ptosis

PTOSIS.
In blepharoptosis, the upper eyelid droops below its normal level. Congenital ptosis is usually a result of a localized dystrophy of the levator muscle in which the striated muscle fibers are replaced with fibrous tissue. The condition may be unilateral or bilateral and can be familial, transmitted as a dominant trait.

Parents often comment that the eye looks smaller because of the drooping eyelid. The lid crease is decreased or absent where the levator muscle would normally insert below the skin surface. Because the levator is replaced by fibrous tissue, the lid does not move downward fully in downgaze (lid lag). If the ptosis is severe, affected children often attempt to raise the lid by lifting their brow or adapting a chin-up head posture to maintain binocular vision. Marcus Gunn jaw-winking ptosis accounts for 5% of ptosis in children. In this syndrome, an abnormal synkinesis exists between the fifth and third cranial nerves; this causes the eyelid to elevate with movement of the jaw. The wink is produced by chewing or sucking and may be more noticeable than the ptosis itself.

Although ptosis in children is often an isolated finding, it may occur in association with other ocular or systemic disorders. Systemic disorders include myasthenia gravis, muscular dystrophy, and botulism. Ocular disorders include mechanical ptosis secondary to lid tumors, blepharophimosis syndrome, congenital fibrosis syndrome, combined levator/superior rectus maldevelopment, and congenital or acquired 3rd nerve palsy. A complete ophthalmic and systemic examination is therefore important in the evaluation of a child with ptosis.

Amblyopia may occur in children with ptosis. The amblyopia may be secondary to the lid's covering the visual axis (deprivation) or induced astigmatisim due to the weight of the lid on the globe (anisometropia). When amblyopia occurs, it should generally be treated before treating the ptosis.

Treatment of ptosis in a child is indicated for elimination of an abnormal head posture, improvement in the visual field, prevention of amblyopia, and restoration of a normal eyelid appearance. The timing of surgery depends on the degree of ptosis, its cosmetic and functional severity, the presence or absence of compensatory posturing, the wishes of the parents, and the discretion of the surgeon. Surgical treatment is determined by the amount of levator function that is present. A levator resection may be used in children with moderate to good function. In patients with poor or absent function, a frontalis suspension procedure may be necessary. This technique requires that a suspension material be placed between the frontalis muscle and the tarsus of the eyelid. It allows patients to use their brow and frontalis muscle more effectively to raise their eyelid. Amblyopia remains a concern even after surgical correction and should be monitored closely.

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Section 7
5 . 1
Chapter 5 - EYELIDS - Blepharoptosis

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Philip L Custer

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INTRODUCTION
Blepharoptosis (ptosis) results from congenital or acquired abnormalities of the levator or Muller's neuromuscular complexes. It can be defined as an abnormally low position of the upper eyelid margin, determined while the eye is looking in primary gaze. Trauma and orbital masses may also cause mechanical ptosis.

Ptosis may present with a variety of symptoms, including superior visual field obstruction, headache, and fatigue. Contact lens patients may report difficulty wearing or inserting their lenses. Ptosis repair is considered in those patients who are symptomatic or displeased with the cosmetic appearance of their eyelid. It is the goal of ptosis repair to adequately elevate the eyelid, while minimizing the risks of lagophthalmos and ocular exposure.

HISTORICAL REVIEW
Surgeons prior to the mid-1800s repaired blepharoptosis by excising upper eyelid skin, essentially suspending the eyelid from the brow. The frontalis suspension was popularized in the nineteenth century when physicians utilized a variety of subcutaneous implants to create a direct connection between the drooping eyelid and the forehead. Sutures, wires, xenografts, and autologous tissue grafts were employed. Motais and Parinaud introduced the superior rectus suspension procedure in 1897 [1] [2] . A portion of the superior rectus muscle was transposed and attached to the eyelid. Unfortunately, the resulting adhesion limited the independent movement of the eyelid and globe, compromising eyelid closure and blinking. Enthusiasm for this procedure declined as patients developed complications from chronic ocular exposure.

Bowman (1857) is credited with the first description of a procedure to shorten the levator-Muller's muscle complex through a conjunctival (posterior) incision [3] . An anterior levator technique was subsequently reported in 1883 by Eversbusch and Snellen [4] [5] . In 1975, Jones et al. determined that many cases of acquired ptosis were caused by a dehiscence of the levator aponeurosis. They described a technique to repair this structure that successfully elevated the eyelid [6] .

