REVIEW URRENT C OPINION
Blepharoptosis following ocular surgery: identifying risk factors Kyle J. Godfrey a, Bobby S. Korn a,b, and Don O. Kikkawa a,b
Purpose of review To evaluate the incidence of blepharoptosis following ocular surgical procedures, to elucidate mechanisms for its cause, and to identify potential risk factors for ocular surgeons to avoid. Recent findings Postoperative blepharoptosis has been a poorly understood concept. In the search for a definitive cause, various technical components of surgery have been implicated. Recent research highlights the importance of individual anatomy and proposes new mechanisms for postoperative ptosis, including excessive eyelid tension from specula, topical prostaglandin analogue use, and direct trauma at the level of the tarsal plate. Summary Blepharoptosis is common following ocular surgery and can occur through multiple mechanisms. Certain individuals are at a higher risk for postoperative blepharoptosis, but all surgeons and patients undergoing ocular surgery should understand this risk when providing informed consent. Operative techniques can be adjusted to decrease rates of postoperative blepharoptosis. Keywords blepharoptosis, cataract surgery, eyelid speculum, ocular surgery, ptosis
INTRODUCTION Blepharoptosis, herein referred to as ptosis, is an abnormally low upper eyelid position relative to the visual axis and corneal light reflex (Fig. 1). It is quantified by the margin-reflex distance 1, which has a normal range of 4–5 mm. Proper eyelid position is dependent on both anatomy and neuromuscular function, primarily an intact connection between the levator palpebrae superioris (LPS) muscle and the tarsal plate and pretarsal orbicularis oculi via the levator aponeurosis, and adequate function of the LPS (Fig. 2). Ptosis is a known complication of ocular surgery. A recent study [1] suggests that nearly one-third of acquired ptosis is postsurgical. This ptosis can be transient or persistent, and may detract from the effectiveness of the primary surgical procedure. Furthermore, despite being well reported, its precise mechanism remains unclear. Here we present a review of the literature.
PTOSIS FOLLOWING CATARACT SURGERY Cataract surgery is among the most common surgical procedures worldwide, and ptosis is a well
described postoperative complication, albeit poorly understood. To this end, multiple mechanisms have been proposed, and theories have evolved in tandem with surgical techniques. Most hypotheses focus on damage to the levator complex. Anatomically, the LPS originates from the lesser wing of the sphenoid bone superolateral to the optic foramen and fans out as it travels anteriorly along the superior orbital wall and above the superior rectus muscle, reaching its maximum diameter of 18 mm at the musculotendinous transition to the levator aponeurosis [2]. The levator aponeurosis descends from Whitnall’s ligament and splits into an anterior and posterior lamella. The anterior lamella becomes confluent with the orbital septum and inserts on pretarsal orbicularis oculi muscle and underlying subcutaneous tissue, whereas the posterior lamella a
Division of Oculofacial Plastic and Reconstructive Surgery, UCSD Department of Ophthalmology and bDivision of Plastic Surgery, UCSD Department of Surgery, La Jolla, California, USA Correspondence to Don O. Kikkawa, MD, FACS, Shiley Eye Institute, 9415 Campus Point Drive, La Jolla, CA 92093-0946, USA. Tel: +1 858 822 5972; e-mail: [email protected] Curr Opin Ophthalmol 2016, 27:31–37 DOI:10.1097/ICU.0000000000000218
1040-8738 Copyright ß 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.co-ophthalmology.com
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Cataract surgery and lens implantation
KEY POINTS Blepharoptosis is common following ocular surgical procedures. Individual patient anatomy may confer the highest risk of postoperative blepharoptosis. Surgical techniques can be adjusted to decrease rates of postoperative blepharoptosis. Levator dehiscence is the most likely mechanism, and can be caused by speculum use alone. Postoperative blepharoptosis can be treated successfully with surgical repair.
