What is blepharoptosis

Blepharoptosis also called ptosis, is defined as drooping of the upper eyelid with the eyes in the primary position of gaze ¹. Blepharoptosis can be bilateral or unilateral and can be difficult to identify unless a proper exam is performed. Blepharoptosis is relatively common in the general population and while frequently regarded as a purely cosmetic issue, blepharoptosis can be visually disabling and may be a sign of underlying systemic disease. Blepharoptosis affects men and women equally and there is little data regarding incidence differences between races ². Comprehensive studies that investigate the incidence and prevalence of blepharoptosis are lacking, but one study looking at individuals 50 years of age and older in England discovered that 11.5% had some form ptosis and that the prevalence of blepharoptosis increased greatly with age ³. While involutional ptosis is the most common cause of blepharoptosis in older populations, there are many causes that affect all age groups.

Blepharoptosis can classify as true ptosis or pseudoptosis. True ptosis is further classified based on the age of presentation into congenital ptosis and acquired ptosis ⁴.

Eyelid anatomy

The opening located between the upper and lower eyelid is elliptical and termed the palpebral fissure. The upper eyelid curvature is maximum at a point just nasal to the mid pupillary point, which is an important point to mark before surgery to get the best cosmetic results. The upper lid covers 1 to 2mm of the superior limbus, while the lower lid lies at the lower limbus.

Structures forming the eyelid ⁵:

1. Skin and subcutaneous tissue
2. Orbicularis oculi
3. Orbital septum
4. Preaponeurotic fat pad
5. Tarsal plate
6. Levator aponeurosis and Muller’s muscle
7. Conjunctiva

Skin

• The eyelid skin is the thinnest layer of skin in the entire body. The eyelid crease forms due to attachment of levator aponeurosis to the skin.

Orbicularis oculi

• It is a circular muscle and consists of three parts namely: preseptal, pretarsal, and orbital orbicularis. Contraction is responsible for gentle and forced closure of the eyelid.

Orbital septum

• It is a multi-layered structure of thin fibrous connective tissue. The septum inserts superiorly to the periosteum over the superior orbital rim. Inferiorly it merges with the fibers of levator aponeurosis above the superior tarsal border.[5]
• In ptosis surgery, the septum is opened to gain access to the levator muscle. Care should be taken to separate septal attachments to the levator muscle to avoid post-operative lid retraction.

Preaponeurotic fat pad

• The fat pad is posterior to the septum and anterior to the levator. This pad of fat can be identified intraoperatively by applying pressure over the globe which causes it to prolapse forward. It helps in identifying the levator muscle which lies immediately posterior to it.

Tarsal plate

• Tarsal plate forms the structural skeleton of the eyelid and is made up of dense connective tissue. The vertical height is 10 to 12 mm in the upper eyelid and 4 to 5 mm in the lower lid. The tarsal plates contain the Meibomian glands, the orifices of which open posterior to the grey line.

Levator Palpebrae superioris muscle

Levator Palpebrae superioris muscle is the main elevator of the eyelid. It originates at the orbital apex from the periosteum over the lesser wing of sphenoid. It travels forward below the roof of the orbit. At the superior orbital rim, it changes direction from horizontal to vertical and forms the tendinous sheath called levator aponeurosis. At this transition, lies the Whitnall’s ligament which is seen as a dense white band of connective tissue and acts as a pulley. It lies 10 to 12 mm above the tarsal plate.

The levator aponeurosis has several insertions. Anteriorly, it inserts into the upper lid skin forming the lid crease. Inferiorly, it inserts onto the anterior surface of the superior one-third of the tarsus. Posteriorly, it has attachments to the superior conjunctival fornix. Medially and laterally, it forms the medial and lateral horns which then insert into the posterior lacrimal crest and Whitnall’s tubercle along with the canthal tendons ⁶.

The levator receives nerve supply by the superior division of the oculomotor nerve.

