FROM JANE

Status: current, with caveats. The source library flags this one as still taught but qualified — read the safety notes on each component before relying on it.

A checklist of the classic clinical findings of infective endocarditis so the disease can be recognized on physical exam.

F — Fever

Most common sign of infective endocarditis

Fever is the single most common finding, present in roughly 90% of patients. It may be low-grade and waxing/waning in subacute disease or high with rigors in acute disease (e.g., S. aureus).

Physiology. Bacteremia triggers inflammatory cytokines (IL-1, IL-6, TNF) that reset the hypothalamic temperature set-point upward.

Safety. Draw 2-3 sets of blood cultures from different sites before starting antibiotics so the organism can be identified.

R — Roth spots

Retinal hemorrhages with a pale center

Retinal hemorrhages with a pale/white center seen on fundoscopy; the white center is a fibrin-platelet plug. They are non-specific (also in leukemia, diabetes, anemia, HIV) and found only on eye exam.

Physiology. Retinal capillaries rupture; a central fibrin-platelet aggregate forms the white-centered appearance.

Safety. Never use the absence of Roth spots to rule out endocarditis - they are uncommon and non-specific.

O — Osler nodes

Painful immune-complex lesions (subacute endocarditis)

Painful, tender, red-purple nodules on the finger/toe pads (and thenar/hypothenar eminences), coming and going over hours to days; more typical of subacute endocarditis.

Physiology. Immune-complex deposition in small skin vessels triggers local vasculitis - hence tenderness. Cultures are usually sterile.

Safety. Osler nodes are painful clues, not emergencies; the real danger is the valve infection and emboli.

M — Murmur

New or changing heart murmur

A new or changing heart murmur (often a new regurgitant murmur) is found in up to ~85% of patients and is the cardiac hallmark. Vegetations destroy valve tissue so a previously normal valve leaks.

Physiology. Vegetations ulcerate leaflets/chordae so valves don't close completely, producing regurgitant flow and an audible murmur.

Safety. Right-sided (tricuspid) endocarditis in IV drug users may present with pulmonary symptoms and little or no murmur - don't be falsely reassured.

J — Janeway lesions

Painless septic microemboli (acute endocarditis)

Non-tender, flat, erythematous/hemorrhagic macules on the palms and soles, more typical of acute endocarditis (especially S. aureus).

Physiology. Septic microemboli (with live bacteria) lodge in skin capillaries and form microabscesses; being embolic rather than inflammatory, they are painless and can grow bacteria on culture.

Safety. Painless doesn't mean harmless - Janeway lesions signal active embolization that can also hit the brain, spleen, or kidneys.

A — Anemia

Normocytic anemia of chronic inflammation

A normocytic, normochromic anemia (anemia of chronic inflammation/infection) develops over weeks in subacute disease.

Physiology. Chronic infection raises cytokines and hepcidin, suppressing red-cell production, blunting the erythropoietin response, and shortening red-cell survival.

Safety. Anemia is a sign, not the disease - don't reflexively transfuse without treating the underlying infection.

N — Nail-bed (splinter) hemorrhages

Microemboli in nail capillaries (non-specific)

Linear, dark-red/brown streaks under the distal nail bed caused by microemboli. Non-specific - trauma is far more common than endocarditis.

Physiology. Small septic emboli lodge in longitudinal capillaries under the nail, producing streaks of hemorrhage.

Safety. A single splinter hemorrhage after trauma means little; multiple new ones with fever and a murmur are concerning.

E — Embolic phenomena

Systemic (or pulmonary) embolization from vegetations

Left-sided endocarditis embolizes to the brain (stroke), spleen, kidneys, and extremities; right-sided disease embolizes to the lungs (septic pulmonary emboli). Embolic stroke is a feared complication.

Physiology. Friable vegetations shed fragments that travel with arterial flow; the syndrome depends on which valve is infected and where the embolus lands.

Safety. A new focal neurologic deficit in a patient with endocarditis is a stroke until proven otherwise - an emergency.

Memory aids

• F = Fever
• R = Roth spots
• O = Osler nodes
• M = Murmur
• J = Janeway lesions
• A = Anemia
• N = Nail-bed (splinter) hemorrhages
• E = Embolic phenomena

Quick review

• F = Fever — Most common sign of infective endocarditis
• R = Roth spots — Retinal hemorrhages with a pale center
• O = Osler nodes — Painful immune-complex lesions (subacute endocarditis)
• M = Murmur — New or changing heart murmur
• J = Janeway lesions — Painless septic microemboli (acute endocarditis)
• A = Anemia — Normocytic anemia of chronic inflammation
• N = Nail-bed (splinter) hemorrhages — Microemboli in nail capillaries (non-specific)
• E = Embolic phenomena — Systemic (or pulmonary) embolization from vegetations