

Dermatophytosis or Tineas

Figure 21. Versicolor pityriasis

Dermatophyte infections aect the skin and keratinized structures, like


hair and nails (there is no mucosa involvement). Clinical diagnosis is
achieved after performing a culture. Woods lamp test normally turns
out to be negative. In general, Trichophyton dermatophyte rubrum is
the most frequent dermatophyte.

Non Inflammatory Tineas

Candidiasis
The most common triggering agent is Candida albicans. It is normally saprophytic, although, under certain conditions, candidiasis may become pathogenic (immunosuppression, humidity, pregnancy and contraceptives).

Non inflammatory tineas do not produce irreversible scarring alopecia, while inflammatory forms do. Tineas are treated with azoles derivatives.

Candidiasis of nail fold is usually associated with periungual inflammation (perionixis) and initial proximal aectation, which dierentiates it from tinea unguium (Figure 22).

The types of tinea are the following:


Ringworm of the scalp (tinea capitis or tinea tonsurans) is characteristic of childhood. It presents with alopecic plaques, broken hair
and desquamation. Infections tend to resolve spontaneously without leaving scars at the onset
of puberty.
Ringworm of the body (herpes
circinatus or tinea corporis) are
erythematous, desquamative
plaques (with more active borders), which are also circinate
and normally pruritic (Figure
23). Plaques grow eccentrically,
with less activity in the center
and more in the borders.
Ringworm of the foot (tinea
pedis): the most frequent is the
athlete foot, with desquamation in interdigital spaces.
Tinea incognito refers to tinea
Figure 23. Herpes circinatus
(tinea corpis)
wrongly treated with corticoids, what makes diagnosis
dicult, as the lesion has been modified Figure 24).

Figure 22. Candidiasis of nail fold

Figure 24. Tinea incognito secondary to treatment with topical steroids

Clinical Forms
Intertrigo: erythematous plaque in cutaneous folds. Atrophy and
fissures are typically deep in the skin fold, as well as satellite and
peripheral lesions (papules and/or pustules).
Mucosa involvement may cause diverse symptomatology, like vulvovaginitis, glossitis, and white papules in the anterior region of the
oral mucosa. Candidal balanitis is characterized by the presence of
punctiform erosions and pustules on gland and balanopreputial
sulcus. Candidal balanitis often appears after sexual intercourse or
after oral antibiotic intake.

Remember
Almost a 100% of HIV patients suffer from muguet throughout their disease
course.

13

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

Ringworm of the groin (tinea cruris or eczema marginatum von


hebra) formed by erythematous desquamative plaque with more
active borders (Figure 25).

mentations appear as a result of a reduction in hemoglobin by a parasite enzyme.

Diagnosis
Diagnosis is clinical and by direct visualization.

Treatment
Pediculosis is treated with malathion, lindane or topical permethrin.

Scabies
Scabies is originated by an acarus known as Sarcoptes scabiei. It has an
incubation period of 1 month.

Clinical Presentation
Figure 25. Ringworm of the groin (tinea cruris)
Tinea unguium: subungual
hyperkeratosis with onycholysis, but without perionixis
(Figure 26).

Diagnosis
Clinical diagnosis is reached after
performing a culture.

Treatment
Treatment involves topical antifungal medication in localized
areas.

Figure 26. Tinea unguium

Scabies produces generalized pruritus, more intense at night. The patient usually catches the infestation, which is passed to the patients
relatives. It is common to find that a recent trip to a tropical country has
been made. Lesions appear between the fingers (Figure 27), in wrists,
feet, genitalia, mammary areola and axilla, but back and face are usually spared. The most specific lesion is the acarine burrow, in whose less
scaly end, the advancing zone, the mite lies. Nodules are frequent in
axilla and genitals (nodular scabies).
Norwegian scabies is typical of the immunosuppressed. Patients
present with generalized hyperkeratosis and scabs. Norwegian scabies produce little pruritus, but it is very contagious because there
are many acari.
Nodular scabies involves the persistence of pruritic nodules despite
treatment. Lesions usually appear in axilla and genitalia. Pruritus is
due to a hypersensitivity phenomenon because of the acarus, already dead. Nodular scabies is treated with corticoids.

Oral antifungal medication is used in extensive forms, nail fold or scalp


involvement.

4.4. Parasitic Infections


Pediculosis
Pediculosis is transmitted by direct contact or by contact with fomites,
which release toxins that produce intense pruritus.

