EXAMINATION OF THE SKIN, HAIR, NAILS, AND MUCOUS MEMBRANES

EXAMINATION OF THE SKIN, HAIR, NAILS, AND MUCOUS MEMBRANES

The skin functions as a sensory organ; as an organ of metabolism that has synthesizing, excretory, and absorptive functions; as a protective barrier against the external environment; and as an important factor in temperature regulation. The clinical examination of the skin is partly an appraisal of these particular functions. In addition, however, the skin is synergistic with internal organ systems, and therefore, it reflects pathologic processes that are either primary elsewhere or shared in common with other tissues. The history of medicine suggests that diseases initially characterized as solely cutaneous (e.g., lupus erythematosus, dermatitis herpetiformis, and urticaria pigmentosa) have often subsequently been found to involve several systems.

In as much as visual appreciation of skin lesions is the sine qua non of dermatologic diagnosis, the examiner's eye is undoubtedly the most important instrument at his or her disposal. Yet the standardization of this instrument is a subject that receives scant attention, even though there are surprising variations in physicians' reports of what has been seen.

Furthermore, variability persists at every step of the diagnostic process, from description to differential diagnosis. The chances for correct recognition improve, of course, as the examiner gains familiarity with the various disorders of the skin. Even with experience, however, the greatest difficulty in diagnosis is often because of a failure to notice pertinent details from the available evidence.

Feinstein has challenged the tendency to favor laboratory tests that give numerical values as opposed to clinical observations. He wrote that clinicians try to be scientific in the use of inanimate objects but not in the use of their own sensory organs and brain. They often believe that their own human equipment is a hindrance instead of an advantage, an apology rather than an incentive for science in clinical work. Feinstein emphasized the need for more attention to sick people and the human methods of evaluating them, not to inanimate technology. Furthermore, the ability to arrive at a diagnosis through the history and physical examination is probably the most ancient, perhaps defining, and often—from an intellectual point of view—most satisfying attribute of being a physician. Physical diagnosis is an art, but no less a science because of it, and nowhere is the skill of physical examination more crucial to accurate diagnosis than it is in dermatology.

The examination of the skin should be made in a well-lighted room with natural light, if possible, or a “daylight” type of lamp. When feasible, the patient should be gowned, and examined completely and systematically in sections or quadrants. Articles of clothing are hindrances during the examination and may even be responsible for the inadvertent concealment of large areas of the skin.

The examination should commence with a general assessment of the patient as a whole—a “low-power” scan of the skin surface, during which rapid stock is taken of the skin, nails, and mucous membranes. The survey should include an appreciation of the color, moisture, the turgor, odor and the texture of the skin. Clothing may give clues to the cause of a suspected contact dermatitis or parasitic infestation (e.g., pediculosis).

Efflorescence Of Skin Disorder

Efflorescence is defined as lesion on skin which are visible for naked eyes and possible for palpation during examination. Efflorescence is divided in two types : primary Lesions and seccondary lesion. Primary lesion, when the lesion appear at the beginning of the disease. Secondary lesion, when the lesion appear as the disease progresses.

Primary Lesions

Descriptions of the basic primary lesions follow:

Macules are up to 1 cm and are circumscribed, flat discolorations of the skin without any elevation or depression. Examples: flat nevi, freckles. Patches are larger than 1 cm and are circumscribed, flat discolorations of the skin. Examples: senile freckles, vitiligo, measles rash.

Papules are up to 1 cm and are circumscribed, elevated, superficial, solid lesions. Examples: warts, elevated nevi, lichen planus. A wheal is a type of papule that is edematous and transitory (present less than 24 hours). Examples: Hives, sometimes insect bites.Plaques are larger than 1 cm and are circumscribed, superficial, elevated,solid lesions. Examples: lichen simplex chronicus,mycosis fungoides.

