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Chapter 87 – Entropion

Chapter 87 – Entropion









• Entropion: an inward rotation of the tarsus and eyelid margin ( Fig. 87-1 ).



• Foreign body sensation.

• Secondary blepharospasm.

• Ocular discharge.

• Epiphora.

• Conjunctival metaplasia.

• Superficial keratopathy.

• Corneal scarring.



• It is progressive.

• Numerous corrective techniques for this anomaly are reported.

• Multiple pathogenic factors, including tarsotendinous instability, capsulopalpebral fascia dysfunction, and preseptal orbicularis muscle override.

• Surgical goals are to normalize eyelid function and appearance.





There are over 400 publications in the medical literature that address entropion and its treatment. Early procedures can be categorized as vertically shortening the anterior lamella (skin and orbicularis muscle), vertically lengthening the posterior lamella (tarsus and conjunctiva), and/or controlling lamellar rotation. The ancient Egyptians and Arabians are credited with the earliest entropion treatment—everting the lower eyelid through skin and orbicularis muscle cautery. Celsus and others described procedures directed at foreshortening the anterior lamella or stabilizing its position. Procedures involving horizontal eyelid tightening were popularized by Fox, Bick, and others.[1] Wies[2] described a procedure that utilized full-thickness blepharotomy and eyelid margin rotation. Despite the nonphysiological basis of this procedure, it gained wide acceptance because of its technical ease and nonreliance upon a knowledge of eyelid anatomy.

The mid-twentieth century heralded an anatomic approach to entropion repair. In 1963, DeRoetth[3] and Jones et al.[4] separately identified the lower eyelid retractor system as pivotal in acquired entropion development. Jones et al.[5] also described a surgical correction via lower eyelid retractor repair. Lower eyelid retractor microanatomy and physiology were further refined by Hawes and Dortzbach, [6] Goldberg et al.,[7] and others.[8] [9] Orbicularis muscle functions in acquired and congenital entropion were clarified by Dalgleish and Smith[8] and Tse et al.,[10] and tarsal plate and canthal tendon physiologies were advanced by Benger and Musch, [9] Shore,[11] and Liu and Stasior.[12] Finally, the importance of autologous tarsoconjunctival support in entropion was contributed by Shorr et al.[13] and Baylis and Hamako[14] and led to improved posterior lamellar substitutes and grafting technique by Silver [15] and others.[16]


A complete ocular history, including all prior eyelid procedures, and physical examination are essential. A general medical history and physical examination may be critical in uncovering systemic manifestations predisposing to entropion development or altering the selection of treatment options.

The Capsulopalpebral Fascia

Capsulopalpebral fascia dysfunction is central to the evaluation of both congenital and acquired entropion (see Box 87-1 and Chapter 82 ). Although many authors suggest that entropion results from disinsertion or dehiscence of the fascia from the inferior tarsus, histological observations disclose only an attenuation of the conjoint capsulopalpebral fascia and orbital septum complex.[6] Clinical observations that identify possible lower lid retractor dysfunction include a higher eyelid resting position in primary gaze, an increased passive vertical distraction, and a reduced vertical eyelid excursion. Benger and Musch,[9] however, could not demonstrate a loss of lower lid excursion in patients who have entropion. They noted that normal lower lid excursion, in the presence of capsulopalpebral fascia disinsertion or attenuation, parallels the normal upper eyelid excursion in patients with aponeurogenic blepharoptosis.

Schwab et al.[17] determined the normal depth of the central inferior fornix to be 11?mm. In cases of retractor dysfunction, the fornix depth often increases. In some cases, a white band, representing the disinserted edge of the capsulopalpebral fascia, can be observed beneath the palpebral conjunctiva.

The Tarsus and Canthal Tendons

The appositional pressure between the eyelid and globe is a factor in entropion development. Bick[1] demonstrated that entropion could be temporarily corrected by the intraconal injection of 2–4?ml of saline. Although an age-related lengthening of the lower eyelid or tarsus remains unproved, some studies suggest that age-related horizontal lower lid laxity occurs, especially in patients who have chronic entropion.[12] This laxity often results from stretching of the lateral canthal tendon. The horizontal eyelid distraction test remains the best way to judge horizontal eyelid laxity. The central eyelid is passively pulled from the ocular surface while the eye is in the primary gaze position. Measurements of greater than 6?mm between the eyelid margin and corneal surface are considered abnormal.


Another determinant of the appositional pressure between globe and eyelid is the relative position of the globe. Although widely discussed in the literature, involutional enophthalmos has not been verified. Kersten et al.[18] demonstrated no association between “involutional” entropion and globe position as measured by Hertel’s exophthalmometry. Lower eyelid medial entropion has been reported following enophthalmos induced by orbital





Figure 87-1 Right lower eyelid entropion. Note the inward rotation of the tarsal plate about the horizontal axis and the resultant contact between the mucocutaneous junction and ocular surface. This patient may have multiple anatomic defects contributing to the eyelid presentation.




Preoperative Assessment of Entropion



• Higher eyelid resting position in primary gaze

• Increased passive vertical eyelid distraction

• Increased depth of inferior conjunctival fornix

• Presence of a white infratarsal band



• Passive horizontal eyelid distraction



• Exophthalmometry



• Height of tarsal plate

• Presence of cicatrizing conjunctival disease





decompression in Graves’ orbitopathy.[19] Enophthalmos alone may be insufficient to cause entropion.

