Sách Giáo Khoa Về Lột Da Hóa Học (Chemical Peels – Ấn Bản 2)

192      Textbook of Chemical Peels
(b)
(a)
(c)
Figure 22.16  (a) Solar lentigines before treatment. (b) Localized frosting from OTP. (c) Results after one OTP treatment and four ETCA
peels.

FACE AND HANDS: ACTINIC KERATOSES AND LENTIGINES      193
can be repeated after 3–6 weeks, depending on whether the
keratosis is on the face or body. ETCA should be applied on
both the face and the body after OTP to reduce the risk of pig-
mentary changes.
Postpeel Care
At the end of treatment, the doctor can apply a corticosteroid
cream to the lesions treated with OTP to limit the inflammatory
reaction. This application should not be repeated until after
more than 72 hours. Between peels and for at least 6 weeks after
the last peel, the patient should apply effective sun protection10
three times a day after Blending Bleaching Cream. The patient
should be warned not to touch or pull off the scabs: these are
normal and to be expected (Figure  22.21). Vaseline can be
applied to the scabs to enhance healing.
After 6 weeks of skin regeneration, the patient should use
daily care products that are suited to his or her skin.
CASE STUDY 5: LARGE ACTINIC
KERATOSES TREATED WITH ETCA DEEP
FOCAL APPLICATION + ETCA FULL-FACE
APPLICATION (ISO-MOSAIC TECHNIQUE)
Figure 22.22 shows general photoaging of the face, lentigines,
and keratosis.
The peeling options are as follows:
•
Deep full-face phenol peel (Lip & Eyelid Formula).
•
Light full-face phenol peel (Easy Phen Light).
•
Medium-depth TCA peel (Unideep).
•
Focal reticular dermis peel (OTP).
•
Regional deep ETCA peel.
•
Focal deep ETCA peel.
•
Full-face papillary dermis peel (ETCA PC).
•
Full-face basal layer peel (ETCA).
The best choice is always the least traumatic and least
dangerous technique that could be effective for a patient,
depending on analysis of his or her skin.
After discussing the technical details and price of the
procedure, the patient did not accept a deep full-face phenol
Figure 22.17  Actinic keratoses of different diameters.
Figure 22.18  Precise application of OTP solution to the lower limb.
Figure 22.19  OTP can be used to treat numerous lesions, as long
as the healthy skin between them is not touched.
Figure 22.20  The speed with which OTP penetrates gives an idea
of how keratinized the lesion is. If there is a lot of keratinization, the
solution penetrates more quickly on the edges of the lesion.

194      Textbook of Chemical Peels
peel. OTP comes with the risk of PIH and depigmentation of the
face. Papillary dermis peels (Unideep, ETCA PC) are options,
but some keratoses are so thick that there is the possibility of
insufficient results.
In this case, preference is given to an “iso-mosaic technique”
using ETCA applied at different depths. A number of touches
will be applied depending on the thickness of the keratosis.
ETCA or ETCA Pain Control is focally applied, by touches,
on the main keratosis (Figure 22.23).
•
Cheeks: Some superficial lesions are treated at depth 5/7:
pink-white frosting.
•
Nose: Larger, thicker keratoses have been touched more
times, up to the end point of pure white frosting (depth 6/7).
•
Eyebrows, upper lip: Still larger and thicker keratoses have
been touched still more, up to the end point of yellowish-
grey frosting (depth 7/7).
•
After that, ETCA or ETCA PC is applied on the whole face
to treat small lentigines and keratoses, up to the basal layer
(depth 3/7); the end point is frosting points.
•
After the peel, the postpeel mask cream is applied.
The full treatment (Figure 22.24) consists of the following:
•
Deep touch (differential depth, depending on the type of
keratoses) of lesions with ETCA immediately before the
first and eventually the fourth ETCA.
•
Four ETCA peels, once a week.
•
Postpeel mask cream.
Daily care:
•
Morning: Blending Bleaching Cream and sun protection
(Melablock-HSP, SPF 50+).
•
1 p.m.: Sun protection is applied again.
•
3 p.m.: Sun protection is applied again.
•
Evening: DHEA-Phyto cream is applied.
At the end of the treatment, keratoses, lentigines, and sun
aging are visibly cured, as seen in Figures 22.25 and 22.26.
COMPLICATIONS
Prolonged Erythema
The erythema that always follows the application of OTP usu-
ally lasts for 2–3 weeks (Figure 22.27). There may be prolonged
erythema if too much OTP has been applied as a result of too
much solution, too much pressure on the cotton bud, or too
long a contact time with the skin. Treatment consists of careful
use of corticosteroids, tyrosinase inhibitors, and effective sun
protection (see Chapter 37).
Pigmented Ring
A full or partial pigmented ring sometimes persists when
the solution has not been applied fully up to the edges of the
lesion: the external part of the lentigo has not been touched
by the acids and remains untreated (Figure 22.27). Treatment
consists of applying OTP to the ring during the next peel ses-
sion. This complication can be avoided by letting the OTP go
(a)
(b)
Figure 22.21  (a, b) Normal scabbing 8 days after the application of OTP.

FACE AND HANDS: ACTINIC KERATOSES AND LENTIGINES      195
slightly beyond the visibly pigmented zone at the end of the
application.
Persistence or Recurrence of the Lesion
An SL or AK will persist without any change unless the acid
goes deeper than the epidermis and penetrates the deep
dermis.
The lesion will recur if it has not been completely
destroyed by the acid as a result of a technical error or because
the lesion is unexpectedly deep. A differential diagnosis
is necessary before more OTP can be applied. Lip & Eyelid
phenol solution can be applied locally, followed by 24 hours’
occlusion, in the case of recurrence or resistance to OTP (see
Chapter 30).
Depigmentation or Scarring
Hypertrophic scars can be treated in the classic manner by
corticosteroid injection and long-term use of a silicone sheet
dressing (see Chapter 37). If OTP has penetrated too deeply
and has destroyed all the melanocytes in the area, it can cause
hypochromic or achromic scarring. The situation depicted in
Figure 22.30 may result either because a pure TCA solution at
80% m/m was applied11 or because the OTP-type solution was
applied too liberally and left too long on the skin. From the
appearance of the patient’s skin in Figure 22.30, it seems likely
that undiluted 80% TCA was used or a low-grade copy of OTP
solution was applied too liberally to areas larger than 1 cm2.
Even if the long-term prognosis is good with the right treat-
ment, surgery is sometimes the only solution when the damage
is extensive (Figure 22.28).
Figure 22.23  ETCA is applied, by touches, on the main kerato-
sis; note different types of frosting colors.
Figure 22.24  Patient about to undergo ETCA deep focal applica-
tion and ETCA full-face application (iso-mosaic technique).
Figure 22.25  Patient after treatment.
Figure 22.22  General photoaging of the face, lentigines, and
keratosis.

196      Textbook of Chemical Peels
Postinflammatory Hyperpigmentation
PIH is relatively easy to treat and tends to fade naturally with-
out sun exposure. For its treatment, see Chapter 37.
Focal treatments should be avoided on phototypes V and
VI: the patient in Figure 22.29, phototype V, suffered PIH after a
focal deep application of TCA.
Remember that nevi, melasma, and patients with photo-
type V or VI are not indications for OTP (Figure 22.31).
PRECAUTIONS
•
OTP is a strong peel, and the indications and application
methods should be followed strictly.
•
Seborrheic keratoses and flat warts do not respond well to
OTP. They can be treated with shave excision followed by a
single application of ETCA.
•
OTP should not be used on lesions larger than 1  cm in
diameter. Larger lesions should not be treated, even par-
tially, with OTP.
•
Concentrated 80% m/m TCA must not be applied to the
skin before it has been mixed with the base solution.
Figure 22.27  Focal redness after OTP application could last for
weeks or months before disappearing, eventually transforming into
PIH.
Figure 22.28  Atrophic, depigmented scars after a focal deep
TCA application. (Courtesy of Dr. Andrew Winter.)
(a)
(b)
Figure 22.26  (a) Before treatment. (b) The results of the full treatment show clear skin rejuvenation, regeneration of normal skin archi-
tecture, and removal of sun lentigines and keratoses.

FACE AND HANDS: ACTINIC KERATOSES AND LENTIGINES      197
•
The contact time between the skin and the cotton bud must
be brief.
•
OTP should always be used in combination with ETCA,
and with Blending Bleaching Cream and sun protection
(50+, then 25+) after the peel.
•
Phototype V and VI patients should not be treated; appli-
cation of OTP should be restricted to phototypes I to III,
or IV.
•
Scabs should not be pulled off in the postpeel period.
•
Aggressive use of OTP can cause scarring and/or pig-
mentation problems. Intense application of OTP can cause
patches of erythema that can persist for up to 3 months.
This prolonged erythema can be treated by the application
of topical corticosteroids and total sunblock.
NOTES

1. Using OTP on patients with phototype IV or dark Asiatic skin
should be discussed with the patient because of the risk of pig-
mentary changes.

2. Three times a day for patients with phototype IV.

3. Presentation boxes vary from country to country; it is best to
read the instructions that come with the box.

4. It is also possible to inject the peel solution directly onto the tip of
the cotton bud. The buds usually take a volume of 0.12–0.14 cm3
of solution, except for cotton buds from Asia, which are finer.

5. There is also a special applicator in the OTP kit.

6. OTP is a solution that is applied only on the lentigines to be
treated and not on the surrounding skin.

7. Bowen’s disease, also called erythroplasia of Queyrat or prickle-
cell carcinoma in situ, is a premalignant lesion.

8. The KIN classification, in which the degree of intraepidermal
invasion by abnormal keratinocytes is classified as (I) slight, (II)
moderate, or (III) severe.

9. Miller SJ, Moresi M. Actinic Keratosis, Basal Cell Carcinoma and
Squamous Cell Carcinoma. In: Bolognia JL, Jorizzi JL, Rapini RP
(Eds.). Dermatology. St. Louis, MO: Mosby, 2004: 1677–96.
10. Melablock-HSP® 50 between sessions and for at least 1 week
after the last peel. Thereafter, Melablock-HSP 25+ is enough for
the 6 weeks of skin regeneration.
11. This can happen if the doctor does not prepare the solution
­himself and an inexperienced assistant is given this essential
task.
Figure 22.29  PIH after focal deep application of TCA.
Figure 22.31  PIH after application of OTP to nevi. Nevi are not
an indication for OTP.
Figure 22.30  A combination of PIH around depigmented areas,
which are in turn centered around a scar, is common when a large
excess of TCA is applied to skin of phototype IV or V.

23
Trichloroacetic acid to the papillary dermis
Unideep
INTRODUCTION
Trichloroacetic acid in a simple aqueous solution (TCA-SAS) is
the peel most widely used to partially or completely remove
the papillary dermis. Strict prepeel preparation is required to
even out penetration, reduce melanocyte activity, and acceler-
ate postpeel reepithelialization. The main purpose of postpeel
care is to counter complications (see Chapter 14).
Unideep was designed to make prepeel preparation as
easy as possible while maintaining rapid reepithelialization
and limiting the risks of postpeel complications. Unideep is a
by-product of Easy TCA (ETCA) “technology” and is a medium-
depth peel that reaches the papillary dermis (Table 23.1).
Unideep is a saponified and stabilized TCA peel that
contains—after mixing Aktivator TCA—25% m/m TCA. It is
a good peel for patients who want quick results with a lower
risk of side effects than TCA-SAS. The Unideep solution coagu-
lates the proteins in the epidermis and the papillary dermis,
but not the proteins of the vessel walls. The resulting frosting
is an even pink-white rather than pure white. The skin is regen-
erated by the keratinocytes that have remained intact in the
deeper dermal papillae, the pilosebaceous units, and the sweat
glands. These keratinocytes regenerate a new epidermis, while
the dermal action of Unideep stimulates fibroblast production:
collagen, elastin, and glycosaminoglycans.
The postpeel mask cream should be applied twice: 50% of
the tube immediately after the peel and the remaining 50% of
the tube the morning of the first day after the peel. The postpeel
mask stimulates the skin, breaks the vicious oxidative cycle
(inflammation ← free radicals), and accelerates healing time. It
also helps to limit the vicious inflammatory circle that follows
any medium-depth peel and counters postpeel pigmentary
changes.
INDICATIONS
Unideep, a Class II medical device, is designed for local or
full-face peelings, depth 5/7, phototypes FZ 1–4. The main
indications for a TCA to the papillary dermis are photoaging,
nonactive acne, hyperpigmentation, melasma, chloasma, kera-
toses, and fine lines. Unideep can also eliminate most freckles.
A single peel is usually enough to achieve deep regeneration of
the skin, but sometimes it may be necessary to repeat the peel
for perfect results.
Unideep can be used:
•
As monotherapy.
•
In combination with Only Touch in the treatment of solar
lentigines or actinic keratoses.
•
In combination with local phenol (Lip & Eyelid Formula)
as an evening-out peel after treating deep wrinkles around
the mouth or eyes (see Chapter 36). The downtime with
lips and eyelids (1 week) is the same as for a peel to the
papillary dermis.
•
As a local application (e.g., on the forehead only) in com-
bination with a more superficial peel (ETCA) on the rest
of the face so that the patient can keep up his or her social
life more easily.
It is sometimes difficult to choose between doing a single
Unideep peel and four ETCA or Easy TCA Pain Control peels.
Overall, these peels offer patients the same results. However,
one Unideep peel is sometimes more effective than ETCA when
treating pigmentation problems originating in the dermis,
whereas the opposite is true in the treatment of photoaging,
when strong stimulation is needed to regenerate healthier-look-
ing skin. The best indication for Unideep is in patients with skin
phototypes I–III. The risk of postinflammatory hyperpigmenta-
tion (PIH) must be discussed with patients who have darker
skin phototypes.
METHOD OF APPLICATION
Preparing the Skin
Weeks before Peeling
Depigmenting preparation is recommended for phototype
FZ > 4. When Unideep is used on skin phototypes 4–6, the
skin requires preparation for 4–6 weeks prior to peeling: Skin
Tech Blending Bleaching Cream twice daily, possibly with a
3% hydroquinone cream. There should be classic herpes pre-
vention for patients with a medical history (3 days before and
3 days after peeling).
Immediately before Peeling
Cleanse the skin with Skin Tech Cleanser, rinse and dry the
skin, and then disinfect and degrease it with a 50% alcohol/50%
acetone solution. To degrease the skin properly, it must be
wiped with acetone several times.
Preparing the Applicator
Dental Cotton Tube:  The ideal applicator is a cotton dental swab
held in a clamp (Figure 23.1); this makes it easier to handle and
to apply the right amount of pressure. The cotton swab in the
kit is too long and needs to be cut into two equal halves for use
as an applicator.
Double-Ear Cotton Bud:  Unideep also can be applied using a
double cotton bud, as for ETCA or phenol application.
Preparing the Peel Solution
Inject into the vial of base solution the entire contents of the
Aktivator TCA 50% vial to obtain a concentration of TCA
25% w/w.

Trichloroacetic acid to the papillary dermis: Unideep      199
Control of Burning Sensation
Most patients can easily tolerate this treatment without nerve
block anesthesia if the peel is done slowly, cosmetic unit by cos-
metic unit. More squeamish patients may prefer to have intra-
venous sedation, along with nerve blocks.
Analgesic Medication
The patient can take an acetaminophen plus codeine tablet half
an hour before going to the doctor. The patient may also benefit
from taking a second tablet 1 or 2 hours after the peel, at the
peak of the discomfort.
Cryoanesthesia
Any pain can be eased considerably by simply chilling the skin
before the first application and between the different coats.
Cold packs (e.g., 3M products: Figure 23.2) or a ventilator can
be used for this. If neither is available, a bag of ice or simply
contact with a cold surface (e.g., an empty bottle) soon eases the
burning sensation. Cold packs can be applied directly on the
acid if they have been dried beforehand.
Nerve Blocks
A local anesthetic (nerve block) may be necessary for sensitive
patients. With nerve blocks, peel application is painless and
quicker. (See Chapter 33 for details on how to perform nerve
blocks.) After nerve blocks have been applied to the area under
treatment, the peel solution is applied to the face. It is first
applied on the forehead and temples, until an even pink-white
frosting is obtained; the postpeel mask cream is applied on the
area that has just been treated before moving on to the next
area. The face is done in three stages: forehead and temples,
nose and cheeks, and the chin. The postpeel cream soon stops
the burning sensation.
Vocal Anesthesia
In many cases, vocal anesthesia or medical hypnosis can allevi-
ate the burning sensation of the acid in Unideep.
Topical Anesthesia
For reasons outlined in Chapter 33, anesthesia with a topical
cream should not be used before a peel to the papillary dermis.
Figure 23.1  Unideep applicator held in a clamp.
Figure 23.2  Cryoanesthesia with 3M’s cold pack.
Figure 23.3  The face is divided into five zones for application.
Table 23.1  Description of Unideep Kit
Base solution
One 4 ml vial of solution containing four alpha
hydroxy acids, antioxidants, trace elements,
and saponines
Trichloroacetic
acid
Aktivator TCA 50%: One 3.2 ml vial containing a
50% w/w TCA solution
Postpeel mask
Two 10 ml tubes of Skin Tech postpeel mask
cream designed to control inflammation and
pain after the peeling
Various
One dosage card for Skin Tech postpeel mask, a
small container for mixing the TCA with the
base solution, cotton buds, and instructions for
use

200      Textbook of Chemical Peels
Application
Unideep peeling solution is applied to five different areas
(Figure 23.3). The physician should complete the application in
one area before moving to the next (Figure 23.4).
The First Layer
Use the applicator included in the kit, held with tweezers. Soak
the applicator in the peeling solution, drain it slightly on the
edge of the small container kit, and apply the Unideep peel-
ing solution to the skin using regular circular movements. A
peeling depth of 5/7 (papillary dermis) needs a uniform pink
frosting.
The Following Layers
Several successive layers are necessary to obtain uniform pink-
white frosting (Figure 23.5). Let each layer dry before applying
the next one. Each of the five areas will be treated sequentially;
when peeling has finished in one area, apply the Skin Tech
postpeel mask and then apply the peeling solution to the next
area. No pause is required between two zones.
The Last Layer
The last layer is the one after which the clinical “sign” appears
that corresponds to the required depth. The “sign” is not a volume
(milliliters) or a temporal concept (minutes), but a clinical concept:
the appearance of a pink-white uniform frosting, associated with
the sign of “sliding” when the skin is pinched (Figure 23.6); it is a
sign of peeling to the papillary dermis (deep 5/7). A gray-white
Figure 23.4  The first coat of Unideep often produces uneven
frosting that will even out with the second coat.
(b)
(a)
Figure 23.5  (a, b) Sequenced application.
Figure 23.6  Epidermal sliding.

Trichloroacetic acid to the papillary dermis: Unideep      201
frosting signals a reticular dermis (depth 6/7) peeling. This depth
is not recommended with Unideep.
Skin Tech Postpeel Mask
Once the uniform pink frosting has appeared in an area, imme-
diately apply 1 g of the Skin Tech postpeel mask on the treated
area before beginning to treat the next area. The postpeel
mask stops the pain, redness, swelling, and burning sensation
of the skin caused by the peeling, in a few minutes. Postpeel
inflammation is quickly controlled and the risk of side effects
is limited, but application of the mask does not eliminate the
possibility of side effects.
After frosting occurs, the solution should not be neutral-
ized. At the end of the peel on the five areas, reapply an addi-
tional 2 g of the postpeel mask on the face with a soft massage.
At the end of the procedure, half a tube of postpeel cream
should have been applied to the face. It should be rubbed in,
and the solution and cream left in place to work until the next
morning. The next morning, the patient should apply the rest of
the postpeel cream to the face, after washing with neutral soap
or cleansing lotion.
POSTPEEL AFTERCARE
From the 1st to the 15th day after the peel, the patient should
generously apply Skin Tech IPLase Mask cream to the face to
reduce erythema (Figures 23.7 and 23.8).
The postpeel daily care recommended by the doctor
is essential to guarantee results and safety. Special atten-
tion should be paid to possible PIH. The patient must apply
Blending Bleaching Cream twice a day for a few months. A
sunscreen such as Skin Tech Melablock-HSP SPF 30 or 50+ is
indicated in all cases, for a minimum period of 3–6 months,
depending on patient’s skin type and sun exposure. The doc-
tor should be able to control, predict, and prevent possible
complications and treatment. He or she should check the
cream and skin tolerance. If a postpeel temporary intolerance
appears, the application of daily care cream should be post-
poned for a few days.
Postpeel Desquamation
Postpeel desquamation can take different forms, depending on
the patient’s phototype: the darker the original phototype, the
darker the skin will appear after peel. A patient with a clear
phototype will exhibit a soft darkening, while a phototype 4 or
5 patient will exhibit dark brown skin during the week after the
peel (Figures 23.9, 23.10, and 23.11).
RESULTS
See Figures 23.12, 23.13, and 23.14 for examples of results.
Day 0:
Afternoon and evening
Apply postpeel mask
Day 6
Apply vaseline
Days 3 and 6
Check if infection
– 2 Weeks
Day 7–8
Makeup allowed
Protective Home care
IPLASE (reduces erythema) 3x/d
Vit E antioxidant (moisturizing) every time the patient feels the skin tensed
Skin Tech Cleanser (Cleanse skin)
if PIH risk, give the patient Blending Bleaching 3 x/day 2 weeks before Unideep.
Blending Bleaching (Pigment control) 2x/d
09 am, 12 pm, 03 pm
09 am, 12 pm, 03 pm
Melablock HSP, SFP 50+
Melablock HSP, SFP 30
0
U
1
2
3
4
5
6
7
8 to 30
After day 30
Smokers, polluted cities:
Pigment control:
Moisturizing:
Dry skin, + 40 years old:
Dermal tensor:
Dermal filling:
Nutritive ACE
Blending Bleaching
Vit E Antioxidant
DHEA Phyto
Actilift
Atrofillin
Specific Home care
Figure 23.7  Postpeel care.
Figure 23.8  Application of a thick coat of postpeel mask.

