Eyelid abnormalities may indicate underlying systemic problems
The diagnosis can take place in the optometrist’s office.
by Leonid Skorin Jr., OD, DO, FAAO, FAOCO
This course is jointly sponsored by PCON, The State University of New York State College of Optometry and Vindico Medical Education. It is COPE-approved for 2 continuing education credits.
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Although the public knows us by the generic term of “eye doctor,” we certainly evaluate and treat more than just eyes. A critical part of the human anatomy that optometrists need to be intimately knowledgeable of is the eyelids and periocular adnexa. Not only do these structures maintain the health and proper functioning of the eyeballs, but diseases of these structures may sometimes point us to other underlying systemic manifestations.
Eyelid anatomy: anterior, posterior lamella
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The eyelid can be grossly divided into two broad structures: anterior and posterior lamella. According to Wobig and Dailey (pages 15 to 29), these, in turn, are further sub-divided into five structural planes: the skin and subcutaneous fascia, the eyelid protractors (orbicularis oculi, corrugator supercilii, procerus), the orbital septum and fat, the retractors of the eyelids (levator muscle with its aponeurosis, Müller’s muscle, capsulopalpebral fascia, inferior tarsal muscle) and the tarsi and conjunctiva.
At the eyelid margin is a strip of orbicularis muscle, the muscle of Riolan, and it is directly associated with the eyelashes. Cahill and Doxanas say this is responsible for the darker coloration of the slightly depressed midsection of the lid margin commonly referred to as the gray line. According to Lambreghts and Melore, the gray line delineates the lid into anterior and posterior lamella.
The eyelids have several functions: they protect the globe and the cornea, they maintain the physiologic integrity and clarity of the ocular surface, they produce and spread tears and help with tear elimination, according to Kronish.
Ectropion: the lid falls away from the globe
Ectropion is a malposition of the eyelid in which the lid falls away or is pulled away from its normal apposition to the globe, say Tse and Neff. According to Eliasoph, this can be of varying degree and may involve only a portion of the eyelid margin. Ectropion, according to Tse and Neff, can be unilateral or bilateral and may affect either the upper or lower eyelids, although the lower eyelid is more commonly affected.
Chronic exposure of the globe and palpebral conjunctiva results in dryness with reflex lacrimation. According to Gladstone (pages 616 to 618), keratinization of the exposed palpebral conjunctiva can occur from chronic inflammation and desiccation. With medial ectropion and secondary punctal stenosis there is epiphora and maceration of the delicate skin from the natural salts found in human tears, says Remington. Tse and Neff report that persistent corneal exposure contributes to epithelial breakdown and increases the risk of infectious keratitis.
Ectropion can be classified as congenital, involutional (senile), cicatricial, inflammatory, mechanical or paralytic, says Gladstone. Involutional ectropion is the most common type encountered. A progressive laxity of the lateral and medial canthal tendons occurs. This laxity, says Laur, is a result of aging as gravity, rubbing and pulling of the eyelids leads to loss of elasticity.
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Cicatricial ectropion is caused by scarring or contracture of the skin and underlying tissues, such as shortening of the anterior lamella, which then pulls the eyelid away from the globe, reported Cahill and Doxanas. Actinic damage, thermal burns, chemical burns, trauma, laser resurfacing, chemical peel or surgery can all be causes of this type of ectropion, according to Tse and Neff.
Mechanical ectropion is due to lid edema, bulky lid tumors, orbital fat herniation or even lid-riding poorly fitted eyeglasses, while paralytic ectropion results from paralysis of the facial nerve, reported Friedman and colleagues. Inflammatory ectropion is secondary to chronic inflammation from dermatologic conditions such as acne rosacea, atopic dermatitis, eczema or herpes zoster infections or may even be drug induced, according to Friedman and colleagues and Hegde and colleagues.
Quantify laxity before treatment
The amount of horizontal lid laxity must be quantified before treatment can be initiated. Physical testing for horizontal laxity involves performing the snap-back test.
In the snap-back test, the patient is asked to look up slightly while the examiner pulls the lower eyelid inferiorly. The eyelid should return to its normal anatomical position within 1 or 2 seconds prior to a blink, according to Nesi and colleagues. In the setting of pathologic laxity, the eyelid will remain below its proper position without globe apposition, said Kronish.
