Homoeopathic management of Eczema

Dr Reshma Radhakrishnan

INTRODUCTION
Dermatitis is a general term that describes an inflammation of the skin, but dermatologists use the term to refer to a specific group of inflammatory skin diseases. Eczema [atopic dermatitis] a Greek word meaning “a boiling out”. Atopy the strange word, coined in 1923 by Coca, means “out-of-place-ness” or “different.” Atopy refers to the predisposition to develop asthma, allergic rhinitis, and an associated skin disease appropriately called atopic dermatitis.

Most, but not all, dermatologists use dermatitis and eczema interchangeably. In general, dermatitis is used more commonly in the United States, and eczema is used more commonly in Europe. Dermatitis and Eczema are non-contagious inflammation of the skin, characterized by are erythema, scaling, oedema, vesiculation and oozing. It is characterized by superficial inflammatory oedema of the epidermis associated with vesicle. Itching varies from mild to severe paroxysms which may even interfere with work and sleep.

Dermatotic lesions pass through:

• Acute (micro vesicular or macro vesicular)
• Subacute (crusting and scaling)
• Chronic (acanthotic, thickening of the epi dermis) phases).

The acute stage: is characterized by itchy erythema followed by oedema, papules, vesicles, oozing and crusting. Most of the typical eczeınas of moderate intensity start with these morphological features. This stage does not last long. In about a couple of weeks the lesions start to heal.

Chronic: If the cause persists, and the eczema lasts over months or years, it becomes chronic. In such cases, the integument appears thickened and pigmented with prominent crisscross markings (Lichenification). This is the end result of all types of long-standing eczemas.

Sub-acute: In between the acute and chronic stages, is the sub-acute stage. characterized by papules and scaling with moderate oedema and erythema. Acute eczema may pass through this stage before it heals completely or becomes chronic.

• Primary lesions may be macules, papules, vesicles, edematous patches, or plaques.
• Secondary lesions from infection or excoriation, marked by weeping, crusting, scaling, fissuring. In chronic cases lichenification [cutaneous hypertrophy and accentuation of normal skin] are frequent.

ETIOLOGY

The exact cause of eczema (atopic dermatitis) is unknown. Basically, two factors cause dermatitis and eczema.

• An allergic or a sensitive skin
• Exposure to an allergen or an irritant.

Darier had correctly said that, “there is no eczema but an eczematous patient. “

The general predisposing causes are:

• Age – usually occurs in infancy, at puberty and at the time of menopause.
• Familial predisposition – Familial sensitiveness is an important factor
• Allergy – There is usually a personal or family history of allergy, viz., asthma. eczema, hay fever, etc. Genetic predisposition is responsible for the preponderance of eczemas in certain families and their absence in others. It arises from interplay of multiple genes with external environmental factors. The more atopic genes that are present, the less environmental initiators are required to produce eczema.
• Debility– General physical debility predisposes to eczema by lowering the resistance of the individual and hence, the threshold.
• Climate – Climatic extremes like heat, dampness and severe cold
• Psychological factors

Multiple precipitating, exciting and aggravating factors

• Irritants Physical, chemical or electrical.
• Sensitizers Plants, cosmetics, clothing, medicaments and occupational hazards.
• External infections-Streptococci, staphylococci. Fungus, etc.
• Mental and emotional conflicts, strains and stresses.
• Internal septic focus shedding toxins or causing bacteremia.
• Diet and state of digestion.
• Allergic, Xero dermic, hyperhidrotic or seborrheic
• Drugs given for the disease, or otherwise.
• State of local or general nutrition.
• Climate temperature and humidity.

CLINICAL FEATURES

There are several patterns of eczema but the clinical features are similar, irrespective of the cause.

• Pruritus and scratching
• Course marked by exacerbations and remissions
• Lesions typical of eczematous dermatitis
• Personal or family history of atopy [asthma, allergy or eczema]
• Clinical course lasting more than 6 weeks
• Lichenifiaction of skin
• Presence of dry skin

CLASSIFICATION OF ECZEMA

ENDOGENOUS ECZEMA

ATOPIC DERMATITIS [Synonym: Besnier’s Prurigo]
The eczematous process is usually the result of endogenous sensitization, but exogenous allergies may also play a part. The latter can be proved by patch tests, and the former, by scratch tests, which show allergy to multiple agents. There is more than normal susceptibility to develop passive transfer antibodies in the blood serum (Prausnitz Kustner reaction).

Besides allergens, emotional stresses and parental attitudes can also cause this condition. (The parents are usually the anxious type, and the patient is usually very sensitive and highly strung but often very intelligent. The atopic patient is also very sensitive to physical stresses like heat, cold and humidity and also infections. There is also vasomotor sensitivity.

Etiopathogenesis: The pathogenesis of atopic eczema is complex and multifactorial, involving an interplay of contributing factors:

• Generalized prolonged hypersensitivity to common environmental antigens, such as pollen and house-dust mite, is the hallmark of atopy, in which there is a genetic predisposition to produce excess IgE.
• Filaggrin gene mutations increase the risk of developing atopic eczema by more than threefold, emphasizing the importance of epidermal barrier impairment in this disease.
• Decreased skin barrier function may also allow greater penetration of allergens through the epidermis, and thus cause immune stimulation and subsequent inflammation.
• The interaction between genes and environment is important; it has been estimated that 60%–80% of individuals are genetically susceptible to the induction of IgE-mediated sensitization to environmental allergens such as food and animal hair.
• There is a complex interaction between skin barrier, genetic, environmental, pharmacologic and immunologic factors. Triggering factors include:
• Skin barrier function is disrupted causing dehydration. Xerosis of the skin is the most important aggravating factor.
• Infection with Staph aureus act as super antigens and stimulate T cells and macrophages
• Auto-allergens are released from damaged tissue.
• Foods- eggs, milk, peanuts, fish, wheat
• Seasonal variation- atopic dermatitis usually improves in hot season and flares in the cold season.
• Clothing- wool and fur aggravate the condition.
• Emotional stress.
• Inhalants- dust mites, pollens
• These allergens are taken up by the antigen presenting cells in the skin and processed and presented to the CD 4 T cells along with class II MHC antigens.
• The activated T cells secrete many cytokines, especially Interleukin-4 (IL-4), (Th 2 type of response).
• There is a relative reduction in the number of CD 4 + T cells that secrete IL-2 and γ-interferon and also a decrease in CD8 + T cells.
• IL-4 activates the B lymphocyte to produce excess of IgE. IgE interacts with the antigen and sensitizes the mast cells and basophils, and causes degranulation.
• Inflammatory mediators are liberated and cause intense itching and eczema.
• The damaged skin provides a good environment for the Staph aureus population to grow and the exotoxins further worsen the eczema, by acting as super antigens.

Pathology

• The connecting link between the causes of eczema and its pathological anatomy is nearly always tropho-neurotic in character, causing a catarrhal inflammation on the skin very similar to the catarrhs of the mucous membranes.
• In general, it may be said that the blood vessels are dilated, that there is a cellular exudation of the tissues with round cell infiltration in the papillary layer of the corium.
• In the papular form, the changes take place around the follicles, especially the hair- follicles, and the rete cells become separated by fluid exudations and swell up.
• In the vesicular form, there is a further liquefaction of the cells, the contents of which unite in small accumulations beneath the corneous layer, while a pustule is formed by the emigration of leucocytes into the cavity formed by the contents of the liquified cells.
• The rete-mucosum is exposed when the horny layer is cast off without vesiculation, as occurs in eczema rubrum. Cell infiltration extends almost to the subcutaneous tissue in chronic indurated eczema, and the papilla become markedly hypertrophied

Clinical features

• They are rather characteristic.
• Itching is a predominant symptom; It is the itch that rashes rather than the rash that itches. The constant scratch leads to a vicious cycle of itch— scratch—-rash—-itch.
• Itching is severe and often interferes with sleep. it usually occurs in spasms.
• Atopic dermatitis may begin at any age, although 60% of patients have an initial outbreak by their first birthday and 90% by their fifth.

Clinically. there are four stages of atopic eczema:

1. Infantile stage, (2 mo-2 yrs): Characterized by intense itching, erythema, papules, vesicles, oozing, and crusting. Patients typically develop eruptions on the cheeks, forehead, and scalp, and less so on the trunk or extremities, The diaper area is usually spared. Dermatitis clears in half of patients by 3 years of age.
2. Childhood type (3- 11 years or continuation of infantile eczema): More chronic, lichenified lesions are present as circumscribed scaly patches with less moist and crusting lesions. Classical areas include the wrists, ankles, backs of the thighs, buttocks, and antecubital and popliteal fossae, although other areas, including extensors, may be involved in early childhood. Two-thirds of patients are clear by age 6
3. Adolescent young adult phase (12-20 yrs): Thick, dry, lichenified plaques, almost to the exclusion of weeping, crusting, or oozing lesions are seen on the face, neck, upper arms, back, and flexures.
4. Adult phase (> 20 yrs) Atopic dermatitis usually resolves in adulthood, but the hands, face, neck, and, rarely diffuse areas of skin with dry lesions may be involved. Only 10% of infantile or childhood cases of atopic dermatitis persist into adulthood.

