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Clinical Management of Eyelid Retraction Dr. Gunda Sridevi Ashok, MS, Aravind Eye Hospital, Madurai Eyelid retraction is a functional and cosmetic disease process that poses a threat to vision and can be psychologically debilitating to patients. Eyelid retraction increases the vertical height of the palpebral fissure, thereby causing poor coaptation of lids and hence lagophthalmos thus leading to exposure keratopathy. The causes of eyelid retraction in the patients can be categorized into a tripartite simplification of Frueh’s system, namely, neurogenic, myogenic and mechanistic1. Comments on selected entities follow. Neurogenic Eyelid Retraction Eyelid retraction can be congenital or acquired. Preterm infants showing upper eyelid retraction is due to immature myelination of vertical eye movement systems and immaturity or dysfunction of the extrageniculocalcarine visual pathways.2 Two common causes of constant lid retraction, are (1) thyroid eye disease, and (2) Collier’s sign1 of the posterior commissure. Dorsal midbrain syndromes can result from several entities. The key features are light – near pupillary dissociation and conjugate upgaze and convergence paralysis; retraction nystagmus on attempted upgaze, downgaze paralysis, vertical nystagmus, skew deviation and fixation disturbances. The most common causes of the Perinaud’s syndrome, by age, are as follows: infants, congenital hydrocephalus and aqueductal stenosis; 13 years, pinealoma; 30 years, subthalamic arteriovenous malformations; 40 years, posterior third ventricle tumors; 55 years or more, basilar artery disease. Eyelid retractions can occur due to loss of supranuclear control of levator inhibition in lesions of non-dominant cerebral hemisphere and coma, Retraction (or pseudoretraction) of an eyelid as a result of contralateral blepharoptosis is seen in patients with acquired ptosis associated with levator aponeurosis dehiscence or disinsertion.3,4 In facial nerve dysfunction, the lower lid sags on the affected side due to paralysis of orbicularis oculi which closes the eyelids and zygomaticus muscles, which elevate the cheeks as well as the corrugator supercilii and procerus muscles, which depress the eyebrow1. Lower eyelid retraction occurs because of the unopposed effects of gravity and lower eyelid retractor contraction. The etiology of facial nerve dysfunction can be: 1. Trauma along its course such as fracture of base of skull involving petrous part of temporal bone. 2. Cerebrovascular accidents involving anterior inferior cerebellar artery causing ischemic damage just proximal to the geniculate ganglion. 3. Bell’s palsy thought to be associated with an acute viral infection or reactivation of herpes simplex virus. 4. Acoustic neuromas in the cerebellopontine angle tumors. 5. Infectious, immune mediated causes such as Lyme disease, Chickenpox, Mumps, Polio, Guillain – Barre Syndrome, Leprosy, Diphtheria and Botulism. 6. Mobius Syndrome: A rare, congenital condition characterized by bilateral sixth and seventh cranial nerve palsies, motility disturbances, limb anomalies and orofacial defects. Myogenic Eyelid Retraction Myogenic eyelid retraction can be congenital or acquired. Congenitally can occur due to Vol. XV, No.1, January - March 2015 fibrosis resulting from an intrauterine infection or periorbital inflammation 5 or due to dense medial and lateral horns of the levator palpebrae superioris, aponeurosis at the level of Whitnall’s ligament and congenital extraocular muscle fibrosis6. Tha acquired causes may include protractor (ie. Orbicularis oculi) weakness as in various periocular myopathies including Myasthenia Gravis, Myotonic Dystrophy and Chronic Progressive External Ophthalmoplegia. Mechanical Eyelid Retraction Mechanical causes of eyelid retraction include prominence of the globe, such as may occur with severe myopia, buphthalmos, proptosis, retrobulbar hemorrhage, craniosynostosis. Cutaneous scarring from