INTRODUCTION
Injection-related vascular complications (IRVC) result from inadvertent arterial occlusion by injectable filler materials used in minimally invasive facial aesthetic procedures.1 IRVC is rare but can lead to severe adverse effects, including skin and tissue necrosis, ophthalmoplegia, partial or complete vision loss, and stroke.1–3 Filler materials implicated in IRVC include hyaluronic acid (HA), calcium hydroxyapatite, human and bovine collagen, poly-L-lactic acid, and autologous fat; among these, HA is the most common filler used worldwide.2 Although rare, the exponential global surge in the popularity of filler injections has correlated with an increase in IRVC, and even more alarming, this number is believed to be underreported.1,2
The glabella, forehead, nasal dorsum, nasolabial folds, tear trough, midface, and temporal fossa are commonly implicated in IRVC.4,5 These facial injection sites are high-risk given the potential for accidental cannulation and occlusion of high-risk vessels, which include the ophthalmic artery, central retinal artery and branches, supratrochlear artery, dorsal and lateral nasal arteries, and temporal artery or vein.4,5 The leading hypothesis for IRVC pathogenesis is that the inadvertent cannulation of high-risk vessels causes retrograde flow and embolization of filler materials into the ocular, cerebral, or facial vasculature, which induces vision loss, stroke, or skin and tissue necrosis.1,3
IRVC-induced skin compromise is an urgent condition, while IRVC-induced vision loss or stroke is a medical emergency.1,3 To minimize the risk of IRVC, fillers should be injected slowly and in smaller aliquots.2 Treatment is aimed at recanalizing the occluded vessels and reperfusing the ischemic tissue.1 High-dose, pulsed hyaluronidase injections of the entire ischemic area are the primary treatment modality administered via retrobulbar, subcutaneous, intralesional, and sub-tendon routes.1,3,6 By degrading HA, hyaluronidase can induce ischemic
The glabella, forehead, nasal dorsum, nasolabial folds, tear trough, midface, and temporal fossa are commonly implicated in IRVC.4,5 These facial injection sites are high-risk given the potential for accidental cannulation and occlusion of high-risk vessels, which include the ophthalmic artery, central retinal artery and branches, supratrochlear artery, dorsal and lateral nasal arteries, and temporal artery or vein.4,5 The leading hypothesis for IRVC pathogenesis is that the inadvertent cannulation of high-risk vessels causes retrograde flow and embolization of filler materials into the ocular, cerebral, or facial vasculature, which induces vision loss, stroke, or skin and tissue necrosis.1,3
IRVC-induced skin compromise is an urgent condition, while IRVC-induced vision loss or stroke is a medical emergency.1,3 To minimize the risk of IRVC, fillers should be injected slowly and in smaller aliquots.2 Treatment is aimed at recanalizing the occluded vessels and reperfusing the ischemic tissue.1 High-dose, pulsed hyaluronidase injections of the entire ischemic area are the primary treatment modality administered via retrobulbar, subcutaneous, intralesional, and sub-tendon routes.1,3,6 By degrading HA, hyaluronidase can induce ischemic
