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Dacryoadenitis
Introduction
Dacryoadenitis refers to inflammation of the lacrimal gland, a key component of the ocular adnexa responsible for tear secretion (see Image. Dacryoadenitis).[1] The condition may present in acute or chronic forms, affect one or both eyes, and arise from infectious, autoimmune, or idiopathic causes.[2]
The lacrimal gland is a bilateral, lobulated, almond-shaped structure located in the superotemporal orbit. This structure consists of palpebral and orbital lobes and produces the aqueous component of the tear film, which is vital for ocular surface protection and homeostasis. Encased in dense connective tissue, the lacrimal gland contains a mix of acinar and ductal cells, along with immune cells such as immunoglobulin A-secreting plasma cells and T lymphocytes.[3]
The course of dacryoadenitis depends on its cause. Acute cases are typically infectious and self-limiting, while chronic forms may indicate an underlying systemic condition such as sarcoidosis or immunoglobulin G4-related (IgG4-related) disease (IgG4-RD).[4] Dacryoadenitis may spread through direct extension from adjacent tissues, hematogenous dissemination, or lymphatic propagation.[5]
Dacryoadenitis presents clinically with eyelid edema, discomfort, and erythema localized to the superotemporal orbit.[6] In more severe cases, ocular motility disturbances, conjunctival chemosis, and proptosis may develop.[7] Chronic dacryoadenitis often leads to persistent glandular hypertrophy and progressive fibrosis, which can result in irreversible dysfunction.[8]
Distinguishing between acute and chronic dacryoadenitis is essential for accurate diagnosis and appropriate treatment.[9] Viral dacryoadenitis resolves spontaneously, while bacterial cases may require antibiotic therapy.[10] Inflammatory disease may respond to steroids or follow a chronic relapsing course, necessitating long-term management to maintain remission.[11]
Ongoing research continues to provide insights into immune-mediated mechanisms and histopathological subtypes of dacryoadenitis. The recognition of IgG4-related dacryoadenitis as a distinct entity has refined the diagnostic criteria, enabling more precise classification and targeted treatment.[12] Future studies aim to elucidate underlying mechanisms further and optimize therapeutic approaches for this complex condition.
Etiology
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Etiology
Lacrimal gland inflammation may be acute or chronic, infectious or noninfectious. Acute dacryoadenitis is frequently infectious and unilateral.[13] Infection most often ascends from the conjunctiva but may also originate from the skin, penetrating trauma, or hematogenous seeding in bacteremia.
Viral pathogens are more common than bacterial causes, particularly in children and young adults. Viruses typically lead to acute nonsuppurative dacryoadenitis. Epstein-Barr virus is the most common viral etiology.[14] Other frequent viral pathogens include the following:
Bacterial infections tend to cause suppuration. Staphylococcus aureus is the primary bacterial pathogen, with Streptococcus pneumoniae and gram-negative rods also implicated.[20][21] Fungal causes, though rare, include Histoplasma, Blastomyces, and Nocardia.[22] Aspergillus and Candida infections are uncommon but severe, primarily affecting individuals with compromised immune function.[23] These infections may present insidiously with chronic inflammation and may require antifungal therapy alongside surgical intervention if tissue necrosis develops.[24] Chronic infectious dacryoadenitis is uncommon, with some cases linked to Mycobacterium tuberculosis.[25][26] Parasitic infections, though rare, have been associated with dacryoadenitis, particularly in endemic regions where protozoal or helminthic infestations are prevalent.[27]
Chronic dacryoadenitis is more often inflammatory. Noninfectious dacryoadenitis is frequently associated with autoimmune disorders, including Sjögren syndrome, sarcoidosis, Crohn disease, and granulomatosis with polyangiitis.[28]