Orbicularis Muscle

The historical subclassification of a spastic entropion variant implied a cause-and-effect relationship with increased orbicularis muscle tone. Dalgleish and Smith[8] demonstrated a superior migration of the preseptal orbicularis subunit toward, but not beyond, the inferior tarsal border in lower lid entropion. It is unclear whether this muscular bunching is a primary phenomenon or epiphenomenon. Clinical evaluation for preseptal orbicularis override is subjective and should be carried out with the eye in primary gaze position, after a spontaneous blink, and following forceful eyelid closure. Eyelids with preseptal override are often described as having a thickened appearance. In contrast to observations in eyelids with isolated capsulopalpebral fascia dysfunction, the inferior tarsal border is not easily visualized in orbicularis override.



Figure 87-2 Epiblepharon. Note the bilaterality, loss of the lower eyelid skin crease, and overriding skin fold. The normal orientation of the tarsal plate distinguishes this condition from entropion.

The Posterior Lamella

Reduced posterior lamellar support in entropion may be more widespread than appreciated. Its vertical contracture in cicatrizing conjunctival disease has been distinctly categorized (cicatricial entropion). Several studies, however, imply a role for tarsoconjunctival loss even in noncicatrizing disease. An age-related decrease in the vertical dimension of the tarsal plate and a reduced tarsal height associated with involutional entropion have been documented.[8] [20]

In the setting of posterior lamellar foreshortening, knowledge of the underlying disease process is paramount in deciding the timing and type of surgery. The majority of these cases involves trachoma, Stevens-Johnson syndrome, ocular cicatricial pemphigoid, chronic meibomian gland inflammation, chemical and radiation injury, and postoperative fibrosis. Additional diagnostic considerations include topical medication toxicity, sarcoidosis, atopic keratoconjunctivitis, ocular rosacea, toxic epidermal necrolysis, membranous conjunctivitis, herpes zoster ophthalmicus, progressive systemic sclerosis, dysthyroidism, and neoplasm. Patients who have progressive processes need preoperative and perioperative immunomodulation to stabilize their disease.[21] [22] When the primary process is uncertain, a diagnostic conjunctival biopsy is indicated. Kemp and Collin[23] offered a grading system for cicatricial change. This system focuses on the position of the meibomian gland orifices, conjunctivalization of the eyelid margin, the position and orientation of the cilia, assessment of tarsal plate structure, keratinization of the palpebral conjunctiva, assessment of posterior lamellar scarring, and symblepharon formation.

Other Factors

Case reports suggest profoundly prolapsed orbital fat as a risk factor for lower eyelid entropion. Both Raina and Foster[24] and Bartley et al.[25] reported entropion in pediatric patients who have either morbid obesity or facial dysmorphism. Carter et al.[26] reported excessive orbital fat prolapse associated with lower eyelid entropion in the Asian population.


Other clinical entities may be confused with entropion and must be eliminated from the differential diagnosis. Epiblepharon, distichiasis, trichiasis, and eyelid retraction arise from different pathophysiologies, follow a different clinical course, and necessitate different therapies.


In epiblepharon, a horizontal fold of redundant pretarsal skin and orbicularis muscle extends beyond the eyelid margin and compresses the eyelashes against the globe ( Fig. 87-2 ). The condition is usually bilateral, prevalent in Asian populations, and



commonly involves the lower lid. Some patients demonstrate the clinical findings at all times, whereas others are symptomatic only in downgaze. Although both epiblepharon and congenital entropion result from lower eyelid retractor defects, their clinical presentation and course contrast sharply.[27] Nearly 80% of children who show epiblepharon have no ocular complaints.[28] The condition frequently resolves with the normal vertical growth of the facial bones. Although the majority of patients can be managed conservatively, treatment should not be delayed in symptomatic cases. A transcutaneous reattachment of the lower lid retractor anterior fibers to the skin and orbicularis is achieved by reforming the lower eyelid crease through the removal of a horizontal skin and orbicularis muscle strip and deep fixational suture closure.[27] [29]


Distichiasis refers to an accessory row of cilia arising from the meibomian gland orifices. It may occur in an autosomal dominant inheritance pattern. The tarsal plate in distichiasis manifests a normal position and orientation. It is the eyelash follicles that emerge from an abnormal position, the result of metadifferentiation of the primary epithelial germ cells originally intent upon meibomian gland development. The lashes are directed posteriorly toward the ocular surface and may not become symptomatic until about 5 years of age. Treatment modalities include mechanical epilation, electrolysis, radiofrequency ablation, laser photoablation, and cryotherapy to the posterior eyelid lamella.


Trichiasis is an acquired condition in which cilia arising from their normal anterior lamellar position are misdirected toward the ocular surface. This usually results from inflammatory disruption and scarring of the eyelash follicles. The underlying inflammation may involve both eyelid lamellae and produce a coexistent entropion. Treatment is usually based upon the number, distribution, and severity of the misdirected cilia. Treatment modalities include epilation, electrolysis, radiofrequency ablation, laser photoablation, cryotherapy to the posterior eyelid lamella, anterior eyelid lamellar recession, and surgical excision of the eyelash bulbs.

Eyelid Retraction

Eyelid retraction may be clinically confused with entropion. The retracted eyelid is pulled toward the orbital rim with the eyelashes obscured by the resulting fold of eyelid skin (pseudodermatochalasis), resembling entropion. Some underlying disease conditions can result in the coexistence of entropion and lid retraction. The key in differentiating eyelid retraction from entropion remains the orientation of the tarsal plate. In isolated lid retraction, the tarsal plate maintains its normal orientation relative to the globe surface, and the eyelid margin is in a normal but vertically displaced position.

