11 The lens is a unique structure that is transparent in its normal state and functions to focus light onto the retina. It is made up of very regularly arranged lens fibers that are derived from the lens epithelium, which continues to produce new fibers throughout the animal’s life. These fibers become densely packed within the lens nucleus (center) in later life which results in nuclear sclerosis, a normal aging change. It is enclosed by a thin lens capsule that isolates it from the body but maintains limited permeability to allow passage of essential nutrients. The lens capsule varies in thickness (anterior > posterior) and is suspended by dozens of tiny zonules (tertiary vitreous) from the ciliary body posterior to the iris. The lens is isolated from the rest of the body and immune system before birth and therefore is not recognized as self. When lens fibers become abnormal (cataractous) or the lens capsule is damaged or breached, a significant immune‐mediated uveitis results, which is referred to as lens‐induced uveitis. Developmental defects in the lens can involve the lens itself, persistent vascular systems designed to provide nutrition to the developing lens that fail to regress, or the zonules. The most common defects are smaller than normal lens (microphakia usually combined with microphthalmia) and cataract formation. Congenital cataracts are discussed later in the section on cataract. Microphakia is a smaller than normal lens, and probably occurs more frequently than reported. Microphakia occurs in most, if not all, microphthalmic globes (Figure 11.1). Congenital cataracts are often also microphakic. In a study on Miniature Schnauzer congenital cataracts, ultrasonographic globe measurements from growing and adult normal and cataractous dogs revealed that the majority of cataractous eyes were slightly smaller than age‐matched controls and the affected lenses were correspondingly reduced in size. In dogs with multiple ophthalmic anomalies, such as those in homozygous merle dogs or breeds with inherited retinal dysplasia and retinal detachments, microphakia is often present (see Figures 4.1 and 10.2). Figure 11.1 Microphakia in a dog. Note the lens periphery is smaller than normal, and elongated ciliary processes surround the lens equator (arrows). A complete hypermature cataract is also present. Examination of an affected lens reveals reduced lens circumference and/or reduced thickness (anteroposterior). Ultrasonography (a‐scan mode) measurements are the most accurate clinical (in vivo) method to measure the lens anteroposterior length (axial length). Other abnormalities include persistent pupillary membranes, persistent hyaloid remnants (persistent hyperplastic tunica vasculosa lentis, PHTVL and persistent hyperplastic primary vitreous, PHPV), and lenticonus or lentiglobus. If the microphakic lens is cataractous, the opacity remains stationary in size or progresses depending on the areas of the lens affected. Treatment is not usually attempted provided clinical vision is present. Colobomas of the canine lens are rare. They appear clinically as a notch or indentation of the lens equator (Figure 11.2). They can be typical (located at the 6 o’clock position) or atypical (all other sites). Lens colobomas appear directly related with the focal absence of zonules and an associated coloboma in the ciliary body and often the iris. Cataract may not be present. Figure 11.2 Lens coloboma in a puppy. The coloboma is a flattened area devoid of zonulary attachments (arrows). An incomplete and immature cataract is also present. In lenticonus and lentiglobus the anterior and/or posterior surface of the lens protrudes in either a conical (conus) or more generalized (globus) projection. Posterior lenticonus is the most common form and occurs occasionally with congenital cataracts (inherited congenital cataracts in the Miniature Schnauzer or persistent hyaloid remnants (PHTVL and/or PHPV) (Figure 11.3). Figure 11.3 (A) Lenticonus in an Old English Sheepdog puppy. The very discrete focal cataract affects the posterior cortex and posterior lens capsule. (B) Slit lamp biomicroscopic view of posterior lenticonus in a Miniature Schnauzer cataract (nuclear and posterior cortex). The posterior protrusion from the caudal lens extends into the anterior vitreous (arrow). The clinical appearance of posterior lenticonus, as viewed anteroposteriorly, is a circular and often cataractous outcropping of the posterior lens and capsule. Posterior protrusion of the polar area of the lens into the anterior vitreous can be confirmed with slit lamp biomicroscopy. If the lens is cataractous, ultrasonography can be used to detect posterior lenticonus. In the evaluation of congenital cataracts for surgery, special attention is directed at the posterior lens. Because posterior lenticonus often signals a thin and weak polar posterior lens capsule and possible anterior vitreal abnormalities, cataract surgery in these eyes presents additional risks. As noted in Chapter 10 on the canine anterior uvea, persistent pupillary membranes (PPMs) are the most frequent anterior uveal anomaly in the dog. They represent an abnormal development of the pupil, and arise from the anterior surface (collarette) of the iris (Figure 11.4; see also Figures 8.3 and 10.3). This distinguishes the PPM from posterior synechia which implies the adherence of the pupillary or posterior surface of the iris to the lens, and