eyelid neoplasms, herpes zoster ophthalmicus, smallpox, atopic dermatitis, scleroderma or burns can cause eyelid retraction. Blowout fractures of the orbital floor may cause upper eyelid retraction on either a neurogenic or mechanical basis. Hypotropia of the globe can stimulate increased innervation to the superior rectus and levator palpebrae superioris7 muscles that elevate the upper lid mechanically.8 Eyelid retraction can result from inadequacy of the vertical dimension of upper and lower eyelid skin from accidental or iatrogenic trauma due to scarring or over excision of the eyelid skin and congenital abnormalities, such as type II blepharophimosis syndrome. Measurement of the vertical dimension of skin between the brow and the upper lid margin should demonstrate at least 20mm to allow complete downward excursion of the upper eyelid during closure. Eyelid retraction can occur due to overcorrection in ptosis surgery due to vertical shortening of levator muscle i.e.”middle lamella” which thus results in upper lid retraction and lagophthalmos. Symblepharon between the bulbar and palpebral conjunctiva may also limit downward excursion of the upper eyelid and cause eyelid retraction. 13 In thyroid – related orbitopathy, a variety of pathophysiologic mechanisms in varying combinations may lead to the retraction. These include inflammatory fibrosis of Muller’s muscle, abnormal sympathetic tone in Muller’s muscle, proptosis, contracture of the inferior rectus muscles with superior rectus hyperactivity, and over medication with thyroid replacement.9-11 In all patients with lagophthalmos, it is crucial to check corneal sensation to rule out a component of fifth nerve dysfunction. Fifth nerve dysfunction is most likely to occur in patients who have had intracranial trauma, surgery, or a neurovascular accident where multiple cranial nerve palsies may be present. Eyelid retraction due to neurogenic, myogenic, mechanical or spastic etiology leads to lagophthalmos due to poor coaptation of the eyelids during attempted closure thus leading to exposure keratopathy. Management of Eyelid Retraction Maintenance of a moist ocular surface is critical, regardless or etiology, initial symptomatic treatment is directed towards increasing ocular surface lubrication and decreasing evaporative drying. Lubricating eyedrops, ointment, moisture shields, tarsorrhaphy are beneficial during acute phase. Differences in tear production and protective Bell’s phenomenon are probably responsible for the variation in corneal breakdown observed in patients with similar degrees of lagophthalmos. Medical Treatment and Supportive Care for Corneal Exposure Nonpreserved artificial tears should be administered frequently (at least four times per day) in order to supplement the patient’s tear film. Ointments can be applied to the cornea once at bedtime or throughout the day in cases of severe corneal exposure. Moisture goggles also may be used. As the corneal surface normalizes, ointments may be replaced with 0.5 percent or 1 percent 14 methycellulose formations. When choosing a lubricant, the patient’s ability to accept visual blurring caused by the viscosity of the lubricant should be considered. Infectious corneal ulcers should be treated with appropriate antibiotic therapy. Also, the surgeon may elect to patch the eye closed or place a Frost suture for temporary protection of the cornea. Prefabricated moisture chambers are commercially available or thin polyethylene film can be taped over an exposed eye in acute cases. II. Tarsorrhaphy When recovery of the eyelid closure is expected which is a few weeks, a temporary tarsorrhaphy achieves narrowing of the interpalpebral fissure. In most cases, the cornea can be protected adequately by suturing the lateral one-third of the eyelids together. Ideally, a small opening remains so that the patient can retain useful vision, the health of the cornea may be assessed and lubrication or antibiotic therapy can be applied to the eye. When a