INTRODUCTION
Lower eyelid ectropion is a well-recognized complication following surgical repair of orbital fractures, particularly when a transcutaneous subciliary approach is employed. Although this approach provides excellent exposure of the orbital floor and is also widely used in aesthetic lower eyelid surgery, it has been associated with a higher incidence of postoperative lower eyelid malposition, including ectropion and retraction, compared with transconjunctival approaches [1-3]. Such malposition may result in ocular surface exposure, epiphora, irritation, and aesthetic dissatisfaction, frequently necessitating secondary corrective procedures.
Postoperative lower eyelid malposition is widely regarded as a multifactorial condition. In addition to surgical approach and trauma severity, patient-related factors—most notably advanced age—have been shown to increase susceptibility to lower eyelid instability after lower eyelid surgery [1-5]. Importantly, clinically significant ectropion may develop even in the absence of substantial anterior lamellar deficiency, suggesting that mechanisms other than skin shortage are instrumental in postoperative eyelid malposition [3,4].
Anatomically, the lower eyelid is composed of anterior, middle, and posterior lamellae, each of which plays a distinct role in eyelid support and mobility. While anterior lamellar shortening has traditionally been emphasized as a primary mechanism of postoperative ectropion, increasing attention has been directed toward pathological changes involving the middle lamella. Scarring or adhesions of the orbital septum may restrict vertical eyelid excursion and contribute to persistent eyelid malposition, particularly in older adults undergoing transcutaneous lower eyelid surgery [2,6].
Despite growing recognition of the role of middle lamellar pathology, objective clinical or radiologic correlation with intraoperative findings has been limited. In particular, the perioperative soft tissue changes that may precede middle lamellar fibrosis remain incompletely characterized. Herein, we present a case of lower eyelid ectropion that developed after orbital floor blowout fracture repair via a subciliary approach in an older adult. The case provides detailed surgical and imaging observations that contribute to a more nuanced understanding of middle lamellar involvement in postoperative lower eyelid ectropion.
CASE REPORT
A 78-year-old woman presented to our department after a ground-level fall, reporting periorbital swelling. Computed tomography revealed a left orbital floor blowout fracture without evidence of globe injury on coronal facial bone images (Fig. 1A). Surgical repair was planned, and open reduction was performed via a transcutaneous subciliary approach. Fracture reconstruction was achieved using a porous polyethylene implant (Medpor; Stryker), which was positioned to restore the contour of the orbital floor.
The immediate postoperative course was unremarkable. Mild swelling of the left lower eyelid was observed during the early postoperative period, without signs of infection, wound dehiscence, or skin compromise. Thus, the patient was managed conservatively. Approximately 3 weeks after surgery, however, progressive eversion of the left lower eyelid became evident. Despite continued observation over the subsequent 3 months, the ectropion failed to improve spontaneously, and the patient reported ocular irritation and tearing (Fig. 2A). Surgical revision was therefore indicated.
Revision surgery was performed through the previous subciliary incision. Dissection in the preseptal plane revealed dense fibrotic adhesions involving the middle lamella, resulting in tethering of the lower eyelid and marked restriction of upward eyelid excursion. Targeted adhesiolysis was performed at the level of the arcus marginalis, allowing adequate mobilization of the lower eyelid. Adequate release was confirmed intraoperatively by restoration of free upward eyelid movement, without resistance, on gentle traction. After complete release, the eyelid could be repositioned without tension, and no skin shortage was encountered.
To reinforce horizontal lower eyelid support, a lateral tarsal strip procedure was subsequently performed. Two drill holes were created in the lateral orbital rim, and the tarsal strip was secured using 4-0 polypropylene sutures (Prolene; Ethicon). Stable and symmetrical eyelid position was confirmed intraoperatively, and skin closure was completed without difficulty.
The postoperative course was uneventful. Complete resolution of the ectropion was achieved, and the lower eyelid position remained stable. At the 1-year follow-up visit, the patient demonstrated a satisfactory eyelid contour without ocular discomfort, tearing, or functional problems (Fig. 2B).
As part of routine postoperative follow-up after orbital fracture repair, coronal computed tomography was obtained 6 months after initial surgery. The scan demonstrated a well-positioned orbital floor implant with bony remodeling along the reconstructed orbital floor, indicating adequate orbital support (Fig. 1B).
To further evaluate perioperative soft tissue changes, a retrospective review of the patient’s imaging studies was performed. One week after the initial orbital fracture repair, magnetic resonance angiography obtained for an unrelated neurologic evaluation incidentally revealed a hematoma in the preseptal area of the left lower eyelid (Fig. 3A). A subsequent brain magnetic resonance imaging study performed approximately 2 months later revealed fibrotic changes involving the septal region on sagittal T1-weighted images (Fig. 3B), as well as signal changes in the anterior lamella (Fig. 4A). These anterior lamellar changes were considered more likely to reflect secondary soft tissue irritation associated with persistent eyelid eversion rather than a primary cicatricial process. In the same examination, the inferior oblique muscle was appropriately positioned over the orbital floor implant, and coronal T2-weighted images demonstrated no abnormal signal intensity or enlargement of the inferior rectus or other extraocular muscles (Fig. 4B). These radiologic findings were concordant with the intraoperative observation of dense middle lamellar adhesions encountered during revision surgery.
