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Chapter 86 – Blepharoptosis

Chapter 86 – Blepharoptosis

 

PHILIP L. CUSTER

 

 

 

 

 

DEFINITION

• An abnormally low position of the upper eyelid margin, determined while the eye is looking in primary gaze.

 

KEY FEATURES

• Blepharoptosis (ptosis) may result from trauma, masses, and congenital or acquired abnormalities of the levator or Müller neuromuscular complexes.

• May present with various symptoms, including visual field obstruction, headache, and fatigue.

• Surgery is considered in patients who are symptomatic or displeased with the appearance of their eyelid.

• The goal of ptosis repair is to elevate the eyelid without causing excessive lagophthalmos or ocular exposure.

 

 

 

INTRODUCTION

Blepharoptosis was initially repaired by excising upper eyelid skin, essentially suspending the eyelid from the brow. The frontalis suspension was popularized in the 19th century, when a variety of subcutaneous implants were used to create a direct connection between the eyelid and forehead. Motais[1] and Parinaud[2] introduced the superior rectus suspension in 1897. A portion of the superior rectus muscle was transposed and attached to the eyelid. Enthusiasm for this procedure declined as patients developed late complications from the resultant lagophthalmos.

Bowman (1857) first described shortening of the levator–Müller’s muscle complex through a conjunctival incision.[3] Anterior levator resection was subsequently reported in 1883 by Eversbusch and Snellen. [4] [5] In 1975, Jones et al.[6] published the successful repair of acquired ptosis by levator aponeurotic reattachment or resection.

Modern physicians use a variety of procedures, depending upon the levator muscle function. Patients with poor levator function usually require frontalis suspension. Anterior levator aponeurotic resection or posterior müllerectomy is often used in patients who have good levator activity.

PREOPERATIVE EVALUATION AND DIAGNOSTIC APPROACH

The Ocular and Medical History

The initial evaluation is directed toward determining the cause of the ptosis. The history should ascertain the onset, duration, severity, and variability of the condition. Reviewing old photographs is helpful in documenting the progression of the disorder. There may be a positive family history in some forms of hereditary ptosis. Prior ocular trauma, surgery, or disease can contribute to the development of ptosis or alter the treatment plan. Ptosis repair is considered with caution in patients who have 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.

Concomitant ocular signs are helpful in making a diagnosis. Ipsilateral miosis is suggestive of Horner’s syndrome, and mydriasis is found in cases of oculomotor paralysis. Patients who have surgically or traumatically enlarged pupils often experience photophobia, a symptom that can be exacerbated by ptosis surgery. Ocular inflammation or dryness may cause reactive ptosis. These conditions must be corrected before considering ptosis repair. A basic tear secretory rate is obtained in adult patients. Surgery is often limited or avoided in patients with dry eyes.

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

Hering’s Law

The levator muscles obey Hering’s law of equal innervation. [7] These muscles are innervated from a single midline nucleus, resulting in equal central neural output. In cases of bilateral asymmetrical ptosis, the less affected eyelid may maintain a normal level of elevation due to excessive innervational stimulation determined by the more ptotic eyelid. This condition can be detected prior to surgery by manually elevating the ptotic eyelid. An immediate fall of the contralateral eyelid confirms the presence of bilateral, asymmetrical ptosis masked by levator “overaction.” [8]

Levator Muscle Function

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

Other Measurements

The upper eyelid margin is normally positioned 1–2?mm below the superior limbus. The location of the lid margin is measured with the patient looking in primary gaze. This may be recorded as the position (in millimeters) of the eyelid margin with respect to the pupillary light reflex (margin-to-reflex distance or MRD).

The amount of redundant skin (dermatochalasis) and the position of the upper eyelid creases are recorded. Ocular motility is assessed. Coexisting strabismus may be present in cases of congenital ptosis, acquired neurological or myopathic disease, and

 

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Differential Diagnosis of Upper Eyelid Blepharoptosis

 

CONGENITAL PTOSIS

Myopathic ptosis

 

Blepharophimosis syndrome

 

Marcus Gunn’s jaw-winking syndrome

 

 

ACQUIRED PTOSIS

Third nerve palsy

 

Horner’s syndrome

 

Myasthenia gravis

 

Chronic progressive external ophthalmoplegia

 

Aponeurotic ptosis

 

Mechanical ptosis

 

 

 

 

orbital masses. Ptosis patients who have hypotropia typically have a component of pseudoptosis. In patients who have reduced or absent Bell’s phenomenon, ptosis repair should be conservative to avoid postoperative exposure.

