Primary Aquired Nasolacrimal Duct Obstruction

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Idiopathic or primary acquired daryostenosis, synonymous with primary acquired nasolacrimal duct obstruction (PANDO), is a syndrome of unknown origin. Of all non-traumatic forms, it accounts for most cases observed in adults. Pathological studies of the nasolacrimal passage have indicated that PANDO is caused by fibrous obstruction secondary to chronic inflammation [4, 13, 14]. Nevertheless, the pathophysiology of functional dacryostenosis, i.e., patients with epiphora despite patent lacrimal passages on syringing (so-called functional dacryostenosis) has still not been understood. Descending pathogens from the conjunctival sac, as well as diverticula of the lacrimal passage, have been suggested to be causal factors. Other specialists claim to have located the origin of idiopathic dacryostenosis in the nose. Here, simple infections of the nasal mucous membrane or diseases of the sinuses have been suggested; however, clinical studies indicate that nasal disease is extremely rare in patients undergoing dacryocystorhinostomy (DCR).

Interestingly, the mucous membranes of the lacrimal passage and nose reveal morphological differences between the nasolacrimal epithelial cells with microciliation only and the nasal epithelial cells with their kinociliae (Fig. 2.1) [24]. This suggests differences in susceptibility to pathogens; however, it has been shown that ectopia of nasal epithelial cells is a more or less common finding in the nasolacrimal ducts [1, 27]. In addition to descending infection from the eye, ascending infection of these atopical cells during nasal inflammation could thus be the starting point of dacryostenosis. In this scenario, the nasal inflammation has long since abated when the dacryo-cystitis passes into a chronic state, causing the changes characteristic for dacryostenosis (see below).

Recent findings have indicated that "functional obstruction" of the lacrimal passage occurs in many more patients than suggested previously (Table 2.1) [25]. Furthermore, some of these patients report a history of acute or chronic dacryocystitis and digital pressure over the sac also reveals mucopurulent reflux in some cases [25].

Squamous metaplasia has been observed during recent analyses in cases of functional dacryostenosis with loss of columnar epithelial cells and goblet cells and with that of lacrimal passage specific mucins and TFF peptides (see Chap. 1) in the stenotic area (Figs. 2.2, 2.3). Moreover, the helically arranged connective tissue fibers undergo remodeling leading to subepithelial fibrosis (Fig. 2.2) [25]. In addition, a reduction and even total loss of specialized blood vessels of the surrounding cavernous body and their replacement by connective tissue occurs (Fig. 2.2) [25].

Nasolacrimal Duct Obstruction
Fig. 2.1. Scanning electron micrograph of the epithelial surface of the nasolacrimal duct reveals a single cell with kinociliae (arrows) between cells with microvilli. Bar=6 ^m
Fig. 2.2. Histology of dacryosenosis. a Section through

t a tissue specimen of a patient shows chronic inflammation with epithelial and subepithelial infiltration of defense cells and incipient subepithelial fibrosis with increased occurrence of fibroblasts (arrows). b Section through a subepithelial blood vessel shows chronic fibrosis with wall thickening and intimal t t proliferation (arrows) c Section through a tissue specimen of a patient shows chronic inflammation with squamous metaplasia, absence of intraepithelial goblet cells, subepithelial fibrosis with basement membrane thickening (arrows), and reduction of wide capillaries. All images are with toluidine blue O ~staining. a-c Bar=27.5 ^m

Table 2.1. Patient case data of a group of 36 patients undergoing endonasal dacryocystorhinostomy in PANDO at the Department of Otorhinolaryngology, Head and Neck Surgery, Christian Albrecht University of Kiel, Germany. DE duration of epiphora (months), LS lacrimal sac, ND nasolacrimal duct, DC dacryocystitis, MD mucous discharge. (From [25])

Table 2.1. Patient case data of a group of 36 patients undergoing endonasal dacryocystorhinostomy in PANDO at the Department of Otorhinolaryngology, Head and Neck Surgery, Christian Albrecht University of Kiel, Germany. DE duration of epiphora (months), LS lacrimal sac, ND nasolacrimal duct, DC dacryocystitis, MD mucous discharge. (From [25])

Case no.

Gender

Age (years)

