Treatment Protocol for Acute Arterial Occlusion Secondary to Facial Revolumization Procedures

Adverse Events

The first recorded manufactured adverse event from an injectable dermal filler was in 1991. At that time, the US Food and Drug Administration warned of adverse events secondary to collagen injections, including open sores, abscess formation associated with delayed healing of the skin, and partial blindness.¹⁰

Arterial Embolization and Cannulation. The most serious complications from dermal fillers are accidental injection and/or embolization of the filler into the arterial system. Since 1991, an increased number of cases of soft tissue necrosis, blindness, and stroke have been reported as a result of injection of fillers in the glabella, forehead creases, temple, crow’s feet, nose, cheeks, nasolabial folds, and lower lip.^11-15

Accidental cannulation and inadvertent injection of fillers into the arterial vessels can have catastrophic complications. The potential of such inadvertent complications occurs despite skill level of the practitioner or surgeon. Therefore, recognition and treatment of a vascular occlusion must be immediate and aggressive to avoid devastating and potentially irreversible complications including blindness, stroke, and death.^11-15

Acute Blindness and Stroke. The issues and concerns associated with local intra-arterial dermal filler injection and distal embolism are well described in the literature. However, the mechanism of retinal artery occlusion is much more complex given the need for deep placement of products and the force necessary to cause distention and elevation of the dermis. Hence, higher g-forces are applied via the plunger, forcing the intra-arterial filler proximally past the origin of the retinal artery. When the clinician stops the injection, the arterial systolic pressure immediately embolizes the filler into the distal branches of the ophthalmic artery. This causes acute pain and blindness (Figure 5). Depending on the g-force applied, filler can enter into the internal carotid artery and embolize resulting in cerebral ischemia. Signs of cerebral ischemia may be mild or overt.^4-9

Intra-arterial placement results in pain out of proportion to the procedure and results in almost immediate skin blanching. Depending upon the duration of ischemia, there is progressive necrosis of the end target tissue (nasolabial dermis, mucosal and dermis lip, alar and nasal tip cartilage with dermis).^14,16-19 Areas of tissue necrosis are also subject to secondary bacterial or viral infections, which is why the patient in Case 2 was given a course of acyclovir and cephalosporin.

Management

Patients with intra-arterial dermal filler injection constitute a medical emergency requiring immediate intervention. We recommend clinicians initiate the treatment protocols outlined in the Box and Table 1.

Hyaluronidase. Injection of hyaluronidase may assist in degrading the HA around the arterial puncture site, relieving compression, which may increase blood flow. There is a risk of distal embolization from a dislodged HA emboli.

Fat Graft Injections. There are no known degradation products for fat, CaHA, PLLA, or PMMA products. The use of normal saline or hyaluronidase has no proven efficacy and may increase the compression pressure in the artery and surrounding tissue, causing further ischemia.

Nitroglycerin. The use of topical nitroglycerin 2% will dilate the superficial vasculature with possible draw of blood from surrounding cross-feeding vessels. The nitroglycerin should be applied for 5-minute intervals every 1 to 2 hours. Adjusting the duration and frequency is necessary if the patient experiences headache or lightheadedness.

Corticosteroids. As corticosteroids help to decrease the inflammatory response in tissue ischemia, including edema, treatment should be initiated immediately. High doses (eg, 60 mg) of an oral corticosteroid for 4 days or a methylprednisolone dose pack for 6 days are both acceptable treatment options. There is no increased efficacy to giving corticosteroids via the intramuscular or intravenous (IV) route. Corticosteroid use in diabetic patients may increase blood glucose levels.

Subcutaneous enoxaparin. A low molecular weight heparin, enoxaparin should be given at a dose of 30 mg SC twice daily in patients in whom there is no known contraindication to heparins. Enoxaparin should not be given in combination with ASA therapy.

Acetylsalicylic Acid Aspirin. Patients should be given 325 mg ASA orally, which may assist fibrinolysis. Prophylactic treatment with an antacid is recommended to prevent gastritis/esophagitis associated with ASA therapy. Acetylsalicylic acid aspirin should not be given to patients in whom contraindications exist, or used in combination with enoxaparin.

Phosphodiesterase Type 5 Inhibitors. Phosphodiesterase type 5 inhibitors (eg, tadalafil, sildenafil, vardenafil) inhibit the degradation of cyclic guanosine monophosphate, allowing arterial muscle wall relaxation and increased vasodilation.

Antibiotic and Antiviral Therapy. Tissue ischemia requires treatment with prophylactic antibiotics and antivirals. Oral broad-spectrum coverage for gram-positive bacteria should be initiated (cephalosporin or penicillin). If the oral mucosa is compromised, the clinician should consider clindamycin.

Consultations. Ophthalmology consultation should be obtained if the patient has symptoms of retinal or ophthalmic artery compromise. Plastic surgery consultation should be obtained for possible HBO therapy and for possible surgical intervention. A neurology consultation should be obtained if the patient has symptoms of cerebral ischemia (Table 2).