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Osler Node and Janeway Lesions
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
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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.
References
Murdoch DR, Corey GR, Hoen B, Miró JM, Fowler VG Jr, Bayer AS, Karchmer AW, Olaison L, Pappas PA, Moreillon P, Chambers ST, Chu VH, Falcó V, Holland DJ, Jones P, Klein JL, Raymond NJ, Read KM, Tripodi MF, Utili R, Wang A, Woods CW, Cabell CH, International Collaboration on Endocarditis-Prospective Cohort Study (ICE-PCS) Investigators. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study. Archives of internal medicine. 2009 Mar 9:169(5):463-73. doi: 10.1001/archinternmed.2008.603. Epub [PubMed PMID: 19273776]
Marrie TJ. Osler's nodes and Janeway lesions. The American journal of medicine. 2008 Feb:121(2):105-6. doi: 10.1016/j.amjmed.2007.07.035. Epub [PubMed PMID: 18261495]
Yee J, McAllister CK. Osler's nodes and the recognition of infective endocarditis: a lesion of diagnostic importance. Southern medical journal. 1987 Jun:80(6):753-7 [PubMed PMID: 3296228]
Gil MP, Velasco M, Botella R, Ballester JE, Pedro F, Aliaga A. Janeway lesions: differential diagnosis with Osler's nodes. International journal of dermatology. 1993 Sep:32(9):673-4 [PubMed PMID: 8407097]
Level 3 (low-level) evidenceFarrior JB, Silverman ME. A consideration of the differences between a Janeway's lesion and an Osler's node in infectious endocarditis. Chest. 1976 Aug:70(2):239-43 [PubMed PMID: 947688]
Level 3 (low-level) evidenceGunson TH, Oliver GF. Osler's nodes and Janeway lesions. The Australasian journal of dermatology. 2007 Nov:48(4):251-5 [PubMed PMID: 17956487]
Level 3 (low-level) evidenceVon Gemmingen GR, Winkelmann RK. Osler's node of subacute bacterial endocarditis. Focal necrotizing vaculitis of the glomus body. Archives of dermatology. 1967 Jan:95(1):91-4 [PubMed PMID: 6016316]
Level 3 (low-level) evidenceAlpert JS, Krous HF, Dalen JE, O'Rourke RA, Bloor CM. Pathogenesis of Osler's nodes. Annals of internal medicine. 1976 Oct:85(4):471-3 [PubMed PMID: 788582]
Level 3 (low-level) evidenceCardullo AC, Silvers DN, Grossman ME. Janeway lesions and Osler's nodes: a review of histopathologic findings. Journal of the American Academy of Dermatology. 1990 Jun:22(6 Pt 1):1088-90 [PubMed PMID: 2370335]
Level 3 (low-level) evidenceSilverman ME, Upshaw CB Jr. Extracardiac manifestations of infective endocarditis and their historical descriptions. The American journal of cardiology. 2007 Dec 15:100(12):1802-7 [PubMed PMID: 18082531]
McDonald JR. Acute infective endocarditis. Infectious disease clinics of North America. 2009 Sep:23(3):643-64. doi: 10.1016/j.idc.2009.04.013. Epub [PubMed PMID: 19665088]
Hoen B, Duval X. Clinical practice. Infective endocarditis. The New England journal of medicine. 2013 Apr 11:368(15):1425-33. doi: 10.1056/NEJMcp1206782. Epub [PubMed PMID: 23574121]
RuDusky BM. Recurrent Osler's nodes in systemic lupus erythematosus. Angiology. 1969 Jan:20(1):33-7 [PubMed PMID: 5762438]
Jennette JC. Overview of the 2012 revised International Chapel Hill Consensus Conference nomenclature of vasculitides. Clinical and experimental nephrology. 2013 Oct:17(5):603-606. doi: 10.1007/s10157-013-0869-6. Epub 2013 Sep 27 [PubMed PMID: 24072416]
Level 3 (low-level) evidenceStevens GL, Adelman HM, Wallach PM. Palpable purpura: an algorithmic approach. American family physician. 1995 Oct:52(5):1355-62 [PubMed PMID: 7572558]
Servy A, Valeyrie-Allanore L, Alla F, Lechiche C, Nazeyrollas P, Chidiac C, Hoen B, Chosidow O, Duval X, Association Pour l'Etude et la Prévention de l'Endocardite Infectieuse Study Group. Prognostic value of skin manifestations of infective endocarditis. JAMA dermatology. 2014 May:150(5):494-500 [PubMed PMID: 24500311]
Level 2 (mid-level) evidenceVanderWielen B, Bose S. Janeway lesions and Osler's nodes: an indication for prompt transesophageal echocardiography. Canadian journal of anaesthesia = Journal canadien d'anesthesie. 2017 May:64(5):542-543. doi: 10.1007/s12630-017-0832-1. Epub 2017 Feb 1 [PubMed PMID: 28150158]