1 s2.0 S001150292030105X Main
1 s2.0 S001150292030105X Main
1 s2.0 S001150292030105X Main
Disease-a-Month
a r t i c l e i n f o
Keywords:
Epiphora
Nasolacrimal Duct Obstruction
Tearing
Lacrimal Duct
Introduction
Epiphora is the overflow of tears, which may occur due to overproduction by the lacrimal
gland or a blockage of the lacrimal drainage system. The lacrimal secretory and drainage sys-
tem is responsible for maintenance of a lubricated ocular surface. The lacrimal drainage system
empties tears produced by the lacrimal gland into the nose. When not functioning properly, the
tears tend to build up in the eye, causing excessive tearing or even infection. This article will
focus on the diagnosis and management of nasolacrimal duct obstruction (NLDO).
∗
Corresponding author at: Department of Surgery, Northshore University HealthSystem, 2050 Pfingsten Rd., Ste. 280,
Glenview, IL 60026, United States.
E-mail address: pphelps@northshore.org (P.O. Phelps).
https://doi.org/10.1016/j.disamonth.2020.101043
0011-5029/© 2020 Elsevier Inc. All rights reserved.
2 E. Avdagic and P.O. Phelps / Disease-a-Month 66 (2020) 101043
Nasolacrimal anatomy
The nasolacrimal drainage system begins with the upper and lower punctum, which are
openings on the mucous membrane portion of the posterior lamella of the eyelid (Fig. 1). These
openings extend into the upper and lower ampulla, which measure approximately 2 mm in
length. The drainage system then sharply angles at approximately 90° and continues as the up-
per and lower canaliculi for another 8 mm until merging to form the common canaliculus.1 The
common canaliculus extends another 3–5 mm before it drains into the lacrimal sac. The lacrimal
sac is approximately 10–15 mm in length and located in the fossa positioned between the an-
terior and posterior lacrimal crest. The anterior crest is formed by the frontal process of the
maxilla, while the lacrimal bone forms the posterior crest. The lacrimal sac subsequently forms
the nasolacrimal duct, which is another 12–18 mm in length. Its intraosseous portion of the na-
solacrimal duct (called the nasolacrimal fossa) is about 12 mm in length. The soft tissue portion
of the nasolacrimal duct extends approximately 5 mm inferior to the bony septum. The distal
end of the duct enters the inferior meatus and is covered by a mucosal fold known as the valve
of Hasner. The valve functions to prevent reflux of air from the nose.1
The lacrimal pump functions via a positive and negative pressure system involving a cycle
of eyelid opening and closure to maintain lubrication of the eye and excrete excess tears into
the nasal sinus. In the relaxed state, the lacrimal puncta lie within the lacrimal tear lake. This
is an area along the medial portion of the lower eyelid where tears collect with gravity when
the head is elevated. At this time in the cycle the lacrimal sac is filled with tears. Eyelid closure
promotes contraction of the pretarsal orbicularis muscle, which closes the puncta and canali-
culi. The preseptal orbicularis fibers insert into the sac and compress it, thus creating a positive
pressure mechanism that then propels the tears through the duct. Eyelid opening then relaxes
E. Avdagic and P.O. Phelps / Disease-a-Month 66 (2020) 101043 3
the orbicularis, causing the puncta and lacrimal sac to open, now creating negative pressure that
then draws tears into the canaliculi and lacrimal sac.2
Clinical presentation
Nasolacrimal duct obstruction can be caused by either congenital or acquired etiology. Both
acquired and congenital obstruction of the nasolacrimal duct can result in tear stasis within the
lacrimal sac. The patient typically first notes excessive tearing, pooling of the tear lake, and a
mucopurulent discharge. In certain instances, tear stasis can result in the development of an
infectious process, such as dacryocystitis, or inflammation of the lacrimal sac.3 Acute dacry-
ocystitis tends to present as localized swelling, pain, and erythema in the medial canthal area.
The area is typically very tender to palpation, and the clinician may express a mucopurulent
discharge with massage along the medial canthal area. The discharge may also be expressed
spontaneously, causing the patient to experience the eyelids being “glued shut” after extended
periods of sleep.1 , 3 A patient can also present with chronic dacryocystitis as a consequence of
nasolacrimal stenosis and subsequent obstruction. Chronic dacryocystitis tends to present as a
palpable, yet nontender mass. Intermittently, it may present with episodic occurrences of acute
dacryocytitis.1
Diagnosis
in the nares. An absence of dye on the cotton tip indicates either a partial or complete obstruc-
tion of the lacrimal drainage system.1 , 3
In addition, the clinician should also examine the nares to evaluate for signs of possible ob-
struction in the distal region of the duct. It is also important to make note of the presence of
bloody tears. A bloody discharge may indicate the development of a lacrimal sac tumor. In cases
in which a tumor is suspected, the clinician should perform computed tomography and refer to
an oculoplastic surgeon for an excisional biopsy.1
Nasolacrimal duct obstruction is commonly seen in pediatric patients. The condition is usu-
ally present since birth, secondary to a failure of canalization of the nasolacrimal duct. The ob-
struction most commonly occurs at the valve of Hasner, the area where the nasolacrimal duct
enters the nose. Recent research demonstrates the obstruction can be caused by persistence of
a membrane, narrowing of the inferior meatus, or due to bony obstruction.4
As expected, the obstruction will lead to an overflow of tears in the newborn. The parents
will note excessive tearing either in one or both eyes, which typically leads to matting of the
eyelashes. Further overgrowth of bacteria in the obstructed duct will lead to crusting of the
lashes and the expulsion of a mucopurulent discharge onto the eyelids.4 A dye disappearance
test is a rapid and efficient way to confirm obstruction in the newborn population. The vast ma-
jority of infants with symptomatic congenital NLD obstruction will have complete spontaneous
resolution by the age of one.4–6
A select number of cases will lead to an overgrowth of bacteria within the obstructed naso-
lacrimal duct, causing not only an overflow of mucopurulent discharge, but conjunctival injec-
tion with possible conjunctivitis or even dacryocystitis. Dacryocystitis will present as an acute
infection of the lacrimal sac and may proceed to cellulitis of the surrounding skin. These pa-
tients should be promptly treated with systemic antibiotics.4 Once the infection has resolved,
the infant should have nasolacrimal duct probing to prevent a recurrence of infection.
Acquired nasolacrimal duct obstruction presents later on in life and can be categorized into
primary or secondary acquired obstruction. Tearing tends to be the most common presenting
symptom. As discussed above it is important for the clinician to determine whether the tearing
is due to nonobstructive causes such as hypersecretion (most often caused by dry eye or ble-
pharitis) or lacrimal pump failure (ectropion or lid laxity). The nasolacrimal duct is the most
common area of primary acquired duct obstruction in adults.3 , 7 , 8 This type of NLDO tends to
occur most commonly in women around the fifth or sixth decade.3 Although still controversial,
the narrower and longer nasolacrimal canal observed in women is believed to contribute to the
higher occurrence in this population.3 , 10 , 11 , 12
Acquired nasolacrimal duct obstruction or stenosis is typically associated with excessive tear-
ing or a mucopurulent discharge. As previously discussed, the duct stenosis leads to a lack of
tear drainage from the lacrimal sac. This tear stasis is a nidus for infection, eventually leading to
a chronic infectious process with an accumulation of mucopurulent material, swelling, pain, and
erythema near the medial canthal area.1 , 13
The underlying pathophysiology of acquired nasolacrimal duct obstruction can be classified
into primary or secondary. Primary obstruction tends to be associated with a fibroinflamma-
tory process.3 Biopsies analyzed during routine dacryocystorhinosotomy cases have shown the
presence of obstructive fibrosis as a consequence of chronic lymphoplasmacytic inflammation.
The degree of inflammation also appeared to correlate with the extent of the obstruction and
duration of clinical symptoms.3 , 15
E. Avdagic and P.O. Phelps / Disease-a-Month 66 (2020) 101043 5
Secondary nasolacrimal duct obstruction can occur due to a variety of acquired causes that
can result from inflammatory, traumatic, mechanical, or infectious etiology.3 , 9 , 16 , 17 In the adult
patient trauma or iatrogenic manipulation can frequently cause nasolacrimal duct stenosis and
obstruction due to the proximity of the nasolacrimal duct to the paranasal sinuses.1 , 15 In partic-
ular, the nasal and maxillary bone may cause obstruction.1 , 18 , 19
Acute and chronic dacryocystitis represents a well-known cause of secondary NLD obstruc-
tion. Acute dacryocystitis tends to present as partial or complete obstruction of the duct, and
typically occurs secondary to acute bacterial infection, most commonly—Staphylococcus aureus
and epidermidis, various species of Streptococcus, Pseudomonas, Hemophilus influenzae and
other bacterial species. Fungal infection by species, such as Candida and Aspergillus can also
cause dacrocystitis.3 , 20
Histologic specimen of acute dacryocystitis tend to display epithelial inflammation in associ-
ation with a combination of cell necrosis and proliferation.3 In contrast, chronic dacryocystitis
tends to present with a protracted clinical course manifested by inflammation and indolent in-
fection of the lacrimal sac. In contrast to acute dacryocystitis, it is less destructive. Histologic
samples show thickening of the lacrimal sac along with distention of its lumen and folds within
the mucosa. The stroma tends to present with a lymphoplasmacytic infiltrate.3
The clinician should inquire about a prior medical history of eyelid trauma or surgery, sinus
disease, head and neck malignancy, radiation and facial nerve palsy. Facial nerve palsy may be a
significant cause of excessive tearing secondary to aberrant regeneration of facial innervation.3
This condition may lead to orbicularis weakness, further producing an ectropion and functional
epiphora due to lacrimal pump failure.3 Additional causes of outflow obstruction should be ex-
plored, such as a history of chemotherapy, radiation, vasculitis, lymphoma, sarcoidosis, ocular
cicatricial pemphigoid, and scleroderma.3
Hypertrophy of the inferior turbinate deviated nasal septum, rhinoplasty, nasal polyps, nasal
tumors, and intranasal foreign bodies can also cause NLDO.1 , 21 Temporary causes include
paranasal sinus infections. Patients with bloody discharge or bloody tearing should be evalu-
ated for a possible neoplastic process, especially if a hard lesion is palpated above the medial
canthal tendon.
Treatment
The treatment of nasolacrimal duct obstruction (NLDO) involves either restoring the natu-
ral path of lacrimal flow or establishing a new channel, depending on the state of the anatomy.
The treatment of congenital and acquired nasolacrimal duct obstruction differs. Congenital NLDO
tends to spontaneously resolve by the first year of life. Initial management involves topical mas-
sage of the medial canthus and topical antibiotics.3 , 4 Massage is performed by applying pressure
in a downward manner on the medial canthus to produce a hydrostatic pressure that may lead
to opening of the obstruction at the valve of Hasner.4 However, nasolacrimal duct probing is the
first-line treatment in cases that do not resolve on their own. The recommendation is to delay
probing until 6–12 months of age due to the high rate of spontaneous canalization.3 The pro-
cedure has a high success rate when performed within the first one to two years of life. Under
general anesthesia, the puncta are dilated, and the lacrimal sac is further cleaned by massage
and irrigation with saline. The pressure from the irrigation can overcome the obstruction caused
by an imperforate valve or debris. If not successful, the surgeon can then proceed to apply a
probe into the lower canaliculus and follow the anatomy of the nasolacrimal duct to attempt to
unblock the obstruction. In cases of failed probing, balloon dacryoplasty with silicone stenting of
the lacrimal system may be successful.22 The last resort in cases of congenital NLDO is surgical
treatment described below.
Acquired NLDO may initially involve a more conservative approach such as use of topical or
oral antibiotics and anti-inflammatory medication. Severe or chronic infections may require the
use of systemic antibiotics prior to considering procedural manipulation.3 Office based canalicu-
lar probing and irrigation procedures are also commonly initially pursued.
6 E. Avdagic and P.O. Phelps / Disease-a-Month 66 (2020) 101043
Nonetheless, in contrast to congenital NLDO, primary acquired NLDO usually does not re-
solve with probing. The treatment of choice for primary NLDO is a surgical procedure called
dacryocystorhinostomy. In this procedure a new passageway is created between the lacrimal
duct and the nose. This can be done through an external or endoscopic approach. The lacrimal
system (canaliculus and neo-ostium) is typically intubated with a silicone stent for 6 weeks to
3 months after the procedure to reduce the probability of re-stenosis of the lacrimal system. If
there is not a patent canaliculus, conjunctivodacryocystorhinostomy can be considered. This is
an advanced treatment that involves the placement of a Pyrex glass Jones tube from the medial
lacrimal cul de sac and into the nose.3 This surgical treatment involves long term follow up for
irrigation and maintenance of the Jones tube.
In summary, NLDO is a common condition which can cause a variety of symptoms from tear-
ing to acute infection of the lacrimal sac. Identification of these symptoms by the primary care
provider and proper referral to the ophthalmologist or oculoplastic specialist can expedite proper
treatment of these conditions.
Disclaimers/sources of support
None.
Acknowledgments
We thank Mira Shiloach, MS, CCRP for her edits and Mary Callahan for her medical illustra-
tion.
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