Sunday, December 19, 2010

Senile Entropion

Signs and Symptoms
Entropion is defined as inversion of the eyelid margin. The phenomenon may occur unilaterally or bilaterally. Although it may involve the upper or lower eyelid, the lower lids are affected more frequently. Clinical features associated with entropion may be observed both in and out of the biomicroscope and include in-turning of the eyelid margin, eyelid skin or eyelashes contacting the cornea creating ocular irritation, foreign body sensation, epiphora, conjunctival hyperemia, superficial punctate epitheliopathy and, in severe or untreated cases, corneal ulceration.

Etiologically, there are four classifications of entropion: senile (or involutional), congenital, cicatricial, and spastic.

Senile entropion is considered to be the most common form. The lower eyelid turns toward the globe because of increased horizontal lid laxity, an over-riding preseptal orbicularis, disinserted or atrophied lid retractors or tendons, and involutional enophthalmos.

Congenital entropion typically effects the upper eyelid and results from structural defects in the tarsal plate, shortened posterior lamellae (tarsal plate and conjunctiva), or eyelid retractor dysgenesis. Epiblepharon (a fold of skin that overlaps the eyelid margin pushing the eyelid margin inward), prominent epicanthus (a fold of skin partially covering the inner canthus, caruncle and plica semiluminaris) and microophthalmos are factors as well.

Cicatricial entropion is produced when there is as a vertical shortening of the tarsus secondary to scarring of ocular tissue brought about by disorders such as Stevens-Johnson syndrome, ocular cicatricial pemphigoid, trachoma, herpes zoster, trauma, chemical injuries, or thermal burns.

Spastic entropion occurs secondarily to neurologic, inflammatory or irritative processes of the eyelids. Blepharospasm and involutional changes following surgery are among the common sources.

While the treatment of choice should be guided by the underlying cause, the fundamental philosophies of management include moving the lid margins and lashes away from the cornea and lubricating and providing antibiotic coverage for a compromised epithelium. Generally, copious artificial tear drops and ointments can be combined with bacitracin or erythromicin ointment, b.i.d. to q.i.d., in all cases.

Solutions for senile or involutional entropion includes eyelid retraction via taping, thermal cautery or Quickert suture placement (a 2 to 3mm double nylon suture placed into the eyelid 2 to 3mm below the lid margin, perpendicular to the lid margin causing the lid to rotate away from the cornea). Other more complicated surgical solutions exist and should referred to the ocular plastic surgeon. Botulinum toxin injection has been demonstrated as a highly effective alternative to lid taping for temporary eyelid reposition in patients awaiting surgery.

In cicatricial cases, surgical repair may include excision of the scar with a tarsal plate graft from preserved sclera, ear cartilage or hard palate (in most severe circumstances) along with conjunctival and mucous membrane grafting using fetal amniotic membrane tissue.

The easiest way to resolve spastic entropion is to remove the offending irritant. In cases that involve the seventh cranial nerve (essential blepharospasm, orofacial dyskinesia, hemifacial spasm, facial myokymia) a neuro-ophthalmic consult is indicated. In some instances these conditions can be managed pharmacologically using anti-seizure medications.

Congenital cases rarely improve on their own and almost always require surgical correction. In cases such as these, a specialist with experience in pediatric oculoplastics is preferred.

Clinical Pearls

A thorough history should be completed on all patients with entropion. Take note of previous eye surgery, trauma, chemical injury, chronic infection and changes in eyelid tonus.
Diagnose entropion by examining the tonus of the eyelid. A sagging lower lid margin, a positive snap back test (the eyelid is loose and snaps back poorly when pulled away from the globe), loose medial and lateral canthal tendons, and an unusually deep inferior fornix indicate the potential for lid to globe congruity problems.
The differential diagnosis of entropion includes eyelash anomalies such as trichiasis (inward turning of the cilia) and distichiasis (multiple rows of eyelashes), neuro-ophthalmic blepharospasm, traumatic etiologies, scarring from chemical injuries, and lid malposition secondary to previous ocular surgeries.

1 comment:

  1. Hi! I'm glad to stop by your site and know more about ocular cicatricial pemphigoid. Keep it up! This is a good read. I will be looking forward to visit your page again and for your other posts as well. Thank you for sharing your thoughts about ocular cicatricial pemphigoid.
    Cicatricial pemphigoid has been referred to by a variety of designations based largely on its site of involvements, with examples of such terminology including "desquamative gingivitis," "ocular pemphigus," and "benign mucous membrane pemphigoid." However, currently "...such designations are thought to be confusing or somewhat misleadings (e.g., pemphigus in this context is a misnomer , and this disorder is hardly benign given the extent of morbidity it can cause)."
    patient's immune system, with the white blood cells becoming "confused" and beginning to attack not only germs but also part of the patient's own body. In rheumatoid arthritis, for example, the white blood cells become confused and begin to attack tissue in the patient's joints. In pemphigoid, the white blood cells attack skin and mucous membrane, particularly mucous membranes of the mouth, eyes, nose, throat, vagina, and rectum. Patients may or may not have more than one site affected by the disease, but 70% of the patients with cicatricial pemphigoid have eye involvement. And because this is a systemic autoimmune disease, it cannot be successfully treated, long-term, with simple topical (drops) therapy. It must be treated systemically, and typically with strategies that "cool down" the immune system, i.e., suppress the immune system sufficiently to stop the autoimmune process. Suppressing the immune system sufficiently to stop the autoimmune process for a short period (one to five years) is usually sufficient to enduce permanent remission of the disease. If this is not done, then continued inflammation, continued scarring, and eventual blindness in both eyes usually occurs.