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Author: Ryan G. Hartman, MS, Northeastern Ohio
Universities Colleges of Medicine and Pharmacy, Class of 2011
Introduction: Infections of cardiac implantable
electronic devices (CIED) are an infrequent complication occurring
with an incidence of 1 to 7%. Extrusion is a recognized
manifestation of CIED infection and is the migration of a device
from its pocket site to the overlying skin with evidence of visible
device or leads. According to a retrospective study conducted in
2007, extrusion of CIEDs complicates CIED infections in 32% of
cases. Of these cases, 89% were attributed to Staphylococcus
infections. We report a case of Pseudomonas aeruginosa
culture proven pacemaker extrusion.
Case Presentation: We present a 51-year-old
African American male with a past medical history significant for
complicated diabetes mellitus, ischemic cardiomyopathy with an
ejection fraction of 35%, a surgically repaired ventricular septal
defect, and pacemaker dependence due to complete atrioventricular
block. His dual chamber pacemaker was initially implanted in 1996
and later upgraded to an implantable cardiac defibrillator (ICD).
Ten months after ICD implantation, he presented with a CIED
extrusion but exhibited no signs of systemic/local infection or
inflammation. A transesophageal echocardiogram was negative for
vegetation. Intravenous vancomycin was started empirically and the
CIED was later extracted on hospital day 7. Cultures of the pulse
generator pocket grew P. aeruginosa, whereas cultures of
the leads cultivated P. aeruginosa and Staphylococcus
epidermidis. Blood cultures remained negative. Vancomycin was
changed to daptomycin and cefepime was added for broader coverage.
The pulse generator was re-implanted on the contralateral chest
wall two days later. He was discharged on a 6 week course of
intravenous cefepime and oral ciprofloxacin.
Discussion: A review of the literature revealed
that Pseudomonas-related CIED infections often coincide with remote
infections leading to hematologic seeding or proximity to exposed
gastrointestinal flora. Our patient had neither. Late onset CIED
infections, occurring 12 weeks to one year post-implant typically
present without systemic manifestations or local inflammation, as
was seen with our patient. However, most were attributed to
Staphylococcal infections. Since a clinical cure was achieved with
cefepime, we suggest that it be used to treat CIED infections
caused by P. aeruginosa when antibiotic susceptibility
data indicate that it is efficacious. It is hoped that an
organization like the American Heart Association will add to their
guideline recommendations about optimal screening, management and
prevention of Pseudomonas-related CIED infections.
June Issue of IMpact