Congenital lacrimal fistula is an uncommon developmental condition consisting of an accessory or anlage canaliculi between the lacrimal system and the skin. In some cases, the course of such abnormal ducts may be blinded and not in communication with the skin, which may render the clinical presentation occult.
Congenital lacrimal fistulae classification is based on the origin point of its tract, which may derive from the common canaliculus, the lacrimal sac, or the nasolacrimal duct.
The normal adult anatomy of the lacrimal apparatus includes the puncta lacimalia, lacrimal ducts, nasolacrimal ducts, sac, and lacrimal glands (See figures of the lacrimal apparatus). To understand the pathogenesis of congenital lacrimal fistula, it is mandatory to refer to the embryology of the lacrimal system.
The nasolacrimal ducts originate from an ectodermal thickening around the naso-optic fissure in the early 32-day-old embryo. Canalization begins in the 60-day-old embryo, progressing in a caudal direction. Puncta lacrimalia can be found in the seventh fetal month. At birth, only 30% or less of infants have a patent distal nasolacrimal duct.
In this developmental process, many hypotheses have been formulated to elucidate the etiopathogenesis of congenital lacrimal fistulae. Some authors have proposed that the fistula derives from excessive growth of the external wall of the nasolacrimal duct, an abnormal closure of the embryonic fissure, and amniotic bands. A phlogistic process may be involved in the formation of acquired fistulae, including purulent dacryocystitis.
Other authors have pointed out that fistula may originate from a failure in the involution process of lacrimal anlage with a possible aberrant canalization of this cord of cells. Other studies emphasized the role of a dysfunctional fusion of surface ectoderm after invagination of the ectodermal thickening. All these hypotheses converge on the assumption that anlage ducts persist when lacrimal duct cells fail to involute and continue to canalize in abnormal sites.
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