¨ ller’s inserts on the anterior tarsus (Fig. 2) [3]. Mu muscle arises from the undersurface of the LPS and inserts into the superior tarsus and is innervated by the sympathetic nervous system [4]. The medial horn of the levator aponeurosis is thought be thinner and structurally weaker than the lateral horn [2]. Ptosis can be caused by injury to any of these structures, their insertions, or the innervation to the eyelid retractors. In 1976, Paris and Quickert [5] defined postcataract ptosis as 2 mm or more of upper eyelid drooping persisting for more than 6 months following the cataract surgery. They reported two cases occurring secondary to levator dehiscence and estimated the occurrence to be 1–2% based on a survey of 27 ophthalmologists [5]. Most subsequent studies use their criteria to define postoperative ptosis, although its incidence varies widely. Studies have reported rates between 0 and 44% with different surgical and anesthetic techniques, although most seem to fall between 6 and 12% (Table 1) [6–10]. Few preoperative factors have been correlated with postcataract ptosis. They include ptosis in the nonoperative eye and a narrow palpebral aperture in the operative eye [6,9]. Conversely, patient age, sex, LPS function, eyelid crease position, dermatochala-
FIGURE 1. Right upper eyelid ptosis after cataract surgery.
32
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sis, and preoperative ptosis in the operative eye have no effect on rates of postoperative ptosis [6,7,9,11]. Operative time may play a role, but there is no consensus in the literature [6,12]. Three primary theories shape our understanding of postcataract ptosis:
Bridle suture effect During embryogenesis, the LPS and superior rectus muscle initially develop as a single muscle before separating. In the adult eye, common fascial bands connect their respective muscle sheaths [13]. As such, the use of a superior rectus bridle suture to pull the globe downward can cause damage to the superior rectus/LPS subunit, resulting in high rates of postoperative ptosis. Randomized prospective studies show that using superior rectus bridle sutures results in more frequent postoperative ptosis than episcleral retraction sutures [11]. Furthermore, use of an eyelid speculum, which forces the eyelid in the opposite direction, concurrently with a superior rectus bridle suture nearly doubles the rate of postoperative ptosis from 23 to 44% [14]. This is likely because of strong opposing forces between the levator complex and bridled superior rectus causing levator dehiscence. However, using an open subconjunctival approach for superior rectus bridling results in substantially decreased rates of postoperative ptosis (from 19 to 4%) when compared with a closed, transconjunctival approach [15]. There is disagreement regarding whether the development of a superior rectus hematoma during placement of the bridle suture leads to increased postoperative ptosis [8,9].
WL LPA OS
MM
FIGURE 2. Schematic illustration of upper eyelid anatomy demonstrating the anterior and posterior lamella of the levator aponeurosis, Mu¨ller’s muscle, Whitnall’s ligament , tarsal plate (thin arrow), orbital septum, and pretarsal orbicularis oculi muscle (thick arrow). Illustration courtesy of Benjamin Erickson, MD.
