Objective. Cranial ischemic complications such as cerebrovascular accidents (CVAs) and acute visual loss are among the leading causes of giant cell arteritis (GCA)-related morbidity. In this retrospective study, we evaluated the effect of treatment with low-dose aspirin on the incidence of cranial ischemic complications in GCA.Methods. Charts of 175 consecutive patients in whom GCA was diagnosed between 1980 and 2000 were reviewed for medical data. Data for 166 patients who were followed up for at least 3 months were also available.Results. At the time of the diagnosis of GCA, 36 patients (21%) had already been receiving low-dose aspirin (100 mg/day). In all cases, the indication for this treatment was ischemic heart disease. There were no significant differences between the aspirin-treated and non-aspirin-treated groups regarding the mean age of patients, the male-to-female ratio, duration of GCArelated symptoms, rates of headaches, systemic symptoms, and jaw claudication, and the mean erythrocyte sedimentation rate, hemoglobin count, and platelet count. Cerebrovascular risk factors (hypertension, hyperlipidemia, or diabetes mellitus) were more common in the aspirin-treated group (38.9% versus 20%; P‫؍‬ 0.03). Cranial ischemic complications were diagnosed in 43 patients at presentation: 30 patients had acute visual loss, 11 had CVAs, and 2 had both conditions simultaneously. Only 3 of the aspirin-treated patients (8%) presented with cranial ischemic complications, compared with 40 (29%) of the non-aspirin-treated patients (P ‫؍‬ 0.01). Despite the use of steroid therapy, cranial ischemic complications developed in 14 of the 166 patients followed up for 3 months or longer. However, cranial ischemic complications developed in only 3% of the aspirin-treated patients, compared with 13% of the patients treated with prednisone only (P ‫؍‬ 0.02).Conclusion. These data suggest that low-dose aspirin decreases the rate of visual loss and CVAs in patients with GCA.

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Cranial ischemic complications (CICs) are among the presenting manifestations of giant cell arteritis (GCA). Yet patients with GCA may develop CICs at a later stage, despite steroid therapy. In the current report we delineate risk factors for CICs, both at presentation and during follow-up, and review the relevant literature. We reviewed charts of 175 patients with GCA. Follow-up data were available for 166 patients. CICs at presentation or developing within 2 weeks of GCA diagnosis were considered GCA related. CICs developing later were considered GCA related only when associated with other GCA-related manifestations or acute-phase reactions. Associations between CICs and other variables were tested by multivariate analysis. At presentation, 43 patients (24.6%) had CICs. Risk factors were transient cerebro-ophthalmic ischemic episodes (COIEs) (odds ratio [OR] 4.3) and male sex (OR 2.5), while the presence of systemic symptoms was "protective" (OR 0.3). During follow-up 8.4% of patients with GCA developed new CICs. Risk factors in these cases were previous CICs at presentation (OR 5.6) and transient COIEs developing during follow-up (OR 14.8). The use of low-dose aspirin was protective (OR 0.2). These data, together with data from the literature review, suggest that GCA patients with transient COIEs and without fever or other systemic symptoms are at increased risk of presenting with CICs. Risk factors for late-developing CICs were CICs at presentation and late-developing transient COIEs.

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Gastroenterologists should adhere strictly to cautionary measures to prevent misplacement of PEG into the colon. In patients with PEG feeding, the clinician should suspect misplacement of the tube into the colon when there is recurrent severe diarrhea of undigested food or fecal content in the tube, particularly after tube replacement. Treatment may be conservative in most cases.