Sophia Lubrin, BS, MD
Henry Ford Hospital
Fort Wayne, Indiana, United States
Disclosure information not submitted.
Randi Connor-Schuler, BA, MD
Emory University School of Medicine
Atlanta, Georgia
Disclosure information not submitted.
Title: Nosocomial Endocarditis of an ASD Occluder Device Caused by Suppurative Septic Thrombophlebitis
Introduction: Atrial Septal Occluder devices are increasingly used for percutaneous repair of ASDs. In this report, we present the first case of nosocomial endocarditis of an ASD closure device caused by septic thrombophlebitis.
Case Summary: A 55-year-old female with remote ASD repair with the Amplatzer septal occluder presented altered and febrile 3 days after recent hospitalization. On arrival to the ER, she was in mild distress. Her physical examination showed mild erythema and edema of the right forearm. Labs were unremarkable. Infectious work-up and computed tomography (CT) chest with contrast were negative. Empiric antibiotics were begun. After admission, blood cultures grew MRSA. The source was identified as septic thrombophlebitis of the right forearm from a peripheral IV placed during previous admission. Bedside I&D was performed. On day 3 of hospitalization, she developed refractory hypoxia requiring intubation due to ARDS with CT chest showing diffuse airspace disease. Repeat cultures remained positive for MRSA. MRI of the spine was negative and TTE without evidence of endocarditis. TEE was obtained with an initial reading negative for vegetations; however, a second review showed a hypoechoic mass on the ASD closure device, confirming endocarditis. The patient was not a surgical candidate for device removal and was treated with 6 weeks of antibiotics.
Discussion: Atrial Septal Occluder devices are increasingly used for less invasive, percutaneous repair of atrial and ventricular septal defects. The Amplatzer occluder is one of the most frequently used devices. Studies have shown it to be safe; however, several case reports have demonstrated delayed endocarditis of the occluder device like our case. Our case is the first reported of nosocomial endocarditis by suppurative thrombophlebitis. Our case highlights the difficulty of detection of endocarditis of ASD occluder devices. TEE sensitivity for vegetation detection is approximately 96% for native valves and 92% for prosthetic valves. There are no studies on its use for detection of ASD closure device vegetations. In conclusion, given the remote history of placement of these devices and the challenge of visualization of vegetations on them, our case highlights the importance of having a high clinical suspicion in order to identify this rare complication.