Presentation of Case: An 88-year-old female of Pakistani origin presented with a 10-day history of right-sided lateral neck and jaw pain radiating to the right temporal region. She reported associated eye pain, but no visual disturbance, and no jaw or limb claudication, although had experienced intermittent paraesthesia of the hands bilaterally. In the days leading up to admission she had intermittent fever and had received a course of erythromycin for a presumed UTI. She denied malaise, anorexia or night sweats, but reported some minimal weight loss over the previous month. Her medical background included asthma and hypertension only, with no additional cardiovascular risk factors. On examination right sided focal jaw and temporal tenderness was elicited, with a prominently palpable, pulsatile right temporal artery. Heart sounds were normal with no murmurs, no carotid bruits, radial pulses were present and equal and there was no brachial blood pressure discrepancy. Cranial and peripheral nerves were intact. Diagnostic Testing: Inflammatory blood markers were elevated with ESR >119mm/Hr, CRP 191 mg/L, and platelets 777 x 109/L at their peak. Blood cultures were negative, as was a vasculitic screen including ANCA, immunoglobulins, hepatitis, HIV and syphilis serology. Urine dip demonstrated 1+ erythrocytes only. CT neck with contrast showed no abscess,but noted a poorly opacified left common carotid artery. Subsequent USS of the carotid arteries demonstrated non-occlusive, hypoechoic atheroma in the right external carotid with 70% stenosis and complete occlusion of the left common carotid by hypoechoic atheroma. CT angiography of the aortic arch and carotids confirmed the USS findings, as well as mural thickening at the origin of the left subclavian artery and the descending aorta. In retrospect mural enhancement of the left carotid artery was evident on initial venous phase CT. CT thorax abdomen pelvis was essentially normal with no evidence of malignancy. Due to isolation requirements, following Covid-19 exposure, transfer off-site for temporal artery ultrasound/PET or temp artery biopsy was not permissible. Differential & Final Diagnosis: Surgical intervention for carotid artery occlusion was considered unnecessary due to adequate cerebral perfusion and lack of evidence of a cerebral vascular accident. The possibility of infection and incidental atherosclerotic disease was considered, but careful evaluation revealed no focus of infection. The presentation of cranial symptoms, systemic features, highly elevated inflammatory markers, and CT imaging findings suggested a diagnosis of large vessel vasculitis (LVV). Discussion of Management: Further diagnostic evaluation was desirable but contact isolation requisites and operational pressures would have resulted in significant time delay. Due to the patient’s precarious cranial blood supply Prednisolone 40mg once daily was commenced for LVV. Symptoms resolved quickly with a concurrent rapid improvement in serum inflammatory marker levels. Conclusions: Temporal artery ultrasound and PET CT are considered the imaging of choice for investigation of LVV, however contrast enhanced CT can also demonstrate mural thickening and enhancement consistent with vessel wall inflammation1. Carotid artery occlusion has been described in LVV, but our patient uniquely had complete unilateral common carotid occlusion without neurological sequelae. Our case highlighted the validity of alternative imaging methods to establish a diagnosis. Disclosures: None Figure 1. A: venous phase CT showing enhancement of occluded left common carotid artery; B: CT angiogram confirming left carotid artery occlusion; C: Duplex ultrasound of left common carotid showing occlusion by hypoechoic matter; D: Mural thickening of descending aorta.