A 31 year old lady presents to you with a history of recent recurrent "bruising". Although she has no active lesions at the moment and looks quite well, pictures taken on her mobile phone show a substantial dark area on the left ring finger and larger, incomplete dark circular lesions on her upper shins. The GP has checked her ANA. It's negative. Inflammatory parameters are normal. She has two healthy children.
A 71 year old man presents with transient dark lesions on his fingers. On his second visit, you are lucky enough to catch sight of some of these dark areas on the fingers. They are tender. The patient is well and apyrexial without audible murmurs. You diagnose Osler's nodes and ask for blood cultures and echo.
All perfectly reasonable. Except that it may not be enough.
The prospect of embolic lesions from the heart valves is terrifying, but not all such cases are infective endocarditis. There are other possibilities.
Young women with SLE often have Libman Sacks lesions on left sided heart valves, particularly the mitral valve. This is three times more common in those with anti-phospholipid antibodies, which can exist independently of lupus. Although subjects with SLE and Libman Sack's lesions tend to have active lupus, often associated with lupus nephritis, subjects with aPL alone may have been hitherto asymptomatic. While it is important to dip the urine for blood and protein to screen for lupus nephritis, immune glomerulonephritis in infective endocarditis can cause an active urinary sediment.
In fact, Glomerulonephritis is one of the four immune manifestations of infective endocarditis, the other three being Osler's nodes, Roth spots and a false positive Rheumtoid factor (aid memoire GORR).
Treatment would be immunosuppression and anticoagulation, although there are no RCTs that support the use of the former in Libman Sacks endocarditis.
The old man with "Osler nodes" may have cancer, with thrombotic, non infective endocarditis. Clots, present on the heart valves (again more common on the left), are thought to be due to hypercoagulability. Such patients may often have occult DVTs or pulmonary emboli. Gastric or pancreatic cancers may have associated portal or mesenteric vein thrombosis. Apart from treatment of the underlying cancer, these patients need clexane. Warfarin would be ineffective.
Cancer and infective endocarditis can co-exist due to Streptococcus bovis septicaemia. These patients often have underlying colon cancer. Others have cirrhosis.
Subjects with left atrial myxoma can present exactly like subacute bacterial endocarditis with fever, lassitude, murmurs and embolic phenomena. Echo may pick up pedunculated lesions on the mitral valve.
A final non-infective cause of cardiac emboli is eosinophilia. Regardless of the underlying cause of eosinophilia, prolonged or high eosinophil counts go through three phases- cardiac microabscesses, a flabby, poorly contractile myocardium and endomyocardial fibrosis. It is in the second stage that clots build up, often in the left ventricle, which can then embolise and cause strokes, renal or splenic infarcts, just like infective endocarditis.
Eosinophilia can also occur secondarily in subjects with cholesterol emboli, usually from the aorta. These often present in the elderly with renal impairment and livedo in the lower limbs following an invasive procedure such as cardiac catheterisation. There are reports of cholesterol emboli occurring after anticoagulation.
It is important to consider these non-infective causes of endocarditis in subjects with cardiac vegetations on echo, who are culture negative and do not have the expected response to antibiotics.
A 71 year old man presents with transient dark lesions on his fingers. On his second visit, you are lucky enough to catch sight of some of these dark areas on the fingers. They are tender. The patient is well and apyrexial without audible murmurs. You diagnose Osler's nodes and ask for blood cultures and echo.
All perfectly reasonable. Except that it may not be enough.
The prospect of embolic lesions from the heart valves is terrifying, but not all such cases are infective endocarditis. There are other possibilities.
Young women with SLE often have Libman Sacks lesions on left sided heart valves, particularly the mitral valve. This is three times more common in those with anti-phospholipid antibodies, which can exist independently of lupus. Although subjects with SLE and Libman Sack's lesions tend to have active lupus, often associated with lupus nephritis, subjects with aPL alone may have been hitherto asymptomatic. While it is important to dip the urine for blood and protein to screen for lupus nephritis, immune glomerulonephritis in infective endocarditis can cause an active urinary sediment.
In fact, Glomerulonephritis is one of the four immune manifestations of infective endocarditis, the other three being Osler's nodes, Roth spots and a false positive Rheumtoid factor (aid memoire GORR).
Treatment would be immunosuppression and anticoagulation, although there are no RCTs that support the use of the former in Libman Sacks endocarditis.
The old man with "Osler nodes" may have cancer, with thrombotic, non infective endocarditis. Clots, present on the heart valves (again more common on the left), are thought to be due to hypercoagulability. Such patients may often have occult DVTs or pulmonary emboli. Gastric or pancreatic cancers may have associated portal or mesenteric vein thrombosis. Apart from treatment of the underlying cancer, these patients need clexane. Warfarin would be ineffective.
Cancer and infective endocarditis can co-exist due to Streptococcus bovis septicaemia. These patients often have underlying colon cancer. Others have cirrhosis.
Subjects with left atrial myxoma can present exactly like subacute bacterial endocarditis with fever, lassitude, murmurs and embolic phenomena. Echo may pick up pedunculated lesions on the mitral valve.
A final non-infective cause of cardiac emboli is eosinophilia. Regardless of the underlying cause of eosinophilia, prolonged or high eosinophil counts go through three phases- cardiac microabscesses, a flabby, poorly contractile myocardium and endomyocardial fibrosis. It is in the second stage that clots build up, often in the left ventricle, which can then embolise and cause strokes, renal or splenic infarcts, just like infective endocarditis.
Eosinophilia can also occur secondarily in subjects with cholesterol emboli, usually from the aorta. These often present in the elderly with renal impairment and livedo in the lower limbs following an invasive procedure such as cardiac catheterisation. There are reports of cholesterol emboli occurring after anticoagulation.
It is important to consider these non-infective causes of endocarditis in subjects with cardiac vegetations on echo, who are culture negative and do not have the expected response to antibiotics.
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