Congenital Entropion

Fewer than 50 cases of true congenital lower eyelid entropion have been reported in the medical literature, and the hypothesized pathophysiology is derived mostly from intraoperative observation.[25] [27] [29] Current belief is that in congenital lower eyelid entropion both the anterior and posterior attachments of the capsulopalpebral fascia are dysfunctional. This accounts for the poorly formed lower lid skin crease in addition to the inward tarsal rotation in affected children. Unlike epiblepharon, congenital entropion does not resolve spontaneously and requires prompt surgical intervention.

A rare form of congenital upper eyelid entropion is known as the horizontal tarsal kink syndrome. In this condition, a fixed right-angled inward rotation of the tarsal margin causes apposition of the eyelid margin to the ocular surface and results in early and severe corneal complications. The cause of this variant remains speculative. Surgical interventions, including tarsal eversion sutures, transverse blepharotomy, and resection of the tarsal kink with eversion sutures, have been advocated. [30] The potential for severe corneal complications requires early recognition and prompt therapy.


Patients who have entropion must be evaluated as possible surgical candidates. The extent of ocular findings, patient’s age, and systemic comorbidities must be considered in devising a treatment plan. The patient should understand the benefits, risks, and treatment alternatives before therapy is initiated. Medical therapy is appropriate prior to surgical intervention and for patients who refuse or are too ill to undergo surgery. Symptoms may be ameliorated through the use of artificial tears, lubricating ointments, or a bandage soft contact lens. Temporary eyelid margin eversion can be obtained by rotating the anterior lamella away from the globe with tape.

Quickert-Rathbun Sutures

Eyelid margin rotation and lamellar migration can be corrected by placing several well-spaced and tightly tied full-thickness sutures.[31] Chromic gut, nylon, and silk sutures are equivalent for scar induction, but silk and nylon sutures unfortunately incite epithelial ingrowth along the suture tract. [32] Despite Quickert and Rathbun’s[33] reported 0% recurrence with up to 5 years of follow-up, the consensus is that suture entropion repair leads to late recurrence.[31] This shortcoming may be acceptable in patients who are poor surgical risks or for whom a temporary repair is adequate.

Botulinum Toxin

Chemodenervation of the orbicularis muscle with botulinum toxin may provide temporary entropion correction when the patient demonstrates significant preseptal muscle override.[34] Subcutaneous or intramuscular injection into the nasal and temporal lower eyelid can be performed in the office setting. Chemodenervation is noted within 3–5 days following administration and may last up to 6 months (see also Chapter 91 ). Injections in the medial lower eyelid may be complicated by temporary medial ectropion, punctal eversion, or inferior oblique muscle paresis.


Entropion surgery is an outpatient procedure usually performed in the physician’s office or in an ambulatory surgical center under local anesthesia. Pediatric patients require general inhalational anesthesia, although local subcutaneous infiltration is often utilized for additional hemostasis.

A 1:1 dilution of lidocaine 2% with 1:100,000 epinephrine (adrenaline) and bupivacaine 0.75% combined with hyaluronidase (150 units per 10?ml of injectable anesthetic) provides excellent anesthesia. Hyaluronidase enhances anesthetic solution diffusion within connective tissues, reduces tissue distortion, and better preserves normal tissue anatomy. When coadministered with epinephrine, it does not reduce the anesthetic duration of action.

For many patients, the pain elicited during the local anesthetic injection is the most distressing aspect of the surgery. Sodium bicarbonate (1?ml of 1?mEq/ml [1?mmol/ml] solution per 10?ml of injectable anesthetic) can be added to local anesthetic solutions to decrease pain upon injection.[35] Sodium bicarbonate, however, decreases the pharmaceutical half-life of the anesthetic agent and admixed epinephrine. Thus, buffered anesthetic-epinephrine mixtures should be utilized within 1 week of preparation.[36] A nonpharmacological method of reducing injection discomfort is



to provide the patient with adequate verbal support and to infiltrate the tissues slowly. Tissue infiltration or a regional nerve block is best performed with a 27- or 30-gauge hypodermic needle on a control syringe. The onset of epinephrine-induced vasoconstriction requires up to 10 minutes, so tissue infiltration should be performed prior to the surgical skin preparation and patient draping.

Monitored anesthesia care combines intravenous sedation with local analgesia. Its principal advantage is the sedative-induced amnesia. Propofol is an intravenous sedative that is neither a benzodiazepine nor a sedative-hypnotic. Its onset of action is equal to that of thiopental and it has a rapid recovery of less than 5 minutes.[37] It is excellent for the induction and maintenance of monitored anesthesia care sedation. It can produce undesirable cardiorespiratory depression, including systemic hypotension, peripheral vasodilatation, and respiratory depression. The use of intravenous sedatives necessitates appropriate preoperative evaluation and intraoperative monitoring of systemic blood pressure, cardiac rhythm, respiratory rate, and oxygen saturation.


