DOI: https://doi.org/10.21203/rs.3.rs-2284011/v1
To analyze the relationship between dermatochalasis and the orbicularis retaining ligament (ORL) and their effect on involutional entropion.
Ninety-two eyelids of 68 patients with involutional entropion underwent surgery to remove the prolapsing fat, plicate the lateral canthal tendon or use a lateral tarsal strip procedure, advance the retractor, resect the excess skin with OOM and tighten the OOM by securing the OOM flap to the periosteum, and had a postoperative follow-up of 12 ~ 18 months.
Eighty-eight of 92 eyelids had a satisfactory outcome with normal eyelid positioning and pleasing cosmetic results. Four eyelids showed ectropion, but all of them improved in three months. No recurrence was observed in this study.
The dermatochalasis may be an aetiology of involutional entropion. The relaxed skin could be retracted upward by the ORL, and the skin is then rolled over the superior tarsal border and pressed against the globe. Our procedure addressed most factors and is a useful technique for involutional entropion.
Involutional entropion is the most common type of lower eyelid malposition in the elderly population. The eyelid margin turns inward against the globe, causing tearing, irritation, foreign-body sensation, corneal ulcers, and subsequent vision loss. The aetiology is complex and includes horizontal lid laxity [1, 2], vertical laxity resulting from lower eyelid retractor disinsertion or attenuation [3], and overriding of the preseptal orbicularis oculi muscle (OOM) [4]. To date, numerous surgical techniques have been reported, and those that addressed a single factor such as everting sutures (ES), and Jones, Wies, and lateral tarsal strip (LTS), have proven effective [5, 6]. Randomised controlled trials (RCT) have shown that combined procedures performed better than a single procedure [7, 8]. We believe that procedures that address more factors will result in lower recurrence rates and found that it was necessary to excise excess skin during our procedures. Many authors have also excised excessive skin during surgery [9–16], and Meadows et al. mentioned that dermatochalasis and orbital fat prolapse were possible causative factors for involutional entropion in 1999 [17]. Dermatochalasis is an aging process aided by gravity and is characterised by loss of elastic tissue, weakening of connective tissue, thinning of the epidermis, and redundancy of the skin [18]. While the relaxed skin should shift downward because of gravity, it becomes pressed upward, which leads to entropion formation. How does this happen?
Ninety-two lower eyelids of 68 patients with involutional entropion underwent surgery from December 2018 to December 2020. Institutional review board approval was obtained and written informed consents were obtained from all participants. The research was adhered to the principles of the Declaration of Helsinki. There were 37 men (48 eyelids) and 31 women (44 eyelids) ranging in age from 51 to 89 years (average age, 66.3 years). And twenty eyelids were recurrent and had previously undergone other surgeries, including nine patients with transcutaneous retractor advancement, two with ES and others with no definite records. All cases were observed for more than 12 months postoperatively (range, 12–18 months).
The location of the incision was marked 1mm below the lashes from the punctum to the lateral canthus and then slightly downward to the orbital rim. The lower eyelid was infiltrated with 2 ml of 2% lidocaine with 1:100,000 epinephrine. The skin and the underlying pretarsal OOM were incised along the mark and dissected to the orbital rim to make the skin-orbicularis flap. The globe was pressed gently and the prolapsing fat removed. The lateral canthal tendon was secured to the lateral orbital rim periosteum with a 5 − 0 Ethibond suture (Figures 1 and 2), or the LTS procedure for the severe horizontal laxity was used. Three double-armed 5 − 0 Ethibond suture were placed through the inferior border of the tarsus and in the retractor 3-5mm below the border༈Figures 1 and 3༉. The sutures were tied to achieve a proper position of the eyelid. The patient was asked to look upward and open their mouth. The flap was draped with gentle upward and lateral traction, and the flap was marked according to the underlying incision. The excess flap was resected, including the skin and the underlying OOM. The OOM flap was tightened by securing to the lateral orbital rim periosteum with a 5 − 0 Ethibond suture. Finally, the wound was closed with a continuous 6 − 0 nylon suture. The surgical video is available.
Of the 92 eyelids, 88 had satisfactory eyelid position and cosmetic results. Four eyelids showed ectropion, but all improved in three months and had a normal position. There was asymmetry in some unilateral entropions, but it was not obvious in most cases. There was no recurrence at more than 12 months of follow-up.
The relaxed skin becomes pressed upward, which leads to entropion formation. And it was necessary to excise excess skin during our procedures. Based on existing literature, we found that the orbicularis retaining ligament (ORL), which arises from the periorbita of the inferior orbital rim, functions as a functional and structural barrier that allows the sagging skin to be retracted upward [19, 20]. ORL can also restrict the OOM and fat in addition to the skin. We hypothesised that the relaxed skin is retracted upward by the ORL, rolled over the tarsus, and pressed against the globe, which may represent the aetiology of involutional entropion.
The skin loses elasticity and tone with aging due to degraded elastic fibres and reduced collagen synthesis [21]. Loss of skin elasticity is a critical feature of eyelid aging and leads to rhytide, colour and texture changes, and festoon formation [22]. Periocular dermatochalasis is a common sign of facial aging [23]. The lower eyelid length increases vertically with age and is measured from the lid margin to the lower eyelid demarcation crease in the midpupillary line. The length increases linearly with each decade, with the greatest increase in the 40-49-year-old group [24].