Volume 27 Number 1 January 2016
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Blepharoptosis following ocular surgery Godfrey et al. Table 1. Reported incidence of postoperative ptosis following selected ocular surgeries and surgical procedures Reported incidence of ptosis (%)
Surgical procedure Extracapsular cataract surgery Bridle suture and speculum
1–44.4
Bridle suture (closed approach)
19–23
Bridle suture (open approach)
4
&&
investigate this, Crosby et al. [20 ] performed mechanical testing of eyelid specula to determine the force required to compress each speculum over a range of displacements. They demonstrated that reusable specula are significantly stiffer than disposable specula, and that the stiffness of each speculum was greatest at the range of displacement corresponding to narrower palpebral apertures [20 ]. This increased force on the eyelid and levator complex may explain why patients with the smallest palpebral apertures are most likely to develop postoperative ptosis. &&
Phacoemulsification cataract surgery Bridle suture and speculum Speculum only
12.9 0–11.5
Glaucoma surgery Trabeculectomy without mitomycin C
12
Anesthesia effect
Trabeculectomy with mitomycin C
19
Bilateral ptosis following bilateral trabeculectomy
7
Some have postulated that postcataract ptosis may develop from damage to the levator complex by local and regional anesthetic agents. Suggestions of myotoxicity from local anesthetics were based primarily on animal models and have not been validated in the ophthalmic literature [21]. One study did show a correlation between the volume of peribulbar anesthetic administered during surgery and the amount of ptosis on postoperative day one. This same study also found that postoperative day one ptosis is the best predictor of persistent ptosis at six months [6]. However, other studies have not found a correlation between the speed or volume of peribulbar anesthetic and postoperative ptosis [22]. If administering a nerve block, the injection location can make a difference: the Van Lint block causes higher rates of ptosis than the Nadbath block [11]. However, there does not seems to be a significant difference between retrobulbar and subconjunctival injection when looking at the postoperative ptosis incidence [23,24]. It has also been suggested that hyaluronidase, an enzyme added to local anesthetic to improve distribution, may reduce the incidence of ptosis [25,26], although this has been disputed [27].
Glaucoma drainage device
Not reported
Vitreoretinal surgery Intravitreal steroid injection
11
Intravitreal anti-VEGF injection þ subTenon’s steroid injection
17
Panretinal photocoagulation with contact lens
9.7
Vitrectomy
Not reported
Intravitreal anti-VEGF injection
Not reported
Corneal and refractive surgery Radial keratotomy
10
LASIK/LASEK/PRK
Not reported
Corneal transplantation
Not reported
LASIK, laser-assisted in -situ keratomileusis; LASEK, laser epithelial keratomileusis; PRK, photorefractive keratectomy; VEGF, vascular endothelial & growth factor. References listed in text: [5–11,14–16,31–33,34 , 35–37,40].
Speculum effect Although the bridle suture theory is a valid mechanism, postcataract ptosis still occurs in the absence of a bridle suture. In some series, even temporal, clear corneal incisions have shown similar postoperative ptosis rates to scleral tunnels with superior rectus bridling, both around 10% [16], and this confirms an alternate mechanism. It has been postulated that a tight eyelid speculum reduces blood flow to the LPS, horizontally stretches the eyelid, and that contraction of the orbicularis against the rigid speculum causes levator dehiscence. It is also thought that sustained compressive forces from the speculum can cause crush injury to the delicate upper eyelid musculature and myoneural or myovascular connections, ultimately leading to muscle injury and subsequent ptosis [2,17–19]. As mentioned, narrow palpebral apertures are a preoperative risk factor for postoperative ptosis. To
PTOSIS FOLLOWING CORNEAL AND REFRACTIVE SURGERY Ptosis has also been reported as a postoperative complication of refractive surgical procedures such as laser-assisted in-situ keratomileusis [28–30] and radial keratotomy [31]. In these procedures, no bridle suture, injectable anesthetics, or conjunctival flaps were used, but an eyelid speculum was used. Although postradial keratotomy ptosis rates have been reported around 10% [31], the incidence of postoperative ptosis following modern refractive techniques has not been studied in depth. Corneal transplants have been included in analyses of ptosis
1040-8738 Copyright ß 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.co-ophthalmology.com
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
33
Cataract surgery and lens implantation
rates following anterior segment surgeries [7], but have not been evaluated independently. Ptosis following these procedures is likely the result of speculum-induced eyelid injury through the aforementioned mechanisms.
