Functional epiphora represents tearing in the context of patent irrigation. The more specific definition includes an absence of dry eye signs, hypersecretion, or eyelid abnormalities. Yet something isn’t functioning or the patient wouldn’t complain of tearing. The problem is that we don’t know what isn’t functioning in many of these patients.

I prefer the term dys functional epiphora for several reasons, including: 1) the term “functional” implies that the lacrimal outflow system is working, which, at least in some cases, it is not; 2) the term “dysfunctional” alerts the clinician to search for a specific anatomic or physiologic abnormality; and 3) to be only somewhat humorous, “dysfunctional” often describes the relationship between patient and surgeon after failed surgery. I begin the conversation with my patients by explaining, “This type of tearing is frustrating to live with,” and as they nod their heads in agreement, I add, “And challenging to treat.”

Calling epiphora “functional” in the setting of patent irrigation contradicts the fact that something isn’t working right to produce it. The term almost admits defeat in that it hinges on the results of irrigation, a severely inadequate test, to determine functionality of the drainage system. Just because the system is patent to forceful irrigation doesn’t mean it is functioning at all under normal circumstances. The term “functional nasolacrimal duct obstruction” carries similar contradictions, and may have an even more prejudicial effect on the clinician’s thinking than “functional epiphora” in that it presupposes the anatomic location of the problem to reside within the nasolacrimal duct. Both terms may lead to cognitive errors, such as “anchoring” and “satisfaction of search.” In this setting, “anchoring” could lead the clinician to proceed down a path of investigation that assumes a normal nasolacrimal outflow system, and “satisfaction of search” could allow neglect of other findings that could indicate more than one pathologic process at work.

Calling epiphora dys functional tells us that we must still search for a cause both in the individual patient and through future study. Dysfunctional epiphora should be defined as epiphora attributable to an unclassified lacrimal outflow abnormality in the setting of patent irrigation. As we elucidate more subtle outflow abnormalities, the diagnosis should dwindle.

Regardless of what we call epiphora occurring with patent irrigation, it is clear that the causes are not completely or accurately characterized and that in some patients no therapy seems to adequately address the epiphora. Our ability to correctly identify and treat the underlying abnormality is limited by current diagnostic methods and by our understanding of tear drainage system physiology.

Current diagnostic methods include biomicroscopy, dye disappearance testing, irrigation/Jones testing, and dacryocystography/scintigraphy. Each provides some information, but not even together do they adequately describe the steady state of a tear production and drainage system. If dysfunctional epiphora is a wastebasket term that includes varied etiologies of epiphora, the first step must be to shrink the wastebasket and eliminate causes not attributable to unclassified lacrimal outflow abnormalities.

Many patients with dysfunctional epiphora have a subtle abnormality of the ocular surface, eyelid, or lacrimal system that underlies the tearing. The clinician must methodically eliminate other possible causes before determining that epiphora is “physiological.” Conditions causing reflexive hypersecretion should be investigated, including dry eye syndrome, rosacea, exposure, conjunctivochalasis, prominent globes, and rhinitis. Nasal speculum examination represents an integral component in the evaluation of the patient with epiphora. The eyelids should be evaluated for subtle signs of eyelid malposition, such as mild ectropion, punctal dystopia, stenosis, signs of previous eyelid surgery, mild seventh nerve dysfunction, and mild lagophthalmos.

Other patients suffer from partial obstruction that the clinician can sometimes infer from dye disappearance testing and irrigation/Jones testing. Some patients suffer from a combination of ocular surface disease and partial obstruction. The two may in fact be causally related in some cases given the dynamism of the production/drainage apparatus and the anatomic continuity and similarity of the ocular surface and lacrimal passages. Surely the lacrimal drainage system participates in the feedback loops of the lacrimal functional unit. Negative feedback loops regarding tear film osmolality in cases of nasolacrimal duct obstruction have already been proposed.

The etiologies of dysfunctional epiphora that remain after careful biomicroscopic examination, dye disappearance testing, and irrigation/Jones testing can be classified into broad categories that include subtle partial duct obstructions, tear pump failure, and other dynamic failures. Though we like to think of drainage system abnormalities as being either pre-sac or post-sac, there is likely significant overlap in this simplified scheme. The dye disappearance test and tear meniscus height do not distinguish between these etiologies. Jones testing possesses high false-positive and false-negative rates. Dacryoscintigraphy and dacryocystography may contribute in select cases if available. However, dacryoscintigraphy doesn’t allow high enough resolution to show the precise anatomic location of a stricture, and dacryocystography involves administering dye under nonphysiologic conditions.

So what should we offer our patients with dysfunctional epiphora when our dysfunctional understanding hasn’t led to an obvious etiology? The surgical options are few and haven’t significantly changed in decades : horizontal eyelid tightening, silicone intubation, and dacryocystorhinostomy (DCR).

Horizontal eyelid tightening may diminish the epiphora in some patients, possibly by improving the pump mechanism. While preoperative eyelid taping may modestly improve predictability of success, we have better odds at predicting which patients may fail—that is, those with no laxity, those with prominent globes, or those with severe actinic or other skin changes producing insufficiency of the anterior lamella. Horizontal eyelid tightening may worsen some types of valve mechanism–induced epiphora, and most tightening procedures involve lacerating the lateral orbicularis sphincter, which could also adversely affect the pump mechanism.