It is marked by ill-defined, lichenoid patches, scratch marks and blood crusts with exacerbations of acute eczema from time to time. The skin is dry and injures easily. This stage is most marked till the age of 25, and may last through life. There may be associated cataract. Intolerance to high temperatures and humidity is fairly common.

Other features

• Stroking leads to blanching and not redness as in normal skin. This unique feature of AD is called white dermographism.
• Cheilitis, conjunctivitis, facial pallor, ichthyosis and nipple eczema are the minor features of AD.
• Extensive skin involvement may cause exfoliative dermatitis.
• Many skin changes may be seen, including dry skin, accentuation of palmar creases, keratosis pilaris (spinelike follicular hyperkeratosis), and ichthyosis vulgaris.
• A double infraorbital fold known as Dennie-Morgan lines, pityriasis alba (hypopigmented scaly patches), dark edematous skin beneath the eyes known as “allergic shiners,” and an exaggerated vertical linear nasal crease caused by rubbing the nose are also common.
• Increased susceptibility to cutaneous infections, especially herpes simplex and Staphylococcus aureus, increased sensitivity of the hands to cold weather, and pallor about the nose, mouth, and ears are often seen.
• Early-onset anterior subcapsular cataracts may be seen.
• It is not difficult in a typical case.
• In every case attempt should be made to establish the specific etiology and the assess the personality of the individual.
• It is so seldom seen in its primary or initial state that it may easily be mistaken for other diseases unless the main points of diagnosis are always borne in mind.
• Most patients have raised total IgE levels and IgE-specific antibodies, this is not a prerequisite for the diagnosis, as a significant minority have normal levels of IgE.

Prognosis: If left alone, eczema tends to continue indefinitely; but under judicious and persistent treatment can cur. Spontaneous and complete remission occurs during childhood. 30-5-% patients may develop asthma or hay fever later in life. Adult-onset AD often runs a severe course.

Management:

• The patient is advised to avoid any predisposing factors like dust, infection or any particular food which aggravates the condition.
• Dry skin management is the most important. The child should be given a quick bath with Luke warm water.
• Soap substitutes like cleansers containing cetyl and stearyl alcohol or super fatted soaps used for bathing, prevents drying of the skin.
• Moisturizers and emollients should be applied immediately after bath and repeated many times to prevent drying.
• Moisturizers should be applied along the direction of hair follicles to avoid folliculitis, within 3 minutes of exiting bath or shower.
• Urea and alpha-hydroxy acids containing moisturizers are particularly effective.
• Creams are preferred in an acute eczema and petrolatum for dry eczema.
• Wet compresses with saline or dilute potassium permanganate solution reduce the oozing associated with acute eczema.
• Oral and topical antibiotics to eliminate the Staph aureus infection promote healing.
• Cotton clothes are preferred.
• Cool and comfortable environment prevents itching.
• Antihistamines such as hydroxyzine should be used without hesitation because it is the ‘itch that rashes.’
• Foods have been implicated by some reducing atopic dermatitis, nuts, soy, wheat, and seafood being the most common allergens.
• The role of food allergies in the induction or exacerbation of atopic dermatitis, however, remains controversial.
• The role of food-elimination diets is debatable, since there are documented cases of these diets inducing malnutrition in children.
• Similarly, there are contradictory studies regarding the efficacy of breastfeeding over cow or soy milk in pre- venting atopic dermatitis.
• Topical calcineurin inhibitors may be used as glucocorticoid-sparing agents but should not be used in infected eczema.
• Secondary infection should be treated but positive skin swabs in isolation, without clinical evidence of infection, do not necessarily require treatment with antibiotics, although antiseptics would be appropriate.
• Sedating antihistamines may help to break the itch/scratch cycle.
• Phototherapy is generally the next step, if topical therapies are insufficient. Narrowband UVB is usually the initial phototherapy of choice and can also be used in children.
• PUVA or UVA1 can also be used if UVB is ineffective, although mainly in adults as PUVA is generally avoided in children.
• Localized phototherapy may be used for eczema on hands and feet and PUVA may be more effective in that situation.
• Systemic immunosuppression with, for example, oral glucocorticoids, intermittent ciclosporin, azathioprine or methotrexate may be needed if the response to topical therapies and phototherapy is inadequate.

SEBORRHEIC DERMATITIS
The term seborrheic dermatitis may be a misnomer because the pathogenic role of sebum has not been established. The lipophilic yeast Pityrosporum, a normal inhabitant of the skin, has been implicated in the etiopathogenesis along with abnormalities of essential fatty acids. It is a common, chronic disorder characterized by greasy scales overlying erythematous patches or plaques. Induration and scaling are less prominent than in psoriasis, but clinical overlap exists between these diseases [sebo-psoriasis].

It has a bimodal occurrence in infancy and adult age unlike AD it does not constitute on to adult life. It may be evident within the first few weeks of life, and within this context it typically occurs in the scalp [cradle cap], face or groin. Most common location

• Scalp
• Eye brows
• Eyelids
• Glabella
• Nasolabial folds
• External auditory canal
• Post auricular areas
• Central chest
• Axilla
• Groin
• Sub mammary folds
• Gluteal cleft

The lipophilic yeast Pityrosporum, a normal inhabitant of the skin, has been implicated recently. This conclusion is based on the finding of higher-than-normal numbers of the organisms in seborrheic areas and the response of seborrheic dermatitis to anti- fungal therapies, such as selenium sulfide and ketoconazole.

An increased incidence and severity of seborrheic dermatitis are seen in persons with Parkinson’s disease, facial paralysis, poliomyelitis, syringomyelia, quadriplegia, and emotional stress, suggesting that the CNS may influence seborrheic dermatitis. The mechanism is uncertain but may relate to increased rates of sebum production reported in some neurologic conditions. Severe or recalcitrant seborrheic eczema can be a marker of immune deficiency, including HIV infection.

Clinical features
It is more common in males and occurs after puberty and the incidence increases with age.

The common clinical patterns are:

• Scalp and face involvement
• Petaloid
• Flexural
• Pityrosporum folliculitis

1. Scalp and face involvement: Greasy or dry scaling, erythematous macules and papules often cause a diffuse involvement of the scalp. Other classical sites are eyebrows, eyelashes, beard, malar region, scalp hairline (corona seborrheica), naso-labial folds, retro-auricular and meatal region.
2. Petaloid: Lesions simulating pityriasis rosacea, occur over the pre-sternal area.
3. Flexural: In the axillae, groins, anogenital and sub-mammary areas, SD presents as diffuse, sharply marginated erythema with erosions and fissuring. Common in the elderly.
4. Pityrosporum folliculitis: Is an erythematous follicular eruption with papules or pustules over the back.

Infantile Seborrheic Dermatitis: It presents in infants between 2-10 weeks of age and clears spontaneously by 8-12 months of age before reappearing at puberty. Distribution in infants includes the scalp (first site involved -cradle cap, 40% children), diaper area (napkin dermatitis), and other intertriginous folds. The primary lesions are round to oval patches of dry scales or yellowish-brown, greasy crusts with variable erythema. It presents as greasy yellowish scales without any hair loss.

Adult Seborrheic Dermatitis: Pityriasis capitis or dandruff is the adult counterpart in its mildest form or the precursor lesion. With progression, the scalp may become inflamed and covered with greasy scale. Dull or yellowish-red, sharply marginated, nonpruritic lesions covered with greasy scales are seen in areas with a rich supply of sebaceous glands. The other areas involved in adults are the central face, retro-auricular and nasolabial folds, glabella, eyebrows and external auditory canal. Lesions may also see in the axillary, pre-sternal and interscapular areas and inguinal folds. It is the one of the most common causes of chronic dermatitis of the genital area.

Management

• Cradle cap responds well to vegetable oils massaged on to the scalp prior to the use of shampoo.
• The oil helps in softening and easy detachment of scales.
• Shampoos active against Pityrosporum orbiculare, such as selenium sulfide, zincpyrithione, or ketoconazole, or shampoos containing keratolytic, such as tar, salicylic acid, or sulfur, can control dandruff.
• Avoid greasy ointments and reduce soap use.
• For extremely thick scalp lesions that may overlap with psoriasis (sebo-psoriasis or seborrhiasis), Baker’s P and S Liquid with Phenol may be left on 8-12 hours be-fore scrubbing to loosen adherent scales, followed by appropriate shampoos.
• Blepharitis responds to warm water compresses, gentle cleansing with dilute nonirritating or baby shampoo, and topical sulfacetamide ointment.
• A short course of ultraviolet Blight or oral ketoconazole may be helpful.

NUMULAR ECZEMA OR DISCOID ECZEMA
It a is a chronic pruritic inflammatory dermatitis, typically affects middle aged or elderly. In Latin nummular, meaning “coinlike”. Clinically characterized by circular or oval “coinlike” lesions of variable sizes ranging from 1cm to 5cm, rapidly beginning as small edematous papules that become crusted and scaly. They are formed by coalescence of minute papulovesicular and are intensely pruritic, with excoriations.

