Wound healing, especially impending skin necrosis is a subject of great interest and involvement for the aesthetic industry. While much of the physiology of wound healing is understood, gaps still exist in our understanding of the phenomenon, especially epithelial formation to prevent dermal scarring. Within the past fifteen years, as facial soft-tissue augmentation with dermal filler products has become increasing popular, this aspect of medicine has become even more important. Without sounding alarmist, these dermal filler products are usually considered safe, having mostly mild and transient adverse events but serious complications related to interrupted blood supply to eyes or the nose can occur with nasolabial fold dermal injection. The exact mechanism of this event is unknown, but it is widely accepted that vascular compromise is probably a function of embolisation and/or compression of material into the vasculature. Rare vascular complications with hyaluronic fillers include either arterial embolus or venous compression during or after the event which results in reticulation some hours later that may lead to total skin necrosis within a few days. Some of these patients show no evidence of vascular compromise during injection and this has led me to postulate the ‘roundabout’ theory of etiology (1).

Because of the recent increase in late vascular occlusion complications that I am seeing, especially those from overseas, it has given me the opportunity to try and prevent dermal scarring by trying to stimulate the restoration of epithelial tissue at the earlier opportunity. We have known for a long time that hypoxia is a vital stimulant for both angiogenesis and subsequent neocollangenesis, but development of adequate capillary network within the damaged skin requires adequate amounts of tissue oxygen concentration. Oxygen is vital for hydroxylation of lysine and proline residues during collagen synthesis and for cross linking and maturation of collagen which is required for strong wound healing. Lack of oxygen is primarily corrected by the use of high concentration hyperbaric oxygen, leading to adequate amounts of mature collagen formation.

Hyperbaric Oxygen Therapy (HBOT)

Hyperbaric Oxygen Therapy HBOT increases the oxygen gradient between the centre and periphery of the wound, thus creating a strong angiogenic stimulus. This along with fibroblastic proliferation leads to increased neovascularisation. Hyperoxia in normal tissues causes vasoconstriction which reduces post-traumatic tissue oedema, contributing to the treatment of necrosis. This vasoconstriction, however, does not cause hypoxia as this is more than compensated by increased plasma oxygen content and microvascular blood flow (2). HBOT increases the generation of oxygen free radicals, which oxidise proteins and membrane lipids, damage DNA and inhibit bacterial metabolic functions. Superoxide dismutase, catalase, glutathione and glutathione reductase keep the formation of these radicals in check until the oxygen load overwhelms the enzymes, leading to the detrimental effects on cell membranes, proteins and enzymes. HBOT is particularly effective against anaerobes which lack superoxide dismutase and facilitates the oxygen-dependent peroxidase system by which leukocytes kill bacteria (3)

Secondary mechanisms of action to provide epithelium include fibroblast proliferation and neocollangenesis by use low level laser light (LLLT) and the use of growth factors from platelet rich plasma (PRP). This results in unwanted angiogenesis that has to be modified later by the use of intense pulsed light.

Re-epithelisation with Platelet-rich plasma (PRP) and Low-level laser (light) therapy (LLLT)

Platelet-rich plasma (PRP) can regenerate tissue regeneration and it is becoming a valuable adjunct to promote healing in many procedures in aesthetic medicine. PRP derives from the centrifugation of the patient's own blood and it contains growth factors that influence wound healing, thereby playing an important role in tissue repairing mechanisms (4). Platelets form a rich source of important growth factors, such as platelet-derived growth factor (PDGF), transforming growth factor-b (TGF-b) 1 and 2, and vascular endothelial growth factor (VEGF); all of these are involved in the angiogenic cascade which assists in hard and soft tissue wound healing (5). I was aware that the repaired tissue would be quite vascular due to factor (VEGF) and that I would possibly have to treat this with a vascular laser later on in the healing process.

It is imperative to restore epithelium to the compromised area as quickly as possible or one will end up with a dermal scar. Low-level laser (light) therapy (LLLT) is a fast-growing technology used to treat a multitude of conditions that require stimulation of healing, relief of pain and inflammation, and restoration of function. The photons are absorbed by mitochondrial chromophores in skin cells. Consequently, electron transport, adenosine triphosphate (ATP) nitric oxide release, blood flow, reactive oxygen species increase and diverse signaling pathways get activated. Stem cells can be activated allowing increased tissue repair and healing (6). We used an Omnilux Revie in the clinic and the patient was given a portable Genosys Omega light for home use.

Technique

HELPIR is an acronym  

H= Hyperbaric oxygen

E= Epithelial stimulation

L= Low level light laser (633nm)

P= PRP

I =IPL

R= Resurfacing laser 

HELPIR technique in practice

Reversal of a nine day old skin necrosis due to dermal filler vascular occlusion

This case involves a 34-year- old woman who received some hyaluronic acid injections to the left nasolabial fold and marionette area. She had an uneventful procedure but reported back to the aesthetic clinic with a blue-black skin discolouration in the nasolabial and malar area on the second day. In view of the colour of the area she was told by a nurse that it was a bruise and for her to take some arnica. When bullae and sloughing occurred on the fourth day she went to her GP who mistakenly thought it was an infective process and he started her on dual antibiotics. Her condition disimproved over the weekend and she eventually presented to a hospital emergency room on the seventh day. Her area of compromise was cleansed and she was referred to plastic out-patients the next day who provided no additional care. I was informed of the problem by a hospital doctor about the problem when nine days had already passed.

