Mr Mark Devlin and Mr Jeff Downie outline a proposed classification system related to labial vascular compromise
Labial vascular compromise (LVC) following lip filler injection is the subject of much discussion and anxiety amongst aesthetic clinicians. Most of the discussion centres on the avoidance and management of this complication, but little about the underlying pathogenesis and mechanisms.1 The aim of this paper is to expand the debate on this subject.
In considering LVC we have also examined the potential underlying process of compartment syndrome (CS). This is a well-recognised clinical phenomenon occurring when the pressure within a tissue compartment rises to exceed perfusion pressure.2 Therefore, it results in vascular compromise with tissue ischaemia and potential necrosis. The syndrome itself represents a spectrum of severity and can present in both acute and chronic forms.2
Whilst CS occurs in many anatomical areas of the body, the vascular compromise specifically seen following labial injection of filler has never been considered, or defined, as a form of this syndrome. In this article, we review the presentation of vascular compromise following lip filler and consider what anatomical, technical and pathogenic considerations may be contributory. In considering CS as a potential endpoint of swelling and inflammation within the aesthetic lip compartment/subunit, we also seek to consider what lessons may be learnt from the management of CS elsewhere in the body. This article represents a theoretical proposal regarding the underlying pathogenesis of LVC. Understanding the potential subtypes of LVC may help in directing treatment algorithms or be beneficial if treatment modalities were to be compared.
Firstly, we carried out a literature search using Medline. We inserted a variety of key words in combination, which included, ‘filler’, ‘lip’, ‘labial’, ‘compartment syndrome’ and ‘labial artery’. Our aim was to determine whether any classification system currently existed. We were also interested to ascertain whether CS had been considered and/or described as one of the specific pathological processes underlying the presentation of post-lip filler vascular compromise.
We also conducted a review of recent cases presented to our clinic in which the diagnosis of LVC was made following aesthetic injection with lip filler. We sought to classify the various presentation types in a simple clinical system. We also reviewed the recent literature on the management of CS to determine if there were areas of commonality which may contribute to the understanding and management of LVC and labial compartment syndrome (LCS), which we discuss later.
Post-filler LVC was reported in the literature, however, we found no current classification system. No comparisons of treatment modalities related to the potential underlying processes which may cause LVC were also found.
In terms of CS, this represents a spectrum of clinical presentations with a consistent underlying pathogenesis.2,3 Typically, CS occurs following trauma or bleeding. Whilst it affects the limbs in most cases, variants within the head and neck have been described, for example, the superior orbital fissure syndrome.4,5 The consistent anatomical elements can be considered as neurovascular anatomy that traverses and is contained within muscular compartments. Any cause of muscle swelling or increased pressure within the compartment may result in a rise in pressure which, if it exceeds the perfusion pressure, will result in vascular compromise and give rise to a predictable pattern of signs and symptoms.
The signs and symptoms of CS are traditionally described as being the ‘six Ps’. These are described as pain, pallor, pulselessness, paraesthesia, paralysis and perishing cold (poikilothermia). The lower limb is the most common site for this to occur and trauma is cited as the most common cause of acute CS. Chronic variants of CS are described, for instance, in relation to exercise. There are acute and chronic presentations of this condition. It does not seem that the definition of CS has been specifically used to define or describe any of the pathological processes underlying the vascular compromise seen in association with lip filler, although the diagnosis has been defined in the head and neck, most notably the orbit.4,5 In the case of vascular compromise following lip injections, the signs and symptoms are somewhat consistent with the above. Immediate pain and blanching of the tissues are commonly described by patients suffering this complication.
The general effects of lip filler on the capillary vasculature have been reviewed and the impact on the capillary system have been suggested as critical.6 This effect on the microvasculature is in keeping with a more general issue with perfusion, rather than that of simple direct intravascular injection.
From our own clinical experience, LVC presents in either one of two ways. For clarity, we have considered these as either Type 1 or Type 2. These can be further subclassified and described as below described, as summarised in Table 1.
Type 1: Immediate
Type 1 typically presents as soon as the injection begins. There is usually severe pain and immediate blanching of the skin and vermillion. Patients who have had treatments before will state that this was unlike any previous experience. Anecdotally, this may be more often seen in patients who are having a first treatment of this region. The following are the potential mechanisms for this presentation:
1. Intravascular injection – this would cause immediate vascular occlusion. The dimensions of the labial artery are such that this is not likely but does remain a possibility. There is evidence of this occurrence in the literature.
2. Intramural injection (mural damage) – this could occur in association with the above but could also occur without intravascular ingress of material. Arterial spasms would result as well as almost immediate mural and extramural swelling.
