Management of Necrosis After Aesthetic Injection: A Clinical…Management of Necrosis After Aesthetic Injection: A Clinical Protocol

Definition

Necrosis is the death of most or all of the cells in an organ or tissue due to disease, injury, or failure of the blood supply^[1]. Unlike apoptosis, which is a programmed and ordered phenomenon, necrosis is the accidental death of the cell caused by mechanisms such as an insufficient supply of oxygen, thermal or mechanical trauma, or irradiation. Cells undergoing necrosis swell and rupture (cytolysis), releasing their contents into the surrounding tissue. The local inflammatory response is characterised by swelling, pain, heat and redness. The necrotic cells are subsequently phagocytosed and removed by the immune system.

Introduction

Necrosis is one of the most severe and feared early complications in aesthetic treatment^[2]. It may occur via four principal mechanisms:

1. Interruption of the vascular supply.
2. Compression of the area around a vessel.
3. Obstruction of a vessel with foreign material.
4. Direct tissue damage from physical, chemical, radiation or laser energy.

Incidence

Necrosis can complicate many aesthetic procedures but is most commonly associated with the injection of dermal fillers. The incidence with collagen has historically been reported at approximately 9 per 100,000 cases, with 50% of events occurring in the glabellar region^[3]. For dermal fillers overall, an incidence of approximately 1 per 100,000 cases has been described^[4]. Necrosis has been reported with all dermal filler classes, including collagen, hyaluronic acid, calcium hydroxylapatite, PMMA and autologous fat^[5].

Signs and Symptoms

Many cases of impending necrosis declare themselves at the time of injection, and the practitioner must be alert to the early signs. Delayed necrosis is also well described, attributed to the hydrophilic properties of hyaluronic acid causing post-treatment swelling and secondary vascular compression, or to intra-arterial deposition producing a platelet nidus that later embolises into a terminal branch^[5,6].

1. Pain

Severe pain is usually experienced by the patient when ischaemia ensues, though this may be masked by topical anaesthesia, nerve block or lidocaine-containing product. Severe pain is not a normal feature of dermal filler treatment: pain that is disproportionate or persistent during or after treatment should prompt urgent review^[2,3,5–7].

2. Prolonged blanching

When vasculature is compromised, the area appears pale, white or dusky. The pattern is often reticulated, following the affected vascular territory. Blanching may be obscured by adrenaline-containing anaesthetics^[2,3,5–7].

3. Dusky purple discolouration

Typically presents several hours later, when tissue death has occurred^[5,7].

4. Coolness

Tissue that is no longer perfused will be cool to the touch, although this is not apparent immediately after injection^[7].

High-Risk Anatomical Zones

Glabellar region

Approximately 50% of reported filler-related necrosis cases occur in the glabella, attributed to its watershed circulation and limited collateral supply^[2,3,4,8].

Nasal tip and alar triangle

The nasal tip and alae are supplied by end arteries with no meaningful collateral flow. The angular artery turns sharply within the alar triangle and is prone to external compression or inadvertent intravascular deposition^[3,4,7].

Minimising the Risk

1. Detailed working knowledge of regional vascular anatomy^[7,9].
2. Aspirate before bolus injection, recognising that a negative aspiration does not exclude intravascular position^[5,7,8,10].
3. Deliver product at the appropriate depth and tissue plane^[2,5].
4. Use the smallest volume needed; consider staged review at 7–14 days rather than overcorrection^[2,7,8].
5. Avoid bolus injection in high-risk zones^[7].
6. Avoid adrenaline-containing solutions that mask early blanching^[6].
7. Recognise that local anaesthesia can blunt the warning sign of pain.
8. Do not inject into the nasal tip.
9. Inject the glabella superficially and medially, with caution^[2,8].
10. Prefer blunt-tipped cannulas in danger zones to reduce intravascular entry^[7].
11. Exercise caution in patients with prior rhinoplasty or surgery and in those with pre-existing filler in situ^[3].
12. Watch the patient: listen to symptoms and observe the skin throughout the procedure.
13. Risk is greater with denser or longer-acting/permanent products.

Management of Necrosis

Necrosis may arise from arterial occlusion — direct intravascular injection or embolisation of product — typically presenting immediately with acute pain and blanching. It may also follow venous occlusion from external compression by filler or post-procedural oedema, more often seen with hyaluronic acid and presenting later with dull pain and dusky discolouration^[2].

1. Stop the treatment immediately

As soon as compromise is suspected (typically pain and blanching in an at-risk area), discontinue injection and, where possible, aspirate product while withdrawing the needle^[2–6,8,9].

2. Massage the area

Firm massage encourages flow and may dislodge filler compressing a vessel. Continue for several minutes^[2–6,8,11].

3. Apply heat

Local warmth encourages vasodilatation and improves perfusion^{[2–6,8–11]}.

4. Tap the area

Tapping may help dislodge intra-arterial emboli at the site or further upstream^[10].

5. Hyaluronidase flooding (HA fillers)

Where a hyaluronic acid filler is implicated and there is no contraindication, high-dose hyaluronidase should be deployed without delay across the entire affected vascular territory, not only the injection site. Re-dose at 60–90 minute intervals until perfusion returns. Always have a documented anaphylaxis protocol and adrenaline immediately available before administration^{[2–5,9–11]}.

6. Topical nitroglycerin paste

Application under an occlusive dressing has been described as an adjunct vasodilator, although evidence remains limited.

7. Aspirin

A loading dose of 300 mg followed by 75 mg daily until resolution has been suggested to limit platelet aggregation, by analogy with established antithrombotic practice, provided there is no contraindication^[7,13].