Muller’s muscle

It is a sympathetically innervated smooth muscle. It originates from the under surface of the levator aponeurosis at the level of the Whitnall ligament and inserts into the superior border of the tarsus. It contributes to 2 mm of eyelid elevation.

Conjunctiva

It is the innermost layer of the eyelid formed by non-keratinizing squamous epithelium. It continues over the anterior surface of the globe. It contains goblet cells, the secretions of which hour of utmost importance in keeping the eyes moist.

Blepharoptosis causes

Blepharoptosis may be congenital or acquired ptosis.

Acquired blepharoptosis can be further categorized as neurogenic, myogenic, aponeurotic, mechanical, or pseudoptosis ⁷:

• Aponeurotic ptosis
• Neurogenic ptosis
• Myogenic ptosis
• Mechanical ptosis
• Traumatic ptosis

Congenital blepharoptosis

Congenital ptosis results usually from isolated localized myogenic dysgenesis levator palpebrae superioris. Very small number of congenital blepharoptosis may result from genetic or chromosomal defects, and neurologic dysfunction ⁸.

• Blepharophimosis syndrome which is characterized by short palpebral fissures, congenital ptosis, epicanthus inversus, and telecanthus.
• Congenital third cranial nerve palsy.
• Congenital Horner’s syndrome which is characterized by mild ptosis, miosis, anhidrosis, and heterochromia.
• Marcus Gunn jaw-winking syndrome which results from misdirected innervations to the ipsilateral levator muscle by the motor nerve to the external pterygoid muscle. Patients have lid elevation with mastication or with movement of the jaw to the opposite side.

Aponeurotic ptosis

Aponeurotic blepharoptosis is the most prevalent form of adult ptosis and usually presents in the 5th or 6th decade of life. It is also known as involutional ptosis. However, it can occur in young individuals following trauma, recent eyelid swelling, ocular surgery or prolonged use of contact lenses. Involutional ptosis has also been described in relatively younger populations, especially in patients that wear hard contact lenses or chronically rub their eyelids ⁹. Soft contact lens wear has also been associated with ptosis in some cases ¹⁰. The incidence of ptosis in postoperative cataract patients was previously reported to be around 6%, but newer techniques have decreased this incidence ¹¹.

The pathogenesis of aponeurotic ptosis is most often due to dehiscence or disinsertion of the levator aponeurosis connection to the tarsal plate ¹². Since this connection is responsible for the formation of the upper lid crease, the crease is often elevated or absent in these cases. In involutional ptosis cases, true dehiscence is sometimes absent, and ptosis occurs due to stretching or thinning of the aponeurosis. Rarely the levator muscle shows fatty infiltration.

Characteristic features of aponeurotic blepharoptosis are that patients have a good levator function with a high lid crease, affected eyelid appears lower on down gaze and a thin upper eyelid with redundant skin.

Neurogenic ptosis

Neurogenic blepharoptosis results from any condition which disrupts the innervation of either the levator muscle or muller’s muscle. The varieties most commonly encountered by an ophthalmologist are 3rd cranial nerve (oculomotor nerve) palsy and Horner syndrome.

Third cranial nerve palsy

Lesions along the oculomotor nerve (3rd cranial nerve) present with ptosis and restriction of adduction, elevation and depression movements of the eyeball. Pupillary involvement may or may not be present. Bell’s phenomenon is usually poor. Pupil-involving third nerve palsy is considered a neurological as it is most often due to a posterior communicating artery aneurysm compressing the nerve. Pupil-sparing third nerve palsy is most often due to an ischemic vascular cause and usually resolves spontaneously in 3 months. Other causes include inflammation, trauma or tumors along the course of the nerve. Lesions of the superior orbital fissure, orbital apex, or cavernous sinus, present in combination with other cranial nerve palsies.

Treatment is challenging as the patients have a poor or absent Bell’s phenomenon placing them at high risk of developing exposure keratopathy post-surgery. Ideally, strabismus surgery is done first to correct the deviation followed by ptosis correction via the frontalis sling technique with planned under-correction.

