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Managing dry skin conditions

It has been estimated that 15% of clinic time in primary care is spent dealing with dermatological problems. In this article Lesley Hickin provides a comprehensive overview of dry skin conditions, from their biology to the best choice for treatment

Lesley Hickin
Sessional General Practitioner
South London

Consultations about skin conditions take up a lot of time both for the practice nurse and family doctor, with up to 15% of clinic time spent dealing with dermatological problems. You will commonly see patients of all ages who for one reason or another are troubled by dry skin. It may be a presenting feature in a generalised skin disease, or secondary to other pathological processes.
You will feel more confident and capable of helping your patients manage their dry skin if you can assess the underlying cause before embarking on treatment. If you also have a good understanding of the different types of emollients and appropriate regimes for applying them your patients will benefit. It is worth giving individually prepared written information to back up your consultation, and keep a supply of emollient samples for patients to try.

The biology of dry skin 
The skin is the largest organ in the body, functioning as a barrier to prevent fluid loss from the dermis and preventing external irritants and pathogens from breaching the skin. When barrier function is compromised the skin can dry out and be damaged by environmental factors. Genetic predisposition to dry skin is common, recent research having identified one of the genes responsible.(1)
The top layer of the skin is the epidermis, attached to the deeper dermis (see Figure 1). From the basement membrane at the bottom of the epidermis keratinocytes (columnar nucleated cells) divide and migrate to the surface gradually changing and maturing. As the process evolves lipids are produced within the keratinocytes and expelled in the lamellar bodies to produce the intercellular lipid which helps enable the barrier function.

The very top layer of flat, dead, non-nucleated keratinocytes (also known as corneocytes) is known as the stratum corneum. The thickness varies from the thinnest on the face to the thickest on the heels. Corneocytes are arranged in sheets held together by lipids, forming a firm but elastic membrane, lubricated by sebum which is produced by the sebaceous glands associated with hair follicles. The surface of healthy skin is smooth, slightly shiny and well hydrated.
The process of epidermal differentiation, from basement membrane to stratum corneum, takes around 14 days, then a further 14 days elapse before the dead cells are sloughed off in the process known as desquamation.
Corneocytes have tough cornified envelope proteins (filaggrin and keratin are the most important) and contain a group of substances known collectively as natural moisturising factor (NMF), made from the breakdown of filaggrin. NMF actively attracts and holds water in the stratum corneum, helping maintain plump well hydrated corneocytes and flexible elastic skin. Also found are proteins called aquaporins which help regulate the flow of water within cells. Thus the skin is not just an inert barrier, but has complex mechanisms in place to maintain hydration and respond to the environment.
Under normal conditions the stratum corneum has a 10-30% water content giving skin its soft smooth and flexible texture. Water is lost from the skin by evaporation, and it is replaced from the dermis and the atmosphere. Sebum and intercellular lipids form a barrier acting as a natural moisturiser and prevent evaporation. Signs and symptoms of dry skin arise when water loss exceeds replacement and the water content falls below 10%. The barrier function is disrupted because dry skin is more permeable and loses more water to the environment, also is less able to resist the absorption of irritants and bacteria.

What causes dry skin?
Heredity and environment

  • Age and aging - the skin's ability to produce sebum and intracellular lipids reduces with age, particularly in women. Skin elasticity also decreases.
  • Genetic tendency - the tendency to develop dry skin can be inherited. The water content of skin is partly determined by genetics, and under similar circumstances different people will have dry, normal or oily skin.
  • Humidity - in low humidity environments (cold dry air of winter , central heating, desert environments, air conditioning) evaporation of water from the skin increases leading to subsequent dryness.
  • Excessive cleanliness - soaps, detergents and cleansers strip oils from the skin so it dries.
  • Dry skin is associated with several disease processes either affecting the skin alone or as part of a generalised pathology.

Intrinsic skin diseases

  • Eczema/dermatitis - atopic eczema usually develops in childhood although may appear for the first time later in life. Varicose eczema is associated with venous hypertension in the lower legs, but can precipitate a generalised eczema. Contact eczema can occur at any age and can complicate other forms of eczema.
  • Psoriasis - dry adherent flaky plaques are characteristic of psoriasis. Scalp and nail abnormalities often coexist.
  • Ichthyosis vulgaris - this is an inherited form of generalised dry skin characterised by generalised thickened and fissured skin.
  • Fungal infections - on the soles and palms dry flaky skin can be caused by fungal infection.
  • Lichen simplex - this condition resembles discoid eczema but is basically caused by persistent scratching of dry skin.