protracted clinical course is evident, a permanent tarsorrhaphy may be performed by abrading the eyelid margins at the site of the sutures to create intermarginal adhesions. The sutures are removed in 10 to 14 days. If the patient regains useful function of the orbicularis oculi muscle, the adhesions can be lysed. A limitation of tarsorrhaphy is that, loosening of the sutures may occur, resulting in inadequate lid coverage of the cornea. Trichiasis and poor cosmetic appearance represent additional risks. III. Eyelid Surgery This is beneficial in improving appearance and ocular protection after acute phase of the disease process has resolved and amount of retraction has stabilized. Definitive treatment of lagophthalmos depends on accurate diagnosis of the underlying cause. A.Eyelid Retraction due to Abnormal Globe Protrusion Patients with proptosis are usually managed best by orbital decompression and repositioning of AECS Illumination the globes within the orbit. Patients who are not candidates for orbital decompression may undergo lid lengthening procedures in an attempt to reposition the lids anteriorly to the corneal apex during closure. Proptosis due to craniosynostosis syndromes requires craniofacial surgery and orbital expansion to reposition the globes posteriorly. Sometimes, traumatic expansion to reposition the globes posteriorly. On occasion, traumatic deformities may cause partial collapse of the orbital skeleton with protrusion of the globe who then require reconstruction of the underlying bony abnormality and reexpansion of the orbit. Patients with a retrobulbar mass or hemorrhage displacing the globe anteriorly require removal or drainage of the retrobulbar lesion to allow the globe to be deposited in the orbit. It is important to determine whether the problem is due to inadequate skin, as in patients following eyelid burns or after aggressive skin removal at blepharoplasty, or is due to increased tightness and shortening of the “middle lamella,” (eyelid retractors). The latter is usually seen following ptosis repair or traumatic scar contracture following full-thickness lid lacterations. Measurement of the upper eyelid skin and observing the lid position in both the primary and downgaze will help to differentiate between shortage of skin and tight middle lamella. If the lower lid is contributing to incomplete closure, inferior scleral show should be obvious. B. Eyelid Retraction due to Inadequate Vertical Skin Requires anterior lamellar replacement with skin flaps or grafts. Eyelid retraction due to a tight middle lamella that resists complete closure requires recession of the eyelid retractors. Lid lengthening procedures, either by releasing Muller's muscle or the levator aponeurosis, may increase the vertical excursion. Surgeons vary in their use of spacers or simple retractor recession in the upper eyelid. In the lower lid, recessing of the retractors is usually performed in combination with placement of a spacer to counteract the effect of gravity. Vol. XV, No.1, January - March 2015 C. Eyelid Retraction due to Lid Globe Adhesion by symblepharon must be treated by releasing the symblepharon and reconstructing the appropriate fornix by placing a fornix deepening suture with mucous membrane grafting. D. Upper Eyelid Retraction in TRO A number of surgical procedures have been described to correct eyelid retraction. 1. Levator Recession: Recession of the upper eyelid retractors (levator and muller’s muscles) is a useful procedure in patients with upper eyelid retraction from thyroid ophthalmopathy. 2. Tarsotomy : is useful in mild cases of retraction due to TRO or ptosis overcorrection. 3. Superior tarsal muscle (Muller’s) excision: Procedure was initially reported by Putterman and Urist who did isolation and excision of temporal part of all of Muller’s muscle, progressing to incision and weakening of the levator muscles if the muller’s muscle excision does not relieve retraction12,13. 