Epiphora (tearing) is a common ophthalmic problem comprising 3% of all clinic visits. The majority of patients presenting to a tertiary care center or oculoplastic specialist have tearing secondary to obstruction at some level in the nasolacrimal system. The most common obstructive etiology is nasolacrimal duct obstruction distal to the lacrimal sac, however there are a subset of patients who present with canalicular obstruction.
The frequency of canalicular obstruction has been reported to be between 16 and 25% in patients presenting with obstructive epiphora. The obstruction can occur either at the upper/lower canaliculus or the common canaliculus.
Many conditions have been associated with canalicular obstruction. It may be congenital or acquired.
Congenital canalicular obstruction:
The lacrimal system is affected in up to 78% of the cases of anophthalmos or severe microphthalmos. This may be seen as punctal atresia or stenosis, canalicular stenosis (58%), or common canalicular stenosis (7.3%).
Acquired canalicular obstruction:
- Inflammatory and infectious: Blepharitis, canaliculitis, infections (viral, bacterial, fungal), ocular cicatricial pemphigoid, Steven Jonson Syndrome, ectropion.
- Traumatic: canalicular laceration, chemical burn; thermal burn
- Drug-induced: Docetaxel, Paclitaxel, Pilocarpine; Timolol, Dorzolamide; Idoxuridine; trifluridine; Fluorouracil, echothiophate iodide, Dipivefrin, Betaxolol, Mitomycin, Isotretinoin, Verteporfin.
- Systemic disease: Malignancy, lichen planus, inflammatory bowel disease.
- Iatrogenic: Prior punctal plugs, punctal cauterization, post-surgical damage, longstanding lacrimal intubation, radiotherapy.
Differentiating between risk factors and etiological factors in canalicular obstruction disease is often difficult. Old age was found to be a risk factor for punctual and canalicular obstruction. However, considering gender as a risk factor for canalicular obstruction was found to be controversial in different studies. Chronic blepharitis, apart from its etiological contribution, was found to be a risk factor for recurrent stenosis.
Canalicular obstructions could be anatomically classified as:
- Proximal: Initial 2–3 mm from the punctal opening
- Midcanalicular: 3–8 mm from the punctum
- Distal: from a membrane at the opening of the common canaliculus to the lacrimal sac
A variety of pathological processes can result in canalicular obstruction. Inflammatory conditions initially cause lacrimal mucosal swelling but may lead to fibrotic narrowing or obstruction. Canalicular stenosis and obstruction related to punctal plugs is associated with accumulation of debris, including inflammatory reactions resulting in scar formation along with injury to canaliculus by the act of probing itself, prior to plug insertion. The mechanical stress on the mucosa might lead to mild chronic inflammation, causing stenosis of the punctum. The histological findings associated with topical anti-glaucoma medications include conjunctival metaplasia, decrease in goblet cells and increased number of sub-conjunctival fibroblasts, macrophages, and other inflammatory cells. These changes may account for punctal and/or canalicular stenosis in this group of patients. Involutional changes such as tissue atrophy, atonicity of the surrounding orbicularis fibers and dense fibrotic structures of the punctum and the canaliculus result in punctal and proximal canalicular stenosis.
Primary prevention of canalicular obstruction includes early ophthalmic consultation and treatment for susceptible patients, especially those with an increased risk for developing stenosis due to topical or systemic treatment with causative medications, treatment of chronic blepharitis, avoidance of frequent canalicular probing which can cause further damage and patients on Docetaxel treatment should undergo insertion of bicanalicular silicone stents to prevent complete closure of the canaliculi, and prevent more complicated surgeries.
History of any concurrent ocular or systemic disease, topical and systemic medications, surgeries, allergy, trauma, previous ocular interventions, including those for dry eye disease, need to be recorded.
Canalicular obstruction symptoms are excessive moisture in eyes, overflow of tears on the cheek and mildly blurred vision.
Signs include increased tear lake, evident epiphora, stenosis of punctum and difficulty in passing lacrimal dilator or probe.
- Clinical diagnosis is reached by a systematic clinical examination of eyelids and lacrimal system.
- A slit lamp examination can identify the presence of a membrane or fibrosis over the punctum, punctum size, tear meniscus height, eyelid margin, conjunctiva around the punctum, eyelid malposition, position of the punctum in the tear lake, and any sign of previous surgery.
- Schirmer test, tear break up time, ocular surface staining, and tear meniscus height will highlight any associated ocular surface abnormalities.