Despite advancements in understanding and diagnostic testing, many inflammatory cases remain idiopathic.[29] Idiopathic dacryoadenitis is a diagnosis of exclusion established when no specific infectious or autoimmune cause is identified.[30] Histopathological evaluation may aid in assessing suspected idiopathic cases. The growing interest in IgG4-related dacryoadenitis has led to its recognition as a distinct entity, accounting for 23% to 35% of cases previously classified as idiopathic orbital inflammation.[31][32]
Epidemiology
The prevalence of dacryoadenitis is not well documented, but it occurs less frequently than dacryocystitis, which involves inflammation or infection of the lacrimal sac. Historical literature estimates its incidence at approximately 1 in 10,000 ophthalmic cases. Acute dacryoadenitis most commonly affects children and young adults, with viral infections being the predominant cause.[33] Bacterial suppurative dacryoadenitis is less frequent and may result from Staphylococcus aureus, Streptococcus, or Haemophilus infections.[34]
In contrast, chronic dacryoadenitis is more common in middle-aged and older individuals with underlying systemic inflammatory conditions. When associated with autoimmune disease, dacryoadenitis appears to be more prevalent in women, reflecting the broader gender predilection observed in systemic autoimmune disorders.[35]
Pathophysiology
Dacryoadenitis results from immune-mediated inflammation, leading to glandular enlargement and dysfunction. In infectious cases, direct microbial invasion triggers an acute inflammatory response characterized by neutrophilic infiltration, tissue swelling, and cytokine-driven immune activation.[36] The ensuing inflammatory cascade obstructs the lacrimal ducts and reduces tear production, causing ocular discomfort and dry eye symptoms.[37] Chronic noninfectious dacryoadenitis is marked by predominant lymphocyte and plasma cell infiltration, leading to progressive fibrosis and glandular shrinkage.[38] The immunopathogenesis varies based on the underlying cause.
In autoimmune-associated dacryoadenitis, such as in Sjögren syndrome cases, autoantibodies and T-cell-mediated inflammation contribute to glandular tissue destruction.[39] In sarcoidosis, granulomatous inflammation alters the lacrimal gland’s structure, progressively impairing function.[40] IgG4-related dacryoadenitis is characterized by extensive lymphoplasmacytic infiltration, storiform fibrosis, and obliterative phlebitis. Elevated serum immunoglobulin 4 (IgG4) levels and histological findings of IgG4-positive plasma cells define this condition.[41] Although its precise pathophysiology remains under investigation, dysregulated immune responses potentially triggered by environmental or genetic factors are thought to contribute to its development.
Histopathology
Nonspecific inflammation of the lacrimal gland can exhibit various histopathological patterns. Infiltration may consist primarily of lymphocytes or a mixture of lymphocytes and neutrophils. The inflammatory cells' distribution pattern may be focal, diffuse, or perivascular. Fibrosis and acinar destruction may also be present. In cases associated with sarcoidosis, nonnecrotizing granulomas composed of epithelioid and multinucleated giant cells may be observed. IgG4-related dacryoadenitis features lymphoplasmacytic infiltration and may develop interlobular fibrosis.[42] Immunohistochemical staining can reveal an increased number of IgG4-positive plasma cells.[43]
Histopathological analysis is crucial for differentiating various forms of dacryoadenitis and guiding treatment decisions. Acute infectious dacryoadenitis typically presents with neutrophilic infiltration, glandular swelling, and localized necrosis. Bacterial dacryoadenitis is often characterized by abscess formation and polymorphonuclear leukocyte infiltration, whereas viral infections generally result in lymphocytic infiltration, sometimes accompanied by plasma cells.[44]
Chronic dacryoadenitis, particularly when linked to autoimmune disorders such as Sjögren syndrome, IgG4-RD, and sarcoidosis, demonstrates distinct histological features. Dacryoadenitis associated with Sjögren syndrome is marked by lymphocyte infiltration, germinal center formation, acinar destruction, and periductal fibrosis.[45] IgG4-related dacryoadenitis is defined by dense lymphoplasmacytic infiltration, storiform fibrosis, and obliterative phlebitis.[46] A diagnosis is supported when IgG4-positive plasma cells constitute more than 40% of the total plasma cell population.[47]
History and Physical
