December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Pathomechanism of Primary Acquired Dacryostenosis
Author Affiliations & Notes
  • D Paulsen
    Christian Albrecht Univ of Kiel Kiel Germany
    Inst of Anatomy
  • AB Thale
    Christian Albrecht Univ of Kiel Kiel Germany
  • S Maune
    Otorhinolaryngology Head and Neck Surgery
    Christian Albrecht Univ of Kiel Kiel Germany
  • BN Tillmann
    Christian Albrecht Univ of Kiel Kiel Germany
    Inst of Anatomy
  • FP Paulsen
    Christian Albrecht Univ of Kiel Kiel Germany
    Inst of Anatomy
  • Footnotes
    Commercial Relationships   D. Paulsen, None; A.B. Thale, None; S. Maune, None; B.N. Tillmann, None; F.P. Paulsen, None. Grant Identification: DFG Pa738/1-2
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 3017. doi:
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    • Get Citation

      D Paulsen, AB Thale, S Maune, BN Tillmann, FP Paulsen; Pathomechanism of Primary Acquired Dacryostenosis . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3017.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: To obtain new insights into the pathophysiology of primary acquired dacryostenosis. Method: Tissue specimens from the human nasolacrimal ducts of thirty-six patients undergoing endonasal dacryocystorhinostomy within a framework of primary acquired dacryostenosis were analyzed employing histology and electron microscopy. Six lacrimal systems of body donors served as controls. One group of tissue specimens from each lacrimal system was prepared and processed with paraffin, sectioned, stained by different methods and finally examined by light microscopy. The other group was processed with araldite following preparation, sectioned semithin and ultrathin and examined by transmission electron microscopy. The degree of dacryostenosis was scored in each tissue specimen by grading the histologic sections as mild (active chronic inflammation), moderate (proliferative sclerotic forms of chronic fibrosis) or severe (total subepithelial fibrosis). Results: Of thirty-six patients with epiphora, thirteen revealed functional obstruction with a patent lacrimal system on syringing; in twenty-three cases, the lacrimal passage was completely obstructed. Different pathologic stages correlating to duration of symptoms were found ranging from active chronic inflammation to proliferative sclerotic forms and total subepithelial fibrosis. Conclusions: Descending inflammation from the eye or ascending inflammation from the nose initiates swelling of the mucous membrane, remodeling of the helical arrangement of connective tissue fibers, malfunctions in the subepithelial cavernous body with reactive hyperemia, and temporary occlusion of the lacrimal passage. In the follow-up, repeated isolated occurrence of dacryocystitis leads to structural epithelial and subepithelial changes, which may lead either to a total fibrous closure of the lumen of the efferent tear duct or to a non-functional segment in the lacrimal passage that is manifest on syringing.

Keywords: 437 inflammation • 324 aqueous • 385 degenerations/dystrophies 

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