PTOSIS FOLLOWING GLAUCOMA SURGERY Ptosis has also been reported following trabeculectomy, with an incidence of 12% in the Collaborative Initial Glaucoma Treatment Study (CIGTS) [32]. Subsequent studies [33] have confirmed this rate, and determined that combining trabeculectomy with cataract extraction does not significantly increase the risk of postoperative ptosis compared with trabeculectomy alone. There is also no significant difference in posttrabeculectomy ptosis for limbus versus fornix-based conjunctival flaps [33]. Trabeculectomy with the antimetabolite mitomycin C causes slightly higher rates of ptosis, affecting 19% of eyes in a smaller prospective study [34 ]. Of note, in the CIGTS trial [32], bilateral ptosis was found in 7% of patients undergoing bilateral trabeculectomy, more than the 2.5% that would have been expected, if the probability of ptosis were independent between the two eyes. Patients of African ancestry were also noted to experience higher rates of postoperative ptosis than Caucasians [32]. There are no specific reports of ptosis rates following surgical placement of glaucoma drainage devices, although this is a difficult population to study because of many confounding variables including prior surgeries, laser procedures, and long-term administration of topical glaucoma medications. &
¨ ller’s muscle. on the sympathetic control of Mu Previous large series of intravitreal injections of ganciclovir did not report the occurrence of ptosis [38]. The occurrence of ptosis following serial intravitreal antivascular endothelial growth factor (antiVEGF) injections has not been reported. There have also been case reports of microvascular third nerve palsy following intravitreal anti-VEGF injections [39], but the significance of this is not clear. One study [40] prospectively evaluated 41 eyes receiving PRP with a contact lens for delivery of the laser treatment. A total of 9.7% of eyes experienced postlaser ptosis, and a correlation was found between decreased tarsal plate height and increased postlaser ptosis, which was hypothesized to be because of greater chance of direct trauma to the LPS as a result of its relatively lower position.
TREATMENT OF POSTSURGICAL PTOSIS Ptosis following ocular surgery can be treated with high rates of success [2,5,7,41–45]. These treatments restore or recreate the structure–function relationships within the upper eyelid using multiple surgical approaches (Fig. 3). The primary procedures for patients with intact LPS function include external levator advancement, whereby the dehisced levator aponeurosis is located and advanced to the tarsal ¨ller’s muscle–conjunctival resection, plate, and Mu whereby the posterior lamella is shortened and the ¨ller’s muscle and LPS are advanced through a Mu transconjunctival approach. If LPS function becomes poor following the ocular surgery, alternative causes for the development of ptosis should be considered.
DISCUSSION PTOSIS FOLLOWING VITREORETINAL SURGERY There are no specific studies of ptosis following vitreoretinal surgery, however ptosis has been described following intravitreal injections and panretinal photocoagulation (PRP). For intravitreal injections, ptosis has been reported primarily as a complication of steroid injections, and one series found a rate of 11% [35,36]. Another series compared eyes receiving intravitreal bevacizumab and subtenon’s triamcinolone plus laser versus laser treatment alone for refractory diabetic macular edema and noted ptosis in 17% of the eyes receiving injections compared with none in the eyes receiving laser alone [37]. It should be noted that not all of the studies commented on their use of specula. The cause of ptosis following intravitreal steroids is not clear, but could be related to effects 34
www.co-ophthalmology.com
When looking at the study as a whole, several findings highlight the underlying importance of individual anatomy, and support levator dehiscence as the primary abnormality. Two examples include: the unexpectedly higher rates of bilateral ptosis seen in the CIGTS trial [32], and the preoperative presence of contralateral ptosis being validated as a risk factor for the development of postoperative ipsilateral ptosis [9]. In tandem, these suggest an individual susceptibility to levator dehiscence and ptosis; however, if the levator aponeurosis has already dehisced, worsening of ptosis usually will not develop. However, if a patient is prone to levator dehiscence, suggested by contralateral ptosis, any ocular procedure may trigger impending dehiscence in the operative eye. There may be a subclinical ptosis with greater susceptibility to dehiscence caused by repetitive trauma from contact lens wear, Volume 27 Number 1 January 2016
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Blepharoptosis following ocular surgery Godfrey et al.
