Ectropion Clinical Presentation
- Author: Edsel Ing, MD, FRCSC; Chief Editor: Hampton Roy, Sr, MD more...
With the exception of patients with acute facial nerve palsy, patients may have ectropion for months or even years before they seek medical attention.
Patients often complain of irritated or red eyes with tearing. They may constantly wipe their eyes, thereby exacerbating lid laxity and the ectropion.
Advanced age may suggest the patient has involutional ectropion.
Eye drop instillation with chronic eversion of the lower lid can lead to involutional ectropion.
A history of facial burns, lid surgery, or lid trauma is usually easily confirmed on cursory examination and may suggest cicatricial ectropion.
In patients with cicatricial ectropion and periocular skin rash, a history of facial skin cancer and topical and systemic medication use should be ascertained (see Causes).
Facial nerve palsy can cause ectropion. Acute facial nerve palsy is consistent with Bell palsy. Chronic, insidious progressive facial nerve palsy may indicate a mass lesion. For patients with facial nerve palsy, the caregiver should be asked if nocturnal lagophthalmos occurs. These patients especially require slit lamp examination of the cornea and testing of corneal sensation.
Gestalt examination of the visage may reveal a connective tissue disorder, prior surgical scars or burns, cancerous skin conditions, parotid mass, or the physiognomy for floppy eyelid syndrome. All of these findings may be important in ectropion evaluation.
Documentation of visual acuity and examination of the cornea and the conjunctiva are part of any complete oculoplastic examination. Corneal exposure, corneal ulceration, and conjunctival keratinization may accompany ectropion.
Because of gravity, ectropion usually involves the lower lid and is described as punctal, medial, lateral, or tarsal (complete). Laxity-related ectropion typically begins medially; with time, the central lid margin and the lateral lid may evert.
Both the distraction test and the snap-back test are usually performed for abnormal horizontal lid laxity. Anterior lid distraction of more than 6-8 mm from the globe suggests horizontal lid laxity. If the lower lid is pulled inferiorly, the lid should quickly return to its previous position. If not, this may be interpreted as an abnormal snap-back test result. The patient should not be allowed to blink the eyelid back into position.
If cicatricial ectropion is suspected, superiorly displace the lower lid margin. If the lower lid margin does not extend 2 mm above the inferior limbus, then cicatricial ectropion should be considered. In patients with skin erythema and cicatricial ectropion, skin cancer or a medication-induced skin rash should be excluded.
Typically, the puncta should not be visible, unless the lid is everted. If this is not the case, punctal ectropion is present.
Chronic punctal ectropion may result in punctal phimosis.
Chronic ectropion may cause keratinization of the lid margin and the palpebral conjunctiva.
In patients with complete tarsal ectropion, a white line in the inferior fornix is often present, indicating a disinserted capsulopalpebral fascia.
In patients with suspected paralytic ectropion, the following should be documented:
Presence or absence of Bell phenomenon
Degree of lagophthalmos - To estimate nocturnal lagophthalmos, the patient should gently close the eyelids when in the supine position.
Disparity between spontaneous and voluntary lid closure
With a lower motor neuron seventh nerve palsy (eg, Bell palsy), the ipsilateral brow and the lower facial musculature are weak. With an upper motor neuron seventh nerve palsy, brow-elevation is relatively spared due to the bilateral innervation of the upper face.
In patients with suspected facial nerve palsy, orbicularis oris dysfunction can be tested for by asking them to show their teeth rather than smile. Compare the elevation of the angles of the lips; ptosis of the lateral lip on the affected side is often present.
If a slow-onset or nonresolving seventh nerve palsy is seen, perform the following:
Palpate the parotid gland for tumor.
Exclude prior malar skin cancer.
Check the patient's hearing to exclude a cerebellopontine angle tumor.
Perform a slit lamp examination for uveitis, which may suggest a disease process, such as sarcoidosis or Lyme disease.
Inferior scleral show should be distinguished from ectropion, especially in patients with prominent globes. Horizontal eyelid tightening will exacerbate the scleral show of a proptotic eye, because the shortest arc between the canthi lies inferior to the cornea.
Patients with involutional ectropion of the lower lid may also have involutional changes of the upper eyelid. Failure to recognize this prior to horizontal tightening of the lower lid may result in the upper lid prolapsing over the lower lid margin with the lower lid lashes rubbing the palpebral conjunctiva of the upper lid (ie, lid imbrication, which can be seen with floppy eyelid syndrome).
Ectropion may be congenital or acquired. Congenital ectropion is rare and usually involves the lower lid. The cause often is a vertical deficiency of the anterior lamella. Congenital ectropion is rarely an isolated anomaly. It may be associated with blepharophimosis syndrome, microphthalmos, buphthalmos, orbital cysts, Down syndrome, and ichthyosis (collodion baby). Occasional congenital ectropion cases are on a paralytic basis.
Acquired ectropion may be involutional, paralytic, cicatricial, or mechanical.
Involutional ectropion is the most common form of ectropion in developed countries.
A major factor is horizontal lid laxity, usually due to age-related weakness (most patients are elderly) of the canthal ligaments and the pretarsal orbicularis. Patients with involutional ectropion have been suggested to have an age-normal or larger than normal tarsal plate, which may mechanically overcome normal or decreased orbicularis tone, in conjunction with canthal tendon laxity.
Patients with an anophthalmic socket may have involutional ectropion due to chronic pressure of the ocular prosthesis.
Disinsertion of the capsulopalpebral fascia may lead to severe tarsal ectropion.
Paralytic ectropion may occur with seventh nerve palsy from diverse causes, such as Bell palsy, cerebellopontine angle tumors, herpes zoster oticus, and infiltrations or tumors of the parotid gland.
Cicatricial ectropion occurs from scarring of the anterior lamella by such conditions as facial burns, trauma, chronic dermatitis, excessive skin excision (or laser) with blepharoplasty, or orbital fracture repair with a transcutaneous approach.
Glaucoma drops (eg, dorzolamide, brimonidine) have been implicated as a cause of cicatricial ectropion.
Less common causes of cicatricial ectropion include cutaneous T-cell lymphoma, pyoderma gangrenosum, and ichthyosis.
Antineoplastic agents (eg, docetaxel) and epidermal growth factor receptor inhibitors (eg, erlotinib, cetuximab) have been reported to cause cicatricial ectropion.
Mechanical ectropion may occur with lid tumors, such as neurofibromas that evert the lower lid. Glasses have been implicated as a "mechanical factor" that causes ectropion.
Acute idiopathic bilateral lower lid ectropion has been described. An uncommon case of bilateral upper lid ectropion from blepharospasm has also been described.
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