Modern physicians use a variety of ptosis procedures, depending upon the levator muscle function (see below). Patients who have poor levator function often require frontalis suspension. Anterior levator aponeurotic shortening is widely employed in patients who have good levator activity. Some surgeons prefer a posterior resection of Muller's muscle in these individuals.

PREOPERATIVE EVALUATION AND DIAGNOSTIC APPROACH
The ocular and medical history
The initial evaluation is directed toward determining the cause of the ptosis. The medical history should ascertain the age of onset, duration, severity, and variability of the condition. Interviewing family members and reviewing old photographs are helpful to document the progression of the disorder. The family history may be revealing in some forms of ptosis with hereditary patterns. Previous ocular trauma, ocular surgery, or eyelid disease may have contributed to the development of ptosis or alter the treatment plan. Ptosis repair should be considered with caution in patients who have prior symptoms of ocular irritation, dryness, photophobia, or diplopia. True eyelid ptosis must be differentiated from the various causes of pseudoptosis including dermatochalasis, contralateral eyelid retraction, enophthalmos, and hypotropia.

The presence of concomitant ocular signs may help make a diagnosis. Ipsilateral miosis is suggestive of Horner's syndrome, while mydriasis may be found in cases of previous oculomotor paralysis. Patients who have surgically or traumatically enlarged pupils often suffer photophobia, which may worsen following ptosis surgery. Significant ocular inflammation or dryness may be responsible for a reactive ptosis; if present, these conditions must be corrected prior to contemplating ptosis repair. A Schirmer's test should be used to measure the basic tear secretory rate in adult patients. In cases of reduced tear function, surgery should be limited or avoided in order to avoid exacerbation of dry eye syndrome.

Preoperative photographs are obtained to document the severity of ptosis. Visual fields with and without elevation of the drooping eyelids are used to determine the degree of visual obstruction. Additional diagnostic studies, such as orbital imaging or neuromuscular testing, may be indicated when clinical examination fails to determine the cause of the ptosis.

Bell's phenomenon
With eyelid closure, reflex innervation to the extraocular muscles result in an upward and slightly outward rotation of the globe. This mechanism protects the cornea in cases of lagophthalmos. In patients who have reduced or absent Bell's phenomenon, ptosis repair should be conservative to avoid postoperative exposure problems. This is especially true in patients who show pre-existing dry eye.

Hering's law
The levator muscles obey Hering's law of equal innervation [7] . Since the levator muscles are innervated from a single midline nucleus, central neural output is equal to both levator muscles. Thus, in cases of bilateral but asymmetric ptosis, the less affected eyelid may be capable of maintaining a normal level of elevation due to excessive innervational stimulation determined by the more ptotic eyelid. This condition may be detected prior to surgery by manual elevation of the ptotic eyelid. An immediate fall of the contralateral eyelid confirms the presence of bilateral, asymmetric ptosis masked by levator 'overaction' [8] .

Levator muscle function
Levator muscle function is determined by measuring the excursion of the eyelid margin as the patient looks from downgaze to upgaze. The eyebrow must be manually fixed against the supraorbital rim during this measurement in order to prevent the frontalis muscle from contributing to the eyelid movement. Many patients subconsciously raise their eyebrow in a compensatory effort to elevate the drooping lid, a beneficial finding in individuals who may require frontalis suspension. Normal adults typically demonstrate 13-16mm of levator function [9] . Lesser measurements may indicate the presence of a developmental or acquired myopathy.

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Section 7
5 . 2
Other measurements
The upper eyelid margin is normally positioned 1-2mm below the superior limbus, well above the pupil. The position of the upper eyelid margin is measured while the patient looks in primary gaze. This may be recorded as the position (in millimeters) of the upper eyelid margin below the superior limbus, or its position (above or below) with respect to the midpupillary light reflex.

The position of the upper eyelid crease in both eyes is measured and recorded, along with the amount of redundant skin (dermatochalasis). This is important, especially in cases of unilateral ptosis, so that a normal lid crease can be reformed at the time of surgery. Ocular motility must be assessed in all patients who have ptosis. A coexisting strabismus may be detected in some patients who have congenital ptosis, acquired neurologic or myopathic disease, or in the presence of orbital masses. A component of pseudoptosis often is present in cases of hypotropia.