202      Textbook of Chemical Peels
(a)
(b)
(c)
Figure 23.9  Postpeel at days 5 (a), 6 (b), and 8 (c) on a clear phototype.

Trichloroacetic acid to the papillary dermis: Unideep      203
(a)
(b)
Figure 23.10  (a) Soft flaking after a peeling depth of 3/7; ETCA basal layer peel (pinpoints of frosting) on phototype FZ 3. (b) Flaking at
day 6, after a peeling depth of 5/7, pink-white frosting on phototype FZ 4.
(a)
(b)
Figure 23.11  (a) Flaking at day 6 after a peeling depth of 5/7. (b) Pink-white frosting on phototype FZ 2.

204      Textbook of Chemical Peels
(a)
(b)
Figure 23.12  (a) Natural darkening of freckles 24 hours after the application of Unideep; they will disappear 5–6 days after the peel.
(b) Freckles 1 month after a Unideep peel.
(a)
(b)
(c)
(d)
(e)
Figure 23.13  (a–c) Combination of peels: Unideep has been applied to the forehead only, and ETCA has been used to treat the rest of
the face that is not as badly damaged by postacne pigmentation. (d, e) Forehead view of a full-face Unideep application.

Trichloroacetic acid to the papillary dermis: Unideep      205
PRECAUTIONS AND COMPLICATIONS
Potential complications from this type of peel are described in
detail in Chapter 37.
General Precautions
Unideep is a peel to the papillary dermis; therefore it is essen-
tial to follow the indications and method of application. Misuse
of Unideep could produce the classic side effects of medium-
depth peels.
The patient should be warned not to scratch the skin after
the peel. Concentrated TCA should not be applied to the skin
without mixing it with the base solution.
Specific Precautions for Dark Phototypes
The techniques described are for patients with phototype
I–III. To treat patients with a higher phototype (IV–VI), extra
precautions should be taken. The patient should prepare the
skin by applying Blending Bleaching Cream twice a day for 2–3
weeks before the peel; use sun protection cream (Melablock-
HSP 50+); and avoid exposure of the skin to daylight. The peel
should be applied carefully, and great care should be taken not
to have any excess solution.
After the peel, Blending Bleaching Cream should be
applied as soon as possible, when flaking has finished, and be
continued for 6 weeks after the peel.
Pigmentary Changes
Pigmentary changes can be treated with three or four ETCA
sessions and Blending Bleaching Cream. Total sun protection
is essential.
(a)
(b)
Figure 23.14  (a) Before peeling and (b) 60 days after one papillary dermis peel: Skin quality is enhanced, fine lines have disappeared,
freckles and lentigines have disappeared, and photoaging generally is solved, but a papillary dermis peel is not indicated for suppressing
wrinkles.

24
Resorcinol
Unna’s paste/Jessner’s solution
CHEMISTRY
Resorcinol (Figure  24.1), also known as resorcin, meta-dihy-
droxybenzene, 1,3-dihydroxybenzene, and 1,3-benzenediol,
has a molecular weight of 110.11 and a relative density of 1.272.
It is slightly more acidic than phenol, with a pKa of 9.15. It is sol-
uble in water, alcohol, ether, and glycerol. It comes in the form
of white needle-shaped crystals. Resorcinol crystals oxidize
easily and turn pink on contact with light, air, or iron.
PROPERTIES OF RESORCINOL
Antiseptic
Resorcinol has antiseptic properties similar to those of phenol1
and was used to dress minor wounds before the era of antibiotics.
It has antifungal properties and was also applied on chancroids
and syphilitic ulcers. Its bactericidal effect is 30% of that of phenol.
Proteolytic and Protein Coagulant
Resorcinol is a phenol derivative, and its proteolytic power is
about 1/40 of that of phenol. It breaks the weak hydrogen links
of keratin and acts as a proteolytic agent, even at concentrations
as low as 5%.2 At higher concentrations, it can also precipitate
skin proteins and become a protein coagulant.
Antipruritic
Resorcinol is used in many antipruritic formulations, especially
in chronic kidney dialysis. It is mainly used in paste form, usu-
ally called Unna’s paste, or in solution form, as Jessner’s solu-
tion or Combes’ solution.
INDICATIONS FOR RESORCINOL
•
Acne: Acne is a good indication for resorcinol.
•
Folliculitis: Resorcinol is effective in this indication, even
on the back.
•
Comedones: Resorcinol eliminates comedones.
•
Scars: Superficial scars can be slightly improved, but deep
“ice-pick” scars or extended scars do not respond to this
treatment.
•
Photoaging: Solar keratoses, pigmentary lesions, epider-
mal atrophy, and solar elastosis are indications for resor-
cinol if their histological origins are not too deep.
•
Dyschromias: Resorcinol has been used with varying suc-
cess to treat melasma, chloasma, postinflammatory hyper-
pigmentation (PIH), and postacne pigmentation. It can
eliminate some freckles. Resorcinol is contraindicated in
patients with phototypes IV–VI because of the risk of pig-
mentary changes.
Obsolete Indications
Manquat’s Elementary Treatise on Therapeutics (1903) describes
the heroic experiments of colleagues who tested, on their own
bodies, the effects of resorcinol taken in ever-increasing doses
until convulsions ensued (ingestion of 10 g of resorcinol in 15
minutes). The indications officially retained in 1903 were the
following:
•
Antipyretic: Resorcinol was considered a dangerous and
rather ineffective antipyretic.
•
Antiseptic: The antiseptic use of resorcinol was recom-
mended for surgery in place of phenol, as it is less toxic
and less caustic.
•
Anesthetic: Resorcinol acts as a mild local anesthetic.
•
Psoriasis and eczema: Unna used it in ointments of 10%–
20% to treat psoriasis, and of 2% to treat pityriasis capitis
and seborrheic eczema.
HISTOLOGICAL CHANGES
Epidermal
After a resorcinol peel, the superficial stratum corneum comes
away from the germinative layer in the stratum granulosum.3,4
The basal layer shows increased mitosis and accelerated turn-
over. The total thickness of the epidermis therefore increases,
to the detriment of the stratum corneum, and the skin appears
more hydrated.
Dermal
The fibroblasts in the papillary dermis are stimulated and pro-
liferate: they synthesize a large quantity of new collagen, which
is deposited in bands beneath the epidermis (in the Grenz
zone). The intercellular matrix is enriched in glycosaminogly-
cans. Further down, short-lived but rapid vasodilation occurs,
signaling the presence of dermal inflammation.
Four months after the peel, the histological changes
in the dermis, apart from vasodilation, are still visible. The
intercellular space has a higher concentration of glycosamino-
glycans, and there are more collagen and elastic fibers in the
dermis.
INGREDIENTS OF RESORCINOL PEELS
Many classic formulas use resorcinol combined with old-fash-
ioned ingredients that may now sound somewhat strange and
mysterious.
Wool Fat (Lanolin)
Wool fat is obtained from extracts of soapy water in which
sheep’s wool has been washed or is extracted with solvents
from grease wool. Lanolin is obtained by purifying the grease
(or suint). This emollient is a yellow and viscous substance, con-
sisting of fatty acids and fatty acid esters.

Resorcinol: Unna’s paste/Jessner’s solution      207
Petrolatum (Vaseline)
This neutral, semisolid unctuous substance, tasteless and odor-
less, is derived by distilling or purifying petroleum. Thin lay-
ers are transparent. Petrolatum is the official generic name;
Vaseline is a (genericized) trademark.
Benzoin Axunge
Axunge is a greasy excipient used to reduce erythema. It is, in
fact, simply lard (i.e., grease extracted from a pig’s epiploon).
Benzoin axunge is prepared by adding 5 g of tincture of ben-
zoin per kilogram of melted axunge and stirring until the mix-
ture has cooled.
Benzoin
Benzoin, or gum benzoin, is a resinous secretion obtained from
cuts made in the trunk or branches of the Styrax benzoin tree.
It contains coniferyl benzoate, benzoic acid, benzyl cinnamate,
vanillin (a phenol aldehyde), and a number of triterpenes.5 (See
Box 24.1)
Benzoin resin is a local irritant. A hundred years ago,
it was considered to be an aphrodisiac when ingested. At the
beginning of the 20th century, benzoin was primarily adminis-
tered as an antiseptic in fumigation to treat chronic respiratory
diseases: small pieces of it were thrown onto a heated metal
plate.6 Tincture of benzoin is obtained from dissolving (1/5)
benzoin in alcohol.
Ceyssatite and Zinc Oxide
Ceyssatite is a white clay (from Ceyssat in France) whose absor-
bent properties, similar to those of kaolin, have been widely
used in cases of hyperhidrosis and eczema. Ceyssatite and zinc
oxide have an exfoliating and desiccant action that is absolutely
essential for resorcinol to act evenly.
Kaolin
Kaolin is a white clay mostly made up of silicon dioxide, alu-
minum oxide, iron oxide, titanium dioxide, magnesium oxide,
and sodium oxide. It was first found in China, in Kao-Ling.
European kaolin is formed by the decomposition of feldspath
in granite rock in Brittany or Limousin. Kaolin has good absor-
bent properties and is gentle on the skin; it is very well tolerated
by patients with very sensitive or reactive skin. It is used for
its healing, antiseptic,7 and anti-inflammatory qualities and its
excellent coverage in Unna’s paste formula.
Benzoic Acid
Benzoic acid is a weak carboxylic acid.8 It is not very soluble
in water (3 g/l at 25°C) and has a molecular weight of 122. It
comes in the form of a white silky-looking solid and is used as
an antiseptic and antifungal agent or as a preservative in some
fizzy drinks.
RESORCINOL PASTES
Formulations of Different Pastes
The formulations for resorcinol paste most often used in the
past are shown in Table  24.1. The preparation of this paste
involves a great deal of work for the pharmacist, who has to
use centrifugation and/or ultrasound. The resorcinol crystals
have to be thoroughly ground in a mortar before making up
the paste to ensure no big crystals remain in it.9 The resulting
mixture will be more homogenous and easier to spread. Unna’s
paste does not remain active very long, as it oxidizes rapidly.
The doctor should therefore always use a freshly made paste.
Another formulation contains resorcinol, olive oil, kaolin, zinc
oxide, petrolatum, and wool fat.
Preparing the Peel
Preparing the Skin
The best results are achieved when the patient’s skin has been
prepared for 15 days beforehand; see Chapter 2. If the skin has
been prepared with tretinoin or alpha hydroxy acids (AHAs),
or if the patient has used products (benzoyl peroxide) or tech-
niques (scrub, or abrasion with a massage glove) that increase
the permeability of the stratum corneum, the resorcinol paste
should not be left on too long.
Allergy Test
An allergy test should be done before each resorcinol peel, by
applying a small bit of paste on the skin behind the ear for
BOX 24.1  Benzyl and Phenyl
• Benzene is a molecule.
• Benzyl is a group that has to be attached to some-
thing else. It is methyl benzene whose methyl
group (CH3–) has lost a (H–)
• Phenol is a molecule; the suffix -ol means that it
has a (–OH) radical.
• Phenyl is a group that has to be attached to some-
thing else. It is a benzene minus a (–H) or a phenol
without its (–OH) group.
Table 24.1  Formulations of Resorcinol Paste
50%a,b
50%c
30%c
Resorcinol
40 g
60 g
30 g
Zinc oxide
10 g
15 g
15 g
Ceyssatite
2 g
3 g
5 g
Benzoin axunge
28 g
50 g
Benzoic acid
2 g
Dermagor cold cream
40 g
a Trauchessec JM, Vergereau R. Les Peelings. In: Bartoletti
CA, Legrand JJ (Eds.). Manuel Pratique de Médecine
Esthétique. 2nd ed. Paris, France: Société Française de
Médecine Esthétique, 159–167.
b Rusciani L, Rossi G, Bono R. Les peelings chimiques.
Journal de Médecine Esthétique et de Chirurgie Derma­
tologique. 1993; XIX (78): 78–80.
c Cohen, L, Préparations Magistrales en Dermatologie. In:
Arnette (Ed.). Collection des Manuels Pratiques de
Médecine Esthétique. Paris, France: 1989.
OH
OH
Figure 24.1  Chemical structure of resorcinol.

208      Textbook of Chemical Peels
20 minutes. This provides a minipeel to evaluate the risk of
allergy. This allergy test should be conducted like a localized
peel. The skin must be allowed to dry and flake; the normal
action of resorcinol on this thinner and more sensitive skin
should not be confused with an allergy. Any hint of an allergic
reaction (e.g., swelling, redness, itching, blistering, or weeping
skin) should rule out this peel immediately.
There is one significant cloud on the horizon: the allergy
test itself can make a patient who was not previously allergic to
resorcinol allergic. It is therefore not wholly predictive.
Clean and Degrease
The skin should be disinfected (with alcohol) and degreased
(with ether or acetone) before applying the paste.
Hydrating the Patient
The patient must be well hydrated to facilitate diuresis and
elimination of the metabolites of the resorcinol. An intravenous
drip of saline solution should be set up, but if this is not pos-
sible, the patient should be asked to drink several glasses of
water before the resorcinol is applied.
Preparing the Paste
Resorcinol paste is compact and difficult to apply. It can be
easily softened by putting it in a water bath at 45° for approxi-
mately 10 minutes. If that is not possible, small blocks of paste
should be applied to the patient’s skin. Heat from the skin will
slowly “melt” the paste and make it easier to spread, although
the resorcinol may penetrate too deeply where contact time has
been longer.
Analgesia and Anesthesia
No analgesia or anesthesia is necessary. Resorcinol has a mild
local anesthetic effect, and a resorcinol peel is neither painful
nor stressful.
Positioning the Patient
The patient lies down during the peel and for half an hour
afterward.
Applying Resorcinol Paste
Application
The patient’s eyelids are protected with Vaseline or damp cot-
ton (makeup remover) pads. A thick coat of paste is applied with
a tongue depressor—enough to make a mask of even thickness.
The paste should not be applied to the eyelids or mucous mem-
branes. The paste has to be applied a little way into the hair, and
should just touch the eyebrows.
On the jaw area, as with phenol, the paste is applied up to
2 cm below the upper jaw. The paste should be rubbed gently
to make it more homogenous. Resorcinol paste is often applied
on the décolletage and back. Great care must be taken in these
areas, however, as the extent of the surface area treated can
induce toxicity. Large surface areas should be treated in several
stages, and a rest period between two applications will help the
body eliminate the metabolites from the detoxification of this
phenol compound.
Contact Time for a Facial Peel
The contact times discussed below are a rough guide only and
should be modified to suit the patient’s skin type, the disorder
being treated, the results desired, and so forth.
First Application (First Day)  The contact time is 10–25 min-
utes. A few minutes after the first application, the patient feels
some heat and then a tolerable burning sensation. This sensa-
tion starts where the resorcinol has penetrated most rapidly.
The cheeks are usually more permeable than the forehead.
The areas where the patient first feels burning are the first to
be cleaned of the resorcinol paste at the end of the peel. The
sensation of acid “burning” can sometimes become intense,
and a yellow serous fluid may be seen to weep through the
partially lysed epidermis. In this case, the patient should be
given an analgesic for the first night: acetaminophen plus
codeine.
After the first application, the skin becomes red in color,
as if sunburned.
Second Application (Second Day)  The contact time is 20–30
minutes. The resorcinol is left to work for longer: 10 minutes
more than the first session, or even 15 minutes more on areas
that did not react as well on the first application, mainly on the
forehead.
After the second application, the skin becomes brownish,
and the patient’s social life is disrupted.
Third Application (Third Day)  The contact time is 30–35 min-
utes. The third application must be conducted with extreme
caution. If the “resorcinol membrane” that is forming has modi-
fied the permeability of the skin, epidermolysis is present, and
the skin has been badly injured, rough handling (or paste that
is too compact) could pull away the skin and sharply increase
the risk of postpeel complications in the form of erythema and
pigmentary changes.
After the third application, the resorcinol membrane
has formed. It is made up of lysed and dried out corneocytes
and keratinocytes, stuck together by any serous fluid seeping
through the epidermis.
Contact Time for a Body Peel
The skin on the body is less permeable than the skin on the face,
and the contact times will therefore be longer.
On the first day, the contact time should be 30–50 min-
utes, on the second day 40–60 minutes, and on the third day
50–70 minutes. Again, extreme caution is recommended for
peels on nonfacial skin because of its limited capacity to regen-
erate and because the extent of the area to be treated increases
the risk of general toxicity.
End of the Peel
At the end of contact time, the paste is removed with a tongue
depressor and a dry gauze pad. A small amount of paste can be
left on the skin at the end of the peel so that a thin layer of res-
orcinol remains to give full results. It is not strictly necessary to
remove the paste in the same order in which it was applied. The
paste can be left to work longer in certain places to increase the
strength of the peel locally—for example, on the more resistant
skin on the forehead.
If the doctor wishes to remove all of the paste, the follow-
ing solution can be used:
•
Tincture of benzoin, 50 ml.
•
Tincture of Quillaja,10 50 ml.
•
Rose water, 100 ml.

Resorcinol: Unna’s paste/Jessner’s solution      209
IMMEDIATE POSTPEEL CARE
The patient remains lying down for approximately half an hour
after the peel. The back of the table is raised to move the patient
gradually from a lying position to a sitting position, and he or
she continues to be hydrated. The patient then goes home, with
an analgesic or an anti-inflammatory to deal with any pain or
unpleasant burning. 3M cold packs can help ease the sensa-
tion of heat. Resorcinol peels owe some of their effectiveness
to the presence of siccative agents.11 Any topical hydration of
the skin must therefore be strictly avoided until flaking has
begun. Actual downtime will start after the second application
of the resorcinol paste and will last for 8 days. It is important to
warn the patient about the downtime and explain clearly how
the face will look during the week it is flaking. The resorcinol
membrane flakes starting on the fourth day. The more mobile
areas of the face, around the face and eyes, will flake first. The
resorcinol membrane slowly cracks, making the skin look
around 100 years old. It grips the skin in a straitjacket, some-
times making it difficult for the patient to speak and eat. The
patient should anticipate a liquid diet for a few days: yogurt,
soup, broth, consommé, purée, and so forth.
The patient must not pull off the strips of peeling skin. At
the most, the strips can be cut off with scissors, without pulling
the skin at all. The skin is pink and sensitive underneath the
resorcinol membrane. As soon as flaking starts, the skin needs
hydration (vitamin E hydrating and antioxidant cream, or even
Vaseline if necessary). Effective sun protection (see Chapters 2
and 3) must be used permanently for 1–3 months. How long
sun protection is used depends on the risk of hyperpigmenta-
tion (skin phototype IV, sunny climate, working outside, etc.).
Repeating the Peel
According to Unna, the resorcinol paste can be applied again as
soon as flaking is complete. Physicians are rarely called upon
to repeat an application of resorcinol paste nowadays. The
results of an Unna’s paste peel remain modest in relation to the
complexity of the treatment and the downtime involved, and
patients are not prepared to accept these conditions.
JESSNER-TYPE RESORCINOL SOLUTIONS
Formulations of Different Solutions
Some authors use m/m instead of m/v, which changes the actual
concentration of the active ingredients. It is also important to
stress the need for the pharmacist to use the crystal form of the
lactic acid and not the solution form. Lactic acid comes in liquid
form with a concentration of 85%. The pharmacist should use
lactic acid crystals and not solution to prepare the Jessner solu-
tion. Moreover, different molecules, many of them unknown,
are used to denature alcohol, to make it unfit for drinking, and
there is a risk of potential chemical interactions with the acids.
The alcohol used by the pharmacist must be pure, not dena-
tured. Resorcinol solutions have been used at concentrations of
10%–50% in alcohol or ether to treat keratoses.
Resorcinol solutions have the distinct advantage of not
having to be neutralized.
Eller and Wolf’s Solution (1941)12
•
Resorcinol (crystals), 17 g.
•
Salicylic acid13 (crystals), 8.5 g.
•
Lactic acid14 (crystals), 8.05 cm3.
•
Rose oil, 0.05 cm3.
•
Alcohol 95°, ad 100 ml.
Five to eight coats are applied one after the other with cot-
ton, depending on the depth of peel desired and the skin type.
Three coats produce frosting and six coats produce edema.
Eller and Wolf recommended constant hydration of the patient
before and after treatment.
Urkov’s Solution (1946)
•
Resorcinol, 38 g.
•
Salicylic acid, 6.6 g.
•
Lactic acid (solution), 13 cm3.
•
Alcohol 95°, ad 100 cm3.
After leaving the solution to rest for 24 hours and fil-
tering it, UV exposure was what made it effective. Solutions
not exposed to UV did not appear to work. The skin was also
prepared by UV exposure, and the solution was applied five
times, allowing each coat to dry before the next application.
Urkov then applied an occlusive mask. This mask allowed the
superficial layers to hyperhydrate by blocking transepidermal
water loss (TEWL). The hyperhydration dissolved the salicylic
acid that would have precipitated on the skin without occlusion
and could not have penetrated, as only the acids in solution can
readily penetrate the skin barrier. He then applied zinc stea-
rate powder (which is antiseptic and anti-inflammatory). The
erythema subsided in 5–6 days and exfoliation was superficial.
The solution can be kept in the refrigerator for 10 days.
Jessner’s15 Solution or Combes’16 Solution (1950s)
•
Resorcinol (crystals), 14 g.
•
Salicylic acid (crystals), 14 g.
•
Lactic acid (crystals), 14 g.
•
Ethanol 95° (not denatured), ad 100 ml.
Jessner’s solution must be kept in a glass, light-protected,
hermetically sealed bottle. It can be kept in the refrigerator for
more than 2 years like this. When the solution oxidizes, it turns
pink. Contact with the fingernails can turn them orange-yellow.
Other Combinations
Resorcinol solutions have been used in combination with glycolic
acid, trichloroacetic acid (TCA), and 5-fluorouracil (5-FU). Many
modified versions of Jessner’s solution have been presented,
containing kojic acid, hydroquinone, and other ingredients. The
effectiveness of these resorcinol solutions depends on skin prep-
aration, skin sensitivity and thickness, the type of applicator and
the force of application, the number of coats applied, the type
of solution used, the quality of the solution’s preparation, and
other factors. Moreover, products with a tyrosinase-inhibiting
action (kojic acid, hydroquinone, etc.) produce their effect only in
the long term. Single application of these products cannot treat
melasma in any way. Only repeated applications, allowing the
gradual absorption of products that inhibit melanocyte metabo-
lism, can be considered as an effective treatment.
Jessner’s Formula
Indications
Jessner’s solution provides an exfoliating peel, effective in the
treatment of acne and dyschromias of superficial origin.
Safety
It is a relatively safe peel. Overpeeling is rare with this treat-
ment, but phototypes IV–VI are still contraindicated because

