In the evaluation of patients with acquired tearing, the first step is to assess whether epiphora (tearing caused by insufficient drainage) or lacrimation (hypersecretion of tears) is the cause of tearing. Systematic examination helps isolate the cause of acquired tearing and distinguish patients with obstruction of the lacrimal drainage system from those with secondary hypersecretion.
This chapter discuss the symptoms, clinical characteristics, causes, and management options of acquired nasolacrimal duct obstruction (NLDO).
Etiology
NLDO is the most common cause of persistent epiphora. Acquired NLDO can be classified in to two categories : primary acquired nasolacrimal duct obstruction (PANDO) and secondary acquired nasolacrimal duct obstruction (SANDO).
Primary Acquired Nasolacrimal Duct Obstruction
PANDO most frequently affects middle-aged adults and more women than men. In studies on the osseous nasolacrimal canal, it been observed that women have significantly narrower dimensions in the lower nasolacrimal fossa and middle nasolacrimal duct (NLD), as well as changes in the anteroposterior dimensions of the bony nasolacrimal canal. These changes coincide with osteoporotic changes throughout the body and may explain the higher incidence of PANDO in women. Menstrual and hormonal fluctuations and a heightened immune status have also been suggested as factors that may contribute to the disease process in lacrimal obstruction. These may explain the prevalence of NLDO in middle-aged and elderly women. Hormonal changes that bring about a generalized de-epithelialization in the body may cause the same within the lacrimal sac and duct. An already narrow lacrimal fossa in women may predispose them to obstruction by sloughed-off debris.
Secondary Acquired Nasolacrimal Duct Obstruction
SANDO may result from several causes, including infection, inflammation, neoplastic, trauma, and mechanical. Bacteria, viruses, fungi, and parasites have been implicated as underlying causes of infectious lacrimal drainage obstruction. SANDO has no sexual or age predilection.
Bacterial infection can be caused by different bacteria, such as Staphylococcus aureus, Actinomyces, Pseudomonas, Propionibacterium, Fusobacterium, Bacteroides, Mycobacterium, Chlamydia, Nocardia, Aeromonas, Enterobacter, and Treponema pallidum . Viral causes of lacrimal obstruction most commonly are seen with herpetic infection. Obstruction is due to the damage to the elastic tissue of the substantia propria as well as to the canalicular elastic tissue and/or the adherence of the inflammatory membranes to the raw epithelial surface of the canaliculus.
Fungi may obstruct lacrimal passages by forming a stone (dacryolith) or cast. This mechanical obstruction has been associated with Aspergillus, Candida, Pityrosporum, and Trichophyton .
Parasitic obstruction is unusual but is reported in patients infected with Ascaris lumbricoides, which enters the lacrimal system retrograde through the valve of Hasner.
Inflammation may be endogenous or exogenous in origin. Wegener granulomatosis and sarcoidosis are two examples of conditions that lead to obstruction caused by progressive inflammation within the nasal and lacrimal sac mucosa. Other endogenously arising inflammations associated with lacrimal obstruction are cicatricial pemphigoid, sinus histiocytosis, Kawasaki disease, and scleroderma.
Neoplasms may cause lacrimal obstruction by primary growth, secondary spread, or metastatic spread. Primary tumors of the lacrimal drainage system are relatively uncommon but may arise in the puncta, canaliculi, lacrimal sac, or NLD. Secondary spread from nearby tissues is more common than primary tumors. This most commonly involves eyelid cancers (e.g., basal cell carcinoma, squamous cell carcinoma), although spread from the maxillary antrum and the nasopharynx also have been reported. Studies have documented lacrimal obstruction from oncocytoma and cylindroma from direct extension. Metastatic spread, an exceedingly rare phenomenon, has been reported with primary sites from the breast and prostate.
Trauma may be iatrogenic in the case of scarring of the lacrimal passages after overly aggressive lacrimal probing. Iatrogenic causes of NLDO also may follow orbital decompression surgery, paranasal, nasal, and craniofacial procedures. Non-iatrogenic traumatic causes are either blunt or sharp and most commonly involve the canaliculus, lacrimal sac, and NLD. Posttraumatic dacryostenosis was found to have a frequent association with delayed treatment of facial fracture repair or bone loss in the lacrimal district.
Exogenous causes may also result in inflammatory obstruction of the lacrimal drainage system. Eye drops, radiation, systemic chemotherapy (e.g., docetaxel anhydrous [Taxotere], Sanofi-Ventis), and bone marrow transplantation are all causes of treatment-related inflammatory obstruction.
Mechanical lacrimal drainage obstruction may be due to intraluminal foreign bodies, such as dacryoliths or casts. These may be caused by infection (e.g., 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 NLDO.
Evaluation
Evaluation should include a detailed general medical history, ocular history, and exact description of the symptoms. The clinical picture of patients with acquired NLDO may include epiphora, mucoid punctal discharge with pressure on the lacrimal sac, or dacryocystitis. Painful swelling of the medial canthus is sometimes present, and in cases of nasal, sinus, or lacrimal sac tumor, bloody tears and epistaxis.
Past medical history may include inflammatory disease such as Wegener granulomatosis, sarcoidosis, ocular cicatricial pemphigoid, Kawasaki disease, scleroderma, neoplastic disease and its treatment, such as lymphoma, previous radiation treatment to the medial canthal area, systemic chemotherapy with fluorouracil, parasitic infection, facial trauma, and previous nasal or sinus surgery.