- The medial canthal region should be palpated and compressed, looking for any regurgitation through the puncta (regurgitation test). Mucopurulent regurgitation signifies NLD obstruction.
- Dye disappearance test (DDT) is useful to differentiate hyperlacrimation from lacrimal drainage obstruction (whether functional or anatomical). In this test, one drop of fluorescein 2% or a fluorescein strip wetted by artificial tears is gently placed or briefly inserted in the inferior fornix of each eye. The tear meniscus height is evaluated with cobalt blue light after five minutes for the clearance of fluorescein and symmetry of dye in both eyes. If dye is absent after five minutes, this indicates a patent system. Presence of dye indicates the anatomical obstruction between the punctum and valve of Hasner.
- Lacrimal probing, lacrimal irrigation and probing of the canaliculi are two investigations that may be part diagnostic and part therapeutic, for example by dislodging a stone. Probing may be used in an attempt to palpate or localize the site of obstruction. With probing, the length of canalicular patency distal to the punctum can be measured, and from that the length of the canalicular blockage can be estimated. Following punctal dilation, a Bowman probe is used to pass through the punctum and ampulla into the canaliculus. A hard stop signifies a patent canaliculus. Usually a gritty sensation or mild resistance while passing the probe implies canalicular stenosis. Soft resistance to the probe that cannot be overcome may signify obstruction. Location of the canalicular stenosis and obstruction can be measured by grasping the punctal end of the probe and withdrawing it from the canaliculus.
- Irrigation of the lacrimal system provides valuable information as to the lacrimal drainage system patency. Return from the same punctum with some passage of fluid to the nose could imply canalicular stenosis. Common canalicular obstruction typically results in the return of clear fluid from the opposite punctum. The return of the fluid along with some mucous through the other punctum signifies the presence of complete nasolacrimal duct (NLD) obstruction. Patients with stenotic NLD feel the passage of fluid to the nose with minimum reflux from the other canaliculus.
- Dacryocystography is of limited diagnostic value in canalicular disorders. Lacrimal scintigraphy may be useful in those patients with presumed functional epiphora. Canalicular endoscopy, if available, can directly reveal the position of the obstruction.
- Laboratory test offer limited value t to be done in canalicular obstruction. Abnormal eye discharge needs to be sent for the different studies (depending on suspected etiologies) such as Gram stain/Giemsa stain, cultures and sensitivities.
- Conjunctival biopsy may be done for patients suspected to have ocular cicatricial pemphigoid. Additionally, blood test can be requested according to the possible etiology such as anticytoplasmic antibodies for granulomatosis with polyangiitis (formerly Wegener's).
Agensis of canalicular system, punctal atresia, Nasolacrimal duct obstruction, evaporative dry eye, conjunctivitis, canaliculitis, trachiasis and eye lid malposition (ectropion or entropion) are distinguishing characteristics of canalicular obstruction.
Management strategies are influenced by the aetiology, obstruction position and extent.
Goals of treatment for canalicular obstruction include: relieving the patients’ symptoms; maintenance of anatomic patency of the canaliculi; preventing progression to complete obstruction, and maintaining the function of the opposite canaliculus.
Medical management can be used for patients at risk of developing canalicular obstruction. It is found that the use of topical steroid drops and artificial tears during use of systemic chemotherapeutic agents especially (5-fluorouracil, docetaxel, idoxuridine) may prevent canalicular scarring and fibrosis. Moreover, successful treatment of eye infectious causes such as conjunctivitis or canaliculitis can maintain the patency of the lacrimal drainage. Conservative treatment
Medical follow up
Timely diagnosis and appropriate management of a canalicular narrowing in patient with risk factors can prevent moving to surgical options for managing canalicular obstruction such as conjunctivodacryocystorhinostomy (CDCR).
- Surgical options are influenced by how distal, proximal or extensive the obstruction is found to be. The full extent of the obstruction may only become full apparent during surgery
- Incomplete obstruction or stenosis can be treated with canalicular stenting and intubation.
- For proximal - mid canalicular obstructions: Reconstruction: the focal canaliculus obstruction near the puctum can be excised. The cut ends of the canaliculus anastomosed over a stent. Dacrocystorhinostomy with retrograde intubation of the lacrimal system has shown some success may avoid the need for a Jones tube.
- For more distal obstruction, trephining of scarred segment can establish a patent lumen. Stenting is then required to prevent contracture and also to provide scaffolding to direct proper epithelialization. Balloon canaliculoplasty can be performed following lacrimal trephination or in cases of stenosis..
