Chemical Peels and Injectables

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Chemical Denervation

Botox: botulinum toxin

  • FDA information:
  • Botox is used to treat overactive bladder, incontinence, prevention of headaches and chronic migraine, upper and lower limb spasticity, cervical dystonia, blepharospasm, hyperhidrosis.
  • Botox Cosmetic is approved to treat glabellar lines and crows feet.
  • Mechanism of botox: inhibits release of acetylcholine at the neuromuscular junction, blocks nerve stimulation of muscular activity and causes muscular paralysis
    • Myobloc vs botox cosmetic: myobloc has shorter duration of action, quicker onset, greater radius of diffusion, and higher pain with injection
  • Muscles treated: 
    • Procerus: stretches from nasal bones to dermis of glabella, contraction promotes horizontal rhytids in the glabellar regions
    • Nasalis: responsible for bunny lines
    • Corrugator supercilii promotes vertical rhytids in the glabella.
    • Orbicularis occuli: serves as a sphincter around the eye and may also contribute to vertical glabellar rhytids. The orbicularis is a brow depressor.
    • Frontalis: responsible for horizontal forehead rhytids above the eyebrows, is a brow elevator.
      • Paralysis can cause brow depression revealing lid ptosis. 
  • FDA approves 20U of Botox for treatment of the glabellar region, 50 for the axilla, 100 for the palm and 150 for the soles of the feet in hyperhidrosis.
    • Each unit corresponds to the calculated median intraperitoneal lethal dose (LD50) in mice
  • Anatomical landmarks for masseteric hypertrophy injections:
    • Masseter originates from the body of the zygoma and inserts on inferior border of the mandible
    • Below transverse line from earlobe to corner of mouth is safe zone
  • Medications that potentiate the effects of Botox include penicillamine, quinine, calcium channel blockers, aminoglycosides.

Dysport: another botulinum toxin. Contraindicated in those with a milk allergy.

Complications of neurotoxins:

  • Eyelid ptosis: from inadvertent effect of Botox upon the levator palpebrae superioris. Most commonly occurs after treatment of the glabellar region.
    • Treated with apraclonidine drops (Iodipine) or phenylephrine. This stimulates Muller’s muscle which is an accessory eyelid elevator that is located deep to levator and can help improve ptosis 1-3mm.
    • Apraclonidine is an alpha adrenergic agonist.
  • Dysphagia: can result from botox administration for platysma banding if placed too deep in cervicomental junction affecting the strap muscles.

Facial Fillers (include calcium hydroxyapatite, poly-L-lactic acid, and hyaluronic acid)
Hyaluronic acid (lasts 4-12 months) 

  • Mid face: for the mid face, use HA that is highly cross linked, with stability, density, cohesivity, and longevity
    • Injected in preperiosteal level to optimize results
  • Tear trough: should inject at the level of the periosteum (safer and has higher longevity)

Calcium hydroxyapatite (radiesse): semipermanent material that can be injected as a soft tissue filler. 

  • Can be prone to nodule formation
  • Lasts 1-2 years
  • Can be prone to nodule formation
    • Treatment includes direct excision, observation, needle disruption (do not respond to steroids!)

Poly-L-lactic acid: Sculptra is utilized for the treatment of HIV retroviral related lipoatrophy.

  • Injected subcutaneously in the cheek, submuscularly in the orbital region, subperiosteally in the temples.

Complications of soft tissue fillers:

  • Intravascular injection and embolization: requires urgent management to preclude tissue necrosis. Signs include blindness, pain, blanching, mottled skin discoloration, and slow capillary refill.
    • Retinal artery occlusion can cause blindness. Most common area of injection is glabella followed by nasal dorsum.
      • Mechanism is injection into the ophthalmic artery from internal carotid artery.
    • Only hyaluronic acid can be dissolved with hyaluronidase. This should be injected immediately locally at the site (retrobulbar for retinal artery occlusion)
      • Can use warm compresses and nitroglycerin paste as adjuncts 
    • Risk reduction mechanisms include using large bore blunt cannulas (27 gauge or larger), injecting less than 0.1 in any single injection site, avoiding high pressure injection, anatomy awareness, and local anesthesia with epinephrine.
  • Tyndall effect: when calcium hydroxyapatite is placed too near the surface and causes a greyish hue

Skin Care
Tretinoin: treats sun damaged and aging skin, vitamin A derivative.

  • Dose is 0.05-0.01%, works starting after 3 months of use.
  • Effects include increased quantity of collagen (type I, III), greater organization of collagen within the dermis, improved organization of elastic tissue, epidermal hyperplasia, increased mucin deposition, decreased melanin, decreases stratum corneum, increases keratinocyte transit rate through dermis.
  • Improves rhytids, smooths skin, corrects dyschromia (not indicated for deep rhytids).
  • Can be used prior to chemical peel or surface lasering
  • Mechanism of treatment of retinoic acid for acne is decreasing corneocyte adhesion in the stratum corneum, resulting in reduced follicular occlusion and comedone formation.
    • Retinoic acid inhibits AP1 transcription factor binding to DNA and reduces protease activity.
  • Systemic isotretinoin mechanism causes atrophy of sebaceous glands and attenuation of the secretion of sebum.

Chemical Peel: (treats fine lines if refractory to tretinoin)

  • Glycolic acid: neutralized with sodium bicarbonate
  • Salicylic (does not need to be neutralized)
    • Complication includes salicylic acid toxicity. Symptoms include rapid breathing, tinnitus, hearing loss, dizziness, abdominal cramps, and central nervous system reactions.
    • Generally well tolerated even over large TBSA <20%.
  • TCA: neutralized with saline
    • Superficial dermis neutralizes TCA peel as well; does not have systemic absorption
  • Jesser’s solution: cannot be neutralized, consists of (resorcinol, salicylic acid, lactic acid, ethanol)
  • Phenol-croton: cannot be neutralized; has systemic absorption
    • Causes more hypopigmentation than other peels (for patients that have higher Fitzpatrick)
    • Protoplasmic toxin that disrupts cell walls and denatures proteins
    • Rapid dermal absorption
    • Can cause cardiac arrhythmias. Patients should have cardiac and respiratory monitoring.


  • Superficial depth peels:(glycolic, salicylic, Jessner’s, TCA <30%) end point is transparent frost with a pink background. Indicates peel has penetrated superficial dermis
  • Medium depth peels: (TCA 35-50%), endpoint is deep white frost. Indicates that the peel has penetrated the upper reticular dermis.
    • Good for moderate to deep rhytids
  • Deep peels: (Phenol +croton oil) penetrate to mid reticular dermis
    • Croton oil dictates depth of peel
    • Deep peels only suitable for Fitzpatrick I

Complications of chemical peels: 

  • Herpetic lesion outbreak: history of perioral herpetic lesions require pretreatment with acyclovir before any chemical peel procedure. Otherwise patients have 50% chance of developing an outbreak.


  • Carbon dioxide laser
    • Can be used for resurfacing. Causes complete ablation of the epidermis and superficial papillary dermis with thermal injury and coagulation through the papillary dermis. This causes edema, exudation, redness, crusting; wound healing is complete in 7-10 days


  • Can only volunteer non-surgical services IE botox
  • Cannot administer patient product if brought from outside the US (even if it is FDA approved)
  • Facial fat grafting: to maximize take, should increase surface area contact of fat to vascularized tissue. This includes placing extremely small amounts of fat with each pass.
    • Has longer down time than filler injection.

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