Ocular history may include dacryocystitis, recurrent conjunctivitis or ocular pemphigus, previous eye surgery (dacryocystorhinostomy [DCR] or eyelid surgery), glaucoma, and the use of antiglaucoma medications, or other topical medications.
Examination begins with evaluation of the eyelid position and blink function. The lower lid should be well opposed to the globe with good snap back tone ( Fig. 12.1 ). Punctal patency and position relative to the tear lake are assessed. Punctal discharge may indicate canaliculitis ( Fig. 12.2 ).
The lacrimal sac fossa is palpated to evaluate tenderness, to determine whether a mass is present, and to elicit reflux from the puncta. A tender lacrimal sac may be indicative of dacryocystitis ( Fig. 12.3 ). Firm canthal masses, bloody reflux from the punctum, and hypervascularity are suggestive of neoplasm. Reflux from the punctum suggests an obstruction in the lacrimal system. A significantly distended sac may not regurgitate with pressure owing to the functional valve of Rosenmüller.
Slit-lamp examination is performed to detect the presence of eyelid, conjunctival, or corneal inflammation that may be associated with hypersecretion, as well as to detect secondary infection.
When evaluating the tear meniscus, the size of the lacrimal lake, the presence of precipitated proteins, and stringy mucus may indicate an abnormal tear film. This in turn may cause reflex tearing.
Tear breakup time can be observed after fluorescein has been placed in the conjunctival cul-de-sac. The patient is asked to open the eyes and refrain from blinking. The ophthalmologist then examines the tear film using a broad beam of the slit lamp. The time before breakup should be at least 10 seconds. A more rapid tear film breakup time may indicate poor function of the mucin or meibomian layer despite an apparently sufficient amount of tears.
The mucin layer of the tear film helps spread the other layers evenly over the corneal surface. The oily layer of the tear film, secreted from the meibomian glands, helps prevent tear evaporation. Topical rose bengal and lissamine green staining can be used to evaluate corneal and conjunctival epithelium. These detect subtle ocular surface abnormalities by staining devitalized conjunctival and corneal epithelium. Fluorescein staining indicates more severe tear film malfunction with epithelial loss.
When evaluating basal tear secretion, topical anesthetic is applied and the inferior cul-de-sac is dried. A Schirmer strip is bent at the notch and placed with the short end resting on the conjunctiva and the fold crease on the eyelid margin at the lateral one-third of the lower eyelid. The strip is left in place for 5 minutes and the amount of wetting is recorded. The normal amount is approximately 10 to 15 mm. Rapid saturation of the filter strip signifies hypersecretion. However, excess secretion may occur in response to irritation from the measuring strips themselves. Serial testing should be performed to confirm this assumption. Two classic but less often performed tests are the Schirmer I and Schirmer II tests. The Schirmer I test allows the physician to evaluate both basic and reflex tearing. The Schirmer II test is used to distinguish between fatigue block (when reflex secretion is suppressed because of chronic irritation) and a lack of function of the reflex secretors circumstances.
Nasal examination may uncover an unsuspected cause of the epiphora, such as an intranasal tumor, turbinate impaction, or chronic allergic rhinitis. These conditions may occlude the nasal end of the NLD.
Diagnostic Tests
The dye disappearance test (DDT) is a noninvasive, rapid, and convenient test that is useful for assessing PANDO, functional NLDO, congenital NLDO, and canalicular laceration. The examiner instills fluorescein into the conjunctival fornix of each eye (using a drop of sterile 2% solution fluorescein solution of a moistened fluorescein strip) and then observes the tear film with the cobalt blue filter of the slit lamp. Persistence of significant dye and asymmetric clearance of the dye from the tear meniscus over a 5-minute period indicate a possible obstruction. The DDT has great value in ruling out conditions if the result is negative; if the DDT results are normal, severe lacrimal drainage dysfunction is highly unlikely. However, it does not rule out other causes of tearing, such as allergy, dacryolith, or intranasal obstruction.
The Jones I and Jones II tests have historically been used in the evaluation of epiphora and are now rarely used in clinical practice The Jones I test investigates lacrimal outflow under normal physiologic conditions, and the Jones II test determines the presence or absence of fluorescein in the irrigating saline solution fluid retrieved from the nose after irrigation in nonphysiologic conditions.
The lacrimal drainage system irrigation is performed to evaluate obstruction of lacrimal drainage system occlusion and the level of obstruction. It is usually performed immediately after the DDT. Using topical anesthesia, the lower eyelid punctum is dilated ( Fig. 12.4 ) and the irrigating cannula is placed in the canalicular system. To prevent canalicular kinking and difficulty in advancing the irrigating cannula, the clinician maintains lateral traction of the lower eyelid. Canalicular stenosis or occlusion should be noted, and if suspected should be confirmed by subsequent diagnostic probing. Once the irrigating cannula has been advanced into the horizontal canaliculus, clear saline solution is injected. Careful observation and interpretation determine the area of obstruction without additional testing. Total canalicular obstruction is suggested when it is difficult to advance the irrigating cannula and impossible to irrigate fluid. Complete blockage of the common canaliculus is suggested when irrigation passes successfully but refluxes through the upper canalicular system and no distension of the lacrimal sac is noted.
