In a study of nearly 25,000 individuals over 60 years old, involutional entropion was found in 2.1% of patients. Prevalence increased with age: 0.9% for patient 60-69 years old, 2.1% for 70-79, and 7.6% for those over 80. Bilateral disease is three times more common than unilateral. Entropion is more common in women, with prevalence 2.4%, than men, prevalence 1.9%. Involutional entropion has a prevalence of 2.4% in whites and 0.8% in blacks.
Patients with involutional entropion are often elderly and have significant comorbidities. The 4-year mortality for patients with involutional entropion is 30%.
Involutional entropion is due to a combination of causative factors: loss of horizontal lid support with canthal tendon laxity; disinsertion, atrophy or dehiscence of lower lid retractors; preseptal orbicularis oculi override of the pretarsal orbicularis oculi; loss of vertical lid support with tarsal atrophy; and orbital fat atrophy leading to enophthalmos that allows inversion of the lid margin.
An understanding of the relevant anatomy is required to explain and treat this mechanical condition. The lower lid derives stability from the orbicularis oculi, lower lid retractors, tarsus and canthal tendons. The canthal ligaments and tarsal plate contribute horizontal lid stability. Loosening of horizontal tension across these structures, especially the lateral canthal tendon, allows the lid margin to rotate. The lower lid retractors provide vertical stability and are analogous structures to the levator aponeurosis and Mueller's muscle in the upper lid. The capsulopapebral head of the retractors surrounds the inferior oblique and forms part of the Lockwood ligament before fusing with the septum at the inferior border of the tarsal plate. Patients with involutional entropion have on average 1.4mm increased distance between the lower lid retractors and the inferior border of the tarsal plate. The posterior layer of the lower lid retractors provides the most traction on the lid. Loosening of these vertical stabilizing structures allows the lid to rotate inward.
The lower lid retractors have fine extensions to the orbicularis oculi and overlying skin. As these connections weaken or dehisce, the preseptal orbicularis can travel superior and override the pretarsal muscle. This rotates the eyelid margin against the globe. Cadaveric research showed that all elderly patients had clear override of the preseptal orbicularis oculi over the pretarsal orbicularis oculi in the lower lid, with the override extending superiorly all the way to the lid margin. However, 10 of 11 upper eyelids showed no orbicularis override, and the single case of override was mild.
Histologic examination of tarsal plates in patients with involutional entropion shows collagen degeneration, disorganized collagen fibers and abnormal elastogenesis. Collagen fibers provide tensile strength to the tarsus, and elastic fibers give the tarsus resiliency. With aging, the population of the tarsus shifts from mainly collagenous fibers to elastic fibers, and the total number of collagen and fibers decreases. This shift in fiber population is associated with increased horizontal eyelid laxity, and tarsal atrophy has been asociated with entropion. Smaller tarsal plates allow for more horizontal lid laxity and orbicularis override. Females have smaller tarsal plates than males, which explains in part why entropion is more prevalent in females.
Orbital fat content and overall volume decreases with age or after trauma, producing enophthalmos. Greater spacing between the globe and eyelid creates lid laxity. In patients with documented lower lid laxity, shorter axial lengths and lower Hertel measurements are associated with entropion, but no difference exists between entropion patients and normal controls. Enophthalmos also allows for greater orbicularis override, which can drive entropion. Asians and females are more enophthalmic contributing to higher rates of entropion observed in these populations.
Elderly and Asian patients have increased anterior protrusion of orbital fat, which creates a force vector acting on the lower lid that predisposes for entropion.
Patients with entropion tend to present with complaints of foreign body sensation, redness, tearing and discharge. Symptoms may be intermittent depending on etiology of the entropion. Dry eye syndrome is present in 72.1% patients with involutional entropion, and punctate epithelial erosions are noted in 61.9%.
A patient suspected to have entropion should undergo a thorough ophthalmologic exam. On gross exam, one should note any facial spasm and signs of skin irritation or infection. The physician should pay close attention to the lid margin structures to evaluate for trichiasis, distichiasis and epiblepahron. These conditions can mimic entropion but do not have improper position of the eyelid margin and have different management.
