Introduction

• Signs: sudden onset blindness or rapidly progressive blindness over a period of days, often accompanied by Cushingoid signs (polydipsia, polyuria, weight gain over preceding months).
• Diagnosis: history, clinical signs, ophthalmoscopy, hematology, biochemistry, adrenal axis testing, sex hormone testing, electroretinography (ERG).
• Treatment: no treatment possible.
• Prognosis: visual prognosis is poor, with permanent loss of sight. Systemic signs (PU/PD) may spontaneously reduce over a period of months in some cases.

Pathogenesis

Etiology

• Etiology is not known. A significant number of cases (40-60%) show Cushingoid systemic signs but the etiopathogenic link with Cushing's is unclear; only 12-17% of cases can be confirmed with Cushing's Hyperadrenocorticism based on adrenal axis testing. However, 85% have elevated sex hormones.

Predisposing factors

• Overweight, middle-aged, female, small breed dogs.
• Association with Cushing's syndrome is some cases.

Specific

• None known.

Pathophysiology

• Sudden loss of photoreceptor function - both rods and cones equally affected.
• Cause is unknown but presumed to be a toxic 'knockout' of rod and cone photoreceptors.
• Retinal toxicity due to aberrant endogenous corticosteroid production has been proposed as a potential mechanism. Corticosteroids have been shown to be retinotoxic in some species, and the link with Cushingoid signs may point to a similar mechanism in dogs.
• In humans, a similar condition of sudden onset blindness may be associated with cancer-associated retinopathy. However, there is no evidence of this in dogs.

Timecourse

• Acute onset.

Epidemiology

• Unknown.

Diagnosis

Treatment

Outcomes