Other underlying medical conditions

  • Hypothyroidism.
  • Chronic renal failure.
  • Diabetes especially with neuropathy.
  • AIDS.
  • Nutritional deficiencies (eg, vitamin B and C deficiency).
  • Malignant diseases - myeloma, lymphomas.
  • Drug reactions - lithium, isotretinoin, etretinate, diuretics.

Signs and symptoms of dry skin

  • Dull appearance.
  • Flaky surface.
  • Cracks and fissures.
  • Signs of inflammation.
  • Feels rough and uneven.
  • Sensory changes - tightness, itching.
  • Roughened and thickened appearance (lichenification).
  • Excoriation and infection from scratching.
  • Shiny finger nails.

Treatment of dry skin
Treatment of dry skin involves advice on environmental change, and the use of emollients in various forms.
How emollients (synonymous with moisturisers) work used not to be well understood by many practitioners. Emollients provide a lipid film on the epidermis, reducing water loss and drying, and take part in the active processes that keep water content in the stratum corneum at a steady state. They reduce irritation/itching and restore barrier function, preventing the penetration of irritants and allergens which may cause atopic eczema.
Emollients have always been regarded as the main treatment for dry skin, although there is a scarcity of good evidence-based research for this.(2) Common practice and apparent clinical effectiveness mean that we continue to use them. Recent work has shown that bath emollients are of questionable benefit in patients with atopic eczema.(3) Sometimes additives to the emollients improve their function. Emulsifying agents and surfactants increase stability and enable less oil to be used in a product. Humectants such as urea, propylene glycol and glycerol are added which attract more water into the stratum corneum. Antibacterial agents are also often added.(4) Some patients develop a sensitivity reaction to these additives leading to contact dermatitis.(5,6)
Many different types of emollient are available and effectiveness depends to a large extent on the ratio of oil to water.(7)

  • Ointments contain mostly oil, have a heavy greasy texture and are the most effective emollients. These should be used on dry skin as the treatment of choice.
  • Creams contain more water are tolerated better on the face and act as good soap substitutes. They are useful for infected skin with exudate.
  • Lotions are more water based and are useful for oozing areas and hair-bearing areas
  • Sprays are mainly water and have very little long-term effect, but are cooling and soothing.
  • Mild/moderate dry skin can be dramatically improved by some simple changes to daily routines.
  • Clean skin regularly to remove debris, dead skin cells and old topical treatment.
  • Bath in lukewarm water rather than hot, shower less frequently - shower dry skin more rapidly.
  • Avoid soap, shower gel and bubble baths, use water alone plus a soap substitute when needed.
  • Dry the skin by gentle patting rather than rubbing.
  • Use emollients directly after bathing to seal in water when the skin is slightly damp.
  • Use moisturisers several times a day.
  • Use the greasiest emollient tolerated.


How to apply emollients

  • Directly to the skin.
  • Thin, quickly and frequently.
  • In a downward motion in the direction of hair growth.
  • Without vigorous rubbing (may plug hair follicles and cause folliculitis).
  • Always after a bath.
  • Even after the condition settles to prevent recurrence.
  • By dabbing on then stroking.

How much emollient should be applied?
Whereas the application of topical steroids is measured by fingertip units directly from the tube, emollients come in large tubs and pump dispensers, so quantities can be measured in pump actions (different brands dispense different amounts) or by using a handy measure such as a spoon. Depending on the dryness of the skin the regime of emollient application can be light, moderate or high dose and the amount of emollient required for each regime can be quantified as teaspoon/dessertspoon/tablespoon measures, or by the number of pump actions required to provide an equivalent amount of emollient. For example one teaspoonful or two pumps (1 g per pump action) will lightly moisturise an arm but a tablespoonful (10 pumps) will be needed for a heavy regime. Although it only takes five minutes to apply the cream/ointment it may take up to 30 minutes for soaking in. The patient can put on some loose clothing meanwhile.