DIFFERENTIAL DIAGNOSIS

Blepharoptosis may be categorized by age of onset (congenital vs. acquired), severity, and physiological etiology. The differential diagnosis of blepharoptosis is shown in Box 86-1 .

Congenital Ptosis

SIMPLE CONGENITAL (MYOPATHIC) PTOSIS.

The majority of children with congenital ptosis have a developmental myopathy of the levator muscle. The ptosis is present at birth and remains stable throughout life. Levator function is decreased in proportion to the severity of the ptosis. The fibrotic levator muscle limits inferior mobility of the eyelid, causing less ptosis in downgaze ( Fig. 86-1 ). The upper eyelid crease is usually indistinct or absent. Compensatory elevation of the eyebrows or a chin-elevated head position is often present.

Simple congenital ptosis is unilateral in 69% of cases. [10] Bilateral involvement may be symmetrical or asymmetrical in appearance. Coexisting strabismus 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] Strabismus and anisometropia may lead to amblyopia, which is found in 20% of patients who have simple congenital ptosis.[17] Occlusion amblyopia is less common and should be considered a diagnosis of exclusion. Early surgery is indicated in cases with obstruction of the visual axis. Treatment is otherwise delayed until the late preschool years.

Children who have good levator function are effectively repaired with anterior levator aponeurotic-muscle resection, whereas children with severe ptosis and poor function often require frontalis suspension. Treatment of severe unilateral congenital ptosis is challenging. Unilateral frontalis suspension may be considered in children who have compensatory elevation of the eyebrow. Maximal levator resection can also be used, although this procedure can be complicated by postoperative lagophthalmos. Bilateral frontalis suspension combined with ablation of the uninvolved levator muscle provides symmetrical eyelid appearance and function. However, many parents are hesitant to consider surgery on the normal eyelid.

BLEPHAROPHIMOSIS SYNDROME.

Approximately 6% of children with congenital ptosis demonstrate the typical findings of blepharophimosis syndrome.[10] There is severe bilateral ptosis with poor levator function. The palpebral fissures are horizontally shortened (blepharophimosis) with resultant telecanthus ( Fig. 86-2 ). True hypertelorism is occasionally present.[18]

 

 

 

 

 

 

Figure 86-1 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.

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.

 

Blepharophimosis is a dominantly inherited condition, although the severity of findings varies among affected family members.[19] Sporadic cases also occur. Blepharophimosis is associated with primary amenorrhea in some family lines.[20]

Treatment of blepharophimosis usually requires a staged approach. The telecanthus and epicanthal folds are initially repaired with medial canthal tendon plication and local skin flaps.[18] [21] Bilateral frontalis suspension is subsequently performed. 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 is typically unilateral and not hereditary. There is intermittent elevation of the ptotic eyelid, coinciding with contraction of the muscles of mastication, resulting in a “winking” movement during eating or chewing ( Fig. 86-3 ). 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 is usually intact. Hypotropia and other forms of strabismus may be seen in the jaw-winking syndrome.[23]

 

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Figure 86-2 Blepharophimosis syndrome. A, With symmetric bilateral ptosis, telecanthus, and epicanthal folds. B, Postoperative appearance following bilateral canthoplasty and frontalis suspension.

 

 

 

 

Figure 86-3 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.

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 that stimulate the synkinesis.[26] Mild cases can be treated with levator aponeurotic-muscle resection. Patients with large-amplitude winking may require ablation of the levator, followed by frontalis suspension.[27]

 

 

Figure 86-4 Horner’s syndrome with ipsilateral right upper eyelid ptosis and pupillary miosis.