4. Levator marginal myotomy of levator and muller’s muscle has been described by Grove in cases with severe upper eyelid retraction3,14. In this procedure retractors are separated from the conjunctiva and from anterior fibrotic adhession to the orbicularis muscle. Two marginal myotomies are made, one from each side of the muscle, which serves to lengthen the muscle. By quantitatively judging the upper eyelid position during the procedure, the dissection and lysis of adhesions can be continued until the upper eyelid is in the described overcorrected position. E. Lagophthalmos due to facial nerve dysfunction: This may occur due to lesions anywhere along the course of the seventh nerve from the central brain stem nucleus to the distal peripheral nerve. Dysfunction may be caused by local compression, traumatic disruption or viral or autoimmue inflammation (as in Bell’s palsy). It is important to determine whether facial nerve 15 dysfunction is anticipated to be permanent (eg. Following removal of the nerve as part of radical cancer resection) or temporary (as experienced by over 75% of patients with Bell’s palsy). Temporizing measures include lubrication and temporary tarsorrhaphy. If exposure is severe or anticipated to be long lasting, more permanent surgical corrections should be considered. The importance of testing corneal sensation in patients with seventh nerve dysfunction of intracranial origin cannot be overemphasized. The combination of a hypoesthetic cornea and incomplete lid closure is particularly threatening to the cornea, and these patients will often require extensive tarsorrhaphy. However, because tarsorrhaphy is cosmetically disfiguring and visually limiting, dynamic closure of the paralyzed upper eyelid should be considered. Various Options Available Include 1. Facial Reanimation Technique – Various techniques have been used to reanimate the facial musculature in seventh cranial nerve paralysis including primary facial nerve repair, cross – facial nerve grafting, hypoglossal facial nerve transfer, temporalis muscle transfer, and free innervative muscle transfer.15 All of these procedures are time-consuming and none will perfectly restore the blink reflex or voluntary closure. 2. Mechanical Aids – Various mechanical aids to eyelid closure have also been used including eyelid weights, palpebral springs, silastic bands, and permanent eyelid magnets. 16-17 All of these various eyelid loading procedures rely on a normally functioning levator muscle to voluntarily open the eyelid. With attempted closure, the levator is inhibited and the gravitational pull exerted on the lid load causes downward excursion and eyelid closure. Recently attention has centered chiefly on loading of the upper lid by subcutaneous placement of a gold weight.15-19 16 Gold Weight Implantation Gold weight can be implanted into the upper eyelid to treat paralytic lagophthalmos. This procedure enhances eyelid closure in a gravity dependent fashion. Gold has been considered an ideal substance because it is inert and tends to not show through the thin skin of the eyelid. In cases of allergy, platinum may be used. Gold weights range from 0.6 to 1.6g increments. Properly chosen, the ideal weight will allow full closing and opening of the lids, while avoiding ptosis in primary gaze. Gold weight implantation is usually well tolerated. The material consists of 99.9% pure 24 carat gold. It is sutured to the tarsus with 7-0 nylon sutures after exposure through an upper eyelid crease incision. It is important to avoid damage to the levator aponeurosis during dissection over the surface of the tarsus to avoid postoperative ptosis. Several series have reported that more than 90% had “success” with a gold weight implantation for paralytic lagophthalmos.15,19 Although some degree of lagophthalmos may often persist after gold weight implantation, it is usually diminished enough for topical lubrication to control the symptoms of exosure. Because of this high early success rate many surgeons now consider initial placement