Acute dacryoadenitis commonly presents with erythema and tenderness over the superotemporal orbit. The glandular enlargement causes the lateral eyelid to droop, producing a characteristic S-shaped curve along the eyelid margin (see Image. Typical Dacryoadenitis).[48][49][48] Suppurative discharge from the lacrimal ducts, pouting of the lacrimal ductules, conjunctival chemosis, and swelling of preauricular and cervical lymph nodes may also be observed.[50] Fever and malaise can accompany these findings.[51] Inflammatory dacryoadenitis often develops more gradually, typically presenting as painless lacrimal gland swelling, which may be bilateral.[52]
A thorough history and physical examination are essential for diagnosing dacryoadenitis. A recent viral or bacterial infection may suggest an infectious cause.[53] Chronic dacryoadenitis may present as a progressively enlarging, painless gland, often with symptoms indicative of an underlying systemic disorder.[54][55] The physical examination should assess for eyelid edema, palpate the lacrimal gland for tenderness and consistency, and evaluate conjunctival injection and chemosis. Signs of orbital involvement, including proptosis, restricted extraocular motility, and vision impairment, require further evaluation to exclude orbital cellulitis or malignancy.[56] Bilateral dacryoadenitis raises suspicion for autoimmune or systemic inflammatory conditions, such as Sjögren syndrome, sarcoidosis, or IgG4-RD.[57]
Evaluation
Acute lacrimal gland swelling associated with a viral illness does not require biopsy or extensive laboratory evaluation. However, an additional workup is warranted if atypical features are present or if the swelling persists despite treatment.[58] Bilateral involvement, systemic symptoms, or occurrence in older adults raises suspicion for malignancy or an underlying autoimmune condition, necessitating further investigation.
Laboratory tests for identifying the cause of dacryoadenitis may include a complete blood count, erythrocyte sedimentation rate, C-reactive protein, anti-nuclear antibody, and anti-neutrophil cytoplasmic antibody. Angiotensin-converting enzyme is an unreliable marker for sarcoidosis. Serological tests for anti-Ro/SSA, anti-La/SSB, and IgG4 levels are important in diagnosing systemic inflammatory disorders. Infectious evaluation may include viral serologies, blood cultures, and tuberculosis testing.[59]
Imaging studies play a vital role in evaluating lacrimal gland involvement and distinguishing inflammatory conditions from neoplastic processes. Ultrasound may be used to assess glandular hypertrophy and internal echotexture.[60] Computed tomography (CT) and magnetic resonance imaging (MRI) provide detailed visualization of soft tissue involvement, osseous erosion, and orbital extension.[61] Contrast-enhanced MRI is particularly effective in differentiating benign inflammatory conditions from malignancy.[62] In acute dacryoadenitis, imaging may reveal adjacent lateral rectus myositis, periscleritis, or scleritis.[63] Chronic inflammatory conditions do not typically exhibit scleral enhancement.
Lacrimal gland biopsy is indicated in cases with atypical features, unclear etiology, or inadequate response to treatment.[64] In a review of 60 cases of lacrimal gland inflammation of unknown origin, histopathologic analysis identified a specific diagnosis in 61.7%, with 38% linked to systemic disease. Systemic steroids should be avoided before biopsy when feasible, as they can alter histologic findings. A biopsy is typically conducted using a transcutaneous approach, targeting the orbital lobe while preserving the tear ducts that drain through the palpebral lobe into the temporal conjunctival fornix.[65] Tissue samples are typically fixed in formalin, while fresh tissue is required for flow cytometry. Coordination with the laboratory before biopsy is essential, as specific handling and transport requirements may vary, particularly for flow cytometry.
Treatment / Management
The treatment of dacryoadenitis depends on its underlying cause. Acute viral dacryoadenitis usually resolves within 4 to 6 weeks and may require only supportive care, including analgesics and warm compresses. If a chalazion or signs of bacterial infection are present, topical antibiotics with warm compresses may be beneficial. The efficacy of oral antiviral therapy remains uncertain.