210      Textbook of Chemical Peels
of the risk of pigmentary changes. Unlike resorcinol paste,
Jessner’s solution does not cause dizziness, tinnitus, or faint-
ness. When applying the solution on large surface areas, how-
ever, it must be taken into account that the potentially toxic
agents that it contains may be absorbed and are likely to be
eliminated via the liver and kidneys. According to Rubin,
applying Jessner’s solution on the face, neck, and décolletage
in a single session remains without danger of salicylism.
Salicylism was described, however, again by Rubin, when
doing Jessner peels together on the face, neck, arms, and lower
limbs.17
Standard Application of Jessner’s Solution (Original Formula)
Preparing the Skin  Standard skin preparation increases the
depth of penetration of Jessner’s solution and improves the
results—while increasing the risk of complications. An allergy
test is essential, especially because of the resorcinol in the
formula.
Cleaning and Degreasing  The skin is cleaned and degreased
with alcohol and acetone. Care should be taken not to abrade
the skin manually with the gauze pad while degreasing.
Applying the Solution  Applying Jessner’s solution is about as
painful as a TCA peel at 15%. It is applied gradually, leaving
each coat to dry completely before applying the next coat. The
strength of the peel depends on the number of coats applied; it
is therefore possible to penetrate the skin gradually. Carelessly
applying one coat immediately after the other would take the
peel beyond the desired effect and increase the risk of compli-
cations. It takes time to do a peel with Jessner’s solution. The
depth of action also depends on the force of application: the
greater it is, the deeper the acids will penetrate. Patients with
thin skin should be treated with lighter hand pressure than
patients with thick skin.
•
Level 1: An even coat is applied to the area to be treated,
regardless of the type of applicator (brush, cotton buds,
cotton balls, gauze pads, etc.18). It is always advisable to
use disposable applicators to avoid any risk of transmit-
ting infection. The first coat usually causes erythema and
occasionally some pinpoint frosting. Some “pseudo-frost-
ing” usually can be seen after the ethanol has evaporated:
this is caused by the ingredients of the solution, especially
the salicylic acid, precipitating on the skin. Unlike genuine
frosting, which is protein coagulation, pseudo-frosting can
be brushed off easily. The patient should be fanned with a
handheld or portable fan to alleviate the “burning” sensa-
tion and eliminate any unpleasant fumes. If the application
remains at level 1, only a very slight drying of the skin will
be observed afterward.
•
Level 2: The skin is left to dry for 4–5 minutes between two
successive coats. The second and third coats trigger more
pronounced erythema and cloudy white frosting, as well
as some pain and discomfort. The discomfort will last for
approximately a quarter of an hour. Trauchessec19 applies
the solution once a week until results are achieved. The
first treatment consists of only one coat, the second of two,
and the third of three coats of solution. After level 2, the
patient’s skin feels dry and tight. The top layers of the epi-
dermis, dried out by the solution, appear transparent but
still stick to the underlying cells. Flaking occurs within 4–5
days. Locally, some areas may turn a brownish color where
Jessner’s solution has penetrated more deeply than antici-
pated. After three coats, the stratum corneum separates
from the skin, there is no blistering or epidermal necrosis,
and the dermis is not directly affected.
•
Level 3: Applying additional coats deepens the effect of
Jessner’s solution. The erythema becomes established and
the frosting tends to spread over a wide area, sometimes
over the whole of the treated area. Flaking is more pro-
nounced, and the skin is brownish and comes away in long
strips. This can last for approximately 10 days. Downtime is
common at this depth, even if there is rarely any scabbing.
Postpeel Care
The skin still feels tight and dry, but it should not be hydrated.
When flaking has finished, the patient can wear makeup and
should use effective sun protection. The patient must not help
the flaking along at the risk of causing erythema and pigmen-
tary changes.
Jessner’s as a Preparation for a TCA Peel
Jessner’s solution can be used as a preparation for a deeper peel.
Monheit Technique
The skin is prepared and cleaned in the usual manner. The
Jessner’s solution is applied to level 1: erythema occurs, along
with some localized pinpoint frosting at most. Five minutes
should be left between each coat. The last coat is left to dry,
and then TCA is applied—this will penetrate more quickly and
more evenly20 because of the breakdown in the epidermal bar-
rier function. It will also be more painful. This technique could
be used on patients with thick and oily skin when better TCA
penetration is needed.
Jessner’s as a Preparation for an AHA Peel
A Jessner’s peel would improve and even out AHA penetration
through the skin.
Moy Technique
The skin is prepared and cleaned in the usual manner. Jessner’s
solution is applied to level 1. The last coat is left to dry for 5
minutes, and then glycolic acid is applied until the erythema
spreads. This is followed by neutralization. Because of the
erythema already caused by Jessner’s solution, it is difficult to
judge the progress of the AHA peel, and it is common for it to
penetrate too deeply, causing unexpected frosting. This more
delicate technique should only be used for treating patients
with very thick and oily skin that can tolerate high concentra-
tions of AHAs being left on the skin for long periods before
neutralization.
Jessner’s for the Neck and Décolletage
Jessner’s solution is applied in the usual manner, but at a rate of
one peel every 2–4 weeks. Under no circumstances should the
patient help the skin to flake, which could leave depigmented
or hyperpigmented patches.
Jessner’s for Keratoses
To treat actinic keratoses with Jessner’s solution, the skin is
first degreased carefully with acetone. Jessner’s solution is then
applied once a week for approximately 8 weeks. This treat-
ment is not very effective, however, as no more than 15% of the
actinic lesions disappear.

Resorcinol: Unna’s paste/Jessner’s solution      211
TOXICITY AND SIDE EFFECTS
J. Andeer tested the toxicity of resorcinol at the end of the 19th
century.6 He consumed gradually increasing doses of resor-
cinol and made objective and careful notes of the sensations
he felt and the symptoms he developed. In this way, he tested
a daily intake of 1 g of resorcinol and gradually increased the
doses until he was taking 10 g of resorcinol in 15 minutes. This
triggered auditory, visual, muscular, and proprioceptive symp-
toms, then convulsions with breathing difficulties and muscle
contractions. He was fortunate enough to be able to report that
all these phenomena disappeared after 5 hours of “resorcinol
agony.” History does not tell us if he repeated the experiment to
evaluate its reproducibility, but we know that other colleagues
have tried the same kind of experiment with resorcinol and
many other toxic agents as well.
Although it belongs to the phenol group of chemicals,
resorcinol has very different exfoliating properties and is far
less toxic than phenol itself. The routes of metabolic detoxifi-
cation are mainly via the liver and kidneys. As a precaution,
patients with liver or kidney deficiencies should be ruled out
for treatment with resorcinol, as should patients with arrhyth-
mia and women who are pregnant or breast-feeding.
Toxicity
Resorcinol is toxic by ingestion of an average dose of 6  g.
Serious accidents have been described after ingestion of 3.5 g,
however.6 It irritates the mucous membranes and the skin, and
ingestion can cause methemoglobinemia, cyanosis, convul-
sions, or even death. Cases of methemoglobinemia have been
described after application on leg ulcers but not after a peel on
normal skin.
The problem raised with the use of Jessner’s solution is
more the fear of salicylism than the toxicity of the resorcinol
itself. Cases of salicylism have been described after application
of Jessner’s solution to the face, chest, arms, and legs.17
The size of the surface area treated, the patient’s body
weight, and the patient’s degree of hydration are all key fac-
tors. The risk of toxicity increases with the surface area treated.
There is a greater risk in patients with low body weight and
patients who are not well hydrated.
Secondary Hypothyroidism
Thyroid injury after chronic skin application of resorcinol has
been reported several times. In 1977, Katin and colleagues21
published a case of hypothyroidism following regular applica-
tion of a 2% resorcinol cream in a chronic dialysis patient suf-
fering from pruritus. The mechanism of action seems to be as
follows: the presence of a hydroxy group in the meta position in
the resorcinol would block the metabolism of iodine by inhib-
iting the peroxidase needed to oxidize iodide into iodine, the
only form that can be assimilated by the body.
Allergies
Unna’s Paste
Allergies to resorcinol have been widely described. It is there-
fore wise to do a skin sensitivity test behind the patient’s ear 8
days before a resorcinol peel. Any contact with resorcinol can
sensitize the patient (or the physician) to it, so the test must be
repeated before each peel. The fact that the first peel does not
trigger an allergic reaction is no guarantee that the next peel
will not trigger one. Allergy to resorcinol is permanent—there
is no point trying again.
In the allergy test, a small quantity of Unna’s paste is
applied to a patch of skin 2 cm × 2 cm behind the ear and left
for 15 minutes. The test is read immediately and then again 48
hours and 5 days later—although Letessier3 recommends just
one reading, after 4 days.
It is important not to confuse an allergy with the skin’s
natural response to the chemical peel applied behind the ear.
A highly localized and normal skin reaction to the peel will
occur: erythema followed by flaking. The appearance of any
blistering or pruritus contraindicates any further contact with
resorcinol completely and definitively. If a patient is allergic,
Unna’s paste causes reversible facial eczema, with no cosmetic
benefit.
Jessner’s Solution
The allergy rate to resorcinol is less than 0.1%.17
Hyperpigmentation
Pigmentation disorders are relatively common after a resor-
cinol peel. Effective sun protection (see Chapter 3) must be used
for 1–3 months after the peel.
The people most prone to pigmentary changes are those
who had pigmentation problems before the peel, those who
take oral contraceptives or are on hormone therapy, and those
who have a record of posttraumatic or PIH or have a high den-
sity of melanosomes (phototypes IV–VI).
Potential problems with pigmentary changes are treated
in the usual manner, as described in Chapter 37. Pigmentation
problems such as ochronosis after a resorcinol peel, also
described in the literature, are more complicated to treat.
Prolonged Erythema
A few areas of mild erythema, which changes color with the
cold, alcohol, or emotion, can very occasionally last for several
weeks. Erythema after a resorcinol peel is usually reversible
without treatment but requires preventive treatment against
pigmentary changes, especially in high-risk patients (see the
preceding paragraph and Chapter 37).
Dizziness and Nausea
Dizziness and nausea can occur during or after application of
the paste. Some authors attribute these symptoms to peripheral
vasodilation and the resulting low blood pressure. This expla-
nation is not satisfactory, however, as facial vasodilation is in
no way correlated with low blood pressure. Other facial peels
produce at least the same degree of vasodilation without caus-
ing low blood pressure or faintness. Furthermore, there would
have to be a great deal of peripheral vasodilation to make blood
pressure so low that a patient in the lying position can feel it.
Blood pressure readings taken after a peel are not low enough
to explain this “dizziness.”
It appears instead that the dizziness and nausea
are symptoms of the beginnings of resorcinol poisoning.
Fortunately, the symptoms soon resolve. Because resorcinol is
a phenol compound, using Unna’s paste and Jessner’s solution
on large areas can theoretically lead to typical phenol compli-
cations. Although resorcinol is usually 40 times less toxic than
phenol itself, 100 g of Unna’s paste contains 40 g of resorcinol.
That is the toxic equivalent of 1 g of phenol. The precautions of
slow application (in 1 hour) that are taken with phenol are not
observed for resorcinol and, with resorcinol, the area treated is
often larger. Resorcinol is a small molecule that, like phenol, is

212      Textbook of Chemical Peels
easily absorbed by the capillaries. Rapid application of a thick
and warm layer of resorcinol can introduce a relatively large
quantity of the substance into the bloodstream and trigger the
start of neurological toxicity typical of phenol compounds. As
a result, the face can be treated in perfect safety, but when large
areas are being treated, as is the case with a peel on the back, it
is essential that the treatment consist of several separate peels.9
Arouette9 reports an unpublished clinical case of an extensive
application of Unna’s paste bringing on coma in a few hours
with full recovery.
Secondary Infections
A recurrence of herpes lesions should be anticipated, and pre-
ventive treatment should be taken if necessary. Scratch lesions22
can trigger impetigo on the face. Scratching is the only expla-
nation for signs of infection after a peel with Unna’s paste or
Jessner’s solution.
Scarring
As with any superficial peel, under normal conditions the risk
of developing scars is very low. Nevertheless, scabs and dry
skin should not be pulled off.
Inadequate Results
If the results are considered inadequate, the patient might ben-
efit from additional peels. A maintenance resorcinol peel can
be done every year, if indicated. According to Unna (quoted by
Arouette9), “under some circumstances, it is necessary to do
several successive exfoliations that can be performed without
interruption.”
NOTES

1. For comparison with phenol, see Chapters 25 and 26.

2. Fintsi Y. Exoderm-lift – liquid formula. 1996.

3. Lettessier S. Chemical Peel with Resorcin. In: Roenigk RK,
Roenigk HH (Eds.). Dermatologic Surgery, Principles and Practice.
2nd ed. Oxford, UK: Marcel Dekker, 1999: 1115–19.

4. Collins PS. Chemical Face Peelings. In: Evaluation and Treatment
of the Aging Face. Springer, 1995: 34–67.

5. Terpenes are a class of compounds whose chemical structures
are based on a number of “isoprene units” derived from the
hydrocarbon CH2 = C(CH3)–CH = CH2; they may themselves
be hydrocarbons but also may contain alcohol (OH), aldehyde/
ketone (CO), and carboxylic acid (COOH) groups. Monoterpenes
are C10 compounds derived from two isoprene units, sesquiter-
penes (C15) are derived from three isoprene units, diterpenes (C20)
from four, and tritepenes (C30) from six. Terpenes are widespread
in plants, where they are largely responsible for the odor, and
they are the major constituents of plant-derived “essential oils.”
Among the best known terpenes are R-pinene (turpentine), cam-
phor, menthol, and citronellal (all monoterpenes), and farnesol (a
sesquiterpene that is a constituent of the essential oils of many
plants). Certain terpenes have important biological roles: vita-
min A, for example, is a diterpene, and steroid hormones have
a structure related to triterpenes (and are biosynthesized by a
similar route).

6. Manquat A. Traité Élementaire de Thérapeutique de Matière Médicale
et de Pharmacologie. 5th ed., tome 1. 1903: 240–60.

7. Kaolin (like ceyssatite) has absorbent properties that allow it to
trap microorganisms.

8. Note the distinction between benzoic acid (C6H5COOH), in
which a carboxylic acid group is attached to the benzene rign,
and phenol (C6H5OH), in which the substituent on the benzene
ring is a hydroxy group.

9. Arouette J. Dermabrasion, Relèvements, Peelings. In: Blackwell
A. (Ed.). Collection des Manuels Pratiques de Médecine Esthétique.
1989, Paris.
10. Quillaja bark is a natural soap containing 9%–10% saponins that
is used in phytotherapy for dandruff, athlete’s foot, and irritated
or sensitive skins.
11. Used alone, a resorcinol peel at 5% triggers light exfoliation. The
real peeling effect starts at 25% and becomes more obvious at 40%.
12. Dr. Eller and his assistant Shirley Wolf described this formula in
New York in 1941.
13. Salicylic acid (3%–5%) triggers light exfoliation. A concentration
of 15% is needed for a superficial peel. A concentration of 50%
(beware of salicylism) produces a dermal peel.
14. Such weak concentrations of lactic acid are ineffective in them-
selves but may enhance penetration of the other ingredients.
15. Max Jessner qualified as a dermatologist in Germany in 1922.
At New York University Hospital in the 1950s, he developed
the solution for the treatment of acne that bears his name. Dr.
Jessner’s aim was to improve the performance of peels while
reducing the risk of side effects, by exploiting the synergy
between the different ingredients.
16. Dr. F. C. Combes made wide use of Jessner’s formula in the 1960s
and is better known in the United States.
17. Rubin MG. Manual of Chemical Peels, Superficial and Medium Depth.
Philadelphia: JB Lippincott, 1995.
18. Frosting is reached more quickly with a brush than with a
double cotton bud, unless greater pressure is applied. Brushes
should be used once only or disinfected with povidone–iodine.
Single-use brushes are preferable: would you like to treat
your skin with a brush that has already been used on acres of
unknown skin?
19. Trauchessec JM. Teoria y practica de los peelings. Med Estet. 1996;
40: 11–21.
20. This would not be the case with AHAs before a TCA peel
(Coleman technique). AHAs do not penetrate evenly and might
cause the TCA to penetrate still more unevenly.
21. Katin MJ, Teehan BP, Sigler MH, Schleifer CR, Gilgore GS.
Resorcinol induced hypothyroidism in a patient on chronic
hemodialysis. Annals of Internal Medicine. 1977; 86(4): 447–9.
22. And overenthusiastic personal hygiene—for example, using a
sponge such as a Buf Puf, nonprescribed cosmetic scrubs, a face
cloth (which is a breeding ground for microbes), etc.

25
Phenol
Chemistry, formulations, and adjuvants
CHEMISTRY OF PHENOL
As a class, phenols are compounds in which a hydroxy group
is attached to a benzene ring. The name phenol also is used
to refer specifically to the simplest compound in this group,
which is also known as hydroxybenzene, benzenol, or carbolic
acid (Figure 25.1).1 Phenol has a molecular weight of 94.11, a spe-
cific gravity of 1.071, and a boiling point of 182°C. It can react
vigorously or even violently with other compounds, including
formaldehyde, acetaldehyde, and trifluroacetic acid, as well as
aluminum chloride, nitrobenzene, some nitrates and nitrites,
and other oxidizing agents. Phenol crystals are white or pink,
and melt at 41°C. Most commercial phenol has a purity of 98%,
but 100% pure phenol is obtainable.2
Phenol was formerly obtained from coal tar but is now
made by hydrolyzing chlorobenzene at 350°C or, more frequently,
by air oxidation of cumene3 and treatment of the resulting
cumene hydroperoxide to yield phenol and acetone (Figure 25.2).
Estimates of the amount of phenol produced worldwide vary, but
since 1980 more than 5,000,000 tons have been produced.
Phenols may have more than one hydroxy group
attached to the same benzene ring—for example, the three iso-
meric4 dihydroxybenzenes catechol (ortho-dihydroxybenzene
or 1,2-benzenediol), resorcinol (meta-dihydroxybenzene or
1,3-benzenediol), and hydroquinone (para-dihydroxybenzene
or 1,4-benzenediol); see Figure 25.3.
Molecules that have a single benzene ring with one or
more hydroxy substituents are known as “simple phenols.”
Examples are phenol itself and the three dihydroxybenzenes
mentioned in the previous paragraph, as well as the cresols
(discussed later). There are also “diphenols” (Figure 25.4) and
polyphenols. Polyphenols are complex molecules containing
several benzene rings with one or more hydroxy substituents.
They are widespread in nature, often lending plants their
color. Polyphenols (flavonoids and anthocyanins) constitute an
important group of antioxidants used in antiaging medications;
flavonoids (Figure 25.5) are a distinctive group of polyphenols
with a specific structure, containing two benzene rings, one of
which is fused to an oxygen-containing ring.
PHENOL DERIVATIVES
Medicine has made wide use of phenols in many indications,
as we shall see later in this book. Medical publications on peels
abound in terms that are no longer in use and names of out-
dated molecules, which makes some texts difficult to read.
It is therefore worthwhile to briefly review these terms and
compounds.
Cresols—Lysol
Cresols are simple phenols in which the benzene ring has one
methyl and one hydroxy substituent. There are three isomers:
ortho-, meta-, and para-cresol5 (Figure 25.6). Coal tar cresol or
cresylol is a mixture of the three isomers and is also called
cresylic acid, hydroxytoluene, or methylphenol. Coal tar and
cade oil are mixtures of cresol and guaiacol (see later dis-
cussion). Lysol is the trade name of a solution of cresols in
saponified vegetable oil, developed to counter the difficulties
of putting cresol in solution form. It was an alkaline deter-
gent containing 47%–50% crysylol (= cresol = cresylic acid =
cresylic phenol) as well as a little guaiacol, xylol, and other
ingredients. Chemically, therefore, it was a poorly defined
solution that nevertheless had the advantage of providing a
clear solution when mixed with distilled water. Crude cresol
comes from coal tar and consists of the three isomers: ortho-
cresol 35%–40%, meta-cresol 35%–40%, and para-cresol about
25%. Cresol mixtures are used as preservatives, deodorants,
and disinfectants. Ortho-cresol is a solvent and disinfectant.
Meta-cresol is mainly used in insecticide chemistry or to pro-
duce antioxidants. Para-cresol is mostly used in perfumery.
Many foods contain cresols: butter, wine, tomatoes, asparagus,
cheeses, bacon, and smoked foods. Cresol is four times as toxic
as phenol.
Cresol mixtures are irritating to the respiratory tract and
the skin. Although only anecdotal information is available on
the potentially carcinogenic effects of cresols in humans, the
US Environmental Protection Agency has classified these mol-
ecules as “possible human carcinogens.” Signs of intoxication
include abdominal pain and vomiting. Other symptoms have
also been described, such as heart, liver, and kidney problems.
Facial paralysis, coma, and death are also possible with higher
concentrations, even through simple skin contact.
Guaiacol
Guaiacol (Figure  25.7) is also called o-methoxyphenol,
1-hydroxy-2-methoxybenzene, or catechol methyl ether. It is
found in Valda lozenges and expectorants, and is also used to
make vanillin. It was originally extracted from a tree (Acacia
catechu Willd) and then distilled from guaiac resin. Nowadays,
pure guaiacol is synthesized from catechol, of which it is the
methyl ether. Guaiacol salicylate has analgesic and anti-inflam-
matory properties. Its analgesic properties are due to the inhi-
bition of cyclooxygenase and prostaglandin synthesis and the
release of bradykinin. Guaiacol salicylate is anti-inflammatory
as it stabilizes the lysosomal membrane and inhibits the action
of the chemical mediators of inflammation.
Halogenated Phenols
Halogenated phenols are more powerful disinfectants than
simple phenols, as they are more lipophilic. They are also more
toxic to the central nervous system. The chlorinated phenols are
the most active. Toxicity is specific to each compound.