Post-surgical ptosis
Persistent (>6 months)
Transient (12 mm)
Poor levator function (
Blepharoptosis following ocular surgery: identifying risk factors Kyle J. Godfrey a, Bobby S. Korn a,b, and Don O. Kikkawa a,b
Purpose of review To evaluate the incidence of blepharoptosis following ocular surgical procedures, to elucidate mechanisms for its cause, and to identify potential risk factors for ocular surgeons to avoid. Recent findings Postoperative blepharoptosis has been a poorly understood concept. In the search for a definitive cause, various technical components of surgery have been implicated. Recent research highlights the importance of individual anatomy and proposes new mechanisms for postoperative ptosis, including excessive eyelid tension from specula, topical prostaglandin analogue use, and direct trauma at the level of the tarsal plate. Summary Blepharoptosis is common following ocular surgery and can occur through multiple mechanisms. Certain individuals are at a higher risk for postoperative blepharoptosis, but all surgeons and patients undergoing ocular surgery should understand this risk when providing informed consent. Operative techniques can be adjusted to decrease rates of postoperative blepharoptosis. Keywords blepharoptosis, cataract surgery, eyelid speculum, ocular surgery, ptosis
INTRODUCTION Blepharoptosis, herein referred to as ptosis, is an abnormally low upper eyelid position relative to the visual axis and corneal light reflex (Fig. 1). It is quantified by the margin-reflex distance 1, which has a normal range of 4–5 mm. Proper eyelid position is dependent on both anatomy and neuromuscular function, primarily an intact connection between the levator palpebrae superioris (LPS) muscle and the tarsal plate and pretarsal orbicularis oculi via the levator aponeurosis, and adequate function of the LPS (Fig. 2). Ptosis is a known complication of ocular surgery. A recent study [1] suggests that nearly one-third of acquired ptosis is postsurgical. This ptosis can be transient or persistent, and may detract from the effectiveness of the primary surgical procedure. Furthermore, despite being well reported, its precise mechanism remains unclear. Here we present a review of the literature.
PTOSIS FOLLOWING CATARACT SURGERY Cataract surgery is among the most common surgical procedures worldwide, and ptosis is a well
described postoperative complication, albeit poorly understood. To this end, multiple mechanisms have been proposed, and theories have evolved in tandem with surgical techniques. Most hypotheses focus on damage to the levator complex. Anatomically, the LPS originates from the lesser wing of the sphenoid bone superolateral to the optic foramen and fans out as it travels anteriorly along the superior orbital wall and above the superior rectus muscle, reaching its maximum diameter of 18 mm at the musculotendinous transition to the levator aponeurosis [2]. The levator aponeurosis descends from Whitnall’s ligament and splits into an anterior and posterior lamella. The anterior lamella becomes confluent with the orbital septum and inserts on pretarsal orbicularis oculi muscle and underlying subcutaneous tissue, whereas the posterior lamella a
Division of Oculofacial Plastic and Reconstructive Surgery, UCSD Department of Ophthalmology and bDivision of Plastic Surgery, UCSD Department of Surgery, La Jolla, California, USA Correspondence to Don O. Kikkawa, MD, FACS, Shiley Eye Institute, 9415 Campus Point Drive, La Jolla, CA 92093-0946, USA. Tel: +1 858 822 5972; e-mail: [email protected] Curr Opin Ophthalmol 2016, 27:31–37 DOI:10.1097/ICU.0000000000000218
1040-8738 Copyright ß 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.co-ophthalmology.com
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Cataract surgery and lens implantation
KEY POINTS Blepharoptosis is common following ocular surgical procedures. Individual patient anatomy may confer the highest risk of postoperative blepharoptosis. Surgical techniques can be adjusted to decrease rates of postoperative blepharoptosis. Levator dehiscence is the most likely mechanism, and can be caused by speculum use alone. Postoperative blepharoptosis can be treated successfully with surgical repair.
