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Why Do I Have Excessive and Continuous Eye Watering?
The Lacrimal System: Anatomy and Function
Causes
Symptoms and Signs
Diagnosis
Treatment and Remedies
References and Bibliography

Why Do I Have Excessive and Continuous Eye Watering?

An increase in tear secretion (lacrimation) can result from a different range of causes:

mechanical injury to the eye.
a wide variety of local and systemic diseases.
pharmacological side effects, and, of course.
emotional states.

When the increased tearing results in a thin, non-sticky, watery fluid that overflows the eyelid margin and runs down the cheeks, the more precise medical term is epiphora. This word comes from the Greek epiphora, meaning “to carry over”, and describes tear overflow beyond the capacity of the drainage system.

The clinical significance of epiphora varies considerably. In many individuals, this condition is a transient and self-limiting nuisance. It can be triggered by cold wind, allergen exposure, or emotional distress, but it typically resolves on its own once the precipitating factor is removed. In others, it is a persistent, chronic, and sometimes debilitating condition that impairs vision, disrupts daily activities, causes social embarrassment, and may signal significant underlying ocular or systemic pathology.

The symptom of excessive tearing can affect one or both eyes and may occur in isolation or in combination with a range of associated features that provide important diagnostic information. These associated symptoms may include:

Eye burning: a sensation of heat or chemical irritation within the eye.
Blurred vision, which can result from distortion of the tear film optics or fluid buildup on the corneal surface.
Eyelid swelling (edema): periorbital swelling that occurs with inflammation or infection.
Photophobia is an abnormal sensitivity to light and often indicates corneal or uveal involvement.
Itching, particularly when linked to allergic causes, is a common symptom.
Redness of the eye and periorbital area typically indicates conjunctival injection, which reflects inflammation.
Increased nasal mucus secretion (which reflects the continuity of the lacrimal and nasal drainage systems) is particularly prominent in allergic rhinoconjunctivitis.

While episodic, situationally explained tearing requires no specific investigation, persistent tearing without an identifiable cause should always prompt evaluation by an ophthalmologist. The prognosis of epiphora depends on the nature and severity of the underlying cause: the more significant the underlying pathology, the more prolonged and complex the treatment required, and the more guarded the prognosis for complete resolution.

The Lacrimal System: Anatomy and Function

To understand why tearing becomes excessive, it is essential to first grasp how the normal lacrimal system works. This system is an elegant anatomical apparatus that produces, distributes, and drains tears to maintain ocular surface health.

Tear Production

Tears are not simply water. They are a complex, precisely formulated biological fluid that coats the ocular surface (the conjunctiva and cornea) as a multilayered precorneal tear film. This tear film has three distinct layers:

Outer lipid layer: Produced by the Meibomian glands located in the eyelid margins. This oily layer reduces evaporation of the tear film and provides a smooth optical surface.
Middle aqueous layer: The main volume of the tear film, produced primarily by the lacrimal gland (located in the superolateral orbit, under the brow) and accessory lacrimal glands (Krause and Wolfring glands, located within the conjunctival fornices). This layer contains water, electrolytes, proteins (including lysozyme, lactoferrin, and immunoglobulins), growth factors, and other bioactive molecules.
Inner mucin layer: Produced by goblet cells in the conjunctival epithelium. This mucin layer allows the watery middle layer to adhere to the hydrophobic corneal epithelium, maintaining stable tear film coverage.

Together, these layers serve the critical functions of:

Protection: Lysozyme and other antimicrobial proteins protect against bacterial and viral infection; the tear film also physically washes away foreign particles and microorganisms.
Lubrication: Reducing friction between the eyelid and the ocular surface during blinking.
Nutrition: Delivering oxygen and nutrients to the avascular corneal epithelium (the cornea has no blood vessels and depends on the tear film for its oxygen supply).
Optical quality: The smooth, regular tear film surface is essential for clear vision. Even small disturbances in tear film quality can cause fluctuating visual blurring.

Tear Drainage

After tears are produced and spread across the ocular surface by blinking, excess fluid drains through the lacrimal drainage system:

Lacrimal puncta: Two tiny openings (one on the upper and one on the lower eyelid margin, near the inner corner of the eye) through which tears are drawn by capillary action
Lacrimal canaliculi: Short channels (the upper and lower canaliculi) leading from each punctum toward the inner corner of the eye
Common canaliculus: Where the upper and lower canaliculi typically join (in about 90% of people) before entering the lacrimal sac
Lacrimal sac: Located in the bony lacrimal fossa at the inner orbital margin; collects tear fluid and propels it downward through the nasolacrimal duct by the pumping action of the orbicularis oculi muscle during blinking
Nasolacrimal duct: Carries tears from the lacrimal sac downward through a bony canal to open into the inferior nasal meatus (the floor of the nasal cavity beneath the inferior turbinate)

This explains why crying causes a runny nose: the excess tears drain through the nasolacrimal duct directly into the nasal cavity.

