Major Review
The BLICK Mnemonic for Clinical–Anatomical Assessment
of Patients With Epiphora
David T. Tse, M.D., Benjamin P. Erickson, M.D., and Brian C. Tse, M.D.
Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine,
Miami, Florida, U.S.A.
Purpose: Evaluation of the tearing patient is often distilled
to a search for ocular surface problems causing reflex
hypersecretion versus lacrimal drainage problems. The literature
does not typically emphasize conditions affecting the function
of the tear distribution system, but neglect of these important
factors can lead to suboptimal treatment outcomes. The intent
of this review is to provide a systemic evaluation of frequently
overlooked conditions that can influence the distribution system
and to offer a mnemonic to ensure an orderly sequence of
inspection during clinical examination.
Methods: Review of clinical literature and experience from
1957 to 2014.
Results: Tearing complaints attributable to problems with the
distribution system can be evaluated, classified, and managed
according to the mnemonic BLICK, which stands for Blink
dynamics, Lid malposition, Imbrication, Conjunctivochalasis,
and Kissing puncta.
Conclusion: The BLICK mnemonic is a useful adjunct to the
workup of epiphora.
(Ophthal Plast Reconstr Surg 2014;30:450–458)
T he lacrimal system comprises 3 integrated components that
are responsible for the production, distribution, and drain-
age of tears. The autonomically innervated lacrimal gland and
the accessory glands of Krause and Wolfring secrete the aque-
ous components of the tear film. Along with lipid from the mei-
bomian glands and mucin from the conjunctival goblet cells,
this aqueous component creates a protective film that prevents
corneal desiccation and optimizes refraction.1,2 While once
conceptualized as occupying discrete layers, the components
interact dynamically according to molecular size, tonicity,
concentration, and charge. These compositional factors, along
with the hydrodynamic factors of eyelid blinking and eyelid
closure, are essential for maintaining a stable precorneal tear
film (Table 1).
Periodic blinking distributes tears across the ocular
surface and propels them along the eyelid margin, toward the
Accepted for publication July 9, 2014.
Supported in part by National Institutes of Health Center Core Grant
P30EY014801; Research to Prevent Blindness Unrestricted Grant, Inc., New
York, NY, U.S.A.; Plum Foundation, Los Angeles, CA, U.S.A. and the Dr.
Nasser Ibrahim Al-Rashid Orbital Vision Research Fund. The sponsor or
funding organization had no role in the design or conduct of this research.
The authors have no financial or conflicts of interest to disclose.
Address correspondence and reprint requests to David T. Tse, M.D.,
Bascom Palmer Eye Institute, University of Miami Miller School of Medicine,
900 N.W. 17th Street, Miami, FL 33136. E-mail: dtse@med.miami.edu
DOI: 10.1097/IOP.0000000000000281
450 Ophthal Plast Reconstr Surg, Vol. 30, No. 6, 2014
puncta at the medial canthus for clearance. The lacrimal excre-
tory system then drains tears from the lacus lacrimalis into the
nasal passages via a pump mechanism driven by dynamic alter-
ations in orbicularis tone.3–10 Proper eyelid closure preserves the
precorneal tear film by minimizing evaporation.
Conditions that alter this complex interplay of anatomy
and physiology result in symptomatic epiphora. Clinical distinc-
tion between anatomic and physiologic dysfunction and accurate
localization of anatomical defects are essential to appropriate
treatment. There are a number of reviews of the diverse condi-
tions that can create an imbalance of tear production and tear
drainage.11,12 Frequently, the evaluation of a tearing patient is
conceptualized as a search for “ocular surface problems” ver-
sus “drainage problems.” While the metaphor of the “kitchen
sink” may be helpful in explaining to patients an imbalance
due to tear over-production or reflex hypersecretion (the faucet
turned too high)13 or tear drainage delay (a blocked drain),11,12
this mental shortcut may result in the neglect of important but
under-recognized causes of tearing attributable to the distribu-
tion system—the sink itself. The subject of tearing is broad; an
exhaustive discussion is beyond the scope of any single review,
and will likely eclipse the simple message this manuscript is
trying to convey. The intent of this article is to focus on causes
of tearing specifically related to abnormalities in the lacrimal
distribution system. The authors believe that reflex hypersecre-
tion resulting from aqueous tear deficiency and evaporative tear
deficiency have been well covered in other commonly available
references,14 and do not wish to stray too far from their stated
purpose.
For the most part, the conditions affecting the tear dis-
tribution system have not been well emphasized in the lit-
erature. In this review, the authors aim to provide a systemic
evaluation of frequently overlooked conditions that can influ-
ence the tear distribution system, and to offer a mnemonic to
ensure an orderly sequence of inspection during the examina-
tion of a patient complaining of epiphora. Their intention is
not to suggest that the average ophthalmologist has an overly
simplistic view of tearing, but rather to suggest a concise
mnemonic-guided approach to looking at causes that—in their
experience—are under-represented in the current literature and
sometimes under-recognized in busy clinical practice. This
mnemonic—BLICK—stands for Blink dynamics, Lid malposi-
tion, Imbrication, Conjunctivochalasis, and Kissing puncta.
TEAR DISTRIBUTION SYSTEM: EYELID
ANATOMY AND TEAR PHYSIOLOGY
The tear distribution system consists of the eyelids and the tear
meniscus that extends along the lower eyelid margin. Proper
tear film circulation across the corneal surface requires normal
dynamic eyelid movement—each blink cycle involves the upper
eyelid acting like a windshield wiper, moving downward to
Ophthal Plast Reconstr Surg, Vol. 30, No. 6, 2014 The BLICK Mnemonic for Epiphora Evaluation
TABLE 1.  Requisites for a stable precorneal tear film
Compositional factors
 Mucin Ocular surface epithelia
 Aqueous Main and accessory lacrimal
glands
 Lipid Meibomian and Zeiss glands
Hydrodynamic factors
 Eyelid blinking Tear distribution
Tear clearance
 Eyelid closure Evaporative loss prevention
Anatomical requisites
 Functional neuromuscular unit
 Strong canthal tendon anchoring
 Appropriate lower eyelid position
touch the lower eyelid margin and to pick up the tear meniscus