Bacterial dacryoadenitis necessitates systemic antibiotic therapy, with coverage for methicillin-resistant S aureus being advisable.[66] Broad-spectrum antibiotics such as trimethoprim-sulfamethoxazole, rifampin, doxycycline, or vancomycin may be considered. In cases of purulent discharge, obtaining cultures can help guide antibiotic selection.[67](B3)
Fungal dacryoadenitis requires systemic antifungal therapy and, in some cases, surgical debridement.[68] Abscess formation may warrant surgical drainage.[69] A lacrimal gland biopsy should be performed following appropriate imaging if the glandular enlargement persists beyond 3 months despite treatment, an abscess develops, glandular atrophy occurs, or malignancy is suspected.[70][71]
Corticosteroids reduce lacrimal gland swelling in nearly all forms of dacryoadenitis, making a steroid trial for diagnostic purposes unwarranted. One study suggests that idiopathic dacryoadenitis may respond well to surgical debulking with a low relapse rate.[72] Corticosteroids remain the primary treatment for noninfectious dacryoadenitis. Autoimmune-associated dacryoadenitis, such as that seen in Sjögren syndrome or sarcoidosis, may require systemic immunosuppressive therapy. The management of IgG4-related dacryoadenitis remains under discussion, but an initial trial of corticosteroids is reasonable, with immunosuppressive therapy rarely necessary.(B2)
Reports indicate that sclerosing dacryoadenitis associated with IgG4-related disease may progress to lymphoma.[73] Refractory inflammatory dacryoadenitis may benefit from orbital radiotherapy, methotrexate, or rituximab. Although IgG4-related disease has a high remission rate with rituximab, the response may be temporary.[74] An interprofessional approach involving ophthalmologists, rheumatologists, and infectious disease specialists is essential for optimizing patient outcomes.(B2)
Differential Diagnosis
Malignancy must be ruled out when focal swelling of the lacrimal gland occurs with a gradual onset, particularly in an older patient. Lymphomatous lesions can infiltrate the lacrimal gland.[75] These conditions exist on a spectrum ranging from reactive lymphoid hyperplasia to atypical lymphoid hyperplasia and malignant lymphoma. Both benign and malignant lymphoid tumors cause diffuse enlargement of the lacrimal lobes on imaging.[76] Epithelial tumors of the lacrimal gland may present similarly, including benign mixed tumors, adenoid cystic carcinoma, mixed malignant carcinoma, and mucoepidermoid carcinoma.[77]
Malignant metastases in this region are rare. However, when present, breast cancer is the most common primary source, spreading via lymphatic or hematogenous routes. Among the causes of lacrimal gland enlargement, approximately 50% are due to infection or inflammation, 25% are from lymphoid tumors, and 25% are due to salivary tumors.[78] Histopathological analysis remains the definitive method for distinguishing inflammatory from neoplastic processes.
Thyroid eye disease can sometimes mimic dacryoadenitis, presenting with diplopia due to restrictive inflammation of the extraocular muscles.[79] Unlike dacryoadenitis, thyroid eye disease typically causes lid retraction rather than mild ptosis.[80] Other infectious conditions, such as preseptal or orbital cellulitis, should be considered when evaluating periorbital swelling, erythema, and pain.[81] Focal swelling of the upper eyelid may also result from a chalazion or hordeolum, neither of which involves true lacrimal gland enlargement.[82]
Staging
Dacryoadenitis is not typically classified using a formal staging system. The extent and severity of the disease are assessed based on clinical presentation and imaging findings. Acute dacryoadenitis is categorized as mild, moderate, or severe based on symptoms such as discomfort, erythema, and associated orbital involvement. Chronic dacryoadenitis is classified by the degree of fibrosis and functional impairment of the lacrimal gland. In IgG4-related dacryoadenitis, the severity is evaluated using the IgG4-RD Responder Index, which considers the number of affected organs, disease burden, and therapeutic response.[83] Determining disease severity is crucial for guiding treatment decisions and monitoring disease progression.
Prognosis
The prognosis of dacryoadenitis depends on its underlying cause and the timeliness of treatment. Acute bacterial dacryoadenitis generally has a favorable outcome with prompt antibiotic therapy, often resolving within days to weeks. Viral dacryoadenitis is typically self-limiting, with full recovery expected in most cases. While infectious dacryoadenitis may necessitate antibiotics, it usually resolves without long-term complications.