Horner’s syndrome

Horner syndrome (oculosympathetic paresis) consists of mild ptosis, pupillary miosis, apparent enophthalmos, and anhidrosis. It occurs due to interruption of the sympathetic nerve supply to the muller’s muscle and dilator pupillae muscle.

Pupillary anisocoria can be well demonstrated in dim illumination. Patients with Horner’s syndrome occurring during childhood also have iris heterochromia due to decreased melanin production in melanocytes which is controlled by the sympathetic pathway.

The diagnosis of Horner syndrome is often made clinically. Pharmacological tests using 4% cocaine, 1% hydroxyamphetamine or 2.5% phenylephrine help confirm the diagnosis.

Myasthenia gravis

Myasthenia gravis is an autoimmune disorder characterized by the presence of antibodies to acetylcholine receptors located at the neuromuscular endplates of voluntary muscles ¹³. This leads to decreased action of acetylcholine which results in muscle weakness and fatigue. Myasthenia may be generalized or localized to the eye (ocular myasthenia). The most common presenting feature is variable ptosis associated with diplopia. Symptoms may be unilateral or bilateral. Patients with myasthenia initially have a good levator function. Prolonged upgaze will cause a worsening of ptosis in these patients due to muscle fatigue.

Cogan lid twitch sign: Rapid saccadic eye movements from downgaze to primary position results in rapid upshoot of the lid followed by a gradual drop to the primary position.

Other tests which help confirm the diagnosis include ice test, edrophonium test (Tensilon test), serum acetylcholine receptor antibody assay, single fiber electromyography, and repetitive nerve stimulation test.

Treatment of such patients involves administration of acetylcholinesterase drugs, oral steroids or immunosuppressants. In patients with severe ptosis, ptosis correction with planned under-correction may be an option.

Myogenic ptosis

Myogenic ptosis arises due to an abnormality in the levator muscle itself. These patients usually present with reduced levator action along with restricted extraocular motility and facial expression.

Oculopharyngeal muscular dystrophy

Oculopharyngeal muscular dystrophy is part of an inherited group of progressive muscular dystrophies and is the most common cause of myogenic ptosis. It is characterized by asymmetric involvement of the levator muscles with progressive dysarthria, proximal limb weakness, and dysphagia. It is typically diagnosed in middle age and is associated with individuals of French Canadian decent. It is also prevalent in the Hispanic population in the U.S. ¹⁴. Oculopharyngeal muscular dystrophy should be suspected in individuals who have an autosomal dominant family history of ptosis and a flat facial expression. Dysphagia is usually not present until later in the course of the disease. Some patients report voice changes but this is rarely documented. The diagnosis of oculopharyngeal muscular dystrophy is confirmed with genetic testing or muscle biopsy.

Chronic progressive external ophthalmoplegia

Patients with chronic progressive external ophthalmoplegia present with symmetric, bilateral ptosis and ophthalmoparesis typically in their 30’s. Chronic progressive external ophthalmoplegia is mitochondrial myopathy and therefore displays a mitochondrial mode of inheritance. Extrinsic eye muscles are particularly vulnerable to certain neuromuscular disorders. These muscles contain a larger volume of mitochondria than any other muscle group, and this results in their preferential involvement in mitochondrial myopathies ¹⁵. Symptoms are initially mild and slowly progress to the point of severe ophthalmoplegia. Patients rarely complain of diplopia due to compensatory head movements. Diagnosis is confirmed by muscle biopsy, which shows ragged red fibers. More information on chronic progressive external ophthalmoplegia can be found in the related article.

Kearns-Sayre syndrome

This syndrome is characterized by early-onset chronic progressive external ophthalmoplegia and retinitis pigmentosa. Other findings include cerebellar ataxia, heart block, diabetes, and cognitive deficits. Patients are at risk of sudden cardiac death and the prognosis is poor, with death usually supervening by the fourth decade.