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 symmetrical, bilateral ptosis. Peripheral third nerve deficits are much more common and are often caused by trauma, ischemia (microvascular disease), inflammation, neoplasm, and aneurysms. Ptosis with decreased or absent levator function, mydriasis, and strabismus typically are present. Spontaneous recovery may occur, although a partial deficit often remains. Aberrant regeneration is frequent and occasionally results in gaze-directed eyelid retraction.

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

HORNER’S SYNDROME.

Müller’s 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. 86-4 ). Weakness of the inferior tarsal muscle elevates the lower eyelid, contributing to a narrowed palpebral fissure. Ipsilateral miosis is uniformly present. Many patients also experience hemifacial anhidrosis. Heterochromia can be seen in patients who have congenital Horner’s syndrome.[29] The ipsilateral iris is lighter in color.

Pharmacological (cocaine) testing confirms the diagnosis of this condition. The neurological deficit may result from ischemia, trauma, neoplasm, or iatrogenic insults. A medical evaluation is indicated in patients who have newly diagnosed Horner’s syndrome of unknown causes. Surgical correction is indicated in patients who have significant, persistent ptosis. External levator aponeurotic-muscle resection and posterior müllerectomy are effective methods of repair.

MYASTHENIA GRAVIS.

Ptosis and diplopia are presenting symptoms in about one half of patients who have myasthenia and subsequently appear in 96% of individuals with this condition.[30] The ptosis may be unilateral, bilateral, or alternating. Levator function is either decreased or variable. There is rapid fatigability of the affected levator muscle. 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 have a purely ocular form of the disease; the majority develop systemic involvement.[32] [33]

This autoimmunological condition affects the neuromuscular junction and has a predilection for muscles innervated by the cranial nerves. Antibodies to acetylcholine receptor protein are present in most patients with systemic disease. [32] The history and clinical findings usually lead the clinician to the diagnosis, which is confirmed by Tensilon testing, electrophysiological studies, or acetylcholine receptor antibody levels ( Fig. 86-5 ). Myasthenia is treated medically. Selected patients may benefit

 

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Figure 86-5 Myasthenia gravis with severe bilateral ptosis. A, Before treatment. B, The same patient after administration of intravenous Tensilon.

from thymectomy.[33] Ptosis repair is reserved for individuals with refractory, visually debilitating disease. Limited frontalis suspension is usually performed. Myasthenia patients are at increased risk for developing postoperative ocular exposure from coexisting orbicularis muscle weakness or a poor Bell’s phenomenon.

CHRONIC PROGRESSIVE EXTERNAL OPHTHALMOPLEGIA.

Chronic progressive external ophthalmoplegia (CPEO) includes a group of conditions that are either hereditary or sporadic in nature. Most patients present with symmetrical, bilateral ptosis in early adulthood ( Fig. 86-6 ). The mitochondrial myopathy results in decreased levator function. Extraocular muscles are affected later, 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 delayed until the patient is visually debilitated. Limited frontalis suspension is often the procedure of choice, avoiding postoperative lagophthalmos and resultant ocular exposure.

APONEUROTIC REDUNDANCY OR DEHISCENCE.

Most patients who have acquired ptosis develop the condition secondary to involutional changes in the levator aponeurosis. Gradual stretching or dehiscence of this structure causes slowly progressive ptosis. Chronic contact lens wearers may also develop ptosis on this basis. Aponeurotic dehiscence may occur following ocular surgery or trauma. Ptosis develops in approximately 6% of patients following cataract surgery.[37]

Levator function is not reduced in this form of ptosis. Loss of the aponeurotic attachment results in an abnormally high or indistinct upper eyelid crease ( Fig. 86-7 ). 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 aponeurosis through an anterior approach corrects the ptosis.

MECHANICAL PTOSIS.

Mechanical ptosis develops from cicatricial processes, tumors, 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

 

 

Figure 86-6 Chronic progressive external ophthalmoplegia (CPEO) with bilateral ptosis and ocular motility abnormality.

secondary to a mass effect, and infiltrative conditions restrict 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.

PTOSIS REPAIR

Ptosis repair is an elective procedure. Surgery should be avoided or limited in individuals who have preexisting ocular irritation or photophobia. Patients who have poor tear production can develop symptomatic dryness following eyelid elevation. Ptosis repair in 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 exposure keratitis should there be postoperative lagophthalmos. Limited surgery can be performed should these patients develop visually debilitating ptosis. Nonsurgical elevation of the eyelid with a ptosis crutch attached to the spectacle frame is occasionally helpful, although these devices often limit blinking, resulting in ocular irritation.