of a gold weight even in those patients who are felt likely to recover seventh nerve function over time. In such patients the gold weight can be easily removed through a small skin incision when it is no longer required. However, astigmatic shift as well as migration and/or extrusion of the gold weight may occur. Because gold weight implantation of the upper lid often results in diminished but persistent lagophthalmos, elevation of the paralytic lower lid is also important in these patients to further narrow the palpebral aperture and minimize tear film evaporation and exposure. Lower Eyelid Tightening and Elevation Laxity of the lower eyelid may occur in conditions such as facial nerve palsy due to paralytic ectropion. AECS Illumination Patients with paralytic ectropion were historically managed by horizontal tightening. A tightening procedure such as a lateral tarsal strip will improve apposition of the lower eyelid to the globe and decrease tearing. Although this procedure will relieve ectropion, it virtually always leaves some degree of residual lower lid retraction and scleral show due to the lack of orbicularis tone. Patients who continue to have exposure of the cornea despite medical therapy and upper eyelid restructuring may benefit from lower eyelid elevation. Patients with paralytic lower lid laxity and ectropion are best managed by placing a spacer interposed posteriorly between the tarsus and lid retractors to elevate and support the lid.21 Here, the lower eyelid retractor muscles may be recessed from their insertion on the inferior tarsal border. An additional spacer graft may be sutured to the tarsal plate to achieve further elevation. Banked sclera, autologous ear cartilage, nasal cartilage, polytetrafluoreothylene (Gore-tex) or hard palate mucosa grafts have been used. In cases with a cicatricial component, a full-thickness skin graft and/or collagen or mucosa membrane graft have been used. Horizontal tightening is also performed if there is significant laxity of the lid. Patient who have unacceptable residual lagophthalmos, despite upper lid loading and placement of a spacer in the lower lid, may benefit from a limited lateral tarsorrhaphy as well. Scleral Spacer Graft in Eyelid Retraction Indications Absolute: • Lagophthalmos in facial palsy • Lagophthalmos in Grave’s orbitopathy • Post enucleation socket syndrome • Exposure keratopathy Relative: • Congenital – idiopathic; maternal thyroid abnormality • Neurologic – midbrain lesions, hydrocephalus, Perinaud’s syndrome, aberrant oculomotor nerve regeneration Vol. XV, No.1, January - March 2015 • Sympathomimetic drugs • Contralateral ptosis • Post-surgical (ptosis repair, eyelid reconstruction, orbital floor fracture repair) • Post – traumatic • Following vertical strabismus surgery • Cosmesis Contraindications: • Chemical injury in acute cases • Cicatrising causes of ectropion such as Steven Johnson Syndrome, ocular cicatricial pemphigoid. Eyelid Scleral Grafts Since the most common problem with eyelid retraction surgery is recurrence of the retraction, the idea of placing a spacer between the recessed levator nuscle and superior tarsal border was conceived 21. Tarsus (either as free graft22,23 or as a rotation flap24, auricular cartilage,25 collagen film26 and Gelfilm27 have been used. Advantages • Readily available from eye banks • Good strength, can be easily cut to size • Gives predictable lid height • Has a curved contour • Is easy to structure • Does not contract significantly in the post – operative period. 17 Complications Operative: • • • • • Button holing Inadequate graft size Haemorrhage Button holing of tarsus Inadvertent injury to cornea Postoperative – Early • • • • Edema Ptosis Inadequate correction Chemosis of conjunctiva Late 1. Thickened eyelid 2. Loss of lashes 3. Dry eye 4. Extrusion of graft 5. Recurrence of retraction 6. Fibrosis of lacrimal gland in repeated procedures 7. Resorption 8. Shrinkage 9. Persistent retraction 10.Cysts28 11.Corneal Damage irritation, erosion28 12.Infection28 13.Graft Exposure28 References: 1. Bartley GB. The differential diagnosis and classification of eyelid retraction. Ophthalmology 1996 Jan; 103 (1):168-176. 