Cataract is an ocular pathology characterized by opacity and consequent lack of transparency of the crystalline or lens. This opacity can involve the internal part and/or the capsule of the lens. The lesion can appear in various ways, presenting in a vacuolar form, or markedly dense and diffuse, but can also involve only some fibres producing linear striae inside the lens. Depending on its site, density and extension, the lack of transparency can cause a partial or total lack of vision. The underlying cataract pathophysiology is determined by changes that some factors produce in components of the lens, rather than a direct inflammatory effect, since this is an avascular structure. The classification of cataracts is based on numerous distinguishing factors, such as anatomical and physical characteristics, onset, development and aetiology. The diagnosis is based on clinical and instrumental findings, exploiting observations made with appropriate, specialised ophthalmological equipment. The incidence of cataract is higher in dogs than in cats and, if not treated, cataracts can give rise to various types of complications besides causing a decrease or loss of vision. The treatment of cataracts in the dog is surgery, as there is no scientifically valid evidence that medical therapy with drugs can be useful for this disease.
CLASSIFICATION
Cataracts can be classified according to a number of criteria. In a classification based on the stage of development, the incipient form is defined by minimal opacity, which is often not noted by the animal’s owner and which has little or no effect on the visual capacity of the animal. A cataract is defined as immature if, despite the opacity present, there is still a hazy view of the ocular fundus and the subject has some residual visual capacity. In a mature cataract (Fig. 1) the opacity is complete, the fundus cannot be seen and the animal has lost its vision. In the hypermature form there is a certain degree of reabsorption of the aqueous and protein content of the lens such that the capsule appears shriveled up and the volume of the lens itself decreases. There can be partial recovery of visual capacity in these cases. A cataract can be defined as morgagnian when all the cortex of the lens has liquefied and only the solid nucleus of the lens remains within its capsular covering.
In a classification based on the anatomy of the lens and the position of the opacity within it, cataracts can be defined as anterior capsular, anterior subcapsular, anterior cortical, equatorial, anterior and posterior nuclear (Fig. 2),foetal nuclear, posterior subcapsular, posterior capsular, axial, andsuture line.
The evolution of the cataract can be predicted on the basis of the localisation of the opacity of the lens. Nuclear and capsular cataracts are usually stationary, whereas cortical and equatorial opacities are very often progressive.
Depending on the age at onset, cataracts can be defined as congenital, neonatal, juvenile andsenile. They can be primary or secondary in relation to whether or not there is a possible triggering cause, and fluid, soft or hard depending on their consistency. Cataracts can also be described as pulverulent, cuneiform, stellate, or punctate on the basis of the shape and appearance of the opacity.
Congenital cataract
Congenital cataracts can be the result of an inherited genetic predisposition or of an infectious disease or exposure to toxic substances affecting the foetus during gestation. Not infrequently, congenital cataracts are associated with other defects such as microphthalmus, lenticonus and persistence of the vascular structures dedicated to blood supply to the lens during embryonic life. In this last case, the persistence of the papillary membrane (persistent papillary membrane - PPM) or of the vascular covering of the lens (persistent hyperplastic tunica vasculosa lentis - PHTVL) can cause opacity of the anterior and posterior capsule of the lens, respectively. A congenital aetiology must be suspected every time opacity is seen in the foetal nucleus.
Senile cataract
Senile cataract is part of a physiological process of ageing of the lens, although some authors believe that there are also hereditary forms of senile cataract. The progression of the opacity in senile cataract tends to be extremely slow, although over time the lesion almost always evolves into a mature cataract. Clinically, opaque lines extend from the nuclear area towards the equatorial cortex like the spokes of a wheel. The senile form differs from nucleosclerosis of the lens, which is a normal process of ageing of the lens that usually starts after the age of 7 to 8 years and is related to the greater density of its nuclear component (Fig. 3). The difference in the refractive index between the periphery (cortex) of the lens and its compressed central nuclear part causes the characteristic grey, mother-of-pearl colour of the internal part of the lens. In the advanced stages of nucleosclerosis there may be some difficulty in appreciating fine details of the fundus, while in the early and intermediate stages the vitreous and retina can be evaluated without problem and the nucleosclerosis does not cause any visual impairment.
Primary cataract
A cataract is defined as primary when it is not possible to find any triggering factor. One of the most common forms of primary cataract is that of a genetic-inherited nature. Indeed, this is probably the most common type of primary cataract in animals. Depending on the age at which the cataract appears, it can be considered congenital, juvenile or senile. From a genetic point of view, most inherited cataracts have a recessive mode of transmission, although in some cases it is thought that there may be one or more dominant genes. Hereditary cataract can be progressive leading eventually to blindness, even though some cases remain stationary or evolve slowly over the years without causing visual impairment. In principle, unless another cause of the cataract can be found, many of the cataracts occurring in not elderly pedigree dogs should be considered inherited until proven otherwise, even in the absence of identification of the gene responsible or of inheritance tests which are based on repeated mating and investigations of results obtained in successive generations. Hereditary cataract is normally characterized by a particular age of onset, initial site of the opacity and speed of progression, which are typical for each breed. The genetics committee of the American College of Veterinary Ophthalmology has identified 145 breeds of dogs in which there is a demonstrated or suspected inherited basis to the disease. Hereditary cataract in the dog can be present in isolation or in association with multiple ocular defects or associated with other genetic disorders as occurs, for example, in chondrodysplasia.
