Skip to main content

Pre- and Postoperative Skin Care

By June 30, 2021November 1st, 2021Peer Reviewed Articles



No matter what type of operation you do, cosmetic surgery alone cannot create a convincingly youthful impression. The patient’s loose skin may be pulled up but often they appear merely as neat, tight-skinned mature people. In the worst case, many surgeons have had the experience of doing a facelift on a severely photoaged patient and it seems that the only distin- guishing changes in comparing the before and after pictures is the date! The skin does not simply have to be smooth; it should be fresh, glowing and show few or no signs of accumulated photodamage. (Fig. 62.1) By understanding the basics of the science of skin care, you can guide your patients to use products that can do this for you and complement your work.

Many surgeons make the mistake of believing that

they can achieve youthful skin by using drastic mea- sures such as laser resurfacing, heavy peels or other techniques that destroy the epidermis. The epidermis is far too important and complex to be destroyed or

tortured into becoming smooth. The epidermis is an extremely thin layer, only 0.2 mm thick, which is thinner              than the average sheet of paper. This fine membrane, made up mainly of differentiated kerati- nocytes, is our only protection from the harsh world outside. It is extremely intricate and is not merely a series of layers of dead or dying skin cells. The destiny of differentiated keratinocytes is to become the com- plex stratum corneum that is our real protection. This layer is even thinner and is only 0.01–0.02 mm thick so we should be very careful about the use of physical or chemical abrasives. The convoluted lipid bilayers that fill the space between the corneocytes create the protective properties of the stratum corneum. Healthy keratinocytes are ultimately responsible for a beauti- ful, resilient skin. Our first aim must be to rehabili- tate photoaged, inefficient keratinocytes to create a normal healthy epidermis that then sets up the possi- bility of improving the dermis (Fig. 62.2).

This chapter will explain how to give your patients

normal healthy smoother skin with a thick epidermis and a dermis that is rich in collagen, elastin and natural moisturising factors. One must use well-formu- lated, honest cosmeceuticals [1] (a term coined by Kligman) based on essential micronutrients to gently nurture and rehabilitate photoaged skin. However, we have to realise that each person’s requirements will be a bit different, and that is why we first have to inspect the facial skin very carefully.


Skin Analysis

At your first consultation with the patient you should carefully notice:

  1. The overall colour of the This will give you a good idea of the care against photoageing that the patient is taking. All of these signs will respond to competent skin care combined with intensive treatments to enhance penetration through the skin. At times it may be necessary to employ serial light peels.
    1. Are they excessively tanned or too pale?
    2. Are there pigmentary blemishes? Check if the patient has been on hydroquinone, which tends to cause secondary, aggressive melanosis that is very difficult to treat. Advise patients not to use hydroquinone.
    3. Check the texture of the cheek skin to the side of the nose to see if the “pores” are
    4. Is the submental area hypopigmented?
    5. Does the patient have poikilodermia of Cervat?
    6. Is there telangiectasia on the cheeks?
    7. Is there rosacea?
  1. The general elasticity of the face
    1. Is the skin thick and firm or is it thin and does it stretch easily? If it is thin and has poor recoil, then intensive skin care will be required and also collagen induction therapy (CIT) [2].
    2. Are there wrinkles around the eyes? Are they there permanently even when the face is in re- pose? A blepharoplasty will not suffice to cor- rect these. (Fig. 6).
      • Are they light or deep wrinkles? Light wrin- kles may respond to skin care alone, or may need iontophoresis and sonophoresis treat- ments. Serial light peels, using low-dose tri- chloracetic acid (TCA) in the region of 5– 5%, are also very useful. Deep wrinkles around the eyes will need intensive CIT [3].
      • Are there radiating wrinkles through the eyebrows? These are usually only found with significant depletion of collagen, and there is reduced subreticular fat even though the skin may feel This will not improve signifi- cantly with skin care alone. CIT is definitely required. Hormonal therapy may also be re- quired.
    3. Are there “crisscross” wrinkles on the cheeks (which indicate more severe photodamage)? This will require intensive skin care treatments and can be alleviated with iontophoresis and so- nophoresis.
    4. Are there wrinkles on the chin? This is found with severe sun damage and usually also indi- cates some degree of hormonal insufficiency. This will respond slowly to skin care, intensive treatments and
    5. Are there signs of elastosis in the lower neck and décolleté? It is good to get an impression of the concentration of the elastotic nodules prior to treatment and surgery. Surgery will not improve Intensive skin care, however, will make a big difference. Are there fine vertical skin creases especially below the laryngeal cartilage? In severe cases the combination of skin care with iontophoresis and sonophoresis can at times yield stunning results (Fig. 62.3).
    6. These changes are not of short duration but with maintenance treatments, the skin can be kept smoother for many years after the initial course of
    7. The presence of lines on the upper lip will give you an idea of the hormonal nourishment of the skin. Check the lip vermilion to see if it is smooth or creased by radiating lines as well as transverse lines, which indicate severe tissue loss which can- not be corrected by simple skin care. Besides tissue augmentation, the best result will probably require percutaneous CIT of the lip skin.Look for actinic keratoses, skin cancers.