2. Kleiman MD, Dimario FJ Jr, Leconche DA, etal: Benign transient downward gaze in preterm infants. Pediatr Neurol 1994 Jun; 10(4):313 -316. 3. Grove AS. Levator lengthening by marginal myotomy. Arch. Ophthalmol 1980 Aug; 98(8):1433-1438. 4. Morel-fatio d, lalardrie JP. Palliative surgical treatment of facial paralysis. Plast. Reconstr. Surg. 1964 May; 33: 446 -456. 5. Leone CR Jr. Lewis R. Congenital upper eyelid retraction. J Pediatr Ophthalmol 1976 Nov-Dec; 13(6): 350-2. 6. Gillies WE, Harris AJ, Brooks AM, et al. Congenital fibrosis of the vertically acting extraocular muscles. A new group of dominantly inherited ocular fibrosis with radiological findings. Ophthalmology 1995 Apr; 102(4):607-612. 18 AECS Illumination 7. Putterman AM, Urist MJ: Upper eyelid retraction after blowout fractures Arch Ophthalmol 1976 Jan; 94(1):112 -116. 8. Conway ST: Lid retraction following blow-out fracture of the orbit. Ophthalmic Surg. 1988 April; 19 (4): 279-281. 9. Buffam FV.Rootman J. Lid retraction: Its Diagnosis and Treatment. International Ophthalmology clinics. 1978 fall; 18: 75-86. 10.Henderson JW. A Surgical procedure for retraction of eyelids in endocrine exophthalmos ( a moving picture). Trans Am Ophthalmol Soc. 1+65; 63:70 -74. 11.Feldon SE, Levin L. Graves’ ophthalmopathy: V. Aetiology of upper eyelid retraction in Graves’ ophthalmopathy. Br J Ophthalmol. 1990 Aug; 74(8):484 – 485. 12.Chalfin, J., and Putterman, A.M. Miller’s muscle excision and levator recession in retracted upper lid. Arch. Ophthalmol. 1979; 97 : 1487 13.Putterman, A.M., and Urist, M. Surgical treatment of upper eyelid retraction. Arch Opthalmos 1972; 87:401 14.Grove AS. Eyelid retraction treated by levator marginal myotomy. Ophthalmology. 1980 Oct; 87 (10):1013-1018. 15.Townsend DJ. Eyelid reanimation for the treatment of paralytic lagophthalmos: historical perspectives and current applications of the gold weight implant. Ophthal plast reconstr Surg. 1992; 8(3): 196-201. 16.May M. Gold weight and wire spring implants as alternatives to tarsorrhaphy. Arch. Otolaryngol. Head Neck Surg. 1987 Jun; 113(6):656-660. 17.Arion HG. Dynamic closure of the lids in paralysis of the orbicularis muscle. Int Surg. 1972 Jan; 57 (1):48-50. 18.Pcikford MA, Scamp T, Harrison DH. Morbidity after gold weight insertion into the upper eyelid in facial palsy. Br J Plast Surg. 1992 Sep; 45 (6) : 460 – 464. 19.Kelley SA, Sharpe DT. Gold eyelid weights in patients with facial palsy : a patient review. Plast. Reconstr. Surg. 1992 Mar; 89 (3); 436 – 440. 20.Kersten RC, Kulwin DR, Levartovsky S, Tiradellis H, Tse DT. Management of lower-lid retraction with hard-palate mucosa grafting. Arch. Ophthalmol. 1990 Sep; 108 (9) : 1339 -1343. 21.Dryden RM, Soll DB. The use of scleral transplantation in cicatricial entropion and eyelid retraction. Trans Sect Ophthalmol Am Acad Ophthalmol Otolaryngol. 1977 Aug; 83 (4 Pt 1) : 669 -678. 22.Harvey JT, Anderson RL. The aponeurotic approach to eyelid retraction. Ophthalmology. 1981 Jun; 88 (6): 513 – 524. 23.Brown, Bernice Z. The use of homologous tarsus as a donor graft in lid surgery. Ophthalmic Reconstr. Surg. 1985; 1 : 91 – 96. 24.Kohn R. Treatment of eyelid retraction with two pedicle tarsal rotation flaps. Am.J.Ophthalmol. 1983 Apr; 95 (4) : 539 – 544. 25.Baylis, H.I., Perman, K.I., Fett, D.R., and sutcliffe, R.T. Autogenous auricular cartilage grafting for lower eyelid reconstruction. Ophthalmic. Plast. Reconstr. Surg. 1988; 1:23. 26.Callahan A. Levator recession with reattachment to the tarsus with collagen film. Arch. Ophthal. 1965 Jun; 73 : 800 – 802. 27.Beard C. Ptosis 3rd ed. St. Louis: Mosby 1981. Pg. 237. 28.Mourits MP, Koornneef L.Lid lengthening by sclera interposition for eyelid retraction in Graves’ ophthalmopathy. Br. J. Ophthalmol. 1991 Jun; 76 (6) : 344 – 347.