Lesion sometimes clear centrally and resemble tinea corporis. Sometimes dry scaly lichenified plaque may be seen. It is considered as a variant of Atopic Dermatitis. Its etiology is unknown, but dry skin is a contributing factor. It occurs more frequently in men and is most common in middle age. Also, women aged 55-65 years. Most patients are seen in winter months. Lesions may be clustered on the extensor surface of lower parts of the legs or trunk in males and hands or fingers in females, are often bilaterally symmetrical. It may be generalized and scattered.

Cause

• Unknown cause.
• Psychogenic stresses, focal sepsis, food allergies, alcohol, debility and drugs are usually held responsible.
• A dry skin and cold weather may be associated with it, but not to atopy.
• It is worsened by wood, soaps, frequent bathing and many over the counter topical medications.
• Up to 95% of patients have Staphylococcus aures colonizing or infecting lesions, which suggests a possible hypersensitivity reaction against bacteria.

It has a chronic course from weeks to months and tends to recur. Secondary bacterial infection is common. Nummular eczema should be distinguished from circular patches of infective eczema and tinea circinate. Both of these are asymmetrical, acute and non-recurring conditions. Sometimes, discoid dermatitis may be associated with dyshidrosis of palms and soles, and discoid patches of keratoderma.

Treatment

• This consists of reassuring the patient, correcting the known etiological factors.
• Dry skins are massaged with oil and the nutritional status of the patient must be improved.
• Limiting baths and soap exposure, avoiding irritants, frequent use of emollients, topical corticosteroids, avoiding dry environments.
• Antihistamines all have a role in treatment.
• With the high rate of staphylococcal colonization, many dermatologists routinely prescribe a 2-3-week course of oral antibiotics.
• Photochemotherapy [PUVA] or narrow band UVB [311nm] are very effective in severe cases with extensive involvement.

STASIS / GRAVITATIONAL ECZEMA
It develops on the lower extremities secondary to venous incompetence. Patients may give a history of deep venous thrombosis and may have evidence of vein removal or varicose veins. Early findings consist of mild erythema and scaling associated with pruritus. Inflammatory edema, papules, scaling, loss of hair, ulceration, old hemorrhages and lipodermatosclerosis are the characteristic features.

There may be concomitant irritant contact dermatitis due to secretion from stasis ulcer and allergic contact dermatitis secondary to topical medications and bacterial colonization. Typical initial site of involvement is the medial aspect of the ankle, often over a distended vein.

Pathogenesis: Incompetence of the deep perforating veins increases the hydrostatic pressure in dermal capillaries. Pericapillary fibrin deposition leads to the pathological and clinical changes.

POMPHOLYX / DYSHIDROTIC ECZEMA
Pompholyx is an acute, chronic or recurrent dermatosis of the lateral aspects of the fingers, palms and soles characterized by sudden eruption of bilaterally symmetrical deep seated pruritic, clear vesicles. These may coalesce to form large multiloculated bullae. Later forms scaling, fissures, and lichenification. It is thought to be related to an atopic background and as a manifestation of nickel allergy.

Pompholyx may have several causes, which include atopic eczema, irritant and contact allergic dermatitis and fungal infection. The underlying cause must be treated or removed. Being deep seated, the lesions do not rupture easily and heal instead with a dry thick scale which gradually peels off. Spontaneous remissions can occur in 2-3 weeks. Recurrence is the rule. Secondary infection may occur. Hyper hidrosis is common

Management: Emollients and topical steroids are needed. Venous insufficiency should be managed.

EXOGENOUS ECZEMA

CONTACT DERMATITIS/ CHEMICAL ECZEMA
Contact dermatitis (CD) is a term applied to acute or chronic cutaneous inflammatory reaction to substances that come in contact with the skin. The eruption develops briskly, spreading far beyond original point of contact it has an ill-defined margin, fading at the periphery. Brisk oedema and uniform vesiculation are the features that dominate the eruption.  These reactions occur through one of two mechanisms:

• Non immunologic irritant contact dermatitis (ICD) – 80%
• Immunologic Allergic CD (ACD) – 20%

1. Allergic Contact dermatitis: Allergic contact dermatitis is dependent on sensitization and thus occurs only in sensitized individuals. Previous allergen exposure is required for sensitization and the reaction is specific to the allergen or closely related chemicals.

A minimum of 8-10 days is needed after sensitization for clinical allergy to manifest. Once sensitization to an allergen occurs, it tends to persist throughout life. However, the degree of sensitivity wanes with time unless repeated exposures occur. Depending on the degree of sensitization, even minute amounts of allergen may elicit a reaction. The eruption starts in a sensitized individual 48 hours or a few days after contact with the allergen.

The eruption worsens on repeated exposures (crescendo reaction). There is intense pruritus. Lesions are initially confined to the area of contact with the allergen and later spread to the surrounding areas. The distribution of eczema can be very informative with regard to possible culprits. Generalized involvement can also occur, if sensitization is strong.

Pathogenesis:

• ACD is a type IV, delayed, cell-mediated, hypersensitivity reaction.
• Initially, a low-molecular weight antigen hapten (500-1000 Daltons) contacts the skin and forms a hapten-carrier protein complex.
• This complex then associates itself with an epidermal Langerhans’ cell, which presents the complete antigen to a T-helper cell causing the release of various mediators.
• Subsequently, T-cell expansion occurs in regional lymph nodes, producing specific memory and T-effector lymphocytes which circulate in the general bloodstream.
• This whole process of sensitization occurs in-approximately 5-21 days.
• Upon re-exposure to the specific antigen, there is proliferation of activated T cells, mediator release, and migration of cytotoxic T cells, resulting in cutaneous eczematous inflammation at the site of contact.
• This phase occurs within 48-72 hours after exposure.

Many allergens are irritants, preceding irritation is common and may enhance allergen absorption. In contrast to irritant reactions, relatively small concentrations of an allergen can be enough to elicit an inflammatory reaction. ACD can be divided into acute and chronic forms.

Acute ACD: is characterized by erythema, edema, vesicle formation, and pruritus. It frequently spreads beyond the areas of contact and becomes generalized. The classic example is poison ivy dermatitis.

Chronic ACD: reactions are pruritic, erythematous, scaly, lichenified, and frequently excoriated. These may mimic chronic ICD.

Patch test: It is the only method available to diagnose ACD and differentiate it from ICD. The most widely used method involves the use of a Finn chamber. A small amount of the allergen, usually in a petrolatum vehicle, is placed into individual aluminum wells affixed to a strip of paper tape.  After 48 hours, the patches are removed and the initial readings recorded. Because these allergic reactions are delayed, a second interpretation must be per-formed at 72 hours, 96 hours, or even at 1 week after the initial test application. Additional readings beyond 48 hours increase the positive patch test yield by 34%.

The classic positive allergic patch test reaction shows spreading erythema, edema, and closely set vesicles that persist after removal of the patch or may appear after 2-7 days. Irritant reactions may have a glazed, scalded, follicular, or pustular appearance that usually fades after the patch is removed. Usually, patients with a suspected ACD are patch tested with a “standard” panel of 20 allergens to screen for the most common sensitivities. However, this panel only detects 75-80% of the most common allergies.

Additional testing with more specialized allergens is frequently warranted. Testing should only be done with known materials in accepted concentrations. The Repeated open application test [ROAT], or usage test, is used when patch testing is negative yet there remains a strong clinical suspicion for ACD. Remember, patch testing is a one-time occlusive test that does not duplicate low-level chronic daily exposure. With the ROAT, patients apply the suspected product to a quarter-sized area on the forearm twice a day for 1 week. If the patient is allergic, a localized dermatitis will occur, confirming the suspected allergy.

In ACD, sensitization is present on all parts of the skin as it is immunologically mediated. Therefore, application of the allergen to any area of normal skin provokes an eczematous reaction.

Management:

• Allergen avoidance is key and may involve a change of occupation, recreational activities or hobbies.
• It is important to ensure that patients are fully informed as to the nature and likely occurrence of allergens and good detective work is required to scrutinize lifestyle and daily activities.
• Treatment with emollients and topical glucocorticoids helps but will not suffice if there is continued allergen exposure.

Irritant contact dermatitis
While over 2800 substances have been identified as contact allergens, almost any substance under the right circumstances can act as an irritant. It is important to note that irritating compounds can be allergenic, and allergenic compounds can be irritating. Irritants produce direct toxic injury to the skin. An irritant substance is one that causes an inflammatory reaction in most individuals when applied in sufficient concentration for an adequate length of time.

The potential for an individual compound to cause contact dermatitis varies greatly. Factors affecting a cutaneous response include the substance’s chemical and physical properties, concentration, vehicle, and duration of exposure; patient age, area of exposure, underlying dermatitis, and genetic makeup; and environmental factors such as humidity and temperature.

