Lower Eyelid and Eyelash Malpositions


Figure. 29.1 Sagittal section of the lower lid demonstrating the anterior, middle, and posterior lamellae. (With permission from Rodriguez ED. Volume 3: Craniofacial, Head and Neck Surgery and Pediatric Plastic Surgery. In: Neligan, PC, editor. Plastic Surgery. 3rd ed. Elsevier, Saunders; 2012.)



Biomechanics of the Lower Lid – the Suspension Bridge


The lower lid position is such that the lid margin is in contact with the globe, the conjunctival mucous membrane is held in a moist environment, and the lashes and keratinized skin are held away from the cornea. Its position is dependent on the net balance between the structural support forces, which act in a superoposterior direction (Fig. 29.2), and the gravitational and other extrinsic distraction forces.


image

Figure 29.2 Main components of structural eyelid support. Medial and lateral canthal tendons and the orbicularis oculi exert posterior and superior vectors. The lower lid retractors afford vertical support that opposes inward rotation of the lid margin. 

A suspension bridge, supported at its two lateral ends (canthal tendons), as well as underneath (lower lid retractors), provides a useful analogy for lower eyelid anatomy and physiology. More horizontal support is provided by a series of motorized cables (orbicularis oculi), which mainly run parallel to its deck (the lid margin). Later in this chapter, we will draw on this analogy to demonstrate how an imbalance can develop between the intrinsic and extrinsic forces.



Orbital Vectors


A patient’s orbital vector is defined at the relationship between the corneal apex and the malar eminence in the sagittal plane (Fig. 29.3).5,6 Its importance in eyelid malpositions arises when considering treatment, particularly canthal ligament tightening procedures. Both ocular and midface factors will determine the vector of the orbit.


image

Figure 29.3 Negative (A), neutral (B), and positive (C) orbital vectors. A patient’s orbital vector is defined at the relationship between the globe (the corneal apex) and the malar eminence in the sagittal plane. Red line, vector joining corneal apex to cheek malar eminence; yellow line, vertical vector parallel to cheek malar eminence. 


The Aging Eyelid


Our current knowledge of the anatomy of aging has evolved with contemporary studies,79 which have suggested that eyelid aging has multiple dynamic components. Changes at the cellular level and macroscopic level in different tissues, as well as in the multidimensional dynamics between them, all contribute to the lax and weakly supported eyelid. The topic of the aging eyelid is discussed in Chapter 38.



Bone


Skeletal support of the eyelid undergoes significant change with age. As described in the Lambros theory, the orbital rims undergo remodeling and the maxilla undergoes retrusion, when viewed in the sagittal plane. The posterior and inferior displacement of the orbital rim (to which the lower eyelid is loosely tethered pulls down eyelid tissues, and the resultant smaller surface area of the maxilla provides reduced support for the midface soft tissues, which follow the same vector of descent. In patients who already have relatively poor maxillary projection, this bony and soft tissue loss can further predispose to developing a negative orbital vector.10,11



Tendons, Sheets, and Plates


Observations on the length of the tarsal plate12 and horizontal lid aperture3,7 suggest that these aspects remain relatively stable while the lateral canthal tendon increases in length.3 The theory that the lateral canthal angle descends as a result of this laxity5 has been supported by some studies and disputed by others.7,9 The septum thins with age, beginning as a thick white layer in youth and evolving into a diaphanous structure in older persons.



Muscle


The orbicularis oculi has long been thought to thin and stretch with age, but some studies contradict this.1316 However, the orbicularis oculi does, indeed, undergo degenerative change,17 and the laxity of its retaining ligament to the bony framework could result in less support.





Assessing the Patient


Effective treatment strategies require thorough understanding of normal anatomy and astute assessment of pathologic changes.18 The patient’s history and general health must be assessed with particular attention to specific questions and observations as discussed below.



Observation


The following factors must be observed during assessment:



Skin: Tight, erythematous, leathery, or flaky skin suggests actinic damage or other dermatologic disorders. Forcible blinking or upgaze with an open mouth may reveal unexpected skin tension. Facial scars, lagophthalmos, and signs of potentially malignant lesions should be noted.


