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The lacrimal drainage apparatus is a system that carries tears, produced by the lacrimal gland, from the ocular surface to the nasal cavity. It is defined by the following structures: the puncta, the canaliculi, the lacrimal sac, and the nasolacrimal duct. Moreover, two one-way valves are physiologically important to prevent tear reflux: the valve of Rosenmüller and the valve of Hasner ( Fig. 9.1 ). Different mechanisms have been proposed to describe tear flow from the ocular surface to the nasal cavity, and the most relevant was theorized in 1960s and named “Jones' pump,” from the name of the ophthalmologist who conceived it.
As for the external oculo-lacrimal anatomy, full knowledge of the endonasal anatomy is fundamental. In particular, the lateral nasal wall in its most anterior part is the area of interest for lacrimal surgery. When introducing the endoscope into the nose beyond the nasal vestibule, the inferior and the middle turbinates are found laterally, inserting onto the lateral wall. In the inferior meatus localized below the inferior turbinate, we find the entrance to the nasolacrimal canal and the valve of Hasner. The middle meatus is below and lateral to the middle turbinate. The most important structures in this region are the uncinate process, the infundibulum with the hiatus semilunaris, and the ethmoidal bulla. In front of the superior insertion of the middle turbinate is the agger nasi, which represents the most anterior ethmoidal cell. Once these structures are recognized, the area that corresponds to the fossa where the lacrimal sac is located should be identified above the insertion of the anterior end of the middle turbinate. In particular, the major portion of the sac (approximately 10 mm) is found above the axilla of the middle turbinate.
Disorders of the lacrimal drainage apparatus arise from abnormalities affecting any point along the tears passageway. Canalicular obstruction may be attributed to several etiologies, either congenital , (e.g., punctal atresia, canalicular obstruction, common canalicular stenosis, in cases of anophthalmia or microphthalmia) or acquired. The latter ones may be inflammatory (e.g., blepharitis), traumatic (e.g., canalicular laceration or chemical burn), drug-induced (e.g., by taxanes or Mitomycin), iatrogenic (e.g., prior punctal plugs, punctal cauterization, postsurgical damage, longstanding lacrimal intubation, radiotherapy), or due to local malignancy. However, most cases of lacrimal disorders are ascribable to abnormalities involving the nasolacrimal duct. Nasolacrimal duct obstructions (NLDO) may be classified as either congenital (CNLDO) or acquired. CNLDO is a common disorder in the pediatric population with a prevalence between 5% and 20% in early childhood, causing impaired drainage of tears through the lacrimal system and clinically presenting with epiphora. The acquired NLDO may be idiopathic (or primary), iatrogenic, or posttraumatic. The primary form is the most common, and its etiology is unknown. However, it is postulated that the primum movens for the occlusion of the lacrimal system is inflammation, even of unknown cause, that results in occlusive fibrosis and consequent epiphora.
Possible additional findings in adults are lacrimal sac mucocele or dacryocele/dacryocystocele ( Fig. 9.2 ). They refer to a dilated lacrimal sac that develops secondarily to the coexistence of a distal NLDO, and a proximal functional or structural obstruction (at the junction of the common canaliculus and lacrimal sac). It commonly presents as a mass in the medial canthal region accompanied by epiphora, and sometimes complicated by episodes of inflammation/infection (dacryocystitis/mucopyocele) ( Fig. 9.3 ). Various hypotheses to describe its pathophysiology have been postulated, with two of them being the most accredited ones. A congenital or acquired (due to inflammation or trauma) obstruction of the distal NLD may cause secretions to accumulate within the sac. The increasing pressure on the sac walls may reach the area of junction between the sac and the two canaliculi, causing them to fold upon themselves and displace, resulting in proximal obstruction. The other postulated mechanism includes kinking of the common canaliculus due to malfunction of the Valve of Rosenmüller, that is the entrance of the common canaliculus into the lacrimal sac, secondary to edema and inflammation. Lacrimal sac mucoceles are known to cause bony erosion and remodeling, probably because of both inflammatory mediators and the pressure effect of the mass on the surrounding walls. Occasionally, this process extends to the overlying skin and spontaneous rupture or fistula formation may occur.
For what concerns treatments of pediatric CNLDO, conservative therapy (e.g., observation, lacrimal sac massage, and antibiotics) seem to be the best option in infants aged less than 1 year. On the other hand, in children older than 1 year, probing is successful for most obstructions, even if the timing for probing remains controversial and debated. In adult patients, surgery (e.g., dacryocystorhinostomy) is the gold standard treatment for acquired NLDO.
Indications to perform lacrimal surgery include cases of clinically significant epiphora or chronic conjunctivitis in the presence of nasolacrimal duct obstruction, recurrent dacryocystitis, or the presence of dacryoliths in the lacrimal sac that cause recurring episodes of nasolacrimal duct obstruction.
Malignancy of the lacrimal sac represents the only absolute contraindication to lacrimal surgery. Active dacryocystitis is a relative contraindication to the ab externo approach (see Section 9.2.2 ).
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