Horizontal lid laxity can be evaluated with the snap back test. The examiner pulls the lower lid down and observes the lid returning to its original position without allowing the patient to blink. Normally, the lid returns promptly without a blink, but in cases of increased laxity a blink may be needed to reestablish proper position. The examiner can also pull the lower lid anteriorly away from the globe. In involutional entropion, the lower lid can be displaced 6-15mm from the globe, compared to only 2-3mm in a normal lid.
Resistance to traction and persistence of entropion with horizontal lid traction can indicate cicatricial component. Eyelid eversion tends to be difficult in cicatricial patients, but is usually easy to achieve in involutional cases.
Lower lid retractor function is evaluated by measuring lower lid excursion in downgaze. Normally, lower lid retractors supply 3-4mm inferior movement of the lower lid margin then the patient moves from primary position to downgaze. If this is absent or decreased, it may be a sign of lower lid retractor weakness, dehiscence or disinsertion. In some cases of lower lid retractor disinsertion, slit lamp examination of the inferior fornix reveals a white line 3-4 mm inferior to the inferior tarsal border representing the disinserted retractor band. Increased distance between the lower lid retractors and inferior tarsal plate is often present in entropion.
Spastic entropion can be elicited by forcefully closing the eyelids, causing override of the pretarsal orbicularis oculi by the preseptal orbicularis. Faria-e-Sousa described a method to induce override. After application of topical anesthetic, the patient is instructed to look down. The central lower eyelid is pinched, and skin is rolled over the superior tarsal border and pressed against the globe. The eyelid skin is then spread against the globe and released. The patient remains in downgaze for the entire test. If the entropion persists with eye movements and blinking for at least 3 minutes, a diagnosis of spastic or intermittent entropion can be made.
problem is the direction of lash growth and not a margin malposition.
Another diagnosis that can be confused with entropion is distichiasis. Distichiasis is the growth of lashes from the meibomian gland orifices, which can irritate and damage the cornea.
Epiblepharon is a horizontal fold of redundant skin and orbicularis at the eyelid margin causing the lashes to be directed vertically or invert to a small degree. This condition is common in Asian populations and is present in 46-52.5% of Asian children less than a year old.(Kim) This condition usually asymptomatic and resolves with age, but in extreme and persistent cases surgical management may be indicated if corneal injury is imminent.
There are four main categories of entropion, each with a different pathophysiology: involutional, spastic, cicatricial and congenital. Treatments are aimed specifically at the particular causes for the condition.
retractor weakness, and orbicularis oculi override. Addressing more contributing factors has a greater chance at achieving resolution.
Management strategies range from conservative, noninvasive measures to more complex surgeries requiring tissue grafts. The approach depends on disease severity, patient comorbidities and goals of care. Numerous repair techniques are described in the literature, each with a slightly different approach to the mechanical issues underlying involutional entropion and various combinations of the strategies discussed below.
Patients can achieve temporary relief with taping of the lower lid to the malar eminence or with application of a cyanoacrylate liquid bandage to evert the lid margin. These treatments are beneficial as temporizing measures until the patient can have surgery for definitive repair, or if the patient is too ill to be a candidate for surgical intervention. Temporary relief from involutional entropion can also be achieved with botulinum toxin injections to the orbicularis, weakening the orbicularis to combat override.
Carbon dioxide laser skin resurfacing has been proposed as a conservative means of managing involutional entropion. This method was described with success in four of five patients followed for 21 months.
Full-thickness eyelid sutures (Quickert sutures) can be placed at the bedside or in the office as a quick procedure to offer patients immediate relief from entropion symptoms. The procedure takes an average of 15 minutes to complete and requires only local anesthesia. A double-armed 4-0 chromic suture is placed from the deep inferior fornix below the inferior tarsal border, through the lower lid retractors, and exits through the skin superior to the level of insertion. Exiting more superiorly causes more lid eversion. This procedure indirectly tightens the lower lid retractors and forms scarring between the retractors, orbicularis and skin to prevent override. Recurrence is common, with Jand et al observing over 21% recurrence at 6 months and nearly 50% by two years. Tsang et al encountered better results with 33% recurrence at 14-40 months.