suggests past or current iridocyclitis. Figure 11.4 Old English Sheepdog puppy with four persistent pupillary membranes (PPMs) which extend from the collarette area of the anterior iris and insert on the anterior lens capsule causing cataract formation. Additional cataract formation is occurring in the lens cortices. PPMs extend from the collarette area to the anterior lens capsule, posterior cornea, or to an adjacent collarette area. PPMs extending to the anterior lens capsule appear as fine gray to white strands or larger bands of pigmented tissue. They can contain blood vessels, which hemorrhage when torn by traction of miosis or mydriasis, or laser or surgical incision. Anterior capsular or subcapsular cataracts, secondary to PPMs, usually do not progress. If small and focal, these cataracts may have limited to no appreciable effect on clinical vision. If larger, dense, and within the pupil, an adverse effect on vision (particularly in bright light, when miosis further limits the axial field of view) can occur; in these patients long‐term drug‐induced mydriasis and/or cataract surgery may be beneficial. Persistent hyaloid remnants (PHPV and/or PHTVL) are an infrequent condition in puppies, and affect one or both eyes (Figure 11.5; see also Figure 12.1). This disease has been investigated in the Doberman Pinscher and Staffordshire Bull Terrier. Other breeds affected include the Bouvier des Flandres and the Standard Schnauzer. Figure 11.5 (A) Persistent hyaloid vascular remnants in a Labrador Retriever puppy. Note the red hyaloid blood vessels (arrow), and posterior cortical and capsular cataract. (B) Persistent hyperplastic tunica vasculosa lentis in a hound dog. The surrounding mat of blood vessels are perfused and posterior capsular cataract is present. Persistent hyaloid remnants, when the sole abnormality, are characterized by a posterior polar cataract with blood vessels extending from the optic nerve head to the polar posterior lens capsule. The cataract is usually limited in size and density, permitting ophthalmoscopy and examination of the ocular fundus. Treatment is usually not indicated unless some daytime vision impairment occurs. Topical mydriatics can permit the dog to see “around” the opacity. The disease in the Doberman Pinscher is more severe and usually includes other developmental anomalies including persistent pupillary membranes, secondary cataracts with anomalous posterior lens capsules, posterior lenticonus, and retinal dysplasia. As a result, cataract surgery in this breed is hazardous and yields low success rates. Cataracts are defined as an opacity of the lens or its capsule. Cataracts are frequently encountered in dogs, and are a leading cause of blindness in purebred dogs. Cataracts are classified clinically by age of onset (congenital, adult, and senile), position within the lens (anterior capsule, anterior cortex, nuclear, posterior cortex, and posterior lens capsule; also polar, axial, sutural, zonular, and equatorial), stage of maturity (incipient, immature, mature, hypermature, Morganian), etiology (inherited, traumatic, toxic, metabolic, inflammatory), and appearance (spike, wedge, spoke, cuneiform, sunflower, stellate, punctate, and purverulent). Cataracts are caused by abnormalities of the lens fibers and/or capsule and must be distinguished from nuclear sclerosis, a normal aging change, and minor lens imperfections which can be detected with slit lamp biomicroscopy (Figure 11.6). These imperfections include zones of discontinuity between the anterior and posterior cortical and nuclear (adult, fetal, and embryonal) regions, anterior and posterior lens sutures, Mittendorf’s dot (remnants of posterior hyaloid on the posterior lens capsule), and arcuate line of Vogt (circular line of the anterior aspects of Cloquet’s canal). Figure 11.6 (A) Cataract formation is first evidenced as the formation of vacuoles (arrows) within the lens. These vacuoles gradually enlarge and form “water clefts.” (B) More extensive cataract formation in a Chesapeake Bay Retriever. The cataract formation is concentrated in the lens nucleus, but has extended into the posterior cortex. Nuclear sclerosis is a normal aging change of the lens produced by the compaction of the central lens fibers (Figure 11.7). It is often confused with cataract formation, but it produces no significant impairment of vision. When it is particularly dense, affected individuals can exhibit subtle decreases in depth perception. The condition produces a gray to bluish color (caused by light scattering) to the center or nucleus of the lens, but does not impede direct or indirect ophthalmology and visualization of the ocular fundus, except when very dense in the very elderly dog. Figure 11.7 (A) Nuclear sclerosis of the lens in a 10‐year‐old dog. The gray translucent zone is confined to the lens nucleus. Cortical cataract formation is also starting (arrows). (B) Nuclear sclerosis in an aged mixed‐breed dog. Note the strand of iris indicating atrophy along the ventral pupil. (C) In this example of nuclear sclerosis, the fundic reflex is easily seen.
Canine Lens and Cataract Formation
Congenital Abnormalities
Microphakia
Lens Colobomas
Lenticonus and Lentiglobus
Persistent Pupillary Membranes and Anterior Cataracts
Persistent Hyaloid and Posterior Cataracts
Cataracts
Lens Changes and Aging
Inherited Cataracts in the Dog
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