Muscle: Facial muscle weakness and asymmetry and attenuated blinks should be assessed, as reviewed in Chapter 31.


Orbital vector: The maxillary skeletal structure is best seen clinically by observing the patient from the side (Fig. 29.3).



Medial Canthal Tendon


A medial distraction test is performed by pulling the eyelid laterally and observing the distance that the punctum can be displaced laterally (Fig. 29.4A). The normal tendon will allow minimal displacement of the punctum, whereas a “lax” MCT will allow the punctum to travel 1 to 3mm;19 if the punctum is drawn past the medial limbus (with the eye in primary position), the MCT may require surgical tightening. More quantitative grading systems for MCT laxity have been described.20


image

Figure 29.4 A, Medial distraction test. B, Lateral distraction test. C, Snap/pinch test. Arrows demonstrate the direction of pull of the eyelid. 


Lateral Distraction Test


The lateral canthal angle may become rounded as a result of lateral canthal tendon laxity, dehiscence, or previous surgery (Fig. 29.4B).


In the lateral distraction test, the canthus is pulled medially and the degree of displacement is measured; up to 2 mm of movement is normal.



Snap-Back and Pinch Tests – Testing Generalized Laxity


The snap-back test is performed by pulling the central lower lid away from the globe and then allowing it to snap back into position (Fig. 29.4C). Upon release, a normal eyelid should snap back against the globe immediately without a blink. A severely lax eyelid may require one or more blinks to return to normal position. The distance that the lid can be pulled away from the globe with the thumb and forefinger can also be measured in millimeters by using a ruler (the “pinch” test). The normal lower eyelid can be distracted no more than 6 to 8 mm from the globe.21



Lower Lid Retractor Dehiscence


Excess vertical mobility is suggestive of dehiscence of the lower lid retractors22 on upward displacement. Other clues of retractor dehiscence include diminished lower eyelid excursion on down gaze owing to absence of attachment of the retractors to the tarsal plate and a deep inferior conjunctival fornix.21



Testing for Cicatricial Elements


Scarring of the middle and posterior lamellae may result in ectropion, entropion, or retraction in the neutral position. It is identified by failure of the lower lid to elevate on upward gaze and tethering of the lid on attempted manual elevation. The normal lower lid can be raised over the pupil with manual distraction. Inability to elevate the lower lid margin by 2 mm above the inferior limbus is suggestive of cicatricial vertical lid shortening in one of the three lamellae. Posterior lamella scarring may present as tarsal kink, tarsal conjunctival scarring, symblepharon, or a resistance to lid eversion.


Cicatricial entropion should be suspected if resistance to downward traction or outward rotation is present or if horizontal traction on the lid does not temporarily improve the eyelid position. Fornix symblepharon may render the eyelid difficult to evert.



Additional Clinical Tests



Slit lamp biomicroscopy of the eyelid and ocular surface


Syringing of the nasolacrimal system


Facial nerve weakness – testing the orbicularis



Lower Eyelid Ectropion


Ectropion can be classified into five main categories depending on the underlying disease process, but ectropion may have more than one concomitant pathology. It is not uncommon for a patient to present with chronic ectropion, the primary pathology being involutional, with cicatricial skin changes from chronic epiphora. The assessment should identify those changes that need correction (Box 29.1).


 



Box 29.1


Classification of Lower Lid Ectropion



Congenital (see Chapter 8)


Involutional


Cicatricial


Paralytic


Mechanical



Involutional Ectropion


Involutional ectropion is the most common subtype, with a prevalence of 2.9%.23


The lid will maintain a functional anatomic position as long as intrinsic supporting forces are strong enough to balance the extrinsic distraction forces (Fig. 29.5). A pathologic imbalance can be created by a weakening of the support structures with additional extrinsic factors such as the repetitive stretching of the lid (e.g., from wiping away tears).


image

Figure 29.5 A, Weakening of supportive mechanisms allowing eversion of the lid margin. B, A right lower involutional ectropion with secondary anterior lamellar cicatrization. 