It was immediately obvious that some level of vascular compromise had occurred to the area mentioned with skin breakdown, demarcation, ulceration and sloughing. I suspected this had occurred secondary to venous occlusion by the dermal filler rather than by the action of direct arterial embolism. My impression was formed because of the patient's late presentation of signs (second or third day), the lack of pain during the period that the lesion was developing and there was no history of immediate blanching during the procedure. I had treated many similar cases and was aware that the golden period of recovery had already passed and there was a deficit of material of physicians who had returned necrotic skin back to full physiological and aesthetic function after such a prolonged period of time.

Methods and Materials

The patient was immediately treated with 750 units of Hyalase (hyaluronidase) in a diluted solution of 2% lignocaine to both increase vasodilation and decrease the burning sensation of the enzyme. She was screened for any allergy to bees (hyaluronidase is present in bee sting) and commenced on oral nitrates (20mgs Cialis (tadalafil)) to increase increases blood flow to the area by vasodilation. I prefer to use oral nitrates rather than nitropaste as it works for 48hrs (including night), whereas topical treatment has to be applied hourly. The patient was given 100mgs of cortisone IV and commenced on 4mgs of Dexamethasone PO because of the possibility of venous occlusion secondary to swelling and to reduce the inflammatory state caused by necrosis. She was left on her antibiotics to cover the possibility of infection and referred for daily hyperbaric oxygen therapy. We decided to start at 75% strength later rising to maximum pressures in view of the fact her nose developed necrosis and the long period that had passed since her initial vascular compromise.

Patient Plan Week 1 (see daily) Day 1, 2

Patient to be treated in clinic every day for one week. 

Hyperbaric Oxygen –75% strength daily  

Hyalase (with lignocaine) 750 iu/12hrly for 2 days 

Dexamethasone 4mgs/day for 2 days 

Cialis 20mgs daily for 2-3 days

Klacid 500mgs bd for 5 days 

Left on Flucloxacillin from GP

Daily Low-level laser (light) therapy (LLLT)

Day 3, 4

Hyperbaric Oxygen –increased to full strength daily

Hyalase (with lignocaine) 750 iu/12hrly for another day to include nasal site  

Dexamethasone 4mgs/day to stop 

Cialis 20mgs daily to continue 

Klacid 500mgs bd to continue 

Flucloxacillin 500mgs qid to continue

Daily Low-level laser (light) therapy (LLLT) 

Commence PRP weekly

Day 5, 6

Hyperbaric Oxygen –increased to full strength daily  

Cialis 20mgs daily to stop 

Klacid 500mgs bd to stop 

Flucloxacillin 500mgs qid to stop 

Daily Low-level laser (light) therapy (LLLT)

Day 7, 8

Hyperbaric Oxygen –increased to full strength daily  

Continue PRP weekly 

Daily Low-level laser (light) therapy (LLLT)

Patient Plan Week 2, 3, 4

Hyperbaric Oxygen – stopped on Day 10  

Continue PRP and Omnilux 633 light weekly 

Low-level laser (light) therapy (LLLT) Omnilux 633 bi-weekly 

Home use Genosys Omega light

Patient Plan Week 4, 5, 6, 7, 8

PRP stopped on Day 36 

IPL commenced to Day 42 to continue every three weeks

Low-level laser (light) therapy (LLLT) Omnilux 633 bi-weekly 

Home use Genosys Omega light

Patient Plan Week 8 and 9

IPL stopped on Day 101 

CO2 laser commenced Day 101 Lumenis ActiveFx at 10w 100mj 3/6/2

Treatment stopped Day 108

Mild exfoliation may later be used 2% Salicylic Acid, 0.3% Retinol etc

Lumenis Ultralase CO2 Laser with ActiveFx settings

Lumenis Quantum IPL Omnilux Revive 633 Genosys Omega Light

References

(1) Dr. Patrick Treacy introduces the 'roundabout' theory of dermal filler induced vascular occlusion http://www.bodylanguage.net/facing-complications/

(2): 316–324. Hyperbaric oxygen and wound healing Sourabh Bhutani and Guruswamy Vishwanath

(3) Hyperbaric oxygen therapy for chronic wounds. Kranke P1, Bennett MH, Martyn-St James M, Schnabel A, Debus SE, Weibel S.

(4) Autologous platelet-rich plasma for treating chronic wounds. Martinez-Zapata MJ, Martí-Carvajal AJ, Solà I, Expósito JA, Bolíbar I, Rodríguez L, Garcia J.

(5) Immun Ageing. 2013; 10: 23. Platelet-rich plasma (PRP) in dental and oral surgery: from the wound healing to bone regeneration Antonino Albanese, Maria E Licata, and Giuseppina Campis

(6) Semin Cutan Med Surg. 2013 Mar; 32(1): 41–52. Low-level laser (light) therapy (LLLT) in skin: stimulating, healing, restoring Pinar Avci, MD, Asheesh Gupta, PhD, Magesh Sadasivam, MTech, Daniela Vecchio, PhD (2) Indian J Plast Surg. 2012 May-Aug; 45