Clinical Presentation
Figure 27. Scabies. Acarine burrow
Pediculosis capitis: intense pruritus predominant in retroauricular and
occipital regions, occasionally with excoriations and impetiginization
secondary to excoriations.
Pediculosis corporis: intense pruritus in patients with poor hygiene or
who live in overcrowded conditions.
Pediculosis pubis: genital and pubic pruritus. Brownish-grey macules,
called maculae ceruleae, are typical on underwear and skin. These pig-

14

Treatment
Permethrin cream at 5% is the treatment of choice. It is little toxic,
so it can be used in children and pregnant women.
Topical lindane at 1% irritates and is neurotoxic; therefore, it is contraindicated in pregnant women and children.
Oral ivermectin is utilized in cases of resistance to prior treatments.
There is still little experience as to its use, but in a first instance, a

De rm ato l ogy

single dose would be enough to cure scabies (already used by veterinarians).

4.6. Miscellaneous
Acanthosis Nigricans

4.5. Ischemia
Decubitus Ulcers
Decubitus ulcers are the result of ischemic necrosis by continuous pressure on an area, which restricts microcirculation in that zone.

Clinical Presentation
Decubitus ulcers are present in patients in bed with scarce mobilization.
It is favored by bone prominences and lack of fat tissue. If sensitivity
decreases, there is more risk of formation of decubitus ulcers.

Diagnosis
Diagnosis is achieved based on medical records and clinical presentation.

Treatment
Prevention is of the utmost importance as well as frequent mobilization of the patient in bed.
Once ulcers have been established, hydrocolloid dressings are used for
healing, but sometimes, surgical debridement is necessary.

Gangrene

Acanthosis nigricans are velvet-like papillomatous brown


plaques in neck, axilla and groin
folds (Figure 28).
It is associated with diabetes
mellitus, Cushings disease, polycystic ovarian syndrome and
obesity.
The malignant form of acanthosis nigricans is a paraneoplastic
syndrome that dierentiates
from the benign form because
the latter has mucosal and palmoplantar involvement.

Figure 28. Acanthosis nigricans

Lichen Planus
Lichen planus is an inflammatory, idiopathic disease that equally aects
both genders, with higher frequency in middle age.
Lichen planus has been related to diverse drugs, like gold salts,
anti-malarial medication and thiazides. It has been also linked to
hepatitis C virus infection; however, this association is currently
doubtful.

Clinical Presentation

Gangrene means tissue necrosis.


There are three types: dry gangrene, wet gangrene and gas gangrene.

Clinical Presentation
Dry gangrene is due to ischemia, generally secondary to atherosclerosis. Clinical presentation involves pain, cold, and paleness of extremities. Once tissue is established, it turns bluish-black in color and dry.

Lichen planus presents with red-violaceous, polygonal flat papules,


quite pruritic, which localizes on the flexor side of wrists, forearms, ankles, and lumbosacral and flank regions. On its surface, a whitish reticulate can be observed (Wickhams striae). About 60 - 70% of the cases
present with lesions in oral and genital mucosa oral, which appear as
whitish reticulated lesions (Figures 29 and 30).

Wet gangrene is owing to bacterial flora. Tissue presents with an edematous appearance, either with blisters or pus.
Gas gangrene caused by C. perfringens. It is normally located on recent surgery. Bacteria precociously destroy tissue, producing gas. It is a
medical emergency.

Diagnosis
Clinical diagnosis is obtained by microbiological culture.

Treatment
Treatment requires surgical debridement, with amputation if necessary,
and association of broad spectrum antibiotherapy.
Figure 29. Lichen planus of oral mucosa with typical whitish
Gas gangrene is treated with hyperbaric oxygen.

reticulate

15

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

Clinical Presentation
Violaceous papules
with white stretch marks

Lichenoid lymphocyte
infiltrate (band formation)

Eruption starts with an erythematous plaque between 2 and 5 cm of


diameter with a desquamative central collarette often localized on the
trunk (heraldic mother patch; Figure 31).

Destruction
of basal layer

Figure 30. Lymphocytic interface reaction (lichen planus)

Treatment
Mild forms are treated with topical corticoids.
Severe cases require oral corticoids, psoralens plus ultraviolet light of
the A wavelength (PUVA) or cyclosporine.

Rosacea
Rosacea is a chronic disease of unknown pathogenesis, characterized
by erythema and acneiform lesions on the face. It aects middle aged
women (between 30 and 50 years of age) more.
Rosacea etiopathogenesis is unknown, although there is involvement of
vasomotor lability, infection by Demodex folliculorum, photo exposure
and genetic predisposition.

Figure 31. Pink pityriasis


Around a week later, oval papules appear on the trunk and extremities. These papules share similar characteristics with the mother patch,
though the first ones are smaller and distributed according to skin tension lines. Pink pityriasis may be asymptomatic; however, it is sometimes linked to pruritus. Lesions may last between 4 and 8 weeks and
disappear without leaving scars.

Clinical Presentation
Diagnosis and Treatment
Rosacea symptomatology comprises facial flushing episodes that end
up by provoking a persistent erythema, telangiectasias and papulopustular lesions without comedos. Over time, ocular lesions and hyperplasia of soft tissue may develop.