Intrinsic skin aging is a naturally occurring process that is characterised by dermal atrophy from loss of collagen, elastic fibre network degeneration, and loss of hydration [25]. Collagen and elastin breakdown, marked chronic inflammation, and the scarring of dermis are observed in the histopathology of involutional entropion [26, 27].
The ORL is continuous from the medial to the lateral canthus [28]. The tear trough ligament (TTL) is a continuation or integral part of the ORL because its organizational structure is the same and its position is continuous [29]. The ORL arises from the periorbita of the inferior orbital rim, travels through the junction of the palpebral and orbital portions of the OOM, and attaches to the dermis [20, 30, 31]. To the best of our knowledge, ORL was first termed the orbitomalar ligament (OL) and investigated in detail by Kikkawa et al. (1996) [30].
The ORL consists of multiple fibroelastic bundles with a multilayered plexiform shape and shows histological continuity from periosteal origin to dermal attachment [20, 30]. The ORL is a particularly important structure for maintaining the eyelid and cheek skin and contouring the characteristic facial appearance [20]. As an osteocutaneous ligament, the ORL limits the descent of the OOM and skin [28–33].
The ORL becomes elongated and its cutaneous insertion decreases inferiorly with advancing age [20, 30]. The ORL is involved in the formation of the palpebromalar groove [19, 20], similar to the TTL for the tear trough [29].
The lower eyelids of Asians have orbital fat that extends anteriorly and superiorly, and the preseptal OOM overrides the pretarsal OOM. This may cause the development of fuller lower eyelids and result in redundant skin and further muscle overriding [34]. Fat prolapses may be caused by excessive fat or weakening of the orbital septum and are aggravated by gravitational descent of the midface, which contributes to double convexity and ORL changes with aging [35]. Overriding of the preseptal OOM does not always produce an inward rotational force on the tarsus [36].
Complex anatomical factors contribute to the involutional entropion. In addition, involutional entropion is a dynamic process that involves interactions between changes in various anatomical structures.
A major anatomical basis for the appearance of festoons seems to be the downward descent of the tissues superior to the ORL, and the ORL acts as a functional and structural barrier that defines the lower extent of several clinical entities [19]. That is, the relaxation of tissue above the ORL (including the orbital septum, fat, OOM, and skin) bulges forward and downward, but the ligament restricts prolapse [29]. The sagging skin can be retracted upward by the ORL [20], and the skin is then rolled over the superior tarsal border and pressed against the globe. This may be one of the aetiologies of involutional entropion. This aetiology can be combined with other aetiologies, such as horizontal eyelid laxity and the degeneration and loss of anchoring support of the ORL to cause OOM instability and overriding [30].
The diagram (Fig. 4) shows dermatochalasis and ORL on involutional entropion. The diagram was based on previously published reports [4, 10, 20, 28–30, 33, 34, 37–41].
A CO2 laser can cause thermal coagulation of proteins within the dermis and dermal contractures. Dr. Babuccu treated involutional entropion in five patients using a CO2 laser, and the results were satisfactory [42]. This implies that dermatochalasis may be the aetiology of involutional entropion.
The ORL itself undergoes an aging process and tends to become lax over time. However, it is probable that in patients with a disparate aging process of the ligaments and the dermal contents in which the ligaments age slower than the cutaneous tissues, beyond that what occurs in the normal population due to probable environmental exposures, the ORL may act to serve as a factor in the pathogenesis of dermatochalasis and by extension, involutional entropion as mentioned in the hypothesis. Only in such patients where the tensile strength of the ligament exceeds the age-appropriate counterparts, and not everyone with a normal aging process, may ligament release offer prospects of a cure for involutional entropion.
Releasing ORL might be an option for treating involutional entropion, but we doubt that this could result in ectropion [43]. At present, we have no experience with releasing the ORL, and additional studies, in addition to our own, are needed in the future to investigate this and improve patient treatment.
The relaxation of tissue above the ORL (including fat, OOM, and skin) bulges forward and downward, but the ligament restricts prolapse. The sagging skin, fat, and OOM can be retracted upward by the ORL and we have solved all these factors during our procedure.
We believe that procedures that address additional factors related to this condition will result in lower recurrence rates. Notably, our procedure can solve most etiological factors of involutional entropion to some degree, to regain normal eyelid position and provide aesthetic rejuvenation of the lower eyelid.
However, we cannot prove that the relaxed skin is retracted upward by the ORL to result in entropion directly, even though we excised excessive skin during our procedure.
We propose that relaxed skin becomes retracted upward by the ORL, rolled over the tarsus, and pressed against the globe with age, which may represent the aetiology of involutional entropion. Further investigations are needed to determine the roles of dermatochalasis and ORL in involutional entropion in the future.
What was known before
● Many authors have excised excessive skin during the surgery for involutional entropion.
What this study adds
● The dermatochalasis may be an aetiology of involutional entropion which is retracted upward by the ORL, rolled over the tarsus, and pressed against the globe.
Conflict of interest
None
Funding
None
Ethical approval
The research was adhered to the principles of the Declaration of Helsinki.
Acknowledgements
We thank Dr. Zhou Feng, Dr. Nie Yu, Dr. Lu Yingying, and Dr. Guo Li for their assistance and help in the manuscript and research.