for vertical distribution. Contraction of the pretarsal and prese-
ptal orbicularis muscle results in a lateral to medial narrowing
of the palpebral fissure, which spreads the tear film, replenishes
areas of dryness, adds fresh lipids and glycoproteins to the
secreted aqueous component, and removes debris from the ocu-
lar surface. This dynamic process results in a vertical distribu-
tion of tears with net movement of the tear meniscus towards the
lacrimal drainage system. Here, the puncta conduct tears into
the ampullae of the canaliculi.
Dynamic narrowing of the palpebral fissure is dependent
on the concentrically arranged fibers of the orbicularis oculi,
which are innervated by cranial nerve VII. The palpebral (pre-
tarsal and preseptal) portions of orbicularis muscle are princi-
pally involved in involuntary blinking, while the orbital portion
is responsible for forceful eyelid closure (e.g., winking and
blepharospasm). Firm anchoring of the medial and lateral can-
thal tendons is required to generate adequate contractile tension
to complete the blink cycle.15
The tear distribution system is intimately linked to the
lacrimal pump. While this is technically a tear drainage mecha-
nism, upstream deficits in the distribution system profoundly
influence its function. Historically, the 2 most prominent lacri-
mal pump theories have been those of Jones4,5 and Rosengren.6
There is agreement that eyelid closure results in compression of
the canaliculi with movement of tears into the lacrimal sac.4–6
These models diverge, however, in their understanding of how
eyelid movement impacts subsequent alterations in pressure
within the lacrimal sac.6,7 Jones4,5 believed that contraction of
the orbicularis then creates a negative pressure, sucking tears
into the sac. In contrast, Rosengren6 suggested that this con-
traction largely serves to force tears into the nasolacrimal duct.
To date, a preponderance of evidence supports the Rosengren
model, though subsequent refinements have been made.9
Using high-speed cinematography, Doane9 contributed
significantly to the authors’ understanding of the mechanisms of
blinking and tear drainage. He posited the following sequence of
events in a blink cycle: At the start of a blink, the lacrimal drain-
age passages already contain tear fluid that entered following
the previous blink. As the upper eyelid descends, the papillae
containing the punctal openings elevate from the medial eye-
lid margin. When the lids are half closed, the papillae meet the
opposing eyelid margin, which effectively occludes the puncta
and prevents fluid regurgitation. Further orbicularis contraction
squeezes the canaliculi and sac, forcing out the contained fluid
via the nasolacrimal duct. With complete eyelid closure, the sys-
tem is compressed and largely empty of fluid.
At the beginning of the opening phase of a blink, the
puncta are still occluded and the valve of Rosenmuller acts to
© 2014 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc. 451
prevent re-entry of fluid or air from the nose. While not a valve
in the true anatomic sense, analysis of cadaveric specimens sug-
gests that the acute angle at which the common canaliculus enters
the lacrimal sac does function to prevent egress.16 As compres-
sion abates, the elastic walls of the passages expand to their rest-
ing configuration. This recoil generates a partial vacuum within
the canaliculi and sac. Suction holding the peripunctal eyelid
margins together is released when the eye is approximately two
thirds open. The punctal papillae suddenly “pop” apart, open-
ing the canaliculi to fluid ingress. The blink cycle then repeats.
The anatomical requisites for this mechanism of tear drainage
are that the punctal papillae are apart at the start of a blink, the
lower eyelid has normal position and tone, and the neuromus-
cular unit (seventh cranial nerve-orbicularis muscle) is intact.
More recently, Becker10 proposed a tricompartmental
model of the lacrimal pump based on video analysis, which is
closely aligned with that of Rosengren6 and Doane,9 but var-
ies slightly in its description of lacrimal sac movement during
the blink cycle. According to this model, contraction of the
deep head of the preseptal orbicularis pulls the superior lacri-
mal sac laterally. This creates negative pressure, drawing tears
into the sac. The valve of Rosenmüller prevents retrograde flow
into the canalicular system. Simultaneously, retropulsion of the
globe and orbital soft tissues induced by orbicularis contrac-
tion increases peri-lacrimal pressure, which compresses the
inferior sac to propel tears down the nasolacrimal duct. When
the orbicularis relaxes, the canaliculi open and the upper sac
moves medially, creating a negative intracanalicular pressure
that draws tears into the lacrimal ampullae.
Familiarity with the complex anatomy and physiology
of tear clearance is critical to evaluation of the tearing patient
and therapeutic strategies must respect these underlying prin-
ciples in order to succeed. The BLICK mnemonic can assist the
clinician in systematically considering all potential sources of
impaired tear distribution (Table 2).
A mental checklist of questions should emerge when
examining a tearing patient:
1. Is innervation to the orbicularis intact?
2. Are there signs of a neurodegenerative disorder affecting
blink frequency?
3. Does the upper eyelid touch the lower eyelid margin with
each blink?
4. What is the lower eyelid position?
5. Is the eyelid skin pliant?
6. Are the canthal tendons appropriately anchored?
7. Is the tear meniscus appropriately positioned?
8. Is punctal apposition appropriate during the various stages
of the blink cycle?
BLICK
Blink Dynamics. Evaluation of a patient with epiphora begins
with an assessment of the integrity of the neuromuscular unit
responsible for blinking. While obtaining the clinical history,
the clinician should observe the patient’s blink frequency and
amplitude of upper eyelid excursion.
In patients with seventh cranial nerve palsy, tearing is
multifactorial.17 The neuromuscular unit is altered because
of the motor innervation deficit. Diminished orbicularis tone
impairs downward excursion of the upper eyelid, such that it
fails to touch the lower eyelid to pick up and efficiently dis-
tribute the tear meniscus. Lower eyelid laxity creates an unfa-
vorable “uphill” gradient, and the absence of dynamic blinking
eliminates the “milking” effect that normally propels tears
D. T. Tse et al. Ophthal Plast Reconstr Surg, Vol. 30, No. 6, 2014