The advances and improved surgical success in entropion management occurred through the appreciation of its pathophysiology and anatomic basis.[38] The preoperative assessment mandates the determination of all contributing defects. The planned surgical procedure is a sequential correction of each underlying defect. In most cases, entropion is multifactorial in origin and requires the correction of a combination of defects. Several authors have demonstrated that a single entropion procedure used for all cases is insufficient in providing adequate short- and long-term results.[39] [40] In broad terms, entropion surgery includes:

• The correction of capsulopalpebral fascia dysfunction

• The reduction of horizontal lower eyelid laxity

• The debulking of significant lower lid fat

• The prevention of preseptal orbicularis muscle shifting

• The reconstruction of posterior eyelid lamellar foreshortening

In cases of capsulopalpebral fascia dysfunction, the fascia must be advanced or reattached to the inferior tarsal border. Transcutaneous and transconjunctival approaches are described for this repair.[39] [41] Both approaches can be combined with techniques to correct horizontal laxity, prolapsed orbital fat, and preseptal orbicularis muscle override. The transconjunctival approach readily lends itself to the synchronous placement of a posterior lamellar graft. Some eyelid surgeons better appreciate the anatomic exposure as viewed through the transcutaneous approach. A recent study suggests a higher surgical success rate with the transcutaneous approach.[42]

The capsulopalpebral fascia can be advanced to the inferior tarsal border with or without its separation from the orbital septum. Separation of the septum from the fascia allows broader fascial exposure and a reduced likelihood of entrapping orbital septum in the advancement.

Surgical approaches to horizontal eyelid laxity address foreshortening by resection of the tarsal plate or plication-resection of the lateral canthal tendon. Evidence suggests that the dysfunction resides in the canthal tendon and its attachments rather than in the tarsal plate itself.[11] A surgical approach directed toward resection and reconstruction of the lateral canthal tendon is therefore preferred over purely tarsal resections performed in the central eyelid. This removes the dysfunctional canthal tendon, preserves the integrity of the healthy tarsus, places the incision within the cosmetically forgiving lateral laugh lines, and reduces the probability of a marginal notch, contour abnormality, or trichiasis.

Orbicularis muscle dysfunction is corrected by creating a fibrous barrier between the skin and deeper eyelid structures at the junction of the pretarsal and preseptal subunits. This can be achieved through a cutaneous incision placed at this level, the stimulation of fibrosis through the use of sutures, or the extirpation of a preseptal muscular subunit.[39]

Knowledge of the underlying disease process is essential in the treatment of posterior lamellar foreshortening. The timing of surgery and selection of the procedure are directly linked to the underlying process and its level of activity at the time of intervention. Progressive processes, such as ocular cicatricial pemphigoid, scleroderma, and sarcoidosis, are likely to require local and/or systemic immunomodulators to stabilize the disease course prior to surgical intervention.[22] [43] In certain disease states, a local inflammatory exacerbation may follow posterior lamellar manipulation.[44] In this instance, deviation from direct correction of the pathophysiological defect may be appropriate. A modest advance of the capsulopalpebral fascia may suffice to correct mild to moderate “cicatricial” entropion and obviate the need for potentially dangerous physical manipulation of the tarsus and conjunctiva.[43]

In most cases of tarsoconjunctival foreshortening, once the process is identified and optimal immunosuppression achieved, a posterior lamellar technique is performed. This usually takes the form of a tarsal out-fracture with marginal rotation or placement of a posterior lamellar graft. The transverse tarsotomy is physiological in that it directly addresses the eyelid structures affected by the underlying disease process.[45] [46] By limiting dissection to these layers, the risks of avascular necrosis of the lid, cutaneous scarring, and levator aponeurosis damage are minimized. The tarsotomy incision location is determined by the eyelid microvasculature and the degree of marginal eversion needed.

When posterior lamellar support or buttressing is needed, the selection of appropriate donor material is essential. Functionally, the posterior eyelid lamella is composed of a semirigid support material (tarsus) and a mucosal lining (conjunctiva). Although an autologous tarsoconjunctival composite flap or graft provides the most exact reconstruction, this tissue may be in short supply, especially if the primary disease process is bilateral. When replacement tissue is selected, an autologous, epithelium-covered, semirigid composite graft is favored. Materials utilized for tarsoconjunctival reconstruction or replacement have included tarsoconjunctival flaps and grafts, hard palate mucosa, nasal chondromucosa, and nasal mucoperiosteum. The hard palate mucosa and nasal mucoperiosteum are the current donor tissues of choice.[16] They are autologous, plentiful, easy to harvest, minimally resorptive, structurally similar to tarsus, and can be harvested repeatedly if necessary. Graft materials that may be used to lengthen the tarsus only include amniotic membrane, periosteum, temporalis fascia, banked sclera, irradiated homologous aorta, porous polyethylene, and polytef.[13] [14] [47] [48] [49]


Retractor Reattachment

In patients who do not demonstrate posterior lamellar foreshortening, the author advocates a transcutaneous surgical approach to lower eyelid entropion repair. A 4-0 silk traction suture is passed horizontally through the central lower eyelid margin and clamped to the drape above the brow ( Fig. 87-3 ). The lid is put on mild vertical traction and a subciliary incision is made 4?mm inferior to the eyelid margin (or 2.5?mm inferior to the lower lid lashes). This is extended from just lateral to the lacrimal punctum to beyond the lateral canthal angle. As vertical traction is increased on the intramarginal suture, the multiple tissue layers of the eyelid are separated and assume a planar orientation. The orbicularis muscle is buttonholed at the junction of the pretarsal and preseptal subunits (see Chapter 82 ) and separated for the full skin incision length ( Fig. 87-4 ). A myocutaneous flap is developed to the inferior orbital rim using blunt and sharp dissection posterior to the orbicularis plane.

The “free edge” of the capsulopalpebral fascia is often visualized several millimeters inferior to the tarsal border. The orbital septum is buttonholed 1?mm inferior to its fusion with the capsulopalpebral fascia and opened the horizontal length of the anterior lamellar incision. The point of fusion between septum and capsulopalpebral fascia may vary within the lid, especially in cases of lower eyelid retractor dysfunction. An important surgical landmark





Figure 87-3 A subciliary incision has been made following the placement of an intramarginal 4-0 silk traction suture.