Side

DE

Pathological stage

Stenosis location

Degree of obstruction

DC

MD Sinusitis or nasal disease

1

F

64

L

21

Severe

LS

Functional

X

2

F

50

R

120

Severe

LS/ND

Complete

X

X

3

M

92

L

12

Severe

ND

Complete

Acute sinusitis

4

F

32

L

6

Mild

ND

Functional

5

F

75

L

157

Severe

ND

Complete

X

X

6

F

48

L

26

Moderate

ND

Functional

X

7

F

69

R

8

Moderate

LS/ND

Complete

X

X

8

F

73

R

27

Severe

LS/ND

Complete

X

X

9

F

39

R

19

Severe

ND

Complete

10

F

57

L

9

Moderate

ND

Complete

11

F

40

R

13

Moderate

LS/ND

Functional

12

F

45

R

36

Severe

ND

Complete

X

X

13

F

67

L

204

Severe

ND

Functional

X

X Chronic sinusitis

14

F

63

R

4

Mild

LS/ND

Functional

15

F

58

L

13

Moderate

LS/ND

Complete

X

X

16

M

76

R

27

Severe

LS

Complete

X

X

17

F

16

L

20

Moderate

ND

Complete

18

F

41

R

7

Mild

LS

Functional

X

19

M

32

R

15

Moderate

LS

Complete

20

M

55

R

24

Severe

ND

Complete

X

X

21

F

60

R

120

Severe

ND

Functional

X

22

F

66

L

240

Severe

LS

Functional

X

X

23

F

28

L

7

Mild

ND

Functional

24

F

61

R

240

Severe

ND

Functional

X

25

M

36

R

49

Severe

LS/ND

Complete

X

X

26

F

55

L

16

Severe

LS/ND

Complete

X

X Nasal sinusitis

27

M

65

L

14

Moderate

ND

Complete

28

F

79

L

36

Severe

ND

Complete

29

F

21

L

20

Severe

LS

Complete

X

X

30

F

88

R

1

Moderate

ND

Complete

31

F

61

L

12

Moderate

ND

Functional

Nasal sinusitis

32

F

60

L

10

Mild

LS

Functional

33

F

51

R

32

Severe

ND

Complete

X

X

34

F

45

L

49

Severe

LS/ND

Complete

X

X

35

F

70

L

29

Severe

ND

Complete

36

F

61

L

59

Severe

LS/ND

Complete

Acquired Nasolacrimal Duct Obstruction

Fig. 2.3. Transmission electron micrograph reveals chronic stage of dacryostenosis. The epithelium shows squamous metaplasia. The metaplastic squamous cells reveal condensed, irregular nuclei (C), reduction of cytoplasm, and reduction of cell organelles. The cell surface shows a loose microciliation projecting into a large extracellular space (E). L lumen of the lacrimal passage. Bar=6 ^m

Fig. 2.3. Transmission electron micrograph reveals chronic stage of dacryostenosis. The epithelium shows squamous metaplasia. The metaplastic squamous cells reveal condensed, irregular nuclei (C), reduction of cytoplasm, and reduction of cell organelles. The cell surface shows a loose microciliation projecting into a large extracellular space (E). L lumen of the lacrimal passage. Bar=6 ^m

All these changes lead to an interruption of the tear-flow mechanism in the stenotic segment. The following pathogenic concept of primary acquired dacryostenosis has been postulated: descending inflammation from the eye or ascending inflammation from the region of the nose (perhaps by way of inflammation of "ectopical" nasal epithelial cells in the nasolacrimal duct; Fig. 2.4) may initiate malfunctions in the cavernous body with reactive hyperemia, swelling of the mucous membrane, and temporary occlusion of the lacrimal passage [25]. Then, repeated isolated episodes of dacryocystitis may lead to structural epithelial and subepithelial changes. Loss of typical goblet and epithelial cells, which plays an important role in the tear-outflow mechanism, as well as fibrosis of the helical system of connective tissue fibers in the area of the lacrimal sac and nasolacrimal duct and reduction and destruction of specialized blood vessels of the cavernous body, may exacerbate malfunctions of the tear-outflow mechanism and start a vicious circle [25]; thus, cases of functional dacryostenosis, i.e., patients with epiphora in spite of patent lacrimal passages on syringing, are explainable as follows:

1. In early cases, the rinsing liquid instilled by hand pressure into the lacrimal passage is forced through the segment of the lacrimal passage obturated by reactive hyperemia and swelling of the mucous membrane.

2. Structural changes (caused by chronic dacryocystitis) result in a non-functioning segment in the lacrimal passage. In this latter case, obstruction is not yet complete, but there is no tear transport in the non-functioning segment [25].

Ample evidence certainly exists that obstructed nasolacrimal systems are colonized by increased numbers of pathogenic microorganisms. The histopathology implies that, besides topical or systemic anti-inflammatory agents, nasal decongestants, such as Afrin, possibly could also be useful tools in the management of early cases of primary acquired dacryostenosis, since they could counteract the hyperemia and swelling of the cavernous body [25].

Fig. 2.4. Transmission electron micrograph reveals an early cation of the surface of an epithelial cell demonstrates microvilli stage of dacryostenosis. a Bacteria are visible on the cell surface that are colonized by bacteria. Underneath the surface four of two epithelial cells and in their cytoplasm infiltrating the cell fat vacuoles are visible. L lumen of the lacrimal passage.

organelles. Mitochondria indicated by arrows. b High magnifi- a Bar=1.2 ^m; b bar=0.4 ^m

Fig. 2.4. Transmission electron micrograph reveals an early cation of the surface of an epithelial cell demonstrates microvilli stage of dacryostenosis. a Bacteria are visible on the cell surface that are colonized by bacteria. Underneath the surface four of two epithelial cells and in their cytoplasm infiltrating the cell fat vacuoles are visible. L lumen of the lacrimal passage.

organelles. Mitochondria indicated by arrows. b High magnifi- a Bar=1.2 ^m; b bar=0.4 ^m

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