Sage is a 7-year-old black male Labrador retriever presented for chronic anorexia, weight loss, and depression. During the past 2 weeks, Sage has been bumping into objects and appears to be blind.
The rectal temperature is 104.7°F, the pulse is 90 bpm and strong, and the respiratory rate is 26 rpm. All peripheral lymph nodes are enlarged three to four times normal size and are not painful. Sage appears to be blind. Both pupils are dilated, the menace response and pupillary light reflexes (PLRs) are absent in both eyes (no direct or consensual reflexes when either eye is tested). Fundus examination reveals active chorioretinitis with retinal detachments in both eyes. The neurologic examination is normal.
Using the problem-oriented approach described in Chapter 1, please identify the major problems in this dog and write an initial plan for each.
Blindness is the loss of vision in both eyes. Blind animals are identified when they begin bumping into objects or have trouble visually locating favorite toys. Unilateral blindness is difficult to recognize. Animals may bump into objects on the affected side. Partial loss of vision is nearly impossible to detect in animals without sophisticated equipment. Tests performed to assess vision include navigation of an obstacle course, menace response, cotton ball test, optokinetic nystagmus, and examination of the eye and nervous system.
There are four general categories for blindness:
The pathways for vision are diagramed in Figure 46-1. All fibers from the medial (nasal) retina and 20–35% of the fibers from the lateral retina (temporal) decussate at the optic chiasm. In the cat, about 65% of fibers decussate, 75% in the dog and 85—90% in horses and cattle. For the purposes of lesion localization, it is best to consider that 100% of the fibers decussate. The afferent pathways for vision and PLRs are similar until just before the lateral geniculate body of the thalamus. At this level, sensory fibers for the PLR leave the optic tracts and enter the midbrain to activate the parasympathetic motor centers of the oculomotor nerve (efferent arm of PLR). The efferent arm of the PLR is independent of vision. Visual fibers synapse in the lateral geniculate body, and second order neurons transmit visual information to the occipital cortex via the optic radiation.
The cause of bilateral blindness should be localized to one of the four categories listed above. This can be done with a combination of assessing papillary light reflexes and ophthalmo-logical examination.
Opacification of the Clear Media of the Eye
Opacity of the cornea, aqueous humor, lens, or vitreous should be evident from ocular examination with a bright light. Opacities severe enough to block the tapetal light reflection are likely severe enough to cause functional blindness and distorted images. The PLR is usually normal since sufficient quantity of light passes to the retina to activate the reflex.
Diffuse bilateral retinal lesions cause the pupils to dilate in room light. The PLR may be normal, slow, or absent. The retinal examination is usually abnormal with a few exceptions. The retina can be viewed easily after dilating the pupils with tropicamide 1%, a short onset and short duration mydriatic. Retinal detachment will appear blurry or out of focus with floating retinal vessels. Retinal hemorrhages can vary from small dots to extensive bleeds in the vitreous, obscuring retinal detail. Inflammatory chorioretinitis will also have blurry rather than clear and crisp fundic detail in the areas of inflammation. If it is a transudative chorioretinitis the tapetal color will still be visible. If it is an exudative chorioretinitis the tapetal color will be blocked by gray or brown exudate or granuloma. In the nontapetal fundus exudative lesions appear white, cream, or gray. Retinal degeneration is characterized by thin retinal vessels and an overall hyperreflectivity to the tapetal fundus due to the marked thinning of the overlying retina. In the nontapetal fundus patchy areas of white or gray depigmentation and adjacent pigment clumping may be visible. Degenerative lesions have clear, distinct margins, whereas inflammatory lesions have blurry, indistinct margins due to surrounding fluid accumulation between the retina and choroid. Sudden acquired retinal degeneration (SARD) is the exception to grossly visible retinal disease. Dogs with SARD present with acute blindness but a completely normal appearing fundus. The acute death of photoreceptors gradually leads to degeneration of the remaining retinal layers so that within months the degeneration becomes apparent on fundic examination. The only means of definitively diagnosing SARD on initial presentation is by electroretinogram testing. The electroretinogram is noninvasive and provides an absolute, reliable assessment of retinal function.
Failure to Transmit the Scanned Image
Bilateral lesions of the conducting system (optic nerves, optic tracts) up to the lateral geniculate body or lesions of the optic chiasm cause blindness and absent PLRs. Pupils are dilated in room light. The optic disk is the only component of the conducting system that can be directly examined. Lesions of the optic nerve may extend to the optic disk, causing changes in color, elevation, and size. With unilateral optic nerve or optic tract lesions, the pupils are usually normal size in room light. When the penlight is directed at the affected side, no PLR will be elicited in either eye. When the opposite side is tested, a normal PLR is present in both eyes.
Failure to Process the Image
Lesions affecting the lateral geniculate body, optic radiations, and occipital cortex produce blindness with normal PLR and normal pupil size in room light. This is clinically referred to as “cortical blindness.” Diseases that cause cortical blindness usually cause other neurologic signs suggestive of forebrain dysfunction.
The etiologies of bilateral blindness are listed in Table 46-1.
The problems identified in Sage are as follows: