January 2024 39 As mentioned above, 25% of diabetic dogs may show these changes within 2 months of being diagnosed with cataracts and frequently this is even earlier. In some cases, the lens swells so rapidly that the lens capsule ruptures, releasing lens proteins into the eye. Diabetic cataracts typically exhibit bilateral sudden onset and symmetry, often described as intumescent, with characteristic “waterclefts” along the “Y” shaped lens suture lines (Fig:1). The anterior-posterior diameter is around 10mm, or more, compared to approximately 7mm in a normal lens (Fig: 2). With intumescent cataracts, ocular ultrasound can be used to demonstrate the enlarged lens volume and the reduced distance between the posterior lens capsule and the retina as the lens increases in size. It is theorised that the healthy lens should normally occupy a third of the space from the anterior lens capsule to the retina, whilst intumescent cataracts reduce this and occupy more of the posterior segment of the globe [Fig:2 and 3] Stage 3: Lens Induced Uveitis [LIU] Ongoing lens swelling leads to the stretching of the lens capsule, which can rupture, resulting in the exposure of lens protein to the rest of the eye, causing what is referred to as lens-induced phacoclastic uveitis. Lens protein can also leak through an intact lens capsule and cause phacolytic uveitis. Intraocular inflammation is usually severe and may cause irreversible damage to the ocular structures. With phacolytic uveitis, the soluble lens proteins are presented to the immune system, which drives a lymphocytic-plasmocytic iridocyclitis, but with phacoclastic uveitis, it is both the soluble and non-soluble lens proteins that cause the uveitis. As mentioned above in the introduction, the lens proteins developed before the foetal immune system, so are in nature considered antigenic. Sustained release of proteins (hypermature cataracts) or massive release (lens capsule rupture) leads to a T-cell response resulting in macrophage production, cytokine IL-2 release and further chemotaxis of neutrophils and release of lymphokines. Local neutrophilia also causes the release of proteolytic enzymes. It is critical to be able to recognise these signs of inflammation in dogs with cataracts in the consulting room. Clinically, one may see scleral injection [Fig: 4 and 5], mild to moderate ocular discomfort, aqueous flare [Fig 6 and 7], perilimbal and corneal neovascularisation [Fig 8], keratic precipitates [WBCs and exudate packed onto the endothelium of the cornea] [Fig 9], corneal oedema [Fig 10] and, eventually, darkening of the iris. In addition, the pupil is usually slightly miotic and the intraocular pressure is moderately reduced [hypotony]. The pupil shape may become irregular [dyscoria] as a result of posterior synechiae. Based on fluorophotometric studies of the aqueous humour of dogs with cataracts, it is suggested that the blood–aqueous barrier breakdown might be present in all the eyes with cataracts, regardless of the degree of maturity. This further emphasises the great importance and necessity for a detailed slit lamp biomicroscopy examination of all dogs with cataracts to establish if subtle signs and changes are occurring in the eyes. Figure 1: The “Y” shaped “waterclefts” along the suture lines. Ultrasound showing the enlarged lens and reduced distance between the posterior lens capsule and the retina. Figure 4 Figure 2: a] Normal lens size [b] A swollen intumescent cataractous lens a b Figure 5 Regulars I Ophthalmology Column >>> 40
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