The Balance of Production and Drainage

The lacrimal system maintains a remarkably precise and dynamic equilibrium between tear production and tear drainage. The tolerances in this system are narrow; even small imbalances in either direction produce symptoms. This balance is continuously challenged by environmental, physical, and biological perturbations:

Environmental factors: Temperature, wind, humidity, air pollution, UV radiation
Physical factors: Blinking rate and completeness, eyelid position, corneal sensitivity
Biological factors: Hormonal status, systemic disease, medications, aging

When this balance is disrupted, whether by excessive production, inadequate drainage, or both, the result is epiphora.

Causes

Excessive tearing can be attributed to three principal mechanisms, which are not mutually exclusive and may coexist in the same patient:

Obstruction or narrowing of the tear drainage system (dacryostenosis)
Overproduction of tears by the lacrimal glands, exceeding the drainage capacity
Abnormal eyelid position or closure, disrupting the pump mechanism that drives tears toward the drainage system

Dacryostenosis (Lacrimal Duct Obstruction)

Dacryostenosis refers to any narrowing, known as stenosis, or complete obstruction of the lacrimal drainage pathway. This condition can affect the area from the puncta to the nasolacrimal duct. When drainage is impaired, tears that cannot be evacuated through the normal pathway accumulate in the lacrimal sac and eventually overflow the lower eyelid margin onto the cheek.

Beyond the mere inconvenience of excess tearing, dacryostenosis carries a clinically important risk: the static pool of tears retained within the obstructed lacrimal sac creates an ideal environment for bacterial colonization and proliferation. This can lead to dacryocystitis, an infection and inflammation of the lacrimal sac. The condition typically presents as painful, red swelling at the inner corner of the eye (the medial canthus), discharge of mucopurulent material from the puncta when pressure is applied over the sac, and sometimes fever or systemic upset. Dacryocystitis may occur acutely (often exquisitely painful) or in a chronic, smoldering form with recurrent episodes of mucopurulent discharge.

The causes of dacryostenosis are numerous:

Progressive narrowing of the lacrimal puncta and canaliculi is a normal (though highly variable) consequence of aging. The connective tissue and epithelium lining the drainage channels become fibrotic and lose elasticity over time, causing gradual stenosis. This is the most common cause of acquired epiphora in older adults. Additionally, age-related changes in eyelid tone and position (see ectropion below) further compromise drainage efficiency.

Inflammatory Conditions

Inflammation affecting the tissues adjacent to or within the lacrimal drainage system can cause secondary narrowing:

Ocular surface inflammation: Chronic conjunctivitis (from any cause) can cause inflammatory fibrosis of the puncta and canaliculi
Scleritis and uveitis: Inflammation of the sclera or the uveal tract (the layer between the sclera and the retina, comprising the iris, ciliary body, and choroid) can cause secondary changes affecting the lacrimal system

Eyelid Position Abnormalities

Ectropion: An outward turning of the lower eyelid margin, away from the globe. This is particularly common in older adults (senile ectropion, caused by laxity of the lower eyelid tissues) and causes epiphora by two mechanisms: the lacrimal punctum is everted away from the tear lake (puddle of tears at the inner corner of the eye), preventing effective tear entry; and the normal orbicularis pump mechanism is disrupted. Ectropion is also a cause of chronic ocular surface exposure and irritation.
Entropion: An inward turning of the eyelid margin, causing the eyelashes to rub against the corneal surface (trichiasis). This causes significant ocular irritation, reflex tearing, and potential corneal damage.

Trauma

Physical trauma to the periocular region can directly damage the lacrimal drainage structures: the puncta, canaliculi, lacrimal sac, or nasolacrimal duct. Even seemingly minor trauma (lacerations of the medial eyelid) can transect a canaliculus, causing permanent epiphora if not promptly and correctly repaired. Blunt trauma can cause bony fractures of the lacrimal groove or nasolacrimal canal, compressing the duct externally.

Viral Infections

Certain viral infections, such as herpes simplex virus (HSV), adenovirus, and varicella-zoster virus, can cause fibrotic scarring of the lacrimal drainage system. This scarring may result in secondary stenosis. Adenoviral conjunctivitis is particularly associated with punctal and canalicular scarring.

