Download Management of Eyelid Retraction

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.