According to Tyers and Collin, the snap-back test can be graded as normal (lid snaps back quickly); mild laxity (slow return); moderate laxity (incomplete return unless patient blinks); and severe laxity (incomplete return even after blink).
Nesi and colleagues outline the dislocation or distraction test as performed by grasping the lower eyelid and pulling it anteriorly away from the globe and measuring the distance the lower eyelid margin separates from the globe. Normally, the eyelid can be manually withdrawn only 2 mm or 3 mm from the globe; however, in cases of poor tendon strength, the gap between the eyelid and the globe may extend 10 mm or more, said Kronish. According to Shorr and Perry, if the lower eyelid can be pulled more than 7 mm from the globe, the distraction test is considered positive.
Medial canthal laxity can be demonstrated clinically by pulling the lower lid laterally and observing the position of the inferior punctum. If the lid is normal, the punctum should not be displaced more than 1 or 2 mm. Laxity is graded as mild if it can be displaced to the limbus and severe if the punctum reaches the pupil, according to Kanski. Lateral canthal laxity will display a rounded appearance of the lateral canthus, and the lid can be displaced medially more than 2 mm.
Any cicatricial changes need to be noted during the eyelid evaluation because a surgical repair using an autologous graft will be needed. The amount of scarring is assessed by pulling on the lid horizontally and observing whether the lid margin becomes apposed against the globe. If the lid does not appose freely against the globe, a cicatricial component is present, says Laur.
Temporary, long-term management
Temporary management of ectropion includes liberal topical lubrication with nonpreserved artificial tears during the day and bland ointment at bedtime. The lateral aspect of the lower eyelid can also be taped upwards, helping decrease the overall aperture. Taping the eyelids closed can also help any lagophthalmos when the patient is asleep.
Definitive treatment of ectropion is surgery. Any lateral canthal laxity and horizontal lid laxity can be repaired by performing a horizontal strengthening utilizing a tarsal strip. A full thickness wedge of lateral eyelid is excised and a fashioned tarsal strip is reattached with suture to the orbital periosteum.
Medial canthal laxity repair consists of a medial spindle procedure where a horizontal fusiform excision of conjunctiva and tarsal plate just inferior to the puncta is made with subsequent suture repair. Cicatricial ectropion involves a three-step procedure: release and relaxation of the scarred tissues, horizontal lid strengthening and anterior lamella lengthening with full thickness skin graft (Tse and Neff, Gladstone, Friedman and colleagues).
Entropion: the lid turns inward
Entropion is a condition in which the eyelid margin turns inward against the globe, according to Kronish. This inversion of the eyelid margin may involve either eyelid, although, according to Friedman and colleagues, the lower eyelid is more frequently affected.
Entropion can be classified as congenital, spastic, involutional (senile) or cicatricial. According to Kronish, five pathophysiologic mechanisms have been proposed that may contribute to the internal rotation of the eyelid margin. In almost all cases, say Kronish and Nesi and colleagues, stretching or loosening of the medial and lateral canthal tendons leads to horizontal laxity of the eyelids. This is aggravated by atrophy of the orbital fat and any enophthalmos, says Collin.
Disinsertion or weakening of the lower eyelid retractors (capsulopalpebral fascia) allows the tarsus to rotate inward on its horizontal axis, according to Myint. Clinically, the disinsertion of the lower eyelid retractors can be seen as a white line below the inferior tarsal border indicating the leading edge of the detached capsulopalpebral fascia, say Nesi and colleagues.
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According to Karesh, another aggravating mechanism is the overriding or migration of a hypertrophic and overactive preseptal orbicularis muscle over the pretarsal orbicularis muscle. Finally, eyelid instability is further exacerbated by the thinning, shortening and degeneration of the tarsal plate, says Kronish.
Both the snap-back test and the dislocation or distraction test used to evaluate ectropion are also used in the analysis of entropion. Additional testing for entropion includes the orbicularis override test, says Myint. In this test, the patient is asked to squeeze the eyes closed. The test is positive if there is superior migration of the preseptal orbicularis. Laxity or disinsertion of the lower lid retractors is present if there is a loss of the normal 4- to 5-mm lower lid excursion when the patient is asked to look down, says Kronish.