TABLE 2.  Conditions altering the tear distribution system

Altered blink dynamics Lid malposition Imbrication Conjunctivochalasis Kissing puncta

Facial nerve Palsy Ectropion Subconjunctival Megalocaruncle Blepharoptosis

Facial akinesia Entropion fat prolapsed Subconjunctival LCT disinsertion
Parkinson disease LCT disinsertion LCT disinsertion oribtal fat prolapse Megalopunctum
Progressive supranuclear palsy Retraction Eyelid disparity Conjuctival chemosis
Botulinum toxin Floppy eyelid
Burns and scars Burns and scars
Scleroderma Scleroderma
Ichthyosis Ichthyosis
Discoid lupus Discoid lupus
Zoster Zoster
LCT, lateral canthal tendon.

medially. Reduced contractility may also prevent punctal occlu- Patients with inflexible eyelid skin secondary to burns,
sion, which is necessary to generate a vacuum within the drain- scar tissue, scleroderma, ichthyosis, discoid lupus, zoster, or
age system. The diminished contractile force of the deep head of a host of other cicatrizing processes may have inefficient tear
the preseptal orbicularis fails to generate negative pressure with drainage as the 3 cardinal anatomical issues commonly affect-
the lacrimal pump to siphon tears into the sac.18 Superimposed ing the distribution system are present: lower eyelid malposi-
on this are exposure keratopathy, meibomian gland dysfunc- tion, ineffective upper eyelid excursion, and suboptimal lacrimal
tion, and tear lake stagnation, which results in the accumula- pump function.
tion of debris and inflammatory mediators.19 The consequence In a patient with ichthyosis, the lower eyelid vertical
is a cycle of reflexive hypersecretion exacerbating an ineffective striae denote the presence of anterior lamella tightness, causing
lacrimal pump for tear clearance. a lower eyelid retraction, and eyelid margin ectropion (Fig. 1).
Appropriate treatments seek to optimize the sequence Anatomically, upper eyelid skin inelasticity prevents full excur-
of events in a blink cycle as outlined by Doane.9 Strategies to sion during the blink cycle. Physiologically, eyelid rigidity
improve tear clearance should address 3 key goals: normalize limits the contractile function of the deep head of preseptal
the lower eyelid position to promote horizontal tear movement, orbicularis, undermining the efficiency of the pumping mecha-
maximize the upper eyelid excursion to combat ocular surface nism. Because of ectropion, the tear meniscus is no longer rest-
exposure and reflex tearing, and promote orbicularis contrac- ing on the eyelid margin, but rather in the inferior fornix. Even
tion to improve lacrimal pumping for tear egress. Options there- if the upper eyelid can touch the lower eyelid, it is ineffective in
fore include tightening of the lower eyelid and/or reinserting retrieving the tear film from the inferior fornix for corneal lubri-
the lateral canthal tendon, placing a gold weight or palpebral cation. Because of anterior lamella cicatrix, there is no punctal
spring to increase blink amplitude, and aggressively lubricat- apposition on eyelid closure, such that negative pressure cannot
ing the ocular surface in order to blunt reflex tearing. Temporal be generated. Nocturnal lagophthalmos and tear evaporation
tarsorrhaphy is another possibility, as it narrows the palpebral exacerbates tear film instability, thus accentuating the irritation-
fissure, protecting the ocular surface, and reducing reflex hyper- reflexive tearing cycle upon awakening.
secretion. This procedure, however, will not reanimate the upper
eyelid or improve the pumping mechanism for tear clearance.
Patients with Parkinson disease and progressive supra-
nuclear palsy present with a decreased blink rate and a loss of
facial expression due to muscular rigidity. The intake of neu-
romodulatory drugs may also provide clues. Blink frequency
is typically modulated through a feedback loop in response to
external stimuli, but this reflex arc is blunted in neurodegen-
erative conditions.20,21 The amplitude of upper eyelid excursion
is also reduced, such that it fails to contact and spread the tear
meniscus. These factors result in precorneal tear film desiccation
and reflex hypersecretion. This is often exacerbated by sebor-
rheic dermatitis and meibomian gland dysfunction. In this group
of patients, tearing can be minimized by medical treatment of
blepharitis and frequent application of artificial tears. In patients
with an inability to apply lubricants because of hand tremor, gold
weight insertion can help to optimize each blink cycle.

BLICK
Lid Malposition. Alterations in the hydrodynamic factors
of blinking and eyelid closure responsible for precorneal tear
film stability can profoundly undermine the effectiveness of
the lacrimal distribution system. Broadly, these abnormalities
can be categorized as problems with anterior lamellar elasticity,
eyelid-globe apposition, and canthal anchoring (Table 2).
FIG. 1.  This patient with ichthyosis exemplifies how altera-
tions of eyelid affect the the physiology of tear clearance.
Note the contracted anterior lamella with vertical tension lines
causing lower eyelid retraction and ectropion. The inelastic
upper eyelid skin limits downward excursion to pick up the
tear meniscus that has receded into the inferior fornix because
of lower eyelid malposition. Ineffective corneal lubrication and
nocturnal lagophthalmos contribute to desiccation and reflex
tearing.