Burns and Tumors

Thermal, chemical, or radiation burns affecting the periocular area can cause fibrotic stenosis of the lacrimal drainage structures. Tumors arising from or adjacent to the lacrimal drainage system (including lacrimal sac tumors, skin cancers of the medial canthus, and nasal/sinus malignancies) can cause obstruction either by direct invasion or by extrinsic compression.

Congenital Dacryostenosis

Failure of complete canalization of the nasolacrimal duct, which in the embryo develops as a solid cord of cells that normally opens at its lower end just before or shortly after birth, results in congenital nasolacrimal duct obstruction (CNLDO). This is the most common cause of persistent epiphora in infants, affecting approximately 6% of newborns. It typically becomes evident in the first few weeks of life as persistent watery or mucopurulent discharge from one or both eyes. This often includes crusting of the lashes. While this presentation is frequently attributed to conjunctivitis, the association is often incorrect.

The critical characteristic of CNLDO is that it resolves spontaneously in the vast majority of cases. Approximately 90% of affected infants will have complete spontaneous resolution by 12 months of age, as the remaining membranous obstruction at the valve of Hasner (at the lower end of the nasolacrimal duct) opens naturally. Management in the meantime involves gentle lacrimal sac massage (Crigler massage: firm downward pressure with a fingertip over the lacrimal sac, applied 5–10 times, 2–3 times daily) to build hydrostatic pressure that may open the obstruction. This is combined with topical antibiotics if mucopurulent discharge is prominent.

If spontaneous resolution has not occurred by 12 months (or 18 months in some protocols), specialist evaluation and consideration of lacrimal probing (gentle probing of the nasolacrimal duct under brief general anesthesia to open the obstruction) is appropriate. Success rates for probing in this age group exceed 90%.

Systemic Inflammatory and Autoimmune Diseases

Several systemic conditions can cause lacrimal drainage obstruction as part of their broader inflammatory and fibrotic effects:

Sarcoidosis: Can cause granulomatous infiltration of the lacrimal system.
Granulomatosis with polyangiitis (Wegener’s granulomatosis): A vasculitic condition that frequently involves the orbit, sinuses, and nasal passages, and can cause secondary lacrimal drainage obstruction.
Sinusitis: Inflammation of the paranasal sinuses, particularly the ethmoid sinuses, can cause swelling and obstruction of the nasolacrimal duct where it opens into the inferior meatus.
Thyroid diseases: Thyroid eye disease (Graves’ orbitopathy) causes orbital tissue expansion that can compress the lacrimal drainage system.
Sjögren’s syndrome: A systemic autoimmune condition primarily targeting exocrine glands (including the lacrimal and salivary glands), causing dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia). Paradoxically, the chronic ocular surface irritation caused by Sjögren’s-related dry eye can trigger reflex tearing, causing epiphora even as aqueous tear production is impaired.
Stevens-Johnson syndrome: A severe mucocutaneous reaction (usually drug-induced) that causes intense inflammation and scarring of mucous membranes including the conjunctiva and lacrimal drainage system, often causing permanent epiphora.

Medications

Several pharmacological agents can cause or worsen lacrimal drainage obstruction:

Chemotherapy agents: 5-fluorouracil (5-FU) is particularly notorious for causing canalicular fibrosis and stenosis, a well-recognized and often severe complication of 5-FU-based chemotherapy regimens. Docetaxel and other taxanes have also been implicated.
Radiation therapy: Radiation to the head, neck, or face (including treatment of nasal, sinus, or orbital tumors) can cause fibrotic damage to the lacrimal drainage system.
Cholinergic agonists: Including pilocarpine (used in glaucoma treatment) and phospholine iodide (echothiophate iodide), these drugs can cause lacrimal system inflammation and stenosis with prolonged use.
Eye drops: Certain topical ophthalmic preparations, including those containing preservatives (particularly benzalkonium chloride, BAK), can cause chronic surface inflammation and punctal stenosis with long-term use.

Surgical Causes

Previous surgery involving the nose, sinuses, orbit, or eyelids can inadvertently damage the lacrimal drainage system, resulting in iatrogenic epiphora. This is a recognized complication of nasal septoplasty, functional endoscopic sinus surgery (FESS), orbital surgery, and medial canthal surgery.

Neonates: A Special Consideration

As described above, persistent epiphora and mucopurulent discharge in newborns and young infants is most commonly caused by congenital nasolacrimal duct obstruction (CNLDO), which is the persistence of a membranous obstruction at the lower end of the nasolacrimal duct. The characteristic presentation is:

Persistent watery or mucopurulent eye discharge, typically unilateral but occasionally bilateral.
Crusting of the eyelashes, particularly upon waking.
A distended lacrimal sac may occasionally be palpable as a swelling at the inner corner of the eye (dacryocele or amniotocele).
No true conjunctival injection, or redness, occurs in uncomplicated cases. The absence of significant redness helps distinguish CNLDO from neonatal conjunctivitis (ophthalmia neonatorum); however, superimposed infection can cause both.