214      Textbook of Chemical Peels
Phenolic Acids
Phenol acids are phenols in which there is also a carboxylic
acid group attached to the benzene ring. They include salicylic
acid (ortho-hydroxybenzoic acid) and para-hydroxybenzoic acid
(Figure 25.8). Acetylsalicylic acid (aspirin) and sodium salicy-
late are derivatives of salicylic acid. Like phenol, they have
OH
Figure 25.1  Chemical structure of phenol.
CH
CH3
CH3
CH3
CH3
OOH
(b)
(a)
Figure 25.2  Chemical structure of (a) cumene and (b) cumene
hydroperoxide.
OH
OH
OH
OH
OH
OH
(a)
(b)
(c)
Figure 25.3  Chemical structures of (a) catechol, (b) resorcinol,
and (c) hydroquinone.
OH
OH
Figure 25.4  An example of a diphenol: 2,3’-dihydroxybiphenyl.
OH
OH
OH
OH
HO
O
Figure 25.5  An example of a polyphenol: the flavonoid catechin.
OH
CH3
OH
CH3
OH
CH3
(a)
(b)
(c)
Figure 25.6  Chemical structures of (a) ortho-cresol, (b) meta-
cresol, and (c) para-cresol.
OH
OCH3
Figure 25.7  Chemical structure of guaiacol.
C
OH
O
OH
C
O
OH
OH
(b)
(a)
Figure 25.8  Chemical structures of (a) salicylic acid and (b) para-
hydroxybenzoic acid.

Phenol: Chemistry, formulations, and adjuvants      215
antipyretic and analgesic properties. The methyl, ethyl, and
propyl esters of para-hydroxybenzoic acid (parabens) are used
as preservatives in pharmaceuticals, cosmetics, and foodstuffs.
Bisphenols
Bisphenols (not to be confused with the diphenols), are formed
by two phenols linked with a bridge (–CH2–, –O– or –S–) in
the ortho position, which makes the product easier to tolerate.
Bisphenols are often chlorinated to increase their disinfectant
power. Dichlorophene, tetrachlorophene, and hexachlorophene
(Figure 25.9) are members of this group of compounds. Septisol
is a hexachlorophene soap used widely as a wetting agent in
old phenol peel formulations.
Picric Acid
Picric acid (Figure 25.10) is 2,4,6-trinitrophenol. It is used in the
treatment of burns in a 1% solution because of its stimulating
effect on keratogenesis. The dry crystals are extremely sensi-
tive to friction or shock6 and were widely used as an explosive
before the discovery of TNT (trinitrotoluene). Picric acid can
be synthesized from phenol, benzene, or aspirin. It is soluble
in water and alcohol. It turns the skin yellow. Applying swabs
with 1.2% picric acid is not irritating to the skin but produces
light flaking within 2–4 days. Using picric acid on open wounds
and ulcers appears to stimulate epidermal regeneration.
Acetaminophen
Acetaminophen (known as paracetamol in the United
Kingdom) is N-acetyl-para-aminophenol (Figure  25.11). It has
the same detoxification pathways as phenol and also carries the
risk of inducing methemoglobinemia. To be on the safe side, it
should not be used as an intravenous analgesic during a full-
face phenol peel, so as not to saturate the detoxification path-
ways. Paracetamol is also an intermediate in the pathway for
detoxification of aniline derivatives, before hepatic glucuronide
and sulfate conjugation allow them to be eliminated in urine.
The aniline derivatives acetanilide and phenacetin were once
used as analgesics and antipyretic agents but turned out to be
excessively toxic; they were replaced by acetaminophen, which
had been shown in 1949 to be their major metabolite.
DIFFERENT FORMULATIONS OF PHENOL PEELS
Peels of the Past
Reviewing publications on phenol peels reveals many different
formulations. The first surgical operation in which phenol was
used as a disinfectant took place in March 1865 (Lord Lister,
1827–1912). At the very beginning of the 20th century, Manquat’s
treatise on pharmacology7 described in detail the use of phenol
as an anesthetic and disinfectant, at concentrations of approxi-
mately 5% in aqueous, oil, or alcohol solutions. Preparation
involved the use of various ingenious tricks to prevent the
solutions from separating into multiple layers and to prevent
the formation of isolated caustic droplets. After a relative lull,
other formulations started to appear in medical publications.
They reflect the constant search for the ideal solution and the
increasingly clear understanding of the mechanisms that lie
behind the excellent results achieved with today’s phenol peels.
From this mass of publications, the author has selected 13 major
authors or groups of authors whose formulas will be surveyed
in alphabetical order.
1.
Ahronson presented a glycerinated phenol formulation:
88% liquid phenol is solubilized in anhydrous glycerol
(glycerin) and a few drops of alcohol. This highly concen-
trated formula, used without occlusion, produces a peel
that is not as deep as a peel with Baker–Gordon solution.
2.
Ayres achieved a medium-depth peel by combining phenol
and trichloroacetic acid (TCA). These two formulas are no
longer used today, as there are many other modern peel
solutions that provide effective medium-depth peels using
other molecules, such as TCA, that are not potentially toxic.
3.
Two Baker solutions are described. The first contains liquid
phenol USP 5 cm3, distilled water 4 cm3, croton oil 3 drops,
and septisol 5 drops. The second contains liquid phenol
USP 3 cm3, distilled water 2 cm3, croton oil 3 drops, and
septisol 8 drops. The water determines the concentration,
which is variable. Baker’s solution has to be stirred con-
stantly, as it is not stable and separates into layers if left to
rest.
4.
Brown and Kaplan presented a more complex solution of
phenol (at varying concentrations between 60% and 95%)
CH2
CI
CI
CI
CI
CI
CI
OH
HO
Figure 25.9  Chemical structure of hexachlorophene.
OH
NO2
NO2
O2N
Figure 25.10  Chemical structure of picric acid.
OH
HN.CO.CH3
Figure 25.11  Chemical structure of paracetamol (acetaminophen).

216      Textbook of Chemical Peels
mixed with saponified cresol in oil at concentrations of
up to 10%. The application technique included a patch
test behind the ear. This test made it possible to assess the
necrotic effect of the solution on the patient. If the necrosis
was too severe, the test was repeated with increasing con-
centrations of oil until the right solution for the patient was
found. They recommended applying the solution area by
area, leaving 2 hours between applications. The peel took 2
days to complete.
5.
Combes, Sperber, and Reisch used an aqueous solution with
a high concentration of phenol, combined with citric acid
and sodium salicylate.
6.
Eller and Wolff, on the other hand, advocated an alcohol
solution with a much lower concentration, around 25%,
with salicylic acid. This was also applied in several stages
(four at the most), with 1 or 2 hours between each applica-
tion depending on how sensitive the skin was.
7.
Grade’s three formulas (aqueous phenol with croton oil),
which had widely varying amounts of phenol and water,
had to be left to rest for 6 weeks before use. This resting time
was needed for “peroxides” to form and buffer the solution.
8.
Klein presented a solution that was largely based on
Baker’s, but with different concentrations.
9.
Karp’s three formulas are well known: the first was almost
80% glycerinated phenol; the second combined phenol with
acetic acid, boric acid, salicylic acid and citric acid, but could
only be applied locally, as it was too strong. Karp called his
third formula “the phoenix”: it was an aqueous solution of
glycerinated phenol combined with acetic acid and sodium
salicylate.
10. Litton proposed using a detergent other than septisol and
recommended using glycerol. He was one of the first to
describe an increase in the thickness of the Grenz zone
after a phenol peel.
11. Litton’s solution, as well as that of Truppman and Maschek,
had the dual advantage over Baker’s of being stable in
space and time. These aqueous and glycerinated solu-
tions with concentrations of approximately 50% in phenol
contained croton oil. Once prepared, they could be kept
for several years when stored away from light and heat
sources. Litton’s solution contains more croton oil than that
of Truppman and Maschek.
12. Urkov used a simple alcohol solution of phenol and treated
deep wrinkles with electrocoagulation after the peel.8 He
then applied an occlusive dressing for up to 3 days. His
postpeel treatment was based on the “dry technique.”
13. Verner Kellson’s aqueous solution uses two types of phenol:
Lysol (an oil solution of cresol) and phenol with various
oils, including croton oil. The water has to be distilled, as
Lysol forms calcium cresate when mixed with tap water.
The solution then becomes opalescent instead of clear.
Peels of Today
Exoderm
The author’s late friend, Yoram Fintsi, deserves special men-
tion in this book, because he was one of the main catalysts for
the current success of phenol peels, thanks to the formula he
developed, Exoderm. According to Fintsi, the Exoderm formula
was made in 1986 and then refined in 1990. Thereafter, Fintsi
in Israel and Benhamou in France improved the formulation.
Several formulations were put forward, one after the other, as
shown in Table 25.1. The elements in common are listed above
the dashed line. The first two formulas used septisol, a disin-
fectant soap with hexachlorophene, while the third formula—
the one used today—simply contains saponins. The first
formula contains TCA, the second salicylic acid, and the third
citric acid. The last two formulas are buffered to stabilize the
pH. Fintsi commented on his own current Exoderm formula in
his article “Exoderm, a Novel, Phenol-Based Peeling Method
Resulting in Improved Safety.”9
Hetter Formulas
In 1996, Hetter put forward a series of formulations based on
the principle that by simply changing the concentration of cro-
ton oil, the depth of the peel could be varied (Table 25.2).
Changing the concentration of croton oil is, indeed, one
way of changing the strength of a phenol peel. It is not, however,
the only way, and it is perfectly possible to do a phenol peel
without croton oil. It is also possible to vary the depth of action
of phenol without changing the concentration in croton oil. It
is not, of course, a matter of questioning the intense cytotoxic
effect of croton oil (see the section on adjuvants later in this
chapter), as Hetter10 stresses in 2000. Nor is it a matter of ques-
tioning Hetter’s legitimate refutation of the dogmas that claim,
on the one hand, that lower concentrations of phenol wound
more deeply (a lower concentration of phenol can penetrate
Table 25.2  Hetter Formulas
Very light peel
Medium light peel
Medium heavy peel
Heavy peel
4 cm3 88% phenol
4 cm3 88% phenol
4 cm3 88% phenol
4 cm3 88% phenol
6 cm3 water
6 cm3 water
6 cm3 water
6 cm3 water
16 drops septisol
16 drops septisol
16 drops septisol
16 drops septisol
1 drop croton oil
1 drop croton oil
2 drops croton oil
3 drops croton oil
Take 3 cm3 of the above mixture
and add 2 cm3 88% phenol and
5 cm3 water
Table 25.1  Exoderm Formulas
Formula 1a
Formula 2
Formula 311
Liquid phenol
Liquid phenol
Liquid phenol
Phenol crystals
Phenol crystals
Phenol crystals
Distilled water
Distilled water
Distilled water
Alcohol
Alcohol
Alcohol
Olive oil
Olive oil
Olive oil
Sesame oil
Sesame oil
Sesame oil
Glycerol
Glycerol
Glycerol
Croton oil
Croton oil
Croton oil
Resorcinol
Resorcinol
Resorcinol
Septisol
Septisol
Saponins
TCA 30%
Salicylic acid
Citric acid
Buffers
Buffers
a Formulation certificate with bottles of Exoderm.

Phenol: Chemistry, formulations, and adjuvants      217
more rapidly11 through an epidermis that is made more per-
meable by protein lysis and can therefore be more toxic) and,
on the other hand, that phenol has an “all-or-nothing” action,
which is clearly untrue as also said by Dr. Hetter. Attempts are
currently being made to market “completely nontoxic” phenol
peels. However, the phenol molecule is clearly defined, and so
is its toxicity, as we shall see later. A “phenol” peel that is called
“nontoxic” cannot, by definition, contain phenol.
Lip & Eyelid Formula
Lip & Eyelid Formula is a phenol peel that the author first devel-
oped to increase dermatological safety and to achieve results
without any occlusion on the sensitive skin of the eyelids. The
same solution was then applied to the wrinkles around the
mouth and then to the whole face, but with 24 hours’ occlusion
in these two indications. It is an oil solution of phenol at more
than 60%. Four different oils are used in the various stages of
the product’s preparation. The aim of the oily formulation is
to slow down the penetration of the phenol through the skin
and to improve dermal and epidermal maceration. It limits the
toxicity of phenol by saturating the biochemical hepatic detoxi-
fication pathways more slowly.
Split-face treatment comparing Exoderm and Lip & Eyelid
Formula showed a higher efficacy of the latter.
STORING PHENOL PEEL SOLUTIONS
Pure phenol is resistant to light, but the presence of impurities,
even in small traces, turns it red due to oxygen fixation. This col-
oring does not change the properties of the product. Exoderm
solution must be stored away from light12 and humidity, how-
ever. It can be stored for 3 years in its original, unopened bottle.
The contents of an opened bottle must be used within 1 year.
Baker’s solution must be prepared for immediate use, unlike
Litton’s solution, which can be kept for 3 years in the refrigera-
tor. Medical publications report using the same solution suc-
cessfully over many years. Lip & Eyelid Formula also remains
stable for at least 3 years if kept in the refrigerator in the origi-
nal, closed bottle.
ADJUVANTS OF PHENOL PEELS
General Remarks
Solutions with a high concentration of phenol cause rapid pro-
tein coagulation, which translates clinically into immediate
frosting of the skin. This opaque coagulation acts as a shield
that increases the skin’s impermeability, stops the surface phe-
nol from penetrating, and prevents it from passing rapidly into
the reticular dermis. A solution with a concentration higher
than 80% therefore produces a more superficial peel than might
be logically expected. Solutions with lower concentrations, of
15%–20% for example, are keratolytic and penetrate the skin
more easily to a depth where they are picked up by the drainage
routes of the skin. The phenol is transferred rapidly for metabo-
lization. A small quantity of free phenol, which can only act on
the dermis for a short space of time, does not make for excellent
results. If larger quantities of these low concentration solutions
are applied to the skin in an attempt to get around this problem,
the increased rate of reabsorption of phenol could saturate the
detoxification pathways and the risk of intoxication is higher. At
both higher and lower concentrations, effectiveness is blocked
and adjuvants are needed to make it more effective.
Everything that surrounds the phenol molecule, from pre-
peel treatments to formulation methods, can be considered an
“adjuvant.” Unlike superficial or medium peels, preparing the
skin before a phenol peel is not intended to enhance or even out
the penetration of the phenol, as it does not need help to pene-
trate the skin. Tretinoin or fruit acids are not necessary in prepeel
preparation, and perfect results are achievable without using
them. Small, benign tumors can be treated with electrocoagu-
lation immediately before the peel. Urkov, for his part, treated
deep wrinkles with electrocoagulation after applying phenol
and before applying the occlusive dressing. The skin must be
cleansed and degreased thoroughly to get rid of any epidermal
lipids and debris that can interact with or partially inactivate
the phenol. Prepeel and postpeel care, which are discussed in
detail in Chapters 32 and 35, help to prevent or treat potential
complications. Adjuvants can, for example, enhance the spread
of the phenol within the epidermis, reduce skin surface tension,
enhance liquefaction necrosis of the epidermis, help the phenol
reach the dermis (where it causes a severe inflammatory reaction
that generates collagen and elastin, and blocks its action in the
upper reticular dermis), and slow down and/or reduce the capil-
lary absorption of the phenol (thus allowing time for sulfate and
glucuronide conjugation of the toxin before its elimination).
Different Chemical Adjuvants
The peel solutions should never be prepared simply by dissolv-
ing phenol in one of its potential solvents. Since phenol was
introduced into treatment, doctors who use it have tried to:
•
Moderate (tame) its systemic toxicity. Different substances
have been combined with phenol to reduce its adverse
effects. It should be noted that the only demonstrated way
to avoid cardiac toxicity lies in the application technique
for a full-face phenol peel.
•
Improve its effectiveness. Different chemical adjuvants have
been combined to modify the action of phenol.
The application technique and prepeel and postpeel care
have very important roles. The latest formulations are therefore
tamed and adjuvanted.
The qualitative formulas of recent products are known,
but the percentages and preparation methods are not revealed.
Fintsi explained that adjuvanted and tamed phenol peels must
be prepared according to a precise method and that he was
afraid that if he revealed the exact proportions of the ingre-
dients, doctors would try to make up the formula themselves
without keeping to the necessarily strict order of preparation,
and that this could lead to disastrous results.
Logic must prevail in the attempt to understand how
adjuvants work: it should be remembered that phenol has an
anesthetizing action on sensitive nerve endings through pro-
tein coagulation; this anesthetizing effect develops within
10–15 seconds after application. This means that 15 seconds
after application, the phenol is already in the dermis: it is there-
fore doubtful that combining it with products that penetrate
more slowly, such as salicylic acid or citric acid, can improve the
already rapid penetration of phenol. On the other hand, there
is no doubt that phenol improves the penetration of these adju-
vants, if they can survive without reacting chemically with the
phenol solution itself.
Resorcinol
See Chapter 24 for more details. Although resorcinol is known
to have allergenic properties, no allergies have been reported

218      Textbook of Chemical Peels
when it has been used in small quantities with phenol. However,
the combined use of these two substances in the same peel solu-
tion does not appear to have any clinical value, as the phenol
will have finished working before the resorcinol has started.
Resorcinol cannot therefore modify the effect of phenol. No
data are available on the potential clinical effect of resorcinol
on skin that has just been coagulated by phenol.
Trichloroacetic Acid
TCA is an acid whose strength of action is proportional to
the concentration used. However, it also depends on numer-
ous other factors that are described in detail in the chapters
on TCA.
Salicylic Acid
Salicylic acid is a keratolytic agent that dissolves the amorphous
intercorneocyte matrix and thus diminishes the barrier func-
tion of the stratum corneum. It is sometimes combined with
phenol but does not improve its action. See also the comments
on resorcinol and TCA above.
Croton Oil
Croton oil is extracted from the seeds of the shrub Croton tig-
lium, of the family Euphorbiaceae. In the past, these seeds were
also called Moluccas seeds, Tilly seeds, or small Indian pine
nuts.
Rubbing 2–10 drops of pure croton oil or croton oil
with olive oil on the skin causes an intense burning sensation
within 5 minutes that lasts for several hours and is followed
by erythema. Clusters of small blisters then form and turn into
pustules that dry, scab, and fall off within a few days without
leaving any scars. If, however, the croton is applied too vigor-
ously, keloid scars may result.7
The crotonic acid (Figure 25.12)13 that it contains is an irri-
tant that accelerates epidermal lysis and enhances the cutane-
ous penetration of the phenol. Some authors maintain that a
phenol peel will only produce good results if croton oil is pres-
ent. The croton oil enhances dermal penetration and epidermal
protein coagulation, and thus lower concentrations of phenol
can be used. We have seen, however, that many phenol peel
formulations do not contain croton oil.
The irritant action of croton oil is used to advantage in can-
cer research to enhance the penetration of carcinogens through
the skin barrier. Croton oil is therefore a co-carcinogen. In 1994,
Wilmer et al.14 showed that keratinocytes can produce interleu-
kin (IL)-type substances, growth factors, and tumor necrosis
factor (TNF). Phenol and croton oil induce keratinocyte produc-
tion of IL-8 (at noncytotoxic concentrations), TNF-α and also a
growth factor. TNF-α is a cytokine synthesized (among others)
by the keratinocytes in the stratum spinosum and the stratum
granulosum. It stimulates the differentiation of keratinocytes
into corneocytes and thus accelerates the full regeneration of
the protective stratum corneum.
Amazonian Indians used croton extracts as a vulnerary15
agent. It appears that an alkaloid, taspine, is (partially) respon-
sible for the healing effect on wounds. Its mechanism of action
is probably due to the chemotaxy of the fibroblasts being stimu-
lated, which improves the efficiency of the first stages of heal-
ing without affecting the following stages.16
At the beginning of the 20th century, the vesicant prop-
erties of croton oil were used to good effect on people with
edema. Rubbing croton oil on large areas created numerous
vesicles, the combined serous fluids from which produced
enough liquid to relieve edema in the lower limbs of heart
patients. Experiments were conducted involving the ingestion
of croton oil: this produced intestinal inflammation with diar-
rhea and weight loss.17
Croton oil is a powerful toxin that taken orally in small
quantities of around 20 drops can cause fatal hemorrhagic
gastroenteritis.18
Septisol
Septisol is a liquid soap with hexachlorophene, a bisphenol
used as a disinfectant. It is also a surfactant. At low concentra-
tions, hexachlorophene uncouples the oxidative phosphoryla-
tion of cells and causes morphological changes in membranes.19
It might be keratolytic.20 Intoxication of infants from hexachlo-
rophene preparations (in France, in 1972) resulted in neuro-
logical (encephalitis) and cutaneous symptoms. These products
have turned out to be dangerous after chronic use if not rinsed
off or if applied to damaged skin or to large areas of the body
with an occlusive dressing.
Saponins
Liquid soap helps to reduce surface tension (Box 25.1) and there-
fore improves the penetration of active agents. It also improves
maceration under an occlusive dressing. Anionic and cationic
soaps, like alcohol, enhance the action of ­phenol.19 Formulation
requirements are strict. If there is too much ­surfactant, the phe-
nol ends up within a micelle and its action is reduced. If there is
not enough, the solutions are not stable.
Cresol—Lysol
In the past, saponified cresol as well as Lysol were used as
wetting agents to increase the penetration and therefore the
BOX 25.1  Surface Tension
The forces of attraction and repulsion are more or less evenly
distributed within a liquid. The surface molecules, however,
are unable to balance the lateral intermolecular forces of
attraction. The tension on the surface of a liquid acts like
an elastic membrane, opposing penetration in the liquid.
Agents called surfactants, wetting agents, or detergents
reduce this elastic surface tension and enhance penetration
in the liquid. Wetting agents also have antiseptic properties.
There are two large groups:

1. Cationic surfactants (cetrimide, lauralkonium, etc.):
Powerful bactericides and fungicides

2. Anionic surfactants (e.g., sodium lauryl sulfate):
Used to sterilize the skin before surgical operations
C
C
CH3
H
C
H
OH
O
Figure 25.12  Chemical structure of crotonic acid.