We know that photoageing is a manifestation of the injury caused by sunlight. High-energy light on the UV and violet side of the spectrum does not penetrate as deeply as lower-energy light on the red side, but most of the damage is done by light ranging from blue through to UV. One can, broadly speaking, say that light on the red side of the spectrum is more benefi- cial and healing, whereas light on the violet side is more destructive. Melanogenesis is stimulated by damage to DNA of skin cells, so in fact a tan is a sign of cellular scarring. Studies have shown that green light induces melanogenesis [4], which means that even green light must be causing some damage to DNA.

62 Pre- and Postoperative Skin Care       

Light damages cells on account of a chemical inter- action either at the molecular or at the subatomic level. Each photon has a specified energy depending on its frequency. Molecular damage occurs when cer- tain molecules in the skin, called chromophores, ab- sorb light energy of very precise frequencies. The in- crease of energy in the molecule may then cause fundamental changes to its chemical structure or may even destroy the molecule. Important examples of chromophores in skin are:

  1. DNA, which absorbs UV-B and gets
  2. Vitamin A, which absorbs UV-A, and becomes in- activated.
  3. Vitamin C, which absorbs blue light and is de- stroyed.
  4. Melanin is an amazing molecule because it can ab- sorb the energy of the whole light spectrum with- out being

Subatomic damage occurs when photons of sufficient energy displace an electron from the outer shell of an atom to create a free radical: UV-A is the main culprit inducing free radicals in the skin. These free radicals set up chain reactions in their search for electron sta- bility and consequently may damage vital cellular structures like DNA, cellular membranes and impor- tant intracellular molecules etc.

Bearing this all in mind, one can start to ratio- nalise the prevention and treatment of photoageing:

  1. We must never forget the dangers of uncontrolled free-radical activity so we should always ensure that our skin is rich in a wide variety of lipid- and water-soluble They have to be includ- ed in the skin care regimen and should be used both day and night.
  2. Obviously we have to focus on damaged chromo- phores and understand that all photolabile vita- mins have to be included. Vitamin A is certainly the dominant chromophore that we have to worry about, but we have to remember vitamins C, E, B1, B2, B6, and B12, folic acid, vitamin K and, paradox- ically, vitamin Everyone knows that UV-B is es- sential in the formation of vitamin D (which takes about 20 min), but it is not generally known that vitamin D is unstable when exposed to UV-A light! That is one good reason why people should not stay longer than 20 min in the sun if they intend to make good doses of vitamin D.

have known that vitamin A, mainly available as reti- nyl palmitate, is vital for healthy skin. Wise and Sulz- berger [5] realised that retinyl palmitate was extreme- ly unstable in light and they suggested in 1938 that there is a localised hypovitaminosis A in wrinkled skin. Almost everyone walks around with a chronic, localised hypovitaminosis A in our exposed skin – mainly in the face and neck. We now know that UV-A rays are responsible for photodecomposition of reti- nyl palmitate, which is the major form of vitamin A in the skin [6]. Retinoic acid (tretinoin) is not the only active form of vitamin A: it is just the acid form of vitamin A and is the end product of the metabolism of retinyl palmitate to retinol and retinyl aldehyde and finally retinoic acid.

UV-A rays are ubiquitous, plentiful and penetrate through clouds and windowpanes. Each day we leave our homes and expose ourselves to varying degrees to light, and that affects our cutaneous vitamin A. Even on an overcast day, UV-A destroys some vitamin A in the exposed areas of our skin. You may think that vi- tamin A can easily be replaced by the blood stream, but this is not true and in fact one slowly builds up a deficit of vitamin A during the day and this is only restored quite slowly during the night. Tanning may lower the epidermal vitamin A (as retinyl palmitate) by 70–90% [7]. Once the skin retinoids are depleted after heavy exposure to sunlight, it takes several days before diet alone can restore the normal cutaneous retinoid levels. With repeated exposure to light almost everyone develops this localised chronic deficiency that permits significant degradation of the skin.