Figure 87-4 Westcott scissors divide the pretarsal and preseptal subunits of the orbicularis muscle.

is the lower eyelid fat, which anatomically rests between the septum and fascia. The three lower lid fat pads are gently dissected from the anterior surface of the capsulopalpebral fascia ( Fig. 87-5 ).

In patients who have marked lower lid fat prolapse, fat debulking should be done at this time. This is performed using a standard lower eyelid blepharoplasty technique. Care is taken to ensure complete hemostasis and to preserve the inferior oblique muscle, which courses between the nasal and central fat pads (see Chapter 89 ).

The capsulopalpebral fascia is then advanced upward and reattached to the inferior tarsal border ( Figs. 87-6 through 87-8 ). Grasping the tissue in toothed forceps and having the patient gaze inferiorly can confirm fascial identification. When an apparent disinsertion or dehiscence is present, the fascia is advanced to the inferior tarsal border. In cases in which the fascia is attenuated but not disinserted, the fascia is surgically disinserted by the surgeon, a narrow horizontal strip excised, and the fascia reattached to the inferior tarsal border. Reattachment to the tarsus is performed with several interrupted 6-0 Prolene sutures. Care is taken to ensure that a sufficient purchase of the tarsal plate is incorporated in the suture and that the fascia is not excessively advanced superiorly along the anterior tarsal surface.

In patients demonstrating preoperative preseptal orbicularis muscle override, the extirpation of a preseptal muscle strip is performed. Dissection and hemostasis are facilitated through diffuse



Figure 87-5 Following opening of the orbital septum, the lower eyelid fat is retracted inferiorly. The capsulopalpebral fascia (open arrow) appears disinserted from the inferior tarsus (closed arrow).



Figure 87-6 The free edge of the capsulopalpebral fascia can be elevated easily from the underlying conjunctiva. In cases in which horizontal eyelid laxity is also present, the fascial advancement is performed following the lateral tarsal strip procedure.

infiltration of the myocutaneous flap with an epinephrine-containing local anesthetic solution. A 6–10?mm wide horizontal strip of muscle is dissected en bloc from the eyelid ( Fig. 87-9 ). The subciliary skin incision can be closed with a running 6-0 mild chromic or nylon suture. Topical antibiotic ointment is sufficient for postoperative infection prophylaxis.

Lateral Tarsal Strip Procedure

A horizontal tightening of the lower lid may be combined with reattachment of the retractors or be done as a separate procedure (see Chapter 88 ). The tightening is best performed using a standard lateral tarsal strip technique. A lateral canthotomy and inferior cantholysis of the canthal tendon are performed. Within the temporal eyelid, the anterior and posterior lamellae must be separated from one another at the gray line and the lid margin de-epithelialized. The palpebral conjunctiva is disinserted from the inferior tarsal border to complete the tarsal strip. The redundant tissues of the strip are determined by gently drawing the strip to the lateral orbital tubercle. The excess tissue is excised and the new lateral border of tarsus is attached to periosteum at the lateral orbital tubercle with either two interrupted sutures or a single horizontal mattress suture. The small-radius, half-circle (P-2, S-2, or D-2) needle facilitates the periosteal anchor at the lateral orbital tubercle.





Figure 87-7 The capsulopalpebral fascia is advanced and sutured to the inferior border of the tarsal plate. Care must be taken to obtain a solid purchase of the inferior tarsus and to avoid advancing the fascia superiorly along the tarsal anterior surface.

Absolute hemostasis should be established prior to closure. An absorbable 6-0 horizontal mattress canthopexy suture creates an acute canthal angulation and prevents imbrication of the upper lid over the temporal lower lid. To enhance esthetics, a small Burow triangle may be excised from the inferior skin wound margin lateral to the canthal angle. The lateral canthotomy is closed in a layered fashion.

Transverse Tarsotomy

In moderate cicatricial entropion, a posterior transverse tarsotomy with eyelid margin rotation is the procedure of choice. A 4-0 silk traction suture is placed horizontally through the central eyelid margin and the lid everted over a Desmarres retractor. A complete transverse tarsotomy is performed through the palpebral conjunctiva using a scalpel blade. The tarsotomy should be made equal to or greater than 3?mm from the eyelid margin to avoid the marginal vascular arcade ( Fig. 87-10 ). The marginal rotation is accomplished using double-armed 6-0 nonabsorbable sutures at multiple sites along the eyelid. The suture is first passed in a horizontal mattress fashion through the anterior edge of the nonmarginal tarsal plate. Each arm of the suture is then passed between the planes of the marginal tarsus and orbicularis muscle exiting the eyelid immediately anterior to the ciliary line. By tying under appropriate tension, the eyelid margin is everted. The immediate postoperative appearance should reveal a mild overcorrection of rotation.

Hard Palate Mucosal Graft

In cases of severe cicatricial entropion, the posterior eyelid lamella often requires buttressing. After everting the nonmarginal tarsal plate over a Desmarres retractor and performing the transverse tarsotomy, a limited dissection is performed in the plane between the tarsus and orbicularis muscle. This releases traction exerted by the eyelid retractors, septum, and conjunctiva. The posterior eyelid lamellar defect is measured and a template fashioned for graft harvesting. The graft should be mildly oversized to allow postoperative contraction.

