Infectious Aortitis on FDG PET/CT

Introduction: Aortitis is the inflammation of the aorta and can result from either an infectious or a non-infectious cause. Its initial clinical presentation can be very similar in both etiologies and inflammatory biomarkers can be normal despite significant aortic inflammation, or non-specifically positive. Patient demographics can play a pivotal role in the diagnosis of aortitis subtypes. Due to the difficulty of in vivo tissue, correctly recognizing the aortitis subtype remains a challenge for the appropriate patient management and long-term disease monitoring as some patients may have a "single-hit" disease if treated appropriately. Using CT, MRI or ultrasound (US) imaging has helped address diagnostic uncertainty with the parietal wall thickening and adjacent fat stranding often used as trustful signs of aortic wall inflammation when found around the aorta. It also helps assess luminal abnormalities (aneurysms and/or stenoses), differentiate between atherosclerosis, aortic wall hematoma and aortic wall inflammation. Positron Emission Tomography (PET) using F18-FDG is also part of diagnostic armamentarium as it provides a functional whole-body map of inflammation, identifying other FDG-avid lesions and a measurable degree of FDG uptake by means of the maximal standardized uptake value (SUVmax) that may be useful to monitor vascular inflammation.

Methods: Patient is a 58-year-old woman with history of opioid use disorder who presented with altered mental status and hypotension.

Results: Initial infectious work-up included a chest CTA that ruled out a pulmonary embolism but demonstrated lower lobe consolidations, no evidence of thickening seen around the aortic arch. The patient’s blood culture grew Streptococcus pneumoniae and a testing for SARS-CoV-2 was positive; thus, remdesivir was started. While her pressor and oxygen requirements and the leukocytosis were rising despite the broad-spectrum antibiotics, a chest CT with contrast, seven days after the prior chest CTA, showed worsened lung consolidations. Four days later, repeat chest CT with contrast showed an appearance of a pericardial effusion with associated wall thickening of the thoracic aorta and great vessels and new perivascular inflammation surrounding the proximal abdominal aorta and the visceral branches. A comprehensive infectious and inflammatory work-up including IgG-4-related disease was negative, except for ANA levels (high: 1:2560) and Anti–Scl-70 antibodies (likely non-specific in systemic inflammation). An F¹⁸-FDG PET/CT demonstrated findings suspicious for large vessel vasculitis involving the thoracic and brachiocephalic arteries extending into the abdominal aorta to below the renal arteries, with an incidental discovery of a subcutaneous abscess located in the right arm. There was no purulence on incision and drainage (I&D) of the abscess. Patient was started on methylprednisolone and colchicine daily. Intravenous immunoglobulin course for 3 days was also completed. Follow-up chest CTA, 2 days after the initiation of IVIG and steroids, showed marked reduction in thickness of the aortic wall. Inflammatory markers down-trended with an overall improvement of the mental status of the patient who was discharged from the hospital after finishing the steroid taper.

Conclusions: Infectious aortitis is a challenging radiographic diagnosis due to the overlapping features with the non-infectious aortitis category. The diagnosis has to be established urgently as any delay in medical therapy can result in deleterious consequences for the patient. This case portrayed an infectious aortitis where both SARS-CoV-2 and Streptococcus pneumoniae bacteremia were detected and imaging revealed findings resembling those of large vessel vasculitis. Standard of care treatment was administered. Within a short interval, a drastic improvement in the aortic wall thickening was noted on imaging, which can be, regardless of the biological markers, a surrogate marker for diagnosing any infectious aortitis.

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