Diagnosis is clinical. Treatment is seldom needed, and recommended


therapies in the past (PUVA, erythromycin or oral antivirals) have not
shown clearly favorable results.

Treatment

Vitiligo

Avoid vasodilator stimuli.

Vitiligo is characterized by achromic macules by melanocyte destruction.

Mild cases require topical metronidazole or azelaic acid.

Clinical Presentation
Moderate cases need doxycycline or oral minocyclines.
Severe cases are treated with oral isotretinoin at low doses.

Pink Pityriasis
Gilberts pink pityriasis is an acute self-limiting dermatosis, which mainly aects young adults. It is of unknown origin; although a viral etiology
is suspected (there is some speculation as to links with human herpesvirus type 7).

16

Vitiligo shows achromic macules of chronic course and variable progression.


Lesions are predominant on acral and periorificial areas. They also show
the Koebner phenomenon.
Patients may have markers of autoimmune diseases (i.e., antithyroid
antibodies and diabetes), but these diseases seldom manifest themselves.

De rm ato l ogy

Treatment

Diagnosis

Localized lesions require topical corticoids.

Diagnosis is clinical.

Extensive or generalized lesions are treated with ultraviolet light B


(UVB) or PUVA.

Treatment

Strict solar photoprotection is indispensable (Figure 32).

Treatment entails application of topical 5-fluorouracil, topical imiquimod, cryotherapy or surgery.


If underlying carcinoma is suspected, a biopsy must be performed to
rule out suspicion.

Epidermoid Carcinoma
Epidermoid carcinoma is the second most frequent cutaneous tumor.
Solar photo exposure is the main etiological factor, which is why epidermoid carcinoma appears in zones of prolonged solar exposure, like the
face. Most carcinomas appear over premalignant lesions (actinic keratosis and leukoplakia, among others).

Clinical Presentation
Clinical presentation reveals erythematous or erythematosquamous
plaques. Over time, these plaques form papules and tumors, which often become ulcerative and bleed.
Figure 32. Vitiligo

Diagnosis
Diagnosis is based on clinical suspicion and histopathological confirmation.

4.7. Neoplasias
Seborrheic Keratosis
Seborrheic keratosis is the most frequent benign tumor in human beings, since it is part of cutaneous aging.

Clinical Presentation
Seborrheic keratosis presents with hyperkeratosic papules with an oily
or velvet-like texture, crests, fissures and horny plugs on their surface.
These papules are normally pigmented, showing a brownish-black color.

Treatment
Surgery with safety margins is the treatment of choice. In carcinomas
in situ, cryotherapy can be used, as well as topical imiquimod, electrocoagulation or CO2 laser techniques in destruction of tumors. Radiotherapy may also be used in some cases.

Basal Cellular Carcinoma


Basal cellular carcinoma is the most frequent cutaneous tumor. Chronic solar photo exposure is the main etiological factor; hence, most of these carcinomas aect the facial zone in patients who are 40 years of age or older.

Treatment

Gorlins syndrome should be considered if multiple basal cellular carcinomas are found in non photo exposed areas.

No treatment is required, as lesions do not become malignant.

Clinical Presentation

Seborrheic keratosis can be addressed with curettage or cryotherapy.

Basal cell carcinoma shows a pearly pink papule and superficial telangiectasias.

Actinic keratosis

It is localized over healthy skin and never aects mucosae.


Actinic keratosis is the most common precancerous lesion and aects
almost a 100% of the population in sunny areas.

Clinical Presentation
Actinic keratosis is characterized by erythematous and desquamative
papules, which are hyperkeratosic and rough on touch, developing a
chronic course.

Treatment
Surgery is the treatment of choice. Mohs surgery is performed in zones
where surrounding healthy tissue needs to be preserved. Other alternatives are cryotherapy, imiquimod, electrocoagulation, radiotherapy,
photodynamic therapy and intralesional interferon. Prognosis is excellent, as growth is slow and metastasis, exceptional.

17

A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)

Melanoma
Melanoma is the most aggressive cutaneous tumor, given its ability to
metastasize.
Risk factors comprise solar photo exposure, clear phototype, the presence of dysplastic nevus or a high number of melanocytic nevi. Family history is quite important, as some genetic mutations determine a
higher risk of developing the disease.

In situ

Extirpation 0.5 cm

Follow-up

Breslow < 1 mm

Extirpation 1 cm

Follow-up

Breslow 1 mm

Extirpation 2 cm

Sentinel ganglion

+
Lymphadenectomy

Interferon

Breslow > 4 mm

Clinical Forms
Figure 34. Melanoma treatment
See Figure 33.

Diagnosis

Kaposis sarcoma

Precocious diagnosis is essential to perform precocious surgical extirpation.

Kaposis sarcoma is the most common cutaneous tumor in HIV patients.