Other clinical features of dehiscence or disinsertion of the lower lid retractors include an absent eyelid crease, a rolled appearance of the eyelid and a deep lower conjunctival fornix, according to Kronish and Tyers and Collin. Friedman and colleagues say that digital eversion at the inferior tarsus can help distinguish involutional from cicatricial entropion (involutional rotates out, cicatricial does not).
Persistent entropion will compromise corneal integrity and can cause permanent vision loss. To give the patient immediate relief and to protect the cornea, the lower eyelid may be taped away from the globe or a bandage soft contact lens can be placed on the eye, say Kronish and Myint. Topical lubricating ointments or epilation of eyelashes that are rubbing against the globe can also give temporary but immediate relief.
According to Kronish, botulinum toxin can be injected into the orbicularis muscle and works by weakening the protractors of the eyelid. Surgery is the best way to achieve a long-lasting correction.
A combination of the horizontal eyelid strengthening utilizing a tarsal strip with the reattachment of the lower eyelid retractors with suture to the base of the tarsal plate can give a more permanent correction, report Kronish, Gladstone and Karesh.
Trichiasis, distichiasis: abnormalities of the eyelashes
Lambreghts and Melore describe the presence of one or more in-turning eyelashes of the upper or lower eyelid as trichiasis. The lashes are misdirected toward the globe after emerging from follicles at bizarre angles or from other areas of the eyelids normally free of eyelash growth, reports Karesh.
In trichiasis, the eyelid margin is normally positioned, whereas in entropion, the eyelids are inverted, causing the lashes to rub against the eye, say Nerad and Chang. In most cases, trichiasis is the result of aging changes of the lid; however, it may also be caused by an inflammatory process or trauma that causes scarring and fibrosis around the eyelash follicles at the lid margin, say Lambreghts and Melore.
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Distichiasis can be an acquired or, rarely, a congenital condition in which an accessory row of lashes is located just posterior to the normal eyelashes and arising from the meibomian gland orifices, describe Lambreghts and Melore and Nerad and Chang.
Acquired distichiasis occurs when normal, non-hair producing meibomian glands of the tarsal plate are transformed into pilosebaceous follicles by mechanical or chemical stimuli, says Gladstone (pages 613 to 615). These stimuli include chronic inflammation such as blepharoconjunctivitis and meibomianitis or cicatricial conditions of the mucosa such as Stevens-Johnson syndrome or ocular pemphigoid.
Treatment of trichiasis and distichiasis depends on the extent and distribution of the aberrant lashes. Epilation of abnormal lashes is a simple but temporary solution to the problem. Almost always the lashes will regrow within 3 to 6 weeks. Early in their growth, the lashes will be short and stubby. These lashes will often cause more irritation than longer more flexible ones, according to Lambreghts and Melore, Nerad and Chang, and Gladstone (pages 613 to 615).
More permanent therapy for areas of limited distribution of misdirected lashes includes electrolysis, laser photoablation or cryotherapy. A pentagonal wedge resection of the lid margin can be used to remove a localized segment of lashes while, for most cases of distichiasis, the portion of the tarsus that contains the abnormal lash follicles is excised using a posterior surgical approach, according to Nerad and Chang and Gladstone (pages 613 to 615).
Floppy eyelid syndrome: a triad of symptoms
Floppy eyelid syndrome (FES) consists of the triad of obesity, easily everted “floppy” upper eyelids and an associated chronic papillary conjunctivitis, according to Lambreghts and Melore. In the majority of cases, the patients are obese males that may suffer from obstructive sleep apnea that results in hypoxia from snoring and obstruction of the upper airway when they sleep on their back, reports Siddens. Because of this, these patients will often sleep on their side with their face pressing into a pillow, everting an already lax upper eyelid and causing mechanical inflammation and irritation to the conjunctival surface.
The upper eyelid is the primary lid involved and is rubbery, floppy and easily everted when the lid is mechanically elevated, say Lambreghts and Melore. According to Siddens, eyelash ptosis, when the eyelashes point downward and curl toward the cornea, is a classic finding in this condition. The most common slit-lamp finding in FES patients is punctate epithelial keratopathy, with keratoconus being the second most common finding.
A variant of FES, lax eyelid syndrome (LES), is thought to be much more prevalent, say Lambreghts and Melore. It is described as having similar characteristics as FES, such as lid hyperlaxity and ocular irritation, but it does not include the other findings of obesity, easily inverted tarsus and papillary conjunctivitis. LES can be associated with obstructive sleep apnea.