Parents should be reassured that this condition almost always resolves spontaneously, and that the gentle massage technique described above can accelerate resolution. Medical attention is warranted if the eye becomes significantly red and inflamed (suggesting secondary infection), if there is a tense, painful swelling at the inner corner of the eye (acute dacryocystitis, which may require systemic antibiotics), or if the condition has not resolved by 12 months of age.

Older Adults: A Special Consideration

In older patients, epiphora is extremely common and often multifactorial. Age-related changes contributing to tearing in this population include:

Lower eyelid laxity and ectropion: As the lower eyelid muscles and connective tissue lose tone with age, the lower lid sags away from the globe. The lacrimal punctum, which should sit in close apposition to the tear lake at the inner corner of the eye, becomes everted. As a result, it cannot effectively collect tears. A patient with mild ectropion will complain of persistent watering despite intact anatomy of the lacrimal drainage ducts.
Reduced blink rate and incomplete blinking: Common in older adults (and greatly exacerbated by screen use at any age), reducing the pumping efficiency of the orbicularis oculi muscle and impairing tear distribution and drainage.
Age-related punctal and canalicular stenosis: As described above.
Concurrent dry eye disease: Paradoxically very common in older adults. Chronic ocular surface dryness triggers compensatory reflex tearing, which can overcome the reduced drainage capacity.

The combination of these factors makes epiphora one of the most frequent ophthalmic complaints in elderly patients, and management often requires addressing multiple contributing factors simultaneously.

Overproduction of Tears

In many cases of epiphora, the lacrimal drainage system remains anatomically intact and functions normally. However, the volume of tears produced simply overwhelms its capacity. This overproduction is usually driven by a stimulus to the lacrimal gland or by a reflex arc triggered by irritation of the ocular surface or cornea.

Transient and Environmental Causes

Many instances of excessive tearing are entirely transient and resolve when the triggering stimulus is removed:

Environmental irritants: Smoke (cigarette smoke, campfire, industrial fumes), dust, chemical vapors, wind, and cold air all stimulate trigeminal nerve endings in the cornea and conjunctiva, triggering the corneal reflex arc and driving reflex lacrimation. The classic experience of watery eyes on a windy day is a direct expression of this reflex.
Strong-smelling substances: Cutting onions releases allicin and propanethial S-oxide, volatile compounds that react with the moisture of the cornea to form a dilute sulfuric acid, triggering immediate copious reflex tearing.
Seasonal allergies (allergic rhinoconjunctivitis): Airborne allergens (pollens, fungal spores, dust mite proteins) bind to IgE antibodies on mast cells in the conjunctival epithelium, triggering degranulation and histamine release. This leads to the classic triad of ocular symptoms: itching, redness, and watering. These symptoms are often accompanied by nasal issues, including a runny nose and sneezing. Watering in seasonal allergic conjunctivitis is typically bilateral and strongly associated with the allergen season, with rapid improvement following allergen avoidance or antihistamine treatment.
Transitional conjunctivitis: Any inflammation of the conjunctiva, whether infectious (bacterial, viral, or chlamydial) or non-infectious, stimulates excess tear production as part of the inflammatory response. Viral conjunctivitis (most commonly adenoviral) is a particularly common cause of sudden-onset watery eye discharge, typically associated with redness, a foreign body sensation, and often preauricular lymph node enlargement. Bacterial conjunctivitis tends to produce more mucopurulent (thick, sticky) discharge.
Emotional states and physical stress: Emotional crying (psychogenic lacrimation) is mediated by cortical pathways projecting to the lacrimal nucleus, and is the most universally recognized cause of tearing. Physical stress responses (yawning, coughing, vomiting) also transiently stimulate lacrimal secretion.
Photostimulation: Bright light stimulates reflex tearing through the optic-trigeminal reflex arc. Individuals with low-grade photophobia may experience persistent tearing in ordinary daylight conditions.

Dry Eye Disease (Paradoxical Tearing)

One of the most clinically counterintuitive causes of epiphora, which is also frequently misdiagnosed, is dry eye disease (keratoconjunctivitis sicca).