The ABCDE criteria can help patients to see if they need to seek medical
consultation (asymmetry of lesion, uneven borders, color, and diameter
greater than 6 mm or abnormal evolution).

Clinical presentation

The Breslow index is the thickness of the lesion measured in millimeters


and is the main prognosis factor.

Kaposis sarcoma has a course with violaceous fusiform macules, which,


over time, may evolve into indurated nodules, with blackberry appearance.
This type of sarcoma has been linked to herpesvirus type 8, both in HIV
and seronegative patients (Table 3).

Treatment
The base of treatment is precocious surgical extirpation. If the Breslow
index is less than 1 mm, margins of 1 cm will be performed. If Breslow
index is greater than 1 mm, margins will be of 2 cm.
For melanomas with a Breslow index greater than 1 mm, the sentinel
ganglion must be located. This is the first draining lymph node of the
territory where the tumor is localized. If the ganglion is positive, regional lymphadenectomy will be performed along with interferon administration (Figure 34).

EPIDERMAL KAPOSIS (HIV)

The elderly

Diffuse and bilateral


(frequently in palate and face)

Unilateral plaques
(lower extremities)

Frequent mucosal and visceral involvement

Not so frequent

Precocious lymphatic invasion


Aggressive

Not so precocious

Table 3. Dierences between epidermal and classic Kaposis sarcoma

Lentigo malignant melanoma

Melanoma of superficial extension

10%

70%

Elderly women

Young women

90% on face/photoexposed
zones of aging skins
(chronic exposure)

Spot that grows


during many years (> 10),
then progresses (nodule)

30% previous nervus


Intermittent exposure
Men: back
Women: legs

Macula with mosaic appearance


in colors that grows 4-5 years
and then infiltrates (nodule)
Metastasis 35% to 70%

Better prognosis
Worst histological prognosis
Nodular melanoma

More frequent
Acral lentinginous melanoma

15%

510 % ( 60% black and Asian race)

Middle-aged men

Elderly men

On healthy skin
Any zone
Sudden onset

Sole (ankle), hands,


mucosa, ungual bed
No relation to photo exposure

Uniform black nodule


Rapidly invasive
(vertical growth without radial)
Frequent ulceration and bleeding

Macule with mosaic appearance


(spot that grows)
Some amelanistic
Bad prognosis due to late diagnosis

Figure 33. Clinical forms of malignant melanoma

18

CLASSIC KAPOSIS

Homosexual youth (95%)

De rm ato l ogy

Diagnosis
Diagnosis relies on clinical suspicion and histopathological confirmation.

Treatment

In more advanced stages of the disease, there is aectation of extracutaneous organs, such as lymph nodes, liver, spleen, lungs and bone
marrow. Besides, there may be blastic transformation. Other possible
complication is sepsis by Staphylococcus aureus.
These three stages usually develop consecutively; nevertheless, there
may patients whose debut starts directly with the tumoral stage.

Treatment of localized forms can include surgical extirpation, radiotherapy or intralesional vinblastine.
If the sarcoma is disseminated, options involve interferon or chemotherapy.

Mycosis Fungoides
Mycosis fungoides is a T-cell lymphoma of low-grade malignancy. Its
clinical course may be very slow and surpass 50 years. Three stages are
clinically dierentiated.
1. Eczematous or macular phase: predominantly truncular erythematous macules with years of evolution. They resemble a chromic eczema. Histology is unspecific at this stage.
2. Infiltrative plaque phase: infiltrated erythematous plaques appear.
Histology is diagnostic at this stage. A dermal infiltrate of atypical
lymphocytes band forms can be observed, composed of CD+4 T
lymphocytes with cerebriform nuclei. There is a marked epidermotropism with the presence of clusters of intraepidermal lymphocytes, called Pautriers microabscesses (Figure 35).

Remember
Microabscesses of mycosis fungoides are due to lymphocytes and are called
Pautriers abscesses. Psoriasis microabscesses result from neutrophils and
are labeled as Munro-Sabouraud.

Szary Syndrome
Szary syndrome can be considered as the leukemic phase of T-cell cutaneous lymphoma. It is defined by the triad: erythroderma (Figure 36,
lymphadenopathies and the existence of more than 1,000 Szary cells
per milliliter in peripheral blood. Szary cells are atypical T- lymphocyte
with cerebriform nuclei.
Very intense pruritus is characteristic. For many authors, Szary syndrome is an aggressive clinical form and a bad prognosis of a mycosis
fungoides.

Figure 35. Mycosis fungoides. Inltrative plaque phase


3. Tumoral phase: erythematous exophytic plaques start to appear
(tumors) with a tendency to ulceration. They can have a large size.
Histology may become unspecific again as epidermotropism disappears.

Figure 36. Erythroderma due to Szary syndrome

19