A hard palate graft may be harvested using a local anesthetic block of the greater palatine and nasopalatine nerves followed by diffuse submucosal infiltration. The palatal mucosa is dried with suction and the graft template applied between the median raphe and alveolar process. The mucosa is outlined with a marking pen, the template removed, and the palate incised with a scalpel blade. The graft is undermined with the scalpel or a sharp periosteal elevator. Avoiding the areas of the greater palatine foramen and palatine vessels minimizes excessive bleeding. The palatal defect is not closed but may be covered with an acrylic retainer or the patient’s upper dentures, if available.



Figure 87-8 The completed lower eyelid retractor advancement. Multiple point fixation with nonabsorbable suture ensures permanence.



Figure 87-9 A strip of preseptal orbicularis muscle is extirpated using Westcott scissors. Muscle manipulation predisposes to hemorrhage; thus, thorough wound evaluation and complete hemostasis are essential.

The graft is thinned of fatty tissue on its submucosal surface and secured in the posterior eyelid lamellar defect with 6-0 absorbable sutures along its nonmarginal and lateral borders ( Fig. 87-11 ). The rotated marginal strip of the eyelid is then secured to the anterior surface of the graft with three double-armed sutures, as previously described for the transverse tarsotomy procedure. In severe entropion, rotational overcorrection is desired. To achieve a more pronounced eversion, the tarsotomy can be placed a greater distance from the eyelid margin or the double-armed rotational sutures can be made to exit the skin more anteriorly than the lash line.

The treatment of upper lid entropion with tarsoconjunctival foreshortening differs slightly from that of the lower eyelid. For mild to moderate entropion, the transverse tarsotomy with marginal rotation is the procedure of choice. For severe cicatricial entropion, a posterior lamellar buttressing procedure is recommended. Postoperative application of a prophylactic topical antibiotic ointment is sufficient, although some authors utilize oral antibiotics following graft placement. When a posterior lamellar graft is placed in either the upper or lower eyelid, a Frost traction suture and pressure dressing are used for 5–7 days to immobilize the lid in a stretched position. When hard palate grafts are placed in the upper lid, corneal protection by copious surface lubrication or a bandage contact lens is frequently necessary.


Most postoperative complications can be avoided through meticulous preoperative planning and intraoperative technique.





Figure 87-10 The transverse tarsotomy of the posterior lamella allows rotation of the marginal eyelid segment. Incision placement preserves the integrity of the marginal vascular arcade.

The best way to prevent recurrent entropion is through the appropriate selection of surgical procedures. When entropion recurs during the early postoperative period, the patient must be reevaluated for overlooked or undercorrected predisposing factors. Recurrences that present a year or more after surgery may be due to progression of underlying pathophysiology. Recurrences in patients who have a cicatrizing conjunctival process may be due to graft failure, graft contracture, or disease progression.


Overcorrection of eyelid margin position, or consecutive ectropion, is desired only in patients who have undergone transverse tarsotomy and marginal rotation procedures. When an unintended consecutive ectropion is present, the patient should be evaluated for excessive advancement of the capsulopalpebral fascia, attachment of the fascia too high on the anterior tarsal surface, uncorrected horizontal eyelid laxity, and incorporation of the orbital septum in the advancement or surgical closure. Postoperative ectropion can also occur following unintended extirpation of the pretarsal orbicularis subunit, excessive skin resection, or skin contracture after orbicularis extirpation. In such instances, if the degree of ectropion is mild and tolerated by the patient, conservative management with time, warm compresses, and massage may suffice. When it is severe, full-thickness skin grafting or the transposition of a preseptal orbicularis strip closer to the eyelid margin may be necessary.


The risk of hematoma can be reduced by appropriately discontinuing medications that impair platelet function and the clotting cascade. Intraoperative hemostasis can be achieved by meticulous cautery. Special attention must be given to the lateral branches of the palpebral arcades following lateral cantholysis. Extirpation of the preseptal orbicularis subunit increases the risk of hematoma. When eyelid hematomas occur, they are usually self-limiting and resolve with conservative management. In the setting of brisk bleeding or neuro-ophthalmic signs, reexploration of the surgical field with evacuation of the hematoma and cautery of vessels is indicated. Hemorrhage that occurs at a hard palate donor site usually originates from the greater palatine or nasopalatine artery. It can be controlled with digital pressure, submucosal epinephrine injection, conservative electrocautery,



Figure 87-11 Posterior lamella buttressing is accomplished through a hard palate graft. Graft bed preparation and marginal segment rotation are performed similarly to those for posterior tarsotomy.

chemical cautery, cellulose sponge, collagen sponge, periodontal putty, or a palatal stent.[50]

Eyelid Retraction

Postoperative eyelid retraction is usually the result of excessive horizontal tightening of the tarsus or excessive vertical advancement of the capsulopalpebral fascia. It is also important to ensure reattachment of the lateral tarsus to Whitnall’s lateral orbital tubercle rather than the lateral raphe of the orbicularis complex. An excessively shortened tarsal strip should be resuspended from either the superior crus of the lateral canthal tendon or a periosteal strip elevated from the lateral orbital wall. When it is performed in the same surgical repair, the capsulopalpebral fascia should be advanced and reattached to the inferior tarsal border following the correction of horizontal laxity.

Exposure Keratopathy

Corneal epithelial damage can develop from exposed conjunctival sutures, lagophthalmos, and keratinized hard palate grafts. This risk is higher following upper lid entropion repair. Treatment includes ocular surface lubricants, collagen shields, bandage soft contact lens, early suture removal, and dermabrasion of the keratinized graft.