ANESTHESIA

Ideally, ptosis repair is performed with local anesthesia. An alert patient facilitates the intraoperative adjustment of the eyelid. Subcutaneous injection of a mixture of 2% lidocaine (lignocaine) with 1:200,000 epinephrine (adrenaline) and 0.75% bupivacaine provides adequate analgesia. A minimal volume (1–2?cm3 per eyelid) of anesthetic is required. Larger volumes or deeper orbital injections may alter levator function, compromising muscle adjustment. General anesthesia is necessary for young children, for apprehensive adults, and when harvesting fascia lata.

GENERAL TECHNIQUES

The type of ptosis and amount of levator function are considered when choosing the best procedure for an individual patient. Anterior levator aponeurotic-muscle reattachment or resection is effective in patients who have moderate to good levator function. Maximal levator resection can be used in cases with poor levator activity, although postoperative lagophthalmos is more common. Some surgeons perform a posterior resection of Müller’s muscle in patients who demonstrate adequate elevation of the eyelid following instillation of topical phenylephrine.[38] [39]

Frontalis suspension is performed in patients who have severe ptosis, poor levator activity, and intact frontalis muscle function. Autologous fascia lata is the preferred implant material in pediatric cases. Donor fascia may also be used, although recurrent ptosis may occur secondary to implant absorption.[40] Alloplastic implants such as silicone rods are placed in patients in whom it is impractical to harvest fascia lata. These implants are occasionally complicated by extrusion, infection, or breakage.

 

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Figure 86-7 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.

The quality of Bell’s phenomenon, lacrimal production, and orbicularis activity are considered when determining the amount of eyelid elevation to perform. Selected patients tolerate mild lagophthalmos, which may be necessary to achieve an acceptable cosmetic result. Marked lagophthalmos should generally be avoided due to the risks of corneal exposure.

The skin incision is placed in the location of the desired eyelid crease. The position of the contralateral crease is matched in cases of unilateral ptosis. Eyelid creases are absent or indistinct in many cases of bilateral disease, in which case the incisions are marked about one third of the distance from the eyelashes to the lower edge of the brow.[41] The central incision is approximately 9–10?mm above the lashes in adult women. The adult male crease is usually placed 1–2?mm lower. Combined blepharoplasty and ptosis repair can be performed in patients undergoing bilateral surgery.

Early surgical intervention may be indicated in infants who have occlusion amblyopia. Ptosis repair in young children is otherwise deferred until 3 to 5 years of age, facilitating both preoperative measurements and postoperative care. It is difficult to obtain sufficient fascia lata in children younger than 3 years.

SPECIFIC TECHNIQUES

Anterior Levator Aponeurosis Advancement

The patient is examined both sitting and supine. Any change in eyelid position is noted because surgery is performed with the patient recumbent. A standard full-face surgical wash is performed. The desired position of the upper eyelid crease incision is marked, and subcutaneous infiltrative anesthesia is administered.

After creating the skin incision ( Fig. 86-8 , A), the orbicularis muscle is divided parallel to its muscle fibers. The septum is divided and the preaponeurotic fat pads are retracted upward to expose the underlying levator muscle ( Fig. 86-8 , B). Hemostasis is maintained throughout the procedure.

The opaque levator aponeurosis may be thin or completely dehisced from the tarsus. Any remaining attachments of the aponeurosis are divided, exposing the tarsus. The aponeurosis is separated from underlying Müller muscle with blunt and sharp dissection ( Fig. 86-8 , C). In severe congenital ptosis, the combined aponeurosis–Müller muscle complex may have to be advanced to achieve adequate lid elevation. The dissection in these cases is performed between Müller’s muscle and conjunctiva. The awake patient is asked to look in primary gaze, allowing the surgeon to determine whether the dissection has altered the preoperative eyelid level.

