Background
Epiphora is defined as the involuntary overflow of tears down the cheek. The clinical spectrum of epiphora ranges from the occasionally bothersome trickle to the chronically irritating overflow. Epiphora is caused by a disruption in the balance between tear production and tear drainage. The lacrimal drainage system is a continuous and complex membranous channel whose function is dependent on the interaction of its anatomy, position of the eyelids, and the physiology of tear drainage.
When faced with a patient who complains of tearing, the first step is to determine whether the epiphora is caused by an increase in lacrimation or a decrease in tear drainage. Trichiasis, superficial foreign bodies, eyelid malpositions, diseases of the eyelid margins, tear deficiency or instability, and cranial nerve V irritation may cause an abnormal increase in tear production. In the absence of these conditions, an abnormality in tear drainage is considered.
Abnormalities of tear drainage may be subdivided further into functional and anatomical disorders. Functional failure is related to poor lacrimal pump function, which may be due to a displaced punctum, eyelid laxity, weak orbicularis, or cranial nerve VII palsy. Anatomical obstruction may occur at any point along the upper and lower lacrimal drainage pathway. Congenital lacrimal obstructions are observed not long after birth, on the 1st to 3rd month of life and are the subject of another article, Nasolacrimal Duct, Congenital Anomalies.
Classification of nasolacrimal drainage obstruction
Acquired nasolacrimal duct obstructions (NLDO) are classified as primary and secondary. In 1986, Linberg and McCormick coined the term primary acquired nasolacrimal duct obstruction (PANDO) to describe an entity of lacrimal drainage disorders caused by inflammation or fibrosis without any precipitating cause. [1] Bartley proposed an etiologic classification system for secondary acquired lacrimal duct obstruction (SALDO) based on published cases. [2, 3, 4]
Pathophysiology
PANDO mainly is caused by inflammation, fibrosis, mucosal edema, vascular congestion, and stasis. [5] A systematic review by Ali and Paulsen focused on vascular theories where recurrent malfunction leads to structural epithelial and subepithelial changes that affect the behavior of perilacrimal cavernous bodies. Middle-aged and elderly females who are the most affected population, were noted to have smaller dimensions in the lower nasolacrimal fossa and middle nasolacrimal duct. [6] Some studies suggest menstrual hormonal changes bring about a generalized de-epithelialization as well within the lacrimal sac and nasolacrimal duct.
Causes of SALDO include infectious, inflammatory, neoplastic, traumatic, and mechanical disorders.
The microbiology of acquired nasolacrimal duct obstruction were reported to be more frequented with gram-positive organisms, followed by gram-negative bacteria, anaerobic bacteria and fungi. Gram-negative organisms were reported to be present in NLDO secondary to chronic dacryocystitis.(ref 64) Fungal causes have been documented, and are suspected when the patient is unresponsive to antimicrobial antibiotics. This may be secondary to chronic sinus and nasal infections. [7] Parasitic obstruction is rare but is reported in patients infected with Ascaris lumbricoides, which enters the lacrimal system through the valve of Hasner. Viral tests have isolated coronaviruses, RSV, adenovirus and SARS-CoV-2, and HSV1. [8, 9]
Inflammation may be endogenous or exogenous in origin. Wegener granulomatosis and sarcoidosis are conditions that lead to obstruction due to progressive inflammation within the nasal and lacrimal sac mucosa. Other endogenously arising inflammations reported are cicatricial pemphigoid, sinus histiocytosis, Kawasaki disease, and scleroderma. Exogenous causes of lacrimal drainage obstruction are chronic use of some anti-glaucoma drops, radiation, systemic chemotherapy, and bone marrow transplantation. The use of Iodine-131 I(131) for thyroid carcinoma is associated with a 3.4% incidence of documented NLDO and an overall 4.6% incidence of documented or suspected obstruction. Weekly use of docetaxel therapy used for metastatic breast cancer and non-small cell lung cancer has been reported to be associated with canalicular and nasolacrimal duct obstruction.
Neoplasms resulting in chronic nasolacrimal duct obstruction occur in 4.6% of cases and were unsuspected before surgery in 2.1% of patients. [10] These may cause lacrimal obstruction by primary growth, secondary spread, or metastatic spread. Primary neoplasms may arise in the puncta, canaliculi, lacrimal sac, or nasolacrimal duct. Lacrimal sac biopsies in acquired NLDO revealed adenoid cystic carcinoma, eccrine spiradenoma and small B-cell lymphoma. [11] Secondary spread from nearby tissues is more common than primary tumors. They are most commonly eyelid carcinomas, maxillary antrum tumors, and the nasopharynx tumors. Rare cases of a nasal oncocytoma, medial canthal cylindroma, and necrotizing sialometaplasia of the lacrimal sac [12] have caused nasolacrimal duct obstruction from direct extension. Metastatic spread, an extremely rare phenomenon, has been reported with primary sites from the breast and prostate.
Naso-orbitethmoidal fractures are the most common etiology for traumatic nasolacrimal duct obstruction. [13, 14] HIgh-velocity blunt injuries from motor vehicle accidents commonly involve the whole lacrimal drainage system. Delayed treatment of postraumatic facial fractures also may cause stenosis or bone loss in the lacrimal district. Scarring of the lacrimal passage after frequent overly aggressive lacrimal probing may be an iatrogenic cause of trauma. Iatrogenic NLDO also may follow orbital decompression surgery, paranasal, nasal, and craniofacial procedures.
Mechanical lacrimal drainage obstructions may be due to intraluminal foreign bodies, such as dacryoliths or casts. These may be caused by infection (eg, Actinomyces, Candida) as well as long-term administration of topical medications. Mechanical obstruction also may be caused by external compression from rhinoliths, nasal foreign bodies, or mucoceles. Dentigerous cyst in the maxillary sinus has been reported to have caused nasolacrimal duct obstruction.
Epidemiology
Frequency
United States
Nasolacrimal drainage obstruction is relatively common, but the exact frequency is not known.
International
Worldwide incidence is unknown.
Mortality/Morbidity
Epiphora can be a nuisance. If untreated, nasolacrimal duct obstruction can cause significant problems.
Race
No predilection to race has been established.
Sex
PANDO is more prevalent in women. SALDO has no predilection to gender.
Age
Previous studies have noted a high incidence of PANDO in individuals aged 50-70 years.
Prognosis
Surgical treatment provides resolution of primary acquired nasolacrimal duct obstruction in 85-99% of cases.
Both external dacryocystorhinostomy and endoscopic laser dacryocystorhinostomy have success rates higher than 90%; external dacryocystorhinostomy is slightly more successful.
Patient Education
Patients should be aware that epiphora caused by nasolacrimal duct obstruction is surgically treatable. Early recognition of secondary causes may provide the patient with more conservative treatment options.
Explain the following to the patient:
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Normal lacrimal drainage process
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Level of obstruction of lacrimal drainage passageway
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Possible diagnostic tests that may be necessary to evaluate the condition and their possible results
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Treatment guidelines and options
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If surgery is necessary, discuss the prognosis and possible intraoperative and postoperative complications.
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Dacryocystitis of the left nasolacrimal system.
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Dacryocystogram. A patent nasolacrimal system on the right side of a patient and a blocked system on the contralateral side at the level of the nasolacrimal duct.
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Endoscopic laser-assisted dacryocystorhinostomy. Courtesy of Jorge G Camara, MD, University of Hawaii John A Burns School of Medicine.
