Diagnosing Acne types
In the previous two articles, (part one and part two) we discussed the different forms of acne, and their respective causes. In this final installment, we will review how to diagnose whether the skin condition you are looking at is in fact acne, and if it is, what type.
When diagnosing acne, it is very important to grade the degree of severity just as you would for Pigmentation disorders, impaired acid mantle and Rosacea.
The first questions to ask of your self when looking at a clients skin are:
Is this an active acne? & What do I see the most of?
- Closed comedones
- Open comedones
Majority rules, and it is what you see the most of that will dictate the grade of acne you are analysing. Is what you are looking at really acne? Sometimes it is not.
In many of my writings and seminars on the subject of acne, you will recall that acne has a place in each of the main diagnostic characteristics of Texture, Colour and Secretion.
This makes the diagnosis more difficult to read and one has to ask the question what comes first: One thing you will notice about the higher grades of acne is the inflammatory response.
What you often don’t think about is the excess keratinisation that blocks the pilosebaceous duct, or the impaired acid mantle that is a result of failing/sluggish skin lipid secretions and constant stripping of the skin surface.
The consultation process will reveal any cosmetic and medical history; so look carefully at the skin care and makeup presently used by the client.
Begin with the basic majority skin type, (oily, sensitive or lipid dry) then break the skin down into diagnostic areas 1-6 as in the example consultation diagram at left.
Be sure to systematically work your way through each area.
In this next section, I have categorised acne according to the type and severity of the lesions:
Grade one – Predominantly closed comedones on the chin, forehead and nose wings, but no inflammatory lesions. (pustules) The T zone may be a little oily, (what I call active) but no true oily areas on the cheeks, neck or back. The majority of skin is clear of blemishes.
Grade two – Mainly open and some closed comedones and papules, with some pustules. Comedones and pustules still located only in the oilier areas of the face, such as the chin and forehead. The majority of skin is still clear of blemishes, but has an inflamed look and scars easily. (Easily aggravated by comedogenic cosmetics)
Grade three – Papules and pustules present throughout the T zone and cheeks, withopen comedones (excess keratinisation) with a heavier texture to the skin overall.
Not necessarily oily, but may have a sluggish more viscous oil flow (oxygenation loss). Most often found in late teens, however could be a problem into the twenties. Scarring may be likely.
Grade four – Hormonal (DHT) Mediated Acne
This female adult variety of hormonal acne is often found around the lower face, particularly along the chin, jaw-line and neck. The basic majority is more likely to be lipid dry or sensitive (permanent diffused redness) but not oily.
Macules (Flattened crusted lesion) are found to be predominant with the acne that has been stimulated by high androgen climate contraceptives or those with androgen sensitivity. Some lesions may be of a papule-nodular type and be very tender.
What is probably the biggest indicator is that there will be no open or closed comedones as is normally found with acne vulgaris.
The lack of comedones will help you establish cause to be hormonal mediated acne.
Grade five – Few comedones, some papules, and many pustules, nodules, cysts and abscesses. This is a severe but not very common form of acne known as acne conglobata (means severe).
Cheeks are most often affected as well as neck, chest and back. Scarring exists and is generally severe.
What you may have noted is that as the grading of acne becomes higher, there are fewer comedones to be found.
There will be a combination of visual cues and consulting evidence that will narrow down the type of acne you are diagnosing. By working through the cues in each diagnostic category, (Texture, Colour, Secretions) you can easily confirm what you are seeing. Because the colour aspect is the first thing you will notice, we will start with this.