Pathogenesis


Horizontal laxity in the eyelid in the form of lateral and MCT laxity is a well-established cause of ectropion. In a recent series, Damanesco et al. found lateral canthal tendon (LCT) laxity in 80% of patients with ectropion and MCT laxity in 20%.23


Previous theories about horizontal laxity included a physical stretching and lengthening of eyelid elements with age. However, several studies have now suggested otherwise,24,25 identifying tarsal plate shrinkage after 60 years of age26 and implicating stretching of the LCT. One study suggested that patients with ectropion have always had larger tarsal plates than the average and that an apparently large tarsus in ectropion is not caused by stretching of the tarsus but is a primary etiologic factor in the development of ectropion over entropion.12 It is unclear whether these patients have undergone a less aggressive atrophic aging process, or perhaps the original size of their tarsal plates was larger than average.


Laxity and dehiscence of the lower lid retractors have also been found in patients with ectropia,23,27,28 but usually with concomitant horizontal laxity.


Histologic studies examining full-thickness eyelid specimens from ectropic eyelids suggest collagen degeneration that may contribute to horizontal laxity. Although some studies also show an increase in tarsal elastosis,17,29 a recent publication identified a decrease in elastic fibers.23,29,30 This study also correlated clinical measurements of horizontal laxity with histologic changes in the eyelid tissues and concluded that an increase in horizontal laxity is associated with the reduction in collagen and elastin fibers, as well as the presence of abnormal elastin in tarsal plate, orbicularis muscle, and skin. One of these studies also demonstrated chronic ischemia in the orbicularis muscle,25 but this has not been shown clinically in involutional ectropion.


Other studies have found that white race and prominent axial globe position are more likely to produce ectropia23,31 (Box 29.2).


 



Box 29.2


Pathogenesis of Ectropion



Horizontal laxity


Canthal tendon laxity


Retractor dehiscence


+/− cicatricial component of the anterior lamella


Additional factors


+/− larger tarsal plates


+/− prominent axial-globe positions



Management


Medical Treatments and Interim Measures.

Use of the following has been recommended as interim measures:



Lubricants for the ocular surface


Skin barriers – vaseline, colostomy cream



Surgical Treatment.

Numerous surgical techniques have been proposed to bolster or restore the intrinsic supporting structures and to identify and correct tissues at fault.



Correction of Horizontal Laxity and LCT.

Since most of the horizontal laxity occurs at the lateral canthal area, resecting central portions of the eyelid (wedge resection) is being supplanted by lateral canthal tightening (Fig. 29.6).


image

Figure 29.6 Principles of canthopexy (A) and canthoplasty (B). (From Cardoso de Castro, C, Boehm K, Codner, MA. Techniques in aesthetic plastic surgery series: midface surgery. Philadelphia, PA: Saunders; 2009.)

The aim of lateral canthal resuspension is to restore the tension and position of the lower lid and to direct the canthus posteriorly towards its normal position.


Lateral canthal surgery may or may not shorten the lid length depending on the snap back test. If the lid is snug and “snaps back” firmly, a nonshortening procedure is recommended. If there is more than 2 to 3 mm of lid movement away from the globe and there is little “snap back” without a blink, then a shortening procedure is appropriate.32,33



Transcutaneous Lateral Canthopexy – Nonshortening.

The suture plicates the LCT against the orbital rim without disrupting the lateral canthal angle.32



Lateral Canthoplasty – Shortening.

For lids with significant laxity, lysis of the LCT and inferior cantholysis are performed. The lid is shortened and reattached to the lateral orbital rim.



Treating Horizontal Laxity in A Patient with the Negative Orbital Vectors.

Lower eyelids in patients with negative orbital vectors are at risk of being displaced below the globe following lateral canthal surgery. Therefore, shortening of the eyelid must be avoided in these patients.



Options for Patients with Negative Vectors.

The following options are available for patients with negative vectors:



Refixate the eyelid onto a higher position on the lateral orbital rim. Patients have to be warned of a change in appearance of the eyes and the fact that the lid may not be tightened to the optimal amount.