Chronic and autoimmune forms, such as those associated with Sjögren syndrome, sarcoidosis, or IgG4-RD, may lead to persistent inflammation, fibrosis, and lacrimal gland dysfunction.[84] In severe cases, these complications may result in significant dry eye disease, negatively impacting quality of life.[85] Inflammatory dacryoadenitis tends to be more refractory to treatment and is influenced by any underlying systemic condition. Management may require prolonged steroid tapering, chronic immunomodulatory therapy, or surgical debulking.
As with any nonspecific orbital inflammation, recurrence or lack of resolution warrants a biopsy or repeat biopsy. Early diagnosis and appropriate immunosuppressive therapy can help prevent long-term complications.
Complications
Complications from infectious dacryoadenitis are uncommon, but a lacrimal gland abscess may form, or the infection may progress to preseptal or orbital cellulitis.[86] If left untreated, severe dacryoadenitis can have ocular and systemic consequences. In bacterial infections, abscess formation may necessitate surgical drainage. Orbital cellulitis and its spread to adjacent structures can result in vision-threatening complications, including optic neuropathy and cavernous sinus thrombosis.
Chronic inflammatory dacryoadenitis may lead to progressive fibrosis of the lacrimal gland, causing permanent gland dysfunction and persistent dry eye symptoms. Individuals with IgG4-RD or sarcoidosis may experience multisystem involvement, often requiring prolonged immunosuppressive therapy.[87]
Deterrence and Patient Education
Patient education is crucial for preventing and managing dacryoadenitis. Proper hygiene and prompt treatment of upper respiratory infections can reduce the risk of infectious dacryoadenitis. Patients should be counseled that infectious dacryoadenitis typically resolves on its own but may require antibiotics.
Monitoring for vision changes, pain with eye movement, or suppuration is important for identifying complications such as orbital cellulitis or abscess formation. When dacryoadenitis is linked to an autoimmune condition, patients should be educated about the disease, potential systemic involvement, and the possible need for an extended steroid taper or long-term immunomodulatory therapy.
Pearls and Other Issues
Dacryoadenitis can arise from viral, autoimmune, or idiopathic origins, requiring a comprehensive evaluation to ascertain the underlying etiology. Bilateral lacrimal gland involvement often suggests an autoimmune disorder, whereas unilateral acute cases are more commonly infectious. Imaging and biopsy are essential for distinguishing dacryoadenitis from neoplastic conditions such as lymphoma. Corticosteroids remain the primary treatment for noninfectious dacryoadenitis, though targeted biological therapy is emerging as an alternative for refractory cases.[88]
Enhancing Healthcare Team Outcomes
Managing dacryoadenitis requires an interprofessional approach involving ophthalmologists, rheumatologists, infectious disease specialists, and radiologists. Effective interprofessional communication ensures accurate diagnosis and timely intervention, reducing the risk of complications. Since dacryoadenitis is an uncommon condition, collaboration among healthcare providers facilitates appropriate diagnosis and treatment. Surgery may be necessary in select cases to obtain a lacrimal gland biopsy for diagnostic purposes.
For inflammatory dacryoadenitis that recurs after steroid tapering, consultation with a rheumatologist to assess the need for immunomodulatory therapy is often beneficial. Coordination with rheumatology and internal medicine is also recommended when extraocular symptoms suggest a systemic disease. An interprofessional team approach involving plastic specialty-certified nurses and specialist physicians for evaluation and follow-up supports optimal outcomes. Ongoing research into the molecular mechanisms of dacryoadenitis and the development of targeted therapies may further refine treatment strategies. Interprofessional collaboration and patient education remain key to improving the management and prognosis of dacryoadenitis.
Media
(Click Image to Enlarge)
Dacryoadenitis. An illustration of the eye highlighting the lacrimal system, middle and inferior turbinates, and the valve of Hasner. The images on the right depict dacryocystitis and dacryoadenitis.
Contributed by C Rowe
(Click Image to Enlarge)
Typical Dacryoadenitis. This 16-year-old female patient tested positive for COVID-19 and exhibited mild respiratory symptoms, pain with ocular movements, and diplopia when gazing to the left. Symptoms improved with a slow taper of oral prednisone.
Contributed by Prof. Bhupendra C. K. Patel MD, FRCS
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