DIFFERENTIAL DIAGNOSIS
Blepharoptosis may be categorized by age of onset, severity, and physiologic etiology. Ptosis is either congenital or acquired. Mild ptosis may not be clinically significant, while moderate or severe disease often results in a cosmetic or functional deficit. A variety of myopathic, neurologic, and mechanical conditions result in ptosis. The accurate determination of the cause clarifies the need for ancillary testing, facilitates treatment, and is of prognostic value. The differential diagnosis of blepharoptosis is shown in Figure 5.1 .

Congenital ptosis
Simple congenital (myopathic) ptosis
The majority of children who have congenital ptosis suffer from a developmental myopathy of the levator muscle. This condition is present at birth and generally remains stable throughout life. Levator muscle function is decreased in proportion to the severity of the ptosis. The affected levator muscle is fibrotic, limiting the inferior mobility of the eyelid. The degree of ptosis usually is less marked in downgaze (Fig. 5.2) . The upper eyelid crease is typically indistinct or absent. Many children demonstrate compensatory elevation of their eyebrows or maintain a chin-elevated head position.

Simple congenital ptosis is unilateral in 69% of cases [10] . Bilateral involvement may either be symmetric or asymmetric in appearance. A coexisting ocular motility abnormality is present in approximately 30% of children [11] [12] [13] . Hypotropia is common, a possible manifestation of developmental failure affecting both the superior rectus and levator muscles [14] . Anisometropia is present in 12% of patients with simple congenital ptosis [15] [16] . The ptotic eyelid may cause corneal molding, which results in with-the-rule astigmatism. Strabismus and anisometropia may lead to amblyopia, which is found in 20% of simple congenital ptosis patients [17] . Occlusion amblyopia is less common,

Figure 5-1 Differential diagnosis of upper eyelid blepharoptosis.

remaining a diagnosis of exclusion. Early ptosis repair is indicated in cases with possible occlusion of the visual axis. Surgery is otherwise delayed until the late preschool years.

Children who have good levator function are effectively treated with an anterior levator aponeurotic-muscle resection, while children who have severe ptosis and poor function often require a frontalis suspension. Severe unilateral congenital ptosis remains a treatment challenge. Unilateral frontalis suspension may be considered in children who have compensatory elevation of their eyebrow. Maximal levator resection also can be employed, although this procedure often is complicated by significant postoperative lagophthalmos. Bilateral frontalis suspension combined with ablation of the uninvolved levator muscle provides symmetric eyelid appearance and function. However, most parents are hesitant to consider surgery on the normal eyelid.

Blepharophimosis syndrome
Approximately 6% of children who have congenital ptosis will demonstrate the typical findings of blepharophimosis syndrome [10] . Severe bilateral ptosis usually is present with poor levator muscle activity. The palpebral fissures are horizontally shortened (blepharophimosis) with resultant telecanthus (Fig. 5.3) . True hypertelorism is occasionally present [18] . Epicanthus inversus is another common finding. Mild ectropion of the temporal lower eyelids is seen in severe cases. The inferior puncta often are displaced laterally and the eyebrows may be abnormally wide. Some patients demonstrate low-set, 'lop' ears.

Figure 5-2 Simple congenital ptosis. (a) Decreased levator muscle function occurs along with an indistinct upper eyelid crease. (b) The ptosis is exaggerated in upgaze due to the poor function of the levator muscle. (c) In downgaze, the ptosis is reduced or absent because the fibrotic levator muscle cannot stretch.

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Section 7
5 . 3
Blepharophimosis is a dominantly inherited condition, with high penetrance [19] . The severity of ocular findings may vary among affected family members. Sporadic cases also may occur. Intelligence is not affected and most patients who have blepharophimosis are systemically healthy. Blepharophimosis is associated with primary amenorrhea in some family lines [20] .

Surgical treatment of blepharophimosis usually requires a staged approach. The telecanthus and epicanthal folds often are initially repaired with medial canthal tendon plication and local skin flaps [18] [21] . Bilateral frontalis suspension subsequently is performed to correct the ptosis. Skin grafting may be necessary to relieve coexisting lower eyelid ectropion

Marcus Gunn's jaw-winking syndrome
The jaw-winking syndrome was initially described by Marcus Gunn in 1883 [22] . This form of synkinetic ptosis typically is unilateral and not hereditary. The ptotic eyelid demonstrates intermittent elevation, coinciding with contraction of the muscles of mastication (Fig. 5.4) . The patient is thus noted to 'wink' during eating or chewing. The synkinesis commonly involves the ipsilateral external pterygoid muscle, which moves the jaw toward the opposite side. The severity of the ptosis and the amplitude of the wink are proportionately related. Measurable levator function is variable or decreased. The upper eyelid crease usually is intact. Hypotropia and other forms of strabismus may be associated with the jaw-winking syndrome [23] .

