Doc, will my pet see again? Assessing acute blindness
Ron Ofri, DVM, PhD, DECVO
Dr. Ofri is a professor of comparative ophthalmology at the Koret School of Veterinary Medicine at Hebrew University of Jerusalem in Rehovot, Israel.
Here’s what you need to know about examination, assessment and differential diagnosis in the blind veterinary patient.
Acute blindness in a pet is distressing for both the animal and the owner. Fortunately, in many cases vision can be restored. However, veterinarians and pet owners should bear in mind that acute blindness can be, and often is, a manifestation of systemic disease. Therefore, all patients that present with blindness—even those that do not regain vision—should undergo a comprehensive examination to reach an ophthalmic and systemic diagnosis, as the latter may have profound and long-term implications for the animal’s health.
As with any patient, begin by taking a history. Ask whether the blindness came on abruptly or gradually. Owners often report sudden loss of vision in the pet, even though ophthalmic examination reveals changes associated with chronic disease. Questioning will likely reveal that the blindness was noticed when the animal’s environment was changed (e.g. while visiting friends). We can assume that even though an animal has been blind for some time, the gradual onset of the disease enabled it to learn to navigate at home. The change in environment causes the animal to bump into objects, misleading the owners into believing that the blindness is acute.
Inquire whether the blindness was associated with preferential loss of night vision. One of the first behavioral signs of inherited, degenerative diseases of the outer retina (commonly known as progressive retinal atrophy) is loss of night vision as rods are affected before cones. Be careful of how you phrase your questions and do not "lead" the owners (that is, ask whether there is a difference between the pet’s daytime and nighttime vision rather than “is your pet seeing worse at night?”). Other rod functions (such as detection of moving objects or objects in the peripheral visual field) are also affected before cone functions (color vision, detection of objects in the central visual field). However, these changes are usually too subtle to be detected by owners.
Next, ask about the animal’s overall health and other signs of illness. Blindness may be caused by numerous systemic or neurologic diseases that frequently are accompanied by additional clinical signs. Therefore, a complete (non-ophthalmic) history of the patient is required. Furthermore, a complete physical examination and a thorough neurologic assessment are part of the workup of every case of blindness. Finally, perform a comprehensive ophthalmic examination, and evaluate the patient’s visual system.
Assessing the visual system in the blind animal
Menace response. This involves making a sudden threatening gesture that is supposed to elicit a blink response. It is important to note that the menace response involves cerebral cortical integration and interpretation, and thus is not a reflex. Rather, it is a cortical response that requires the entire peripheral and central visual pathways, as well as the visual cortex and the facial nucleus of cranial nerve VII, to be intact.
To avoid false-positive responses from the visual, contralateral eye (in cases of unilateral blindness), evaluate the menace response in one eye while the other eye is covered. False-positive responses can also result from touching the patient’s eyelashes or hair, or causing air movement near the patient’s eyes. False-negative responses may be caused by facial nerve paralysis. Therefore, in the absence of a menace response always test the blinking reflex by touching of the skin at both the lateral and medial canthi. The menace response is absent in animals younger than about 10 to 12 weeks and may also be affected by the patient’s mental state.
Additional visual tests. Vision also can be assessed using an obstacle course, navigated by the patient in both light and dim environments and with one eye patched. Be consistent in the obstacle course you construct, and make sure it can be navigated by normal animals. The visual placing response is useful when results of the obstacle course and menace response are equivocal. For this test, lift the animal toward the table, allowing it to see the approaching surface. A normal animal will extend its legs toward the surface before its paws touch the table (Figure 1).
Vision can be assessed in young puppies and kittens that may not yet have learned the menace response, and occasionally in stoic older animals, by throwing cotton balls in the air in front of the animal. A normal, alert animal that may not respond readily to a menace gesture will follow the cotton ball. Avoid throwing heavier objects that cause significant air movement or noise, because the animal may respond to these stimuli. Some animals, especially cats, will follow the red light emitted by a laser pointer.
The pupillary light reflex and dazzle reflex. Unlike the menace response, the pupillary light reflex (PLR) is a subcortical reflex. Therefore, it does not test vision, and a normal PLR may be found in a cortically blind animal. Furthermore, as the PLR does not require much afferent input, it is usually present (although it may be diminished or slow) in animals suffering from progressive retinal atrophy, cataracts and other causes of subcortical blindness. Nevertheless, the PLR is a very important test that helps localize the lesion that is causing blindness.
