Lagophthalmos is the inability to close the eyelids completely on attempted closure. The term lagophthalmos is derived from the Greek word ‘lagos’ which means ‘hare’, since the hare was believed to sleep with its eyes open.
Incomplete closure results in
Increased evaporation of tears.
Poor tear film distribution.
Disruption of mucin layer component of tear film.
Drying of cornea.
Breakdown of ocular surface.
Lagophthalmos may be due to
Forward protrusion of eyeball.
Vertical upper or lower eyelid shortening.
Protractor orbicularis oculi muscle dysfunction.
Seventh intracranial nerve dysfunction.
Symblepharon formation (adhesion between eyeball and eyelid).
Closure of eyelids is primarily a function of the descending upper eyelid. The lower eyelid exhibits very little upward movement during closure of eyes. Because of this, many patients tolerate lower eyelid retraction with minimal or no symptoms, as long as the upper eyelid retains normal movement.
Some patients without peri-ocular abnormalities may sleep with their eyes partially open, yet very few of these people suffer symptoms of eye exposure. The majority of them are probably protected by Bell’s phenomenon (up-rolling of eyeballs on closure of eyelids). A number of patients with nocturnal lagophthalmos may have symptoms of ocular surface breakdown.
Comatose patients often exhibit lagophthalmos due to inadequate central seventh intracranial nerve tone. In addition, these patients with concomitant fifth intracranial nerve dysfunction are at particular risk for breakdown of corneal epithelium.
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Patients present with symptoms such as
Foreign body sensation.
Burning of eyes.
Patient may be asymptomatic if there is corneal hypo-aesthesia.
Lagophthalmos is produced due to following three main causes
Failure of function of the orbicularis oculi muscle. This is the most common cause. It may be paralytic, because of facial intracranial nerve involving the orbicularis oculi muscle, or spastic, as is seen in thyrotoxicosis.
Excessive protrusion of the globe in the orbit. Lagophthalmos may accompany proptosis or buphthalmos (enlarged cornea due to elevated intraocular pressure in small children), in spite of normal eyelids, which fail to cover the proptosed eye.
Inadequate vertical dimension of either upper or lower eyelid. It may be structural when retraction or shortening of the eyelids results from scarring or atrophy following injury (e.g. burns) or a disease. Infants with a collodion membrane may have temporary lagophthalmos due to restrictive effect of the membrane on the eyelids.
A degree of physiologic lagophthalmos may occur normally during sleep. Functional lagophthalmos in an unconscious patient may be very problematic.
Diagnosis of lagophthalmos is primarily clinical.
Slit lamp examination by an eye specialist may show inter-palpebral punctate epithelial keratopathy, which is diagnostic of lagophthalmos or incomplete blink. Distribution of the punctate epithelial keratopathy depends upon the position of cornea during sleep in patients with nocturnal lagophthalmos.
External examination for complete eyelid closure should be done with patient gently closing the eyes.
Acute seventh intracranial nerve dysfunction, due to Bell’s palsy, trauma, or iatrogenic injury, may cause lagophthalmos. In cases with subtle orbicularis oculi muscle weakness, manual distraction of the eyelids during forced closure may expose weakness that may cause nocturnal lagophthalmos or incomplete blink.
It is important to check corneal sensation to rule out any component of fifth intracranial nerve dysfunction.
The vertical dimension of upper and lower eyelid skin must be evaluated in patients with suspected lagophthalmos. In the lower eyelids, vertical shortage will be apparent usually and will manifest as ‘sclera show’ and eyelid retraction. However, in upper eyelids the eyelid margin often rests at normal height, and only with downward distraction of the eyelid does the vertical skin shortness becomes apparent.
Function of levator palpebrae superioris muscle (during excursion of the eyelid from up to down), should be measured in all patients suspected of lagophthalmos. Patients with inadequate mobility of the upper eyelid retractors may have lagophthalmos despite a normal vertical amount of skin.
Symblepharon between the bulbar and palpebral conjunctiva in superior fornix may also limit downward excursion of the upper eyelid thereby causing lagophthalmos.
Globe protrusion increases the amount of eyelid excursion necessary to cover the cornea fully during closure of eyes. Lagophthalmos associated with proptosis may lead to exposure keratopathy.
Nocturnal lagophthalmos causes foreign body sensation and watering of eyes on awakening.
Comatose patients often show lagophthalmos due to inadequate tone of central seventh intracranial nerve.
Management should be carried out under medical supervision.
Ocular surface lubrication: Initial symptomatic management is directed towards ocular surface lubrication. Viscous artificial tears are used.
Prevent evaporative drying: Prefabricated moisture chamber or thin polyethylene film may be applied over the eyes to reduce evaporative drying. Temporary or permanent tarsorrhaphy may be required in some cases.
Definitive treatment depends upon accurate diagnosis of the underlying cause of lagophthalmos.
Proptosis: Patients with proptosis are usually best managed by orbital decompression and repositioning of eyeball within the orbit. Patients who cannot have decompression may be helped by lid lengthening procedures in an attempt to reposition the eyelids anteriorly to the corneal apex during closure of eyes. Patients with retro-bulbar mass or haemorrhage require removal or drainage of the retro-bulbar lesion.
Lid shortening: Lagophthalmos due to trauma or iatrogenic shortening of the upper eyelids usually require reconstructive soft tissue surgery.
Inadequate vertical skin: Lagophthalmos due to inadequate vertical skin requires replacement with skin flaps or grafts.
Symblepharon: Lagophthalmos due to eyelid-globe adhesion by symblepharon are treated by releasing the symblepharon and reconstructing the appropriate fornix (junction between palpebral and bulbar conjunctiva) with mucous membrane grafting.
Paralysis of orbicularis oculi muscle: Measures to reduce evaporation and increase lubrication may be sufficient with limited exposure keratopathy of anticipated short duration. If exposure is severe or anticipated to be long lasting, tarsorrhaphy may be done.
Lower lid retraction: Patients with paralytic lower eyelid laxity and ectropion are best managed by placing a spacer to elevate and support the lid. Spacer material may be donor sclera or fascia, autogenous ear or nasal cartilage, acellular human dermis, or mucosa from the hard palate. Hard palate mucosa has become increasingly more common for the relief of lower lid retraction.