The cause of this condition is unknown, although there appears to be misdirection of either the efferent motor innervation or afferent proprioceptive fibers of the third and fifth cranial nerves [24] [25] . The wink often becomes less noticeable with age, as patients learn to limit oral movements which stimulate the synkinesis [26] . Surgical therapy of the ptosis is challenging. Mild cases can be treated with levator aponeurotic-muscle resection. Patients who have large amplitude winking may require ablation of the levator, followed by frontalis suspension [27] .

Figure 5-3 Blepharophimosis syndrome. (a) With symmetric bilateral ptosis, telecanthus, and epicanthal folds. (b) Postoperative appearance following bilateral canthoplasty and frontalis suspension.

Acquired ptosis
Third cranial nerve palsy
The levator muscle is innervated by the superior division of the third cranial nerve. The levator subnucleus is central and unpaired. Intranuclear lesions thus result in symmetric, bilateral ptosis. Peripheral third nerve deficits are much more common; they result from a wide variety of insults including trauma, ischemia (microvascular disease), inflammation, neoplasm, and aneurysms. Ptosis with decreased or absent levator function, pupillary mydriasis, and paralytic strabismus typically are present. Spontaneous recovery may occur, although a partial deficit often remains. Aberrant regeneration is not infrequent and occasionally results in gaze-directed eyelid retraction.

Repair of paralytic ptosis usually requires frontalis suspension. Surgery should be delayed for 6-12 months until it is certain that spontaneous recovery will not occur [28] . Coexisting strabismus should be corrected prior to ptosis repair, otherwise eyelid elevation may result in intractable diplopia.

Horner's syndrome
Muller's smooth muscle is sympathetically innervated and provides several millimeters of eyelid elevation. Sympathetic denervation (Horner's syndrome) results in moderate ptosis with preserved levator function (see Fig. 5.5) . An abnormally high lower eyelid contributes to the narrowed palpebral fissure, secondary to involvement of the inferior tarsal smooth muscle. A relative ipsilateral miosis is uniformly present and many patients also demonstrate hemifacial anhidrosis. Heterochromia may be noted in patients who have congenital Horner's syndrome [29] in which the ipsilateral iris is lighter in color.

Pharmacologic (cocaine) testing facilitates the diagnosis of this condition. The neurologic deficit may result from ischemia, trauma, neoplasm, or iatrogenic insults. A medical evaluation is indicated in patients with newly diagnosed Horner's syndrome without an apparent cause. The ptosis in acute cases should be observed. Surgical correction is indicated in patients who have significant, persistent disease.

Figure 5-4 Marcus Gunn' s jaw- winking syndrome. (a) In primary gaze with the mouth closed, there is right upper eyelid ptosis. (b) With the jaw opened the right upper eyelid elevates due to synkinesis.

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Section 7
5 . 4

Figure 5-5 Horner' s syndrome with ipsilateral right upper eyelid ptosis and pupillary miosis.

External levator aponeurotic-muscle resection or a posterior mullerectomy are effective methods of repair.

Myasthenia gravis
Ptosis or diplopia are the presenting symptoms in about one half of patients who have myasthenia, and subsequently appear in 96% of all individuals with this condition [30] . The ptosis may be unilateral, bilateral, or alternating. Levator function is either decreased or variable. The affected levator muscle usually demonstrates rapid fatigability, where the eyelid twitches or slowly falls with prolonged upgaze [31] . This finding is distinct from the increased ptosis associated with systemic fatigue, suffered by all ptosis patients, irrespective of cause. A minority of myasthenic patients maintain a purely ocular form of the disease, while the remainder develop systemic involvement [32] [33] .

This autoimmunologic condition affects the function of the neuromuscular junction and has a predilection for muscles innervated by the cranial nerves. Antibodies to acetylcholine receptor protein are present in the majority of patients with systemic disease [32] . The history and clinical findings usually lead the clinician to the diagnosis, which is confirmed by Tensilon testing, electrophysiologic studies, or acetylcholine receptor antibody levels (Fig. 5.6) . Myasthenia is treated medically. Selected patients may benefit from thymectomy [33] . Ptosis repair is reserved for those individuals with refractory, visually debilitating disease. A limited frontalis suspension is usually performed. Myasthenia patients are at an increased risk for developing postoperative ocular exposure, secondary to coexisting orbicularis muscle weakness or a poor Bell's phenomenon.

