DIABETIC CATARACTS IN DOGS. DIAGNOSIS AND TREATMENT

Cataratas diabéticas en perros

 

Author: Elena Fenollosa Romero.

Lda Vet CertVOphthal DECVO EBVS® MRCVS. European Specialist in Veterinary Ophthalmology. Elena is a European diplomat/specialist in veterinary ophthalmology. She is head of the Ophthalmology Service at the Reference Hospital of the Catholic University of Valencia and support specialist in the ophthalmology service at The Ralph center in Marlow, Buckinghamshire.

In this article, Elena Fenollosa Romero reviews the clinical-pathological characteristics as well as the diagnosis and treatment of diabetic cataracts in dogs.

Cataract formation is a frequent and one of the most important complication in diabetic dogs. Diabetic cataracts have been reported to be present in almost 60% of diabetic dogs, but not in cats. Beam et al reported that 75% of the canine population diagnosed with diabetes mellitus developed cataracts by approximately 12 months while 80% developed cataracts by 16 months.

Other ocular manifestations of diabetes mellitus in dogs include loss of endothelial cells, presence of intrastromal haemorrhages and retinal vascular damage such as microaneurysms Diabetic dogs also have reduced corneal sensitivity and a reduced Schirmer’s test. All this must be taken into account to maintain good long-term ocular health.

Pathogenesis of cataract formation in diabetic dogs

Patogénesis cataratas diabéticas en perros
Figure 1. Physiological enzymatic process where glucose in the lens is metabolised by hexokinase to lactic acid.

Figure 2. Increased blood glucose causes increased glucose in the lens.

Cataratas diabéticas en perros
Figure 3. When there is an increase in blood glucose and thus in the lens, hexokinase becomes saturated and there is a change in metabolism by the enzyme aldose reductase. As a result, there is a production of sorbitol resulting in an influx of fluid into the lens.

Diagnosis and treatment of diabetic cataracts in dogs

As the fluid content within the lens increases, the fibres become disorganised and the size of the lens increases. The disarrangement leads to cataract formation and the increase in size can lead to a rupture of the capsule. These changes occur very quickly (they can occur within hours) and our patients become acutely blind. When these cataracts are observed with the slit lamp, they usually show a separation of the anterior lens sutures, which is called water clefts (Photo 1). It is therefore very important to act quickly in these cases, i.e., to consider cataract surgery in the early stages of diabetic disease. An erroneous assumption is to attempt to stabilise the diabetic patient before considering cataract surgery. We know some diabetic patients take months to stabilise, so if they are referred for surgery too late after cataract onset, they may no longer be good candidates for surgery due to the presence of severe lens-induced uveitis (Photo 2 and 3), secondary glaucoma or retinal detachment.

Remember that the presence of diabetes must always be considered as a cause of the cataract origin in acute onset cataracts.
If surgical treatment is not an option, these cataracts must be treated chronically with topical non-steroidal anti-inflammatory drugs to control lens-induced uveitis.

Photo 1
Photo 2
Photo 3

 

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