Myotonic dystrophy

Myotonic dystrophy is a hereditary condition with autosomal dominant inheritance. It is the most common form of adult-onset muscular dystrophy. A defining feature of the disease is myotonia, or a failure of the muscle to relax. The classic description is a patient who is unable to release their grip after a handshake. The condition eventually leads to facial and peripheral muscle weakness. Patients present with bilateral ptosis and a flat facial expression. Myotonic dystrophy can be distinguished from oculopharyngeal dystrophy by the associated systemic findings such as “Christmas tree” cataracts, frontal balding, intellectual impairment, and heart block. In addition, the orbicularis weakness and ocular motility deficits are more prominent in myotonic dystrophy compared to oculopharyngeal muscular dystrophy. Diagnosis is confirmed by genetic testing for an expanded CTG repeat in the DMPK gene.

Mechanical ptosis

Mechanical blepharoptosis is caused by excess weight of the upper lid. There are a multitude of causes that can be easily distinguished on physical exam. A few common causes are edema, inflammation or blepharochalasis, tumors, chalazia, dermoid cysts, neurofibromas, cicatrization or scarring of the conjunctiva and amyloid deposits.

Traumatic ptosis

Ptosis occurs due to direct or indirect trauma to the levator muscle. Penetrating injuries involving the levator can be repaired immediately. However, ptosis secondary to blunt trauma may resolve spontaneously over time. Ptosis which does not improve after 6 months can have surgical repair.

Pseudoptosis

It is not true ptosis but apparent ptosis due to abnormalities in structures other than the levator muscle or aponeurosis. A very common cause of pseudoptosis is dermatochalasis, or redundant eyelid skin, that droops beyond the eyelid margin creating the appearance of ptosis. If this skin is manually lifted, one can assess the position of the underlying eyelid margin to assess for the presence of true ptosis. Asymmetric lid heights due to unilateral upper lid retraction might give the impression of ptosis in the contralateral eye. Enophthalmos may also create the appearance of ptosis due to reduced upward forces on the eyelid. Enophthalmos is the posterior displacement of the eyeball within the orbit due to changes in the volume of the orbit (bone) relative to its contents (the eyeball and orbital fat), or loss of function of the orbitalis muscle. Hypotropia may also result in pseudoptosis due to connections from the superior rectus muscle to the upper eyelid.

Other causes of pseudoptosis the eyelid include brow ptosis, microphthalmos, anophthalmos (complete absence of the ocular tissue), phthisis bulbi, and contralateral eyelid retraction.

It is very important to distinguish true ptosis from a pseudoptosis before embarking upon any surgical correction for drooping.

Blepharoptosis symptoms

Patients usually complain of:

• Drooping of eyelids
• Feeling of heaviness in the eyes
• Visual obscuration due to drooping
• Cosmetic complaints

Blepharoptosis complications

Congenital ptosis may lead to amblyopia secondary to deprivation or uncorrected astigmatism. Acquired blepharoptosis results in decreased field of vision and frontal headaches. Blepharoptosis causes significant psychosocial effects and may lead to poor performance in school and at work.

Surgical correction of blepharoptosis may be complicated by bleeding, infection, edema, undercorrection or overcorrection of the ptosis, eyelid asymmetry, granuloma formation, corneal foreign body sensation, and exposure keratopathy. Majority of these complications can be managed easily if discovered early and the appropriate treatment provided.

Blepharoptosis diagnosis

A thorough history taking and clinical examination help determine the cause of blepharoptosis and plan appropriate treatment.

History taking should include the age of onset of ptosis, progression, duration, and any aggravating or relieving factors. Any associated symptoms such as diplopia, diurnal variation, pain, lid swelling, dysphagia or muscle weakness help provide a provisional diagnosis.

Predisposing factors such as trauma, ocular or eyelid surgery, contact lens use, and botulinum toxin injection should be carefully ruled out. A family history of ptosis should be looked for to rule out hereditary disorders. In patients where the history is inconclusive, assessment of old photographs gives an idea about the time of onset.

