The present implications of these findings on Fluoroquinolones for treatment of patients with Aortic Aneurysm
In some comments, more clinical data or more experimental data about Fluoroquinolones (FQ) and the aorta are asked for. However, the growing evidence is that FQ are deleterious for patients with Aortic Aneurysm (AA). In this setting, I would like to raise some issues which are directly connected with the care of those patients with an AA who are treated for whatever reason with FQ. The goal is to discuss practical clinical situations while waiting for more evidence or for binding recommendations.
1/ Should patients with known AA be treated with FQ in case of infection elsewhere?
The answer is not in the literature as no prospective study has been completed to date in such a population. But due to the high risk of a fatal issue in case of rupture or fissure, such a pre-existing condition should be searched for by anamnesis, physical exam or through EHR before filling out a prescription for FQ. Only severe sepsis caused by resistant bacteria to other antibiotics than FQ is a balanced risk indication. In all other cases, FQ should be avoided, especially in pneumonia and UTI without antibiogram. This hazard is not well known and a new regulation is waited (https://www.fda.gov/Drugs/DrugSafety/ucm511530.htm) to include this information in FQ label.
2/ What about patients treated with FQ and presenting with a growing AA?
In those patients, the first diagnosis suspected depends on the infectious context. If the patient is febrile with active infection and inflammation, a mycotic aneurysm is usually suspected either a true native AA if sacciform or a bacterial graft on a pre-existent AA. If the patient is apyretic and infection is healed, growth is usually considered to be a consequence of local inflammation in the arterial wall contemporary with the septic episode (https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.117.028433?u...). Indeed the role of FQ is rarely raised, and this bias of reasoning can impede fast and efficient treatment. In case one, considering the AA as mycotic induces a delay to reintroduce antibiotics before the operation and possibly changes the usual treatment for more aggressive and risky techniques. In case two, the increased risk of rupture which persists 60 days (as nicely shown by Pasternak) could be under-evaluated in the absence of FQ incrimination. This strategy based on non-FQ-aggravated AAs is not appropriate as repairing without delay an AA either by the endovascular or open technique is lifesaving if the threshold diameter of the AA is reached.
3/ Can FQ cause an AA in patients with a normal aorta?
It is not possible to answer this question in humans. However, experimental data suggest mechanistic evidence. Pre-existing conditions or peculiar genomics could define a high-risk group but it is too early for any advice except perhaps for patients with Marfan disease.
These three questions and others remain open, but the clinician cannot ignore accumulating data when choices must be made.
Eventually, the different prospective clinical studies on FQ are of great value for clinicians as sadly tendon rupture is still the main well-known side effect of FQ but not the worst.
Competing interests: No competing interests