Chronic progressive external ophthalmoplegia
Chronic progressive external ophthalmoplegia (CPEO) is a diffuse spectrum of conditions which may either be hereditary or sporadic in nature. Most patients present with symmetric, bilateral ptosis in early adulthood (Fig. 5.7) . The mitochondrial myopathy results in decreased levator function. Extraocular muscles are later affected, resulting in diffuse ophthalmoplegia. Associated systemic findings are present in some forms of this disease, including cardiac conduction defects (Kearns-Sayre syndrome) and dysphagia (oculopharyngeal dystrophy) [34] [35] [36] .

Muscle biopsy may be necessary to confirm the diagnosis of CPEO. Ptosis repair is typically deferred until the patient is visually debilitated. Limited frontalis suspension is usually the procedure of choice, avoiding postoperative lagophthalmos and resultant ocular exposure.

Aponeurotic redundancy or dehiscence
The majority of patients who have acquired ptosis develop the condition secondary to involutional changes in the levator aponeurosis. A gradual stretching or dehiscence of this structure occurs, which leads to a slowly progressive ptosis. Chronic contact lens wearers also may develop ptosis on this basis. Aponeurotic dehiscence suddenly may

Figure 5-6 Myasthenia gravis with severe bilateral ptosis. (a) Before treatment. (b) The same patient after administration of intravenous Tensilon.

Figure 5-7 Chronic progressive external ophthalmoplegia (CPEO) with bilateral ptosis and ocular motility abnormality.

occur following ocular surgery or trauma. A significant ptosis develops in approximately 6% of patients following cataract surgery [37] .

Levator function remains excellent in this form of ptosis. Loss of the aponeurotic attachment results in an abnormally high or indistinct upper eyelid crease (Fig. 5.8) . The superior sulcus deepens and the upper eyelid may appear to be unusually thin, occasionally allowing visualization of the iris through the eyelid tissue. Surgical repair of the aponeurotic dehiscence effectively corrects the ptosis and is best performed with an anterior approach.

Mechanical ptosis
Mechanical ptosis may develop from cicatricial processes, orbital or eyelid masses, or enophthalmos. Scarring involving any of the anatomic layers of the upper eyelid or symblepharon between the lid and globe may limit eyelid mobility and cause ptosis. Encapsulated orbital lesions may alter levator function secondary to mass effect, while infiltrative conditions restrict the muscle activity. The relative severity of mechanical ptosis often varies in different gaze positions. Effective treatment of mechanical ptosis requires correction of the underlying abnormality. Orbital mass lesions may require surgery, radiation, or medical therapy.

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Section 7
5 . 5
Enophthalmos or phthisis alter the normal anatomic relationship between the eye and upper eyelid. The loss of upper eyelid support from the recessed globe results in ptosis and a smaller palpebral fissure. Enucleation or the fitting of a scleral shell often improve ptosis in patients who have phthisis. Restoration of the normal orbital volume usually reduces ptosis in patients who have enophthalmos.

ALTERNATIVES TO SURGERY
Ptosis repair always is considered an elective procedure. Surgery should be avoided or limited in individuals who have preoperative ocular irritation or photophobia. Patients who have poor lacrimal production are at risk for developing symptomatic dryness following eyelid elevation.

Figure 5-8 Levator function. (a) Bilateral ptosis from levator aponeurosis dehiscence demonstrating a high indistinct lid crease. (b) In upgaze, levator muscle function is of normal amplitude.( c) The indistinct eyelid crease and ptosis remain in downgaze. (d) Normal lid height following levator aponeurosis advancement.

Raising the ptotic eyelid of a patient who has an enlarged pupil or sector iridectomy may cause intractable light sensitivity. Individuals who have poor Bell's phenomena are at an increased risk for developing exposure keratitis, should postoperative lagophthalmos be present. Visually debilitating ptosis in the above patients can be repaired with limited surgery in an attempt to undercorrect the eyelid position. Nonsurgical elevation of the eyelid with a ptosis crutch attached to the spectacle frame can occasionally be helpful, although these devices usually limit the blink, which often results in ocular irritation.

