Trauma, can be secondary to fractures to the skull base or mandible, or from surgery (particularly neurosurgery). It can be damaged by trauma, cerebrovascular accidents, Bell’s palsy, tumors, infections, immune-mediated causes, and congenital cranial dysinnervation syndromes. The facial nerve (CN VII) controls most of the eyelid muscles, and facial nerve dysfunction will therefore lead to weakened eyelid closure (Figure 2). Paralytic lagophthalmos is most commonly due to facial nerve dysfunction. Medication effect (particularly sedatives or neuromuscular blockers).Physiologic lagophthalmos (as in the case of nocturnal lagophthalmos).Excessive scar tissue or excessive eyelid removal during surgery (cicatricial lagophthalmos).Facial nerve dysfunction (paralytic lagophthalmos).The etiologies of lagophthalmos can be divided into the following subcategories: Because of this, a portion of the eye remains open during a blink and during sleep, and is subject to damage from exposure. Lagophthalmos is the inability to close the eyelids completely. A summary of risk factors and conditions is listed below. Patients at risk for EK include those who suffer from conditions that interfere with the ability to protect the cornea such asincomplete eyelid closure, inadequate blink reflex, inadequate blink rate and/or decreased protective lubrication of the cornea. The corneal epithelium serves as a barrier to the outside world through the use of tight junctions and damage to the integrity of this structure can facilitate penetration of microbes and external debris. Disruption to this system may lead to an epithelial defect. Several factors help maintain an adequate distribution of the tear film these include an intact blink reflex, normal blink rate, and complete eyelid closure during sleep and blinking. The tear film, a composite fluid of three layers, has several important roles: it nourishes and lubricates the cornea, aids in crisp visual acuity, and protects the cornea from bacterial invasion (Figure 1). Under normal circumstances, the eyelids and tear film protect the cornea, an avascular, nonkeratinized epithelium, from trauma, desiccation, and microbial attack. Lastly, the mucinous layer, which is supplied by both the conjunctiva and the cornea (conjunctival goblet and epithelial cells and corneal epithelial cells) stabilizes the aqueous layer (by providing a viscous medium), maintains attachment of the tear film to the corneal epithelium through the use of glycoproteins, and helps uniformly distribute the tear film layer through the creation of a low surface tension environment. This layer has many functions including but not limited to corneal antimicrobial defense, lubrication, nutrition and supply of oxygen, mechanical clearance of debris, and regulation of cellular functions. The proteins in this layer include lysozyme, lactoferrin, transferrin, ceruloplasmin, metalloproteinases, defensins, and immunoglobulins. The aqueous layer comprises the middle layer of the tear film and contains proteins, cytokines, growth factors, electrolytes, oxygen, and glucose and is supplied by the main and accessory lacrimal glands. This layer is responsible for lubrication and ensuring uniform spread of the tear film, prevention of evaporation, and stabilization of a smooth ocular surface for refraction. The outermost layer consists of lipids that are secreted by the meibomian glands. The tear film consists of three layers (although a contemporary model proposes a gradient model rather than distinctly layered model).
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