Diagnostic Ophthalmology

History and clinical signs

A 7-year-old, 7 kg, neutered male domestic shorthair cat was examined at the ophthalmology service at the Western College of Veterinary Medicine for evaluation of sudden onset of blindness that occurred 3 d previously. Previous medical history was unremarkable, and he was current for routine vaccinations. General physical examination was normal except for the ocular abnormalities. The menace responses were absent bilaterally. Both pupils were dilated at rest, and the direct and consensual pupillary light reflexes were absent in both eyes. The palpebral, and oculocephalic reflexes were present bilaterally. Schirmer tear test (Schirmer Tear Test Strips; Alcon Canada, Mississauga, Ontario) values were 15 and 18 mm/min in the right and left eyes, respectively. The intraocular pressures were estimated with a rebound tonometer (Tonvet, Tiolat, Helsinki, Finland) and were 12 mmHg, bilaterally. Results from fluorescein staining (Fluorets; Bausch & Lomb Canada, Markham, Ontario) were negative, bilaterally. On direct examination, billowing, vascularized tissue was visualized through the pupil in each eye. Biomicroscopic (Osram 64222; Carl Zeiss Canada, Don Mills, Ontario) and indirect ophthalmoscopic (Heine Omega 200; Heine Instruments Canada, Kitchener, Ontario) examinations were completed. A photograph of the cat is provided for your assessment (Figure 1).

Figure 1.

Photograph of both eyes of a 7-year-old domestic shorthair cat.

What are your clinical diagnosis, differential diagnoses, therapeutic plan, and prognosis?

Discussion

Our clinical diagnosis was bilateral serous retinal detachments. Differential diagnoses for serous retinal detachment in the cat include: systemic hypertension secondary to chronic renal disease, hyperthyroidism, diabetes mellitus, hyperaldosteronism, or chronic anemia; primary or essential hypertension; hyperviscosity syndrome; chorioretinitis, secondary to systemic infection such as toxoplasmosis, feline infectious peritonitis (FIP), feline leukemia virus (FeLV), feline immunodeficiency virus (FIV), and disseminated mycotic disease; as well as neoplasia.

Indirect blood pressure (BP), measured using Doppler-shift ultrasonic sphygmomanometry was elevated at 200 mmHg. Complete blood (cell) count (CBC) revealed a mildly increased hematocrit (0.495; normal range: 0.285–0.477) but was otherwise within normal limits. Serum biochemistry showed no significant abnormalities, and urinalysis was unremarkable with a urine specific gravity of 0.1036. Serum thyroxin (T4) was within normal limits, and abdominal ultrasound showed no significant abnormalities. The diagnosis was idiopathic systemic hypertension, as no underlying cause was discovered. Treatment for hypertension was initiated with Amlodipine (Norvasc; Pfizer Canada. Kirkland, Quebec) 0.625 mg, PO, q24h. Upon re-evaluation 3 d later, the systolic BP measurement remained elevated at 190 mmHg and the retinal detachments were unchanged. The medication dosage was increased to 1.25 mg q24h. Re-evaluation 7-d later revealed a BP of 170 mmHg. The retinal detachments were resolving and vision was improving. Over the next 4 wk the BP returned to normal range, the retinal detachments completely resolved, and vision returned. The cat remains on this dose of Amlodipine (Norvasc; Pfizer Canada) to maintain normal BP.

Systemic hypertension in cats is defined as an indirect systolic pressure > 160–170 mmHg (1,2). It occurs most commonly secondary to chronic renal disease, with a frequency of up to 65% and hyperthyroidism with a frequency of 23% (1). Primary or essential hypertension is considered rare in animals and is a diagnosis of exclusion (2). In this cat, however, further testing would be required to rule out all other causes of hypertension including measurement of plasma aldosterone, renin, and catecholamines; creatinine clearance; renal arteriogram; and renal biopsy.

Clinical signs of hypertension are referable to damage to target organs with a rich arteriolar blood supply. The commonly affected areas are renal, cardiovascular, cerebrovascular, and ocular (3). Renal changes secondary to chronic hypertension include glomerulosclerosis, glomerular atrophy, and interstitial fibrosis. Left ventricular hypertrophy and valvular insufficiency may occur due to increased cardiac afterload resulting in ventricular remodeling. Cerebrovascular hemorrhages (accidents or strokes), cerebral edema, and neurological signs such as seizures, head tilt, and depression are associated with hypertension. The most commonly described ocular lesions in hypertension are retinal detachment, edema, retinal hemorrhage, hyphema, and retinal degeneration (1–5). Retinal hemorrhage and edema result from retinal vascular damage (hypertensive retinopathy), while detachment is associated with choroidal vascular damage (hypertensive choroidopathy) (6,7). The vascular system supplying the retina and choroid differ anatomically and physiologically. Retinal arterioles exhibit autoregulation to ensure a constant blood flow despite changes in intraocular pressure and local arterial BP. Increased BP results in vasoconstriction of the precapillary arterioles and sustained vasoconstriction leads to ischemic damage to the vascular smooth muscle and endothelium. Vasodilation and increased vessel permeability ensue, causing leakage of plasma and cells into the surrounding retinal tissue, manifesting as retinal edema and hemorrhage (6). Choroidal capillaries supply the outer layers of the retina. They are fenestrated, allowing leakage of plasma protein into the interstitium. Tight junctions between the cells of the retinal pigmented epithelium (RPE) normally prevent this fluid from entering the subretinal space. Choroidal vessels do not exhibit autoregulation, rather, they are under autonomic control. During hypertension, elevated circulating vasopressor substances may leak into the choroidal extra-vascular space, producing vasoconstriction, ischemia, and infarction of the choriocapillaris and RPE. Retinal pigmented epithelium disruption results in breakdown of the blood-retinal-barrier, fluid leakage into the sub-retinal space, and retinal detachment (7).

The goal of hypertension therapy is to reduce BP to < 170 mmHg. A variety of drugs including diuretics, beta-adrenergic blockers, angiotensin-converting enzyme inhibitors, alpha-adrenergic blockers, and calcium channel blockers can be used to treat hypertension, all with mixed results (2,3,5). Amlodipine is a calcium channel blocker that reduces vascular smooth muscle tone, and is often effective in lowering BP in cats as a single agent (8). The recommended dose is 0.625 mg/d; however, cats that are > 5 kg often require higher doses to control BP, as did this cat (8). Ideally, once BP is normalized, follow-up evaluation of BP, cardiac status, ocular lesions, and progression of renal disease should continue at least every 3 mo.

The prognosis for hypertensive cats remains guarded over the long-term; vision loss and retinal degeneration are common (2,5). Acute vision loss is usually associated with retinal detachment, and recovery generally occurs with reattachment. Detachment causes degeneration of the outer retina, the degree of which depends on the duration of detachment. Despite reattachment, retinal degeneration may progress in some hypertensive cats due to chronic retinal ischemia induced by retinal and choroidal vascular damage (9). It is important to note that controlling BP may help to decrease the risk of severe secondary organ damage that can lead to death such as cerebrovascular accident, heart failure, and progressive renal failure. Compliance with administration of medications and regular veterinary monitoring are extremely important in determining the outcome of the individual hypertensive cat.