Cluver [8]  recognised that vitamin A plays an  essential role in counteracting sun damage. He showed that every time we go out into sunlight, the photosen- sitive vitamin A molecule is denatured not merely in the skin, but also in the blood [9]. Women have an added disadvantage because blood levels of vitamin A drop when they menstruate [10, 11]. That means that during menstruation their skin is more vulnerable to photodamage [12]. Deficiency of vitamin A results in an inefficient epidermis with a thick horny layer, de- layed healing, keratoses, irregular pigmentation, mel- anosis, elastosis, disordered collagen production, im- paired hydration and lax inelastic yellowish skin, i.e. all the signs of photoageing! With time, investigations have demonstrated that vitamin A is not merely good for ageing skin [13, but is actually essential to prevent problems [14, 15]. We also know from experience that topical vitamin A can restore the normal levels within


Vitamin A

Vitamin A deserves special attention because it is not well understood by clinicians, who generally regard only retinoic acid as the active form. For decades we hours, and with continuous use for many months re- verses almost all the signs of photoageing [16, 17].

We do not know precisely how retinoids work but we have some clues:

– In the tissues vitamin A of all forms passes into the cell wall through retinoid binding sites and all of it is metabolised from retinyl palmitate into retinoic acid. Retinoic acid is the essential active metabolite that controls mitochondrial and nuclear DNA. By supplying retinyl palmitate, one automatically also increases the amount of retinoic acid.

– All-trans-retinoic acid and only two other isomers are the key signalling hormones for normal growth and differentiation that regulates between 350 and 1,000 genes and modulates photoageing [18]. It is essential for normal function of all the important cells of the skin [19].

Keratinocytes [20], melanocytes [21], Langerhans cells [22–25] and fibroblasts [26–30] can only func- tion normally with adequate amounts of cellular vita- min A. Vitamin A is a powerful inhibitor of the re- lease of matrix proteinases [31, 32] that are induced by UV irradiation and would destroy collagen and elas- tin. One need not use pharmacological doses of reti- noic acid to treat photoageing because retinoic acid is rather aggressive in pharmacological doses. On the other hand, when one uses retinyl aldehyde, retinol or retinyl palmitate, only physiological doses of retinoic acid are produced and presented to the nucleus, while the excess is stored as retinyl palmitate. More than 90% of cellular vitamin A is retinyl palmitate and as- sociated esters, and it seems that the larger the store of retinyl palmitate, the healthier the skin, which be- comes less prone to skin cancers [33]. Our under- standing of retinoid physiology indicates that we should all maintain high levels of retinyl palmitate in our skin to keep it as young and fresh as possible. Vi- tamin A also prevents tissue atrophy [34] and the de- struction of collagen generally found with intrinsic ageing.

Vitamin A reduces pigmentation by about 60% or more in some cases. Even fairly deep dermal pigmen- tation may be reduced. The best results are seen after many months – even 18 months.

One constantly hears a rumour that retinoids make the skin thinner. In fact the skin is always thicker but is smoother because the horny layer becomes more compact. This has alarmed some dermatologists be- cause the horny layer is the most important protec- tion against UV irradiation. The fact that it is more compact, may well act as a greater physical barrier to UV light! Reassure your patients that these negative rumours about vitamin A are untrue.

working optimally and will repair any wounds as rap- idly as possible. We have to focus our attention on very few special cells:

  1. Stem cell keratinocytes, and differentiated kerati- nocytes
  2. Melanocytes
  3. Langerhans cells
  4. Differentiated fibroblasts and their stem cells

Because their genetic code is most likely damaged to some degree, we have to nourish each of these cells back into optimal health and normalise the DNA as much as we can.

Basically we should be able to treat most of our pa- tients by using combinations of the following:

  1. Adequate, but not excessive UV light protection ev- ery day – remember your patients must make as much vitamin D as they safely can to avoid poten- tial problems like breast, bowel and prostatic can- cer.
  2. Replenishment of the essential skin vitamins that are unstable when exposed to sunlight, particular- ly (but not only) vitamins A, B12, C and
  3. Replacement of carotenoids and other free-radical scavengers.
  4. Active peptides, e.g. Matrixyl, Dermaxyl and cop- per peptides, to promote collagen and elastin pro- duction.
  5. Use of the A-hydroxy acids (AHAs) periodically only when necessary.
  1. A light repetitive TCA/AHA peeling system when indicated.