Silicone intubation may treat partial obstructions or subtle pump/valve abnormalities. The tubes may increase the effective diameter of the system to reduce resistance to tear outflow. Double stents have been reported to improve partial obstructions and theoretically may exponentially decrease the outflow resistance compared to a single tube. The stents may confer improvement after removal because of a “riverbed” phenomenon whereby increased flow maintains the passageway. Given that a significant portion of the common canaliculus resides within the lacrimal sac wall, it is possible that silicone tubes may straighten or otherwise alter morphology at these valve structures to decrease outflow resistance. In this regard, a circular bicanalicular stent could produce different valve changes than an intranasal stent. However, silicone intubation can result in granuloma formation, which could worsen epiphora. The tubes also represent a substrate for bacterial growth, which could cause inflammatory narrowing of the duct lumen. The recent demonstration of bacterial biofilms in culture-negative tubes may reveal further adverse consequences of silicone intubation. Finally, scant data exists to guide stent retention interval.

Dacryocystorhinostomy should easily treat at least that subset of dysfunctional epiphora attributable to partial duct obstructions. Yet even here the results perplex us, as they are significantly worse than for treatment of complete duct obstruction. This suggests overlap of mechanisms even in cases of so-called partial duct obstruction. Interestingly, an external approach seems to give better results in this setting than an endoscopic approach, even though both approaches should effectively bypass a partial duct obstruction. This could be attributable to well-known factors such as the size of the osteotomy and construction of mucosal flaps. However, a recent study showing better postoperative dye clearance after suturing the lacrimal diaphragm to the periosteum in external DCR suggests that the dissection, manipulation, and repair of the structures violated during external DCR may impact function of the tear pump in ways not yet elucidated.

Published success rates vary widely for each of these surgeries given the lack of standard inclusion criteria or outcome measures. However, each seems to provide long-term success in a limited majority of patients at best, and each incurs at least theoretical chances of worsening the epiphora in some patients. Our imperfect understanding of the factors causing normal and abnormal lacrimal outflow limits current treatment results.

Despite these limitations, we can successfully determine and treat the dysfunction in a majority of cases. Once epiphora in the setting of patent irrigation is determined, the clinician should return to the history and physical examination, including detailed slit-lamp examination and nasal speculum examination, to specifically eliminate the myriad causes of epiphora not attributable to “dysfunctional epiphora.” If physical examination does not reveal any subtle structural abnormalities such as punctal or canalicular stenosis, lower eyelid malposition, prominent globe, or mild seventh nerve paresis, then a low threshold for treatment of ocular surface conditions or nasal conditions that could produce hypersecretion should be considered. Epiphora that remains can be divided into three main causes: subtle partial duct obstructions, tear pump/valve failures, and other dynamic failures. A multifactorial etiology should also be considered. Repeated irrigation with careful attention to increased resistance or reflux through the opposing punctum may suggest a partial obstruction. Completely free irrigation suggests a tear pump failure or multifactorial etiology. Lacrimal scintigraphy or dacryocystography may confirm the diagnosis but will rarely guide management. Ultrasound biomicroscopy may reveal a canalicular stone in proximal obstructions, but physical examination should reveal this as well.

Silicone intubation represents a good first surgical option for most patients with presumed partial obstruction or tear pump failure, because intubation carries less morbidity than DCR, and early success rates may be over 90%. Adjunctive balloon dacryoplasty in cases of presumed partial obstruction attempts to engage the “riverbed” phenomenon, though the data supporting its use in this setting are admittedly weak. Adjunctive horizontal eyelid tightening in cases of presumed tear pump failure may slightly improve success rates in patients motivated to relieve epiphora at one surgical setting, even in patients with no demonstrable horizontal eyelid laxity. Double silicone tubes and wider silicone tubes can be used in cases of late recurrence, as can DCR. In cases with greatly increased resistance or significant reflux through the opposing punctum on irrigation, forgoing silicone tubes and proceeding directly to DCR seems reasonable, depending on patient commitment to greater surgical intervention.

Unfortunately, despite many reasonable algorithms to treat that subset of patients with epiphora in the setting of patent irrigation, surgical failures often occur. Advances to improve characterization of this type of tearing and its treatment will come from a better understanding of lacrimal microanatomy and physiology and innovations in instrumentation and wound healing manipulation. Lacrimal canalicular/duct endoscopy represents a powerful tool, still in its infancy, to improve diagnostic and surgical accuracy. Nanotechnology will offer changes in intubation materials and surfaces to improve their effects. Lacrimal stents impregnated with antimetabolites, anti-inflammatory agents, and other biologic agents will address the causes of obstruction on a cellular level. More accurate devices to measure lacrimal resistance may identify cases of subtle partial obstruction to guide treatment. Advances in microanatomy will reveal subtle causes of epiphora that still elude us, which will aid in designing new therapies. Until then, however, the lacrimal surgeon must admit a dysfunctional understanding leading to dysfunctional surgery in many patients with dysfunctional epiphora.