The most common area of involvement is the hands, where dermatitis is initiated or aggravated by chronic exposure to water and detergents. Features may include skin dryness, cracking, erythema to vesiculation, and edema. Erosion, crusting and scaling follows. Papules are not seen. ICD can be divided into acute toxic and cumulative insult subtypes.

Acute toxic: Eruptions occur from a single exposure to a strong toxic chemical, such as an acid, chloroform, methanol, phenol or propylene glycol, and cause toxic reactions after a short exposure. inducing erythema, vesicles, bullae, or skin sloughing. Reactions occur within minutes to hours after exposure, localize to the areas of maximal contact, and have sharp borders. In most cases, healing occurs soon after exposure.

Chronic cumulative insult: It is the more common type of ICD. These are due to multiple exposures of many low-level irritants, such as soaps and shampoos, over time. This dermatitis may take weeks, months, or even years to appear. It is characterized by erythema, scaling, fissuring, pruritus, lichenification, and poor demarcation from the surrounding skin.

Strong irritants have acute effects, whereas weaker irritants commonly cause chronic eczema, especially of the hands, after prolonged exposure. It is dependent on the concentration of the offending agent and occurs in all those who are exposed, depending on the penetrability and thickness of the stratum corneum. There is a threshold concentration for these substances above which they cause acute dermatitis and below which they do not. Individual susceptibility varies and older adults, atopic and fair skinned individuals are predisposed. Irritant eczema accounts for most occupational cases of eczema and is a significant cause of time off work. In chemical burns, necrosis of tissues leads to ulceration.

There is no reliable confirmatory skin test for irritants. Diagnosis is based on the exposure history and clinical picture.

Photosensitive/photo dermatitis
Photosensitivity is an abnormal response to sunlight and affects the sun exposed parts of the body like:

• Forehead
• Malar region
• Nose
• Rim of ears
• ‘V’ area of the chest

In normal persons pigmentation of the skin increases with exposure to sunlight, depending on its intensity, duration of exposure and type of skin. Ultra violet A (UVA 320-400 nm) and ultra violet B (UVB 290-320 nm) are the primary inducers of most photosensitivity reactions. The photon energy is absorbed by molecules such as skin cells (chromophores) and then either dispersed harmlessly or results in clinical disease. The chromophore can be

• Exogenous (topical or systemic)
• Endogenous (DNA is the most important skin chromophore)
• Endogenous or exogenous allergen causing an immune reaction activated by photo radiation.

Eruption develops, or becomes aggravated on exposure to light. Seasonal variations are an Important consideration, particularly more so, in countries with extremes of climate. The common causes of photodermatitis are:

• Drugs like sulphonamides, chlorpromazine, promethazine, declamycin, Terramycin, chlorothiazides, diuretics, different hypotensive and antidiabetic drugs.
• Foods like figs, buckwheat
• External application of:
• Chemicals like sulphonamides, acridine dyes, tar, soaps containing bithionol, tetrachlorsalicylanilide, etc.,
• plants and their products like parsnips, cow parsnips, meadow grass, mustards, lime oil, psoralea, celery, bur clover, bergamot oil, etc.,
• Vit B Complex deficiency, porphyrinuria, seborrheic diathesis and liver disorders predispose to photodermatitis.

Photo dermatosis is broadly classified into:

1. Photo toxicity– sunburn, drug/chemical induced, plant induced (Phyto photo dermatitis).
2. Photo allergy– drug/chemical, chronic actinic dermatitis, solar urticaria.
3. Idiopathic– Polymorphous light eruption, actinic prurigo, hydroa vacciniform
4. Miscellaneous- Metabolic, nutritional, genetic, photo aggravated dermatosis, chronic photo damage.

Sunburn: is a transient inflammatory response of normal skin due to exposure to UVB rays. It is common in fair skinned individuals. There is uniform erythema, edema, vesicles and bullae strictly confined to the sun exposed areas. Erythema is visible 2-6 hours following exposure and reaches a maximum at 24-72 hours and fades in 3-5 days, followed by pigmentation.

Drug / chemical induced photo toxic reactions: In this condition interaction occurs between drugs /chemical with ultra violet rays in the skin and manifests like an ICD (e.g. dyes, coal tar derivatives, psoralens, tetracyclines, phenothiazines, thiazides, sulfonamides and others).

Phytophotodermatitis: Photo-sensitization of the skin after contact with plants which have either phototoxic or photo allergic action. Clinically the lesions consist of a linear erythematous, bullous rash which heals in a week or two. On healing, pigmentation is left behind which takes several months to disappear. The rash develops after contact with the plant during, or followed by, exposure to sunlight.

Photo allergic reactions: A photo allergen such as fragrances like musk ambrette, PABA, phenothiazines and halogenated salicylanilides in deodorant soaps, formed in the skin initiates a type IV hypersensitivity reaction and manifests like an ACD.

Idiopathic- Polymorphous light eruption: Polymorphous light eruption (PMLE) is the most common photo dermatosis. This is common in women. UVA and UVB can evoke PMLE, UVA being more common. Lesions are papular, papulovesicular or urticarial plaques that begin within 24 hours of exposure. In the individual patient, usually one type of lesion predominates.

Photodermatitis must be differentiated from contact dermatitis due to pollens, particularly congress grass. Both occur on the exposed parts. While the former is seen in winter, the latter, is seen at least to begin with, in the pollinating season, in parthenium growing areas. Both get aggravated by exposure to sun, the former more than the latter. In some cases, it is difficult to distinguish the two.

Diagnosis of photodermatitis is based upon:

• Affection of exposed parts
• Worsening by exposure to sun
• Seasonal variation
• Eruption is followed by hyperpigmentation.
• Photodermatitis is a clinical diagnosis, and a search should be made to establish the cause.

Management:

• Strict avoidance of sunlight is necessary.
• Sun block creams like zinc oxide or titanium dioxide, broad spectrum sunscreens, topical glucocorticoids and antihistamines are used in the treatment of PMLE.
• Severe eruption may necessitate systemic steroids.

UNCLASSIFIED ECZEMA

1. Asteatotic Eczema / Eczema Craquele / Xerotic Eczema

This occurs in dry skin and is common in older adults. Low humidity caused by central heating, over-washing, excessive use of soap, malnutrition, diuretics and decrease in skin lipids/cholesterol lowering drugs predispose. The most common site is the lower legs especially shin, and a ‘crazy paving’ pattern of fine fissuring on an erythematous background is seen. Dry winter climate, over washing and hypothyroidism exacerbates the condition.

Emollients are a mainstay, in combination with topical glucocorticoids. Patients must be advised to use caution with flammable emollients and to avoid bathroom slippages related to emollients on floor and feet, and this is particularly relevant for older individuals.

2. Lichen simplex chronicus / Neurodermatitis

LSC is a localized form of lichenification due to rubbing or scratching as a habit or due to stress or anxiety. The skin becomes highly sensitive and hyperexcitable in response to minimal external stimuli. Any emotional conflicts particularly those arising from sex, financial and social problems, may initiate itching: scratching produces further irritation, and a vicious cycle is established resulting in lichenification.

LSC is common in elderly females [menopausal women] and neurotic people. These patients tend to tear off their skin when they cannot get at others for social reasons. It usually occurs as a single plaque of lichenification with exaggerated skin markings and hyper pigmentation associated with paroxysms of pruritus.

Common sites are the lower parts of the legs, back of the knee, ankles, wrists, back of the neck, scrotum and anogenital region. Sometimes a nodular lichenification known as prurigo nodularis develops on the shins and forearms. It should be explained to the patient that the rubbing and scratching must be stopped.

Neurodermatitis should be distinguished from lichenified eczemas, atopic dermatitis, lichen planus hypertrophicus and lichen scleroses et atrophicus. Prognosis is good if the primary emotional conflict can be resolved satisfactorily. Treatment consists of psychotherapy.