Cosmetic surgeons can use cosmetics as though they are pharmaceutics by examining the declaration of ingredients and then selecting products that have suitable active ingredients.


Sun Protection

Make sure that the sunscreen contains dedicated UV- A and UV-B components. Methoxycinnamate, de- spite some adverse press in recent years, remains the best UV-B screen at this stage. Methoxydibenzoyl methane (Avobenzone, Parsol 1789), is a far superior UV-A screen compared with benzophenone (oxyben- zone) which is commonly used. Newer UV-A screen- ing agents (like Mexoryl SX or Tinosorb-M ) are photostable and give better and continuous UV-A



Principles for Treating Facial Skin Preoperatively

The reason for preoperative treatment of skin is to make sure that the skin is as elastic as possible before treatment and also to make sure that the skin cells are protection.

To facilitate vitamin D production, a low sun pro- tection factor (SPF) of 4–8 is all that is necessary in most parts of the world to prevent photoageing [35] under average “working-day” sun exposure. This will also minimise the potential long-term problems from exposure to sunscreens over many years. Of course, for outdoor activities, SPF 16–20 is required and the patient has to be told to reapply sunscreen every 2 h. We must remember that UV-A protection is much more important than UV-B protection and this is not related to the SPF rating. It is absolutely essential that the sun protection product also contain antioxidants to deal with UV rays that are not blocked from pene- trating into the skin.

62 Pre- and Postoperative Skin Care

Pycnogenol, coenzyme Q10, A-lipoic acid, Resve- ratrol and many other chemicals are important anti- oxidants and phytonutrients that increase the general spectrum of antioxidant protection.

We should boost the levels of these essential anti- oxidants prior to sun exposure to minimise the subsequent depletion.



Active Peptides



Vitamin C (L-Ascorbic Acid)

Ascorbic acid is extremely unstable and should not be used in cosmeceutics unless the ascorbic acid solution is made up by the patient. Magnesium (and sodium) ascorbyl phosphate is a water-soluble version of ascor- bic acid that is somewhat more stable but generally only lasts at its intended concentration for 6 months. Ascorbic acid cannot easily penetrate the skin, so es- ters of ascorbic acid have been created to penetrate better and also be more stable. At this time, the most effective form of vitamin C is ascorbyl tetraisopalmi- tate, which is more effective than ascorbyl palmitate or ascorbyl dipalmitate and can deliver large doses of ascorbic acid into the cell itself. Ascorbic acid upregu- lates the production of collagen and is an essential coenzyme for the inclusion of lysine and proline into collagen.


Vitamin E (DA-Tocopherol)

Vitamin E plays an essential role as an antioxidant in safeguarding cellular membranes and when it is ap- plied topically it augments photoprotection; however, this advantage only becomes clear a day or two after sun exposure. Patients using topical vitamin E get less sunburn and a lighter tan. Vitamin E is also light-sen- sitive and can be oxidised into an inactive form.


Other Antioxidants

B-Carotene is the plant form of vitamin A, but is a most powerful free-radical quencher. Estimates sug- gest that one molecule of B-carotene can cope with 1,000 free radicals.

Lutein is another carotenoid which has particular value because besides being an antioxidant, it is also a powerful absorber of blue light that can damage cells quite severely. There are many other carotenoids that can also protect the skin.

Panthenol is a coenzyme in fat and carbohydrate metabolism. It has other soothing effects on skin and is also a free-radical quencher.

Recent research has shown that active peptides such as palmitoyl pentapeptide (Matrixyl) and palmitoyl hexapeptide (Dermaxyl) have a special value in stim- ulating the production of collagen and elastin. They are both peptides made of a sequence of amino acids normally found in collagen and elastin, respectively, and their results have been favourably compared with those of retinol. Palmitoyl pentapeptide stimulates about 16 genes in skin cells, which is only a fraction of the number of genes that vitamin A favourably stimu- lates in the skin. For that reason one should not make the mistake of believing that these peptides can be an alternative to vitamin A. They should be used in con- junction with vitamin A.

Copper peptides facilitate healing of tissues and

may assist in remodelling of collagen. Probably the best indication for copper peptides is when the skin has been injured by peeling, laser or dermabrasion.

With current research, many more molecules will likely come into prominence on account of their stim- ulating effects on healing and collagen and elastin deposition.