Phenol: Chemistry, formulations, and adjuvants      219
strength of phenol. See the discussion of cresols earlier in this
chapter.
Acetic Acid
For a description of acetic acid, see the beginning of Chapter 12.
Oil Formulations21 versus Aqueous Formulations
A cell membrane is a “fluid mosaic” of phospholipids in two lay-
ers. The hydrophilic poles face outward, and the hydrophobic
poles form the inside of the membrane. The lipid cell surface is
strewn with proteins. If we compare a cell membrane to a choc-
olate cream sandwich cookie, the hydrophilic poles would be
the cookies on the outside and the hydrophobic poles would be
the chocolate cream in the middle. The surface proteins would
be found in the small holes on the surface of the cookies. If we
compared a cell membrane to a jam sandwich, the hydrophilic
poles would be the slices of bread and the lipophilic, hydropho-
bic poles would be the jam. The surface proteins would be set in
the air bubbles in the bread.
At the beginning of the 20th century, the relative imper-
meability of cell membranes to many water-soluble components
had already been attributed to the lipid nature of the mem-
branes. Molecules that are soluble in nonpolar solvents (e.g.,
olive oil, sesame oil, and ether) enter cells more rapidly than
water-soluble molecules with the same molecular weight.22 Fat-
soluble molecules “dissolve” in the lipophilic layers and readily
penetrate the interior of the cell. The ratio of the solubility of a
substance in olive oil in relation to its solubility in water pro-
vides the oil/water partition coefficient.
Phenol has a good oil/water partition coefficient.19 The
ability of a molecule to penetrate the cell membrane is pro-
portional to its partition coefficient. Adding oils to phenol
enhances its action in the epidermis and papillary dermis and
slows down the penetration of the oil-bound phenol through
the skin so that it reaches the deeper dermal layers more slowly.
Phenol is also soluble in water and has a low molecular weight
(94.11). Very small molecules that are water-soluble and non-
polar pass through cell membranes much more quickly than
one might expect given the molecular structure of the actual
membrane and the partition coefficient. These small mole-
cules appear simply to pass between two adjacent molecules
in the membrane, without really dissolving in the pole taken
up by the fatty acid. It is also possible that the proteins set in
the membrane are highly permeable to these tiny water-solu-
ble molecules. With increasing molecular weight, membrane
permeability decreases and stops molecules with a molecular
weight greater than 200 from getting through. Phenol’s low
molecular weight and its high partition coefficient would allow
it to pass through the membrane rapidly if it were not bound
to oily components. Moreover, phenol coagulates membrane
proteins.
The vascular endothelium has two absorption pathways.
There are 4 nm pores that form the intercellular spaces. These
pores represent only 0.02% of the capillary surface. Diffusion is
the main pathway, and the principles set out above also apply
to the capillaries.
The antiseptic derivatives of phenol have structural mod-
ifications (halogenation and alkylation) that, by increasing their
liposolubility, improve their antiseptic action.
Brown and Kaplan made use of the “buffering” property
of oils in phenol solutions. Their formulation contained up to
95% phenol combined with oils. A patch test behind the ear
had to be conducted before the facial peel. If there was skin
necrosis, they reduced the strength of the phenol by gradually
adding oil in small quantities until the right dose was found
for the patient’s skin. To increase the strength of the mixture,
on the other hand, soap (saponified cresol) was added or the
concentration of phenol was increased.
Glycerol
Adding glycerin to phenol makes it less irritating. Glycerinated
phenol at 10% is no longer an irritant.
Buffers
Buffers keep the pH of a solution stable. Phenol is more aggres-
sive in an acid environment. The presence of buffers keeps the
solution at an appropriate pH. The pH of today’s phenol solu-
tions is usually close to the skin’s physiological pH.
Alcohol and Water
Alcohol is used at different points during preparation to help
products solubilize more efficiently in the aqueous solution.
Phenol, for example, is more soluble in alcohol than in water.
The purer the phenol crystals, the more soluble they are in
water. Alcohol also enhances the action of phenol.21 Water is
also used as a solvent for certain products or to modify the con-
centration of the phenol.
NOTES
1. In this book, phenol is used in this sense; the plural phenols refers
to the group of compounds in general.
2. Material Safety Data Sheet. Fisher Scientific, Waltham, MA.
3. Cumene (isopropylbenzene, 2-phenylpropane, cumol), molecular
weight 120.2, is a colorless liquid with a strong depressant effect
on the central nervous system.
4. Isomeric compounds (isomers) have the same empirical formulas
but different chemical structures.
5. Also known as ortho-methylphenol and ortho-hydroxytoluene, etc.
6. This is fortunately not the case with solutions.
7. Manquat A. Traité Élémentaire de Chérapeutique de Matière Médicale
et de Pharmacologie. 5th ed. 1903: 240–60.
8. Was this to make up for the inadequate results of this formulation?
9. American Journal of Cosmetic Surgery. 1997; 14: 49–54.
10. Hetter G. An examination of the phenol–croton oil peel: Part III.
The plastic surgeon’s role. Plastic and Reconstructive Surgery. 2000;
105: 725–63.
11. Quicker
penetration
is
not
synonymous
with
greater
effectiveness.
12. To limit the risks of photochemical reactions. Storing the solution
at low temperatures slows down the chemical reactions and is
the best way to store any chemical.
13. Crotonic acid is also known as 2-butenoic acid and has a molecu-
lar weight of 86.09.
14. Wilmer JL, Burleson FG, Kayama F, Kanno J, Luster MI. Cytokine
induction in human epidermal keratinocytes exposed to con-
tact irritants and its relation to chemical-induced inflamma-
tion in mouse skin. Journal of Investigative Dermatology. 1994; 102:
915–22.
15. Vulnerary means promoting the healing of wounds.
16. Porras-Reyes BH, Lewis WH, Roman J, Simchouritz L, Mustoe
TA. Enhancement of wound healing by the alkaloid taspine
defining mechanism of action. Proceedings of the Society for
Experimental Biology and Medicine. 1993; 203: 18–25.
17. Pol O, Ferrer I, Puty MM. Diarrhea associated with intestinal
inflammation increases the potency of mu and delta opioids

220      Textbook of Chemical Peels
and the inhibition of gastrointestinal transit in mice. Journal of
Pharmacology and Experimental Therapeutics. 1994; 270: 386–91.
18. Klein DR, Little JH. Laryngeal edema as a consequence of chemi-
cal peel. Annual Meeting of the American Society for Esthetic
Plastic Surgery, Las Vegas, 1982.
19. Giroud JP, Mathé G, Meyniel G. Pharmacologie Clinique. Expansion
Scientific Français, 2003: 1590–91.
20. Ashen S. Unoccluded Baker–Gordon phenol peels—Review and
update. Journal of Dermatologic Surgery and Oncology. 1989; 15:
998–1008.
21. See also Chapter 27.
22. Bene RM, Levy MN. Physiology. 3rd ed. Mosby Yearbook, Inc.,
1993.

26
Phenol
Properties and histology
MISCIBILITY WITH WATER
Phenol is not completely miscible with water; to obtain a homo-
geneous solution, an excess of water is required.1
NEUROLYSIS AND LOCAL ANESTHESIA
Phenol has been widely used to treat a large number of disor-
ders, including spasticity and chronic pain, because of its neu-
rolytic and local anesthetic properties (5% solution). Topically
applied, phenol has a lasting local anesthetic action that can
affect all the layers of the skin and occurs at the same time as
frosting (Box 26.1 and Figure 26.1). Phenol has been used as a
surface anesthetic to perform small operations. It is neurolytic;2
it coagulates the sensitive nerve endings at the base of the epi-
dermis and in the superficial papillary dermis. During a phe-
nol peel, the first application of acid causes an intense burning
pain that can be alleviated by prior or immediate application
of something cold. After frosting, the anesthetic effect takes
hold and spreads beyond the frosted area by up to a centime-
ter. During a phenol peel, after an initial period of analgesia,
patients complain of renewed pain that they all describe differ-
ently, however. The second wave of pain is more likely to come
from the rapid onset of inflammatory edema; this distends the
tissues and stimulates the deeper nerve endings. This pain
wears off during the first night after the procedure, when the
edema is at its height and is no longer actively distending the
tissues.
CARCINOGENICITY
Phenol is not considered to be carcinogenic.3 On the contrary,
long-term histological studies show that phenol (even when the
formula contains croton oil) has a protective effect against skin
cancers (Box 26.2). A logical explanation of this protective effect
may lie in the fact that the cells that take the brunt of UV rays
are the keratinocytes closest to the stratum corneum, the ones
that form, for example, the top of the dermal papillae. On the
other hand, the keratinocytes that are in the lower regions of
the dermal papillae are protected compared with those higher
up: the UV photons have been partially absorbed or diffracted
by the epidermal layers above them. In addition, the sebocytes4
or keratinocytes that make up the shaft of the hair are anchored
more deeply in the skin, at a depth where the harmful effects of
the sun are not as severe.
The cells that are most active in skin regeneration after
a deep peel are those that are least damaged by the sun’s rays,
the cells that have undergone the least UV-induced genetic
mutation. After a phenol peel, the skin is much healthier than
the skin that the acid coagulated, and statistically will develop
fewer cancers. Moreover, phenol may well coagulate and elimi-
nate any intraepidermal cancer in situ.
PROTEIN COAGULATION
Phenol coagulates proteins simply by combining with them,
and this produces frosting similar to that occurring when the
normally transparent proteins of an egg white become cloudy
on cooking, as a result of their three-dimensional structure
being modified (Box 26.3). The coagulated proteins and phenol
can be separated by the action of alcohol.5 For the phenol and
proteins to form a stable bond, the temperature must be raised.
When phenol comes into contact with the skin or mucous mem-
branes, it causes immediate proteolysis if the concentrations
are high enough, with protein coagulation occurring at higher
concentrations.
DISINFECTION
Phenol is a powerful disinfectant that is more active in vivo than
in vitro, because it coagulates the proteins of living organisms.
It is bacteriostatic (at a concentration of 2 g/l) and bactericidal
(at a higher concentration of 10 g/l). From 13 g/l (about 1.3%), it
is tuberculostatic and fungistatic. It is not considered to be viru-
cidal,6 although one commercial formulation containing 0.13%
of glutaraldehyde and sodium phenate has a virucidal activity
(according to AFNOR Norm T727). Some more lipophilic phe-
nol derivatives have been declared virucidal against HIV and
the hepatitis B virus.1 The fragility of the HIV envelope would
explain this action, though the action against the hepatitis B
virus is not so clear. Many patients report that labial herpes
outbreaks are less frequent or even disappear altogether after
a phenol peel (Box 26.4). Phenol is found in bactericidal, tuber-
culostatic, and fungistatic concentrations in all phenol peel for-
mulas. Even after 24 hours’ contact, no phenol derivative has
shown any sporicidal action.
HISTOLOGY OF PHENOL
A study8 on guinea pigs showed that the reticular dermis
reacts to injury as if it were made up of two distinct layers,
whereas histologically there is no evidence that these two lay-
ers exist, and the reticular dermis appears to be homogenous.
(Figure 26.2 is a schematic illustration of the layers of the skin.)
When the uppermost part of the reticular dermis is attacked, it
reacts by reorganizing the tissues, while the deeper part forms
scars. It must be remembered that the deeper dermis contains
fibroblasts that can react phenotypically as “conventional”
fibroblasts as well as myofibroblasts. Myofibroblasts are dif-
ferentiated (in response to cytokines) fibroblasts that can both
synthesize a strong collagen bundle and activate a cytoplasmic
motor running on actin. This transforms them into “nonmus-
cular” motor cells that can activate a contractile capacity com-
parable to that of a smooth muscle cell.
The myofibroblasts interact among themselves, as if they
were holding hands across their thick and resistant collagen

222      Textbook of Chemical Peels
bundles and, after taking each other’s hands, were bending
their arms to draw closer to each other and thus contract the
skin. Myofibroblasts (Box 26.5) are the skin’s final bulwark, the
last defense against physical, chemical, and biological attack.
When a peel injures the dermis to a depth where there are
fibroblasts capable of turning into myofibroblasts, it means that
there are many keratinocytes (that have been destroyed) upon
which the body can no longer count to regenerate the skin, and
BOX 26.3  Tip about Phenol Penetration
A fast and strong proteinic coagulation, as occurs after appli-
cation of 80% phenol on the skin, can act as an impermeable
shield that prevents further penetration of more acids.
BOX 26.4  Tip about Herpes Labialis
Antiherpes prevention is recommended before a phenol
peel. Nevertheless, it seems that people with a history of
herpes labialis show much less herpes activity after a phe-
nol peel on the lips.
BOX 26.2  Tip about Carcinogenicity
Studies show that peelings are not carcinogenic. More
recent studies demonstrate that even superficial peelings
have a protective anticancer activity.
BOX 26.1  Tip about Pain
Phenol has anesthetic properties that appear together
with the frosting, on average 15 seconds after application.
Inflammatory pain—a local pulsatile, painful hot sensation—
occurs 15–20 minutes later.
Stratum corneum disjunctum
Stratum corneum compactum
Keratinocytes
Epidermal basal layer
Grenz zone
Papillary dermis
Reticular dermis
Hypodermis
GZ
GZ
GZ
GZ
GZ
K
K
K
K
Figure 26.2  Schematic diagram of the layers of the skin adapted to peelings.
Figure 26.1  Immediately after application of phenol to the upper
lip, the anesthetic effect is enough to be able to pinch the skin and
draw blood without any feeling of pain (note the red spots in the
photograph, taken during a chemical cheiloplasty).

Phenol: Properties and histology      223
that skin regeneration will be slow and therefore dangerous for
homeostasis. The activation of the myofibroblast actin-based
contractile motor, which alone can draw the edges of the wound
together, increases the entire organism’s chances of survival.
The deep reticular dermis therefore reacts like an entrenched
guard that has nothing to lose and prefers to produce a scar
rather than undergo extensive necrosis. When a peel injures the
reticular dermis, the safety margin is therefore narrower and
the risk of scarring is greatly increased. In 1985, Kligman stud-
ied and documented the long-term aftereffects of a phenol peel
in his remarkable study “Long-Term Histologic Follow-Up of
Phenol Face Peels.”9 Fintsi also studied the histological effects
of phenol peels.
It is still very difficult, however, to tally the clinical results
and the histological changes of the different types of peels: the
formulations, adjuvants, and concentrations are different, as
are the methods of preparation and application of the various
active agents used. Each patient has different cell characteris-
tics, in either the quality or the quantity of phospholipids, ste-
rols, and proteins embedded in the cell membranes. Doctors
are guided by their own experiences and follow the applica-
tion protocol they have gradually developed in the course of
their practice. This disparity makes it difficult to compare the
results of different studies. Some general principles can, how-
ever, be drawn: we can consider that all peels produce compa-
rable histological effects. The differences arise from the extent
of the inflammation caused and how this inflammation is con-
trolled, as well as the relative depth reached. As far as medium
and deep peels are concerned, effectiveness increases when the
injury is close to the deep reticular dermis. The risk of retrac-
tile scars developing is greatly increased at this depth. There is
therefore a fine line between achieving excellent results and the
incidence of scarring. At the same peel depth, however, phenol
peels produce the most significant changes and the most spec-
tacular results (Figure 26.3).
BOX 26.5  Tips about Myofibroblasts
Normally, fibroblasts do not exert much tension on the
matrix of noninflammatory tissue, but when all the layers of
the skin are affected by an injury, local growth factors send
fibroblasts to colonize the fibrin plug closing the wound and
forming the temporary matrix. The fibroblast invasion and
neoangiogenesis form the granulation tissue. The fibro-
blasts that have invaded the temporary matrix already exert
a certain amount of traction on this tissue. The mechani-
cal stress then stimulates the fibroblasts to produce more
collagen and to turn themselves into “protomyofibroblasts.”
The persistent stress induces the phenotypic transformation
of the protomyofibroblasts into differentiated fibroblasts, the
myofibroblasts, which secrete actin fibers and increase their
contractile force while producing collagen and releasing pro-
teases. Usually, the myofibroblasts disappear via apoptosis
(programmed cell death) as soon as the scar is solid, but
where stress persists, they do not disappear and gradually
form a hypertrophic scar.
(b)
(a)
Figure 26.3  (a) Full-face phenol peel immediately after 24 hours’ occlusion. The darker patches are the areas that have not undergone
liquefaction. This makes no difference to the overall result, as can be seen in (b), which shows the same patient 12 days after the full-face
phenol peel with Lip & Eyelid Formula. The skin tone is completely even, even in the nonliquefied areas.

224      Textbook of Chemical Peels
EPIDERMAL CHANGES
A phenol peel usually produces complete epidermolysis in
keratinocytes and all other living cells in the epidermis. The
Langerhans cells, which play an important role in the skin’s
immune defenses, are also affected. There is a certain amount
of dermolysis accompanying the destruction of the epidermis
(Table 26.1).
DERMAL CHANGES
On contact with the papillary dermis, phenol destroys the
entire elastotic layer within it. Thereafter, the architecture of
the dermis is spectacularly restored. Immediately underneath
the basal membrane, in the Grenz zone, a dense new layer of
collagen fibers is formed, arranged parallel to the basal mem-
brane and interspersed with good-quality elastic fibers in an
effective network.10 Brown described this histological reac-
tion as early as 1960. The new collagen and elastin that is
formed covers the sun-damaged structures that have not been
destroyed by the phenol and pushes them deeper down. The
fibroblasts are strongly stimulated and secrete all the compo-
nents of the extracellular matrix: ground substance, collagen,
elastin, and so forth.The morphology of the fibroblasts varies
widely depending on their location (Table 26.2).
The blood vessels that are newly formed after a phenol
peel provide an effective and lasting supply of nutrients to the
new skin.
After a deep peel, the body takes 4–6 weeks11 to regener-
ate a structurally normal skin. During these 6 weeks, the skin
appears very red, as the many newly formed blood vessels are
showing through an incomplete, thinned, and pale epidermis.
Six weeks is usually the minimum time that erythema lasts
after a phenol peel. After this time, inflammation may persist
and the skin can still appear red for several more months.
Dermal lymphocyte infiltration associated with photoag-
ing is reduced after a phenol peel. On the other hand, there is
significant lymphocyte infiltration in the reticular dermis 2–5
days after a phenol peel.
Overall, the wrinkled superficial layers are liquefied and
replaced by structurally young and homogenous tissue. The
inefficient elastotic dermal layers are renewed and/or pushed
Table 26.1  Action of Phenol on Epidermis
Superficial
epidermal
layers
The epidermal layers are dissolved down to the
basal layer in 24–36 hours under an occlusive
mask. Thereafter, the architecture of the cells
returns to normal and the histological coloring
evens out. After a peel, the palisade structure
of the keratinocytes is more even.
Basal layer
Phenol restructures the architecture of the basal
layer. It does not completely destroy the
melanocytes; they are still found in the basal
layer after peeling. In some histological studies,
the density of melanocytes is sometimes
higher overall. The melanocytes have,
however, become incapacitated or partially
incapacitated: melanin synthesis is reduced,
as is the ability to transmit melanosomes to the
neighboring keratinocytes. This histological
observation explains any hypopigmentation or
depigmentation following a phenol peel. How
much the phenol damages the melanocytes
largely depends on the formulation of the
solution used and the application technique,
which explains why total achromia occurs more
often with some formulations than others. For
example, with Baker’s formula, the risk of
developing “porcelain skin” is higher than with
Lip & Eyelid Formula. PIH is more frequent
than achromia when using today’s phenol
formula.
Table 26.2  Action of Phenol on Dermis
Papillary dermis
The fibroblasts are small and have horizontal
dendritic processes; each fibroblast is in
contact with several collagen fibers. These
observations explain the dense horizontal
arrangement of the new collagen in the
papillary dermis after a phenol peel.
Mid and deep
dermis
The fibroblasts are larger and are in contact
with just one bundle of collagen fibers.
Deep dermis
and hypo­
dermis
The fibroblasts are even larger here (four times
bigger than in the papillary dermis), and the
dendritic processes are long and form a
continuous network. Collagen synthesis by
the fibroblasts causes scars to contract.
Myofibroblasts (see Box 26.1) are cells
produced by fibroblast differentiation. They
contain myofilaments that make them look
like smooth muscle cells and are involved in
the phenomena of scar retraction.
Depending on the depth reached by a peel,
different types of fibroblasts are stimulated
and will react in a specific way because of
their different genetic programming. All of
these histological changes explain how the
skin becomes thicker and the sometimes
dramatic face-lift effect of deep peels.
Figure 26.4  The skin of a 78-year-old patient 10 years after a
full-face phenol peel and 1 year after a medium-depth TCA main-
tenance peel.

Phenol: Properties and histology      225
deep down by the synthesis of new fibers. The quality of the new
collagen is not quite as good as the collagen that had been pres-
ent since birth. However, it is produced in sufficient quantities,
along with new elastin, to provide better support to the newly
rebuilt epidermis.12 The newly formed blood vessels supply the
dermis with the nutrients it had slowly been deprived of because
of the gradual vascular degeneration caused by photoaging.
LONG-TERM HISTOLOGICAL FOLLOW-UP
AFTER A PHENOL PEEL
The changes described in this chapter last a long time. In histo-
logical sections taken 15 years after a phenol peel (Baker’s for-
mula), the difference between the treated and nontreated skin
is incredible, and this explains why, most of the time, only one
phenol peel is necessary for long-lasting rejuvenation of the face.
Other authors13 have confirmed these histological results
after 15–20 years and even talk about permanent results in
some patients. In 1985, Kligman10 showed that dermal recon-
struction lasts for 20 years at least and that the risk of cancer is
reduced. Clinically, the rejuvenated appearance of the skin can
be maintained for a great many years (Figure 26.4).
NOTES

1. Dauphin A, Darbord JC. Hygiène Hospitatière Pratique. 2nd ed.

2. It is used in the treatment of pain in certain cancers to achieve
neurolysis of the nerve routes responsible for transmitting the
sensation of pain.