Any systemic illness, mental health issues, and medication history require documentation. Patients on blood thinners such as aspirin should be advised to stop medications 1 week before surgery.

Clinical examination

Clinical examination starts from the moment the patient walks into the doctor’s clinic. It is essential to look for any facial asymmetry, frontalis overaction, chin up or head tilt posture.

Ocular examination

1. Visual acuity and refraction
2. Cover test to look for any hypotropia and rule out any component of pseudoptosis
3. Extraocular motility disturbance and any aberrant eyelid movements
4. Pupillary examination to look for Horner syndrome or 3rd cranial nerve palsy
5. Examination to look for any giant papillary conjunctivitis or symblepharon
6. Corneal sensation and dry eye evaluation as they can predispose to post-operative keratopathy.
7. Fundus examination for features of retinal pigmentary degeneration

Specific examination of ptosis

Lid measurements should be done positioning the face in the frontal plane, negating the action of frontalis muscle with the thumb, and eyes in the primary position of gaze. The examiner should be seated at the eye level of the patient to avoid parallax error.

1. Palpebral fissure height (PFH): It is the vertical palpebral aperture height between the upper and lower eyelid margin in the pupillary plane with eyes in the primary position of gaze. Average palpebral fissure height (PFH) is around 10mm.
2. Marginal reflex distance 1 (MRD 1): MRD 1 is the distance between the center of the pupillary light reflex and the upper eyelid margin with the eye in primary gaze. Normal MRD 1 is 4-5mm. The difference in MRD 1 between the two eyes helps classify ptosis as mild, moderate or severe in patients presenting with unilateral ptosis.
   • The difference in MRD 1 between two eyes:
     • 2mm – Mild ptosis
     • 3mm – Moderate ptosis
     • 4mm – Severe ptosis
3. Marginal reflex distance 2 (MRD 2): MRD 2 is the distance between the center of the pupillary light reflex and the lower eyelid margin with the eye in primary gaze. Normally MRD 1 + MRD 2 = PFH.
4. Levator action: It is the amount of excursion measured with a millimeter scale when the eyelid moves from extreme downgaze to extreme upgaze with frontalis action negated. Normal levator action is greater than 15mm. It is the single most important measurement in a patient with ptosis as its value determines the choice of surgical procedure.
   • Grading of levator action ¹⁶:
     • Less than 4 mm – Poor
     • 5 to 9 mm – Fair
     • 9 to 11 mm – Good
     • Greater than 12 mm – Excellent
     • In patients with poor levator action (less than 4mm), frontalis sling surgery is the preferred procedure.
5. Margin crease distance (MCD): It is the distance between the lid margin and skin crease in downgaze. Normal margin crease distance (MCD) is 7 to 8mm in men and 8 to 10 mm in women. In congenital ptosis, margin crease distance (MCD) is usually absent or faint, whereas in aponeurotic ptosis MCD is higher than normal. During surgery, it is very important to reform the crease identical to the contralateral eye to maintain symmetry and achieve good cosmesis.
6. Bell’s phenomenon: This is another very important factor to be considered before ptosis correction. The patient is asked to close the eyes gently, and an attempt is made to open them. In patients with poor bell’s, ptosis correction should be avoided or undercorrected to avoid the risk of post-operative exposure keratopathy.
7. Assess presence of lagophthalmos and lid lag on downgaze which if present will worsen post-surgery.
8. Any brow ptosis or dermatochalasis if present should be documented. In involutional ptosis, blepharoplasty procedure is often combined with ptosis repair.
9. Hering test: In patients with unilateral ptosis, the ptotic lid is gently elevated manually, and the contralateral eyelid observed. Due to Hering’s law of equal innervation, the contralateral eyelid may drop (See-saw effect). It is important to demonstrate this to the patient preoperatively and warn them about the possibility of requiring ptosis surgery in the contralateral eye. In such cases, a planned under-correction may be the treatment.
10. Phenylephrine test: It is a useful test in patients with mild ptosis or ptosis due to Horner syndrome; instill 2.5% phenylephrine drops in the superior fornix. Ptosis measurements are repeated after 10 minutes. Patients in whom the ptotic lid elevates due to stimulation of Muller’s muscle are ideal candidates for posterior approach ptosis correction (conjunctival – mullerectomy surgery).
11. Tests to rule out myasthenia gravis
    • Fatigue test: The patient maintains fixation in upgaze for 30 seconds. In patients with myasthenia, the eyelid gradually drops down due to muscle fatigue.
    • Ice test: An ice pack is placed over the closed ptotic eyelid for 2 minutes. Ptotic measurements are repeated after 2 minutes. Improvement in palpebral fissure height (PFH) by 2mm or more is considered positive for myasthenia. This is because cooling improves neuromuscular transmission.
12. Hertel exophthalmometry: A Hertel reading helps rule out any proptosis or enophthalmos and thus excludes pseudoptosis.