Nodules range to 1 cm and are solid lesions with depth; they may be above, level with, or beneath the skin surface. Examples: nodular secondary or tertiary syphilis, xanthomas, basal cell cancers. Tumors are larger than 1 cm and are solid lesions with depth; they may be above, level with, or beneath the skin surface. It is a common term to describe any non algnant or malignant mass. Examples: larger basal cell cancers,  tumor stage of mycosis fungoides.

Vesicles range to 1 cm and are circumscribed elevations of the skin containing serous fluid. It forms erosion when rupture  and join with the likes to form bulla. Examples:  herpes zoster, early chickenpox, contact dermatitis.

Bullae are larger than 1 cm and are circumscribed elevations containing serous fluid. Examples: second-degree burns, pemphigus,.

Pustules  is similar to vesicle except that it is filled with pus.   vary in size and are circumscribed elevations of the skin containing purulent fluid. It appears on inflammatory skin. Examples: acne, impetigo.

Petechiae range to 1 cm and are circumscribed deposits of blood or blood pigments. Examples: thrombocytopenia ,dengue fever and drug eruptions.

Purpura is a larger than 1 cm circumscribed deposit of blood or blood pigment in the skin. Examples: senile purpura and vasculitis.

Urticaria , a flat elevation of skin due to edema of upper dermis. It is characterized by itches, rapid onset, rapid resolution, widened pores and pallor.

Secondary Lesions

Secondary lesions include the following:

Scales are shedding, dead epidermal cells that may be dry or greasy. Examples: dandruff (greasy), psoriasis (dry).

Crusts are variously colored masses of skin exudates. Examples: impetigo, infected dermatitis.

Excoriations are abrasions of the skin, usually superficial and traumatic. Examples: scratched insect bites, scabies.

Fissures are linear breaks in the skin, sharply defined with abrupt walls. Examples: congenital syphilis, athlete's foot.

Ulcers are irregularly sized and shaped excavations in the skin extending into the dermis or deeper. Examples: stasis ulcers of legs, tertiary syphilis.

Scars are formations of connective tissue replacing tissue lost through injury or disease. Keloids are hypertrophic scars beyond the borders of the original injury.

Lichenification is a diffuse area of thickening and scaling with resultant increase in the skin lines and markings.

Several combinations of primary and secondary lesions commonly exist on the same patient. Examples: papulosquamous lesions of psoriasis, vesiculopustular lesions in contact dermatitis, and crusted excoriations in scabies.

Special Lesions

Some primary lesions, limited to a few skin diseases, can be called specialized lesions.

Comedones or blackheads are plugs of whitish or blackish sebaceous and keratinous material lodged in the pilosebaceous follicle, usually seen on the face, the chest, or the back, rarely on the upper part of the arms. Example: acne.

Milia are whitish nodules, 1 to 2 mm in diameter, that have no visible opening onto the skin surface. Examples: in healed burn or superficial traumatic sites, healed bullous disease sites, or newborns.

Telangiectasias are dilated superficial blood vessels. Examples: spider hemangiomas, chronic radiodermatitis.

Burrows are very small and short (in scabies) or tortuous and long (in creeping eruption) tunnels in the epidermis.

In addition, distinct and often diagnostic changes in the nail plates and the hairs are discussed in the chapters relating to these appendages.

Distribution of Skin Lesions

Although it is possible to recognize some skin eruptions by their patterns of distribution, the type and shape of the lesion, which have already been discussed, are much more reliable criteria in diagnosis. Inasmuch as the type, shape, and arrangement of lesions and their distribution pattern constitute the important tetrad in dermatologic diagnosis, it is important that the physician be acquainted with some of the more characteristic distribution patterns that are presented in the discussions of individual diseases throughout this book. Skin disorders can be classified as localized (isolated), regional, or generalized; the term total (universal) denotes involvement of the entire skin, the hair, and the nails.

As a first step in the examination of the skin, the physician should view the disrobed patient from a distance. After a survey of the entire skin surface and a close-up inspection of the type and shape of lesions, the distribution pattern can be put in perspective. For example, if eczematous patches are found on the wrist, earlobes, and neck, there is a clue to a metal contact dermatitis from a metal watchband, metal earrings, and a metal necklace.