Secondary cataract
Secondary cataract is an acquired form of the disease and always has a trigger, which may be trauma, toxic factors, physical causes, metabolic problems, or dietary deficiencies, or is secondary to other ocular disorders such as glaucoma, uveitis, lens luxation and hereditary progressive retinal atrophy. It has not been determined whether the opacity that occurs during progressive retinal atrophy is related to the genetic problems of this disease or to the release of cataract-inducing substances by the affected retina. In the case of cataract secondary to trauma, the trauma may be a blunt injury or wound penetrating the eyeball. In the former case the shock wave produced by the trauma can cause changes in the epithelium or crystalline lens cortex which then give rise to secondary opacities. In the case of penetrating wounds such as a cat scratch, bite, gunshot wound, or entry of metallic foreign bodies, involvement of the lens can give rise to some severe forms of phacoclastic uveitis with serious repercussions for both the function and anatomy of the eyeball. The many toxic substances that can induce the development of cataract include antibiotics (aminoglycosides-paromomycin), antiparasite products (disophenol), antihypertensive drugs (diazoxide, phenylpiperazine) and other substances such as dimethylsulphoxide and ketaconazole.
Cataract may also be secondary to ionising radiation such as that used for the treatment of some forms of cancer or secondary to electric shock. There are numerous causes of metabolic cataract, including cataracts secondary to diabetes mellitus, hypocalcaemia or high copper levels. In puppies fed with artificial milk instead of maternal milk, a brownish-coloured lesion, probably due to a poor supply of arginine, can start to form from the third week of life in the zone that separates the posterior nuclear part of the lens from the cortical part; this lesion may progress, causing a dense, whitish perinuclear opacity.
DIAGNOSIS
The diagnosis of cataract involves the use of instruments suitable for evaluating the extension, features and precise site of the opacity. A slit lamp or biomicroscope is the best instrument for a full diagnostic evaluation and is used after an agent inducing papillary dilatation has been instilled into the eye in order to optimise the examination of the lens, in particular the peripheral equatorial part. The examination may be carried out under direct illumination or retro-illumination. In the case of a mature cataract, ultrasonography may be useful for examining details of the posterior part of the lens and, thereby, identifying disorders such as lenticonus or persistence of embryonic vascular structures.
COMPLICATIONS
A lens affected by cataract can develop secondary complications including a chronic inflammation known as phacolytic uveitis, phacoclastic uveitis, vitreous degeneration, retinal detachment, and subluxation or luxation of the lens. No studies have so far been carried out on the frequency of these complications and for this reason it is difficult to make a prognostic evaluation of the effect of the various factors.
TREATMENT
On the basis of current knowledge and despite numerous attempts to find a medical treatment for cataract the therapy of choice for this disorder is surgery.
Over the years many drug treatments have been used in the management of cataracts but so far none has given scientifically valid results. It should be appreciated that there are problems stemming from subjectivity of the clinical evaluation of the real therapeutic effect and the impossibility of calculating the degree of reabsorption of opacity of the lens. Many of the active principles used derive from agents given to humans which, over the years, have included topical and systemic treatments based on selenium and tocopherol, carnosine and N-acetylcarnosine, zinc citrate ascorbate and orgotein. In diabetic cataract, aldose reductase inhibitors have perhaps shown the greatest potential efficacy from among the various medical treatments.
The surgical treatment of the cataract is very similar to that used in humans and involves intracapsular cataract extraction (ICCE) or extracapsular cataract extraction (ECCE), this latter through the method of phacoemulsification. With the ECCE technique, an intracapsular lens of various shapes and materials can be inserted. When the intracapsular technique is used, an intraocular lens can be implanted within the sulcus.
Suggested readings
- Daniel WJ, Noonan NE, Gelatt KN. Isolation and characterization of the crystallins of the normal and cataractous canine lens.Curr Eye Res.1984 Jul;3(7):911-22.
- Van Der Woerdt A. Lens-induced uveitis.Vet Ophthalmol. 2000;3(4):227-234.
- Williams DL, Heath MF, Wallis C.Prevalence of canine cataract: preliminary results of a cross-sectional study.Vet Ophthalmol. 2004 Jan-Feb;7(1):29-35.
- Gelatt KN, Mackay EO. Prevalence of primary breed-related cataracts in the dog in North America.Vet Ophthalmol. 2005 Mar-Apr;8(2):101-11.
- Slatter D. Disease of the canine lens and cataract formation. In: Slatter D, ed. Fundamentals of Veterinary Ophthalmology. 4rd ed. Philadelphia: Saunders WB, 2007: 859-887.
- Slatter D. Surgery of the canine lens. In: Slatter D, ed. Fundamentals of Veterinary Ophthalmology. 4rd ed. Philadelphia: Saunders WB, 2007: 888-931.
- Rubin L Inherited eye diseases in purebred dog. Baltimore:Williams and Wilkins 1989.