3. Extramural – in this case the vascular occlusion would be related to external pressure. This is perhaps most likely in the case of smaller diameter vessels or where there is an intramuscular course at the point of the injection, leading to an immediate compression of this ‘compartment’.
Type 2: Delayed
This type typically presents at some point beyond the initiation of the injection itself (hours or even days). It may be preceded by increasing pain, swelling and bruising. The signs and symptoms tend to be initially milder than those seen in Type 1. If these processes continue, then we postulate that a common end point may be LCS.
1. Haematoma formation – this could result from direct injury to the labial artery or a branch of this, which falls short of causing an immediate vascular compromise.
2. Oedema – any tissue damage may result in swelling post-treatment. If this is significant, in the lip, a CS may result within the aesthetic compartment.
3. Secondary infection – this could be either viral or bacterial. This is more likely in the presence of a relative vascular compromise and may worsen the symptoms.
|Type 1 (immediate)||Type 2 (delayed)|
|Underlying processes||Intravascular injection||Compartment haematoma|
|Intramural injection||Compartment oedema|
|Extramural injection||Compartment infection|
Table 1: Summary of the proposed classification subtypes
Type 2 pathogenesis may result in a milder form of vascular occlusion. We would expect simple conservative management, with no active intervention, to result in a complete resolution. There would be a risk of sudden deterioration of this group resulting in signs and symptoms of a Type 1 presentation.
This type of variable presentation has been described previously and the role of hyaluronidase as a treatment modality reviewed for its efficacy.7 We have also considered the various independent factors that may influence the risk of either type of LVC. These factors include labial artery anatomy, volume of injection, depth of injection, speed of injection or concurrent pathology/infection, such as herpes simplex or staph aureus, all seem likely to contribute to the relative risk for any patient or treatment episode.
Labial artery anatomy has been the subject of considerable interest in literature. Studies have described these variations topographically and in cadavers, whilst others have used imaging (surface and cross-sectional) to describe the course of the arteries within the lip.8-11 The practical clinical question raised by these studies is whether these variations are contributory to the underlying risk of LVC or even subsequent LCS.
CS is most likely when the neurovascular structures are at risk to the effects of increased pressure within a relatively fixed compartment. The one variant of the labial artery that would seem to increase the theoretical risk of both Type 1 and Type 2 is LVC being the intramuscular variant. Where the artery lies in the loose areolar tissue deep (oral mucosal side) to the orbicularis oris muscle, the risk of LCS would theoretically be significantly lower, especially to Type 1. LVC could still develop in this situation if large volumes are injected or if significant post-treatment swelling were to occur. Bleeding and haematoma formation might also contribute to the development of LVC. In this sense, the depth of injection may have an influence in the development of LVC.
The speed of injection may also be significant in relation to trauma and subsequent tissue oedema, thus constituting a relative contributory factor. Any factor contributing to inflammation and swelling would also be seen as a risk factor for Type 2 LVC. These would include traumatic technique, infection and haemorrhage. It is clearly good practice to avoid filler injections in the presence of active infection, but there may be pathogens present without any obvious signs or symptoms. The delayed presentation may therefore be due to the reduction in perfusion pressure within a compartment of the facial anatomy. Given the various compartments of the face, it seems possible that a CS could develop.
We also reviewed the published treatment algorithms, but only found the Aesthetic Complications Expert (ACE) Group World guidance.12
This provided a sensible approach to the management of LVC and potential lip necrosis. It has been developed from current published evidence, but does not seek to classify the underlying mechanism of VC. As we have considered the possibility of LCS being a common endpoint of untreated LVC of either main subtype, we sought lessons in relation to possible treatments of LVC and LCS from the general scientific literature. Whilst these lessons need careful consideration, it does seem clear that any treatment algorithm to manage LVC and potential lip necrosis should bear these in mind.
To that end, we would think it appropriate to add corticosteroids, botulinum toxin-A and surgery to any future debate regarding the treatment of LVC.2,3
LVC can occur following injection of filler in the lip. The exact mechanism in each individual case is unknown, but there would appear to be a small, predictable number of these which we might define from first principles. The mechanism of injury is significant when considering treatment/management options, but no current classification exists.
In proposing this classification system, we hope that it may expand the debate regarding the management of LVC given the anxiety and morbidity caused. CS has not yet been proposed as an endpoint in cases of delayed onset LVC, and by doing so in this article, we also seek to expand the debate regarding the true pathogenesis of LVC in this subset of patients. By considering this possible underlying process, we can extrapolate from the evidence-based treatment options of CS elsewhere in the body.
Upgrade to become a Full Member to read all of this article.