Management of a Vascular Occlusion Associated with Cosmetic Injections.

Abstract

The three proposed mechanisms of vascular occlusion associated with cosmetic injection are:3 1. Intravascular embolism 2. Extravascular compression 3. Vascular spasm. A study by Chang et al4 failed to show that vascular compression was reproducible in an animal model, although a case report by Lima et al5 showed that tissue hypoperfusion occurred following vascular compression identified using high frequency ultrasound. Vascular occlusion is possible via several mechanisms following cosmetic injections; however, intravascular embolism is the pathophysiology best supported by the evidence.3 When a blood vessel is inadvertently injected with filler material, the normal circulation can become impaired, leading to reduced tissue perfusion and compromise of the tissue relating to its angiosome.6 Most soft tissue fillers used in cosmetic practice consist of hyaluronic acid, and although hyaluronic acid is well-tolerated outside the vessel wall, it is highly inflammatory within blood vessels. Using histopathologic analysis of tissue obtained from rabbit ears, experimental study demonstrated that biphasic hyaluronic acid globules within an arterial vessel lumen produces intense vessel wall inflammation and spasm.6 It is speculated that this inflammation and spasm restricts blood flow and leads to further dispersal of foreign material into the adjacent vascular territory. It is apparent that complications associated with hyaluronic acid injection into an artery involve not just embolus with inflammation of the vessel wall, but spasm of the surrounding anastomoses to limit further spread and protection against wider areas of necrosis.6 Many cases of vascular compromise occur immediately with injection1 and the practitioner needs to be aware of the signs of this. However, there are several published papers that describe delayed onset of symptoms of vascular occlusion.1,7,8,9 Although the exact mechanism for a delayed onset of presentation is not properly understood, there are several proposed mechanisms: 1. Due to the hydrophilic nature of hyaluronic acid fillers in attracting water molecules, this can lead to delayed swelling posttreatment and a subsequent external compression of a vessel. 2. An embolus might obstruct a vessel in an area of skin that has a poor collateral circulation, and, although immediate signs of occlusion fail to manifest, the poor collateral supply fails to deliver enough nutrition to the skin over the following hours when signs of vascular compromise occur.1 3. Delayed vascular occlusion might be due an intra-arterial injection, which does not initially occlude the vessel but creates a nidus for platelet aggregation, subsequently leading to a blockage. 4. An intra-arterial injection might initially occur in a larger vessel or at a bifurcation point where it can later become dislodged, leading to an occlusion in a terminal branch. INCIDENCE Although necrosis can occur as a result of many aesthetic treatments, it is most commonly associated with the injection of soft tissue fillers. The incidence of necrosis related to the injection of collagen has been reported at 9 in 100,000 cases, of which 50 percent of cases were in the glabellar region,10 and for all dermal fillers, an incidence of 1 in 100,000 cases.11 However, it is widely recognized that although the incidence of vascular occlusions following injection of soft tissue filler is increasing, likely due to increasing popularity of these treatments and procedures being performed by less experienced practitioners, incidence data is very poor due to under-reporting. In an internet-based survey completed by 52 experienced injectors worldwide, 62 percent reported one or more intravascular events.12,13 Skin necrosis has occurred as a result of injection of all types of dermal filler, including collagen, hyaluronic acid, Polymethylmethacrylate beads (PMMA), calcium hydroxylapatite, and autologous fat.7

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