A-Hydroxy Acids

AHAs have been the most misused and misunder- stood molecules in skin rejuvenation. Very largely they are simply exfoliants and should mainly be used as penetrant enhancers. In patients with thick rough skin, AHAs have a place to help refine the skin. Once the natural qualities of the horny layer have been re- stored, then the use of AHAs should fall away. Care should be taken because they do impair the natural protection from the sun and they should always be used in conjunction with vitamin A. Lactic acid is an exception because it has a particularly useful effect on restoring natural moisturising factors and is less irri- tating than glycolic acid.

Your patient should use a “cocktail” of vitamin A, vitamin C, other antioxidants and active ingredients such as palmitoyl pentapeptide every morning and evening for a minimum of 3 weeks prior to surgery. Remind them to use these products on the areas where incisions are planned. This will ensure that the skin will heal rapidly and the patient will make the finest and strongest scars. It will also start to help to increase the elasticity of the skin, which will ensure a longer- lasting result as well as younger-looking skin. The longer the patient is on the ideal cocktail, the better the skin will be. However, some patients need more intensive treatment.


Low-Frequency Sonophoresis

Low-frequency sonophoresis (about 20 kHz) was first described in 1996 and has become the most effective way to enhance penetration. Up to 4,000% better pen- etration may occur after only 3 minutes of treatment

Low-frequency sonophoresis should not be con-



Intensive Treatments

When home-care alone is not sufficient we can re- sort to iontophoresis and low-frequency sonophoresis to enhance penetration through skin. By getting higher concentrations of vitamin A, vitamin C and various other molecules, e.g. active peptides, one can reasonably expect significant rejuvenation and tight- ening of skin. Serial light peels can also make a sig- nificant difference.

fused with ultrasound (about 1.1 MHz), which does not have the same powerful properties. The advan- tage of low-frequency sonophoresis is that it can be used on nonpolar molecules as well. Cavitation devel- ops rapidly and is maintained for several hours after the treatment, so significant improvement of skin can be seen in a relatively short time. Treatments are best done once or twice a week for about 24–30 times and the best results seem to occur in combination with iontophoresis [39] (Figs. 62.3, 62.4)




Galvanic current is useful if the selected molecule like vitamin A or ascorbic acid can be ionised into positively and negatively charged ions. A positive electrical current repels positively charged ions into the skin and vice versa. This can cause about 400% better penetration than simple topical applications. Treatments should be done for a minimum of 20 min once or twice a week for 24–30 treatments [36, 37]. This is a very successful method for treating photo- ageing but has to be done by an experienced therapist/ nurse.

Microneedling of Skin

Not everyone can manage to have the specialised treatments of iontophoresis and sonophoresis, so mi- croneedling offers an important way for patients to enhance penetration. Minute holes are made through the stratum corneum only, so this is not a painful procedure. I have designed a special instrument to do this and patients are requested to use it daily before applying their skin care [3]. Significant improvement may be achieved in those patients who are diligent about using the tool every day for about 3–5 min. The results are not due to the microtrauma, but are due to enhanced penetration of vitamin A, vitamin C and other active agents (Fig. 62.5). The use of simple mois- turisers will not cause any tightening of skin.



Repetitive Light Peels

As mentioned before, deep peels (e.g. the classic phe- nol peel, 35% TCA) should be avoided because of the destruction of the epidermis. Medium-depth peels (e.g. 15% TCA, Jessner’s peel ) that do not destroy the basal layer of the epidermis are much safer, though one treatment will not give the smoothening that peo- ple demand from a peel, but the recovery might be almost as great as that for a deep peel. On the other hand, serial light peels done once a month in conjunc- tion with daily applications of vitamin A, vitamin C and  other  active  ingredients  will  give  results  at   6 months that match those of one heavy peel.

Low concentrations of TCA, as low as 2.5%, have been used with gratifying results. This form of peel is safe to use repeatedly on the upper eyelids (Fig. 62.6). The advantage of peeling in these types of cases is that one can smooth out the fine wrinkles of the upper- eyelid skin that can spoil even the best blepharoplasty. Sometimes the improvement is so great that it mimics an upper blepharoplasty as in the case shown.

Repetitive peeling allows the patient to continue with their daily lives with minimal  telltale  signs, and as the skin becomes refined, the need for continuing the peels disappears. Patients with thick rough skins should be treated to a peel at the be- ginning of their skin care programme so that the vitamin A can express its beneficial effects. One advantage of serial light peels in conjunction with vitamin A based cosmeceutics is that  the  patient  will get a better result than expected. Less invasive surgery may then give results that mimic those of bigger operations (Fig. 62.7). tive result. Intense pulsed light (IPL) may be extreme- ly effective in treating melanosis but preventing re- currence becomes important. Vitamin A based and antioxidant-based cosmeceutics should be used for a



Oral Supplements

Most antioxidants can be safely prescribed to patients before operations except for vitamin E, which may ex- aggerate bleeding and bruising. It is not recommend- ed to prescribe oral vitamin A in areas where patients do not get enough sun exposure on account of a risk of osteoporosis. Topical vitamin A cannot be equalled in its effects on skin.