452 © 2014 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc.
Ophthal Plast Reconstr Surg, Vol. 30, No. 6, 2014 The BLICK Mnemonic for Epiphora Evaluation

Normal eyelid configuration and proper positioning of

the puncta relative to the tear meniscus is required for physi-
ological tear clearance. Abnormal apposition of the lower eye-
lid to the globe or displacement of the punctum will affect tear
distribution and clearance (Fig. 2A,B). Lower eyelid eversion
displaces the tear lake from the eyelid margin, and laxity creates
an abnormal gradient for the tear to migrate “uphill” along the
eyelid margin toward the punctum with each blinking action.
Exposed palpebral conjunctiva may keratinize, causing foreign
body sensation and reflex hypersecretion. In severe cases, the
presence of exposure and lagophthalmos further compromises
the precorneal tear film stability. The malpositioned puncta can-
not appose in order to seal the lacrimal drainage system, nor
can tears enter the canaliculi between each blink. This violates
a key anatomical requisite for tear clearance as suggested by
Rosengren6 and Doane.9
Six elements of pathology may be present in an ectropic
eyelid.22 These factors include horizontal eyelid laxity, medial
canthal tendon laxity, punctal malposition, vertical tightness of
the skin, orbicularis paresis secondary to seventh nerve palsy,
and lower eyelid retractor disinsertion. The presence of each
factor is determined by clinical examination. One or more of
these components may be present in an ectropic eyelid. Proper
recognition of the underlying anatomic defect will enable the
surgeon to select the appropriate surgical procedure for correc-
tion. The surgical aim is to restore eyelid anatomy and function
so that the sequence of events in tear clearance is preserved.
Entropion and secondary trichiasis can result in ocular
irritation and reflex tearing that can overwhelm an appropriately
functioning drainage system (Fig. 2C). Furthermore, the entro-
pic eyelid places the inferior punctum in an unfavorable position
to receive tears and prevents proper apposition with the upper
punctum. Six elements of pathology may be present in an entro-
pic eyelid. These factors include horizontal eyelid laxity, dehis-
cence of lower eyelid retractors, posterior lamella cicatrix, and
overriding preseptal orbicularis. One or more of these elements
may coexist in an entropic eyelid. As with ectropion, the aim is
to restore eyelid anatomy and function so that the sequence of
events in tears clearance is preserved.
Eyelid retraction in the presence of exophthalmos associ-
ated with Graves ophthalmopathy affects 2 of the 3 cardinal ana-
tomical issues involving the distribution system; the retracted
lower eyelid creates an abnormal gradient for tear migration
toward the puncta, and an incomplete blink cycle due to the
widen eyelid fissure disrupts corneal lubrication. Incomplete
nocturnal eyelid closure, coupled with reduced Bell’s reflex
secondary to fibrotic inferior recti, exacerbates exposure kera-
topathy and reflex tearing. Associated bulbar conjunctival che-
mosis may disrupt tear migration along the lower eyelid; it also FIG. 2.  A, Ectropion. Lower eyelid eversion displaces the tear lake
contributes to and is in turn worsened by lagophthalmos. The and creates an unfavorable gradient for tears to migrate toward the
lacrimal pump function is unaffected in most cases. punctum. Because the punctum is not in apposition to the globe,
In the presence of an intact neuromuscular unit, adequate tears cannot enter the canaliculi with each blink. B, A tightening
palpebral orbicularis contractile tension is generated when its procedure restores the ectropic lower eyelid to an optimal position
fibers are firmly anchored to the bony orbit via the canthal ten- and supports the tear meniscus. The inferior punctum is in apposi-
tion to the globe and in vertical alignment with the upper punctum,
dons. Laxity of the lateral canthal tendon renders the concentri- such that eyelid closure will form a sealed system to siphon tears
cally arranged orbicularis fibers ineffective in completing each into the lacrimal sac. Overzealous tightening of the eyelid will dis-
blink. Lateral canthal tendon disinsertion is a seldom-recog- place the inferior punctum temporally, altering its vertical alignment
nized anatomical defect that can alter the mechanics of blinking with the superior punctum—an anatomical requisite for proper tear
and lacrimal pump function. It often results in ocular irritation drainage. C, Entropion. Eyelashes of the entropic eyelid cause ocular
and epiphora. irritation and reflexive hypersecretion. The inturned punctum is not
The clinical features of lateral canthal disinsertion are as in an optimal position to receive tears into the excretory system.
follows: 1) a blunted or vertically displaced lateral canthal angle,
2) medial and inferior movement of the lateral commissure with imbrication on attempted eyelid closure, and 5) pseudoupper
eyelid closure, 3) incomplete apposition of the eyelid margins in eyelid retraction (Fig. 3A,B).23 A cotton-tipped applicator may
the absence of an anterior lamellar shortage, 4) temporal eyelid be used to distract the lateral commissure toward the lateral

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D. T. Tse et al. Ophthal Plast Reconstr Surg, Vol. 30, No. 6, 2014

FIG. 3.  Lateral canthal tendon disinsertion. A, A patient presents with incomplete blink and eyelid closure following orbicularis myec-
tomy for essential blepharospasm. A clinical feature of lateral canthal disinsertion is superior displacement of the lateral canthal tendon
complex due to unopposed retraction by the levator. The lateral canthal tendon is not in horizontal alignment with the medial canthal
tendon. B, On attempted eyelid closure, note the medial and inferior displacement of the lateral commissure. Insufficient palpebral
orbicularis contractile tension is generated to effect complete closure when the lateral canthal tendon is not firmly anchored to the
bony rim. C, The disinserted lateral canthal tendon is secured to the lateral orbital rim with a permanent suture through 2 drill holes.
Note the horizontal alignment of the canthal tendons. D, On eyelid closure, note the stability of the lateral commissure and complete
eyelid apposition.

