Definition/Introduction

Osler nodes and Janeway lesions are cutaneous manifestations of endocarditis, a disease most commonly arising from a bacterial or fungal infection of the cardiac endocardium.[1] Osler nodes are tender, purple-pink nodules with a pale center and an average diameter of 1 to 1.5 mm.[2] They are generally found on the distal fingers and toes, though they can also present on the lateral digits, hypothenar, and thenar muscles.[3] The pain usually proceeds nodule development, and they disappear in hours to days, leaving no sequelae. Janeway lesions are irregular, non-tender, erythematous, or hemorrhagic macules or papules commonly found on the palm and soles, lasting days to weeks.[4] The presence of pain is conventionally a means to differentiate Osler nodes from Janeway lesions since accurate differentiation may be challenging, secondary to overlap in the appearance and histology of these two lesions.[5][6]

Dr. William Osler first described Osler nodes in 1893 and Janeway lesions by Dr. Edward Janeway in 1899. The hypothesis is that Osler nodes and Janeway lesions share similar pathogenesis and arise from micro-emboli embedding in different anatomical sites.[2] Pain from Osler nodes is associated with emboli lodging in the glomus apparatus of the dermis.[7] Histologically, Osler nodes and Janeway lesions show septic micro-emboli with dermal micro-abscess formation.[8] Bacteria may not be visualized on histology, in which case tissue culture can help confirm the diagnosis.[9]

As per the modified Duke criteria, Osler nodes are considered immunologic phenomena of infective endocarditis, and Janeway lesions, vascular phenomena. Osler nodes more commonly correlate with subacute endocarditis, whereas Janeway lesions typically occur in acute infective endocarditis.[10] The most common cause of acute infective endocarditis is Staphylococcus aureus.[11] Other common causative pathogens include viridians streptococci, enterococci, and coagulase-negative staphylococci. Risk factors for infective endocarditis include prosthetic cardiac valves, structural or congenital cardiac disease, intravenous drug use, or a recent history of invasive procedures.[12] Osler nodes can also present in non-bacterial thrombotic endocarditis (found in disorders such as systemic lupus erythematosus – Libman Sacks, anti-phospholipid antibody syndrome, and chronic cachectic and chronic infectious diseases), sepsis, and in patients with intravascular grafts.[3][13]

Osler nodes and Janeway lesions are typically differentiated based on their morphology, location, distribution, histology, and, importantly, clinical context. The differential diagnosis includes palpable purpura as found in various types of small and medium vessel vasculitis, including microscopic polyarteritis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis, immunoglobulin A vasculitis, cutaneous small-vessel vasculitis, leukocytoclastic vasculitis, and polyarteritis nodosa. Palpable purpura may also be a finding in paraneoplastic or malignancy-associated-vasculitis, disseminated gonococcal disease, disseminated intravascular coagulation, meningococcemia, Rocky Mountain spotted fever, and Buerger disease. Other causes of purple macules and patches include drug eruptions (glucocorticoid-induced purpura), arthropod bites, sun exposure (actinic/senile purpura), and rarely calciphylaxis.[14][15]

Issues of Concern

The pathogenesis of Osler nodes and Janeway lesions is a contested topic in the literature. Universally accepted clinical definitions for both skin findings do not exist either. Earlier studies of Osler nodes revealed perivasculitis with no bacteria or micro-emboli.[9] This finding led to the belief that a localized immunological mediated response caused Osler nodes. Conversely, other studies have shown micro-abscesses and micro-emboli within the surrounding arterioles of the dermis, with no vasculitis.[8] The timing of the biopsy may affect the histology. Biopsies taken earlier may show micro-emboli and abscesses that are later replaced by immunologic phenomena, similar to Janeway lesions.[6] Further research may be necessary to standardize the definition and pathology of these lesions.

Clinical Significance

Identification of Osler nodes and Janeway lesions may aid in diagnosing the underlying condition, often infective endocarditis. As per the modified Duke criteria, cutaneous manifestations are minor supporting criteria for infective endocarditis. In the pre-antibiotic era, the presence of Osler node reportedly presented in 40 to 90% of infective endocarditis cases.[3] Recent data report ranges from 3 to 5% to 10 to 23%, though skin manifestations of infective endocarditis may go underreported.[1][16] The prevalence of Janeway lesions in infective endocarditis is unclear. Cutaneous manifestations of infective endocarditis may indicate a worse prognosis of infective endocarditis.[16] Early diagnosis and treatment of infective endocarditis are important in reducing disease morbidity and mortality. The identification of cutaneous manifestations of infective endocarditis may aid in the diagnosis.[17]

Nursing, Allied Health, and Interprofessional Team Interventions

In the appropriate clinical context, patients presenting with Osler nodes and Janeway lesions should have blood cultures immediately and echocardiography. The lesions may also undergo biopsy if blood cultures are negative, and the suspicion of infective endocarditis remains high. All health care professionals need to examine the skin thoroughly when performing an assessment. If there is any uncertainty, prompt dermatology consultation is in order.