When an eruption occurs in a bilateral and symmetric distribution, the cause is often endogenous or systemic. This pattern suggests hematogenous dissemination of the pathologic stimulus and is most often indicative of hypersensitivity reactions (e.g., drug sensitization and “allergic” vasculitis), viral exanthems, and certain other skin disorders, such as atopic eczema, dermatitis herpetiformis, etc.

In most cases, the reason for the localization of skin lesions to certain areas is unknown. A few factors, however, account for sites of predilection. Diseases caused or exacerbated by exposure to sunlight are localized to exposed areas such as the dorsa of the hands and arms, the neck, and face, a so-called “photo-distribution.” Areas of the face that are usually spared include the skin of the top part of the upper eyelids and the skin of the hair-covered scalp. Cutaneous (discoid) and systemic lupus erythematosus are predominantly localized in exposed areas but may also appear in completely light-shielded areas, such as the skin of the hair-covered scalp, ears, mouth, and feet.

Areas of minor and repeated trauma and areas where skin rubs against skin account for the distribution of lesions of epidermolysis bullosa and some of the lesions in vitiligo and psoriasis. Trauma in combination with light exposure accounts for the skin fragility and bullae localized to the backs of the hands and the face in porphyria cutanea tarda.

Hidradenitis suppurativa consists of abscesses of apocrine sweat glands and is therefore localized to axillae, nipples (in females), and anogenital areas.

Rosacea is usually confined to the “blush” area of the face, and factors that induce blushing are thought to be precipitative; these include alcoholic beverages, certain spicy condiments, hot beverages, and possibly emotional stress.

Candidiasis (moniliasis) is predominantly localized to areas where the skin is warm and moist (axillary, inframammary, and inguinal regions, the intergluteal cleft, the vaginal area, and the mouth). Candida albicans is a frequent resident of the gastrointestinal tract and reaches some of these sites by direct contact.

Herpes zoster occurs in a dermatomal pattern because the virus moves along the sensory nerves to the skin.

Lesions may be associated with openings of follicles, as in the follicular keratoses of keratosis pilaris, pityriasis rubra pilaris, and vitamin A deficiency. There is a follicular pattern of involvement in acne, lichen planopilaris, psoriasis, some drug eruptions, fungal infections (particularly Trichophyton rubrum and Trichophyton verrucosum), various forms of bacterial folliculitis, and some cases of atopic eczema.

During the time taken to survey the distribution pattern of the dermatosis, it is pertinent to review the history, occupation, various forms of exposure (e.g., to light or to airborne and contact allergens), and history of drug ingestion.

CONGENITAL RUBELLA

Gregg, in 1941, 5 was the first to record the devastating effects of rubella infection in the fetus and to describe the congenital rubella syndrome. Approximately 50 percent of infants who acquire rubella during the first trimester of intrauterine life will show clinical signs of damage from the virus. The earlier the infection, the more severe the fetal damage. In such infants, multiple congenital defects include low birth weight, microcephaly with mental retardation, cataracts, nerve deafness, and congenital heart disease (usually patent ductus arteriosus or ventricular septal defect). Following completion of organ development in the fetus, infection with rubella may produce a variable clinical picture, which may include hepatitis, splenomegaly, pneumonitis, myocarditis, encephalitis, and osteomyelitis. When the bone marrow is affected, the infant may be born with thrombocytopenia and bleeding into the skin, producing a striking picture of petechiae and ecchymoses given the colorful term “blueberry muffin baby.” In congenital rubella, a retinopathy consisting of a diffuse deposit of black pigmentation is commonly found.

