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Ординатура / Офтальмология / Английские материалы / Essentials in Ophthalmology Oculoplastics and Orbit Aesthetic and Functional Oculofacial Plastic Problem-Solving in the 21st Century_Guthoff, Katowitz_2009.pdf
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Table 4.2. Causes of nontraumatic canalicular obstruction and their approximate incidence

Cause of canalicular obstruction

Average annual

 

caseload (%)

Postherpetic

8/23 (35%)

Iatrogenic

6/23 (26%)

Cicatricial conjunctival diseasea

6/23 (26%)

5-Fluorouracil chemotherapy

2/23 (9%)

Lichen planus

1/23 (5%)

Based on cases presenting to Moorfields Eye Hospital over an 8-year period

aIncluding risk factors such as topical glaucoma therapy, severe blepharitis

There are many causes for canalicular dysfunction (Table 4.2), and symptoms vary according to the extent, severity, and duration of the underlying disease. Unfortunately, irreversible canalicular fibrosis is often present at presentation due to delayed diagnosis (e.g., retained punctal plugs or stents), misdiagnosis (as with chronic canaliculitis [34]), or the rapid onset of disease (herpes simplex canaliculo-conjunctivitis). Restoration of canalicular function is hampered by the challenge of providing effective immunosuppression for local disease,

a

c

4.3 Infective Causes

69

such as ocular cicatricial pemphigoid, and the very small caliber of the canaliculi, with surgery failing due to both annular fibrosis and disruption of the dynamic (lacrimal “pump”) function of the orbicularis oculi muscle.

4.3Infective Causes

Severe ocular surface infections can cause canaliculitis either by a direct infection or by spillover of the toxic tear film from an “upstream” hyperacute conjunctivitis.

4.3.1Periocular Herpes Simplex Infection

Apart from trauma, primary periocular infections with herpes simplex virus (Fig. 4.2a) are probably the most common cause of canalicular obstruction (Fig. 4.2b). In 160 patients presenting with lacrimal symptoms after primary herpetic blepharo-conjunctivitis, canalicular block was typically unilateral and significantly more common in women [10, 20]. Primary open lacrimal surgery-DCR with anterograde or retrograde intubation—was undertaken in 94 eyes, of which fewer than a quarter required subsequent bypass tube insertion, emphasizing the role for primary canalicular surgery before resorting to placement of a glass bypass tube.

b

d

Fig. 4.2 Microbial canaliculitis. (a) Primary periocular herpes simplex infection: blepharoconjunctivitis with vesicles; (b) probe identifying proximal lower canalicular block; (c) Actinomyces canaliculitis with large granuloma bulging out of punctum; (d) expression of stones and debris after canaliculotomy

70

4 Lacrimal Canalicular Inflammation and Occlusion: Diagnosis and Management

4.3.2Bacterial Canaliculitis

Numerous microbes may infect the canalicular epithelial surface (Table 4.3), but the most characteristic is due to

4Actinomyces species. Such patients usually present after many months of a painless chronic discharge at the medial canthus, this typically being misdiagnosed as conjunctivitis, chalazion, or nasolacrimal duct obstruction [1, 3]. Although rare, microbial canaliculitis may also lead to chronic or recurrent nasolacrimal obstruction in children [26], and may also be a cause of blood-stained tears. Typically, there is swelling with mild inflammation, centered on the midcanaliculus, and the characteristically stringy yellow discharge at a pouting punctum (Fig. 4.2c). Pressure over the canaliculus may lead to discharge of pus or gritlike “granules,” but in most cases the debris is typically not expressible (unlike that of a lacrimal sac mucocele). Actinomyces, especially A. israelii, is a cast-forming gram-positive filamentous anaerobe that can be difficult to isolate, and the organism has a propensity for colonizing hollow spaces and forming “stones,” such as canaliculiths (Fig. 4.2d).

In all but the mildest cases, Actinomyces canaliculitis is resistant to topical antibiotics alone. Antibiotic syringing of the affected canaliculus is well described [23], but this tends to be ineffective [35] and, more importantly, carries the risk of microbial dissemination into the lacrimal sac and nasolacrimal duct. Definitive treatment entails canaliculostomy with expression of all inflammatory and infective debris; a 6-mm incision is made along the conjunctival border of the affected canaliculus, and the canalicular contents are expressed with firm pressure on either side of its walls. Although a large chalazion spoon may be used to curette stones, this instrument is best avoided as it is liable to damage the severely inflamed canalicular mucosa and result in canalicular occlusion. Chronic infection may lead

Table 4.3. Microbial isolates in canaliculitis

Actinomycetes spp.

Arcanobacterium haemolyticum

Eikenella corrodens

Haemophilus aphrophilus

Lactococcus lactis cremoris

Molluscum contagiousuma

Mycobacterium chelonae

Nocardia asteroides

Propionobacterium propionicum

Staphylocococcus spp.

aPrimary involvement of the conjunctiva or cornea by molluscum is rare and is often associated with HIV infection

to gross distension of the canaliculus by the large number of stones, all of which require removal. The canaliculotomy incision heals spontaneously, and the patient should be placed on a week’s course of a topical antibiotic, such as ofloxacin; because the incision lies along, rather than across, the canaliculus, ring contracture is rare and postoperative epiphora most unusual [1]. Recurrence of symptoms is a likely indication of persistent canalicular stones, and a further canaliculotomy should be performed if necessary; occasionally, such recurrent infection is centered on the lacrimal sac rather than the canaliculi.

4.4Systemic Inflammatory Disease

4.4.1Lichen Planus

Lichen planus (LP), an idiopathic autoimmune disease of the skin and oral or genital mucosa, may rarely affect conjunctiva [15, 28] and lead to severe canalicular obstruction [10, 22]. Etiological mechanisms include autoreactive T cells to keratinocytes and activated tissue matrix metalloproteinases and mast cells. Systemic lesions show suband intraepithelial lymphocytic infiltration with degeneration of basal keratinocytes, and although conjunctival disease is less well characterized, case reports describe reticular subconjunctival scarring, forniceal shortening, and symblepharon formation. These features resemble those seen in ocular cicatricial pemphigoid [21, 25], but immune complex deposition within the conjunctival basement membrane—pathognomonic for ocular cicatricial pemphigoid—is absent in LP.

Canalicular LP leads to extensive bilateral, bicanalicular occlusion in three quarters of patients with symptomatic disease [10]; these changes probably reflect inflammation within the subepithelial substantia propria of the canaliculus, with consequent deep fibrosis “throttling” the canaliculus (Fig. 4.3a). LP patients with proximal or midcanalicular block are offered DCR with retrograde canaliculostomy [36] but are warned of the high likelihood of requiring secondary placement of a Jones bypass tube.

4.4.2Ocular Cicatricial Pemphigoid

Distal spillover of the severe conjunctival inflammation of ocular cicatricial pemphigoid will often cause proximal canalicular blockage (Figs. 4.3c, d). Retention of inflammatory debris will, in some cases, be associated with an exacerbation of ocular surface disease, and consideration will be given to the reestablishment of tear drainage; in