REPERTORIAL APPROACH

• BBCR

SKIN AND EXTERIOR BODY, ERUPTIONS: MOIST, HUMID, ECZEMATOUS: CHRONIC ECZEMA: (13) 1 Am-c, 1 Bar-c, 1 Calc-f, 1 Cupr, 1 Cur, 1 Guai, 3 Nat-c, 3 Psor, 1 Sec, 1 Sep, 1 Sul-i, 3 Sulph, 1 Viol-t

SKIN AND EXTERIOR BODY,MILK-CRUST: (27) 1 Ambr, 3 Ant-c, 2 Ars, 2 Bar-c, 2 Bell, 2 Bry, 4 CALC, 2 Carb-an, 1 Carb-v, 1 Cham, 3 Cic, 3 Dulc, 3 Graph, 2 Hep, 3 Led, 2 Lyc, 3 Merc, 2 Mez, 2 Nat-m, 1 Phos, 4 RHUS-T, 4 SARS, 3 Sep, 2 Sil, 3 Staph, 2 Sulph, 2 Viol-t,

SKIN AND EXTERIOR BODY, SUNBURN: (3) 2 Camph, 3 Lyc, 3 Sulph,

SKIN AND EXTERIOR BODY, ULCERS: ECZEMATOUS (SALT-RHEUM): (16) 3 Ambr, 4 ARS, 2 Calc, 1 Chin, 3 Graph, 4 LYC, 1 Merc, 1 Nat-c, 2 Petr, 2 Phos, 3 Puls, 4 SEP, 2 Sil, 2 Staph, 1 Sulph, 1 Zinc,

SKIN AND EXTERIOR BODY,TETTERS (INCLUDING HERPES AND ECZEMA):IN GENERAL: (81) 1 Agar, 2 Alum, 1 Am-c, 2 Ambr, 1 Anac, 4 ARS, 1 Aur, 2 Bar-c, 2 Bell, 1 Bor, 4 BOV, 3 Bry, 1 Bufo, 1 Calad, 4 CALC, 1 Caps, 1 Carb-ac, 1 Carb-an, 2 Carb-v, 3 Caust, 1 Chel, 1 Cic, 4 CLEM, 1 Cocc, 4 CON, 2 Cupr, 1 Cycl, 4 DULC, 3 Fl-ac, 4 GRAPH, 1 Hell, 1 Hep, 1 Hyos, 1 Kali-c, 1 Kali-n, 3 Kreos, 2 Lach, 3 Led, 4 LYC, 2 Mag-c, 1 Mag-m, 1 Mang, 4 MERC, 1 Mez, 1 Mosch, 2 Mur-ac, 3 Nat-c, 2 Nat-m, 2 Nit-ac, 1 Nux-v, 2 Olnd, 1 Op, 1 Par, 3 Petr, 2 Ph-ac, 3 Phos, 1 Plb, 1 Puls, 2 Ran-b, 1 Ran-s, 4 RHUS-T, 1 Ruta, 1 Sabad, 2 Sars, 4 SEP, 4 SIL, 1 Spig, 1 Spong, 1 Squil, 1 Stann, 3 Staph, 1 Sul-ac, 1 Sulph, 1 Tarax, 3 Tell, 1 Teucr, 1 Thuj, 1 Valer, 1 Verat, 2 Viol-t, 2 Zinc,

• TPB

AGGRAVATION SUN-BURN: (5) 1 Acon, 4 BELL, 2 Camph, 1 Clem, 3 Hyos,

SKIN]ERUPTIONS:MILK CRUST: (28) 1 Ambr, 3 Ant-c, 2 Ars, 3 Bar-c, 2 Bell, 2 Bry, 4 CALC, 2 Carb-an, 1 Carb-v, 1 Cham, 3 Cic, 3 Dulc, 3 Graph, 2 Hep, 3 Led, 2 Lyc, 3 Merc, 3 Mez, 2 Nat-m, 2 Olnd, 1 Phos, 4 RHUS-T, 4 SARS, 3 Sep, 2 Sil, 3 Staph, 2 Sulph, 3 Viol-t,

SKIN ULCERS: SALT RHEUM: (16) 3 Ambr, 4 ARS, 2 Calc, 1 Chin, 3 Graph, 4 LYC, 1 Merc, 1 Nat-c, 2 Petr, 2 Phos, 3 Puls, 4 SEP, 2 Sil, 2 Staph, 1 Sulph, 1 Zinc,

SKIN TETTER:IN GENERAL (HERPETIC): (75) 1 Agar, 2 Alum, 1 Am-c, 2 Ambr, 1 Anac, 4 ARS, 1 Aur, 2 Bar-c, 1 Bell, 4 BOV, 3 Bry, 1 Calad, 4 CALC, 1 Caps, 1 Carb-an, 2 Carb-v, 3 Caust, 1 Chel, 1 Cic, 4 CLEM, 1 Cocc, 4 CON, 2 Cupr, 1 Cycl, 4 DULC, 4 GRAPH, 1 Hell, 2 Hep, 1 Hyos, 1 Kali-c, 1 Kali-n, 3 Kreos, 2 Lach, 3 Led, 4 LYC, 2 Mag-c, 1 Mag-m, 1 Mang, 4 MERC, 1 Mez, 1 Mosch, 2 Mur-ac, 3 Nat-c, 2 Nat-m, 2 Nit-ac, 1 Nux-v, 2 Olnd, 1 Par, 3 Petr, 2 Ph-ac, 3 Phos, 1 Plb, 1 Puls, 2 Ran-b, 1 Ran-s, 4 RHUS-T, 1 Ruta, 1 Sabad, 2 Sars, 4 SEP, 4 SIL, 1 Spig, 1 Spong, 1 Squil, 1 Stann, 2 Staph, 1 Sul-ac, 3 Sulph, 1 Tarax, 1 Teucr, 1 Thuj, 1 Valer, 1 Verat, 2 Viol-t, 2 Zinc,

• KENT

SKIN, ERUPTIONS: ECZEMA: (68) 1 Alum, 1 Am-c, 1 Am-m, 1 Anac, 1 Ant-c, 1 Arg-n, 3 Ars, 3 Ars-i, 1 Astac, 1 Aur, 2 Aur-m, 3 Bar-m, 1 Bell, 1 Bor, 1 Brom, 1 Bry, 2 Calad, 3 Calc, 3 Calc-s, 1 Canth, 1 Carb-ac, 2 Carb-v, 1 Carbn-s, 2 Caust, 3 Cic, 1 Clem, 1 Cop, 3 Croto-t, 1 Cycl, 3 Dulc, 1 Fl-ac, 3 Graph, 3 Hep, 1 Hydr, 2 Iris, 3 Jug-c, 3 Jug-r, 2 Kali-ar, 1 Kali-bi, 1 Kali-c, 2 Kali-chl, 2 Kali-s, 1 Lach, 1 Led, 2 Lith, 2 Lyc, 2 Merc, 3 Mez, 1 Nat-m, 1 Nat-p, 1 Nat-s, 1 Nit-ac, 3 Olnd, 3 Petr, 1 Phos, 2 Phyt, 3 Psor, 2 Ran-b, 3 Rhus-t, 1 Rhus-v, 2 Sars, 2 Sep, 2 Sil, 2 Staph, 3 Sul-i, 3 Sulph, 2 Thuj, 2 Viol-t.

SKIN, ERUPTIONS: CRUSTY: MOIST: (26) 1 Alum, 1 Anac, 2 Anthr, 3 Ars, 2 Bar-c, 3 Calc, 3 Carbn-s, 2 Cic, 1 Clem, 3 Graph, 2 Hell, 2 Hep, 2 Kali-s, 3 Lyc, 3 Merc, 3 Mez, 2 Olnd, 1 Phos, 1 Plb, 1 Ran-b, 3 Rhus-t, 1 Ruta, 1 Sep, 2 Sil, 3 Staph, 3 Sulph,

SKIN, ERUPTIONS: DRY: (61) 2 Alum, 1 Anac, 1 Anag, 3 Ars, 3 Ars-i, 3 Aur, 3 Aur-m, 3 Bar-c, 2 Bor, 2 Bry, 1 Bufo, 2 Cact, 1 Calad, 3 Calc, 3 Calc-s, 2 Carb-v, 2 Carbn-s, 1 Caust, 1 Clem, 1 Cocc, 1 Corn, 2 Cupr, 2 Dulc, 2 Fl-ac, 2 Graph, 2 Hep, 1 Hydr-ac, 1 Hyos, 2 Kali-ar, 2 Kali-c, 2 Kali-chl, 1 Kali-i, 1 Kali-s, 2 Kreos, 3 Led, 2 Lyc, 2 Mag-c, 2 Merc, 3 Mez, 1 Nat-c, 1 Nat-m, 1 Nat-p, 1 Par, 2 Petr, 2 Ph-ac, 3 Phos, 2 Psor, 1 Rhus-t, 2 Sars, 1 Sel, 3 Sep, 3 Sil, 1 Stann, 2 Staph, 2 Sulph, 1 Teucr, 1 Thuj, 1 Valer, 3 Verat, 2 Viol-t, 2 Zinc,

• COMPLETE REPERTORY

SKIN, ERUPTIONS: ECZEMA: CHRONIC: (39) 1 Am-c, 1 Bac, 1 Bar-c, 1 Bell, 2 Berb, 1 Calc, 1 Calc-f, 1 Carb-ac, 1 Carb-v, 1 Carbn-s, 2 Chaul, 1 Clem, 1 Cupr, 1 Cur, 2 Euph-cy, 1 Graph, 1 Guai, 1 Ign, 1 Iris, 3 Kali-ar, 1 Kali-m, 1 Mang, 1 Merc, 1 Merc-pr-a, 1 Merc-pr-r, 1 Mez, 3 Nat-c, 4 PETR, 3 Psor, 2 Rib-ac, 1 Sec, 1 Sep, 3 Sin-n, 1 Skook, 2 Solid, 1 Sul-i, 3 Sulph, 2 Vero-o, 3 Viol-t,

