In , there were about two million procedures using dermal fillers, according to the American Society of Plastic Surgeons, five percent more than in and percent more than in , second only to botulinum toxin type A. These minimally invasive and nonsurgical cosmetic procedures were the two most commonly performed in this range of time studied.
The growing use of dermal fillers, specifically the use of hyaluronic acid HA , can be explained by their effectiveness and versatility as well as their favorable safety profiles.
Injection necrosis is a rare, but important, complication associated with dermal fillers. Necrosis can be attributed to one of two factors—an interruption of vascular supply due to compression or frank obstruction of vessels by direct injection of the material into a vessel itself.
The glabella is the injection site commonly believed to be at greater risk for necrosis, but it can also occur at the nasolabial fold. The initial presentation of vascular events may include pain and discomfort disproportionate to what is typically experienced following filler treatments and clinical findings, including blanching, livedo pattern, or violaceous discoloration.
Case 2: Necrosis and secondary infection 48 hours after the HA injection a. Discrete scars in the affected area after treatment b. Case 1: Edema, erythema, and progressive violaceous reticulated patch, livedoid area were observed on the left cheek 36 hours after the injection a.
Complete healing five days after hyaluronidase application and nine days after the HA injection b. Case 3: Necrosis and secondary infection 48 hours after the HA injection a. Erythema, hipercromia, and discreet scars in the affected area after treatment b.
Every aesthetic procedure has its limitations and potential risks, and every aging face is unique. Certain regions of the face are at a higher risk for complications due to critical structures and the vascular system. It can be considered a dermatologic emergency and must be dealt with immediately. Small vessels branching from the supratrochlear and supraorbital arteries provide the blood supply to the glabellar region and the collateral circulation is limited. Care should be exercised when injecting near the alar groove because large volumes of material or direct injection into the vessel can lead to obstruction of the angular artery and cause necrosis of the nasal ala, which has limited collateral circulation.
As more clinicians adopt fillers compounded with local anesthetics and epinephrine, they may confuse the clinical picture and hide symptoms. Therefore, the immediate picture must be assessed as well as the progression of the signs and symptoms, with the objective of learning to recognize the adverse events early enough to circumvent sequelae of vascular obstruction.
Vessel embolization of filler begins with immediate changes visible in the vascular system—initial blanching, followed by mottled discoloration called livedo reticularis.
This is accompanied by pain, unless there is a nerve block or local anesthetic blocking the pain pathways. The resulting ischemia produces a dusky discoloration associated with sluggish or absent capillary refill after digital compression, as well as possible loss of function.
The three patients in the cases presented had delayed-type presentation. None of them complained of symptoms or showed signs of ischemia during the filler injection or on the day of the procedure. The authors raised the hypothesis of an embolus after the injection and poor collateral circulation to supply nutrition to the area, resulting in late necrosis. It may result from retrograde flow of intravascular injected material into the ophthalmic artery, obstructing the blood flow of distal branches that supply the retina and cornea.
Clinically, patients may present with a sudden blind spot or visual field deficit. Physicians can take certain measures to minimize the risk of local necrosis and embolization from injecting dermal fillers by doing the following 3 :. In the presence of immediate pain or skin discoloration, stop the injection.
The topical nitroglycerin paste can be applied as frequently as every 1 to 2 hours initially. The authors have used mg aspirin under the tongue immediately and lOOmg daily thereafter as an antiplatelet agent.
Prostaglandin E1 PGE1 has also been a clinical treatment to promote vasodilation. Systemic treatment is usually done in the hospital with the patient carefully monitored, as with all potent vasoactive drugs. Cytoplasmic hypereosinophilia seen in left half of image. Avascular necrosis Frostbite Gangrene Necrotizing fasciitis Osteonecrosis of the jaw Toxic epidermal necrolysis.
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