Diagnosis

Infants with congenital rubella may be chronically infected for many months. Virus can be cultured from the nasopharynx, urine, CSF, and even the lens of infants with congenital cataract. As time passes, the amount of virus shed in the nasopharynx and urine gradually declines and disappears. Approximately 85 percent of infants infected in utero will excrete virus in the first month of life; 1 to 3 percent continue to excrete virus in the second year of life. The large amounts of virus from congenitally infected infants are very hazardous to pregnant women working with such infants who may be susceptible to infection. The infant with congenital infection will usually have elevation of IgM as a result of antibody produced by the infant itself, together with elevated IgG caused by passive transfer of antibodies in the maternal blood. IgG traverses the placenta, in contrast to IgM, which does not. The IgG antibodies disappear over the first few months of life. Passively acquired IgG by the fetus from an immune mother may explain the rarity of acquired rubella in early infancy. The antibodies against rubella consist of neutralizing, complement-fixing, and hemagglutination-inhibition antibodies. Neutralizing and hemagglutination-inhibition antibodies usually persist for life. The hemagglutination-inhibition antibodies are easily and quickly measured and serve to determine whether a recent infection can be attributed to rubella by an increase in titer in the convalescent period over the titer in the acute stage. A fourfold increase or more is considered diagnostic of the infection. Testing for these antibodies also enables the physician to determine whether a woman of childbearing age is immune or susceptible to German measles.

More sensitive tests—latex agglutination, fluorescence immunoassay, passive hemagglutination, hemolysis in gel, and enzyme immunoassay—are now available.

IMMUNITY AND IMMUNIZATION

Lifelong immunity usually follows an attack of rubella. Reinfection can occur but is usually not accompanied by clinical signs and symptoms. A rise in antibody level can occur; viremia from subclinical reinfection is very rare. Thus, congenital rubella is very unlikely in an infant whose mother has had an attack of rubella in the past and acquires a reinfection during pregnancy. In these instances, evaluation of fetal blood obtained by cordocentesis for specific rubella IgM antibodies or for evaluation by newer techniques using polymerase chain reaction (PCR) may help to confirm a diagnosis of fetal infection. 6 , 7 The availability of rubella vaccine 8 , 9 and its widespread use has markedly reduced the frequency of congenital infection.

In the United States, rubella vaccine is usually given together with mumps and measles vaccines in a single injection [mumps, measles, rubella (MMR)] at the age of 12 to 15 months and again at school entry (4 to 6 years of age).

Recommendations have been that rubella vaccine should not be given to a pregnant woman. Recent studies indicate that no cases of congenital rubella syndrome were seen among infants born to women who had been inadvertently vaccinated against rubella within 3 months of or early in pregnancy. Based upon this evidence the recommendation now is that pregnancy should be avoided for 28 days rather than 3 months following immunization. 10 Asymptomatic infections have occurred, but as noted, no cases of congenital defects have been documented. Interruption of pregnancy is not indicated.

The child or adult to whom rubella vaccine is administered does not shed sufficient virus to infect susceptible individuals in close contact. As a result, it is safe to immunize children in a family in which the mother is pregnant.

CLINICAL STADIUM OF AIDS

Adult

Divided into four stadiums:

Stadium 1 :

1. Asymptomatic
2. GL
3. Performance scale 1 : asymptomatic, normal activity

Stadium 2:

1. Weight loss of less than 10%
2. Minor mucocutaneus manifestation (e.g oral ulceration, nail fungal infection)
3. Herpes zoster in the last 5 years
4. Reccurent upper respiratory infection (e.g bacterial sinusitis) and/or
5. Performance scale 2 : symptomatic, normal activity

Stadium 3:

1. Weight loss of more than 10%
2. Chronic diarrhea of unknown origin for more than 1 month
3. Fever of unknown cause for more than one month
4. Oral candidiasis (oral thrush)
5. Oral hairy leucoplakia
6. Lung TB
7. Severe bacterial infection (pneumonia, pyomisitis) and/or Performance scale of 3: not getting up of bed<50% in a day for a month

Stadium 4:

1. HIV wasting syndrome (weight loss>10%, with diarrhea of unknown origin for more than one month or chronic frailty and fever of unknown origin for more than one month)
2. Pneumocytosis carinii pneumonia
3. Brain toxoplasmosis
4. Cryptosporidiosis with diarrhea of more than a month
5. Extrapulmonary cryptococcosis
6. Cytomegalovirus disease in organs other than liver, spleen, and lymph. Nodes
7. Mucocutaneus herpes virus infection , for more than one month or in any visceral organs at any duration
8. Progressive multifocal leukoencephalopathy (PML)
9. Other disseminated endemic fungal infections (e.g hystoplasmosis)
10. Esophageal, tracheal, bronchial or lung candidiasis
11. Disseminated atypical mycobacteriosis
12. Non-thyphoid Salmonella septicemia
13. Extrapulonary TB
14. Lymphoma
15. Kaposi Sarcoma

HIV encephalopathy (clinical mental and motor dysfunctions that affect daily activities and progress through weeks and months, without any causing disease or condition other than HIV infection)

And/or performance scale of 4: not getting up of bed>50% in a day for the last one month.

Children

Clinically, children with HIV are divided into three stadium:

Stadium 1:

1. Asymptomatic
2. PGL

Stadium 2:

1. Chronic diarrhea of  unknown origin
2. Severe or  reccurent persistent candidiasis after neonatal period
3. Weight loss or growth failure
4. Persistent fever
5. Recurrent severe bacterial infecction

Stadium 3:

1. Opportunistic infection due to AIDS
2. Severe growth failure
3. Progressive encephalopathy
4. Malignancy
5. Septicemia or recurrent meningitis.

Basic Principle to treat Skin Disorder

Treatment on the skin is an art, why? Because many unique condition of patient’s skin need specific regiment, not only basic chemical substance but also topical substances. Below we describe the principle to treat the skin disorder. Treatment of most of the common skin conditions is simpler to understand when the physician is aware of three basic principles:

First, The type of skin lesion, more than the cause, influences the kind of local medication used. The old adage, “If it's wet, use a wet dressing, and if it's dry, use an ointment,” is important in most cases. For example, the physician should prescribe wet soaks, to treat a patient with an acute oozing, crusting dermatitis of the dorsum of the hand, whether due to poison ivy or soap,. An ointment is indicated for a chronic-looking, dry, scaly patch of psoriasis on the elbow, because an aqueous lotion or a wet dressing would only be more drying. Bear in mind, however, that the type of skin lesion can change rapidly under treatment. The patient must be followed closely after beginning therapy. An acute oozing dermatitis treated with soaks can change, in 2 or 3 days, to a dry, scaly lesion that requires a cream or an ointment. Conversely, a chronic dry patch may become irritated with too strong therapy and begin to ooze.

The second basic principle in treatment is never do any harm and never overtreat. It is important for the physician to know which of the chemicals prescribed for local use on the skin are the greatest irritants and sensitizers. It is no exaggeration to say that the most commonly seen dermatitis is the overtreatment contact dermatitis. The overtreatment is often performed by the patient, who has gone to the neighborhood drugstore, or to a friend, and used any, and many, of the medications available for the treatment of skin diseases. It is certainly not unusual to hear the patient tell of using a strong athlete's foot salve for the treatment of the lesions of pityriasis rosea.

The third principle is to instruct the patient adequately regarding the application of the medicine prescribed. The patient does not have to be told how to swallow a pill but does have to be told how to put on a wet dressing. Most patients with skin disorders are ambulatory, so there is no nurse to help them. They are their own nurses. The success or the failure of therapy rests on adequate instruction of the patient or person responsible for the care. Even in hospitals, particularly when wet dressings or aqueous lotions are prescribed, it is wise for the physician to instruct the nurse regarding the procedure.

With these principles of management in mind, let us now turn to the medicine used. It is important to stress that we are endeavoring to present here only the most basic material necessary to treat most skin diseases. For instance, there are many solutions for wet dressings, but Burow's solution is good choice. Other physicians have preferences different from the drugs listed, and their choices are respected.