ANESTHESIA
Ptosis repair ideally is performed under local infiltrative anesthesia. An alert, awake patient facilitates the intraoperative adjustment of eyelid position and contour. The subcutaneous injection of a mixture of 2% lidocaine (lignocaine) with 1:200,000 epinephrine (adrenaline) and 0.75% bupivacaine provides adequate intraoperative and postoperative analgesia. A minimal volume (1-2cm3 per eyelid) of anesthetic is required. Larger volumes or deeper orbital injections may alter levator function, which compromises muscle adjustment. General anesthesia is necessary for young children, certain apprehensive adults, and when harvesting autologous fascia lata.

GENERAL TECHNIQUES
The type of ptosis and amount of levator function determine which procedure to perform. Patients who have moderate-good levator function have their disorder effectively corrected with an anterior levator aponeurotic-muscle reattachment or resection. This same procedure may be employed in cases with poor levator activity, although large resections are necessary, which result in postoperative lagophthalmos. Some surgeons perform a posterior resection of Muller's muscle in patients who demonstrate adequate elevation of the eyelid following instillation of topical phenylephrine. [38] [39]

Frontalis suspension often is the procedure of choice in patients who show severe ptosis, poor levator activity, and intact frontalis muscle function. Autologous fascia lata remains the preferred implant material in pediatric cases. Preserved donor fascia is available, although absorption with subsequent recurrent ptosis may occur [40] . Silicone rods often are employed in patients in whom it is impractical to harvest fascia lata. Alloplastic implants occasionally are complicated by extrusion, infection, or breakage.

The quality of the Bell's phenomenon, lacrimal production, and orbicularis activity are all considered when determining the amount of eyelid elevation that is ideal in each case of ptosis repair. Selected patients tolerate mild lagophthalmos, which may be necessary to achieve an acceptable cosmetic result in those who have severe congenital ptosis. Marked lagophthalmos generally should be avoided, due to the risks of early or chronic corneal exposure.

The upper eyelid skin incision usually is placed in the location of the desired eyelid crease. The position of the uninvolved eyelid's crease is matched in cases of unilateral ptosis. The creases often are absent or indistinct in cases of severe, bilateral disease. The normal crease is usually positioned one third of the distance from the eyelashes to the lower edge of the brow, measured in downgaze [41] . The central incision is approximately 9-10mm above the lashes in adult women. The adult male crease is usually placed 1-2mm lower. Dermatochalasis can be simultaneously corrected in older patients who undergo bilateral ptosis repair. Redundant skin is excised from above the eyelid crease incision prior to elevating the eyelid.

Occasionally, children who show severe congenital ptosis are at risk for developing occlusion amblyopia. Early surgical intervention may be indicated in these individuals. Ptosis repair in young children is otherwise deferred until 3 to 5 years of age, allowing maturation of the eyelid and facilitating both preoperative measurements and postoperative care. It is difficult to obtain sufficient fascia lata in children less than 3 years of age.

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Section 7
5 . 6
SPECIFIC TECHNIQUES
Anterior levator aponeurosis advancement
Immediately prior to surgery the patient is examined while sitting and supine. Any variation in eyelid position is noted, since the eyelid adjustment will be performed while the patient is recumbent. A standard full-face surgical wash is performed to allow intraoperative comparison of both orbits. The desired position of the upper eyelid crease incision is marked on the ptotic eyelid(s). Subcutaneous infiltrative anesthesia is administered.

The incision is created with a scalpel blade ( Fig. 5.9a ). Sharp-tipped Westcott scissors may be employed for the remaining dissection. The fine subcutaneous tissue is divided to expose the underlying orbicularis muscle (see Chapter 7 .1). A buttonhole is cut through the center of the muscle and the layer is incised medially and laterally parallel to the muscle fibers. Hemostasis is maintained throughout the procedure with bipolar, wetfield cautery. The orbital septum and underlying orbital fat usually are visible at this point. Superior retraction of these structures may occur in cases of marked aponeurotic dehiscence. The septum is divided and the preaponeurotic fat pads are retracted upward to expose the underlying levator muscle ( Fig. 5.9b ).

The opaque levator aponeurosis may be very thin and stretched or completely dehisced from its tarsal attachments. The conscious patient is now asked to open his or her eyes to allow the surgeon to determine if the surgical dissection has altered the preoperative eyelid level. Any remaining distal attachments of the aponeurosis are divided, exposing the tarsus. The aponeurosis is separated from the underlying Muller's muscle using both blunt and sharp dissection ( Fig. 5.9c ). In patients who have marked attenuation of the aponeurosis, such as in severe congenital ptosis, the combined aponeurosis-Muller's muscle complex may have to be advanced as a unit to achieve adequate lid elevation. The dissection in these cases is performed between Muller's muscle and conjunctiva.