¨ ller’s inserts on the anterior tarsus (Fig. 2) [3]. Mu muscle arises from the undersurface of the LPS and inserts into the superior tarsus and is innervated by the sympathetic nervous system [4]. The medial horn of the levator aponeurosis is thought be thinner and structurally weaker than the lateral horn [2]. Ptosis can be caused by injury to any of these structures, their insertions, or the innervation to the eyelid retractors. In 1976, Paris and Quickert [5] defined postcataract ptosis as 2 mm or more of upper eyelid drooping persisting for more than 6 months following the cataract surgery. They reported two cases occurring secondary to levator dehiscence and estimated the occurrence to be 1–2% based on a survey of 27 ophthalmologists [5]. Most subsequent studies use their criteria to define postoperative ptosis, although its incidence varies widely. Studies have reported rates between 0 and 44% with different surgical and anesthetic techniques, although most seem to fall between 6 and 12% (Table 1) [6–10]. Few preoperative factors have been correlated with postcataract ptosis. They include ptosis in the nonoperative eye and a narrow palpebral aperture in the operative eye [6,9]. Conversely, patient age, sex, LPS function, eyelid crease position, dermatochala-
FIGURE 1. Right upper eyelid ptosis after cataract surgery.
32
www.co-ophthalmology.com
sis, and preoperative ptosis in the operative eye have no effect on rates of postoperative ptosis [6,7,9,11]. Operative time may play a role, but there is no consensus in the literature [6,12]. Three primary theories shape our understanding of postcataract ptosis:
Bridle suture effect During embryogenesis, the LPS and superior rectus muscle initially develop as a single muscle before separating. In the adult eye, common fascial bands connect their respective muscle sheaths [13]. As such, the use of a superior rectus bridle suture to pull the globe downward can cause damage to the superior rectus/LPS subunit, resulting in high rates of postoperative ptosis. Randomized prospective studies show that using superior rectus bridle sutures results in more frequent postoperative ptosis than episcleral retraction sutures [11]. Furthermore, use of an eyelid speculum, which forces the eyelid in the opposite direction, concurrently with a superior rectus bridle suture nearly doubles the rate of postoperative ptosis from 23 to 44% [14]. This is likely because of strong opposing forces between the levator complex and bridled superior rectus causing levator dehiscence. However, using an open subconjunctival approach for superior rectus bridling results in substantially decreased rates of postoperative ptosis (from 19 to 4%) when compared with a closed, transconjunctival approach [15]. There is disagreement regarding whether the development of a superior rectus hematoma during placement of the bridle suture leads to increased postoperative ptosis [8,9].
WL LPA OS
MM
FIGURE 2. Schematic illustration of upper eyelid anatomy demonstrating the anterior and posterior lamella of the levator aponeurosis, Mu¨ller’s muscle, Whitnall’s ligament , tarsal plate (thin arrow), orbital septum, and pretarsal orbicularis oculi muscle (thick arrow). Illustration courtesy of Benjamin Erickson, MD.