Pupil size and reaction to light are assessed after the menace test. First, evaluate the size of the pupils at rest (without stimulation) in normal room light. Next, evaluate pupil size and dilation symmetry in dim light, without stimulating the eyes. Unless a cataract or some other opacity is present in the ocular media, the pupils will be retroilluminated by the tapetal reflection. The size of each pupil is assessed and compared to determine whether anisocoria (unequal-sized pupils) is present. If anisocoria is noted, determine which pupil is abnormal by comparing the degree of anisocoria first in the light and then in the dark. The abnormal pupil is the one that changes less in response to the change in stimulus. In other words, if the degree of anisocoria decreases in the dark, then the mydriatic pupil is abnormal; if the degree of anisocoria increases in the dark, then the miotic pupil is abnormal.
Next, test the animal’s reaction to strong light. Because of the decussation in the optic chiasm and pretectal nucleus, stimulating the retina of one eye with a bright source of light causes constriction of both pupils. First, evaluate the direct PLR by shining a bright light into one eye while observing the reaction of its pupil. To evaluate the indirect (or consensual) PLR—constriction of the pupil in the unstimulated eye—shine a bright light into one eye while observing the reaction of the contralateral pupil.
The dazzle reflex is another subcortical reflex. It is manifested as a partial blink reflex in response to a bright light. The anatomic pathway responsible for this reflex is poorly understood. However, this test is a very useful substitute for the PLR in cases when the pupil can't be seen, such as in cases of severe corneal edema or hyphema (Figure 2).
Localizing the lesion in the blind patient
Based on the results of the ophthalmic examination and PLR, the patient may be categorized into one of five general groups:
• Light does not reach the retina. The most common causes of blindness in this category, which are usually evident based on the ophthalmic examination, include severe blepharospasm, extensive corneal edema or pigmentation, hyphema or hypopyon in the anterior chamber, and cataract. In most cases, vision will be restored if the primary ocular disease is treated successfully (Figure 3).
• Retinal disease with a normal/diminished PLR. The two leading differentials in this category are inherited retinopathies and chorioretinitis (or posterior uveitis). The diseases are often diagnosed based on ophthalmoscopic signs. Patients with inherited retinopathy frequently present with attenuation of the retinal vasculature and tapetal hyperreflectivity (Figure 4); the diagnosis may be confirmed with an electroretinographic recording (Figure 5). In chorioretinitis, inflammatory changes are evident in the fundus. The PLR is often normal, since (as noted previously) it requires little afferent input.
• Retinal disease with no PLR. Common causes of blindness in this category include glaucoma, retinal detachment and optic neuritis involving the proximal optic nerve. Glaucoma is discussed in more detail elsewhere. A detached retina can be visualized as a vascular gray veil floating behind the lens (Figure 6), and the diagnosis may be confirmed with ultrasound. Proximal optic neuritis can be confirmed ophthalmoscopically, as the optic nerve head appears congested, elevated and blurry (Figure 7).
• In patients with a normal ophthalmic examination and an absent PLR, blindness is most often caused by sudden acquired retinal degeneration syndrome, optic neuritis involving the distal optic nerve, or neoplasia compressing the optic nerve or chiasm. The former is diagnosed using electroretinography, while advanced imaging (Figure 8) and a neurologic workup are used to diagnose optic nerve and chiasm disease.
• Blind patients with a normal ophthalmic examination and PLR are usually neurologic cases. The blindness is due to central lesions affecting the visual pathways from the lateral geniculate nucleus to the contralateral visual cortex. These may be congenital, metabolic, infectious, inflammatory, toxic or neoplastic central nervous system disease.
Glaucoma, retinal detachment, optic neuritis and sudden acquired retinal degeneration syndrome should be considered in patients presenting with acute blindness and fixed, dilated pupils. In many cases, especially when posterior uveitis, retinal detachment or optic neuritis is present, a systemic disease may be the underlying cause. Therefore, patients should undergo a comprehensive physical examination. Successful diagnosis and treatment of the primary cause may lead to restoration of vision and may even save your patient’s life.
Dr. Ofri is a professor of comparative ophthalmology at the Koret School of Veterinary Medicine, Hebrew University of Jerusalem in Rehovot, Israel.