orbital rim, simulating surgical tightening of the canthal tendon;
when significant dehiscence is present, one can see an imme-
diate improvement in blink dynamics and eyelid closure. This
maneuver is a simple test to verify that a lateral canthal tendon
disinsertion is the underlying anatomical element of the pathol-
ogy. It also serves as a good predictor of functional outcome
following lateral canthal tendon tightening (Fig. 3C,D).23
Patients with floppy eyelid syndrome typically complain
of chronic unilateral or bilateral eye irritation, foreign body
sensation, tearing, and stringy mucoid discharge.24,25 These
symptoms are often worse upon awakening.26 Floppy eyelid
syndrome is more prevalent in overweight male patients who
tend to habitually sleep on one side or face down against the
pillow. In many cases, there is a history of loud snoring or a
diagnosis of obstructive sleep apnea.27
Clinically, the lax upper eyelid everts easily when dis-
tracted superotemporally with finger pressure (Fig. 4A). The
soft and rubbery tarsal plate can be folded upon itself (Fig. 4B).
Spontaneous eyelid eversion subjects the palpebral conjunctiva
to repeated mechanical trauma, causing papillary conjunctivi-
tis as well as direct traumatic keratopathy (Fig. 4C). Eyelash
ptosis with loss of parallelism and pleomorphism (eyelashes
protruding in multiple directions) may develop due to chronic
compression against the pillow (Fig. 4D).28 Slit lamp examina-
tion frequently will show a stagnant tear lake admixed with ropy
discharge at the eyelid margin.
Tearing in floppy eyelid syndrome is caused by a com-
bination of reflex hypersecretion and inadequate distribution of
the tear film by a lax upper eyelid, and stasis due to an ineffective
lacrimal pump. While decrease in tarsal elastin is the putative
mechanism of eyelid scaffold instability, lateral canthal tendon
dehiscence due to mechanical factors is often an unrecognized
finding.29 Interventions include nocturnal patching, treatment of
concomitant sleep apnea, and eyelid tightening with pentagonal
wedge resection or lateral canthal tendon plication.30–33
In discussing conditions affecting the eyelid malposi-
tion component of the mnemonic, the authors have attempted to
walk the line between being overly inclusive and overly exclu-
sive, and many of the judgments of what to discuss are no doubt
informed by their own specific biases. Distinctions are blurred,
but they tend to categorize upper eyelid cicatricial entropion,
trichiasis, and aberrant seventh nerve regeneration (croco-
dile tears) as more related to reflexive hypersecretion than an
alteration in the tear distribution system. Eyelid tumors, eyelid

454 © 2014 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc.
Ophthal Plast Reconstr Surg, Vol. 30, No. 6, 2014 The BLICK Mnemonic for Epiphora Evaluation

FIG. 4.  Floppy eyelid syndrome. A, The lax and rubbery upper eyelid is everted easily as it is distracted toward the eyebrow. Hypertro-
phy and inflammation of the tarsal conjunctiva is present, in addition to a mucoid discharge. B, The rubbery tarsal plate can be folded.
Conjunctival injection, ropy discharge, and pooling of tears along the eyelid margin are present. C, Nocturnal eyelid eversion while side
sleeping places the palpebral conjunctiva in contact with the pillow, causing chronic irritation. This finding suggests mechanical injury
as the primary cause of the papillary conjunctivitis. D, Eyelash ptosis and polymorphism.

notches, pinguecula, and pterygia can certainly alter tear distri-
bution over the corneal surface and along the eyelid margin, but
their experience has been that they are usually quickly and ade-
quately recognized. Keratinization of the eyelid margin exacer-
bating reflexive hypersecretion is often secondary to a number
of primary eyelid malposition conditions. Similarly, forniceal
conjunctival symblepharon can cause secondary eyelid malpo-
sition, leading to lagophthalmos and poor blink—anatomical
issues affecting the distribution system. The consequential
physiological dysfunction is reflexive hypersecretion due to
corneal irritation.
BLICK
is either lateral canthal disinsertion or prior lower eyelid
shortening resulting in eyelid length disparity.29 Up to one
third of patients may have coexisting floppy eyelid syndrome.
Clinical findings include papillary conjunctivitis and occasional
frank tarsal ulceration (Fig. 5B).29 Rose Bengal staining of the
tarsal conjunctiva along the upper eyelid margin confirms the
diagnosis, and the amount of staining typically correlates with
the severity of imbrication.36
Treatment ranges from aggressive lubrication to horizon-
tal eyelid shortening of the upper eyelid. The aim is to restore
eyelid dimension parity. Common techniques include full-thick-
ness upper eyelid pentagonal wedge resection or lateral canthal
tendon plication.29