Several interrupted 6-0 polyester (Mersilene) sutures are placed through partial thickness of the tarsus medially, centrally, and laterally. The surgeon must examine the posterior surface of the lid to insure these sutures are not exposed on the conjunctiva. These sutures are used to reattach or advance the aponeurosis ( Fig. 5.9d ). Multiple adjustments may be needed to achieve the appropriate eyelid position and contour, and compensate for any alteration of lid position that may have been noted either when the patient was placed supine or during the surgical dissection. The eyelid level is adjusted empirically in patients under general anesthesia, considering the preoperative levator function and severity of disease. Redundant aponeurotic tissue is excised. It is advisable to recreate the eyelid crease by suturing the cut edge of either the pretarsal orbicularis muscle or subcutaneous tissue to the aponeurosis with interrupted 7-0 polyglactin (Vicryl) sutures ( Fig. 5.9e ). The skin incision is closed with a running 7-0 polypropylene (Prolene) suture ( Fig. 5.9f ).

Patients are observed for 30-60 minutes following surgery to detect early postoperative hemorrhage or other complications. Cold compresses may be applied while awake for the first 48 hours to minimize edema and ecchymosis. Subsequent wet and warm compresses assist in wound hygiene. A topical antibiotic ointment is placed on the incision several times daily. Suture removal is performed 5-7 days following surgery. Mild lagophthalmos and poor blink often are noted in the early postoperative period, even in appropriately positioned eyelids. This finding may be attributable to orbicularis underaction, which typically improves several weeks after surgery. A variable period of time is required for complete resolution of the postoperative edema and stabilization of the eyelid level.

Frontalis suspension
The pattern of frontalis action, whether diffuse or segmental, is noted prior to surgery. The availability of suspensory material and the brow contour dictate the incision location and the pattern of threading the implanted sling. Common implant materials include autologous fascia lata and silicone rods. The usual patterns for threading these materials are either in one continuous pentagonal polygon or with a triangular sling. A pentagonal-shaped sling usually is placed in patients who have diffuse brow elevation. Medial and lateral horizontal incisions are marked at the superior border of the brow. A central forehead incision

Figure 5-9 Key steps in levator aponeurosis advancement.

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Section 7
5 . 7
is placed approximately 10mm above the brow and between the other two incisions. Triangular slings may be more ideal in individuals who have segmental brow elevation, as they utilize a single incision above the area of the brow that exhibits maximal movement.

Regardless of the sling configuration, brow stab incisions are cut through the skin and subcutaneous tissue, exposing the frontalis muscle in the appropriate locations. Generally, these are located just outside the medial and lateral corneal limbus ( Fig. 5.10a ). A crease incision is created in the eyelid. The subcutaneous tissue, orbicularis muscle, and orbital septum are opened in separate layers ( Fig. 5.10b ). The anterior surface of the tarsus is exposed and hemostasis achieved with bipolar, wetfield cautery.

Fascia lata next must be harvested in patients who undergo autologous grafting. A 3cm incision is made on the lower thigh, just above the lateral condyle of the femur. The white, glistening fascia lata is visible underneath the subcutaneous fat. Blunt dissection is performed along the anterior surface of the fascia, up the lateral aspect of the leg for about 15-20cm. A strip of fascia 6-8mm wide and 15-20cm long is harvested using fascial stripper and cutter. The fascia is cleaned of adherent subcutaneous fat and divided into 2-3mm wide strips.

The autologous fascia or alloplastic implant material (silicone rods, permanent sutures) is sutured to the upper anterior surface of the central tarsus with several partial thickness 6-0 polyester sutures ( Fig. 5.10c ). Eyelid contour can be adjusted by altering the width of this attachment. A Wright fascial needle is then used to pass each end of the sling material first through the peripheral brow incisions and then from these to the central brow incision. The implant is positioned deep to the orbital septum within the lid and superficial to the periosteum over the superior orbital rim. It is best to recreate the eyelid crease by suturing the edge of the pretarsal orbicularis muscle to the aponeurosis with 7-0 polyglactin sutures. The eyelid crease incision is then closed with 7-0 polypropylene in adults or 7-0 chromic sutures in children prior to adjusting the eyelid height ( Fig. 5.10d ). Tensions on the two ends of the sling are adjusted by pulling up on the free ends together at the central brow incision in order to achieve the proper lid height and contour. The ends then are joined with either permanent sutures (fascia) or a silicone sleeve (silicone rods), prior to being buried underneath the subcutaneous tissue of the forehead. The brow and leg incisions are closed in a layered fashion. A light elastic leg dressing may minimize the risk of postoperative hematoma. Postoperative wound care is similar to the regimen described for anterior levator surgery.