Two partial-thickness 6-0 polyester (Mersilene) sutures are placed in the central third of the tarsus. The posterior surface of the lid is examined to ensure that the sutures are not exposed. These sutures are used to reattach or advance the aponeurosis ( Fig. 86-8 , D). Any change in the lid position noted from supine to upright positioning or resulting from surgical dissection is considered when determining the amount of lid elevation to perform. The eyelid is adjusted empirically in patients under general anesthesia, considering the preoperative levator function and amount of ptosis. Redundant aponeurotic tissue is excised. The eyelid crease is reformed by suturing the cut edge of the pretarsal orbicularis muscle or subcutaneous tissue to the aponeurosis (7-0 polyglactin sutures) ( Fig. 86-8 , E). The skin incision is closed with a running 7-0 polypropylene suture ( Fig. 86-8 , F).

Patients are observed after surgery to detect early postoperative hemorrhage or other complications. Cold compresses are used during 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. There may be transient lagophthalmos and poor blink after surgery, attributable to orbicularis underaction. These findings usually improve 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

Incision location and pattern of the implanted material are determined by brow contour. A pentagonally shaped sling is used in patients who have diffuse brow elevation. Medial and lateral incisions are marked at the superior border of the brow, just outside the medial and lateral corneal limbus ( Fig. 86-9 , A). A central forehead incision is placed approximately 10?mm above the

 

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Figure 86-8 Key steps in levator aponeurosis advancement.

brow, between the other two incisions. Triangular slings are more ideal in individuals who have segmental brow elevation. They utilize a single incision above the portion of the brow exhibiting maximal movement.

The brow incisions are created through skin and subcutaneous tissue, exposing the frontalis muscle. A crease incision is used to expose the tarsus ( Fig. 86-9 , B). Fascia lata must be harvested in patients who undergo autologous grafting. A 3?cm incision is made on the lower thigh, just above the lateral condyle of the femur. The white, glistening fascia lata is visible underneath

 

 

Figure 86-9 Key steps in frontalis suspension.

the subcutaneous fat. Blunt dissection is performed on the anterior surface of the fascia, up the lateral aspect of the leg for about 15–20?cm. A strip of fascia 6–8?mm wide and 15–20?cm long is harvested using a fascial stripper and cutter. The fascia is cleaned of adherent subcutaneous fat and divided into strips 2–3?mm wide.

The implant material is sutured to the upper anterior surface of the central tarsus with several partial-thickness 6-0 polyester sutures ( Fig. 86-9 , C). Eyelid contour is adjusted by altering the width of this attachment. A Wright fascial needle is then used to

 

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pass each end of the sling, first through the peripheral brow incisions and then from these to the central brow incision. The implant is passed deep to the orbital septum and superficial to the periosteum of the superior orbital rim. The eyelid crease is recreated by suturing the edge of the pretarsal orbicularis muscle to the aponeurosis with 7-0 polyglactin sutures and the lid incision is closed (7-0 polypropylene, 6-0 gut) prior to adjusting the eyelid height ( Fig. 86-9 , D). The two ends of the sling are adjusted to achieve the proper lid height and contour. The ends 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 layer. A light elastic leg dressing minimizes 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

Persistent ptosis is a common complication, seen after about 10–15% of cases. These patients should be observed until edema has resolved and the eyelid position has stabilized. Some patients require further evaluation because an unsuspected acquired myopathy may be responsible for recurrent or poorly corrected ptosis. Surgical revision is considered in patients who have persistent symptomatic ptosis.

Overcorrection

Patients who have mild overcorrection following surgery should be observed until the lid position has become stable. Digital massage or “squeezing” exercises occasionally lower the eyelid, improving mild overcorrection. Surgical revision with recession of the levator or suspension material is indicated in cases with persistent overcorrection. Early surgical revision should be performed in patients who have marked postoperative overcorrection and ocular exposure.

Eyelid Crease Abnormalities

Incorrect incision placement or failure to create the eyelid crease may result in 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 at the location of the new crease. The subcutaneous tissue is sutured to the aponeurosis prior to skin closure.

It is 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, should then be mobilized between these layers in an effort to minimize the establishment of a new adhesion in the same location. The new crease is then established at a lower level.