SKIN, ERUPTIONS: ECZEMA: DRY: (28) 3 Alum, 4 ALUM-SIL, 3 Am-c, 1 Ars, 1 Bar-c, 1 Berb-a, 1 Bov, 3 Bry, 1 Calc, 1 Calc-s, 1 Canth, 2 Cortico, 1 Eur-p, 1 Fl-ac, 1 Foll, 1 Kali-c, 1 Lob-e, 1 Lyc, 1 Morg, 3 Petr, 2 Platan-a, 1 Por-m, 1 Rad-br, 1 Sars, 1 Sep, 1 Sil, 1 Sulph, 3 X-ray,

SKIN, ECZEMA: MOIST: (94) 1 Aethi-a, 3 Alum, 1 Am-c, 2 Ange-a, 1 Ars, 1 Ars-i, 2 Atro, 1 Bac, 3 Bar-c, 1 Bell, 4 BOV, 1 Brom, 1 Bry, 3 Calc, 1 Calc-f, 1 Calc-s, 1 Canth, 1 Carb-an, 3 Carb-v, 1 Caust, 2 Cham, 1 Chlol, 3 Cic, 3 Clem, 1 Con, 1 Cupr, 1 Cur, 1 Dulc, 1 Erig, 2 Galeg, 2 Genist, 2 Gnaph, 4 GRAPH, 1 Guai, 1 Harp, 1 Hell, 3 Hep, 2 Hoch, 1 Iod, 1 Iris, 3 Kali-br, 1 Kali-c, 1 Kali-chl, 1 Kali-sil, 1 Kreos, 1 Lach, 3 Lappa, 1 Led, 4 LYC, 1 Merc, 1 Merc-c, 1 Merc-pr-a, 1 Merc-pr-r, 3 Mez, 3 Morg, 1 Mut, 1 Nat-c, 3 Nat-m, 3 Nat-s, 1 Nit-ac, 3 Olnd, 4 PETR, 1 Ph-ac, 1 Phos, 1 Phyt, 2 Pot-t, 1 Pras, 1 Prim-o, 3 Psor, 1 Rad-br, 3 Rhus-t, 3 Ruta, 1 Sabin, 1 Sanic, 1 Sars, 2 Scab-s, 1 Sec, 3 Sel, 3 Sep, 3 Sil, 1 Squil, 3 Staph, 1 Sul-ac, 1 Sul-i, 3 Sulph, 1 Tarax, 1 Tere-ch, 1 Thuj, 1 Tub, 1 Vinc, 3 Viol-o, 1 Viol-t, 1 Wies, 1 Zinc,

HEAD, ERUPTIONS: MILK CRUST, CRUSTA LACTEA: (86) 1 Acon, 1 Aethi-a, 3 Alum, 3 Ambr, 3 Ant-c, 1 Ant-t, 3 Ars, 1 Ars-i, 3 Astac, 1 Aur, 4 BAR-C, 2 Bell, 2 Betul, 1 Bor, 1 Brom, 2 Bry, 4 CALC, 1 Calc-i, 1 Calc-p, 3 Calc-s, 1 Canth, 3 Carb-an, 1 Carb-v, 1 Cham, 1 Chel, 4 CIC, 3 Clem, 3 Croto-t, 4 DULC, 3 Euph, 3 Graph, 1 Hell, 4 HEP, 1 Hydr, 1 Iod, 1 Iris, 3 Jug-r, 1 Kali-c, 1 Kali-chl, 1 Kali-m, 1 Kreos, 3 Lappa, 3 Led, 3 Lyc, 3 Mag-c, 2 Med, 2 Melit, 4 MERC, 1 Merc-i-f, 4 MEZ, 1 Mur-ac, 3 Nat-m, 1 Nat-p, 3 Nit-ac, 1 Ol-j, 4 OLND, 1 Onis, 1 Par, 3 Petr, 1 Ph-ac, 4 PHOS, 1 Phyt, 1 Plb-i, 3 Psor, 4 RHUS-T, 3 Ruta, 1 Sarr, 4 SARS, 1 Scroph-n, 1 Seneg, 3 Sep, 4 SIL, 4 STAPH, 1 Still, 1 Sul-ac, 3 Sulph, 2 Tarent, 3 Trif-p, 3 Tub, 2 Ust, 1 Vac, 1 Verat, 3 Vinc, 1 Viol-o, 3 Viol-t, 3 Zinc,

GENERALITIES SUN: AGG.: SUNBURN: (49) 3 Acon, 3 Agar, 3 Ant-c, 3 Astac, 4 BELL, 3 Bov, 1 Bry, 1 Bufo, 1 Cadm-s, 3 Camph, 3 Canth, 1 Carc, 1 Chlorpr, 3 Clem, 2 Cortiso, 1 Cyt-l, 1 Epig, 1 Euphr, 1 Germ, 1 Gink, 1 Hist, 1 Hydrog, 3 Hyos, 2 Hyper, 1 Ignis, 1 Kali-c, 1 Lach, 3 Lyc, 1 Mangi, 1 Morg, 3 Mur-ac, 3 Nat-c, 2 Nelu, 1 Op, 1 Pitu-a, 4 PULS, 1 Rob, 2 Ros-d, 1 Sel, 1 Seq-g, 3 Sol, 3 Sulph, 1 Tam, 1 Tax, 1 Toxop-p, 1 Tub, 1 Uv-lux, 3 Valer, 1 Verat,

CLINICAL, ALLERGY: CREMES, COSMETICS:(2) 1 Ars, 1 Puls,

CLINICAL, ALLERGY: CHEMICALS: (5) 1 Antipyrin, 3 Asar, 1 Ba-tn, 1 Carc, 1 Dpt,

CLINICAL, ALLERGY: METAL DERMATITIS: (3) 1 C-di-o, 1 Morg-g, 1 Pitu-a,

SKIN, ERUPTIONS: ALLERGIC: (56) 4 ANT-C, 1 Apis, 3 Ars, 3 Astac, 1 Bell, 2 Bov, 1 Bry, 1 Calc, 1 Calc-ar, 1 Camph, 1 Cann-s, 1 Carb-v, 3 Chlol, 1 Chol, 1 Coloc, 3 Cop, 1 Dulc, 1 Dys-co, 1 Euph, 1 Fic, 1 Frag, 1 Galph, 4 GRAPH, 1 Hep, 1 Hom, 1 Ind, 1 Levo, 1 Lyc, 1 Mand, 1 Med, 1 Medus, 1 Morg, 1 Morg-g, 1 Nat-s, 1 Neod-c, 1 Pall, 1 Parth, 1 Petr, 1 Pot-a, 1 Prim-o, 3 Puls, 1 Rad-br, 1 Rhus-t, 1 Ruta, 1 Sep, 1 Sil, 1 Stroph, 1 Syc-co, 1 Tela, 3 Ter, 1 Terb-s, 1 Tet, 1 Thuj, 4 TUB, 1 Urea, 3 Urt-u,

• SYNTHESIS REPERTORY

SKIN – ERUPTIONS – chronic: (4) mang. sul-i. syph. vac.

SKIN – ERUPTIONS – crusty – moist: (33) alum. anac. Anthraci. ARS. Bar-c. CALC. CARBN-S. Cic. clem. dulc. GRAPH. Hell. Hep. Kali-s. LYC. maland. med. MERC. MEZ. nit-ac. Olnd. petr. phos. plb. ran-b. RHUS-T. ruta sep. Sil. STAPH. SULPH. vinc. viol-t.

SKIN – ERUPTIONS – eczema – discharging: (36) alumn. AMBR. ARS. calc. calc-s. chin. cic. con. dulc. graph. hep. kali-m. kreos. lach. lap-a. lappa lyc. maland. merc. merc-c. merc-pr-r. mez. nat-c. petr. phos. puls. rhus-t. sep. Sil. staph. sul-i. sulph. tub. vinc. viol-t. zinc.

SKIN – ERUPTIONS – eczema – discharging – salt rheum: (20) AMBR. ARS. calc. calc-s. chin. Graph. hep. lach. lyc. merc. nat-c. petr. phos. puls. rhus-t. sep. Sil. Staph. sulph. zinc.

SKIN – ERUPTIONS – eczema – chronic: (21) am-c. asthm-r. bar-c. calc-f. com. cupr. cur. guaj. ichth. lev. mang-c. merc. Nat-c. psor. sec. sep. sul-ac. sul-i. Sulph. tub. viol-t.

SKIN – ERUPTIONS – eczema – Folds of the Skin: (2) moni. tub.

SKIN – ERUPTIONS – eczema – sun, from: (1) Mur-ac.

SKIN – ERUPTIONS – eczema – dry: (7) calc-s. dulc. frax. sep. streptoc. tarent. viol-t.

SKIN – ERUPTIONS – eczema – children; in: (12) calc. calc-m. calc-s. carc. dulc. frax. med. psor. sep. staph. strept-ent. viol-t.

SKIN – ERUPTIONS – eczema – children; in – infants: (3) frax. med. strept-ent.