Conservative treatment of FES has included using a bland topical ointment for lubrication and wearing a plastic or metal eye shield at night. According to Siddens, treatment of any accompanying obstructive sleep apnea is imperative to reduce the sleep abnormalities and resultant ocular findings. This treatment includes using nighttime continuous positive airway pressure (CPAP), weight reduction and changing sleep habits.
Surgery of the involved eyelid in chronic nonresponding cases involves the eyelid horizontal tightening techniques such as a full thickness pentagonal wedge resection or a lateral canthal strengthening procedure.
Dermatochalasis: a normal part of aging
Dermatochalasis is redundant or loose skin of the lower or, more commonly, upper eyelids and is considered part of the normal aging process. It is bilateral but often asymmetric and may be cosmetic or cause functional visual impairment. Weakened connective tissue, gravity, decreased skin elasticity and systemic conditions such as thyroid disease can all play a part in this excess skin.
Dermatochalasis must be differentiated from the less common blepharochalasis, which is the expansion of the orbital septum and preseptal orbicularis muscle secondary to repeated angioneurotic edema and is seen more commonly in younger patients. According to Putterman, this recurrence causes loose skin and orbital fat herniation. Involvement of the lower eyelids in blepharochalasis can be quite dramatic, and this protruding tissue is known as malar bags or festoons.
Wobig and Dailey (pages 34 to 53) report that dermatochalasis and blepharochalasis are both corrected by blepharoplasty. Visual field assessment should be performed before the surgery to demonstrate any visual field loss, typically superior or superotemporal periphery, caused by hooding from the redundant eyelid tissue, says Putterman. The visual field test should also be repeated with the lids taped to simulate postoperative results to verify that blepharoplasty will improve any field loss. In addition, the patient should have a dry eye evaluation and preoperative photography to document any preexisting conditions.
Eyelid ptosis: congenital and acquired
Ptosis of the upper eyelid is a condition in which the upper eyelid margin is in an abnormal inferiorly displaced position and results in obstruction of the cornea and pupillary aperture so as to impair vision and the visual field, reports Dresner.
Ptosis may be classified into two categories: congenital and acquired. According to Siddens and Skorin, acquired ptosis may be further subdivided into aponeurotic, neurogenic, myogenic, mechanical, pseudoptosis, traumatic or miscellaneous.
Congenital ptosis results from a dystrophic levator muscle that is fibrotic and deficient in striated muscle fibers, say Simons and Tse. It is most commonly unilateral and may be associated with strabismus, amblyopia or anisometropic refractive error. Other related anomalies include ipsilateral superior rectus palsy, double elevator palsy, jaw-wink phenomenon or blepharophimosis (ptosis, epicanthus inversus and telecanthus).
Aponeurotic ptosis is also known as involutional ptosis and is seen with aging. It is caused by a gradual loss of tone of both the levator aponeurosis muscle and Müller’s muscle. This weakness may be a localized dehiscence or disinsertion or a more generalized attenuation or stretching. Patients have a compensatory elevation of the brow, a high or absent upper lid crease and a lateral shift of the tarsal plate, according to Howard.
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Neurogenic ptosis may be caused by a variety of neurologic disorders, including multiple sclerosis, Guillain-Barré, third-nerve palsy, Horner’s syndrome and ophthalmoplegic migraine, report Siddens and Skorin.
Myogenic ptosis may overlap with neurogenic causes but may result from myasthenia gravis, chronic progressive external ophthlamoplegia and myotonic dystrophy.
Mechanical ptosis can occur when tumors or edema force the lid to droop. Often the mobility of the eyelid is impaired. Trauma may indirectly (blunt trauma) or directly (penetrating trauma) cause the levator to disinsert from the tarsal plate.
In blunt trauma injuries, the traumatic ptosis usually resolves as the accompanying edema subsides. Occasionally, traumatic ptosis can last for months before lid function returns.
Pseudoptosis mimics true ptosis. It is an apparent ptosis caused by insufficient posterior support of the eyelid, as seen in phthisis bulbi, microphthalmos, anophthalmos and enucleation; hysterical ptosis, excessive skin on the brow and dermatochalasis, contralateral lid retraction such as occurs in thyroid disease, apraxia of lid opening and blepharospasm and ipsilateral hypotropia.