Dimethylaminoethanol (DMAE) can be useful for treating lipofuscin marks on the face and the hands. A daily dose of 100 mg DMAE for 3 months often re- duces the yellowish brown pigmentation. At times when treatments for melanosis do not work, lipofus- cin may in fact be the real cause.


Preoperative Preparation for Peels, Dermabrasions, Laser, Intense Pulsed Light,

Radio-Frequency (Thermage) and Collagen-Induction Therapy (Skin Needling), etc.

minimum of 3 weeks prior to the procedure, though even better effects will be obtained if the patient has used this regime for 3 months prior to the treatment (Fig. 62.5) By combining these traumatic treatments with the chemical effects of vitamin A, vitamin C and antioxidants, one can expect:

  1. Healthier keratinocytes with faster healing of the epidermis
  2. A thicker epidermis eventually
  3. Better control of pigmentation and the prevention of postinflammatory hyperpigmentation (espe- cially in conjunction with antioxidants such as the “softer” magnesium – or sodium – ascorbyl phos- phate)
  4. More intense collagenosis from DNA stimulation
  5. Healthier collagen with topical vitamin C
  6. Thicker dermis with better support for blood ves- sels
  7. Healthier blood supply to facilitate healing and growth
  8. Greater elastin and collagen formation with added peptides such as palmitoyl pentapeptide and pal- mitoyl hexapeptide


All of these treatment aim to induce tightening of the skin and or lightening of the skin. They all work by controlled damage to either individual cells or all the cells of the epidermis or the dermis. Their benefits arise from the induction of the natural healing pro- cess with the release of various growth factors. The safest use of these various treatments is when the trauma or energy is the lowest to give the most effec-


Postoperative Skin Care

All patients should continue their normal cosmeceu- tic regime as soon after the procedure as they feel comfortable to do so. With peeling, IPL, radio-fre- quency, light nonablative laser and skin needling this is done immediately after the treatment. For ablative laser treatments, the cosmeceutics can be used even on the “raw” areas, though the dosage of topical vita- min A should be rather drastically reduced for the initial 10 days. A soothing vitamin A based gel not only helps to cool the skin but can also supply vitamin A at a suitable level.

Patients who have had a facelift etc., can apply cos- meceutic creams as soon as their bandages are re- moved. Cosmeceutics may be applied even onto the

The combination of cosmeceutics, including light peeling systems, has an important place in cosmetic surgery of the face because one has to remember that cosmetic surgery does not restore youth to the skin. By using cosmeceutics, we can more effectively mimic youthful skin. We also live in an era where more of our patients believe that “less is more” and we can give them good results by including an intelligent cos- meceutic agent for routine daily skin care.


facelift scars themselves. There is no danger of infection and the scars heal rapidly and eventually become much less visible than untreated scars (personal expe- rience). Another method that has been used is to treat the scars with a low-dose peeling agent, e.g. 2.5–5% TCA gel or cream for about 10 min at each visit after the operation. The TCA probably sterilises the wound and treats subclinical infection and hence reduces the inflammation. I have used this and generally scars heal faster and uninformed clinical observers have of- ten been surprised to see that wounds at 2 weeks post- operatively seem to be similar to conventional scars at 6–12 weeks (personal experience). I have used peeling directly on the scars within 2 days after a facelift for the past 10 years and I think that my scars are now the best I have made.

Weak acids are extremely effective at treating topical infections without destroying the surrounding normal tissue.

