CHEMICAL PEELS

DR. ASHNA MALHOTRA

INTRODUCTION
■ Chemical peeling or chemical rejuvenation is a procedure where a
chemical agent or combination of agents of defined strength is applied to
the skin, causing a controlled destruction of the layers of the skin. This is
followed by regeneration and remodeling of the skin with improvement
of texture and surface abnormalities.
■ The objective of chemical peeling is to cause controlled destruction at the
required depth, followed by remodeling without scarring. It can
accelerate the natural processes of exfoliation or destroy the epidermis
and dermis, essentially by protein coagulation or lysis.
INDICATIONS OF CHEMICAL PEELS:
■ Pigmentary disorders Melasma Postinflammatory hyperpigmentation
Freckles Lentigines Facial melanoses
■ Acne Superficial acne scars Postacne pigmentation Comedonal acne
Acne excorie Acne vulgaris-mild to moderately severe acne
■ Aesthetic Photoaging Fine superficial wrinkling Dilated pores
Superficial scars
■ Epidermal growths Seborrheic keratoses Actinic keratoses Warts
Milia Sebaceous hyperplasia Dermatoses papulosa nigra
CONTRAINDICATIONS:
i. Active bacterial, viral, fungal or herpetic infection
ii. Open wounds
iii. H/O (history of) drugs with photosensitizing potential.
iv. Preexisting inflammatory dermatoses such as psoriasis, atopic
dermatitis.
v. Uncooperative patient (patient is careless about sun exposure or
application of medicine).
vi. Patient with unrealistic expectations.
vii. For medium depth and deep peels-history of abnormal scarring, keloids,
atrophic skin, and isotretinoin use in the last six months.
■ Peeling should be performed by a trained dermatologist with the
knowledge of the skin and subcutaneous tissue, including structural and
functional differences and variations in skin anatomy of the facial
cosmetic unit.
■ The physician should have knowledge of the basic chemistry of peels,
such as acids, bases, pH and pKa of peeling solutions and the mechanism
of action of peels.
■ The physician should be well versed with early recognition, prevention
and treatment of postoperative complications such as prolonged
erythema, postinflammatory hyperpigmentation, impending scarring etc.
PREPEEL ASSESSMENT:
■ History including general medical history, degree of sun exposure,
occupation to judge the level of sun exposure, history of herpes simplex,
recent isotretinoin treatment in the last six months (for medium depth and
deep peels), keloidal tendency, tendency for postinflammatory
hyperpigmentation, current medications, any previous surgical treatment,
immunocompromising conditions, and smoking.
■ Examination should include general physical and cutaneous examination
including skin type, degree of photoaging, degree of sebaceous activity
(oily or dry skin), presence of postinflammatory hyperpigmentation,
keloid or hypertrophic scar, infection, and preexisting inflammation.
■ No specific investigations are indicated for superficial peels.
■ In patients in whom deep (phenol) peels are planned, hemogram,