Use spacer grafts (hard palate, donor sclera, ear cartilage grafts, porcine intestine, donor dermis) to elevate the eyelid from the inferior orbital rim. This graft is placed between the inferior tarsal border and the released lower lid retractors.


Reposition the eyelid and move more supportive soft tissue into the malar region with a midface lift. Synthetic fillers have been described for this purpose.


Use malar implants to provide a projection ledge for the lower lid and cheek tissues. This changes the vector of the lower lid when tightened.



Correction of Medial Ectropion.

Fig. 29.7.


image

Figure 29.7 A, Schematic drawing demonstrating tarsoconjunctival diamond excision with lacrimal probe protecting the inferior canaliculus. B, Inverting sutures being placed. C–E, Sagittal schematics demonstrating variations of inverting suture placement. 


Retropunctal Cautery.

A row of cautery burns in the conjunctiva may be sufficient to cause contraction and shortening of the posterior lamellar to treat mild punctal ectropion but is usually of transient benefit.



Tarsoconjunctival Diamond (+/− Wedge Resection).

This “medial spindle technique” may be combined with horizontal shortening. The aim is to shorten the posterior lamella vertically below the punctum to create an inward rotation of the punctum toward the globe.



Correction of MCT Laxity.

MCT laxity is notoriously difficult to correct (see the section on treatment of paralytic ectropion). There has been a constant evolution of techniques for MCT plication because of the complex medial canthal anatomy and problems in achieving a lasting effect.



Correction of Retractor Dehiscence.

The Jones retractor plication involves locating the lower lid retractors via a subciliary incision beveling the dissection to avoid disrupting pretarsal orbicularis. The retractors are sutured to the lower border of tarsus.34



Correction of Cicatricial Component.

If a cicatricial element is found related to secondary epiphora, medical measures using barrier ointments and gentle massage may be tried first. If, however, any tension remains on the lid when the patient looks up with the mouth open, anterior lamellae augmentation may be required (see following section).



Cicatricial Ectropion


Pathogenesis


The pathophysiology of cicatricial ectropion depends on its numerous causes.18 Contracture and fibrosis of either the middle or anterior lamella of the lower lid cause a vertical shortening with subsequent lid eversion (Fig. 29.8). The posterior lamella may also be affected and should be examined as part of a comprehensive assessment.



Actinic damage – loss of normal skin elasticity


Dermatitis (e.g., reaction to topical medications, eczema)


Thermal burns and trauma


Radiotherapy


Infiltrative tumors (e.g., morpheaform basal cell carcinoma)


Dermatologic disorders (e.g., scleroderma, ichthyosis)


Iatrogenic (e.g., post–lower lid blepharoplasty, post–laser treatment)


image

Figure 29.8 A left lower lid ectropion secondary to a thermal burn. A, Open eyes with left lower lid cicatricial ectropion. B, Closed eyes with lagophthalmos. 


Management


The treatment should identify and eliminate the cause of the anterior lamella or middle lamella contracture, for example, by treating eczema or withholding or changing topical medications. Following burns, trauma, and irradiation, it is prudent to wait until the cicatrization phase has stabilized, as long as the ocular surface is protected.



Surgery.

Surgical correction involves addition or transfer of tissue into the area where there is shortage and contracture and to resolve the anterior and inferior distraction forces placed on the lower lid.



Treating Anterior Lamellar Shortage.

The following measures are advocated to treat anterior lamellar shortage:



Moving tissue – heteropalpebral flap (Fig. 29.9A and B) /bucket handle flap, midface lift


image

Figure 29.9 Use of a heteropalpebral flap from the left upper lid to the lower lid (A, pre-op, B, post-op) and skin graft (C, pre-op, D, post-op). Both methods are used to treat a cicatricial left lower lid ectropion. 

Addition of tissue – skin graft (Fig. 29.9C and D)


Expansion of existing tissue (e.g., osmotic tissue expanders)

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

May 14, 2017 | Posted by in OPHTHALMOLOGY | Comments Off on Lower Eyelid and Eyelash Malpositions

Full access? Get Clinical Tree

Get Clinical Tree app for offline access