Postoperative mechanical lagophthalmos most commonly results from incorporation of the orbital septum into the capsulopalpebral advancement or skin closure—appreciation of the anatomic layers is necessary during wound closure. Treatment



ranges from conservative observation to surgical exploration and release of the septum.

Granuloma Formation

Conjunctival granulomas may develop following manipulation or incision of the posterior lamella. Exuberant granulation tissue often develops as a result of chronic inflammation initiated by suture material or another surgical foreign body. Granulomas may resolve spontaneously but frequently necessitate treatment using topical or intralesional corticosteroids, cautery, excision, or removal of the inciting foreign body.


Symblepharon results from tissue manipulation that allows apposition of two or more abraded epithelial surfaces. The conjunctiva is at risk for symblepharon development if not handled with care intraoperatively. Its occurrence can be reduced through the use of symblepharon rings, fornix reformation sutures, or topical and systemic immunomodulators.


Aponeurogenic ptosis can complicate the repair of cicatricial upper lid entropion. The posterior fibers of the levator aponeurosis attach to the inferior one third of the tarsal plate anterior surface. These fibers can be inadvertently disrupted during posterior tarsotomy with a resultant postoperative aponeurogenic ptosis.

Other Complications

Eyelash loss and eyelid necrosis can occur after entropion surgery and are most often due to vascular insufficiency of the marginal arcade. Patients who undergo transverse blepharotomy or repeated surgery are at particular risk. Tissue necrosis and atrophy are often segmental. The damaged segment can be excised and the defect closed directly or reconstructed using typical eyelid reconstructive techniques (see Chapter 94 ).


Appropriate patient evaluation and surgical procedure selection should result in the immediate correction of the eyelid malposition. Most patients report symptomatic relief as early as their first postoperative day. Except in cases of posterior lamellar foreshortening, the appropriate surgical management of entropion has a success rate of 97% or greater.[41] When tarsoconjunctival contraction is present, surgical success still exceeds 90%. An exception occurs in ocular cicatricial pemphigoid, where lower success is predicted. [23] [45] Advances in the understanding of entropion have provided surgeons with improved, more reproducible, and longer lasting treatment options. A systematic approach to the evaluation and treatment of this condition ensures that patients will benefit from these therapeutic outcomes.





1. Bick MW. Surgical management of orbital tarsal disparity. Arch Ophthalmol. 1966;75:386–9.


2. Wies FA. Spastic entropion. Trans Am Acad Ophthalmol Otolaryngol. 1955; 59:503–5.


3. DeRoetth A. Mechanism of senile entropion. Trans Pacific Otoophthalmol Soc. 1963;44:173–7.


4. Jones LT, Reeh MJ, Tsujimura JK. Senile entropion. Am J Ophthalmol. 1963; 55:463–9.


5. Jones LT, Reeh MJ, Wobig JL. Senile entropion: a new concept for correction. Am J Ophthalmol. 1972;74:327–9.


6. Hawes MJ, Dortzbach RK. The microscopic anatomy of the lower eyelid retractors. Arch Ophthalmol. 1982;100:1313–18.


7. Goldberg RA, Lufkin R, Farahani K, et al. Physiology of the lower eyelid retractors: tight linkage of the anterior capsulopalpebral fascia demonstrated using dynamic ultrafine surface coil MRI. Ophthalmol Plast Reconstr Surg. 1994;10:87–91.


8. Dalgleish R, Smith JLS. Mechanics and histology of senile entropion. Br J Ophthalmol. 1966;50:79–91.


9. Benger RS, Musch DC. A comparative study of eyelid parameters in involutional entropion. Ophthalmic Plast Reconstr Surg. 1989;5:281–7.


10. Tse DT, Anderson RL, Fratkin JD. Aponeurosis disinsertion in congenital entropion. Arch Ophthalmol. 1983;101:436–40.


11. Shore JW. Changes in lower eyelid resting position, movement, and tone with age. Am J Ophthalmol. 1985;99:415–23.


12. Liu D, Stasior OG. Lower eyelid laxity and ocular symptoms. Am J Ophthalmol. 1983;95:545–51.


13. Shorr N, Christenbury JD, Goldberg RA. Tarsoconjunctival grafts for upper eyelid cicatricial entropion. Ophthalmic Surg. 1988;19:316–20.


14. Baylis HI, Hamako C. Tarsal grafting for correction of cicatricial entropion. Ophthalmic Surg. 1979;10:42–8.


15. Silver B. The use of mucous membrane from the hard palate in the treatment of trichiasis and cicatricial entropion. Ophthalmic Plast Reconstr Surg. 1986;2:129–31.


16. Bartley GB, Kay PP. Posterior lamellar eyelid reconstruction with a hard palate mucosal graft. Am J Ophthalmol. 1989;107:609–12.


17. Schwab IR, Linberg JV, Gioia VM, et al. Foreshortening of the inferior conjunctival fornix associated with chronic glaucoma medications. Ophthalmology. 1992;99:197–202.


18. Kersten RC, Hammer BJ, Kulwin DR. The role of enophthalmos in involutional entropion. Ophthalmic Plast Reconstr Surg. 1997;13:195–8.


19. Goldberg RA, Christenbury JD, Shorr N. Medial entropion following orbital decompression for dysthyroid orbitopathy. Ophthalmic Plast Reconstr Surg. 1988;4:81–5.