3. Fisher Scientific. Phenol [Material Safety Data Sheet].

4. Sebocytes are in fact keratinocytes that have been differentiated
phenotypically into cells capable of producing sebum. When
under attack, they can quickly dedifferentiate, turn back into
keratinocytes, and regenerate the skin.

5. By separating the phenol from the protein that it has coagulated,
alcohol can enhance the action of the acid on another protein.

6. Giroud JP, Mathé G, Meyniel G. Pharmacologie Clinique. Expansion
Scientifique Français, 2003: 1590–91.

7. Regelson W. DHEA, Melatonin and Hormone Replacement. In:
Updates, Anti-aging Medical Therapeutics, Vol 1. Modesto, CA:
Health Quest Publishers, 1997: 75–81.

8. Hayes DK, Berkland ME, Stombaugh KI. Viability of skin flaps
subjected to simultaneous chemical peel with occlusive taping.
Laryngoscope. 1989; 99: 1016–19.

9. Kligman AM, Baker TJ, Gordon HL. Long-term histologic fol-
low-up of phenol face peels. Plastic and Reconstructive Surgery.
1985; 75: 652–9.
10. Petes W. The chemical peel. Annals of Plastic Surgery. 1991; 26:
564–71.
11. Dembinstri M. Exoderm Method, the Non Surgical Face Lifting.
In: Proceedings of the 44th Congrezzo Nazionale della Società Italiana
di Chirurgia Plastica Ricostructiva ed Estetica. Bologna, Nov. 1995.
12. Asken S. Unoccluded Baker–Gordon phenol peels—Review and
update. Journal of Dermatologic Surgery and Oncology. 1989; 15:
998–1008.
13. Matarasso SL. Glogan RG. Chemical face peels. Dermatologic
Clinics. 1991; 9: 131–50.

27
Phenol
Skin penetration and detoxification
SKIN PENETRATION OF CHEMICALS
The skin has many different functions: it can be the site of
action of a product or the reservoir for a product, it can simply
be a transit site, or it can be an impermeable barrier. The skin’s
main role is to form a barrier limiting the transfer of molecules
in and out. It is especially adapted for this thanks to the mul-
tiple external layers of corneocytes. For the stratum corneum
to be impermeable to both chemical and physical agents,1 it is
essential for it to be intact. It is this layer that forms the main
barrier to the penetration of active products through the skin.
Corneocytes are made up of α-keratin filaments, buried in an
amorphous matrix rich in disulfide bonds. There is a thick pro-
tein envelope of involucrin around each corneocyte, and the
intercellular spaces are full of extremely hydrophobic lipids.
The outer layer of the plasma membrane is hydrophilic. The
outer layer of skin can be described as a hydrophilic “brick
wall” sealed with hydrophobic “mortar.”2 The whole forms an
efficient barrier against both hydrophilic and hydrophobic mol-
ecules. This barrier is so efficient that chemicals can penetrate
living or dead skin to the same degree, just as there is the same
degree of penetration through the whole skin or the stratum
corneum alone.2
Consequently, eliminating all or part of the stratum
corneum drastically enhances the absorption of physical and
chemical agents that could not have penetrated an intact pro-
tective stratum corneum. The ability of a product to penetrate
the skin also depends on how it interacts with the corneocytes
and the intercellular matrix. At the same molecular weight, a
proteolytic product will penetrate the skin more readily than a
product that is not proteolytic. The more liposoluble a molecule
is, the greater its partition between the vehicle and the skin bar-
rier and as a result its ability to penetrate is improved. Another
factor to be taken into account is how solvents interact: ethanol
diffuses better in the stratum corneum when it is mixed with
oil rather than water.2 How well hydrated3 the stratum cor-
neum is also plays an essential role in the skin’s absorption
capacity. When the stratum corneum is hydrated, products can
be absorbed up to 10 times more efficiently.2 Hydration swells
the corneocytes and makes them less dense and less resistant
to diffusion. The fact that on facial skin the stratum corneum is
not very thick means that molecules are absorbed more quickly.
The skin on the face is more permeable than the skin on the
limbs and the torso, but less permeable than the skin on the
genital organs.
WHAT HAPPENS TO PHENOL
AFTER PENETRATION
Lymphatic Absorption
The lymphatic system, which is highly permeable even to large
protein molecules, slowly collects some of the phenol in the
interstitial fluid. The total daily volume carried by the lymphatic
system is approximately equal to the volume of blood of the
same individual. This absorption route is very slow and there-
fore negligible from a toxicological point of view (Figure 27.1).
Capillary Absorption
Phenol penetrates rapidly through the skin and is immediately
absorbed by the dermal blood vessels. The metabolization and/
or excretion sites immediately pick up the phenol that has pen-
etrated into the bloodstream.
Metabolization and Elimination
Twenty-five percent of phenol is metabolized into water and
carbon dioxide and eliminated directly through the lungs. The
remaining 75% is eliminated in free and conjugated form or
undergoes oxidation. Phenol is oxidized to hydroquinone in
the liver. Still in the liver, it is esterified by the transfer of the
sulfuryl group of 3’-phosphoadenosine 5’-phosphosulfuric acid
to the hydroxy group of the phenol and produces phenylsulfu-
ric acid: this is sulfate conjugation. Phenol also undergoes gluc-
uronide conjugation through exchanges with glucuronic acid.
The conjugated phenol is no longer toxic to the organism, and
can be eliminated by the kidneys. Other detoxification enzymes
have been identified, such as phenol 2-monooxygenase, phenol
O-methyltransferase, and phenol Β-glucosyltransferase.4
Active transport processes excrete organic acids such
as glucuronide, and phenol sulfate conjugates in the proximal
tubule. All forms of free or detoxified phenol are therefore
found in urine.
Hepatic and Renal Integrity
Because of the way in which phenol is metabolized, hepatic and
renal integrity is a prerequisite for a phenol peel. Applying phe-
nol more quickly than it can be detoxified and eliminated by
a deficient liver or kidneys could result in severe intoxication.
An interesting study in 1953 by Ruedmann and
Deichmann5 concluded that hepatic and renal integrity were
absolutely vital when using phenol. They wanted to draw the
attention of practitioners to the potential dangers of applying
phenol to large surface areas of the body, even though this type
of treatment previously had presented only minor drawbacks.
A patient did die, however,6 after a phenol solution with
a concentration of 2.3%7 was applied under an occlusive dress-
ing8 on one-third of the body surface area and on flesh burnt by
kerosene.9 This death led the authors to study the metabolism
of phenol by applying 1 g of phenol to 75% of the body sur-
face area in a first group of human “guinea pigs.” Three other
groups were given total doses of up to 4 g on the same body
surface area (75%). A rest period of 90 minutes was left between
successive applications of 1 g.

Phenol: Skin penetration and detoxification      227
Toxic Phenolemia
Doses of free and conjugated phenol show the following
results: the levels of free circulating phenol do not vary much
whether 1, 2, 3, or 4 g of phenol is applied on the skin or if a
rest period of 90 minutes is left between each gram applied.
The peak values in free phenol recorded were approximately
0.60–0.80  mg/100  ml. Benatar10 describes a reassuring 1962
study by Litton in which he recorded the following blood con-
centrations after applying 3 ml of 50% phenol on the face: after
1 hour, 0.68  mg/100  ml; after 2 hours, 0.19  mg/100  ml; and
after 3 hours, 0.10 mg/100 ml. According to the same author,
phenol only becomes systemically toxic at a concentration of
23 mg/100 ml, which, for a total blood volume of 4 l, requires
a total of 1 g in the blood at any given moment. Detoxification
by conjugation is initiated immediately after applying phenol
on the skin.
Aqueous or Oil Vehicle
Phenol in aqueous solution is absorbed very differently
from phenol in oil solution. Maximum blood levels reached
0.9 mg/100 ml when phenol was applied in an oil solution and
1.1  mg/100  ml in an aqueous solution. In 1950, Deichmann11
published a study on the reabsorption of phenol in an aqueous
and an oil vehicle: 71 mg of phenol was absorbed by the skin of
a rat in 1 hour’s contact with an aqueous solution of phenol at
4.7%, whereas only 15 mg was absorbed when the same concen-
tration was present in (mineral) oil solution. Phenol penetrates
the skin more slowly from an oil solution than from an aqueous
solution. In this way, it also becomes less toxic. Applying 4 g
of phenol to the skin does not make the blood concentration of
the free form or conjugated form of phenol any higher than if
3 g were applied. Deichmann did not offer any explanation of
this phenomenon, but the rest period of 90 minutes between
100 - E
100 - (E+D)
100 - (E+D+L)=T
100% phenol
Renal elimination of conjugates
Active transport of detoxified
phenol in the proximal tubule
Pulmonary metabolism
Elimination of H2O and CO2
About 20–25% (T)
Elimination of non-conjugated free
phenol
Diuresis, hydration
Phenol + 3′-phosphoadenosine 5′-phosphosulfuric acid
phenylsulfuric acid (sulfate conjugation)
Phenol + glucuronic acid phenyl glucuronide
(alucuronide conjugation)
Quinone and catechol subsequently undergo
renal elimination
Hepatic detoxification
About 70–75% (T)
Capillary resorption slowed
down by oils, edema, etc.
Epidermis
Dermis
Oily? Dry? Thick? Thin? Prepared? etc.
Thick? Hydrated?
Rich in proteins?
Rich vascularization?
Occlusion?
Slow lymphatic elimination
Concentration? Adjuvants?
Formulation, phenol
Sequestered in applicator, etc.
E = quantity of phenol
sequestered in the epidermis
D = quantity of phenol
sequestered in the dermis
L = quantity of phenol
eliminated by the lymphatic system
T = quantity of potentially
toxic phenol
Figure 27.1  Metabolization of phenol.

228      Textbook of Chemical Peels
each 1 g application most probably allowed enough time for the
phenol to be detoxified. After 3 g, the phenol levels returned to
normal within 48 hours. A little longer was needed to elimi-
nate 4 g. On the third day, the blood levels of phenol reached
doses lower than that of any normal individual, that is, around
0.15 mg. No sign of systemic intoxication was detected in the
course of this study. It must be noted, however, that control
mechanisms were not as sophisticated as they are today and
continuous Holter electrocardiogram recording monitors were,
for example, not yet available.
EFFECTS OF OCCLUSION
In the past, it was thought that applying a dressing was the
cause of local necrosis. In fact, the necrosis occurred when very
tight, thick dressings soaked in phenol were applied to the
wounds. According to studies by Ruedemann and Deichmann,5
applying a dressing (unsoaked) after applying phenol actu-
ally reduces the speed with which the phenol is absorbed—
although not the total quantity. There are two advantages to a
dressing: it allows surface maceration and increases the contact
time with the epidermis. In this way, it can improve the cos-
metic results. Impermeable occlusion reduces the rate at which
phenol is absorbed through the skin and increases the chances
of hepatic metabolization, as the organism is not overloaded or
saturated by a massive influx of phenol. Peaks of free phenol
are lower under occlusion.
The literature is unclear on whether occlusion improves
the results of phenol. In 1980, McCollough and Hillman12
reported that the results of phenol (Baker’s solution) without
occlusion were comparable to those of phenol under occlu-
sion. They went on to say that not using occlusion improves
patient comfort and lowers the risk of complications. What
is true for Baker’s solution is not necessarily true for other
formulas, however. In 1989, Baker published a study show-
ing that occlusion with Vaseline produces the same results as
occlusion with impermeable tape. Stegman,13 Alt, and Brody
published studies that show that phenol is more active under
occlusion.
Occlusion can therefore be used to increase the depth of
action of a peel when the practitioner wants the penetration to
be deeper. This is the case with Lip & Eyelid: occlusion is recom-
mended when treating wrinkles around the lips and chin, but
not for the treatment of eyelid wrinkles. Occlusion with Vaseline
appears to be as effective as an impermeable occlusive dressing.
There is one small practical problem with using Vaseline: heat
from the skin makes it more liquid, and as it liquefies it tends
to drip onto the eyes and neck, and onto the clothes, hands, and
anything else the patient touches. The presence of Vaseline also
rules out spot application the day after the peel.
The duration of occlusion has also been discussed at great
length, with Baker recommending 48 hours’ occlusion. When
I use occlusion, I leave it on for 24 hours. I have not noticed
any difference with longer occlusion times—which seems logi-
cal, as after 24 hours all the phenol applied has had plenty of
time to be reabsorbed by the skin; leaving it for more than 24
hours merely increases the risk of secondary infections. The
importance of the question of occlusion becomes clear when it
is considered that many surgeons take off the occlusion under
anesthetic or sedation, which increases the cost and the risk for
the patient. On the first day, there are very few nerve endings
left that have survived the phenol, and taking off the whole
occlusive mask at once, pulling it downward, is painful only
very briefly. Another question is whether the occlusion should
be applied immediately after the phenol or not. Phenol is a vola-
tile compound, and applying occlusion immediately after it has
been applied will stop it from partially evaporating and will
therefore allow for longer maceration of a greater quantity of
phenol. The sooner occlusion is applied after phenol, the deeper
the effect will be.
URINARY ELIMINATION
The by-products of phenol are rapidly eliminated in the urine.
After intoxication with phenol, these by-products make the
urine a dark color—anything from light olive green to dark
brown. The intensity of the color has no direct relation to the
severity of intoxication.
SPECIFIC PHENOL SENSITIVITIES
Very young children are particularly sensitive to phenol, and
incidents of intoxication were recorded at the beginning of the
20th century after simply applying phenol dressings on the
intact skin of infants and after ingestion of 0.25 g of phenol.14
In the early 1900s, Nothnagel and Rossbach described alcohol-
ism as a situation that improves resistance to phenol. A logi-
cal explanation can be found in the ways in which alcohol and
phenol are metabolized. Alcohol is oxidized to acetic acid in the
body. Certain conjugation mechanisms bring acetic acid into
play through acetylation of the phenol function. The detoxi-
fying conjugation could be between the phenol and the acetic
acid. Deichmann studied basal blood phenol levels before and
after application of phenol to the skin. Basal blood phenol lev-
els were lower than before treatment, showing that the body
adapts to the detoxification process. Wine is known to contain
numerous aromatic molecules, including polyphenols. Wine
drinkers15 develop a more effective polyphenol detoxification
metabolism than nondrinkers, which could explain their rela-
tive resistance to intoxication with phenol.
NOTES
1. All peels remove the stratum corneum, at least partially, and
make the skin permeable to chemical, physical, and environmen-
tal attacks. Total sun block is essential after any kind of peel.
2. Guzzo CA, Lazarus GS, Werth VP. Dermatological Pharmacology.
In: Hardman JG, Limbird LE, Molinoff PB, Ruddon RW,
Gilman AG, Chren MM, Bickers DR. Goodman & Gilman’s The
Pharmacological Basis of Therapeutics. 8th ed. New York: McGraw-
Hill, 2000: 1572–88.
3. Young and well-hydrated skin is more sensitive to a peel than old
and sun-damaged skin.
4. Kyoto University Ligand Chemical Database:
hcage.ch/cgi-bin/get-enzyme-entry? 2.4.1.35/2.1.25/1.14.13.7.
5. Ruedmann G, Deichmann WR. Blood phenol level after topical
application of phenol-containing preparations. JAMA. 1953; 152:
506–9.
6. Deichmann WB. Local and systemic effects following skin con-
tact with phenol: A review of literature. Industrial Hygiene and
Toxicology. 1949; 31: 146–54.
7. This proteolytic concentration means the solution penetrates
rapidly.
8. Occlusion stops phenol from evaporating and enhances macera-
tion in the flesh exposed by the burns.
9. Loss of skin impermeability means that the solution penetrates
rapidly.

Phenol: Skin penetration and detoxification      229
10. Benatar D. Lee peeling au phenol. Journal de Médecine Esthétique et
de Chirurgie Dermatologique. 1988; XV(60): 319–23.
11. Deichmann WB, Miller T, Roberts JB. Local and systemic effects
following application of dilute solutions of phenol in water and
in camphor-liquid petrolatum on the skin of animals. Archives of
Industrial Hygiene and Occupational Medicine. 1950; 2: 454–61.
12. McCollough EG, Hillman RA. Chemical face peel [Symposium
on the Aging Face]. Otolaryngology Clinics of North America. 1980;
13: 353–65.
13. Stegman SJ. A comparative histologic study of the effects of three
peeling agents and dermabrasion on normal and sundamaged
skin. Aesthetic Plastic Surgery. 1982; 6: 123–35.
14. Manquet A. Traité Élémentaire de Thérapeutique de Matière Médicale
et de Pharmacologie. 5th ed, Vol. 1. 1903: 240–60.
15. It should be noted that when this observation was made in
France, at the beginning of the 20th century, the majority of cases
of alcoholism were due to wine.

28
Phenol toxicity
Causes, prevention, and treatment
When phenol is dumped into river water, it is very toxic to
aquatic fauna and lethal at a concentration of 1 ppm. The genu-
ine toxicity of phenol and the almost apocalyptic descriptions
of its side effects, which can even lead to death by cardiovascu-
lar collapse, severely limited its cosmetic use until the second
half of the 1990s, especially in Europe. English-language pub-
lications state that, even so, a phenol peel is “one of the most
frequently used techniques in the treatment of photoaging.”1
As discussed in Chapter 27, phenol is rapidly absorbed by
the skin and mucous membranes. It is also rapidly eliminated
by the lungs in the form of water and carbon dioxide, and by
the kidneys in free form and in sulfate- and glucuronide-conju-
gated form. Detoxification starts immediately after phenol has
been applied.2
Phenol vapor enters the pulmonary circulation very rap-
idly, and because of this respiratory absorption, doctors who
use it (regularly) have to wear a mask. The treatment room
must also be properly aired and ventilated to prevent the
patient, who is already absorbing phenol through the skin,
from absorbing any significant amount through the respira-
tory route. Keeping the patient well hydrated (with a saline
drip) promotes diuresis and therefore renal elimination of free
phenol as well as conjugated or oxidized phenol. Some authors
recommend intravenous hyperhydration before and during the
peel and sometimes forced diuresis with an intravenous injec-
tion of furosemide. This hyperhydration is not necessary when
phenol is applied carefully.
DATA OBTAINED FROM LABORATORY ANIMALS
In rats, the oral LD50 is 530  mg/kg.3 In rabbits, 70% of the
phenol applied to the skin is absorbed in 30 minutes and 99%
within 24 hours.4 In 1944, Deichmann and Witherup5 published
the results of their experiments on the toxicity of phenol in lab-
oratory animals.
Their conclusions were as follows: “the rate of absorption
of phenol/skin surface unit is not closely dependent on the con-
centration of the phenol, but is largely dependent on the total
surface area of skin exposed to the product.”
MEDICATIONS CONTAINING PHENOL
There are many pharmaceutical products widely used in medi-
cine and dentistry that contain phenol, sometimes in fairly high
concentrations. Bonain’s local anesthetic mixture, combining
menthol, cocaine, and phenol, is well known, and is used, for
example, as an intranasal analgesic treatment for certain facial
pains. Other products containing phenol include hemorrhoid
creams, chilblain solutions, ear drops or wax remover drops,
psoriasis treatments, and mouth sprays with phenol in con-
centrations ranging from 3 mg/ml to 50 mg/g. Applying these
products locally introduces only a small quantity of phenol into
the organism at well-spaced intervals, and does not appear to
cause intoxication.
Phenol Soap
Phenol soap with a concentration of 5 g/100 g introduces a small
amount of the active product into the organism with each wash.
Even if resorption, and therefore phenol toxicity, depends more
on the surface area covered than on the concentration of the
product,6 each wash delivers only a small quantity of phenol,
which is soon rinsed off.
Gargles
Tercinol is a phenol solution with a concentration of 15 g/100 g.
It is recommended to dilute a teaspoon of concentrated solution
in a glass of water and to gargle three or four times a day. One
teaspoon is generally equivalent to 5 ml and therefore contains
about 0.75 g of phenol. It is applied to irritated mucous mem-
branes, and a small amount of the product will be swallowed
every time it is used unless the user is an expert at gargling.
Some 2–3 g could come into contact with the irritated mucous
membranes every day. The package notice warns patients of the
potential side effects of phenol.
Dental Wick
Some dental wicks contain up to 375 mg/g of phenol. They are
introduced into the dental cavity being treated and are reap-
plied every 10 minutes. The explanatory notice simply recom-
mends not touching the mucous membranes. Nevertheless, it
is possible for the patient to accidentally ingest a total of 1 g,
although the time lapse allows any phenol that might have
been ingested to be eliminated without toxicity. The products
with the highest concentrations of phenol benefit from its anti-
septic and local anesthetic properties.
Mouthwash
Argentofenol is a disinfectant mouthwash recommended to be
dabbed on the mucous membranes every other day. It contains
up to 35% phenol. Phenol is still used in medicine and den-
tistry, sometimes at high concentrations. Side effects remain
rare, as the product is relatively diluted, applied in small quan-
tities or to small surfaces and therefore readily eliminated,
even when applied repeatedly during the day. There is plenty
of time for the liver to detoxify and the kidneys to eliminate
the phenol.
Phenol Peel
During a full-face phenol peel, 2.5–5  ml of phenol solution
is usually applied on the skin. The conventional formulas
(Litton and Baker) use concentrations of around 50%. Applying
3–4 cm3 of solution therefore leaves 1.5–2 g of phenol on the