In dry eye disease, the tear film is abnormal. This can happen for two main reasons: either aqueous tear production is insufficient, known as aqueous-deficient dry eye (as seen in Sjögren’s syndrome), or the lipid layer is abnormal, causing tears to evaporate too rapidly. The latter, called evaporative dry eye, is the more common form and is typically caused by Meibomian gland dysfunction. The chronically inadequate or unstable tear film leads to persistent irritation of the corneal and conjunctival surfaces. This irritation, in turn, stimulates reflex lacrimation. As a result, a paradox occurs: the patient with dry eyes experiences frequent or constant tearing.

Critically, this reflex tearing does not resolve the underlying problem: the reflex tears are of different composition from the baseline tear film, lacking the mucin and lipid components needed to maintain a stable precorneal film, and therefore do not effectively lubricate the eye. The patient continues to experience burning, irritation, intermittent blurring, and watering simultaneously.

Dry eye disease is extremely common. It affects an estimated 5–34% of adults in various populations, and its prevalence increases sharply with age. Risk factors include female sex, older age, post-menopausal hormone changes, extended screen use (which dramatically reduces blink rate and completeness), contact lens wear, systemic diseases (Sjögren’s syndrome, rheumatoid arthritis, diabetes, thyroid disease), and numerous medications (antihistamines, antidepressants, antihypertensives, diuretics, and others with anticholinergic effects that reduce all secretions).

Blepharitis

Blepharitis, a chronic inflammation of the eyelid margins, is another extremely common cause of both ocular surface irritation and poor tear film quality. The Meibomian glands within the eyelid margins produce the oily lipid layer of the tear film; when these glands become chronically inflamed and their secretions become thick and abnormal (Meibomian gland dysfunction, MGD), the tear film lipid layer is disrupted, causing accelerated evaporation and tear film instability. The result is a picture that closely resembles dry eye disease: burning, irritation, grittiness, intermittent blurring, and paradoxical epiphora. Blepharitis is typically associated with redness along the eyelid margins, crusting or scaling of the lashes, and a frothy or foamy tear film.

Insufficient or Absent Eyelid Closure

The blinking mechanism plays an essential and often underappreciated role in normal lacrimal function. Each blink:

Spreads the tear film evenly across the ocular surface, replenishing the tear film and preventing evaporative dry spots
Pumps tears toward the inner corner of the eye (the medial canthus) through the action of the orbicularis oculi muscle compressing the lacrimal canaliculi
Pumps tears from the lacrimal sac into the nasolacrimal duct through the same muscular compression

Any condition that impairs normal blinking, whether by reducing its frequency, completeness, or force, therefore disrupts both tear film maintenance and lacrimal drainage. This disruption contributes to a complex picture: simultaneous dry-spot formation and tear overflow.

Conditions causing abnormal eyelid closure or blinking include:

Congenital Malformations

Congenital abnormalities affecting eyelid structure or neuromuscular control of the orbicularis oculi may impair eyelid closure from birth. These include coloboma of the eyelid (a congenital notching or gap in the eyelid margin), congenital ptosis affecting eyelid mechanics, and various craniofacial syndromes.

Facial Nerve Palsy (Bell’s Palsy)

The facial nerve, also known as cranial nerve VII, innervates the orbicularis oculi muscle. This muscle acts as a sphincter and is responsible for eyelid closure and the lacrimal pump action. Paralysis of the facial nerve (most commonly idiopathic, as in Bell’s palsy, but also from tumors, trauma, infections, or stroke) causes lagophthalmos (inability to fully close the eye) and loss of the lacrimal pump. The resulting epiphora is worsened by severe ocular surface exposure and evaporative dry eye, both of which accompany lagophthalmos. This creates a particularly debilitating combination: constant tearing paired with a serious risk of corneal damage, known as exposure keratopathy.

Orbicularis Oculi Muscle Injury

Direct trauma to the orbicularis oculi muscle from periocular lacerations, surgical injury, or radiation damage can disrupt the lacrimal pump mechanism even when the facial nerve itself is intact, producing persistent epiphora.

Symptoms and Signs

Excessive tearing may present as an isolated symptom or in association with other signs and symptoms that provide important diagnostic information about the underlying cause. The key associated features are:

Conjunctival redness (hyperemia): Present in most inflammatory, infectious, and allergic causes; absent or minimal in simple lacrimal drainage obstruction
Eyelid swelling: Significant periorbital edema suggests allergic (angio)edema, preseptal or orbital cellulitis, or dacryocystitis
Ocular itching: Intense itching is the hallmark of allergic conjunctivitis; itching is minimal or absent in most non-allergic causes
Photophobia: Sensitivity to light suggests corneal involvement (corneal abrasion, keratitis, iritis) or severe ocular inflammation
Eye burning: Characteristic of dry eye disease, blepharitis, and chemical irritation; also common in viral conjunctivitis
Pain: Severe pain suggests corneal pathology (abrasion, ulcer, foreign body, acute keratitis), acute dacryocystitis, or orbital disease; epiphora from drainage obstruction is typically painless
Mucopurulent discharge: Thick, sticky, yellow-green discharge indicates bacterial infection (bacterial conjunctivitis, acute dacryocystitis); thin watery discharge is typical of viral conjunctivitis and lacrimal drainage obstruction; stringy mucus discharge is characteristic of allergic conjunctivitis and dry eye
Increased nasal mucus secretion: Reflects the anatomical continuity of the lacrimal and nasal drainage systems; prominently increased nasal secretion accompanying tearing suggests an allergic rhinoconjunctivitis or upper respiratory viral infection
Swelling at the inner corner of the eye: A tense, tender swelling at the medial canthus is the characteristic finding of acute dacryocystitis (infection of the obstructed lacrimal sac), a condition requiring urgent treatment
Skin changes: Periorbital dermatitis (redness and scaling of the skin around the eye) may indicate allergic contact dermatitis or seborrhoeic dermatitis
Facial asymmetry or weakness: Suggests facial nerve involvement (Bell’s palsy, tumor, or other neurological cause)

Diagnosis

When tearing is not an isolated, occasional, or clearly explained episode, particularly if it is persistent, recurrent, bilateral, or associated with other symptoms, thorough ophthalmological evaluation is essential. The following diagnostic approaches are employed:

Clinical History

A systematic history should address:

Duration and character of the tearing (constant vs. intermittent, watery vs. mucopurulent, unilateral vs. bilateral)
Associated symptoms (itching, burning, redness, discharge, pain, photophobia)
Environmental or situational triggers (seasonal pattern, wind/smoke exposure, screen use)
Medication history (particularly chemotherapy, eye drops, and anticholinergic agents)
History of nasal or sinus disease, prior ocular or nasal surgery, trauma
Systemic diseases (autoimmune conditions, thyroid disease, atopy)
History of skin conditions or periocular lesion changes

Slit-Lamp Biomicroscopy

The fundamental ophthalmic examination tool, allowing detailed magnified inspection of the:

Eyelid margins (blepharitis, eyelid position, punctal anatomy and position)
Conjunctiva and sclera (injection, follicles or papillae indicating inflammation type, scarring)
Cornea (fluorescein staining to detect epithelial defects, erosions, ulcers, foreign bodies)
Tear film (quality, break-up time, meniscus height)
Lacrimal puncta (size, position, patency)

Tear Film Assessment

Tear Break-Up Time (TBUT): After instillation of fluorescein dye, the time until the first dark spot appears in the tear film (reflecting a dry spot) is measured under the slit lamp’s cobalt blue light. Normal TBUT is >10 seconds; <5 seconds indicates significant tear film instability.
Schirmer’s test: A standardized paper strip placed in the inferior conjunctival fornix measures the volume of tears produced over 5 minutes. Results below 5 mm suggest aqueous-deficient dry eye.

Lacrimal Drainage Assessment

Fluorescein dye disappearance test (FDDT): A drop of fluorescein dye is placed in both eyes; after 5 minutes, the tear meniscus is inspected. Persistence of the dye in one eye compared to the other suggests drainage dysfunction on that side.
Lacrimal irrigation (lacrimal syringing): A cannula is inserted into the lacrimal punctum and saline is gently injected to assess patency of the entire drainage system. This both confirms the presence of obstruction and approximates its location within the system.
Lacrimal probing: A fine metal probe is passed through the punctum and canaliculus to assess patency and localize the level of obstruction.
Dacryocystography (DCG): X-ray or CT imaging of the lacrimal drainage system following injection of contrast dye, providing detailed anatomical information about the site and nature of an obstruction.
Dacryoscintigraphy: A physiological test using technetium-labeled eye drops and gamma camera imaging to assess the dynamic function of the lacrimal drainage system under normal blinking conditions.
Nasal endoscopy: Examination of the nasal cavity, particularly the region of the inferior meatus where the nasolacrimal duct opens, to identify intranasal causes of obstruction or to plan surgical dacryocystorhinostomy.

Microbiological Investigations

Conjunctival swabs for bacterial culture and sensitivity, viral PCR testing, and Chlamydia testing are indicated when an infectious cause is suspected or when standard treatment has not resolved presumed infectious conjunctivitis.

Systemic Investigations

When a systemic cause is suspected (Sjögren’s syndrome, sarcoidosis, thyroid disease, vasculitis), appropriate blood tests and specialist referral are indicated. Biopsy of accessible tissue (minor salivary gland biopsy for Sjögren’s diagnosis, skin or conjunctival biopsy for sarcoidosis) may be necessary.