Horizontal lid laxity can be addressed surgically with a tarsal strip. A lateral canthotomy and inferior cantholysis is performed to release the lower lid. The mucocutaneous junction is removed from the lid margin, and the anterior lamella is excised off the tarsus. Conjunctiva is debrided from the posterior tarsus. A horizontal incision through the superior tarsal plate creates a strip that is trimmed to achieve the desired amount of tightening. The strip is attached to the internal aspect of the lateral orbital rim.
A small case series of 15 patients treated with tarsal strip only showed no recurrence of entropion at an average of 13 months follow-up. A series of 42 eyelids with involutional entropion without canthal tendon laxity used full-thickness excision and repair to treat entropion. This study reported 8% recurrence at 14 months, with average time to failure of 13 months. As an independent measure, addressing the horizontal dimension of the lower lid is more successful in correcting entropion than targeting lid rotation.
There is only one randomized control trial comparing entropion repair techniques, examining everting sutures against everting sutures with tarsal strip. This study found 21% recurrence of entropion by 18 months for patient’s with only everting sutures and no recurrences in the combined group.
Lower lid retractor disinsertion can be reversed surgically with posterior advancement of the retractors. After lateral canthotomy and inferior cantholysis, an incision is made through the conjunctiva and lower lid retractors spanning from the lateral canthus to just lateral to the inferior punctum, taking advantage of the bloodless plane just below the inferior tarsal border. The conjunctiva and retractors are then separated from the anterior lamella to expose the orbital septum overlying orbital fat. A strip of orbicularis is excised or ablated inferior to the tarsus, reducing the effect of preseptal orbicularis override. The lower lid retractors are immediately posterior to the fat compartments and adherent to the conjunctiva. The patient can look up and down to assist in locating the retractors. The retractors are separated from the conjunctiva with cautery, and sharp dissection allows for exposure of the anterior surface of the inferior tarsal plate.
Using 6-0 vicryl, the retractors are reattached to the anterior inferior tarsus to evert the lid margin. Tarsal strip can be combined with this procedure after the retractors are attached, as adequate exposure is already obtained. Combining tarsal strip with retractor advancement takes an average of 13 minutes more than retractor advancement alone, and gives a 96.7% success rate. The dual procedure is more effective in treating involutional entropion with horizontal lid laxity than retractor advancement alone. External approach can be used if there is absent lid laxity, significant festoons or prominent lower lid dermatochalasis.
Everting sutures can also be placed along with tarsal strip and retractor reinsertion with recurrence rate of 2.2% at 22.6 months, much less than the rate of 29% for everting sutures alone.
Spastic entropion is thought by some to be a subset of involutional entropion. Muscle spasm of the orbicularis can induced by local irritation or infection can unmask asymptomatic involutional changes that make the eyelid more susceptible to override, resulting in temporary entropion.
First line treatment is to relieve the instigating condition by treating any infection or local reaction present on the eyelid. Hubbard and Kanski in 1973 described injecting 80% alcohol into the orbicularis oculi to quell spasm with high rates of success. Presently, botulinum toxin injection to the orbicularis and full thickness eyelid sutures have been used to treat this entity.
Cicatricial entropion results from chronic inflammation leading to fibrosis, scarring and shortening of the posterior lamella. These cases are associated with other stigmata of chronic inflammation such as symblepharon, forniceal shortening, keratinization, and loss of normal margin structures. This is unique from other causes of entropion because it is usually secondary to a systemic and progressive inflammatory condition such as ocular cicatricial pemphigoid, Stevens-Johnson syndrome, trachoma, and herpetic disease.
Cicatricial entropion may also be the result of trauma and can be iatrogenic from surgery or radiation therapy. Cicatricial entropion has also been noted to develop after treatment with glaucoma medications, especially miotic agents, and some chemotherapy drugs.
Treatment of cicatricial entropion should always include medical control of the underlying pathologic condition when present. Surgical management poses a challenge of lysing the scar tissue responsible for margin malposition without the corrective surgery inciting additional inflammation. Surgical technique depends on the severity of disease and etiology of symptoms.