HEAD – ERUPTIONS – milk crust: (70) Alum. am-c. ambr. ant-c. ant-t. ars. astac. aur. BAR-C. bell. brom. bry. calc. calc-i. calc-s. Carb-an. carb-v. cham. chel. Cic. clem. con. Dulc. euph. graph. hell. HEP. kali-c. kali-chl. kali-m. kreos. lappa Led. Lyc. mag-c. med. melit. merc. merc-i-f. merc-pr-r. Mez. mur-ac. nat-m. nat-p. Nit-ac. ol-j. olnd. par. Petr. ph-ac. phos. psor. rhus-t. Ruta SARS. scroph-n. seneg. Sep. sil. Staph. sul-ac. sulph. Trif-p. tub. ust. vac. verat. vinc. Viol-t. Zinc.

GENERALS – SUN – sunburn: (35) acon. Agar. am-m. Ant-c. apis ars. BELL. bov. bry. bufo Camph. canth. choc. clem. cortiso. cyt-l. euphr. hist. Hyos. ignis-alc. kali-c. lach. Lyc. Mur-ac. Nat-c. Nat-m. op. PULS. rob. sel. sol Sulph. Valer. vanil. verat.

• BOERICKE REPERTORY

HEAD SCALP: ERUPTIONS: CRUSTA LACTEA: (27) 2 Astac, 2 Bar-c, 3 Calc, 2 Calc-i, 2 Calc-s, 2 Cic, 2 Clem, 3 Dulc, 2 Graph, 3 Hep, 2 Kali-m, 2 Lappa, 3 Lyc, 2 Merc, 3 Mez, 2 Olnd, 2 Petr, 2 Psor, 2 Rhus-t, 2 Sars, 2 Scroph-n, 3 Sep, 2 Sil, 2 Sulph, 3 Trif-p, 3 Vinc, 3 Viol-t,

HEAD SCALP: ERUPTIONS: ECZEMA: (15) 2 Astac, 3 Calc, 2 Clem, 3 Graph, 2 Hydr, 3 Lappa, 2 Lyc, 2 Mez, 3 Olnd, 3 Petr, 2 Psor, 2 Sel, 2 Sulph, 2 Tell, 2 Viol-o,

SKIN PRURIGO: (25) 2 Acon, 2 Aln, 3 Ambr, 2 Anthro, 3 Ars, 3 Ars-i, 2 Ars-s-f, 2 Carb-ac, 3 Chlol, 2 Dios, 3 Dol, 2 Kali-bi, 3 Lyc, 3 Merc, 3 Mez, 3 Nit-ac, 3 Olnd, 2 Ov, 2 Ped, 3 Rhus-t, 3 Rhus-v, 3 Rumx, 2 Sil, 3 Sulph, 2 Ter,

SKIN SEBORRHOEA: (27) 3 Am-m, 3 Ars, 3 Bry, 2 Bufo, 3 Calc, 2 Cinch, 2 Graph, 3 Iod, 2 Kali-br, 3 Kali-c, 2 Kali-s, 2 Lyc, 2 Merc, 2 Mez, 3 Nat-m, 3 Phos, 3 Plb, 2 Psor, 3 Raph, 2 Rhus-t, 2 Sars, 3 Sel, 2 Sep, 2 Staph, 2 Sulph, 2 Thuj, 3 Vinc,

• MURPHY

SKIN ECZEMA, SKIN: (177) 1 Acon, 1 Aethi-a, 2 Aethi-m, 1 Aln, 1 Alum, 1 Alum-p, 1 Alum-sil, 1 Am-c, 1 Am-m, 1 Ammc, 1 Anac, 1 Ant-c, 1 Anthro, 1 Aq-mar, 1 Arbu, 1 Arg-n, 1 Arist-cl, 3 Ars, 3 Ars-i, 3 Ars-s-f, 1 Astac, 1 Aur, 1 Aur-ar, 2 Aur-m, 1 Aur-s, 1 Bac, 1 Bar-c, 3 Bar-m, 1 Bell, 2 Berb, 1 Berb-a, 1 Bor, 2 Bov, 1 Brom, 1 Bry, 2 Calad, 3 Calc, 1 Calc-f, 1 Calc-i, 1 Calc-p, 3 Calc-s, 2 Calc-sil, 1 Cand-a, 2 Canth, 1 Caps, 1 Carb-ac, 1 Carb-an, 2 Carb-v, 1 Carbn-s, 1 Carc, 1 Cast-eq, 2 Caust, 1 Cere-b, 1 Chin-s, 1 Chlol, 1 Chrysar, 3 Cic, 1 Cist, 1 Clem, 1 Com, 1 Con, 1 Cop, 1 Corn, 1 Corn-a, 1 Cosm, 3 Croto-t, 1 Cupr, 1 Cur, 1 Cycl, 3 Dulc, 1 Euph, 1 Fago, 1 Ferr-ar, 1 Fl-ac, 1 Foll, 1 Form-ac, 1 Formal, 1 Frax, 1 Fuli, 3 Graph, 1 Guai, 1 Hell, 3 Hep, 1 Hippoz, 1 Ho, 1 Hydr, 1 Hydrc, 1 Insulin, 2 Iris, 3 Jug-c, 3 Jug-r, 2 Kali-ar, 1 Kali-bi, 1 Kali-br, 1 Kali-c, 2 Kali-chl, 1 Kali-m, 2 Kali-s, 1 Kali-sil, 1 Kreos, 1 Lac-ac, 1 Lach, 3 Lappa, 1 Led, 2 Lith-c, 2 Lyc, 1 Maland, 2 Mang, 2 Merc, 1 Merc-c, 1 Merc-d, 1 Merc-pr-r, 3 Mez, 1 Morg, 1 Mur-ac, 1 Mut, 1 Nat-ar, 1 Nat-c, 1 Nat-m, 1 Nat-p, 2 Nat-s, 1 Nit-ac, 1 Nux-v, 3 Olnd, 1 Osm, 1 Pers, 3 Petr, 1 Ph-ac, 1 Phos, 2 Phyt, 1 Pic-ac, 1 Piloc, 2 Plb, 1 Podo, 1 Polyg-pe, 1 Prim-o, 1 Prim-v, 3 Psor, 2 Ran-b, 3 Rhus-t, 1 Rhus-v, 1 Rumx, 1 Ruta, 1 Sabin, 1 Sanic, 2 Sars, 1 Sec, 1 Sel, 2 Sep, 2 Sil, 1 Skook, 1 Squil, 2 Staph, 1 Stry, 1 Stry-ar, 1 Stry-p, 1 Sul-ac, 3 Sul-i, 4 SULPH, 1 Tarax, 1 Tarent, 1 Tarent-c, 1 Tell, 1 Tere-ch, 2 Thuj, 1 Thyr, 1 Titan, 1 Tub, 1 Ur-ac, 1 Urea, 1 Ust, 2 Vinc, 2 Viol-t, 1 X-ray, 1 Xero, 1 Zinc, 1 Zinc-p,

SKIN PRURIGO, SKIN: (24) 1 Acon, 1 Aln, 2 Ambr, 1 Anthro, 2 Ars, 2 Ars-i, 1 Ars-s-f, 1 Carb-ac, 2 Chlol, 2 Dol, 1 Kali-bi, 2 Lyc, 2 Merc, 2 Mez, 2 Nit-ac, 2 Olnd, 1 Ov, 1 Ped, 2 Rhus-t, 2 Rhus-v, 2 Rumx, 1 Sil, 2 Sulph, 1 Ter,

SKIN ECZEMA, SKIN: ACUTE, FORM: (10) 1 Acon, 1 Anac, 1 Bell, 1 Canth, 2 Chin-s, 2 Croto-t, 1 Mez, 1 Pic-ac, 2 Rhus-t, 1 Sep,

SKIN ECZEMA, SKIN: CHRONIC: (14) 1 Am-c, 1 Bar-c, 1 Calc-f, 1 Cupr, 1 Cur, 1 Guai, 1 Mang, 2 Nat-c, 2 Psor, 1 Sec, 1 Sep, 1 Sul-i, 2 Sulph, 1 Viol-t,

SKIN ECZEMA, SKIN:MOIST: (70) 1 Alum, 1 Am-c, 1 Ars, 1 Ars-i, 2 Bar-c, 1 Bell, 2 Bov, 1 Brom, 1 Bry, 1 Calc, 1 Calc-f, 1 Calc-s, 1 Canth, 1 Carb-an, 2 Carb-v, 1 Caust, 1 Chlol, 1 Cic, 2 Clem, 1 Con, 1 Cupr, 1 Cur, 1 Dulc, 2 Graph, 1 Guai, 1 Hell, 2 Hep, 2 Kali-br, 1 Kali-c, 1 Kali-chl, 1 Kreos, 1 Lach, 1 Lappa, 1 Led, 2 Lyc, 1 Merc, 1 Merc-c, 1 Merc-pr-r, 1 Mez, 1 Nat-c, 1 Nat-m, 2 Nat-s, 1 Nit-ac, 2 Olnd, 2 Petr, 1 Ph-ac, 1 Phos, 1 Phyt, 1 Prim-o, 2 Psor, 2 Rhus-t, 2 Ruta, 1 Sabin, 1 Sanic, 1 Sec, 2 Sel, 2 Sep, 2 Sil, 1 Squil, 2 Staph, 1 Sul-ac, 1 Sul-i, 2 Sulph, 1 Tarax, 1 Tere-ch, 1 Thuj, 1 Tub, 1 Vinc, 1 Viol-t, 1 Zinc,

