Title:   Bullae from the Heart, Infective Endocarditis to Blame

Authors: Yazan Alzu’bi MD, Michelle Goodwin MD, Timothy Barreiro DO

Email: yalzubi@mercy.com

Introduction: Infective endocarditis (IE) commonly presents with fever, bacteremia, and valvular vegetations (3). IE can sometimes have complications, mainly cardiac and neurologic, as the first presentation. On examination, cutaneous manifestations may include petechiae, palpable purpura, splinter hemorrhages, and less commonly Osler nodes and Janeway lesions (1,2). However, cutaneous septic emboli presenting as bullous lesions is very rare.

Case Report(s): A 50-year-old female with past medical history of hypertension, diabetes mellitus type 2, hyperlipidemia, ischemic cardiomyopathy, mitral and tricuspid regurgitation presented 16 days after coronary artery bypass graft surgery and mitral and tricuspid valve replacement with altered mental status and skin lesions on both hands. Examination was also pertinent for holosystolic murmur. Investigations were significant for Staphylococcus aureus bacteremia, multiple small acute cerebral infarcts, and mitral annulus vegetation on echocardiography. On physical exam, large red-purple bullous lesions were found on bilateral hands, roughly measuring 5 cm x 2 cm. There was no surrounding erythema or induration, no purulent discharge visualized. Imaging of the brain revealed septic emboli.

Discussion: Typically, dermatologic manifestations of IE include palpable purpura, petechiae, hemorrhagic plaques, digital cyanosis and livedo reticularis (1,2). Osler node and Janeway lesions can also be found; however, bullous cutaneous septic emboli are rare. For our patient, the cutaneous lesions are most consistent with septic emboli given location, lack of signs of local infection, and timing. On MRI, she had multiple ischemic infarcts spanning several vascular territories consistent with septic cerebral emboli. There have been a few case reports of bullous lesions associated with heparin induced thrombocytopenia, however, in our patient, platelets remained normal throughout course of treatment.

Conclusion: Cutaneous septic emboli as a complication of bacterial endocarditis are well documented in case literature. However, they typically appear as purpura, petechiae, or via other hemorrhagic mechanisms. We present a patient with bullous lesions of distal extremities without associated obvious hemorrhage, which is a rare finding. Given the lack of evidence for secondary skin and soft tissue infection coupled with MRI brain findings of septic embolic infarcts, it is reasonable to attribute these new bullous lesions as a unique presentation of septic emboli in bacterial endocarditis.