Imbrication. The authors acknowledge that imbrication is an BLICK

eyelid malposition, but feel that it is common and important
enough to merit independent inclusion in their mnemonic—
particularly because it is often neglected in the mental algorithm
that guides visual inspection. Eyelid imbrication syndrome is
an abnormality in which a lax upper eyelid overrides the lower
eyelid during closure, permitting the lower eyelid margin and
lashes to chronically abrade the upper eyelid tarsal conjunctiva
(Fig. 5A).34,35 The everted upper eyelid also fails to come in
contact with the tear meniscus, causing suboptimal corneal
lubrication. The rough tarsal conjunctiva rubs against the
corneal surface, producing foreign body sensation and reflex
tearing (Fig. 5B). The lower eyelid can override the upper
eyelid (Fig. 5C). Frequently, the underlying anatomical defect
Conjunctivochalasis. Conjunctivochalasis (CCh) is typically
a bilateral condition in which redundant, nonedematous bulbar
conjunctiva billows over the lower eyelid margin (Fig. 6A).37 This
tissue redundancy causes epiphora by mechanically displacing
the normal tear meniscus and impeding flow along the eyelid
margin toward the punctum.38 Occasionally, redundancy is severe
enough to mechanically obstruct the lower eyelid punctum.39
Conjunctivochalasis also obliterates the normal tear reservoir
in the fornix.39 Wiping of tears across the eyelids mechanically
irritates the redundant bulbar conjunctiva billowing over the
eyelid margin, further exacerbating conjunctival inflammation
and perpetuating a vicious cycle.

© 2014 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc. 455
D. T. Tse et al. Ophthal Plast Reconstr Surg, Vol. 30, No. 6, 2014
FIG. 5.  Eyelid imbrication. A, The medial upper eyelid over-
rides the lower eyelid. Note the presence of punctal eversion,
tarsoconjunctival injection, and keratinization. B, On eversion of
the upper eyelid, diffuse conjunctival injection and keratinization
corresponding to area of imbrication is visualized. The keratin-
ized conjunctiva rubs against the corneal surface, causing reflex
hypersecretion. C, The lower eyelid overrides the upper eyelid.
The etiology of CCh has not been well characterized, but
it appears histologically as a thinning and loss of anchoring of
the bulbar conjunctiva to the underlying Tenon’s capsule.40,41
Once CCh is manifested, it is thought that proinflammatory
cytokines and matrix metalloproteases accumulate as a result of
delayed tear clearance, potentiating further collagenolysis and
elastotic degeneration.38,42–44 Conjunctivochalasis can occur in
isolation or coexist with eyelid laxity, lagophthalmos or blink-
ing abnormality.
Medical management of CCh-related symptoms may
start with lubricants, topical anti-inflammatories or antihis-
tamines, and nocturnal patching.38 Conjunctivochalasis that
456 © 2014 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc.
FIG. 6. Conjunctivochalasis. A, A redundant pleat of bulbar
conjunctiva overlies the lower eyelid margin and inferior limbus.
This loose, excess conjunctiva may mechanically irritate the eye
as well as disrupt the tear film and its outflow, leading to epiph-
ora. B, Subconjunctival fat prolapse. Prolapse of orbital fat from
the central surgical space under the temporal bulbar conjunc-
tiva displaces the tear film and disrupts its flow along the eyelid
margin. Note the pooling of tears at the convex leading edge of
the subconjunctival lesion.
is refractory to conservative treatments can be corrected with
an elliptical resection of the redundant bulbar conjunctiva.38,45
Strategies incorporating fibrin glue, suture fixation to the sclera,
amniotic membrane placement, and thermal cautery have also
been described.37,40,46,47
The presence of an enlarged caruncle, a megalocaruncle,
can be considered a form of CCh, and may cause functional lac-
rimal drainage obstruction.48 Anatomically, a megalocaruncle
is an enlarged caruncle that extends to or beyond the inferior
lacrimal punctum.48 An uncommon finding in young adults, it
is therefore thought to represent a senile hypertrophic change in
the majority of patients.49 An enlarged caruncle physically cov-
ers the inferior punctum and interferes with the apposition of the
upper punctum to the lower on eyelid closure thus abolishing the
vacuum in the lacrimal system.49 Carunculectomy will remove
the physical obstruction of the inferior punctum to restore punc-
tal apposition. Mombaerts and Colla48 reported alleviation of
epiphora in 77% of patients with a 2 to 3 week latency.
Subconjunctival herniation of orbital fat from the central
surgical space can encroach on the temporal lower eyelid, dis-
placing the tear meniscus and mechanically interfering with tear
propagation along the eyelid margin. The anatomical defect is
most likely caused by Tenon’s capsule dehiscence (Fig. 6B). An
effective treatment is a transconjunctival incision to expose the
Ophthal Plast Reconstr Surg, Vol. 30, No. 6, 2014 The BLICK Mnemonic for Epiphora Evaluation

prolapsing fat for direct excision. The aim is to debulk the her-
niating fat to eliminate its mechanical interference of tear flow.
Care should be taken to avoid amputating the palpebral lobe of
the lacrimal gland.
BLINK
Kissing Puncta. The punctal apposition syndrome, or “kissing
puncta,” is a condition in which the upper punctum remains in
apposition to the lower punctum even with the eye open.12,50 The
normal medial canthal architecture, including the caruncle and
lacrimal papillae, is not visible in primary gaze (Fig. 7A–C). The
punctal openings are effectively occluded throughout the blink
cycle, impeding inflow of tears into the canalicular system.51
Punctal apposition when the eyelids are apart violates the
anatomical prerequisite based on Doane’s9 proposed mechanism
of lacrimal drainage.
The exact etiology of this malposition remains unclear,
but in the majority of cases, medial displacement of the inferior
punctum due to laxity of the lower eyelid appears to be impli-
cated. Francis and Wan51 reported successful treatment of 7 eyes
in 5 patients with lateral tarsal strip procedures. Glatt50 described
the management of a single case of punctal apposition syn-
drome with ptosis repair; the upper punctum was successfully
elevated out of contact with the lower punctum. Blepharoptosis
does not appear to be a consistent feature of punctal apposi-
tion syndrome. This condition has also been reported in patients
with Graves orbitopathy.52 In this instance, prolapse of orbital
fat into the upper and lower eyelids resulted in punctual apposi-
tion, and the condition was successfully treated with transcuta-
neous orbital fat decompression.
Applying lateral eyelid traction with tape may separate
the kissing puncta and reveal the medial canthal structures, con-
firming this diagnosis. Patients who respond to this maneuver
are effectively treated by lower eyelid tightening procedures.
Careful attention should also be directed towards identifying
blepharoptosis or other structural abnormalities of the eyelids
that may contribute to punctal apposition. Occasionally, CCh
may coexist with punctal apposition syndrome, such that both
conditions need to be addressed simultaneously to alleviate the
tearing symptom.48
An inferior punctum that is grossly enlarged due to an
aggressive 3-snip punctoplasty or to cheese wiring of the infe-
rior canaliculus from placement of a tight silicone stent also vio-
lates the anatomical principle of appropriate punctual occlusion
(Fig. 7D). The papillae meet with eyelid closure but the puncta
are unable to occlude and therefore cannot generate a partial
vacuum within the canaliculi. Rather than active siphoning of
tears into the lacrimal drainage system, tear clearance becomes
passive and epiphora supervenes.