A few causes of ptosis do not fit any one category and therefore can be called miscellaneous. They include ptosis during pregnancy and ptosis from contact lens or ocular prosthesis wear.
Diagnosing ptosis
Ptosis of the upper eyelid is determined by measuring the palpebral fissure width and margin-reflex distance. Palpebral fissure width is the vertical distance from the central lid to the central upper lid margins and is measured with the patient’s eyes in primary gaze. The patient’s brow and forehead muscles must be relaxed. The normal fissure height can range from 7 mm to 12 mm, with the average being 10 mm, according to Putterman.
In unilateral ptosis, the difference in the palpebral fissure is considered to be amount of ptosis while in bilateral cases, the measurement is subtracted from the average palpebral fissure width of 10 mm, says Gladstone.
The margin-reflex distance (MRD) is a more sensitive measurement of ptosis than the vertical palpebral fissure width. The MRD is the distance between the corneal light reflex in the center of the pupil and the margin of the eyelid as the patient looks straight ahead, according to Putterman and Howard.
The MRD1 denotes the distance from the light reflex to the upper eyelid margin and is normally 4 mm to 5 mm. MRD1 measurements of 4 mm OD and 1 mm OS indicate that the left eye has 3 mm of upper eyelid ptosis. If there is no corneal light reflex, the number of millimeters the eyelid must be raised is then recorded as the MRD in negative numbers, Wobig and Dailey (pages 30 to 33) explain.
The MRD2 denotes the distance from the pupillary light reflex to the lower eyelid margin. This measurement is helpful in identifying lower eyelid retraction or elevation. Siddens and Skorin report that MRD2 averages 4 mm to 5.5 mm. According to Dresner, the MRD1 plus the MRD2 should equal the palpebral fissure measurement.
Measuring function in ptosis
According to Wobig and Dailey (pages 30 to 33), levator function is measured by the direct method of measuring the distance of upper eyelid excursion from extreme downgaze to upgaze. This is the single most important measurement in deciding which surgical procedure should be used to correct the ptosis, says Howard.
To perform this measurement, the examiner presses his or her thumb firmly against the patient’s brow to immobilize the frontalis muscle from contributing to any eyelid elevation. The patient is instructed to look down at the floor. When the patient’s eyes are in downgaze, the upper lid margin is lined up against a millimeter ruler and mentally marked. The patient is then told to look upward at the ceiling and the level is again marked. According to Howard and Wobig and Dailey (pages 30 to 33), the difference between the downgaze and the upgaze measurements represents the levator function. The excursion is graded as normal (15 mm or more), good (12 mm or more), fair (5 mm to 11 mm) and poor (4 mm or less), says Kanski.
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Another measurement includes the assessment of the upper lid crease. The upper eyelid crease is found by lifting the eyebrow and asking the patient to look downward first, then slightly upward and then downward again. The distance from the central upper lid margin to the central crease as the patient looks down determines the margin crease distance measurement, says Putterman. In females, it measures about 10 mm and in males, 8 mm, according to Kanski. Absence of the crease may indicate congenital ptosis, while a high crease suggests and aponeurotic-involutional defect.
Müller’s muscle performance is evaluated by instilling one or two drops of 2.5% phenylephrine into the eye with the ptotic eyelid. The eyelid level is then examined after 15 minutes. A 1.5 mm or greater elevation of the ptotic eyelid is considered a positive test, according to Howard.
Repair of eyelid ptosis may be performed alone or may be combined with other eyelid procedures such as blepharoplasty for dermatochalasis. The basic premise of repair is to reattach the disinserted levator aponeurosis to the tarsal plate, Siddens and Skorin reported. According to Dresner, ptosis caused by levator aponeurotic dehiscence is easily repaired and yields a stable eyelid position with a low rate of recurrence.
For more information:
Leonid Skorin Jr., OD, DO, FAAO, FAOCO, practices in Albert Lea, Minn., and writes and lectures on ocular disease and neuro-ophthalmic disorders. He underwent fellowship training in neuro-ophthalmology. Dr. Skorin performs all of the surgical procedures described in this article. He may be contacted at the Albert Lea Medical Center, Mayo Health System, 404 West Fountain St., Albert Lea, MN 56007; (507) 373-8214; fax: (507) 373-2819; e-mail: skorin.leonid@mayo.edu.
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