A 78-year-old man with a history of a monitored abdominal aortic aneurysm presented after symptomatic COVID-19, investigators reported. He initially developed fever and tested positive by nasopharyngeal PCR. Seven days later he returned with recurrent fever, cough, poor appetite, and elevated inflammatory markers; these findings prompted hospital admission. His past medical history included hypertension, heavy smoking, advanced chronic kidney disease, and diffuse atherosclerotic disease, which the authors identified as relevant comorbid conditions. On admission the patient’s C-reactive protein (CRP) initially fell, but then rose again on hospital day 11. Around that time he developed new-onset, mild low back pain without overt hypotension or other hemodynamic collapse.
Serial imaging had shown a stable maximum short-axis diameter of approximately 43 mm over the prior 2 years, the case report noted. Repeat non-contrast abdominal computed tomography (CT) obtained 18 days after the initial COVID-19 diagnosis demonstrated an increase in the aneurysm diameter from 43 mm to 51 mm compared with prior studies. The CT also demonstrated periaortic fat stranding adjacent to the aneurysm, which the study team interpreted as inflammatory change consistent with impending rupture. The authors reported the timeline and imaging findings as the basis for urgent intervention; the article did not provide additional contrast-enhanced imaging details or histologic correlation.
The care team elected to perform urgent endovascular aneurysm repair (EVAR) prior to hemodynamic deterioration. The decision was driven by the observed rapid growth over a short interval and the presence of periaortic inflammatory signs on CT. The case report did not include detailed procedural metrics, device models, or intraoperative hemodynamics. It did state, however, that intervention occurred before overt rupture or circulatory collapse, reflecting a strategy of early operative management when imaging suggested an imminent threat.
Postoperative recovery was described as stable. The patient was discharged without ischemic complications or procedural adverse events, the authors noted. The report did not supply long-term follow-up beyond the immediate postoperative hospitalization, nor did it report on serial postoperative imaging beyond hospital discharge. No thrombotic, infectious, or graft-related complications were recorded in the inpatient period described.
The authors observed that a previously quiescent abdominal aortic aneurysm may destabilize after recent COVID-19 infection. They recommended that clinicians consider repeat imaging when inflammatory markers rise or when new symptoms—such as low back pain—appear, even if symptoms are relatively mild and hemodynamic parameters remain stable. The case points to a low threshold for reassessment in patients with known aneurysms who develop systemic inflammation from recent infection, according to the report. The article did not attempt to quantify risk across populations, and it did not propose specific imaging intervals or standardized protocols for post-COVID surveillance.
This is a single-patient case report; the authors did not present mechanistic data linking COVID-19 to aneurysm destabilization, nor did they include histopathology or laboratory studies that would explain the rapid enlargement. The report omitted detailed procedural information about the EVAR devices used and lacked longer-term follow-up imaging after discharge. Causality between SARS-CoV-2 infection and aneurysm expansion cannot be established from this report alone. Remaining clinical questions include the incidence of similar events after COVID-19, the pathophysiology connecting systemic inflammation to aneurysm wall weakening, and whether standardized surveillance protocols after infectious insults would alter outcomes. The authors limited their conclusions to the single observed clinical course and advised clinicians to consider repeat imaging when inflammatory markers rise or new symptoms develop.