Janeway Lesions and Cerebral Hemorrhage in Staphylococcal Endocarditis

 A 65-year-old male with end stage renal disease requiring hemodialysis, presented with high grade fever accompanied by rigors and chills, lethargy and joint aches for five days. His white cell count was 18700/µL (normal range 4000-11000/µL) and C-reactive protein level was 475 mg/L (normal range up to 5 mg/L). On the second day of his admission, he developed sudden loss of vision in his left eye and blurring of vision in the right. Blood cultures grew Methicillin-resistant Staphylococcus aureus (MRSA). A computed tomography (CT) scan of the head revealed small hematomas in the right occipital and left temporal lobes of the brain and magnetic resonance imaging (MRI) confirmed findings of a hemorrhagic infarct in the right occipital lobe (Figure 1). Ophthalmoscopy and B scan ultrasound of the left eye found absent red reflex and vitreous hemorrhage. The same day, he developed reddish/purple, macular and non-tender lesions on his palms and left foot as shown in Figure 2. Patient fulfilled Duke’s criteria for endocarditis and was started on vancomycin and rifampicin. Trans-esophageal echo revealed small vegetations on the mitral and tricuspid valves. There was remarkable improvement in the constitutional symptoms and inflammatory markers. Vision in the left eye improved partially with bevacizumab. First reported by Edward G Janeway in 1898, Janeway lesions are a classic but uncommon manifestation of infective endocarditis [1]. These lesions signify septic embolization, are macular, non-tender and found on the palms and soles. These lesions are most commonly associated with acute endocarditis secondary to Staphylococcus aureus.  Histologically, lesions consist of small abscesses in the dermis with thrombosis of small vessels [2]. These lesions are uncommonly seen in current clinical practice due to early and rigorous management of infective endocarditis but were more commonly observed in the pre-antibiotic era. Cerebral hemorrhage accounts for 12 to 30% of all neurological complications of infective endocarditis [3]. This complication is much more common with Staphyloccocal bacteremia, thrombocytopenia and anticoagulant use [4]. Mechanisms postulated for cerebral hemorrhages include transformation of ischemic infarcts by septic emboli, rupture of intracranial mycotic aneurysms and septic erosion of the arterial walls without a well-defined aneurysm. Cerebral hemorrhage secondary to MRSA endocarditis is most commonly associated with the last mechanism [5].

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