20. Bashour M, Harvey J. Causes of involutional ectropion and entropion—age-related tarsal changes are the key. Ophthalmic Plast Reconstr Surg. 2000;16:126–30.


21. Tauber T, de la Maza MS, Foster CS. Systemic chemotherapy for ocular cicatricial pemphigoid. Cornea. 1991;10:185–95.


22. Shore JW, Foster CS, Westfall CT, Rubin PA. Results of buccal mucosal grafting for patients with medically controlled ocular cicatricial pemphigoid. Ophthalmology. 1992;99:383–5.


23. Kemp EG, Collin JRO. Surgical management of upper lid entropion. Br J Ophthalmol. 1986;70:575–9.


24. Raina J, Foster JA. Obesity as a cause of mechanical entropion. Am J Ophthalmol. 1996;122:123–5.


25. Bartley GB, Nerad JA, Kersten RC, Maquire LJ. Congenital entropion with intact lower eyelid retractor insertion. Am J Ophthalmol. 1991;112:437–41.


26. Carter SR, Chang J, Aguilar GL, et al. Involutional entropion and ectropion of the Asian lower eyelid. Ophthalmic Plast Reconstr Surg. 2000;16:45–9


27. Jordan R. The lower lid retractors in congenital entropion and epiblepharon. Ophthalmic Surg. 1993;24:494–6.


28. Noda S, Hayasaka S, Setogawa T. Epiblepharon with inverted eyelashes in Japanese children. I: Incidence and symptoms. Br J Ophthalmol. 1989;73:126–7.


29. Millman AL, Mannor GE, Putterman AM. Lid crease and capsulopalpebral fascia repair in congenital entropion and epiblepharon. Ophthalmic Surg. 1994; 25:162–5.


30. Sires BS. Congenital horizontal tarsal kink: clinical characteristics from a large series. Ophthalmic Plast Reconstr Surg. 1999;15:355–9.


31. Wright M, Bell D, Scott C, Leatherbarrow B. Everting suture correction of lower lid involutional entropion. Br J Ophthalmol. 1999;83:1060–3.


32. Seiff SR, Kim M, Howes EL Jr. Histopathological evaluation of rotation sutures for involutional entropion. Br J Ophthalmol. 1989;73:628–32.


33. Quickert MH, Rathbun E. Suture repair of entropion. Arch Ophthalmol. 1971; 85:304–5.


34. Steel DH, Hoh HB, Harrad RA, Collins CR. Botulinum toxin for the temporary treatment of involutional lower lid entropion: a clinical and morphological study. Eye. 1997;11:472–5.


35. McKay W, Morris R, Mushlin P. Sodium bicarbonate attenuates pain on skin infiltration with lidocaine, with or without epinephrine. Anesth Analg. 1987;66:572–4.


36. Stewart JH, Cole GW, Klein JA. Neutralized lidocaine with epinephrine for local anesthesia. J Dermatol Surg Oncol. 1989;10:1081–83.


37. Marshall BE, Longnecker DE. General anesthetics. In: Gilman AG, Rall TW, Nies AS, Taylor P, eds. Goodman and Gilman’s pharmacological basis of therapeutics, 8th ed. New York: Pergamon Press; 1990:285–310.


38. Boboridis K, Bunce C, Rose GE. A comparative study of two procedures for repair of involutional lower lid entropion. Ophthalmology. 2000;107:959–61.


39. Nowinski TS. Orbicularis oculi muscle extirpation in a combined procedure for involutional entropion. Ophthalmology. 1991;98:1250–6.


40. Jordan DR. Ectropion following entropion surgery; an unhappy patient and physician. Ophthalmic Plast Reconstr Surg. 1992;8:41–6.


41. Dresner SC, Karesh JW. Transconjunctival entropion repair. Arch Ophthalmol. 1993;111:1144–8.


42. Cook T, Lucarelli MJ, Lemke BN, Dortzbach RK. Primary and secondary transconjunctival involutional entropion repair. Ophthalmology. 2001;108:989–93.


43. Elder MJ, Dart JK, Collin R. Inferior retractor plication surgery for lower lid entropion with trichiasis in ocular cicatricial pemphigoid. Br J Ophthalmol. 1995; 79:1003–6.


44. Mauriello JA, Lopresti-Solis AE, DeRose DA, et al. Conjunctival scarring after eyelid surgery as first sign of ocular cicatricial pemphigoid. Ophthalmic Plast Reconstr Surg. 1994;10:142–5.


45. Kersten RC, Kleiner FP, Kulwin DR. Tarsotomy for the treatment of cicatricial entropion with trichiasis. Arch Ophthalmol. 1992;110:714–17.


46. Al-Rajhi AA, Hidayat A, Nasr A, al-Faran M. The histopathology and the mechanism of entropion in patients with trachoma. Ophthalmology. 1993;100:1293–6.


47. Jordan DR, McDonald H, Anderson RL. Irradiated homologous aorta in eyelid reconstruction. Part II: Human data. Ophthalmic Plast Reconstr Surg. 1994;10:227–33.


48. Levin PS, Dutton JJ. Polytef (polytetrafluoroethylene) alloplastic grafts as a substitute for mucous membrane. Arch Ophthalmol. 1990;108:282–5.


49. Matsuo K, Hirose T. The use of conchal cartilage graft in involutional entropion. Plast Reconstr Surg. 1990;86:968–70.


50. Mauriello JA, Wasserman B, Allee S, Robinson L. Molded acrylic mouthguard to control bleeding at the hard palate graft site after eyelid reconstruction. Am J Ophthalmol. 1992;113:342–4.

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