What to look for in the diagnostic characteristic of COLOUR
- Visual erythema around cheeks, centre of the face or lesions
- Slow healing lesions with underlying redness
- Pigmentation or loss of pigmentation around scarring
- Will be easily aggressed, and at times feels hot, itchy and dry
- Uses foaming cleansing agents or wrong cleanser for basic majority skin type causing redness, stinging and tightness after cleansing
What to look for in the diagnostic characteristic of TEXTURE
- Scaly-crusted macules
- Papules, pustules macules and cysts, the majority of which will determine the grade of acne
- Build up of dead skin cells (excess keratinisation)
- Micro, open, closed comedones
- Family history of Keratosis Pilaris
- No comedones (or minimal) with hormonal mediated acne
- Loss of structural integrity and skin density, scars, marks & tears easily
- Small pillows of glycation, (Check if diet consists of high GI index foods)
What ask about/determine regarding SECRETIONS
- May have a medical/family history of acne or androgen sensitivity, superfluous hair
- Could be a mature skin that was once oily
- Irregular menstruation
- Taking or taken medication like Roaccutane that has diuretic side effects, or antibiotics that alter the surface pH and alter acid mantle formation and micro flora balance
- Looks shiny and oily, but feels taut. Check for a fat free diet (EFAD)
- Sluggish/viscous oil flow
- May have a basic majority skin type of oily
- Works/lives in high humidity or artificial atmospheres
- Impaired lymphatic system
- Fat Free diet or poor nutrition may result in Essential Fatty Acid Deficiency
- Poor fluid intake or high tea/coffee/alcohol intake
Review: Causes of acne or hormonal mediated acne
The causes of acne or hormonal mediated acne are enzymes, hormones, and the immune system. These cause changes in a number of cells and systems with the following effects:
Primary effects will be TEXTURE related
- Excess keratinisation & poor desquamation due to poor dissolution of desmosomes in granular layer. This is generally caused by impaired enzyme activity, which can be linked back to a lack of free water in epidermis
- Keratinocyte proliferation aggravating closed comedones caused by Ultra Violet Radiation
- Oxygenation loss will cause slow cell turnover & desquamation of keratinocyte. Will also affect dermal cells fibroblasts & proteins collagen & elastin
- Sluggish, viscous sebaceous secretions combined with EFAD will cause an impaired acid mantle resulting in the skin surface feeling dry, taut and having a build up of dead skin cells
- Proteosomal dermal enzymes will also be affected, resulting in the slowing down of wound healing/repair and replacement of collagen & elastin
Secondary effects will be COLOUR related
- Loss of structural integrity/density of collagen fibrils will also reduce wound healing, skin will tear, mark or scar easily as a result
- Constant removal or loss of acid mantle results in loss of eco system for micro flora. This will be visible as erythema with inflammatory response, and may result in secondary infection
- Slow wound healing; scarring and pigmented lesions are often a result if this response is left unattended
- Weakened capillary walls caused by constant inflammatory response will be apparent as visible erythema, diffused redness or permanently dilated microcirculation. (Angiogenesis)
- Impaired vascular/lymphatic systems will also contribute to poor immune system responses
Resulting characteristics will be SECRETION orientated
- Peroxidation of lipids in cell membranes can cause damage by disrupting fluidity and permeability. Lipid peroxidation can also adversely affect the function of membrane bound proteins such as enzymes and receptors
- Essential fatty acid deficiency (EFAD) increases Trans Epidermal Water Loss (TEWL) will contribute to sticky corneocytes/corneodesmosomes in the Stratum corneum, increasing excess keratinisation and more quickly blocking the pilosebaceous duct
- EFAD will inhibit cellular nourishment and oxygenation/waste exchange. (Cellular/circulatory)
- Essential Fatty Acid Deficiency (EFAD) will result in a compromised cell membrane of dendritic cell melanocyte & langerhan cell affecting immune response and pigmentation
- Sluggish, viscous, little or no sebaceous secretions combined with Essential Fatty Acid Deficiency (EFAD) reduces the formation of skin barrier defence systems like the formation of bilayers & acid mantle
- These will all result in impairment of all systems responsible for the creation of the acid mantle and micro flora habitat and supporting immune system cells like the langerhans cell
- Reduction in the acid mantle and bilayer will increase trans epidermal water flow/loss reducing the amount of free water needed in the epidermis for the enzyme activity to dissolve desmosomes and complete the formation of bilayers. (Oil sits on top of water)
- Impaired lymphatics/toxin build-up, or low dermal reserve will impair proteosomal enzymes required for dermal protein health. Reduced dermal reserve poor or low fluid intake will also affect the wound healing/inflammatory processes
- Impaired lymphatic system could prevent the absorption of fats and fat-soluble vitamins like Vit A and E from the digestive system and the subsequent transport of these substances
For more detailed information refer the book “Advanced Skin Analysis”
Learn more about this topic with an online course from Pastiche Training