FIG. 7.  Kissing puncta. A, A patient with punctual apposition in primary gaze. Note eyelid ptosis and tear stasis along the inferior
eyelid margin. B, Restored medial canthal configuration with separation of the puncta following ptosis repair and blepharoplasty. C, A
patient with kissing puncta and laxity of the lower eyelid. Note the temporal sagging and ascending slope of the medial lower eyelid.
In such cases, tightening of the lower eyelid may suffice to restore the separation of the puncta. D, Megalopunctum. An excessively
tight silicone stent cheese wired through the inferior canaliculus, preventing proper punctal occlusion and leading to epiphora.

© 2014 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc. 457
D. T. Tse et al. Ophthal Plast Reconstr Surg, Vol. 30, No. 6, 2014
SUMMARY
A broad range of eyelid abnormalities and alterations in
blinking mechanics can disturb the physiology of tear clearance,
resulting in symptomatic epiphora. In many instances, a compre-
hensive evaluation of factors affecting the tear distribution sys-
tem in patients complaining of tearing is neglected. The authors
proffer the BLICK mnemonic to ensure an orderly sequence of
inspection of underlying anatomical elements of pathology con-
tributing to the symptom, highlight important clinical clues, and
suggest treatment options guided by the principle of normalizing
eyelid anatomy in order to optimize dynamic blinking action for
physiologic tear distribution and clearance.
REFERENCES
1. Bron AJ, Tiffany JM, Gouveia SM, et al. Functional aspects of the
tear film lipid layer. Exp Eye Res 2004;78:347–60.
2. Tiffany JM. The normal tear film. Dev Ophthalmol 2008;41:1–20.
3. Jones LT. An anatomical approach to problems of the eyelids and
lacrimal apparatus. Arch Ophthalmol 1961;66:111–24.
4. Jones LT. Epiphora. II. Its relation to the anatomic structures and sur-
gery of the medial canthal region. Am J Ophthalmol 1957;43:203–12.
5. Jones LT. Anatomy of the tear system. Int Ophthalmol Clin 1973;
13:3–22.
6. Rosengren B. On lacrimal drainage. Ophthalmologica 1972;164:
409–21.
7. Maurice DM. The dynamics and drainage of tears. Int Ophthalmol
Clin 1973;13:103–16.
8. Doane MG. Interactions of eyelids and tears in corneal wetting and
the dynamics of the normal human eyeblink. Am J Ophthalmol
1980;89:507–16.
9. Doane MG. Blinking and the mechanics of the lacrimal drainage
system. Ophthalmology 1981;88:844–51.
10. Becker BB. Tricompartment model of the lacrimal pump mecha-
nism. Ophthalmology 1992;99:1139–45.
11. Bartley GB. Acquired lacrimal drainage obstruction: an etiologic
classification system, case reports, and a review of the literature.
Part 1. Ophthal Plast Reconstr Surg 1992;8:237–42.
12. Bartley GB. Acquired lacrimal drainage obstruction: an etiologic
classification system, case reports, and a review of the literature.
Part 3. Ophthal Plast Reconstr Surg 1993;9:11–26.
13. Scott KR, Tse DT. Lacrimal system disorders. In: Parrish RK II,
ed. The University of Miami Bascom Palmer Eye Institute Atlas
of Ophthalmology. Philadelphia, PA: Butterworth-Heinemann,
1999:627–37.
14. Pflugfelder SC, Solomon A, Stern ME. The diagnosis and manage-
ment of dry eye: a twenty-five-year review. Cornea 2000;19:644–9.
15. Patrinely JR, Anderson RL. Anatomy of the orbicularis oculi and
other facial muscles. Adv Neurol 1988;49:15–23.
16. Tucker NA, Tucker SM, Linberg JV. The anatomy of the common
canaliculus. Arch Ophthalmol 1996;114:1231–4.
17. Lee V, Currie Z, Collin JR. Ophthalmic management of facial nerve
palsy. Eye (Lond) 2004;18:1225–34.
18. Shah CT, Blount AL, Nguyen EV, et al. Cranial nerve seven pal-
sy and its influence on meibomian gland function. Ophthal Plast
Reconstr Surg 2012;28:166–8.
19. Madge SN, Malhotra R, Desousa J, et al. The lacrimal bypass
tube for lacrimal pump failure attributable to facial palsy. Am J
Ophthalmol 2010;149:155–9.
20. Biousse V, Skibell BC, Watts RL, et al. Ophthalmologic features of
Parkinson’s disease. Neurology 2004;62:177–80.
21. Reddy VC, Patel SV, Hodge DO, et al. Corneal sensitivity, blink
rate, and corneal nerve density in progressive supranuclear palsy
and Parkinson disease. Cornea 2013;32:631–5.
22. Frueh BR, Schoengarth LD. Evaluation and treatment of the patient