Volume 27 Number 1 January 2016
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Blepharoptosis following ocular surgery Godfrey et al. Table 1. Reported incidence of postoperative ptosis following selected ocular surgeries and surgical procedures Reported incidence of ptosis (%)
Surgical procedure Extracapsular cataract surgery Bridle suture and speculum
1–44.4
Bridle suture (closed approach)
19–23
Bridle suture (open approach)
4
&&
investigate this, Crosby et al. [20 ] performed mechanical testing of eyelid specula to determine the force required to compress each speculum over a range of displacements. They demonstrated that reusable specula are significantly stiffer than disposable specula, and that the stiffness of each speculum was greatest at the range of displacement corresponding to narrower palpebral apertures [20 ]. This increased force on the eyelid and levator complex may explain why patients with the smallest palpebral apertures are most likely to develop postoperative ptosis. &&
Phacoemulsification cataract surgery Bridle suture and speculum Speculum only
12.9 0–11.5
Glaucoma surgery Trabeculectomy without mitomycin C
12
Anesthesia effect
Trabeculectomy with mitomycin C
19
Bilateral ptosis following bilateral trabeculectomy
7
Some have postulated that postcataract ptosis may develop from damage to the levator complex by local and regional anesthetic agents. Suggestions of myotoxicity from local anesthetics were based primarily on animal models and have not been validated in the ophthalmic literature [21]. One study did show a correlation between the volume of peribulbar anesthetic administered during surgery and the amount of ptosis on postoperative day one. This same study also found that postoperative day one ptosis is the best predictor of persistent ptosis at six months [6]. However, other studies have not found a correlation between the speed or volume of peribulbar anesthetic and postoperative ptosis [22]. If administering a nerve block, the injection location can make a difference: the Van Lint block causes higher rates of ptosis than the Nadbath block [11]. However, there does not seems to be a significant difference between retrobulbar and subconjunctival injection when looking at the postoperative ptosis incidence [23,24]. It has also been suggested that hyaluronidase, an enzyme added to local anesthetic to improve distribution, may reduce the incidence of ptosis [25,26], although this has been disputed [27].
Glaucoma drainage device
Not reported
Vitreoretinal surgery Intravitreal steroid injection
11
Intravitreal anti-VEGF injection þ subTenon’s steroid injection
17
Panretinal photocoagulation with contact lens
9.7
Vitrectomy
Not reported
Intravitreal anti-VEGF injection
Not reported
Corneal and refractive surgery Radial keratotomy
10
LASIK/LASEK/PRK
Not reported
Corneal transplantation
Not reported
LASIK, laser-assisted in -situ keratomileusis; LASEK, laser epithelial keratomileusis; PRK, photorefractive keratectomy; VEGF, vascular endothelial & growth factor. References listed in text: [5–11,14–16,31–33,34 , 35–37,40].
Speculum effect Although the bridle suture theory is a valid mechanism, postcataract ptosis still occurs in the absence of a bridle suture. In some series, even temporal, clear corneal incisions have shown similar postoperative ptosis rates to scleral tunnels with superior rectus bridling, both around 10% [16], and this confirms an alternate mechanism. It has been postulated that a tight eyelid speculum reduces blood flow to the LPS, horizontally stretches the eyelid, and that contraction of the orbicularis against the rigid speculum causes levator dehiscence. It is also thought that sustained compressive forces from the speculum can cause crush injury to the delicate upper eyelid musculature and myoneural or myovascular connections, ultimately leading to muscle injury and subsequent ptosis [2,17–19]. As mentioned, narrow palpebral apertures are a preoperative risk factor for postoperative ptosis. To
PTOSIS FOLLOWING CORNEAL AND REFRACTIVE SURGERY Ptosis has also been reported as a postoperative complication of refractive surgical procedures such as laser-assisted in-situ keratomileusis [28–30] and radial keratotomy [31]. In these procedures, no bridle suture, injectable anesthetics, or conjunctival flaps were used, but an eyelid speculum was used. Although postradial keratotomy ptosis rates have been reported around 10% [31], the incidence of postoperative ptosis following modern refractive techniques has not been studied in depth. Corneal transplants have been included in analyses of ptosis
1040-8738 Copyright ß 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.co-ophthalmology.com
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
33
Cataract surgery and lens implantation
rates following anterior segment surgeries [7], but have not been evaluated independently. Ptosis following these procedures is likely the result of speculum-induced eyelid injury through the aforementioned mechanisms.
PTOSIS FOLLOWING GLAUCOMA SURGERY Ptosis has also been reported following trabeculectomy, with an incidence of 12% in the Collaborative Initial Glaucoma Treatment Study (CIGTS) [32]. Subsequent studies [33] have confirmed this rate, and determined that combining trabeculectomy with cataract extraction does not significantly increase the risk of postoperative ptosis compared with trabeculectomy alone. There is also no significant difference in posttrabeculectomy ptosis for limbus versus fornix-based conjunctival flaps [33]. Trabeculectomy with the antimetabolite mitomycin C causes slightly higher rates of ptosis, affecting 19% of eyes in a smaller prospective study [34 ]. Of note, in the CIGTS trial [32], bilateral ptosis was found in 7% of patients undergoing bilateral trabeculectomy, more than the 2.5% that would have been expected, if the probability of ptosis were independent between the two eyes. Patients of African ancestry were also noted to experience higher rates of postoperative ptosis than Caucasians [32]. There are no specific reports of ptosis rates following surgical placement of glaucoma drainage devices, although this is a difficult population to study because of many confounding variables including prior surgeries, laser procedures, and long-term administration of topical glaucoma medications. &
¨ ller’s muscle. on the sympathetic control of Mu Previous large series of intravitreal injections of ganciclovir did not report the occurrence of ptosis [38]. The occurrence of ptosis following serial intravitreal antivascular endothelial growth factor (antiVEGF) injections has not been reported. There have also been case reports of microvascular third nerve palsy following intravitreal anti-VEGF injections [39], but the significance of this is not clear. One study [40] prospectively evaluated 41 eyes receiving PRP with a contact lens for delivery of the laser treatment. A total of 9.7% of eyes experienced postlaser ptosis, and a correlation was found between decreased tarsal plate height and increased postlaser ptosis, which was hypothesized to be because of greater chance of direct trauma to the LPS as a result of its relatively lower position.
TREATMENT OF POSTSURGICAL PTOSIS Ptosis following ocular surgery can be treated with high rates of success [2,5,7,41–45]. These treatments restore or recreate the structure–function relationships within the upper eyelid using multiple surgical approaches (Fig. 3). The primary procedures for patients with intact LPS function include external levator advancement, whereby the dehisced levator aponeurosis is located and advanced to the tarsal ¨ller’s muscle–conjunctival resection, plate, and Mu whereby the posterior lamella is shortened and the ¨ller’s muscle and LPS are advanced through a Mu transconjunctival approach. If LPS function becomes poor following the ocular surgery, alternative causes for the development of ptosis should be considered.
DISCUSSION PTOSIS FOLLOWING VITREORETINAL SURGERY There are no specific studies of ptosis following vitreoretinal surgery, however ptosis has been described following intravitreal injections and panretinal photocoagulation (PRP). For intravitreal injections, ptosis has been reported primarily as a complication of steroid injections, and one series found a rate of 11% [35,36]. Another series compared eyes receiving intravitreal bevacizumab and subtenon’s triamcinolone plus laser versus laser treatment alone for refractory diabetic macular edema and noted ptosis in 17% of the eyes receiving injections compared with none in the eyes receiving laser alone [37]. It should be noted that not all of the studies commented on their use of specula. The cause of ptosis following intravitreal steroids is not clear, but could be related to effects 34
www.co-ophthalmology.com
When looking at the study as a whole, several findings highlight the underlying importance of individual anatomy, and support levator dehiscence as the primary abnormality. Two examples include: the unexpectedly higher rates of bilateral ptosis seen in the CIGTS trial [32], and the preoperative presence of contralateral ptosis being validated as a risk factor for the development of postoperative ipsilateral ptosis [9]. In tandem, these suggest an individual susceptibility to levator dehiscence and ptosis; however, if the levator aponeurosis has already dehisced, worsening of ptosis usually will not develop. However, if a patient is prone to levator dehiscence, suggested by contralateral ptosis, any ocular procedure may trigger impending dehiscence in the operative eye. There may be a subclinical ptosis with greater susceptibility to dehiscence caused by repetitive trauma from contact lens wear, Volume 27 Number 1 January 2016
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Blepharoptosis following ocular surgery Godfrey et al.
Post-surgical ptosis
Persistent (>6 months)
Transient (12 mm)
Poor levator function (