- Canaliculodacryocystorhinostomy: if there is total obstruction at the common canaliculus, the common canaliculus is removed and the remaining of the canalicular system directly anastomosed to the lacrimal sac mucosa over the silicone stent. Using silicone stent with large diameter may increase the success of the surgery.
- Conjuctivodacryocyctorhinostomy (CDCR): when the canaliculi are severely obstructed and cannot be reconstructed, a Pyrex glass tube (Jones tube) is placed through an opening created at the inferior half of the caruncle and then through the osteotomy site into the middle nasal meatus. Many modifications of the original Jones tube exist.
Surgical follow up
Canalicular stents may be left in situ for several months to ensure proper canalicular epithelialization. A Lester-Jones tube requires regular follow up for cleaning of the tube.
Canalicular obstruction may recur following the stent removal. Conjunctivitis with or without granulation due to pressure from the collar of the tube against the upper lid or conjunctiva may complicate Jones tube placement. Diplopia and ectropion of the lower lid may occur due to abnormal Jones tube placement. For cases where Jones tube comes out, it should be treated immediately as it is not possible to re-insert the tube if it is delayed.
The successful treatment of canalicular obstructions continues to represent a therapeutic challenge. CDCR with a Lester Jones bypass tube is the standard treatment in situations where there is extensive canalicular obstruction. Although a high rate of anatomic success can be achieved with this procedure, many studies have reported a relatively high rate of complications affecting patient’s satisfaction. Despite these drawbacks, many patients with otherwise intractable epiphora are helped by this procedure.
1. Mohsen Bahmani Kashkouli, Farzad Pakdel, Victoria Kiavash. Assessment and Management of Proximal and Incomplete Symptomatic Obstruction of the Lacrimal Drainage System. Middle East Afr J Ophthalmol. 2012 Jan;19(1):60-9.
2. Vasilios S. Liarakosa , Kostas G. Boboridisb , Emmanouil Mavrikakisa and Ioannis Mavrikakis. Management of canalicular obstructions. Current Opinion in Ophthalmology 2009, 20:395–400.
3. Orbit, Eyelids, and Lacrimal System, section 7. Basic and Clinical Science Course, AAO, 2013-2014
4. Kai E. Wilhelm, Ulrich Hofer, Hans J. Textor, Thorsten Böker, Holger Strunk, Hans H. Schild. Nonsurgical fluoroscopically guided dacryocystoplasty of common canalicular obstructions. CardioVascular and Interventional Radiology January 2000
5. White WL, Bartley GB, Hawes MJ, Linberg JV, Leventer DB. Iatrogenic complications related to the use of Herrick Lacrimal Plugs. Ophthalmology. 2001 Oct;108(10):1835-7.
6. Farzad Pakdel, MD; Mohsen Bahmani Kashkouli, MD. Lacrimal Drainage Obstruction Associated with Topical and Systemic Medications. Journal of Ophthalmic and vision research 2009; Vol. 4, No. 4.
7. B. Esmaeli1, G. Hortobagyi, F. Esteva, V. Valero, M. A. Ahmadi, D. Booser, N. Ibrahim,E. Delpassand & R. Arbuckle. Canalicular stenosis secondary to weekly docetaxel: a potentially preventable side effect. Annals of Oncology 13: 218–221, 2002
8. Athanasiov PA, Prabhakaran VC, Mannor G, Woog JJ, Selva D. Transcanalicular approach to adult lacrimal duct obstruction: a review of instruments and methods. Ophthalmic Surg Lasers Imaging. 2009 Mar-Apr;40(2):149-59.
9. Tao H, Xu L-P, Han C, Wang P, Bai F. Diagnosis of lacrimal canalicular diseases using ultrasound biomicroscopy: a preliminary study. International Journal of Ophthalmology. 2014;7(4):659-662.
10. Suk-Woo Yang , Hae-Young Park , and Don O. Kikkawa. Ballooning canaliculoplasty after lacrimal trephination in monocanalicular and common canalicular obstruction. Jpn J Ophthalmol. 2008 Nov-Dec;52(6):444-9.
11. Wearne MJ, Beigi B, Davis G, Rose GE. Retrograde intubation dacryocystorhinostomy for proximal and midcanalicular obstruction. Ophthalmology. 1999 Dec;106(12):2325-8; discussion 2328-9.
12. Steele EA.Conjunctivodacryocystorhinostomy with Jones tube: a history and update. Curr Opin Ophthalmol. 2016 Sep;27(5):439-42.