Intracameral moxifloxacin and anterior uveitis

Pubblicato il

Wednesday, 18 January 2023

Argomento

Surgical Area

Moxifloxacin is a third-generation, broad-spectrum fluoroquinolone used in ocular surgery. However, several studies have associated intracameral use of moxifloxacin with the occurrence of anterior uveitis, a complication that should not be underestimated.

Acute anterior uveitis

L'uveitis acute anterior uveitis (AAU), an inflammation of the iris and ciliary body, is a condition that has an incidence of 17-52 patients per 100,000 each year and accounts for approximately 50%-60% of all uveitis observed in tertiary care. AAU typically presents with ocular pain, red eyes and photophobia. Blurred vision and pupil irregularity may occur due to the formation of synechiae, i.e., adhesions between the iris and lens.

Examination by slit-lamp biomicroscopy also reveals the presence of cells and glows (a haze of aqueous humour caused by protein loss) in the anterior chamber.

If left untreated, acute anterior uveitis can develop into serious complications, such as oedema, cataracts and glaucoma, which subsequently lead to loss of vision.

Acute anterior uveitis as a consequence of intracameral use of moxifloxacin: studies

Several recent studies have described clinical cases in which anterior uveitis occurred as an adverse effect, following theintracameral use of moxifloxacin.

In one of these studiesa 64-year-old Colombian male patient presented to the emergency department with severe ocular pain and photophobia in his left eye, 15 days after cataract surgery. On specialist evaluation in ophthalmology, pigment dispersion in the anterior chamber and chamber angle, severe anterior segment inflammation and elevated intraocular pressure were observed. The poor response to treatment for a condition with suspected viral origin and the exclusion of other possible aetiologies led to the conclusion that the anterior uveitis diagnosed in the patient was induced by treatment with intracameral moxifloxacin during cataract surgery.

In another study, intracameral use of moxifloxacin was associated with a particular form of anterior uveitis, bilateral acute iris transillumination (BAIT), characterised by acute bilateral loss of the pigmented epithelium of the iris, transillumination of the iris, dispersion of pigment in the anterior chamber and paralysis of the iris sphincter. BAIT presents with symptoms similar to those of other types of anterior uveitis, i.e., pain, photophobia and red eyes. BAIT can also cause a severe increase in intraocular pressure (IOP), which sometimes requires surgery.

Finally, in a further studiobilateral acute uveitis developed in a 56-year-old patient after moxifloxacin was administered, this time systemically, following severe pneumonia. Shortly after starting antibiotic treatment, the patient developed bilateral eye pain, which allowed AAU to be diagnosed. Furthermore, 3 years after the event, the patient was diagnosed with iris atrophy and limited pupillary dilation, indicative of paralysis of the iris sphincter muscle. This case provided further support for the evidence that moxifloxacin can also cause collagen degradation in ocular muscles, as well as in other body districts and blood vessels.

Moxifloxacin: possible mechanisms of adverse effects

Moxifloxacin has been shown to have a high tissue affinity and is absorbed, in particular, in pigmented tissue, such as the iris, compared to other fluoroquinolones, such as levofloxacin. Sampling of the aqueous humour after moxifloxacin administration demonstrates high concentrations of the drug. Although the exact mechanisms of moxifloxacin-induced uveitis are still unclear, it is hypothesised that the drug exerts direct toxicity towards the iris pigment, based on studies demonstrating skin sensitisation and phototoxicity following administration of this antibiotic. Direct toxicity may explain iris atrophy, pupil mydriasis and iris sphincter muscle paralysis, which gives rise to the clinical findings reported in patients with moxifloxacin-induced uveitis.

An alternative hypothesis is that moxifloxacin causes collagen damage to the smooth muscles of the pupil sphincter muscles. Indeed, fluoroquinolones are known to cause collagen degradation and can lead to conditions such as tendinopathy and Achilles tendon rupture, and even aortic aneurysm by dissection, due to the same mechanism. Therefore, it is possible that a similar process occurs with the iris collagen.

The choice to use moxifloxacin, therefore, must be made taking into account the potential adverse effects it may have on several levels and considering that safer and equally effective alternatives are available.

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