Treatment and Remedies

The management of excessive tearing is directed entirely at the underlying cause. Because the spectrum of causes ranges from trivially transient to surgically complex, treatment approaches vary enormously in their nature and intensity.

Self-Resolving and Environmental Causes

In many cases, the tearing is transient and resolves spontaneously when the precipitating stimulus is removed: leaving a smoky environment, completing a bout of emotional crying, or waiting out the pollen season. No specific treatment is required beyond the removal of the triggering factor.

Paradoxical epiphora caused by dry eye disease responds well to regular artificial tear supplementation. By restoring a stable, adequate tear film, the chronic corneal surface irritation driving reflex tearing is reduced, and overall tearing volume decreases. A wide variety of formulations is available:

Preservative-free drops: Preferred for frequent use (more than 4–6 times daily), as the preservatives in multidose bottles (particularly benzalkonium chloride) cause cumulative surface toxicity with frequent application
Viscous gels and ointments: Provide longer contact time and are particularly useful for nighttime application or for more severe dry eye
Lipid-supplementing drops: Particularly effective for evaporative dry eye (Meibomian gland dysfunction) by replenishing the deficient lipid layer
Anti-inflammatory eye drops: In moderate to severe dry eye, topical cyclosporine (ciclosporin) or lifitegrast eye drops reduce the inflammatory component of dry eye disease, improving tear film quality over 3–6 months of use

Blepharitis Management

Warm compresses: Applied to the closed eyelids for 10 minutes daily, softening the thickened Meibomian gland secretions and facilitating their expression
Lid margin hygiene: Gentle cleaning of the eyelid margins with a diluted baby shampoo solution or commercial lid wipe preparations to remove debris and biofilm
Topical or oral antibiotics: Low-dose oral doxycycline (50–100 mg daily for 6–12 weeks) or topical azithromycin eye drops are effective for Meibomian gland dysfunction associated with blepharitis; topical antibiotics (fusidic acid, chloramphenicol) for bacterial blepharitis
Intense Pulsed Light (IPL) therapy: An emerging, evidence-supported treatment for chronic Meibomian gland dysfunction, particularly in patients with associated skin rosacea

Pharmacological Treatment of Allergic Causes

Topical antihistamine eye drops: Combined antihistamine/mast cell stabilizers (e.g., olopatadine, ketotifen) are the first-line treatment for allergic conjunctivitis, rapidly reducing itching and tearing.
Oral antihistamines: Second-generation, non-sedating antihistamines (cetirizine, loratadine, fexofenadine) provide systemic control of allergic symptoms including ocular features.
Allergen avoidance: The most effective long-term strategy is minimizing exposure to known triggers.
Topical mast cell stabilizers: Sodium cromoglicate and nedocromil are effective when used prophylactically before allergen exposure.
Allergen immunotherapy (desensitization): For patients with clinically significant, documented allergen sensitization causing persistent symptoms despite pharmacological management, subcutaneous or sublingual immunotherapy can induce long-term immunological tolerance.

Treatment of Infectious Conjunctivitis

Bacterial conjunctivitis: Topical antibiotics (chloramphenicol, fusidic acid, fluoroquinolones for more severe cases). Most cases of bacterial conjunctivitis are self-limiting within 7–10 days even without treatment, but antibiotics shorten the symptomatic period and reduce contagiousness.
Viral conjunctivitis: Largely supportive. Use cold compresses and lubricating drops for comfort. Topical antiviral agents (aciclovir) are indicated for herpetic conjunctivitis.
Chlamydial conjunctivitis: Systemic antibiotics (oral doxycycline or azithromycin) are required, as topical antibiotics alone are insufficient.

Corticosteroids (topical or systemic) are indicated for allergic or inflammatory causes when first-line treatments are insufficient. Topical corticosteroids require careful ophthalmological supervision due to the risks of cataract formation, elevated intraocular pressure, and masking of infectious conditions.

Surgical Management of Lacrimal Drainage Obstruction

When pharmacological measures fail to resolve epiphora caused by lacrimal drainage obstruction, surgical intervention is required.

Dacryocystorhinostomy (DCR)

The definitive surgical treatment for nasolacrimal duct obstruction is dacryocystorhinostomy (DCR). This procedure creates a new drainage pathway directly between the lacrimal sac and the nasal cavity, bypassing the obstructed nasolacrimal duct entirely.