Phenol toxicity: Causes, prevention, and treatment      231
skin. It is important to be aware of the fact that the toxicity of
phenol solutions appears to be paradoxical, as, up to a certain
point, diluted solutions can be more toxic than concentrated
ones. Publications report that simple aqueous dilutions of 2
parts phenol to 1 part water (i.e., solutions with a concentration
of around 33%7) are usually the most dangerous. Some phenol
peel formulations still use this concentration, however, confus-
ing speed of penetration with cosmetic effectiveness.
PARADOXICAL TOXICITY
At a concentration higher than 80%, phenol is a keratocoagulant.
The first applications of phenol precipitate the skin proteins
and thus create a biological barrier that prevents further appli-
cations of phenol from penetrating too rapidly. Concentrations
lower than 80% are keratolytic,8 as they break the disulfide
bonds between the keratin molecules and allow more of the
solution to penetrate more rapidly. Reducing the concentration
of a phenol solution can therefore make it more dangerous, both
locally and systemically. Lowering the concentration of phenol
in a peel solution is therefore not enough to make it nontoxic,
and quicker penetration should not be confused with improved
results. Solutions with lower concentrations penetrate more
rapidly through the skin and are more rapidly absorbed: they
are therefore more toxic at the same time as being less effective
from a cosmetic point of view.
The distinction between keratolytic and keratocoagulant
must be given careful consideration. It is clinically obvious that
solutions that are assumed to be keratolytic cause protein pre-
cipitation, or coagulation. Roenigk9 published an interesting
article on this subject: in spite of the concentration of approxi-
mately 50% (48.5% to be precise), phenol acts as a keratocoag-
ulant in Baker’s solution because of—according to him—the
combination with croton oil and septisol. Other protein coagu-
lating peels do not use septisol or croton oil, however.
Stone8 performed a histological study of the depth of pen-
etration of various phenol formulas: the Gordon–Baker formula
at 48.5% phenol, the Verner–Dickinson formula at 67%, and liq-
uid phenol at 88%. The results, in keeping with the principles
set out above, show that Baker’s formula penetrates twice as
deeply as Verner’s and four times as deeply as liquid phenol at
88%. Although phenol is absorbed rapidly by skin tissue, only
a part of it will gradually reach the innermost regions, as the
skin proteins flocculate almost immediately, and this creates a
physical catchment area for the phenol as well as a natural dam
that prevents it from penetrating the deeper layers too quickly.
LESSONS FROM MEDICAL HISTORY
General Remarks
The average fatal dose (death within 24 hours) in humans is
8–15 g by ingestion (according to Nothnagel and Rossbach in
Manquat10). Individual predisposition largely explains the
variations in the toxic dose. In 1903, Manquat10 reported two
extreme cases: his colleague, Bouchard, had “by mistake
injected” (sic) two patients with enemas containing 48 g of phe-
nol. Their temperatures fell to 35°C, went up to 41.8°C in the
evening, returned to normal the next day, and remained stable
the following days. There is no information available on the
long-term outcome of this accident: chemical intestinal necro-
sis, fistulization, secondary infection, survival, death, or liver
and kidney toxicity?
Ingesting just 0.5  g of phenol can lead to symptoms
of toxicity, and sometimes an oral dose of 5  g is enough to
cause death. The patient shows signs of corrosive esophagitis
and gastritis, then signs of kidney damage, cardiac collapse,
breathing difficulties, and a feeling of inebriation followed by
coma. Medical history tells us that the “Lister” technique took
the life of many patients. Lord Lister, born in England in 1827,
was the first surgeon to use phenol to disinfect the air in the
operating theater (1867). This technique saved many patients,
but others started to die when phenol was first used to dis-
infect wounds or when catgut was disinfected with phenol
oil. Phenol proved toxic when applied directly in too great
a quantity to skin that was unprotected by the stratum cor-
neum. Lysol, used as a household disinfectant for toilets and
bathrooms, is an oil mixture of cresols and other ill-defined
phenols dating from before the First World War. Even if Lysol
is less toxic and less irritating than phenol, it was the method
of choice for suicide11 and abortion12 at the beginning of the
20th century.
Phenol Administration Routes in the Past
Every possible route (apart from perhaps intra-arterial injec-
tion) was used to administer phenol:
•
Oral or rectal routes (0.5–1  g of phenol in enemas, 6–12
times a day in the case of typhoid fever); the rectal route
was preferred.
•
Topical route (diphtheria).
•
Intrapleural injection (3 g).
•
ENT route: gargles or ear drops.
•
Intravenous route (treatment of varicose veins).
•
“Tissue” route (neurolysis, etc.).
•
Inhalations (whooping cough).
Authors at the beginning of the 20th century knew all about
the toxic effects of phenol and described the symptoms in detail.
It is obvious that the doses used caused frequent and serious acci-
dents. Doctors then became more cautious and used a maximum
concentration of 0.5 g of phenol in enemas, to be repeated every 3
hours, so as not to reach a total daily dose of 4 g. Doses of 4–20 g/
day were considered dangerous or lethal. Manquat10 reported:
“inside the body, we have nearly always administered phenol in
enemas (0.5 to 1 gram of phenol to 200 to 500 grams of vehicle)
that have sometimes been repeated every three hours (Desplats).
A dose of 4 grams has brought the patient’s temperature down
as low as 34° (Van Oye). Caution dictates that we should not go
beyond 0.5 g per enema,” and that “We sometimes prescribe a
dose of 1 to 4 grams in a potion; patients have difficulty tolerating
this preparation.”
Desplats recommended the following “lemonade”:
•
Phenic acid:  2 to 4 grams
•
Lemon water:  100 grams
•
Simple syrup:  100 to 150 grams
•
Water:  q.s. for one liter
Take 100 grams of this solution every 3 hours.
A simple calculation shows that patients at the beginning
of the 20th century were supposed to ingest 800 g of this “lem-
onade”: every 24 hours, that is, 1.6–3.6 g of phenol per day. Toxic
accidents, however, were described when a dressing soaked
in phenol left some of the product in a cavity that was having
difficulty draining, and in the majority of serious cases phenol
was injected into perirectal cell tissue.10 Reading these old texts

232      Textbook of Chemical Peels
provides access to a whole theory of symptoms that today are
only seen in cases of industrial poisoning.
All this—and even the fact that phenol was considered
highly toxic by inhalation—did not stop Bethene and Court13
from suggesting the inhalation of liquid phenol fumes to treat
whooping cough in 1954. The plasma concentrations reached
were far higher than those described by Litton during full-face
peels.
SYMPTOMS OF PHENOL INTOXICATION
Gastrointestinal Symptoms
Ingesting more than 0.5 g of phenol triggers anorexia, nausea,
and belching. Symptoms of gastroenteritis (colic, vomiting, and
diarrhea) occur with slightly higher concentrations. Massive
ingestion destroys the mucous membranes in the upper diges-
tive tract. It has been reported that gastric problems can occur
after applying phenol dressings externally.
Experience of conventional14 phenol peels also shows that
a small percentage of patients complain of nausea or even vom-
iting shortly after a deep peel. This nausea and vomiting occur
within a few hours after the application of an occlusive mask.15
The cause-and-effect relationship between these symptoms
and excessive phenolemia has not been officially established.
Neurological Symptoms
Generally, there are no neurological symptoms when doses of
less than 1–2 g have been ingested. The neurological symptoms
are headaches, tinnitus, hypoacusis, paresthesia, muscular
hypotonia, and stupor. If the dose is fatal, the patient falls into a
coma after a feeling of inebriation and dies without convulsions.
Phenol stimulates the motor neurons of the anterior horn.16
Cardiovascular Symptoms
Cardiovascular complications have been known since the
19th century: the pulse was described as becoming irregular
and weak, slowing down to become extremely weak or imper-
ceptible. Hemoglobinuria and methemoglobinemia were also
described.
Details of these complications are considered later in this
chapter, as well as techniques for avoiding and treating them.
LESSONS FROM TOXICOLOGY CENTERS
In 1993, a retrospective study was conducted over 5 years at
the Poison Center Philadelphia.17 It involved 96 cases of poison-
ing with Creolin, a disinfectant containing 26% phenol. This
concentration is known to be potentially toxic, as it enhances
penetration through keratolysis. Exposure was oral in 60 cases,
dermal in 2 cases, and both oral and dermal in 12 cases. Only 1
case of inhalation was recorded.
•
Oral exposure: Eleven patients (14%) experienced rapid cen-
tral nervous system (CNS) depression that was rapidly
reversible. Fourteen patients experienced vomiting, cough-
ing, and stridor.
•
Dermal exposure: Seven patients (100%) also had respiratory
symptoms. On contact with the skin, phenol precipitates
keratin and forms a white film, followed by redness and
then necrosis. A 5% solution causes a burning sensation
and then local anesthesia.18
•
Antidotes to phenol: Isopropanol (isopropyl alcohol) and
polyethylene glycol seem to be the most effective local
antidotes, both histologically and because they slow down
blood penetration.19 Immediately rinsing the area of skin
that has come into contact with the phenol with plenty of
water gets rid of some of the toxin and prevents precipita-
tion of some of the epidermal proteins.
•
Mixed exposure (oral plus dermal): Four people experienced
vomiting, coughing, and stridor. Skin and mucous mem-
brane burns were recorded in approximately 25% of the
poisonings.
It is remarkable that no cardiovascular complications were
recorded in this study. Medical publications report that when a
person is exposed rapidly to a sufficient quantity of phenol (in
general, 3–4 g of phenol applied quickly to the face), abnormal
heart rhythms may occur. These abnormalities appear 15–20
minutes after the beginning of the peel and are often rapidly
reversible. If any arrhythmia had developed during these
cases of poisoning, it would no doubt have occurred rapidly
and disappeared again by the time the patient arrived at the
hospital. This argues in favor of the autonomous reversibility
of arrhythmias with phenol. The authors cautiously conclude:
“The absence of serious toxicity and major chemical burns in
this series does not eliminate concern with the corrosive and
systemic risks of phenol poisoning.”
It should also be noted that phenol was widely used
for 112  years between 1867 (Lister) and 1979 (in a study by
Truppmann and Ellenby20) without any cardiovascular moni-
toring and with relatively few serious or fatal complications
considering that very often it was applied in nonmedical cir-
cumstances (by lay peelers). Baker6 himself asserted that in
5000 cases of full-face or partial treatments, he did not note
any abnormal heart rhythms—or any systemic toxicity—that
could be attributed conclusively to phenol. McCollough and
Maloney21 pointed out that in 25 years of using phenol, they
came across a certain number of arrhythmias of toxic origin,
but that none of these cases needed any specific treatment apart
from waiting for the sinus rhythm to return and adding 15 min-
utes to be on the safe side. Asken22 confided that in 15 years
of performing phenol peels using the Baker–Gordon method,
he never came across a case of arrhythmia that needed treat-
ment. However, in 1997, the author of this book was faced with
a patient who experienced relatively severe arrhythmia when a
full-face phenol peel was applied. How this arrhythmia devel-
oped is described later in this chapter.
The fear of arrhythmic complications is the main brake
on the use of phenol peels today. It is therefore worthwhile
studying this problem in detail. The conclusions that can be
drawn from reading about these complications in medical lit-
erature help us understand how to apply phenol with greater
safety, though the possibility of arrhythmias occurring cannot
be avoided.
CARDIOVASCULAR COMPLICATIONS
For more than 50 years, lay peelers used phenol in full-face
peels for cosmetic purposes without any medical monitoring.
Cases of deaths related to phenol peels date from this era until
the 1960s.
In 1973, Litton, Fournier, and Capinpin23 published the
results of a survey covering cardiovascular complications
(Figures 28.1–28.7) during phenol facial peels. In the 493 ques-
tionnaires returned by plastic surgeons, only 3 cases of cardiac
arrhythmias were reported. It should be noted, however, that

Phenol toxicity: Causes, prevention, and treatment      233
heart monitoring was only (very) rarely used in this era and in
this indication. Reading all the works on the cardiac toxicity of
phenol clearly shows that arrhythmias (easily triggered by the
rapid application of large quantities of phenol) were only rarely
diagnosed or published, and the fact that they tend to resolve
spontaneously allowed practitioners to sleep peacefully.
Truppmann and Ellenby routinely used cardiac monitor-
ing when doing phenol peels and detected many arrhythmias. In
1979, they published the results of a study on 48 patients treated
with phenol peels.20 Saponified and nonsaponified Baker or
Litton formulas were studied. They report that 23% of patients
treated with phenol showed arrhythmia, on average 17.5 min-
utes after the phenol was first applied. These arrhythmias were
often premature ventricular (Figure 28.3) or supraventricular
contractions, bigeminy, or supraventricular (Figure  28.2) or
ventricular tachycardias (Figure  28.7). Tachycardia, which in
extreme cases can sometimes reach 220–230 beats per minute,
can turn into ventricular fibrillation and lead to cardiac arrest.
These seem to be the first documented reports of car-
diac arrhythmias that definitely can be attributed to phenol in
humans. The authors also state that when they applied phenol
Figure 28.1  Sinus rhythm.
Figure 28.2  Supraventricular tachycardia.
No P wave
T
wave
P
T
Atrial
QRS complex
Ventricular
QRS complex
Figure 28.3  Premature ventricular contraction.
Figure 28.4  Bigeminy.
Figure 28.5  Trigeminy.
Figure 28.6  Quadrigeminy.
Figure 28.7  Ventricular tachycardia.

234      Textbook of Chemical Peels
slowly, taking more than 1 hour, no incidence of arrhythmia
was detected.
The types of arrhythmia encountered were the following:
•
Ten patients of the 48 treated with facial peels showed
arrhythmia.
•
Four patients showed premature ventricular contraction;
aged 30, 36, 59, and 71.
•
Two patients showed bigeminy; aged 24 and 43 (Figure 28.4).
•
Two patients showed paroxysmal tachycardia; aged 55
and 67.
•
Two patients showed ventricular tachycardia; aged 36
and 73.
To refine their conclusions, the authors studied the poten-
tial influence of different parameters:
•
Products used in anesthesia: No correlation could be found.
•
Oxygenation before and during the peel: No correlation could
be found.
•
Saponified or nonsaponified formula: No correlation could be
found.
•
Preexisting arrhythmia: No correlation could be found (other
authors24 have confirmed this lack of correlation).
•
Age of the patient: No correlation could be found.
•
Speed of application: Fifty percent of patients who received
a phenol peel in less than 30 minutes developed arrhyth-
mia, with the average time for arrhythmia to occur being
approximately 17.5 minutes; no patient developed arrhyth-
mia when the peel was applied over a minimum period of
60 minutes.
•
Surface area treated: No arrhythmia occurred before phenol
was applied on at least half of the face.
Lotter in 1980 and Litton in 1981 published the results of
two countersurveys. Lotter25 highlighted the fact that only 23%
of doctors performing phenol peels use cardiac monitoring to
check the progress of the application. Litton recorded in his
study26 that after reading Truppmann and Ellenby’s article,20
13% of plastic surgeons who had answered his questionnaire
now reported arrhythmias under phenol and that 51% of prac-
titioners now monitored phenol peels with a cardioscope.
The question asked of the plastic surgeons was: Have
you seen any cardiac complications during a phenol peel? The
answers were as follows:
Yes:  5%
No:  87%
Tachycardia:  6%
Arrhythmia:  1%
Premature ventricular contraction  1%
Of the doctors questioned, 51% said they used monitor-
ing, while 42% never used it and 7% only sometimes monitored
their patients.
The conclusion that can be drawn from these studies is:
putting the patient on cardiac monitoring is a legitimate pre-
caution that allows the doctor to act immediately in case of car-
diovascular complication. On the other hand, not monitoring
the patient does not necessarily make the prognosis for com-
plications any worse, and most of the time they seem to resolve
spontaneously.
In response to these studies, Baker27,28 claimed that, in
the course of 5000 phenol peels, he never came across a case
of arrhythmia. His observation was based on the following
evidence:
•
Complications can take practitioners by surprise during
any cosmetic procedure, and facial peels are no exception
to this rule.
•
The most common complications involve pigmentation,
and through careful patient selection these complications
can be avoided.
•
Hypertrophic scars are extremely rare after a chemical
peel.
•
Systemic toxicity also is extremely rare.
Nevertheless, Baker recommended that all patients
should be monitored during full-face phenol peels, which
seems obvious to us nowadays. Baker stated that he only
observed “normal” irregularities during his phenol peels and
never had a patient die. He considered the cases of premature
supraventricular contractions and the two cases of paroxysmal
tachycardia reported by Truppmann and Ellenby20 to be epi-
phenomena, not very serious and fairly frequent during minor
procedures, especially if an anesthetic containing adrenaline
(epinephrine) is used. The two cases of bigeminy reported
by Truppmann and Ellenby did not bother him either, as he
often came across bigeminy during routine procedures and
drew the logical conclusion that phenol should not automati-
cally be blamed for everything. He was, however, alarmed by
the two cases of ventricular tachycardia in the patients who
received a “rapid” application of phenol in less than 1 hour,
and stressed the importance of taking time over the peel. Baker
also recommended taking at least 1 hour to apply any phenol
peel. Finally, he concluded that phenol peels produce results
that no other surgical technique can rival and that an experi-
enced practitioner, aware of the complications and risks, can,
by carefully selecting his patients, apply phenol peels without
any fear of dire consequences. In 20 years of using phenol, he
did not observe any cardiac complication that could be directly
attributed to phenol with certainty.28 Nevertheless, all of these
opinions, even when they come from such well-known medical
experts, cannot aspire to the status of scientific facts.
Gross29 decided to reproduce the study by Truppmann
and Ellenby, using the same nonsaponified formula in 100 con-
secutive peels on the face and neck (up to the clavicles in the ante-
rior region and up to the 7th cervical vertebra in the posterior
region). Given the number of arrhythmias that occurred after
the 54th patient, the method of application had to be changed.
Out of 54 patients, 31 (57%) developed cardiac arrhythmia
(supraventricular and/or ventricular). Unfortunately, Gross did
not reveal the quantities of phenol used. Logically, it was used
in large quantities, because the surface area treated included
the face and neck up to the 7th cervical vertebra. Moreover, the
premedication contained substances that change the heartbeat,
such as beta-blockers.
The rest of the patients were therefore treated in two ses-
sions with a 24-hour interval in between: the face was treated in
the first session and the neck in the second. In this series, “only”
22% of the patients developed arrhythmia. No correlation was
found between the age of the patients, their gender, the preexis-
tence of cardiovascular diseases, and the incidence of arrhyth-
mias. On the other hand, the blood concentrations reached

Phenol toxicity: Causes, prevention, and treatment      235
in this study seem to be very high, up to 33.29  mg/100  ml.
These figures differ enormously from those in Deichmann’s
or Litton’s studies (see discussion later in this chapter). We
know that the systemic toxicity of phenol can manifest from
23 mg/100 ml.30 The arrhythmias seem to occur in the follow-
ing order: tachycardia and premature supraventricular con-
tractions that develop into atrial fibrillation (pulsus irregularis
perpetuus). Arrhythmias lasts on average 2–19 minutes and are
spontaneously reversible, depending on the clearance of the
phenol and the gradual lowering of blood concentrations after
hepatic detoxification and renal elimination. This study did not
show any relation between blood levels and the occurrence or
severity of arrhythmias. Each patient appears to have his or her
own particular sensitivity to phenol. In conclusion, Gross rec-
ommended dividing the face into different sections and leaving
a rest period of 20 minutes between each zone (see Chapter 33).
Baker’s point of view is fully shared by Cortez,31 who,
in a retrospective study of hundreds of phenol peels that he
performed between 1983 and 1990, did not observe any cardiac
toxicity when the precautions for use were followed.
A study by Wexler et al.4 on rabbits found a correlation
between the rapid onset of arrhythmia and the speed with
which phenol is absorbed through the skin: 70% of phenol is
absorbed in 30 minutes in rabbits. Forced diuresis (intravenous
furosemide) while the peel is being applied prevents cardiac
arrhythmia by increasing renal elimination of free phenol,
even before the conjugation and oxidation processes of detoxi-
fication could protect the organism. In addition, slow applica-
tion of the solution in at least 1 hour meant that no arrhythmia
was observed, as this leaves enough time for the phenol to be
detoxified.
A study on humans, limited to 10 patients, was pub-
lished in 1990.32 Continuous electrocardiogram (ECG) record-
ings (halters) were taken before, during, and after the peels.
Many ectopic beats were recorded, but no direct relation with
the application of phenol was established, although one case of
arrhythmia was found to be suspicious. Despite a review of the
study documents, the author of this book is unable to analyze
the different factors that might have influenced this study with
any precision.
In 1985, Warner and Harper33 published an article report-
ing a suspect case of multifocal premature ventricular contrac-
tions and bigeminy in a child34 weighing 36 kg who received
a dose of 2.4 g of 40% phenol in 0.8% of croton oil, hexachloro-
phene, and water.35 This large quantity36 was applied to 1.9%
of the body surface area (we know that the absorption surface
is at least as important, if not more, than the total quantity of
phenol applied) and under general anesthetic. Arrhythmias
from phenol usually occur rapidly, in approximately a quar-
ter of an hour, and in this case they occurred after 55 minutes.
Phenolemia was not measured and, according to the authors,
there was nothing in the case history that could have attributed
the arrhythmia to phenol. The child had already had several
phenol peels in the past for dermatological problems and had
never experienced any problems, but because of Truppman’s
and Ellenby’s descriptions, the authors assumed that phenol
was the culprit.
Another study37 compared the toxicity of trichloroacetic
acid (TCA) and phenol (Baker’s solution); the conclusion was
that “it would appear advisable” to set up a cardiac monitor
during a full-face peel with Baker’s solution, whereas TCA does
not cause any type of arrhythmia.
Previous studies have shown that cardiac monitoring
is an essential prerequisite when doing a phenol peel on the
face, even if serious arrhythmia can be avoided by applying the
product in at least 1 hour. Applying phenol without any cardiac
monitoring is not good medical practice, and any subsequent
complications could be considered professional malpractice
based on negligence. It should be remembered that vagal reac-
tions are not uncommon during any treatment that is stressful
for the patient and that they need to be detected in order to be
treated correctly.
PREVENTION OF CARDIAC ARRHYTHMIAS
By observing the following seven points, the risks of cardiovas-
cular complications can be significantly reduced:4,38
1.
Prepeel checkup: ECG, liver, and kidney (blood analysis).
2.
Application over more than 1 hour.
3.
Monitoring (ECG and pulse oximetry).39
4.
Good general health.
5.
Good patient selection.
6.
Good hydration.40
7.
Lidocaine as a preventive.41 This point is highly debatable,
because arrhythmia can be avoided simply by taking more
than 1 hour to apply the phenol. Simple lidocaine used to
do nerve blocks before the phenol peel should be consid-
ered a cautious technique.
TREATING ARRHYTHMIA DURING A PEEL
There are several articles describing the appropriate treat-
ment for heart arrhythmias occurring in the course of a phenol
peel.20,24,26,33
At the First Signs of Arrhythmia
If the ECG shows the least sign of arrhythmia—even slight,
seemingly insignificant, and supraventricular—the application
of phenol should be stopped immediately and the intravenous
drip speeded up to hydrate the patient more and force diuresis
to eliminate not only the conjugated phenol but also free phe-
nol. Under these conditions, the arrhythmia should show rapid
signs of improvement and not get any worse. Fifteen minutes
after the last arrhythmia, the phenol can be reapplied again
carefully. It is essential for the anesthetist, the doctor doing the
peel, and/or an assistant to read the ECG constantly. A certain
amount of competence in ECG reading is therefore recom-
mended before doing a full-face phenol peel. There would be no
point plugging in an ECG monitor and being unable to detect
basic heart rhythm abnormalities.
Some authors4 recommend the use of furosemide to
increase diuresis, but furosemide can cause abnormal ionic
plasma levels, which can in turn cause arrhythmias or make
them more likely. Be that as it may, furosemide rapidly
increases the elimination of free phenol in urine, even before
the processes of hepatic conjugation, which come into play very
rapidly, have been able to detoxify it.
Experiments undertaken by Wexler et al.4 show the
following results in animals. When 2  ml of Baker’s solution
is applied quickly on the skin of rabbits weighing 3  kg and
sedated with pentobarbital, on a surface area proportionally 5–8
times larger than the human face, numerous heart arrhythmias
are observed. It is interesting to note that the doses required to
induce arrhythmias in rabbits are high. Forced diuresis with

