Learnt about aesthetic medicine in the past 1 year, so in this section, I will make a summary on what I learned so far, divided into botox, filler, laser, chemical peel, anatomy and clinical dermatology, total of 6 sections
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Fillers
Classifications of fillers
Temporary : which last 6-8 months
semi-permanent - 1-2 years
permanent > 3 years
Site of placement
intradermal
subdermal
supraperiosteal
Rheology of fillers
cohesivity
low cohesitivity - better tissue intregration
elasticity ( g prime )
higher resistance to force eg gravity
higher tissue lifting properties
viscosivity ( double g prime )
higher double g prime filler is better for area where tissue mobility is high
*indication: scrulptra FDA approved, indicated for HIV related atrophy
Safety properties of fillers
Reversibility ( able to be diluted / dissolved )
less cross linking
less modification from native source
liquid like consistency that support aspiration
Materials :
HA fillers : restylane, juvederm
Autologus : fat and collagen
non HA / synthetic : sculptra ( poly-lactic acid - collagen stimulator) , aquamid, radiesse ( calcium hydroxyapatite - collagen stimulator )
Classification of HA
crosslink
monophasic ( monodensified and polydensified )
biphasic
non cross-link
high molecular weight
low molecular weight
HA good modification
minimal cross linking with modification degree 1/9 - 4.0 %
HA with excessive modification
high crosslinking
rigid struccture
high risk of complication
Types of HA crosslinking
NAHSA
vycross
CPM
RHA
'Injection techniques for fillers
retrograde linear thread - most common
anterograde linear thread
fanning
cross hatching
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Managing complications of fillers
early ( < 24 hours ) and late ( > 24 hours to 2 weeks )
life threatening and non life threatening
Early non life threatening complications
abscess
pain
rash
itch
tyndall effect - due to superficial injection
swelling
Early life threatening complications
anaphylaxis
infection
embolism
compartment syndrome
arterial occlusion
Late life threatening complications
carcinogenic response
Late non life threatening complications
granuloma
biofilm
migration
inflammatory nodule
Filler induced necrosis signs and symptoms
pain
skin discloration
temperature changes
blanching
Early necrosis and Late necrosis
Early necrosis
arterial occlusion
late necrosis mechanism :
hydrophilic nature of filler causing compression of vessel
compartment syndrome
intravascular injectuon causing embolism
Minimise risk of necrosis by managing patient factor, product factor, procedure factor and practitioner factor
Patient contraindications
previous silicon injection
repeated filler injection( biofim formation - limited speace for filler placement and risk of abscess formation )
previous trauma / surgery - changes on vasculature
Product
filler for augmentation not used to terminal end ( eg tip of nose )
Practitioner factor
Aspiration technique
Procedure factor
Avoid lignocaine if posssible, avoid adrenaline
use cannula
Managing necrosis
warm compress for 10-15 mins, every 1-2 hour
Regardless of type of filler use, hyaluronidase 1500 u
for alganess - vit c / normal saline
Aspirin PO 325mg daily - avoid taking with enoxaparin, take with antacid esomaprazole 40mg daily
corticosteroid 40mg daily for 5 days
Cephalosporin 500mg QUD, add clindamycin if oral mucosa involvement, acyclovir 800mg for 5 days
ibuprofen 400mg daily to reduce inflammation - avoid co-taking with aspirin
hyperbaric oxygen
nitroglycerin paste - possible s/e : dizziness
refer: opthal, neuro if suspected cerebral ischemia, plastic
In conclusion: dilute/ dissolve and remove the filler
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Retrograde embolism secondary to intravascular injection of filler
Possible complications of embolism
cardiac complications
opthalmic complications
pulmonary complications
cerebral complications
Types of visual complications in facial related retrograde embolism
Type I blindness without opthlmoplegia and ptosis
Type II blindness with ptosis and without opthalmoplegia
Type III blindness with opthalmoplegia and without ptosis
Type IV blindness with opthalmoplegia and ptosis
CRAO
loss of cherry red spots ( retina opacification )
2/3 loss vision
permanent loss of vision in CRAO can occur as soon as 2 minutes
Treatment of CRAO secondary to filler induced retrograde embolism
Retrobulbar injection of hyaluronidase into infraorbital foramen and supraorbital notch via SO/ ST /IO under USG
Opthalmic artery
diameter 2mm
artery of the orbit - major arterial shunt between ICA and ECA
originates from internal carotid artery within the middle cranial fossa, travel through optic foramen, and divides into multiple arterial branches within the orbital cavity
Opthalmic artery branches DR MCLESSI
D orsal nasal artery - external nasal artery that supplies lateral wall of the nose
R. Central Retinal Artery
M. uscular artery ( inferior and superior ) that supply extraocular muscle.
C entral retinal artery - first branch of OA
L acrimal artery - second and largest branch of OA
E thmoidal artery - anterior and posterior ethmoidal artery
S upraorbital artery - an end artery
S upratrochlear artery - terminal branch of OA
Internal palpabrel artery
both supraorbital and suprotrochlear arteries provides minor branches to medial and middle portions of upper and lower eyelids via medial palpabral arteries
Supraorbital artery
end artery with diameter 1mm
terminal branch of OA with diameter of 1mm
both SO and ST supplies upper and lower eyelids via medial palpebral arteries
The supraorbital artery ( SOA) supplies periosteum of the frontal bone, skin of forehead, superior rectus and levator palpebrae superoris muscle
The terminal branches of SOA form anastomoyic networks with contralateral counterparts of supratrochlear and superficial temporal arteries
Supratrochlear artery
terminal branch of ophthalmic artery which is the first intracranial branch of ICA
After exisitng the orbit, ascending to forehead, approximately 2cm from the midline
accidentally cannulation result in embolization of CRA in retrograde fashion, which leads to retinal injury and permanent blindness
Injecting fillers in SO/ ST/ glabellar region poses high risk for the following reasons:
they are both end artries
in direct connection with OA which gives out CRA
Their distances are <5cm away from CRA
There are several variation to their anastomosis with branches of facial artery
Dorsal nasal artery
emerges from orbit above the medial palpebral ligament
divide into two branches :
1. one branch crosses root of nose, and anastomoses with lateral nasal branch of the angular artery
The other branch runs along the dorsum of the nose, supplies its outer surface and anstomoses with the artery of the oppoiste side, and with lateral nasal branch.
Lateral Nasal Artery ( anterior and posterior )
is the remaining branch of facial artery after it gives off the superior labial artery near oral commisure
as the anterior lateral nasal artery turns anteriorly along the nasal ala, it gives off the angular artery, which courses superiorly along the lateral aspect of the external nose
There is anastomosis between LNA of the ECA and DNA of the ICA which if given off the by OA
Infraorbital artery
terminal branch of maxillary artery
exits infraorbital canal at infraorbital foramen and divides into several branches supplying skin of lower eyelid, lateral aspects of the nose, and upper lips
Superior labial zone
the golden ratio between upper lip and lower lip vertical distance is 1: 1.6
the upper lip protrude 1-2mm anterior than lower lip
Superior labial artery
15mm from lateral corner of the lips
run between oo muscle and labial mucosa / within the muscle itself
depth is about 3mm, injection must be kept superficial to it
Inferior labial artery
Mental artery
main artery of the chin
usually has only one main perforator, which penetrates the platysma
mental foramen is at the level of second premolar, parellel to mid pupillary line
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