COMPLICATIONS
Successful ptosis repair requires a complete understanding of the surgical anatomy and function of the upper eyelid. Meticulous surgical technique minimizes the occurrence of many surgical complications, such as hemorrhage, infection, poor wound healing, and visual loss. Excessive dissection of the levator may traumatize the superior oblique muscle or lacrimal gland ductules. Appropriate preoperative evaluation and patient selection reduce the risks of postoperative ocular irritation, keratitis, and photophobia.

Undercorrection
Persistence of some postoperative eyelid droopiness is the most common complication of ptosis repair, seen in about 10-15% of patients. These patients should be observed until the surgeon is certain that all edema has resolved and the eyelid position has stabilized. In some cases a surgical revision is needed to obtain an ideal position of the eyelid. Further levator resection or brow suspension may limit lid closure in some patients. An unsuspected acquired myopathy may be responsible for recurrent or poorly corrected ptosis. Such patients may require repeated ptosis correction over many years.

Overcorrection
Patients who have mild overcorrection following ptosis repair also should be observed until the lid position has become stable. Digital massage or 'squeezing' exercises occasionally provide a slight lowering of the eyelid, which improves mild overcorrection. Surgical revision with recession of the levator or suspension material is indicated in cases with persistent overcorrection. Emergent, early surgical revision should be performed in patients who show marked postoperative overcorrection and ocular exposure.

Figure 5-10 Key steps in frontalis suspension.

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Section 7
5 . 8
Eyelid crease abnormalities
Incorrect incision planning or failure to adequately create the eyelid crease may result in either an indistinct or a poorly positioned crease. An absent or abnormally low crease may be reformed by placing an incision through skin and orbicularis muscle in the location of the new crease. The subcutaneous tissue or orbicularis muscle is sutured to the aponeurosis, prior to skin closure.

It is very difficult to lower an abnormally high crease. The attachment between the skin-orbicularis muscle and the aponeurosis must be separated. Soft tissue, such as orbital fat, then should be mobilized between these layers, in an effort to minimize the establishment of a new adhesion in the same location. The new crease then is established at a lower level.

Abnormalities of eyelid margin contour
Distortions of the eyelid margin contour result from uneven advancement of the aponeurosis. If mild, segmental massage of the higher portion may be helpful. However, in many cases a surgical revision is required, with tightening or loosening of individual sutures. This often can be accomplished at the 1-week follow-up visit, before the skin wound flaps are firmly united.

Lagophthalmos and exposure keratitis
Keratitis following ptosis repair may be related to overcorrection, lagophthalmos, inadequate blink, decreased tear production, or a poor Bell's phenomenon. Nighttime lubricating ointment and topical artificial tears are employed to treat minor cases. Bandage soft contact lenses occasionally can be helpful. Punctal occlusion may be indicated in patients who have severe dry eyes. Persistent keratitis in patients who have poor blink or lagophthalmos may require lowering of the upper eyelid. Alternative procedures, such as elevating the lower lid, canthoplasty, and tarsorrhaphy, can be considered for patients in whom reversal of the ptosis repair would be visually disabling.

Prolapse of the superior conjunctival fornix
With excessive advancement of the aponeurosis or Muller's muscle the superior conjunctiva may prolapse into the palpebral fissure. This results from failure to separate the fine attachments between the aponeurosis and the superior fornix suspensory ligaments. If the conjunctival is easily reduced, a pressure patch for several days may correct the condition. Once fibrosis supervenes, direct excision is necessary.

OUTCOME
The vast majority of ptosis procedures are successful and restore a normally functioning eyelid and improve superior visual field. The new eyelid position usually remains stable, with recurrences being uncommon. Patients who have congenital ptosis, acquired myopathies, or postoperative lagophthalmos require continued evaluation after surgery to detect possible ocular exposure or the development of associated ophthalmic conditions.

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