Many patients believe that they should be careful with using topical vitamin A soon after surgery



Cosmeceutic skin care is essential to complement fa- cial cosmetic surgery and achieve rejuvenation. A brief explanation of the action of the major cosmeceu- ticals precedes their method of use. Vitamin A, espe- cially in its ester form, gives all the benefits without the irritation of retinoic acid, and should be used on every patient both before and after surgery. Its role is both preventative against photoageing as well as re- generative. Antioxidants work hand in hand with vi- tamin A and also complement sun protection but act only in preventing photoageing to a degree. Iontopho- resis and sonophoresis enhance penetration of vita- min A and active peptides and can help surgeons achieve realistic rejuvenation. Serial light peels may also be useful, giving a fresher appearance to the skin.


because of the popular misconception that vitamin A makes the skin thinner. Retinoic acid I believe  is  not the best form of vitamin A soon after surgery or surface treatments because it is rather harsh. Clini- cians who are used to the dry, pink, uncomfortable skin may see the reaction as a good sign, but to the patient this is extremely inconvenient and, in fact, unpleasant. It becomes a good reason to stop using it or to use it irregularly. When one uses the storage forms of vitamin A, one gets compliant patients with all the benefits of vitamin A etc. but without the discomfort, sun sensitivity and often disturbing appearance. Even postoperatively, persuade your pa- tients to increase the levels of vitamin A etc. until they are using up to 50,000 IU of vitamin A twice daily if possible (it might take many months and episodic mi- nor retinoid reactions!). This will ensure the healthi- est, most radiant skin to complement your surgery. Intensive treatments like iontophoresis, sonophoresis and physically enhanced penetration will also ensure that your results are maintained in the best  way  (Fig. 62.3c). Encourage all your patients to continue using cosmeceutics postoperatively and you will be rewarded with happier patients who have had real rejuvenation.