DISCUSSION
Postoperative lower eyelid ectropion following orbital fracture repair is a multifactorial complication that cannot be explained solely by anterior lamellar shortening. Although cutaneous deficiency has traditionally been emphasized as a primary cause, restriction or scarring of the middle lamella may play a critical role in limiting eyelid mobility, even when skin involvement is minimal [3,4]. The present case underscores the clinical importance of recognizing middle lamellar pathology as a distinct mechanism of postoperative ectropion and addressing it directly during revision surgery.
In this patient, retrospective imaging demonstrated a preseptal hematoma in the early postoperative period, followed by fibrotic changes along the septal region on follow-up imaging. Although these findings do not establish a direct causal relationship, the temporal sequence provides contextual support for the intraoperative identification of dense adhesions at the level of the arcus marginalis. Such adhesions likely contributed to tethering of the lower eyelid and restricted upward excursion, ultimately resulting in persistent ectropion. These observations reinforce the concept that secondary soft tissue changes involving the middle lamella, rather than anterior lamellar deficiency alone, may play a pivotal role in the pathogenesis of postoperative eyelid malposition [2,6,7]. In the setting of blowout fracture repair using a subciliary approach, insufficient hemostasis during lower eyelid dissection or closure may predispose to postoperative hematoma formation, which in turn can promote an inflammatory response and subsequent fibrotic contracture of the middle lamella. Accordingly, meticulous intraoperative hemostasis and consideration of adjunctive measures, such as temporary drain placement in selected high-risk cases, may be important preventive strategies to reduce the risk of cicatricial complications.
Although muscle-related factors, including inferior rectus dysfunction or extraocular muscle injury, have been proposed as potential contributors to postoperative lower eyelid malposition [7], no radiologic evidence of extraocular muscle abnormality was identified in this case. Magnetic resonance imaging obtained 2 months postoperatively demonstrated normal position and signal intensity of the inferior oblique and inferior rectus muscles, suggesting that extraocular muscle pathology was unlikely to be a primary contributor to the observed ectropion.
In addition, subciliary incisions may theoretically pose a risk of transient or partial denervation of the orbicularis oculi muscle through injury to terminal branches of the facial nerve [8]. However, subtle lower eyelid muscle weakness is difficult to assess objectively in this clinical context. Although a minor neuromuscular component cannot be entirely excluded, the intraoperative identification of dense middle lamellar adhesions and the complete resolution of ectropion following targeted middle lamellar release with lateral canthal reinforcement suggest that middle lamellar restriction was the principal mechanism in this patient. Even if a degree of orbicularis oculi dysfunction had been present, it would likely have functioned as a secondary contributor rather than the dominant cause of eyelid malposition. Accordingly, these findings support the interpretation that middle lamellar restriction, rather than neuromuscular imbalance or extraocular muscle involvement, was the dominant mechanism underlying the patient’s eyelid malposition [2].
From a surgical standpoint, the key principle in this case was restoration of eyelid mobility through targeted release of restrictive middle lamellar adhesions before horizontal tightening. Adhesiolysis at the level of the arcus marginalis effectively re-established vertical eyelid excursion, after which lateral tarsal strip fixation was performed to reinforce horizontal support. Although isolated lateral tightening may be sufficient in cases of pure involutional horizontal laxity, failure to address vertical restriction in the presence of cicatricial components may compromise surgical outcomes. This consideration is particularly relevant in older adults, in whom age-related tissue laxity and reduced elasticity further predispose the lower eyelid to instability [6,9,10]. In addition, meticulous layer-by-layer repair, including accurate re-approximation of the periosteum, orbicularis oculi muscle, and skin, may help minimize postoperative fibrosis and reduce the risk of lower eyelid malposition by preserving normal anatomical relationships and limiting excessive scar formation.
Consistent with this approach, several studies have reported suboptimal outcomes when isolated tightening procedures are performed in the presence of cicatricial or restrictive pathology [11,12]. The favorable outcome in the present case, with stable eyelid position maintained at 1-year follow-up, supports a stepwise revision strategy consisting of initial release of middle lamellar restriction followed by reinforcement of horizontal eyelid support. In this context, preoperative imaging—even when obtained for unrelated indications—may provide valuable insight into underlying septal pathology and assist in surgical planning.
The implications of this case extend beyond orbital fracture repair. Older adults undergoing transcutaneous lower eyelid procedures, including aesthetic lower blepharoplasty, may encounter similar challenges related to age-associated laxity and postoperative soft tissue changes [1-5]. In such settings, persistent eyelid malposition should prompt careful evaluation for restrictive middle lamellar pathology and adequacy of lateral support, rather than reliance on prolonged observation or isolated tightening alone. Accordingly, the surgical principles demonstrated in this case may be applicable to both reconstructive and aesthetic lower eyelid surgery.
This report is limited by its single-case nature and the absence of quantitative eyelid measurements. In addition, the imaging studies were not dedicated orbital examinations, which may limit precise characterization of periocular soft tissues. Because these imaging studies were obtained for unrelated neurologic indications, the findings should be interpreted as supportive rather than diagnostic. Nevertheless, the concordance among radiologic findings, intraoperative observations, and postoperative outcomes suggests that careful assessment of the middle lamella should be incorporated into the evaluation of postoperative lower eyelid ectropion, particularly in older adults undergoing transcutaneous lower eyelid surgery.
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