urinalysis, liver and renal function tests and electrocardiograph should be
done.
■ Documentation
Informed consent after counseling as below
Photographic record
■ Proper counselling including realistic expectations, Explanation about the
nature of treatment, expected outcome, time taken for recovery of normal
skin and importance of maintenance regimens, side effects, likely and
unlikely complications.
Preprocedure treatment:
■ Priming is essential for at least 2-4 weeks prior to the procedure.
■ The advantages are as follows
 Decreased chances of PIH
 Uniform & better penetration of the peel
 Decreasing the wound healing time
 Assessing the tolerance of topical agents used for maintenance
 Evaluate patient compliance
■ It includes:
i Control any active infection or preexisting dermatoses.
ii Broad-spectrum sunscreens.
iii Hydroquinone (2-4%) in patients prone to postinflammatory
hyperpigmentation.
REAGENTS:
i. Correctly labeled peeling agents in various concentrations
ii. Alcohol to clean the skin
iii. Acetone to degrease the skin
iv. Cold water
v. Syringes filled with normal saline for irrigation of the eyes, in case of
accidental spillage.
vi. Neutralizing solutions: Specific neutralizers are mentioned under
description of individual peels.
EQUIPMENTS:
i. Glass cup or beaker in which the required agent is poured.
ii. Head band or cap for the patient.
iii. Gloves
iv. Cotton-tipped applicators or swab sticks
v. 2 x 2 cotton gauze pieces
vi. Fan for cooling
vii. Timer for alpha-hydroxy acid peels
PEELING AGENTS:
1. Alpha-hydroxy acids, AHA
a) Monocarboxylic acids: Glycolic acid, Lactic acid,
b) Bicarboxylic acid: Malic acid,
c) Tricarboxylic acid: Citric acid
2. Beta-hydroxy acids, BHA (salicylic acid)
3. Trichloroacetic acid (TCA)
4. Alpha-keto acids (pyruvic acid)
5. Resorcinol
6. Jessners solution (Salicylic acid 14 g, Lactic acid 14 g, Resorcinol 14 g
with Ethanol to make 100 mL)
7. Retinoic acid
8. Phenol
TYPE
TypesOF accordingHISTOLOGICAL
to depth: AGENTS
PEEL LEVEL
A. Very Superficial
Very light peels:
Exfoliation Necrosis up
of stratum to the level
Glycolic of stratum for 1-2
acid 30%-50%
corneum. Agents
superficial used: TCA
corneum, without10%,
anyGA 3050%,
minutes;Salicylic acid 20-30%,
Jessners solution 1-3 coats,
epidermal Tretinoin 1-5%
necrosis Jessner’s solution in 1-3 coats;
B. Superficial light peels: Necrosis through Low
the conc.
entireResorcinol
epidermis up20%-30%
to for 5-
basal layer. Agents used: TCA 1030%, GA 10 50-70%,
minutes; Jessners solution 4-7
TCA 10% in 1 coat
coats
Superficial Necrotic of part or all of Glycolic acid 50%-70% for 2-20
C. Medium depth thepeels: Necrosis
epidermis up to upper
anywhere reticular dermis. Agents
minutes;
used: TCA 35-50%,
between GA 70% plus TCA 35%,
stratum 88%solution
Jessner’s phenol un-occluded,
in 4-10 coats;
Jessners solution plus TCA
granulosum to35%,
basalsolid
cell CO2 plus TCA
Resorcinol 35% for 30-60
40%-50%
layer up to mid-reticularminutes;
D. Deep peels: Necrosis dermis. Agents used: Baker-
Gordon phenol peel TCA 10%-30%
TYPE OF PEEL HISTOLOGICAL LEVEL AGENTS