  1. Kligman AM, Dagadkina D, Lavker Effects of topical tretinoin on non-sun-exposed protected skin of the elderly. J Am Acad Dermatol 1993, 29(1):25–33
  2. Fernandes D. Percutaneous Collagen induction: an alterna- tive to laser resurfacing. Aesthetic Surg J 2002, 22(3):307– 309
  3. Fernandes D. Minimally invasive collagen induction thera- py. Oral Maxillofac Surg Clin N Am 2004, 162(17):1
  4. Parrish JA, Jaenicke KF, Anderson Erythema and me- lanogenesis action spectra of normal human skin. Photo- chem Photobiol 1982, 36(2):187–91
  5. Wise F, Sulzberger Yearbook of Dermatology (1938) 282
  6. Berne B, Nilsson, M, Vahlquist A. UV irradiation and cuta- neous vitamin A: an experimental study in rabbit and hu- man J Invest Dermatol 1984, 83:401–404
  7. Tang G, Webb AR, Russel RM, Holick HF. Epidermis and serum protect retinol but not retinyl esters from sunlight- induced photo-degradation. Photodermatol  Photoimmu- nol Photomed 1994, 10:1–7
  8. Cluver EH. Sun-trauma prevention. S Afr Med J 1964, 38:801–803
  9. Cluver EH, Politzer WM. Sunburn and vitamin A deficien- cy. S Afr J Sci 1965, 61:306–309
  10. Cluver EH, Politzer WM. The pathology of sun S Afr Med J 1965,39(41):1051–1053
  11. Ahmed F, Khan MR, Karim R, et Serum retinol and bio- chemical measures of iron status in adolescent schoolgirls in urban Bangladesh. Eur J Clin Nutr 1996, 50(6):346–351
  12. Lithgow DM, Politzer WM. Vitamin A in the treatment of menorrhagia. S Afr Med J 1977, 51(7):191 – 193
  13. Varani J; Warner RL, Gharaee-Kermani M, et Vitamin A antagonizes decreased cell growth and elevated colla- gen-degrading matrix metalloproteinases and stimulates collagen accumulation  in  naturally  aged  human  skin.   J Invest Dermatol 2000, 114(3):480–486
  14. Saurat Skin, sun, and vitamin A: from aging to cancer. J Dermatol 2001, 28(11):595–598
  15. Kligman Current status of topical tretinoin in the treatment of photoaged skin. Drugs Ageing 1992, 2(1) 7–13
  16. Kligman AM, Grove GL, Hirose R, et Topical tretinoin for photoaged skin. J. Am Acad Dermatol 1986, 15:836– 859
  17. Bhawan J. Short- and long-term histologic effects of topi- cal tretinoin on photodamaged Int J Dermatol 1998 37:(4)286–292
  18. Fuchs J, Huflejt ME, Rothfuss LM, et Acute effects of near ultraviolet and visible light on the cutaneous anti- oxidant defence system. Photochem Photobiol 1989, 50(6): 739–744
  19. Reichrath J, Münssinger T, Kerber A, et In situ detec- tion of retinoid-X receptor expression in normal and pso- riatic human skin. Br J Dermatol 1995, 133(2):168–175
  20. Diaz BV, Lenoir MC, Ladoux A, et Regulation of vascu- lar endothelial growth factor expression in human kerati- nocytes by retinoids. J Biol Chem 2000, 275(1):642–650
  21. Rosdahl I, Andersson E, Kágedal B, Törmä H. Vitamin A metabolism and mRNA expression of retinoid-binding protein and receptor genes in human epidermal melano- cytes and melanoma Melanoma Res 1997, 7(4):267– 274
  22. Murphy GF, Katz S, Kligman Topical tretinoin re- plenishes CD1a-positive epidermal Langerhans cells in chronically photodamaged human skin. J Cutan Pathol 1998, 25(1):30–34
  23. Meunier L, Voorhees JJ, Cooper KD. In vivo retinoic acid modulates expression of the class II major histocompat- ibility complex and function of antigen-presenting mac- rophages and keratinocytes in ultraviolet-exposed human J Invest Dermatol 1996, 106(5):1042–1046
  24. Meunier L, Bohjanen K, Voorhees JJ, Cooper Retinoic acid upregulates human Langerhans cell antigen presenta- tion and surface expression of HLA-DR and CD11c, a beta 2 integrin critically involved in T-cell activation. J Invest Dermatol 1994, 103(6):775–779
  25. Dunlop KJ, Halliday GM, Barnetson All-trans retinoic acid induces functional maturation of epidermal Langer- hans cells and protects their accessory function from ul- traviolet radiation. Exp Dermatol 1994, 3(5):204–211
  26. Francz PI, Conrad J, Biesalski HK. Modulation of UVA- induced lipid peroxidation and Suppression of UVB-in- duced ornithine decarboxylase response by all-trans-ret- inoic acid in human skin fibroblasts in vitro Biol Chem 1998, 379(10):1263–1269
  27. Varani J, Fisher GJ, Kang S, Voorhees Molecular mech- anisms of intrinsic skin aging and retinoid-induced repair and reversal. J Investig Dermatol Symp Proc 1998, 3(1):57– 60
  28. Lee X, Si SP, Tsou HC, Peacocke M. Cellular aging and transformation suppression: a role for retinoic acid recep- tor beta Exp Cell Res 1995, 218(1):296–304
  29. Edward Effects of retinoids on glycosaminoglycan syn- thesis by human skin fibroblasts grown as monolayers and within contracted collagen lattices. Br J Dermatol 1995, 133(2):223–230
  30. Shigematsu T, Tajima S. Modulation of collagen synthesis and cell proliferation by retinoids in human skin fibro- blasts. J Dermatol Sci 1995, 9(2):142–145
  31. Bizot-Foulon V, Bouchard B, Hornebeck W, et Uncoor- dinate expressions of type I and III collagens, collagenase and tissue inhibitor of matrix metalloproteinase 1 along in vitro proliferative life span of human skin fibroblasts. Regulation by all-trans retinoic acid. Cell Biol Int 1995, 19(2):129–135
  32. Moon TE, Levine N, Cartmel B, Bangert Retinoids in prevention of skin cancer. Cancer Lett 1997, 114(1–2):203– 205
  33. Bauer EA, Seltzer JL, Eisen Retinoic acid inhibition of collagenase and gelatinase expression in human skin fi- broblast cultures: evidence for a dual mechanism. J Invest Dermatol 1983, 81:162–169
  34. Harrison JA, Walker SL, Plastow SR, et Sunscreens with low sun protection factor inhibit ultraviolet B and A pho- toaging in the skin of the hairless albino mouse. Photoder- matol Photoimmunol Photomed 1991, 8(1):12220
  35. Schmidt JB, Binder M, Macheiner W, Bieglmayer New treatment of atrophic acne scars by iontophoresis with es- triol and tretinoin. Int J Dermatol 1995, 34(1):53–57
  36. Schmidt JB, Donath P, Hannes J, Perl S, Neumayer R, Reiner A. Tretinoin-iontophoresis in atrophic acne Int J Dermatol 1999, 38(2):149–153
  37. Mitragotri S, Blankschtein D, Langer Transdermal drug delivery using low-frequency sonophoresis. Pharm Res 1996, 13(3):411–420
  38. Fernandes D. Understanding and treating In: Peled IJ Manders EK (eds) ; Esthetic surgery of the face., Taylor & Francis 2004, pp 227–240
  39. Fernandes D. Minimally invasive percutaneous collagen induction. Oral Maxillofac Surg Clin N Am 2005, 17:51– 63
Des Fernandes

Author Des Fernandes

More posts by Des Fernandes

Leave a Reply

Skip to content