If there is mild disease with symptoms from lashes abrading the corneal surface, skin resection may be sufficient to rotate the margin. If offending lashes are arranged in a sectoral pattern, cryotherapy can be offered. If a larged portion of the lid has offending lashes follicle excision can be performed. Follicle excision is achieved by splitting the lamella posterior to the lashes and excising the lashes with Westcott scissors. The base of the lash follicles is then cauterized to prevent regrowth. 90% of eyelids treated with this procedure had functional success with no return of trichiasis at 6-24 months.
In moderate disease affecting the upper lids, tarsal infracture is a viable surgical option that preserves the lashes and can deliver acceptable cosmesis. An external partial tarsectomy is performed through a lid crease incision. A double-armed 6-0 vicryl is placed partial thickness through the tarsus and externalized. A full-thickness tarsotomy is then performed to direct the lid margin away from the globe. Everting sutures are placed to keep the lid margin rotated anteriorly, and the skin is closed.
Transverse blepharotomy and marginal rotation has also been used to treat cicatricial entropion. In this procedure a full-thickness incision is made 4mm from the lid margin and 5-0 absorbable suture is passed partial-thickness through the anterior tarsus and lower lid retractors of the proximal lid and then through the orbicularis and skin of the distal lid. The suture is tied in horizontal mattress fashion over a bolster near the lash line, and skin is closed. The sutures and bolster remain in place for 10 days. This procedure has an 85% success rate for upper and lower lid cicatricial entropion repair.
For severe cicatricial disease, the posterior lamella must be lengthened while releasing scar tissue and lid retractors. In these instances the posterior lid retractors can be weakened by recession or lysis with a spacer. Hard palate graft, other mucous membrane graft or allograft can be used to support and bolster the posterior lamella. Graft choice is especially important when operating on the upper lid, as the graft will be in constant contact with the cornea, and free tarsoconjunctival grafts may provide good results.
Congenital entropion is a rare condition in which the lower lid margin is rotated inward since birth. This results from disinserted lower lid retractors, posterior lamella vertical insufficiency or kinking of the tarsal plate. Children may also develop entropion following facial paralysis, a condition that typically leads to ectropion in adults. In pediatric patients, the orbicularis acts to counter the inturning force of the lower lid retractors, and facial paralysis results in unchecked retractor function rotating the eyelid margin toward the globe surface. Eyelid retraction may be confused with congenital entropion.
Treatments include lubrication to limit mechanical trauma, taping the lower lid to the malar prominence to correct lid margin position, or injecting low doses of botulinum toxin into the orbicularis to weaken the muscle and prevent override. Surgical therapy provides definitive treatment.
The most common complication following entropion repair is recurrence. As mentioned prior, transconjunctival involutional entropion repair has a recurrence of 3.3%. Cicatricial entropion repair poses a more challenging treatment picture, and has a higher rate of recurrence. Recurrence can be prevented by aiming for over-correction at time of surgery, but overly aggressive correction of lid rotation may lead to punctual eversion. Ectropion can also result from repairs that attach the inferior lid retractors to the anterior surface of the tarsus rather than the inferior aspect. Overly aggressive shortening of the lower lid retractors or excessive skin removal can produce lower lid retraction and inferior scleral show. Using local anesthesia allows the surgeon to assess lid height, motility and contour during the procedure and make any necessary adjustments promptly to prevent induction of ectropion. Simultaneous correction of horizontal lid laxity can also prevent postoperative ectropion. Erb et al, noted no incidences of retraction, inferior scleral show or ectropion in a series of 151 eyelid repairs for involutional entropion.
Lid-splitting surgical approaches risk fistula formation. If encountered, these should be excised and repaired.
The surgeon should be cognizant of the marginal arcade during entropion repair to prevent necrosis at the lid margin. Any full-thickness incisions through the lid should be made inferior to the inferior margin of the tarsus, at least 4mm inferior to the lid margin, to avoid vascular compromise.
Overall, transconjunctival entropion repair has a low rate of complications, with Erb et al noting a 4% rate: stitch abscess and conjunctivochalasis 0.7% each and lateral tarsal strip dehiscence and lateral canthal dystopia.
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