Medium depth Necrosis of the epidermis Glycolic acid 70% for 3-30
& part or all of the minutes;
papillary dermis TCA 35%
TCA 50%
Augmented TCA (CO2+TCA
35%, Jessner’s + TCA 35%,
glycolic 70% + TCA 35%)

Deep Necrosis of the epidermis Phenol 88%

& papillary dermis, which
extends into the reticular
dermis
 Mechanism of action:
■ ALPHA HYDROXY ACIDS
– Small molecular size, penetrates easily.
– Work by reducing enzymes like sulfotransferase, phosphotransferase &
kinase.
– These enzymes fix sulfate & phosphate groups to the surface of corneocytes.
– Reduction of the enzymes decreases the cohesion between corneocytes &
cause exfoliation.
– This action is possible only at an acidic pH.
– At high pH they work as moisturizers.
– Popular AHA’s are weak acids, neutralized by water or a weak buffer like
sodium bicarbonate.
– As they need to be neutralized, they have a higher risk of inflammation,
hypo or hyperpigmentation or even scars.
■ AZELAIC ACID
– Saturated dicarboxylic acid found in wheat, barley & rye.
– Bacteriostatic for
• Staphylococcus aureus
• E coli
• Pseudomonas aeruginosa
• Candida albicans
– Bactericidal for
• Propionibacterium acnes
• Staphylococcus epidermidis
– In vitro, acts as a scavenger of free radicals & also inhibits 5 alpha reductase
enzymes.
– Decreases the free oily acid in lipids on the skin & regularizes the
keratinization process.
■ SALICYLIC ACID
– It is a beta hydroxy acid.
– It is highly soluble in ethanol & minimally in water.
– Works in acne because of its high affinity for lipids & keratolytic action.
■ RETINOIC ACID
– Belongs to terpene family.
– Present in food in the form of beta carotene & gets converted in the skin
into retinaldehyde.
– 95% of this is converted to retinyl ester & 5% into all trans & 9-cis
retinoic acid.
– Most commonly used retinoids are all trans retinoic acid, 13-cis retinoic
acid, retinaldehyde/ retinal.
– All trans retinal & retinoic acid are strong agents, should be used
cautiously.
■ TRICHLOROACETIC ACID
– Hygroscopic white crystals, very strong acid.
– Self neutralises by coagulation of proteins in the skin, which is
visible as frosting.
– More the acidity, deeper the penetration.
– Thicker the coat applied, more intense the side effects.
■ PHENOL & RESORCINOL
– Both work in similar fashion.
– Work by enzymatic inactivation & denaturation of proteins.
– Increase the cell permeability & ultimately cause cell death.
Skin preparation before peeling
i. The patient is asked to wash the face with soap and water.
ii. The hair is pulled back with a hair band or cap.
iii. The patient lies down with head elevated to 45” with the eyes
closed.
iv. Using 2 x 2 gauze pieces, the skin is cleaned with alcohol and
then degreased with acetone.
POSTOPERATIVE CARE:
The aim is to prevent or minimize complications and ensure early recovery.
i. In the post-peel period, edema, erythema and desquamation occur. In
superficial peels, this lasts for 1-3 days, whereas in deeper peels, it lasts for
5-10 days.
ii. Mild soap or a non-soap cleanser may be used. If there is crusting, a topical
antibacterial ointment should be used to prevent bacterial infection.
iii. Clear instructions must be given to the patient for the postprocedure period.
iv. Cold compresses or calamine lotion may be used to soothe the skin.
v. They should be told to use broad-spectrum sunscreens and only bland
moisturizers until peeling is complete.
vi. They should avoid peeling or scratching the skin.
vii. Analgesics are not usually needed but may be advised in case of burning
sensation.
COMPLICATIONS:
i. Pigmentary changes: Postinflammatory hyperpigmentation and
hypopigmentation. These can be very persistent and often difficult to
treat. They may be treated with broad-spectrum sunscreens, topical
corticosteroids, tretinoin, hydroquinone or alpha-hydroxy acids.

ii. Infection: Bacterial (Staphylococcus, Streptococcus, Pseudomonas),

viral (Herpes simplex) and fungal (Candida). They should be treated
aggressively and appropriately.
iii. Scarring is rare in superficial peels. Proper priming, proper choice of
peeling agent and postoperative care can help in prevention of this
complication.
iv. Allergic reactions
v. Milia
vi. Acneiform eruptions
vii. Lines of demarcation
viii. Textural changes
ix. Persistent erythema: Erythema persisting for more than three weeks after
a peel, is indicative of early scarring and should be treated with potent topical
corticosteroids for ≤ 2 weeks.
x. Toxicity: Although rare, it may occur with resorcinol, salicylic acid and
phenol.
IMMEDIATE DELAYED
COMPLICATIONS COMPLICATIONS
– Hyperpigmentation
– Pain, burning sensation – Hypopigmentation
– Pruritus – Persistent erythema
– Erythema – Herpes simplex infection
– Bacterial infection
– Epidermal or dermal burns
– Fungal infection
– Edema – Acneiform eruption
– Ocular injuries – Scarring
– Skin textural changes
– Demarcation lines
– Milia
– Systemic toxicity
COMBINATION PEELS:
■ Combination of peeling agents enhances the depth of the peel without
using a higher concentration of the peeling agent.
i. Glycolic acid 70% combined with TCA 35% (Colemans Peel).In darker
skins, lower concentrations of TCA (10-25%) may be used.
ii. Solid CO2 combined with 35% TCA (Brodys peel)
iii. Jessners solution with 35% TCA (Monheits Peel).
■ Two procedures can also be combined to blend cosmetic units and avoid
demarcation lines:
i. Chemical peeling combined with dermabrasion: This procedure was
originally used by combining application of 50% TCA followed by
dermabrasion for post-acne scarring.
ii. Chemical peeling can also be combined with laser resurfacing for
skin rejuvenation. First, a chemical peel is performed and then, the
deeper wrinkles in the periorbital and perioral areas are treated with
pulsed CO2 laser.
iii. Chemical Peel with derma-sanding using sandpaper
iv. Chemical peeling with Botulinum Toxin.
v. Chemical peeling with fillers.
THANK YOU