Nariman S. Boyle and Eli L. Chang

Abstract  The objective of this chapter is to review the various etiologies and management of traumatic blepharoptosis. Iatrogenic causes constitute the most common category of factors in traumatic ptosis. This includes ptosis postintraocular surgery and posteyelid and adnexal procedures. Contact lens wear, various systemic interventions, and birth trauma are other iatrogenic causes reported in the literature in association with upper lid blepharoptosis. Lacerations and blunt traumatic injuries to the upper eyelid are frequently associated with various degrees of blepharoptosis. Neurogenic ptosis secondary to head trauma can occur secondary to third nerve injury, superior orbital fissure syndrome, or traumatic facial nerve palsy. The prognosis and management of traumatic ptosis depends on the underlying mechanism of injury.

Introduction

Traumatic blepharoptosis is an abnormally low upper eyelid following trauma. There are a multitude of mechanisms resulting in traumatic blepharoptosis. Ptosis can be mild, moderate, or severe depending on the complexity of injury to

E.L. Chang (*)

Doheney Eye Institute, University of Southern California, Los Angeles, CA, USA

e-mail: echang@doheny.org

the eyelid structures, including the levator muscle and aponeurosis. Nearly half of the traumatic cases are iatrogenic in nature with inadvertent injury to the levator muscle or aponeurosis [1]. Iatrogenic causes are numerous and are secondary to a large repertoire of surgical and nonsurgical interventions.

Etiology and Mechanisms

of Traumatic Ptosis

Iatrogenic Causes of Ptosis

Ptosis Postintraocular Surgery

One of the most common causes of blepharoptosis is the iatrogenic category, which encompasses a broad range of etiologies and mechanisms. Ptosis postintraocular surgery is commonly observed. The incidence of ptosis after cataract surgery has been quoted to be approximately 5–7% [2, 3]. By comparison, glaucoma filtering surgery and other types of complicated intraocular surgeries have a slightly higher incidence of ptosis when compared to simple cataract extraction. Although the mechanism of ptosis postintraocular surgery is uncertain, there are numerous articles pointing to the use of a speculum during ocular surgery [4]. The exact mechanism is unknown, but it is thought to be secondary to levator aponeurosis dehiscence. Bridle suture and anesthesia myotoxicity have also been implicated in postcataract ptosis [5]. The type of local

anesthesia used in cataract surgery does not seem to affect the incidence of postoperative ptosis [2]. A randomized, double-masked study of 317 patients revealed the incidence of ptosis at 90 days to be 5.5% in patients who received retrobulbar anesthesia and 5.8% in the peribulbar anesthesia group [2].

Ptosis Posteyelid and Adnexal Procedures

Ptosis may occur as a complication of a wide range of eyelid and adnexal procedures, through various mechanisms. Ptosis as a consequence of blepharoplasty can be transient secondary to postoperative eyelid edema or hematoma. Inadvertent levator dehiscence during resection of a wide strip of pretarsal orbicularis may result in permanent ptosis with a high lid crease [6, 7]. Direct repair of the ptosis secondary to an aponeurotic defect in the immediate postoperative period is instrumental in correcting ptosis after blepharoplasty [7].

Resection of conjunctival or eyelid tumors with violation of the levator complex or Müller muscle may cause ptosis. Excision of conjunctival tumors with or without cryotherapy may result in scarring or symblepharon between the bulbar conjunctiva and the posterior surface of eyelid. This may lead to ptosis secondary to mechanical limitation of the eyelid excursion. In these cases, release of the symblepharon and grafting the defect with mucous membrane or amniotic membrane may improve the ptosis and prevent recurrence of the symblepharon. Use of antimetabolites, such as mitomycin C, is useful in patients who are predisposed to exuberant scar formation [8, 9]. Young patients who sustain a chemical burn are a good example in this category.

Excision of eyelid tumors resulting in large full thickness lid defect necessitates reconstruction. The lid may be tight for many weeks. Lid elevation may be mechanically restricted by a horizontally tight eyelid, a vertical traction band, a swollen eyelid, or a bulky scar or skin graft. Limited lid elevation secondary to a horizontally tight eyelid gradually resolves with time. On the

other hand, vertical traction bands, bulky scars, and skin grafts may necessitate surgical revision to resolve the mechanical restriction and improve lid elevation.

Ptosis is commonly observed in patients with an anophthalmic socket [10, 11]. It can be true ptosis or pseudoptosis. True ptosis can be due to levator muscle damage during enucleation, scarring of the levator secondary to socket surgery or preexisting involutional ptosis. Pseudoptosis, on the other hand, is due to the loss of volume in the anophthalmic socket or inadequate prosthesis size. It is also due to the abnormal mechanical forces in the anophthalmic socket with loss of support of Whitnall’s ligament and straightening of the course of the levator [10]. Inferior migration of the orbital implant is another mechanism for pseudoptosis (Fig. 13.1). This can be verified in clinic by applying digital pressure on the implant to push it superiorly and noticing the improvement of the ptosis. Enucleation technique may contribute to the development of ptosis. Imbrication of the rectus muscles after enucleation over spherical implants may lead to upper lid ptosis in addition to implant migration [12]. The imbricated muscles over a spherical implant may slip off the implant, usually inferonasally, resulting in migration of the implant to the supero-temporal tenon space in the orbit. As a result, the superior fornix and upper lid are pulled forward and downward which may explain the ptosis [12].