236      Textbook of Chemical Peels
furosemide significantly reduces the arrhythmias. By applying
the product slowly, arrhythmia is avoided altogether, in spite
of the extremely high doses and the extent of the surface area
treated.
“Benign” Arrhythmias
Simple, isolated supraventricular extrasystoles can occur fre-
quently during any type of procedure, simply because the
patient is under stress. The right reaction to these benign
arrhythmias is to stop applying the phenol and wait for the
sinus rhythm to return “naturally.” These seemingly benign
extrasystoles can in fact be a sign of more serious arrhythmias.
It is best to be prepared by having all the necessary equipment
ready and to keep a close eye on the ECG to pick up any more
significant changes in rhythm. It is a bit late at this stage to be
wondering whether the lidocaine is at hand or if the battery in
the laryngoscope is charged.
More Serious Arrhythmias
Bradycardia
In the case of bradycardia, intravenous atropine is indicated. In
cases of severe phenol poisoning, it has been reported that the
pulse rate can at first increase and then drop off.
Tachyarrhythmias
Arrhythmia can evolve rapidly: within a few seconds, benign
supraventricular arrhythmias can turn into other types of
rhythm disorders, such as nodal tachycardia, atrial fibrillation,
and multiple ventricular extrasystoles, in doublets or triplets.
It is important to act quickly, which is easy to do when every-
thing that is needed to deal with these arrhythmias (which for-
tunately are very rare) is readily available and the patient is on
a drip.
The patient should be put on oxygen to maintain good
blood oxygen levels. Treatment consists of slow intravenous
injection of 50 mg of lidocaine without adrenaline (epinephrine).
Usually, the arrhythmia rights itself in less than 10–15 minutes.
A total maximum dose of 100  mg, in two slow intravenous
injections of 50 mg (in 1 minute), provides a strong and rapid
antiarrhythmic effect (50 mg of lidocaine may be sufficient to
get the patient back into a regular sinus rhythm). If lidocaine
does not bring the rhythm back to normal, bretylium tosylate
may be indicated42 (if in an area equipped for resuscitation).33
Other antiarrhythmics are now available and can of course be
used, depending on the type of arrhythmia and the compe-
tence of the doctor injecting them.
Blood Pressure
In cases of severe phenol poisoning, blood pressure can rise
slightly and then drop significantly afterward.43
Collapse and Cardiac Arrest
To the best of the author’s knowledge, collapse, ventricular fibril-
lation or flutter, torsade de pointes, and other extremely serious
arrhythmias have not been described during peels. However,
they can occur with severe phenol poisoning, usually caused by
accidental intravascular injections of phenol. In Truppmann’s
and Ellenby’s study, none of these serious arrhythmias were
described, and cardioversion and defibrillation were not nec-
essary if more than 1 hour was taken to perform the peel. If
medication proved insufficient and the arrhythmia led to col-
lapse, external heart massage and/or an electric shock of 200 J
would resuscitate the patient. Again, however, there is no risk
of this level of arrhythmia when a phenol peel is applied cor-
rectly, and as already noted, a full-face phenol peel performed
in more than 1 hour does not trigger any arrhythmia. The
author of this book has come across only case of arrhythmia.44
It occurred when influenced by a highly respected colleague
who claimed that he performed all his full-face peels in 30 min-
utes, without any ECG monitoring, as he had never had any
patients feel unwell. The absence of an ECG obviously meant
that he could not pick up on any arrhythmias. His experience
could lead to the conclusion that the arrhythmias potentially
caused by a full-face phenol peel remain benign and resolve
without treatment. However, this conclusion would be hasty
and irresponsible.
In 1994, Lalanne et al.24 described two cases of cardiac
arrest after the injection, in 3 minutes, of 1.4 and 1.8 g of phenol
in an aqueous solution with a concentration of 6% (2 × 15 ml).
The injections were strictly extravascular but were near the
aorta. The injections were made into the semilunar ganglia and
were given as painkillers to patients with inoperable pancreatic
cancer. These patients were in a poor state of health generally,
on numerous drugs, and under general anesthesia.45 There is
an accumulation of numerous risk factors here, and the phe-
nol peels were applied under completely different conditions.
The complications occurred almost immediately, 2–3 minutes
after the injection, and started with a drop in arterial oxygen
saturation to 92%. The arrhythmia began with polymorphous
ventricular extrasystoles that rapidly turned into ventricular
tachycardia, ventricular fibrillation, and cardiac arrest. The
treatments described earlier got the patients back to normal
rhythms.
In 1993, Gaudy et al.46 described the same type of acci-
dent, in which 30 ml of 6.6% phenol solution (around 2 g) was
injected for palliative splanchnic neurolysis in a patient with
cancer of the pancreas. It seems obvious that, in spite of the fact
that the injection was extravascular and given by a competent
practitioner, there was massive vascular absorption, which can
cause accidents that are fortunately reversible after treatment. It
is most likely that the injections were made in edematous tissue
that had been damaged by surgery beforehand and that this
enhanced penetration.
When intoxication has been severe and death narrowly
avoided, jaundice and oliganuria43 follow—a sign of the hepatic
and renal toxicity of phenol. These cases do not fall within the
strict framework of a phenol peel performed correctly: hepatic
and renal toxicity are complications linked to acute poisoning.
OTHER TYPES OF TOXICITY
Toxicity by Inhalation
Phenol vapors are heavier than air (vapor density 1.2). The
best way to ventilate a room where a phenol peel is being per-
formed is therefore at ground level and not higher up. This is
important, as phenol vapors can travel considerable distances
at ground level. Care should be taken with electric heaters, as
there is a risk of the vapors coming into contact with a source of
heat that can start a fire: the mixture of phenol vapors and air
has a flashpoint of 79°C (174°F).43
The olfactory sensitivity threshold is 0.047  ppm.
Therefore, it is difficult to eliminate phenol vapors from a
room; it can take hours. The presence of 250 ppm in inhaled
air poses an immediate danger to health and life. Acute poi-
soning from phenol vapors can produce the same symptoms as

Phenol toxicity: Causes, prevention, and treatment      237
oral poisoning. Chronic exposure47 to phenol vapors produces
the following symptoms: vomiting, difficulty swallowing,
excessive salivation, diarrhea, anorexia, headaches, dizziness,
weakness and myalgia, mental disturbances, dark urine, and
sometimes skin eruptions. Postmortem examinations of ani-
mals given fatal doses of phenol vapors show the presence of
myocardial necrosis and acute pneumonia, as well as vascular,
liver, and kidney damage.43
Ophthalmic Toxicity
Direct contact with phenol crystals, concentrated solutions, or
vapors (45 ppm) causes serious damage to the eyes: hyperalgesic
chemical conjunctivitis, severe iritis, and possibly corneal opaci-
fication with loss of vision and edema of the eyelids. In some
cases of poisoning through direct accidental eyelid contact, the
seriousness of the injury to the eyelids has required surgery.48
The results of phenol coming into direct contact with the
eye can vary from complete recovery of vision to loss of the eye,
depending on the severity of the lesions. Chronic, repeated, or
prolonged exposure to phenol vapors can cause conjunctivitis.
A gray discoloration of the sclera along with brown patches
of pigmentation at the insertion of the rectus muscle tendons
of the eye have been described after chronic exposure.43 Any
direct contact between phenol and the eyes requires raising
the eyelids and rinsing immediately with copious amounts of
water or saline solution. The eye should be flushed with saline
solution for 30–60 minutes, while waiting for the opinion of
an ophthalmologist. Ophthalmic Vaseline or a Vaseline-based
antibiotic eye ointment should always be put in the eyes before
applying phenol, as Vaseline largely deactivates phenol.
Hepatic and Renal Toxicity
Some cases of hepatic and renal toxicity after severe poisoning
with phenol derivatives have been reported in the literature,
but the author has not been able to find any such record in med-
ical publications dealing with phenol peels.
NOTES

1. Glogau RG, Matarasso SL. Chemical peels: Trichloroacetic acid
and phenol. Dermatology Clinics. 1995; 13: 263–76.

2. Ruedemann R, Deichmann WR. Blood phenol level after topical
application of phenol-containing preparations. JAMA. 1953; 152:
506–9.

3. Rats seem to be resistant, as this LD50, applied to an average
human weight of 65 kg, would give a figure of 34.45 g of phenol.

4. Wexler MR, Halon DA, Teitelbaum A, Tadjer G, Peled IJ. The pre-
vention of cardiac arrhythmias produced in an animal model
by the topical application of a phenol preparation in common
use for facial peeling. Plastic and Reconstructive Surgery. 1984; 73:
595–8.

5. Deichmann WB, Witherup S. The acute and comparative toxic-
ity of phenol and o-, m-, and p-cresols for experimental animals.
Journal of Pharmacology and Experimental Therapeutics. 1944; 80,
233–40.

6. Baker TJ. Chemical Rejuvenation of the Skin.

7. Arouette J. Dermabrasion, Relèvements, Peelings. In: Blackwell
A. (Ed.). Collection des Manuels Pratiques de Médecine Esthétique.
Paris: Arnette, 1989.

8. Stone PhA. Peelings au phénol Baker–Gordon et modifies. J Med
Esth Chir Derm. 1996; XXII(90): 93–7.

9. McCulloch EG, Langsdon PR, Maloney BP. Chemical Peel with
Phenol. In: Roenigk RK, Roenigk HH (Eds.). Dermatologic Surgery,
Principles and Practice. 2nd ed. Oxford, UK: Marcel Dekker, 1996:
1147–60.
10. Manquat A. Traité Élémentaire de Thérapeutique de Matiére Médicale
et de Pharmacologie. 5th ed., Vol. 1. 1903: 240–60.
11. After voluntary ingestion of Lysol, death occurs within 3–4 hours;
at autopsy, corrosive esophagitis and gastritis were of course noted.
12. Backstreet abortionists readily used irritant solutions, phenol
and Lysol solutions among them, as uterine enemas to induce
abortions. It is likely that this method was just as dangerous for
the mother as for the fetus, because of the rich vascularization of
the uterus. Autopsy would show a high concentration of phenol
in the right side of the heart, which drains all the veins of the
body and therefore the phenol-laden blood.
13. Bethune M, Court D. Vaporizing fluids containing phenols.
British Medical Journal. 1954; i: 1494.
14. As opposed to “tamed” formulations.
15. Vomiting can cause reversible petechiae (see Chapter 37).
16. Dauphin A, Darkord JC. Hygiène Hospitalière Pratique. 2nd
ed. Association de Pharmacie Hospitalière de l’lle de France.
Editions médicales internationales.
17. Spiller HA, Quadrani-Kushner DA, Cleveland P. A five-year
evaluation of acute exposure to phenol disinfectant (26%). Journal
of Toxicology—Clinical Toxicology. 1993; 31: 307–13.
18. Giroud JP, Mathé G, Meyniel G. Pharmacologie Clinique: Bases de la
Théapeutique. 2nd ed. Paris: Expansion Scientific Français, 1978.
19. Hunter DM, Timerdery BL, Leonard RB, McCalmont T, Schwartz
E. Effects of isopropyl alcohol, ethanol and polyethylene glycol/
industrial methylated spirits in the treatment of acute phenol
burns. Annals of Emergency Medicine. 1992; 21: 1303–7.
20. Truppman E, Ellenby JD. Major electrocardiographic change
during chemical face peeling. Plastic and Reconstructive Surgery.
1979; 63: 44–8.
21. McCulloch EG, Langsdon PR, Maloney BP. Chemical Peel
with Phenol. In: Roenigk RK, Roenigk HH (Eds.). Dermatologic
Surgery, Principles and Practice. 2nd ed. Oxford: Marcel Dekker,
1996: 1147–60.
22. Asken S. Unoccluded Baker–Gordon phenol peels—Review and
update. Journal of Dermatologic Surgery and Oncology. 1989; 15:
998–1008.
23. Litton C, Fournier P, Capinpin A. A survey of chemical peeling of
the face. Plastic and Reconstructive Surgery. 1973; 51(6): 645–7.
24. Lalanne B, Baubion O, Sezeur A, Tricot C, Gaudy JH. Circulatory
arrest after splanchnic neurolysis with phenol in unrespectable
cancer of the pancreas. Annals de Chirurgie. 1994; 48(11): 1025–8.
25. Lotter cited in Botta SA, Straith RE, Goodwin HH. Cardiac
arrhythmias in phenol face peeling: A suggested protocol for
prevention. Aesthetic Plastic Surgery. 1988; 12(2): 115–17.
26. Litton C, Trinidad G. Complications of chemical face peeling as
evaluated by a questionnaire. Plastic and Reconstructive Surgery.
1981; 67: 738–43.
27. Discussions following Litton and Trinidad.
28. Baker TJ. The voice of polite dissent. Plastic and Reconstructive
Surgery. 1979.
29. Gross BG. Cardiac arrhythmias during phenol face peeling.
Plastic and Reconstructive Surgery. 1984; 73: 590–4.
30. Benatar D. Le peeling au phénol. Journal de Médecine Esthétique et
de Chirurgie Dermatologique. 1988; XV(60): 319–23.
31. Cortez E. Chemical face peeling. Otolaryngology Clinics of North
America. 1990; 23: 947–60.
32. 1990 study.
33. Warner MA, Harper JV. Cardiac dysrhythmias associated with
chemical peeling with phenol. Anesthesiology. 1985; 62: 366–7.
34. We have already seen that infants are more sensitive to phenol
than adults.
35. This keratolytic concentration makes for rapid penetration, and
blood vessel uptake of the phenol is quicker in a formula that
does not contain any oils other than croton.
36. More than is usually applied during a facial peel.
37. Stagnone GJ, Orgel MG, Stagnone JJ. Cardiovascular effects
of topical TCS 50% and Baker’s phenol solution. Journal of
Dermatologic Surgery and Oncology. 1987; 13: 999–1002.

238      Textbook of Chemical Peels
38. Botto SA et al. Cardiac arrhythmias in phenol face peeling: A
suggested protocol for prevention. Aesthetic Plastic Surgery. 1988;
12: 115–17.
39. Both are essential, as the onset of arrhythmia is often preceded
by a significant drop in oxygen saturation. Besides, arrhythmia
cannot be detected by a pulse oximeter.
40. 500 ml of saline solution before the peel to trigger diuresis.
41. The lidocaine used to carry out any facial nerve blocks should be
taken into account.
42. Note that 2 ml intravenous vials contain 100 mg. 5 mg/kg should
be injected and repeated after 15–30 minutes, 10 mg/kg if neces-
sary. The total maximum dose is 30 mg/kg.
43. Fisher Scientific. Phenol [Material Safety Data Sheet].
44. This arrhythmia occurred before the research that allowed the
author to write this book was undertaken.
45. General anesthesia is not always considered to be an additional
risk factor during phenol peels.
46. Gaudy JH, Tricot C, Sezeur A. Troubles du rythme cardiaque
graves après phènolisation splanchnique peopèratoire. Canadian
Journal of Anesthesia. 1993; 40: 357–9.
47. This has no relation to what a doctor performing phenol peels,
even on a regular basis, can inhale.
48. A phenol peel always causes severe edema in the eyelids.
Scarring, however, is very rare.

29
Phenol
Choice of peel and combination treatments
INFLUENCE OF THE PATIENT’S
AGE AND GENDER
Age
A phenol peel is mainly indicated to treat facial skin for severe
photoaging. It is the only type of peel that can eliminate
deep wrinkles1 and regenerate elasticity and firmness in the
treated skin in a single treatment. Phenol peels are therefore
usually aimed at people who are (well) past their 40s. There
is no real age limit, and phenol has been used on patients
of advanced years (Figure  29.1) as well as on other much
younger patients. Old age is not in itself a contraindication to
phenol,2 and it is remarkable to note that the skin regenerates
perfectly well at any age. The oldest patient that the author
has treated was 82 when she had a phenol peel, and she was
not the oldest patient to ever receive a phenol peel. Phenol
has been used on children to treat specific disorders. Young
adults have also been treated with phenol for acne scars or
scars of other origins. However, because of its toxicity and
the profound changes it makes to the skin, phenol should not
be used without a good reason. Phenol should not be used to
treat something that alpha hydroxy acids (AHAs) or trichlo-
roacetic acid (TCA) can treat just as well. The strength of a
peel should always be adapted to the problem being treated:
there is no point in applying a peel that is too superficial or
too deep.
Gender
Thickness of the Skin
A man’s skin is often more resistant, thicker, and oilier
(Figure 29.2) than a woman’s skin. Sagging skin is more com-
mon than photoaging in men, and men are often better candi-
dates for a face-lift than a peel. It is the type of skin more than
the gender that determines the results of a phenol peel. If aging
has resulted in a thick skin sagging, without dyschromia (see
also Figure 29.7), and if the folds are more pronounced than the
wrinkles and fine lines, a peel is not at all indicated either in a
man or a woman, as, even if phenol produces a “three-dimen-
sional face-lift” effect, the extent of the retraction is no substi-
tute for surgery (Figures 29.2 and 29.3).
When aging has resulted in sun-damaged thinning skin
with wrinkles and age spots, a peel is an excellent indication
and produces surprising results, in both men and women
(Figure 29.4). Men with light skin phototypes and thin and sun-
damaged skin respond very well to phenol. The gender-based
distinction is purely statistical: in general, women can be said
to respond better to phenol than men, but this does not rule out
men for this treatment.
The only problem that proves awkward after treating
a man’s skin is postpeel erythema (Figure  29.5). Women can
easily use makeup to hide it, but this is difficult for men. Men
can, however, wear a tinted sunblock to hide the redness.
Shaving
The question of shaving often comes up, and it is true that
stubble can pose a technical problem for a patient who wants
to shave at all costs. This is a minor concern, however, as the
patient has to wait for only 10 days after a phenol peel before
shaving. On the 11th day, the doctor might allow the patient to
shave carefully, after evaluating the condition of the patient’s
skin. Wearing a beard can even be an advantage and make the
demarcation line less visible (Figure 29.5).
Makeup
Patients regularly ask about wearing makeup after a phenol
peel. Patients who usually wear foundation can go back to
using it when the skin has finished flaking, around the 8th day
and with the doctor’s permission. The first time makeup is used
signals the long-awaited return to a normal social life.
Some patients do not usually wear makeup, and it is
important to tell them that it will probably be essential for them
to wear foundation after the peel to hide the erythema, which
can last up to several months. The reddest areas should be
covered with a green (to counteract the redness) makeup stick
before foundation is applied.
If the patient refuses to use makeup, she should be
advised to use a tinted sunblock, and this should be discussed
with her before the peel.
INFLUENCE OF THE PATIENT’S PHOTOTYPE
Although phenol has been used successfully on patients with
a “Mediterranean” skin type or on Asian patients with a fair
skin, it is nevertheless aimed at patients with a light skin pho-
totype. Patients with Fitzpatrick skin type I—III are excellent
candidates. Patients with Fitzpatrick skin type IV and patients
with severely sun-damaged skin will have to accept the pos-
sibility of a visible demarcation line3 on the neck.
This demarcation line (Figure  29.6) can be made less
obvious both by a good peeling technique and by combination
with other peels on the neck.4 Darker skin types are not such
a good indication, because of the change in skin tone after the
peel. Most patients with a lot of wrinkles, however, prefer to
exchange their wrinkles for a difference in skin color that can
easily be disguised with makeup.
Skin phototype is even more important when using phe-
nol locally; a local5 phenol peel can only be applied on light skin
phototypes that will not show any significant and visible differ-
ence in color on the eyelids and around the mouth. The same
applies to patients with a lot of freckles, keratoses, or lentigines,

240      Textbook of Chemical Peels
Figure 29.2  A patient 8 years after a full-face phenol peel: the
quality of the skin has remained much improved, but the wrinkles
and sagging did not really benefit from the peel. A face-lift would
be indicated for this patient.
Figure 29.3  Two years after a full-face phenol peel on a patient
with thick and oily skin, the quality of the skin has improved but the
folds and sagging remain unchanged. A face-lift would have been
a better indication for this patient.
(b)
(a)
Figure 29.1  An 82-year-old patient (a) before and (b) after a full-face phenol peel.