Abnormalities of Eyelid Margin Contour

Distortions of the eyelid margin contour result from uneven advancement of the aponeurosis. Surgical revision is often required. The lid contour is adjusted by tightening or loosening individual aponeurotic sutures.

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 daytime artificial tears are used in minor cases. Punctal occlusion may be indicated in patients who have severe dry eyes. Persistent keratitis may require lowering of the upper eyelid. Alternative procedures, such as elevating the lower lid, canthoplasty, and tarsorrhaphy, can be considered in patients in whom reversal of the ptosis repair would be visually disabling.

Prolapse of the Superior Conjunctival Fornix

Excessive advancement of the aponeurosis or Müller’s muscle may cause prolapse of the superior conjunctiva. This results from failure to separate the fine attachments between the aponeurosis and the superior fornix suspensory ligaments. If the conjunctiva is easily reduced, a pressure patch for several days may correct the condition. Once the prolapsed tissue becomes fibrotic, 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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1. Motais M. Opération du ptosis par la greffe tarsienne d’une languette du tendon du muscle droit supérieur. Ann Oculist (Paris). 1897;118:5–12.

 

2. Parinaud H. Nouveau procédé opératoire du ptosis. Ann Oculist (Paris). 1897;118:13–17.

 

3. Bader. Report of the chief operations performed at the Royal London Ophthalmic Hospital for quarter ending 25th September 1857. R Lond Ophthalmic Hosp Rep. 1857;1:33–5.

 

4. Beard CH. Ophthalmic surgery, 2nd ed. Philadelphia: P Blakiston’s and Sons; 1914:230–52.

 

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6. Jones LT, Quickert MH, Wobig JL. The cure of ptosis by aponeurotic repair. Arch Ophthalmol. 1975;93:629–34.

 

7. Gay AJ, Salmon ML, Windsor CE. Hering’s law, the levators, and their relationship in disease states. Arch Ophthalmol. 1967;77:157–60.

 

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9. Fox SA. The palpebral fissure. Am J Ophthalmol. 1966;62:73–8.

 

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12. Berke RN. Congenital ptosis—a classification of two hundred cases. Arch Ophthalmol. 1948;41:188–97.

 

13. Carbajal UM. An analysis of 142 cases of ptosis. Am J Ophthalmol. 1958;45: 692–704.

 

14. Sevel D. Ptosis and underaction of the superior rectus muscle. Ophthalmology. 1984;91:1080–5.

 

15. Beneish R, Williams F, Polomeno RC, et al. Unilateral congenital ptosis and amblyopia. Can J Ophthalmol. 1983;18:127–30.

 

16. Merriam WW, Ellis FD, Helveston EM. Congenital blepharoptosis, anisometropia, and amblyopia. Am J Ophthalmol. 1980;89:401–7.

 

17. Anderson RL, Baumgartner SA. Amblyopia in ptosis. Arch Ophthalmol. 1980;98:1068–9.

 

18. Callahan A. Surgical correction of the blepharophimosis syndromes. Trans Am Acad Ophthalmol Otolaryngol. 1973;77:op687–op695.

 

19. Briggs HH. Hereditary congenital ptosis with report of 64 cases conforming to the Mendelian rule of dominance. Am J Ophthalmol. 1919;2:408–17.

 

20. Townes PL, Muechler EK. Blepharophimosis, ptosis, epicanthus inversus, and primary amenorrhea—a dominant trait. Arch Ophthalmol. 1979;97:1664–6.

 

21. Mustarde JC. Experiences in ptosis correction. Trans Am Acad Ophthalmol Otolaryngol. 1968;72:173–85.

 

22. Gunn RM. Congenital ptosis with peculiar associated movements of the affected lid. Trans Ophthalmol Soc UK. 1883;3:283–5.

 

23. Oesterle CS, Faulkner WJ, Clay R, et al. Eye bobbing associated with jaw movement. Ophthalmology. 1982;89:63–7.

 

24. Lewy FH, Groff RA, Grant FC. Autonomic innervation of the eyelids and the Marcus Gunn phenomenon. Arch Neurol Psychiatry. 1937;37:1289–97.

 

25. Spaeth EB. The Marcus Gunn phenomenon. Am J Ophthalmol. 1947;30: 143–158.

 

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