Osler Nodules: Causes, Treatment and Pathogenesis

They are small lumps in purple, slightly raised, soft to the touch, often with a pale center.

The pain usually precedes the development of the visible lesion up to 24 hours.

Osler Nodules are typically found on the fingers and / or toes. They can occur at any time during the course of endocarditis (usually subacute) and last from hours to several days.

How did they get their name?

The lesions were first described by French doctors as “Nodosites Cutanees Ephemeres” which means “short skin nodules” and by Dr. Mullen of Hamilton.

Parkes Weber later suggested that they be known as Osler’s nodes in recognition of the fact that Sir William Osler (1849-1919) had “first called attention to its complete diagnostic importance”.

His first description of these injuries was in 1893. Sir William Osler, a physician of Canadian origin, wrote 1344 publications on a wide range of medical subjects.


The underlying cause of the nodes has been debated since Osler first proposed microembolization as a cause (this is the dispersion of small particles around the bloodstream).

Early reports favored an allergic or immunological cause, but more recent reports have isolated bacteria within the nodules.

A skin biopsy (histology) may reveal a neutrophilic vasculitis (inflammation of the blood vessels) that affects the glomus apparatus of the ends of the fingers, or microabscess formation without evidence of vasculitis.

It has been postulated that biopsies taken early show the bacteria within the microabscesses and as time progresses, the ganglia become sterile and a hypersensitivity or vasculitis of small vessels develops, mediated by the immune system.

What tests should be done?

A careful search for endocarditis is performed. This includes multiple blood cultures, other blood tests, urine tests, ECG, chest x-ray, and an echocardiogram (cardiac ultrasound). The diagnosis can be elusive.

A skin biopsy may be useful to confirm the diagnosis of Osler’s nodules.


The treatment is aimed at bacterial endocarditis and involves intravenous antibiotics and sometimes valvular surgery. Skin lesions tend to heal spontaneously without scarring.

A particular case

Four patients in whom endocarditis had been verified at autopsy had the pathogenic organism isolated from Osler’s nodules. In three cases the responsible organism was identified in the Gram spots.

The etiological agent was Staphylococcus aureus in three cases and Candida albicans in one case. The histological examination of an Osler node of one of the patients with endocarditis showed a microabscess in the papillary dermis together with microembolism in nearby dermal arterioles.

Workers have previously interpreted similar histological findings as consistent with perivasculitis resulting from an immunological reaction to the pathogenic organism.

The present findings support Osler’s original claim that the skin lesions that bear his name are “in all likelihood caused by tiny emboli.”

Osler nodules are found in the context of infective endocarditis and represent the deposition of the immune complex. These painful nodules are seen on the palms of the hands and on the palms of the feet.

Osler nodules should be distinguished from Janeway lesions that are not painful and are produced by microembolization causing microabscesses in the palms of the hands and soles of the feet.


The pathogenesis of Osler’s nodules and Janeway’s lesions remains a mystery despite a vigorous debate over the past 113 years. They are given great emphasis among the clinical signs of bacterial endocarditis, but are rarely seen in practice.

Two cases of subacute bacterial endocarditis are presented. A 66-year-old woman with Bartonella henselae endocarditis developed Osler’s nodules on her hands postoperatively and a 23-year-old man with Streptococcus oralis endocarditis developed sensitive macules with a suggestive appearance of Janeway heel lesions.

The dermatopathology was similar in both cases, consisting of a leukocytoclastic vasculitis without formation of micro-abscesses or visible organisms.

Although appearance is generally consistent, it is not always possible to distinguish Osler’s nodules from Janeway lesions based purely on clinical presentation.

In addition, the histology of both clinical signs may appear similar.

Other reports are necessary before stronger conclusions can be drawn.

However, it may be that the histological appearance of Osler’s nodules and Janeway’s lesions is determined primarily by the nature of the causative organism, while the clinical aspect may be determined by the anatomic site.

Classically, Osler’s nodules are on the tip of the finger or toes and are painful. Janeway injuries occur in the palm and soles of the foot and are not painful.

It is believed that Osler’s nodules are caused by a localized mediated immune response, whereas Janeway’s lesions are thought to be caused by septic microembolism.

These findings often overlap and are difficult to differentiate. These appeared in 40-90% of cases of infectious endocarditis in the preantibiotic era, however, recent prospective data report that the incidence is 3-5%.

Splinter hemorrhages are usually oriented in the distal third of the nail. Other causes of splinter hemorrhages include, minor trauma, atrial myxoma, and rheumatoid arthritis.

The appearance of Osler’s lymph nodes, Janeway’s lesions and splinter hemorrhages often coincide with systemic embolization.

It is important to recognize these classic physical findings of infective endocarditis, a condition with high morbidity and mortality in which early diagnosis is the key.

Points to take into account

Janeway lesions and Osler’s lymph nodes are found in 3-5% of cases of infective endocarditis.

Osler’s lymph nodes, Janeway lesions and splinter hemorrhages often coincide with systemic embolization.

It is important that doctors recognize these physical findings.