with ectropion. Ophthalmology 1982;89:1049–54.
23. Tse DT, Shriver EM. Lateral canthopexy. In Tse DT, ed. Color Atlas
of Oculoplastic Surgery. 2nd ed. New York, NY: Wolters Kluwer/
Lippincott Williams & Wilkins, 2011:76–81.
24. Ezra DG, Beaconsfield M, Sira M, et al. Long-term outcomes of
surgical approaches to the treatment of floppy eyelid syndrome.
Ophthalmology 2010;117:839–46.
458 © 2014 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc.
25. Ezra DG, Beaconsfield M, Sira M, et al. The associations of
floppy eyelid syndrome: a case control study. Ophthalmology
2010;117:831–8.
26. Culbertson WW, Ostler HB. The floppy eyelid syndrome. Am J
Ophthalmol 1981;92:568–75.
27. McNab AA. Floppy eyelid syndrome and obstructive sleep apnea.
Ophthal Plast Reconstr Surg 1997;13:98–114.
28. Netland PA, Sugrue SP, Albert DM, et al. Histopathologic fea-
tures of the floppy eyelid syndrome. Involvement of tarsal elastin.
Ophthalmology 1994;101:174–81.
29. Karesh JW, Nirankari VS, Hameroff SB. Eyelid imbrication. An
unrecognized cause of chronic ocular irritation. Ophthalmology
1993;100:883–9.
30. Bartsich S, Swartz KA, Spinelli HM. Lateral canthoplasty using the
Mitek anchor system. Aesthetic Plast Surg 2012;36:3–7.
31. Kang H, Takahashi Y, Ichinose A, et al. Lateral canthal anatomy: a
review. Orbit 2012;31:279–85.
32. Kannan RY, Chuah JL, Burns J, et al. The “leicester lasso” lateral
canthoplasty. Ophthal Plast Reconstr Surg 2014;30:186.
33. McCord CD, Boswell CB, Hester TR. Lateral canthal anchoring.
Plast Reconstr Surg 2003;112:222–37; discussion 238–9.
34. Burkat CN, Lemke BN. Acquired lax eyelid syndrome: an unrecog-
nized cause of the chronically irritated eye. Ophthal Plast Reconstr
Surg 2005;21:52–8.
35. Holbach LM. Diseases of the eyelid-conjunctival complex and
corneal complications of lid disease. Curr Opin Ophthalmol
1995;6:39–43.
36. Donnenfeld ED, Perry HD, Schrier A, et al. Lid imbrication syn-
drome. Diagnosis with rose Bengal staining. Ophthalmology
1994;101:763–6.
37. Meller D, Tseng SC. Conjunctivochalasis: literature review
and possible pathophysiology. Surv Ophthalmol 1998;43:
225–32.
38. Petris CK, Holds JB. Medial conjunctival resection for tearing as-
sociated with conjunctivochalasis. Ophthal Plast Reconstr Surg
2013;29:304–7.
39. Huang Y, Sheha H, Tseng SC. Conjunctivochalasis interferes
with tear flow from fornix to tear meniscus. Ophthalmology
2013;120:1681–7.
40. Doss LR, Doss EL, Doss RP. Paste–pinch–cut conjunctivoplasty:
subconjunctival fibrin sealant injection in the repair of conjunctivo-
chalasis. Cornea 2012;31:959–62.
41. Gumus K, Pflugfelder SC. Increasing prevalence and sever-
ity of conjunctivochalasis with aging detected by anterior seg-
ment optical coherence tomography. Am J Ophthalmol 2013;155:
238–242.e2.
42. Li DQ, Meller D, Liu Y, et al. Overexpression of MMP-1 and MMP-
3 by cultured conjunctivochalasis fibroblasts. Invest Ophthalmol Vis
Sci 2000;41:404–10.
43. Ward SK, Wakamatsu TH, Dogru M, et al. The role of oxidative
stress and inflammation in conjunctivochalasis. Invest Ophthalmol
Vis Sci 2010;51:1994–2002.
44. Zhang XR, Zhang ZY, Hoffman MR, et al. The effect of age and
conjunctivochalasis on conjunctival thickness. Curr Eye Res
2013;38:331–4.
45. Liu D. Conjunctivochalasis. A cause of tearing and its management.
Ophthal Plast Reconstr Surg 1986;2:25–8.
46. Nakasato S, Uemoto R, Mizuki N. Thermocautery for inferior con-
junctivochalasis. Cornea 2012;31:514–9.
47. Otaka I, Kyu N. A new surgical technique for management of con-
junctivochalasis. Am J Ophthalmol 2000;129:385–7.
48. Mombaerts I, Colla B. Partial lacrimal carunculectomy: a simple
procedure for epiphora. Ophthalmology 2001;108:793–7.
49. Mourits MP, Koornneef L, Wiersinga WM, et al. Clinical criteria
for the assessment of disease activity in Graves’ ophthalmopathy: a
novel approach. Br J Ophthalmol 1989;73:639–44.
50. Glatt HJ. Epiphora caused by blepharoptosis. Am J Ophthalmol
1991;111:649–50.
51. Francis IC, Wan MK. The punctal apposition syndrome: a new sur-
gical approach. Br J Ophthalmol 2002;86:1256–8.
52. Cheema MM, Meyer DR. Epiphora secondary to punctal apposition
in the setting of Graves’ orbitopathy. Ophthal Plast Reconstr Surg
1995;11:122–4.