Blepharoptosis treatment

Management of blepharoptosis is primarily surgical. Observation is only required in mild cases of congenital ptosis if no signs of amblyopia, strabismus, and abnormal head posture are present. If there is risk for amblyopia, strabismus, and substantial abnormal head posture, surgery is done as soon as possible. Blepharoptosis surgical correction can be done at any time for improving the field of vision or the aesthetic appearance.

If blepharoptosis represents a sign of systemic disease such as myasthenia gravis and Kearns-Sayre disease, the patient should be referred to the appropriate physician for further management.

External photographic documentation is good to obtain especial before attempting surgical correction.

Patients with myasthenia gravis may improve with medical treatment. Sympathomimetic topical eye drops such as apraclonidine and phenylephrine provide short temporary lift of the upper eyelid in some patients.

Blepharoptosis surgery contraindications

• Severe dry eye
• Patients suffering from myogenic ptosis like chronic progressive external ophthalmoplegia – in these patients, if ptosis correction is planned, a conservative surgery should be the choice to clear the visual axis
• Poor Bell’s phenomenon
• Ptosis associated with oculomotor nerve palsy
• Myasthenia gravis: These patients should be treated medically first with anticholinesterase agents

Blepharoptosis surgery

Most patients undergoing ptosis correction seek surgery due to visual obscuration and loss of peripheral field of vision caused by the drooping eyelid. Heaviness in the eyelids is another common concern. A significant proportion seeks surgery for cosmetic concern as the drooping eyelid creates a tired-looking appearance.

Surgery is appropriate for patients who have limited visual fields or for cosmetic reasons ¹⁷. Surgical correction of congenital ptosis can be done at any age depending on the severity of the disease and early intervention is required if there is a risk for development of amblyopia or significant abnormal head position. There are three surgical approaches to ptosis repair ¹⁷:

1. Muller’s muscle conjunctival resection,
2. Levator advancement and
3. Ffrontalis sling.

Depending on treatment goals, the underlying diagnosis, surgeon preference, and the degree of levator function, the appropriate technique is chosen. Patients need to be aware that symmetry is not easy to achieve. Great care should be taken for patients with dry eyes, decrease corneal sensation, absent Bell phenomenon, double elevator palsy, or progressive external ophthalmoplegia to avoid exposure keratopathy postoperatively. If the patient has strabismus and blepharoptosis, strabismus needs to be corrected first.

Müller’s muscle conjunctival resection

The Müller’s muscle conjunctival resection (MMCR) procedure utilizes an internal approach to ptosis repair, thereby leaving no visible external scars after the procedure. Resection of Müller’s muscle typically provides 1-2 mm of lift. After flipping the upper eyelid, the palpebral conjunctiva and Müller’s muscle are resected and the resected ends are sutured together. The advantages of Müller’s muscle conjunctival resection include predictable results, lower rates of reoperation, rapid recovery, less post-operative bleeding, and no intraoperative adjustment ¹⁸. Phenylephrine drops, often used for pupillary dilation, are a sympathetic agonist and stimulate Müller’s muscle. They are instilled during the pre-operative evaluation to approximate the results of an Müller’s muscle conjunctival resection operation and determine if the procedure would provide sufficient lift.