8. Antibiotics

Necrotic tissue is prone to secondary infection; topical and/or oral antibiotics may be required depending on extent. Anti-herpetic cover should be considered in susceptible patients with perioral involvement^[2,3,4].

9. Superficial debridement

Plastic surgical referral may be needed for debridement to promote healing^[2,3,5,8,9].

10. Wound care management

Ongoing wound care, dressings and scar management form the longitudinal arm of treatment^[3,8].

11. Adjuncts of emerging or limited evidence

Hyperbaric oxygen therapy has been reported in case series^[14]. Low molecular weight heparin has been used to limit thrombosis and embolisation in isolated reports^[4,15]. Oral vasodilators including PDE5 inhibitors have also been suggested, but evidence is insufficient to recommend routine use^[4]. Adequate analgesia, including opioids where required, must not be overlooked.

Stepwise Algorithm

Follow-Up and Documentation

All patients presenting with necrosis require active follow-up until full resolution, often on a daily basis initially. Practitioners should be contactable out of hours via a documented emergency number. Detailed clinical notes, photographic evidence and clear patient communication are the most effective safeguards against a complication progressing to a complaint or clinical negligence claim.

Necrosis Following Sclerotherapy

Necrosis following injection of sclerosant during vein treatment is reported at approximately 1 in [series-dependent] cases^[16], typically attributable to extravasation, inadvertent intra-arterial injection, high-pressure delivery, or underlying vasculitis. Presentation mirrors that described above: pain, pallor and discolouration within the first 24 hours, dermal sloughing within 24–72 hours, and frequent ulceration. Management is supportive — measures to improve perfusion, compression, occlusive dressings, antibiotics where infection develops, and superficial debridement as required. Once healed, residual dermal scarring should be addressed. Prognosis is good where the extent of necrosis is minimal^[16,17].

Practical Insights for Clinic

• Keep a sealed complications kit in every treatment room: hyaluronidase ampoules, sterile water for reconstitution, syringes and needles, GTN paste, aspirin, anaphylaxis kit with adrenaline, warm compress and dressings.
• Pre-procedure: confirm indemnity, document informed consent including necrosis risk, and photograph the area.
• Use the smallest effective bolus, prefer cannulas in vascular zones, and avoid injecting on top of long-standing filler without imaging or caution.
• If unsure whether you are seeing impending necrosis, treat as if you are. The cost of unnecessary hyaluronidase is low; the cost of delay is not.

Conclusion

Tissue necrosis remains a rare but devastating complication of aesthetic injection. Outcomes are determined less by initial severity than by the speed and structure of the clinical response. A rehearsed protocol — recognition, cessation, mechanical measures, prompt hyaluronidase flooding and adjunct therapy — combined with rigorous documentation and follow-up, is the evidence-supported standard for every injector.

References

1. Oxford English Dictionary.
2. Sclafani AP, Fagien S. Treatment of injectable soft tissue filler complications. Dermatol Surg 2009;35:1672–1680.
3. Grunebaum L, Allemann I, Dayan S, Mandy S, Baumann L. The risk of alar necrosis associated with dermal filler injection. Dermatol Surg 2009;35:1635–1640.
4. Tracy L, Ridgway J, Nelson JS, Lowe N, Wong B. Calcium hydroxylapatite associated soft tissue necrosis: a case report and treatment guideline. J Plast Reconstr Aesthet Surg 2014;67:564–568.
5. Ozturk CN, Li Y, Tung R, Parker L, Peck Piliang M, Zins JE. Complications following injection of soft-tissue fillers. Aesthet Surg J 2013;33(6):862–877.
6. Cohen JL. Understanding, avoiding, and managing dermal filler complications. Dermatol Surg 2008;34(Suppl 1):S92–S99.
7. Hirsch RJ, Cohen JL, Carruthers JD. Successful management of an unusual presentation of impending necrosis following a hyaluronic acid injection embolus. Dermatol Surg 2007;33:357–360.
8. Glaich AS, Cohen JL, Goldberg LH. Injection necrosis of the glabella: protocol for prevention and treatment after use of dermal fillers. Dermatol Surg 2006;32:276–281.
9. DeLorenzi C. Complications of injectable fillers. Aesthet Surg J 2013;33:561–575.
10. DeLorenzi C. New high dose pulsed hyaluronidase protocol for hyaluronic acid filler vascular adverse events. Aesthet Surg J 2017;37(7):814–825.
11. Inoue K, Sato K, Matsumoto D, Gonda K, Yoshimura K. Arterial embolisation and skin necrosis of the nasal ala following injection of dermal fillers. Plast Reconstr Surg 2008;121(3):127e–128e.
12. Beleznay K, Carruthers JD, Humphrey S, Jones D. Avoiding and treating blindness from fillers. Dermatol Surg 2015;41:1097–1117.
13. Antithrombotic Therapy: A National Clinical Guideline. SIGN Guideline No. 36. Scottish Intercollegiate Guidelines Network.
14. Impending necrosis after injection of hyaluronic acid and calcium hydroxylapatite fillers: report of cases treated with hyperbaric oxygen therapy. Dermatol Surg 2014;40(9):1049–1052.
15. Schanz S, Schippert W, Ulmer A, Rassner G, Fierlbeck G. Arterial embolization caused by injection of hyaluronic acid. Br J Dermatol 2002;146:928–929.
16. Goldman MP. Overview of complications of sclerotherapy. Australasian College of Phlebology.
17. Consensus paper on venous leg ulcer. The Alexander House Group. J Dermatol Surg Oncol 1992;18(7):592–602.

Selected sources cross-indexed with PubMed and NICE clinical knowledge summaries. Where individual case series are cited, the reader is directed to the primary literature for full methodology.