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The common complaint of a watering eye may be caused by a variety of problems, including lacrimal hyposecretion, lacrimal hypersecretion, or blockage of the lacrimal drainage system. This system is a complex membranous channel whose function depends on the interaction of anatomy and physiology. Effective tear drainage depends on a variety of factors, including the volume of tear secretion, eyelid position, and anatomy of the lacrimal drainage passages. Epiphora is defined as an abnormal overflow of tears down the cheek. The patient with symptomatic tearing may have a normal lacrimal drainage system overwhelmed by primary or secondary (reflex) hypersecretion or a drainage system that is anatomically compromised and unable to handle normal tear production. On the other hand, a patient with partial drainage obstruction may have a concomitant reduction in tear production and therefore be completely asymptomatic or may even suffer from symptomatic dry eye syndrome. Epiphora is determined by the balance between tear production and tear drainage, not by the absolute function or dysfunction of either one. The causes of lacrimal drainage problems can be divided into two categories: anatomic and functional. Anatomic obstruction refers to a mechanical or structural abnormality of the drainage system. The obstruction may be complete, such as punctal occlusion, canalicular blockage, or nasolacrimal duct fibrosis, or partial, caused by punctal stenosis, canalicular stenosis, or mechanical obstruction within the lacrimal sac (i.e., dacryolith or tumor). In patients with functional obstruction, epiphora results not from anatomic blockage but from a failure of lacrimal drainage physiology. This failure may be caused by anatomic deformity such as punctal eversion or other eyelid malpositions, but can also result from lacrimal pump inadequacy caused by weak orbicularis muscle action. It is helpful to determine whether the patient’s complaint is true epiphora or a “watery eye.” Detailed history-taking and careful examination will help direct the evaluation of a tearing eye. A host of clinical tests have been described, and the selection of appropriate tests will depend on the initial history and ophthalmic examination. 13-1-1 History-Taking. Any clinical evaluation should begin with a thorough history. A complaint of watery eye does not necessarily imply a lacrimal drainage problem.

Tearing is a common presenting complaint in infants referred to an ophthalmologist and may be the first sign of something as benign as an impermanent anatomic defect or as grave as congenital glaucoma. When tearing is chronic, parents of an affected infant are often frustrated by the persistent accumulation of fluid and mucopurulent material in the eye and on the eyelids and anxious that the condition may be a sign of a more serious problem. The best initial management of tearing in an infant is to take a detailed history, which often provides important clues as to the cause of tearing, and then to perform a thorough, systematic ophthalmic examination. Tears serve four main functions: (1) they form a tear film to keep the eye moist, (2) they lubricate the eye, (3) they keep the eye clear of particulate matter and debris, and (4) they provide a refractive surface on the corneal epithelium. The tear film comprises three layers: a thin inner layer of proteinaceous mucin coats and protects the eye, an aqueous layer keeps the eye moist and lubricated, and an outer lipid layer slows evaporation of the aqueous layer. Basal tears are produced by the accessory lacrimal glands located in the conjunctiva and keep the eye moist under steady-state conditions; normal patients have a tear meniscus (or “tear lake”) visible along the inner lower eyelid as a result of basal tear production. Irritation or emotional extremes can trigger reflex tear production by the main lacrimal gland in the superotemporal quadrant of the orbit, “flooding” the tear lake. The level of the tear lake is highest when the rate of tear production by the lacrimal glands exceeds the rate of tear drainage into the nasolacrimal system. Tears normally drain out of the eye through puncta located on the nasal portion of the upper and lower eyelids. They then enter the upper and lower canaliculi, which run inferiorly and medially before joining to form the common canaliculus, which conducts tears through the valve of Rosenmuller and into the lacrimal sac.

Obstruction of the tear outflow system can occur anywhere along its course from the tear lake to the inferior meatus of the nose. Surgical techniques designed to relieve this functional or complete obstruction have been available for a long time. Toti of Italy described the dacryocystorhinostomy (DCR) procedure in 1908 as a treatment modality for obstruction of the nasolacrimal duct. His technique did not make use of mucosal flaps. Dupuy-Dutemps of France, on the other hand, encouraged the use of flaps. He recommended suturing together the nasal mucosal and lacrimal sac flaps. The success rate of the operation improved dramatically. Today the external DCR procedure makes use of modifications of both of these historically described procedures. In recent years, intranasal DCR has enjoyed renewed popularity. This procedure had been performed by Lester Jones and others for years but was dropped because the success rate was 80% at best. Although the use of endoscopic techniques and laser technology has been advocated by some authorities, the success rate (approximately 70%) with relatively short-term follow-up has limited its acceptance. More recently, Javate and associates reported a series of patients undergoing endoscopic DCR with the radiofrequency Ellman unit. Their reported success rate of 90% compared favorably with a 94% success rate in 50 age-matched patients undergoing external DCR with a follow-up of 9 months. This rate also compares favorably to the present authors’ success rate of approximately 95% in uncomplicated cases undergoing external DCR and a similar rate with the endoscopic approach without use of a laser. Therefore, the laser does not appear to offer any significant advantage over more traditional intranasal approaches, and the cost may actually be a financial disincentive to its use. The benefit of mitomycin continues to be debated. You and associates performed a prospective study showing favorable long-term success rates with the use of mitomycin. On the other hand, Liu and associates performed a prospective study that demonstrated no benefit. While the DCR works well for lacrimal sac or nasolacrimal duct obstruction, it does not address obstructions of the puncta and canaliculi.

Once feared for its deadly properties, Botulinum toxin is now revered for its effectiveness as a treatment in minimally invasive facial rejuvenation. The injection of Botulinum toxin is the most frequently performed nonsurgical cosmetic procedure, with at least 4.8 million procedures in 2009. First approved by the U.S. Food and Drug Administration (FDA) in 1979 for the treatment of strabismus, Botulinum toxin was shown to be both safe and effective for use to decrease muscle function. Botulinum toxin’s cosmetic applications were first recognized when it was noted that facial rhytides improved in the areas of treatment with the toxin when it was used for noncosmetic applications in the late 1980s and early 1990s. FDA approval for cosmetic treatment of the glabellar furrows was announced in 2002, and off-label aesthetic indications have continued to evolve. Botulinum toxin is produced by the gram-positive, anaerobic Clostridium botulinum. The neurotoxin acts on the peripheral nervous system, where it inhibits release of acetylcholine from the presynaptic terminal at the neuromuscular junction. There are seven distinct antigenic Botulinum toxins (BTX-A, B, C, D, E, F, and G) produced by different strains of C. botulinum. The human nervous system is susceptible to only five of these serotypes (BTX-A, B, E, F, G), and types A and B are currently available for human injection. In the United States, there are four commercially available Botulinum toxin preparations: three types of Botulinum toxin type A, OnabotulinumtoxinA or Botox Cosmetic® (Allergan, Inc., Irvine, CA), IncobotulinumtoxinA or Xeomin (Merz, Frankfort Germany), and abobotulinumtoxinA or Dysport (Medicis, Scottsdale, AZ). There is one preparation of Botulinum toxin type B, RimabotulinumtoxinB or Myobloc® (Elan Pharmaceuticals, San Diego, CA). Other Botulinum toxin type A products are anticipated to come to the U.S. market in the next decade as well. Different formulations of Botulinum toxin type A are biochemically unique and are not necessarily equivalent in dosing. The Botox unit is three times as potent as the Dysport unit, but this conversion ratio does not take into consideration safety or antigenic potential. Practically speaking, a range of 2.5 to 3 to one has been recommended to make Dysport dosing approximate the effects of Botox.