SKIN ECZEMA, SKIN: DRY: (5) 3 Alum-sil, 1 Berb-a, 1 Calc-s, 1 Foll, 1 Morg,

SKIN ECZEMA, SKIN: CHILDREN, IN: (9) 1 Calc-s, 1 Carc, 1 Frax, 1 Graph, 1 Lappa, 1 Morg, 2 Nat-m, 1 Sulph, 1 Viol-t,

CLINICAL SUNBURN, AILMENTS FROM: (31) 1 Acon, 2 Agar, 2 Ant-c, 2 Apis, 3 Bell, 1 Bov, 1 Bry, 1 Bufo, 2 Calen, 2 Camph, 3 Canth, 1 Clem, 1 Cortiso, 1 Cyt-l, 1 Euphr, 1 Hist, 2 Hyos, 1 Kali-c, 1 Lach, 2 Lyc, 2 Mur-ac, 2 Nat-c, 1 Op, 3 Puls, 1 Rob, 1 Sel, 3 Sol, 2 Sulph, 3 Urt-u, 2 Valer, 1 Verat,

CLINICAL BURNS, GENERAL, FIRE, CHEMICALS, AILMENTS, FROM: (88) 1 Acet-ac, 2 Acon, 1 Agar, 1 Aloe, 1 Alum, 1 Alumn, 1 Anac, 1 Ant-c, 2 Apis, 1 Arist-cl, 1 Arn, 3 Ars, 2 Bar-c, 2 Bell, 1 Both-l, 2 Bry, 1 Calc, 1 Calc-f, 1 Calc-p, 1 Calc-s, 3 Calen, 1 Camph, 4 CANTH, 1 Carb-ac, 2 Carb-v, 2 Carbn-s, 2 Caust, 1 Chin, 1 Cic, 1 Cosm, 1 Crot-h, 1 Cycl, 1 Des-ac, 1 Echi, 1 Eucal, 1 Euph, 1 Ferr, 1 Gaul, 1 Grin, 2 Ham, 1 Hed, 2 Hep, 1 Hoit, 1 Hyos, 2 Hyper, 2 Ign, 1 Jab, 2 Kali-bi, 1 Kali-c, 1 Kali-chl, 2 Kreos, 1 Lach, 1 Mag-c, 2 Mag-m, 2 Merc, 1 Mom-b, 2 Nat-c, 2 Nux-v, 1 Op, 1 Par, 1 Paraf, 1 Passi, 1 Petr, 1 Phos, 2 Pic-ac, 2 Plan, 1 Plat, 1 Plb, 2 Puls, 1 Rad-br, 1 Ran-b, 2 Rhus-t, 1 Ruta, 1 Sabad, 2 Sec, 1 Semp, 1 Sep, 1 Sieg, 2 Sil, 3 Sol, 1 Spira, 2 Stram, 2 Sul-ac, 2 Ter, 1 Thuj, 3 Urt-u, 1 Verat, 1 X-ray,

CLINICAL SUNBURN, AILMENTS FROM: CHRONIC: (3) 1 Nat-c, 1 Nat-m, 2 Sol,

CLINICAL SUNBURN, AILMENTS FROM: SUNBURNS, EASILY: (2) 1 Nat-m, 2 Sol,

CHILDREN CRUSTA, LACTEA: (1) 3 Staph,

 MANAGEMENT [HOMOEOPATHIC]

General Management

• All local or exciting causal elements should be removed as soon as possible.
• If no exciting features are apparent, a careful search should be made in every possible direction to ascertain a possible systemic cause so that the proper constitutional treatment may be instituted.
• A careful examination of the patient’s bathing, diet, exercise and sleep, in fact all details that contribute toward the habits of everyday living should be investigated.
• In any case, the individual should be treated rather than the disease eczema.
• There is no combination of symptoms found exactly alike in two individuals; hence it is useless to look for specifics in the treatment of eczema.
• The quantity and quality of food is again an individual question. some patients requiring no restrictions, in fact must be urged to eat.
• A reduction in quality is found just as desirable as a reduction in quantity, and the regulation of meal hours and sufficient chewing are important considerations.
• Speaking broadly, all stimulants should be prohibited, and liquids should be indulged in sparingly at meals, while a reasonable amount of pure water should be drunk between meals.
• Fresh articles of food, such as the light lean meats, fowl, fish, vegetables, salads, and unsweetened fruit may be urged, while starchy and sugary foods, such as candy, pastry, pie and confections, and shell-fish, salt meats, salt fish, dried or preserved foods of all kinds, and condiments should be avoided.
• Physiological treatment further demands that the patient have sufficient amount of bodily exercise, especially if it can be pleasurable, to further the elimination of poisonous accumulations within the system because retention of these is supposed to be a fundamental cause of eczema.
• Often passive exercise, if not applied to the surface involved, is the easiest means of accomplishing the object.
• Bathing, like many useful habits, must be regulated to the needs of each individual but the ordinary soaps should never be employed.
• Hot water is best employed both for its cleansing and therapeutic effects, especially if only used for a few minutes, as it will often relieve irritation and cause a beneficial reaction.
• The drying of the skin should be more in the nature of a patting than a rubbing, as irritation of all description should be avoided.
• It is seldom that the addition of alcohol, salt, bran, starch, borax or soda will benefit, and long contact with water nearly always aggravates eczema.
• Masks, gloves, bandages and even immobilization of various parts may aid to prevent scratching.
• Occasionally the subject of fresh air and ventilation, especially of sleeping rooms, should be investigated, and the occupation of an individual may need to be radically changed to improve his general hygiene.
• Clothing should be selected with care so as not to be too warm, too thin or too irritating.
• Flannel or wool invariably irritates an’ eczematous surface, although they be worn over linen or cotton.

Therapeutic management

• Homoeopathic Approach: “Treat the patient and respect the skin” should be the golden rule of thumb whilst treating an eczema, that is to say, there is no eczema, but an eczematous patient.

Acute Eczema

• It is not true that always one should prescribe an acute drug in acute phase of eczema; many times, one gets a picture of deep acting drugs like Sulphur or rare occasional nosodes like Tuberculinum.

We build the acute totality with the help of the following:

(1) Ailments from, if any

(2) The look of eczema

(3) The discharge

(4) Itching with modalities

(5) Concomitants, if any, associated with It

(6) Any other P.Q.R. symptoms available.

• If the selected remedy is a short acting drug, then one should start with giving it 3-4 times a day and a following remedy every 3rd day.
• Further repetition should be considered only after enquiring in detail about the symptoms just mentioned in the totality.
• Never start with a deep acting drug in acute eczemas as far as possible until you are too sure.
• Once the acute eczema gets completely cured, do not forget to evolve the constitutional drug and interpose either a constitutional remedy or a nosode, depending on the dominant miasm present at that time.
• This is chiefly to prevent recurrence or suppression of the eczema if at all by the acute remedy.

Chronic Eczema

The main reasons for the eczema to become chronic are:

• Non-elimination of exciting, predisposing and complicating causes.
• Treatment of acute eczema with suppressive measures like faulty selection of similimum using strong topical ointments, local application of strong acids to burn the skin.

Two things should always be kept in mind while treating a case of chronic eczema:

• In cases of infective eczema resistance of the patient should be built up against the infection by repeated administration of intercurrent remedies like nosodes and constitutional remedy wherever applicable.
• In cases of allergic eczema, one should try to desensitize the individual by giving the allergies in potentized form on the principle of Isopathy, e.g. in cases of congress grass eczema. Congress grasses in 30 potencies to be given repeatedly over a prolonged period.

Examples of Occupational Dermatitis

Occupation	Causative Agent	Occupational Drugs
Agriculture	Plants, Insecticides.	Anacardium, Rhus tox, Petroleum
Automobiles	Oil Petrol, Paints	Petroleum
Buildings Workers	Cement Lime	Calc – Sulph Calc-carb
Pharmaceutical	Dyes, Chemicals Solvents	Sulph, Psor, Graph, Carbo-Veg
House wife	Soaps Vegetables Artificial flavour	Calc-s Graph Nat-m
Painters	Printer’s ink	Plb-met, Carb-v, Sulph
Rubber workers	Dyes, Glues	Sulph
Tar workers	Tar	Carb – an
Doctors	Iodine Streptomycin Sulphonamide	Iodium Streptomycin

BIBILOGRAPHY

• Davidsons principles of practice of medicine
• K V Krishna Das – Textbook of Medicine
• API Text book of Medicine
• Dermatology secrets
• Diseases of the skin (including of exanthemata)
• Diseases of the skin by Frederick m Dearborn, A B
• Repertories – Synthesis, Complete, BBCR, TPB, Boericke, Kent, Murphy

Dr Reshma Radhakrishnan
PG Scholar, Homoeopathic Repertory & Case Taking, GHMC, Kozhikode,
E-mail: dr.reshmaradhakrishnan@gmail.com