Actually, I am concerned with the association between the use of contrast agents and rupture of thoracic aortic dissection (Stanford A type).
Here is the case I experienced recently. A 57-year-old male with a history of hypertension and atrial fibrillation visited our department with a complaint of chest pain. His consciousness was clear and his systolic blood pressure was 100 mmHg. TTE revealed dilated ascending aorta along with moderate aortic regurgitation. Immediately, contrast-CT was performed. Contrast enhanced CT revealed Stanford A type aortic dissection. There was no retention of pericardial effusion. Within a few minutes after that, he fell into CPA. TEE revealed massive retention of pericardial effusion. PCPS was introduced. However, PCPS did not work efficiently probably because of collapse in the right heart. Immediately, pericardial drainage was performed; drainage was not effective because of coagulated blood.
In this case,
Should we have performed pericardiotomy to save this patient?
May contrast agents trigger the rupture of thoracic aortic dissection (Stanford A type)? Actually, I know several cases that thoracic aortic dissection ruptured immediately after contrast CT. I want a paper discussing this point.