Levator advancement

This procedure has the ability to offer greater lift than Müller’s muscle conjunctival resection (MMCR) and can be performed in patients who had unsatisfactory Müller’s muscle conjunctival resection procedures in the past. An incision is made in the upper eyelid crease to expose the levator aponeurosis. The aponeurosis is dissected off Müller’s muscle, advanced toward the tarsal plate, and sutured in place. The height and contour of the eyelid can be adjusted intraoperatively after examining the lid appearance with the patient sitting upright. This procedure is effective in patients with at least moderate levator function as the levator muscle is still required to lift the eyelid. An eyelid with poor levator function is also at risk for recurrence of ptosis due to replacement of the normal muscle fibers with fat and fibrous tissue resulting in dehiscence of the suture ¹⁹.

Frontalis sling

Slings are indicated for patients with severe ptosis and poor levator function and for patients with progressive myogenic ptosis (oculopharyngeal muscular dystrophy, chronic progressive external ophthalmoplegia, and myotonic dystrophy). In this procedure the eyelid is suspended by either fascia lata (harvested from the thigh), suture, or alloplastic materials (such as silicone). The sling is sutured to the tarsus using an upper eyelid crease incision. It is then passed under the fascia of the brow and secured to the frontalis muscle superiorly using three small incisions above the brow. The eyelid heights are adjusted intraoperatively and the slings are secured. A frontalis sling is indicated in patients with poor or absent levator function because the mechanical movement of the eyelid in such cases is effected solely by the frontalis muscle.

Blepharoptosis repair complications

Undercorrection

This phenomenon may occur with any technique. In the immediate post-operative period, the lid appears undercorrected due to the lid edema. Patients may be reassured. However, if the under-correction persists then revision surgery may be required. The wound can be reopened and aponeurosis re-advanced.

Overcorrection

Overcorrection is more often encountered following advancement for aponeurotic/involutional ptosis. Mild overcorrection in the immediate postoperative period may be tackled with eyelid traction. The patient may be asked to look downward and pull on the eyelashes with the thumb and forefinger; this may be done for a few minutes 3 to 4 times a day. Severe overcorrection will require immediate revision. The wound can be reopened and the sutures cut. The levator is then placed at a more recessed position or secured to the tarsal plate using hang back sutures.

Lagophthalmos and exposure keratopathy

All patients are counseled pre-operatively about post-operative lagophthalmos and decreased blink rate. Management of lagophthalmos in the immediate post-operative period is with copious lubricants. A temporary frost suture may be applied. In cases where severe exposure keratopathy develops a revision surgery is done to lower the lid height.

Eyelid contour defects

Contour defects occur due to improper placement of sutures on the tarsus. Patients presenting with small contour defects usually settle down with time. Lid massage and eyelid traction exercises are advised. Persistent or severe contour abnormalities require revision surgery and proper placement of sutures on the tarsus.

Conjunctival prolapse

Extensive dissection between the conjunctiva and levator can disrupt the suspensory ligaments of the superior fornix and produce conjunctival prolapse. Mild prolapse can be treated conservatively with lubricants. Severe prolapse requires repositioning of the conjunctiva with pang sutures; suture is passed through the prolapsed conjunctiva and secured at the skin crease.

Eyelash ptosis

Excessive dissection of the orbicularis from the tarsus results in lash ptosis, which can be corrected by anterior lamella repositioning sutures.

Suture granuloma

Small granulomas can form at the suture site. They can be excised with Wescott scissors and the base cauterized. The suture causing the granuloma also requires removal.

Blepharoptosis prognosis

Good results are usually achieved by the medical and surgical approaches availabe for managing blepharoptosis. Recurrence over time is not uncommon. More than one surgery may be needed to achieve this result, especially in congenital ptosis.

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