The procedure has evolved significantly over the decades:

External DCR (traditional approach): Performed through a small skin incision at the inner corner of the eye, the lacrimal sac is identified and opened, a window is made in the underlying bone, and the nasal mucosa is incised. Flaps of lacrimal sac mucosa and nasal mucosa are sutured together to create a permanent opening. Silicone tubes (stents) are typically placed through the new passage and left for several weeks to maintain patency during healing before being removed in the office without anesthesia. This approach has high long-term success rates (>90%) but requires general anesthesia in most settings and leaves a small facial scar.
Endoscopic (endonasal) DCR: Performed entirely from within the nasal cavity using an endoscope introduced through the nostril, without any external skin incision. The lacrimal sac is identified through the nasal mucosa and a new ostium is created endoscopically. Silicone stents are placed as in the external approach.
Laser-assisted DCR: Using laser energy (typically diode or holmium:YAG laser) via an endoscopic or transcanalicular approach to create the bony window and mucosal opening. This can often be performed under local anesthesia or sedation rather than general anesthesia, and the precision of laser technology ensures excellent surgical control and outcomes. This minimally invasive approach is increasingly favored, particularly in elderly or medically complex patients who are poor candidates for general anesthesia.

The choice between external, endonasal endoscopic, and laser DCR depends on the patient’s anatomy, the specific nature and level of the obstruction, the surgeon’s expertise, and patient preference. All approaches aim to achieve the same result: a patent, permanent new tear drainage pathway.

Additional Surgical Considerations

Punctal dilation and probing: For isolated punctal stenosis (narrowing of the punctal opening), dilation of the punctum using graduated probes can be effective. This procedure may also involve placing a punctal plug or a mini-Monoka stent to maintain the newly enlarged opening during healing.
Canalicular repair: Traumatic transection of a lacrimal canaliculus requires prompt surgical repair (ideally within 24–48 hours of the injury) using fine monofilament sutures and intubation of the repaired canaliculus with a silicone tube to maintain patency during healing.
Eyelid surgery: Ectropion repair (tightening the lower eyelid through lateral canthal fixation procedures) and entropion repair are effective, well-tolerated procedures with high success rates for their respective indications.
Lagophthalmos management: In Bell’s palsy and other causes of facial nerve palsy, various approaches to protect the cornea and improve eyelid closure are available: lubricating eye drops and ointments (used intensively), moisture-chamber spectacles, gold weight implantation in the upper eyelid (to allow gravity-assisted closure), tarsorrhaphy (partial surgical closure of the eyelid margins), or dynamic procedures to restore orbicularis oculi function.
Surgery for foreign body penetration: Significant penetrating ocular trauma requires urgent surgical management by an ophthalmologist. Attempting to remove a penetrating foreign body without specialist care risks catastrophic intraocular injury.

Lacrimal Sac Massage (for Neonatal Dacryostenosis)

As noted above, parents of infants with congenital nasolacrimal duct obstruction should be taught the Crigler massage technique: using the tip of a clean finger, applying firm, rhythmic downward pressure over the lacrimal sac (located at the inner corner of the eye, just below the medial canthus) 5–10 times, 2–3 times daily. This creates hydrostatic pressure within the lacrimal sac that can open the membranous obstruction. Parents should also be taught to clean any discharge from the lashes with a clean damp cloth and to apply prescribed topical antibiotics if mucopurulent discharge is present.

References and Bibliography

Ernst D, Witte T. Sjögren’s syndrome. Dtsch Med Wochenschr. 2016 Apr;141(8):544-50. doi: 10.1055/s-0041-111436. https://pubmed.ncbi.nlm.nih.gov/27078243/
American Academy of Ophthalmology. Tearing. https://www.aao.org/eye-health/symptoms/tearing
Hurwitz JJ. The Lacrimal System. Lippincott-Raven Publishers, 1996.
Olver JM. Functional Anatomy of the Choroidal Circulation: Methyl Methacrylate Casting of Human Choroid. Eye. 1990.
Kashkouli MB, et al. External versus endoscopic dacryocystorhinostomy: a systematic review and meta-analysis. Ophthalmic Plastic and Reconstructive Surgery. 2014;30(4):275-280.
Ali MJ. Principles and Practice of Lacrimal Surgery. Springer, 2015.
MacEwen CJ, Young JD. Epiphora during the first year of life. Eye (London). 1991;5 (Pt 5):596-600.
Pflugfelder SC, Baudouin C. Challenges in the clinical measurement of ocular surface disease in dry eye. Expert Opinion on Medical Diagnostics. 2011;5(2):145-158.
DEWS II Report (Dry Eye Workshop II). TFOS DEWS II Pathophysiology Report. The Ocular Surface. 2017;15(3):438-510.

Excessive and Continuous Eye Watering (Epiphora): Causes, Symptoms, and Treatment