Lacrimal Gland Prolapse: Key Causes and Management

The lacrimal gland is essential for tear production, maintaining eye health and comfort. In some cases, it may shift from its normal position, resulting in lacrimal gland prolapse. This condition often appears as swelling in the upper eyelid and can be mistaken for other eyelid disorders. While typically asymptomatic, it may cause discomfort or cosmetic concerns. Identifying its causes and recognizing key features are crucial for effective management.

Gland Location And Anatomy

The lacrimal gland is located in the superotemporal orbit, resting in a shallow depression called the lacrimal fossa of the frontal bone. This positioning protects the gland while allowing it to perform its primary function—producing the aqueous component of the tear film. It consists of two lobes: the larger orbital lobe, positioned deeper in the orbit, and the smaller palpebral lobe, which lies closer to the eyelid and is more involved in tear secretion. These lobes are separated by the lateral horn of the levator aponeurosis, a fibrous structure that helps maintain the gland’s position.

Tears are secreted by acinar cells and transported through ducts that open into the superior conjunctival fornix, ensuring even distribution across the ocular surface. The gland receives blood from the lacrimal artery, a branch of the ophthalmic artery, while venous drainage occurs through the superior ophthalmic vein. Lymphatic drainage involves the preauricular and parotid lymph nodes, which contribute to immune surveillance.

Neural control is mediated by parasympathetic and sympathetic pathways. Parasympathetic fibers, originating from the superior salivatory nucleus and traveling via the greater petrosal nerve, primarily stimulate tear production. Sympathetic innervation, derived from the superior cervical ganglion, regulates vascular tone, indirectly affecting secretion. This dual autonomic regulation allows tear production to adjust based on environmental and physiological needs.

Common Factors Leading To Prolapse

Lacrimal gland prolapse occurs due to structural weakening of orbital tissues supporting the gland. A primary cause is age-related atrophy of connective tissues, particularly the lateral horn of the levator aponeurosis. As these structures lose elasticity, they become less effective at anchoring the gland, allowing it to descend anteriorly. Studies suggest collagen degradation and reduced fibroblast activity contribute to this process.

Mechanical forces also play a role. Chronic eye rubbing, common in individuals with allergic conjunctivitis or habitual behaviors, exerts repeated pressure on the gland, encouraging displacement. Ocular trauma, including blunt force injuries or complications from eyelid surgery, may weaken fascial attachments. Procedures like blepharoplasty, if not carefully performed, can inadvertently disrupt support structures, increasing the risk of prolapse.

Genetic predisposition is another factor. Individuals with conditions such as Ehlers-Danlos or Marfan syndrome, which affect collagen synthesis, are more prone to early-onset prolapse. Hormonal changes, particularly declining estrogen levels in postmenopausal individuals, may also accelerate connective tissue weakening.

Distinctive Clinical Features

Lacrimal gland prolapse typically presents as a painless, soft mass in the superolateral quadrant of the upper eyelid, often creating asymmetry. Unlike inflammatory or neoplastic lesions, it lacks erythema, tenderness, or rapid progression. The gland may become more prominent when looking downward, a useful diagnostic clue.

Patients may experience a sensation of fullness in the affected eyelid, though functional impairment is rare. In some cases, excessive displacement can contribute to mechanical ptosis, where the prolapsed gland exerts downward pressure on the eyelid margin, partially obstructing vision. Unlike aponeurotic ptosis, which results from levator dysfunction, this drooping arises from the gland’s mass effect.

Cosmetic concerns often prompt medical evaluation, as asymmetry can become more noticeable over time. Unlike orbital fat prolapse, which allows more dynamic tissue movement, the prolapsed gland remains relatively fixed. Palpation typically reveals a firm, mobile structure that can be repositioned into the lacrimal fossa, distinguishing it from tumors or fibrotic conditions.

Relationship With Blepharochalasis

Blepharochalasis, a rare eyelid disorder marked by recurrent edema and progressive skin laxity, is associated with lacrimal gland prolapse. Repeated swelling episodes, often beginning in adolescence or early adulthood, weaken periorbital tissues, including the lateral horn of the levator aponeurosis. This loss of structural support makes the gland more susceptible to displacement.

Unlike age-related dermatochalasis, which results in excess skin, blepharochalasis leads to thinning and fragility, making the prolapsed gland more visible. This can create an irregular eyelid contour. Additionally, compromised levator attachments may exacerbate prolapse severity. Some patients also develop concurrent ptosis due to levator dehiscence, further complicating the presentation.

Methods For Diagnosis

A structured clinical approach is necessary to differentiate lacrimal gland prolapse from other orbital and eyelid conditions. A thorough patient history should assess the duration of swelling, prior trauma or surgery, and systemic conditions affecting connective tissue integrity. Direct visualization often reveals a soft, mobile mass in the superolateral eyelid, becoming more pronounced when looking downward. Unlike inflammatory or neoplastic lesions, it maintains a consistent size without tenderness. Palpation can confirm mobility and repositioning into the lacrimal fossa, distinguishing it from fixed masses.

Imaging aids in ambiguous cases. High-resolution orbital ultrasound can delineate the gland’s position and rule out infiltration. When deeper pathology is suspected, MRI or CT scans provide detailed visualization. MRI is particularly useful for assessing soft tissue integrity, while CT imaging helps identify bony abnormalities or fat herniation that may mimic prolapse. These tools ensure an accurate diagnosis and guide treatment decisions.

General Management Approaches

Treatment depends on symptom severity and glandular displacement. In mild, asymptomatic cases, observation may be sufficient. Monitoring assesses progression, particularly in patients with connective tissue disorders or recurrent eyelid edema. Patients should be advised to avoid behaviors that exacerbate prolapse, such as frequent eye rubbing.

For significant cosmetic or functional concerns, surgical intervention is preferred. Lacrimal gland resuspension repositions the gland into the lacrimal fossa using sutures anchored to the periosteum or surrounding connective tissue, restoring eyelid contour while preserving function. If prolapse coexists with severe ptosis or dermatochalasis, concurrent procedures such as blepharoplasty or levator advancement may be performed for optimal results. Addressing underlying tissue laxity is essential to prevent recurrence.