Temporal, or giant cell, arteritis is associated with significant morbidity, including permanent vision loss and stroke, if it is not promptly treated. González-Gay and colleagues performed a retrospective study of patients with giant cell arteritis to identify clinical features that would serve as predictors of vision loss and stroke.

A total of 239 patients were included in the study. Giant cell arteritis was confirmed by biopsy in each patient. Clinical features of the disease included thickening, swelling or tenderness of at least one temporal artery, recent onset of headache that was atypical for the patient, jaw claudication, vision changes, fever and weight loss. Cerebrovascular involvement was characterized by a transient ischemic attack or stroke. All of the patients received treatment with oral corticosteroids (prednisone at dosages ranging from 45 to 80 mg daily or the equivalent [60 mg in the majority of patients]) after the diagnosis was established.

Ocular symptoms occurred in 69 (28.9 percent) of the 239 patients. As a group, these patients had a higher frequency of cerebrovascular involvement than the 170 patients without ocular involvement. Ocular involvement did not relate to a delay in diagnosis; the time to diagnosis was somewhat shorter in patients with ocular manifestations. Permanent vision loss occurred in 34 (14.2 percent) of the patients and was due to ischemic optic neuritis in 31 patients, retinal artery occlusion in two patients and retrobulbar optic neuritis in one patient. Eleven patients had bilateral vision loss. Interestingly, eight of the 34 patients had partial recovery of vision after treatment with corticosteroids. However, if treatment was instituted more than two days after the onset of vision symptoms, there was no improvement. The eight patients with improvement in vision differed only in terms of a shorter interval between the onset of vision loss and the initiation of treatment (a median of 1 day versus 4 days).

Predictors of permanent vision loss in this study included a history of transient vision loss and jaw claudication. Eight patients (3.4 percent) sustained a cerebrovascular accident, with neurologic symptoms usually appearing an average of seven days after the onset of ocular symptoms. Symptoms of arteritis preceded the ischemic event by a median interval of 1.5 months. The stroke involved the vertebral-basilar territory in four patients and the carotid system in four patients. The best predictors of stroke were permanent vision loss and jaw claudication. There were two deaths in patients who sustained a stroke in the vertebral-basilar territory.

The authors conclude that the risk of permanent vision loss from temporal arteritis is increased in patients with transient vision loss or jaw claudication. Vision loss may be prevented or partially improved by prompt diagnosis and administration of corticosteroids. The authors recommend that high-dose corticosteroid therapy be instituted without delay, before biopsy confirms the diagnosis of giant cell arteritis, in patients who present with transient vision loss. Arteritis can be demonstrated in a temporal artery biopsy specimen even after two weeks of corticosteroid therapy.