Vertical rectus muscle surgery is known to affect upper and lower lid position [13]. Recession of the superior or inferior rectus leads to widening of the palpebral fissure. On the other hand, resection or advancement of the vertical rectus muscles may lead to narrowing of the palpebral fissure. Resection of the superior rectus is less likely to result in upper eyelid blepharoptosis if careful dissection is performed [13]. It is advised that all intermuscular septum and fascial connections to be dissected about 12–15 mm posterior to the muscle insertion to separate the superior rectus from levator and Müller muscles.

Botulinum toxin has a broad array of cosmetic and functional applications. While it has

been safely and effectively used, adverse reactions are possible. Transient upper lid blepharoptosis is the most common example. Ptosis results from inadvertent injection or diffusion of the botulinum toxin behind the orbital septum, affecting the levator muscle function [14]. The effect typically lasts about 3 months. A careful history, inquiring about any recent botulinum toxin injections around the eyes, may spare these patients unnecessary surgery.

Contact Lens Wear

Usage of contact lenses, particularly rigid gas permeable and hard is another cause of iatrogenic ptosis. Several reports suggest the association of acquired nonsenile ptosis with prolonged use of contact lenses [15, 16]. In one series, contact lens use was identified in 47% of patients

with acquired ptosis in the young to middle aged group [15]. It is often progressive and bilateral in 58% of cases and unilateral in the remaining 42% [15]. Levator aponeurosis dehiscence and thinning was found in the majority of those patients who underwent surgery [15, 16]. Another histopathology study showed fibrosis of Müller muscle and levator aponeurosis in patients with blepharoptosis and a history of prolonged hard contact lens use [17]. In comparison, patients with involutional ptosis were found to have mild Müller muscle fibrosis and substantial fatty degeneration of the levator muscle.

The mechanism of ptosis in contact lens wearer is attributed to recurrent traction on the levator aponeurosis during contact lens removal with lateral pulling of the lids. Another unusual and rare mechanism for ptosis associated with contact lens wear is intrapalpebral migration of the contact lens by eroding into the tissue. It is a

rare complication. Clinical presentation may vary from simple upper eyelid ptosis to more unusual findings, such as a conjunctival mass in the superior fornix, a movable hard mass simulating a neoplasm, or an orbital mass [18–23]. Another manifestation of contact lens migration can be pseudochalazion, where the contact lens is embedded in the tarsal conjunctiva [24]. Patients often have unilateral ptosis and may recall losing a contact lens on the same side. Double lid eversion may reveal the retained contact lens. Imaging may be required in cases where there is an encysted mass.

A more common complication of contact lens use is giant papillary conjunctivitis (GPC). Papillary changes in the tarsal palpebral conjunctiva can occur as part of an immunoglobulin E (IgE)-mediated hypersensitivity reaction. Patients with GPC may present with ptosis attributed to local inflammation and edema. The ptosis is usually reversible once contact lens use is discontinued and the GPC is treated [19].

Ptosis Following Systemic Interventions

Horner syndrome has been well described as a complication in thoracic and neck surgery [25, 26]. It has been reported following coronary bypass surgery with a frequency ranging from 1.3 to 7.7% [27, 28]. It tends to be isolated and unrelated to a C8-T1 plexopathy. In a study of 248 patients, hypertensive and diabetic patients had a higher incidence of Horner syndrome than normotensive patients (10.6 vs. 2.9%); there was no correlation with the cardiopulmonary bypass time. Horner syndrome persisted in 4% of patient at 6 months after surgery [27]. Another study revealed Horner syndrome in 1.3% of patient undergoing a variety of thoracic procedures, including thoracotomy, chest tube insertion, and thoracic trauma [25]. Transient Horner syndrome has been reported in patients with tension pneumothorax. Chest tube insertion relieved the tension pneumothorax and reversed the ptosis and miosis on the same side [29]. On the other hand, chest tube insertion itself can precipitate a transient or permanent Horner syndrome [30, 31]

due to damaged preganglionic sympathetic fibers. In one case, CT scan showed that the tip of the chest tube was resting against the stellate (cervicothoracic) ganglion. Repositioning of the chest tube led to resolution of the Horner syndrome [31]. Thoracoscopy and internal jugular venous cannulation have also been associated with Horner syndrome [26, 32, 33]. Surgical procedures involving the neck, including radical neck dissection for tumors, parathyroid surgery, thyroidectomy, carotid endarterectomy, and cervical spine fusion, may cause Horner syndrome secondary to sympathetic denervation from damage to the cervicothoracic ganglion [26, 34].

Another iatrogenic cause of Horner syndrome is epidural anesthesia [35], which may or may not display associated cranial nerve palsies. Horner syndrome has been described following lumbar epidural analgesia for labor with low concentration (0.04%) bupivacaine [35, 36]. Therefore, if patients become symptomatic following epidural infusion, a diagnostic work up may be unnecessary. Transient Horner syndrome has also been reported in a patient who underwent thoracic epidural analgesia for multiple rib fractures [37].

Birth Trauma

Birth trauma secondary to forceps delivery, vacuum extraction, fetal rotation, and shoulder dystocia may result in ptosis manifesting at birth [38]. Ptosis can be secondary to a stretched or dehiscent levator aponeurosis [39]. Horner syndrome is another potential cause of ptosis in newborns (Fig. 13.2). A study conducted to define the etiologies of Horner syndrome in the pediatric age revealed a history of birth trauma in 53% of patients [38]. Ptosis due to congenital Horner syndrome may be differentiated from garden-variety congenital ptosis based on history of birth trauma, as well as the absence of anisocoria and the presence of lid lag in downgaze in congenital ptosis. Children with congenital Horner syndrome and a history of a forceful delivery may not require the extensive work up otherwise mandated in the absence of a history of birth trauma [38].