Should topical steroids/immune modulators be applied before or after emollients?
There is conflicting advice regarding this common problem. Theoretically applying the emollient before the steroid will improve penetration by the steroid, but if the steroid is applied too soon after the emollient the steroid will be diluted. The British Association for Dermatology guidelines for atopic eczema advise that at least 30 minutes should elapse between emollient and steroid application. Since most topical steroids only need to be applied once daily the emollient regime can be adjusted around this. NICE guidelines for tacrolimus (a steroid-sparing anti-inflammatory topical treatment for eczema and psoriasis) state that emollients should not be applied for two hours before or after tacrolimus.(8)

The economics of emollients
In general patients should use the cheapest emollient that is effective, cosmetically acceptable and which they are prepared to use regularly. When possible cheaper generics should be offered, and patients should be made aware that lower cost products may be available over-the-counter (OTC). Costs can vary enormously, eg, Oilatum cream is many times more expensive than cetomacrogel cream BP. However, the most important factor is patient acceptability and continued use.

So what do I do when I see a patient with dry skin?
Dry skin can usually be diagnosed on the basis of the signs and symptoms noted during a history taking and physical examination. Ask about existing medical conditions, family history, occupation, prescribed and OTC drugs, and daily skin care. If you suspect contact sensitivity make sure you know which creams and dressing have been used already.
Blood tests may be needed to distinguish simple dry skin from conditions for which dry skin is a symptom. Examine all the skin, not just the part the patient shows you, and look at nails and hair, which may give you a clue as to other skin conditions. Take scrapings for mycology if you suspect fungal infection. Wood's light, which uses UV wavelengths, may show some fungal infections, but the most common are not visible (eg, tinea tonsurans).
When you have made an assessment of the patient's needs the next step is to decide the most suitable emollient regime, and advise on changes in daily living that will be effective. Try to keep the regime simple and give the patient a written copy of what they are going to do, demonstrating how to apply emollients if necessary. Warn them that it will take several weeks for the treatment to work to its maximum benefit, and bring them back for regular progress reviews.
Common pitfalls with emollients:

  • Make sure you prescribe enough emollient. An adult will need at least 500 g a week, and a child 500 g every two weeks.
  • Patients commonly stop using their emollients when the skin is better - they should continue, and this will prevent flares of eczema.
  • Bath additives can be slippery and dangerous particularly for children and the elderly. In view of recent research this age group will be better advised to use emollients after the bath.(9)
  • Antiseptic additives can be irritant and cause contact dermatitis so avoid as far as possible.

What is the latest research
Research has identified the gene that causes dry scaly skin in common ichthyosis and predisposes to atopic eczema.(1) The gene produces filaggrin which is found in large quantities in corneocytes. About 10% of North Europeans carry a mutation that switches off the filaggrin gene to varying degrees causing ichthyosis vulgaris. In the UK about five million people make 50% of normal amounts of filaggrin, leading to a milder form of the disease. One in 500 have both copies of the gene out and have severe dry skin problems. Other studies have shown that people with filaggrin abnormalities are also more likely to develop eczema and asthma.
Patients with atopic eczema have also been found to have altered amounts of the protein aquaporin 3 which is thought to be important in water transport. This may explain why people with eczema develop dry skin so severely and rapidly.


  1. Nomura T, Sandilands A, Aklyama M, et al. Unique mutations in the filaggrin gene in Japanese patients with ichthyosis vulgaris and atopic dermatitis. J Allergy Clin Immunol 2007;119:434-40.
  2. Rees M. Managing atopic eczema. Primary Health Care 2002;12(8):27-37.
  3. Bath emollients for atopic eczema: why use them? Drug Ther Bull 2007;45(10):73-5.
  4. Fan W, Kinnunen T, Nilinimake A. Skin reactions to glycols used in dermatological and cosmetic vehicles. Am J Contact Dermatitis 1991;2:181-3.
  5. Cork MJ. The role of Staphylococcus aureus in atopic eczema: treatment strategies. J Eur Acad Dermatol Venereol 1996;7 Suppl 1:S31-3.
  6. Flohr C, Williams H. Evidence based management of atopic eczema. Arch Dis Childhood Educ Practice 2004;89(2):35-9.
  7. Clark C. How to choose a suitable emollient. Pharmaceutical J 2004;273:351-3.
  8. National Institute for Health and Clinical Excellence. Atopic dermatitis (eczema): pimecrolimus and tacrolimus. Technology Appraisal Guidance 82. London: NICE; 2004.
  9. Antiseptic/emollient combinations. Drug Ther Bull 1998;36(11):84-6.