This patient is suspected to have endocarditis; would you like to examine him'?



Fever, malaise, anorexia, weight loss, rigors: non-specific symptoms of inflammation.

· Progressive heart failure: due to valve destruction (can be dramatic).

· Stroke, pulseless limb, renal infarct, pulmonary infarct: caused by embolization of vegetations.

· Arthralgia, loin pain: due to immune-complex deposition.

· Obtain a history of recent dental procedures.

· History of valvular heart disease, history of intravenous drug abuse.


· Look for the following signs:

- Anaemia.

-Clubbing (seen in one fifth of the cases).

Splinter haemorrhages in the nails (vasculitic phenomenon; probably due to embolic phenomena in

the nail bed).

-Osler's nodes (vasculitic phenomenon; tender, erythematous, pea-sized nodules seen in the pulp of the

fingers; caused by inflammation around the site of the infected emboli lodged in distal arterioles).

Janeway lesions (vasculitic phenomenon; fiat, non-tender red spots found on the pahns and soles;

they blanch on pressure).

- Petechiae - conjunctiva, palate and skin.

· Record the temperature.

· Listen to the heart for murmurs and look for signs of cardiac failure.

· Examine the fundus for Roth's spots (vasculitic phenomena). "

· Examine the abdomen for splenomegaly.

· Look for embolic phenomena: stroke, viscera or occlusion of peripheral arteries

· Test urine for microscopic haematuria (vasculitic phenomena).

Remember that ostium secundum atrial septal defects almost never have infective endocarditis.


This patient has Janeway lesions and Roth's spots (lesions) confirming infective endocarditis and is in

severe heart failure (functional status).


How would you investigate such a patient?

· Test the urine for microscopic haematuria.

· Take a full blood count (FBC) to show normocytic, normochromic anaemia and raised white cell


· Test for raised erythrocyte sedimentation rate (ESR).

· Blood culture: take three samples from different sites in 24 hours. It is the most important test for

diagnosing endocarditis and cultures are negative in more than 50% of cases of fungal aetiology.

· Echocardiography may show vegetations. A negative study does not rule out endocarditis as

vegetations less than 3-4 mm in size cannot be detected. Further-more, all the leaflets of the aortic,

tricuspid and pulmonary valves may not be visualized in every patient.

What are the major manifestations of bacterial endocarditis?

· Manifestations of a systemic infection: fever, weight loss, pallor, splenomegaly.

· Manifestations of a vasculitic phenomenon: cardiac failure, changing murmurs,

petechia , Roth's spots , Osler nodes , Janway lesions , splinter hemorrhages,

stroke, infarction of viscera, mycotic aneurysm.

· Manifestations of immunological reactions: arthralgia, finger clubbing, uraemia.

Name the common organisms found in infective endocarditis.

Streptococcus viridans, Staphylococcus aureus, Strep.faecahs, fungi.

What precautions would you take to prevent bacterial endocarditis?

Antibiotic prophylaxis before any dental, gastrointestinal, urological or gynaeco-logical procedure is

recommended in rheumatic valvular disease, most congenital heart lesions (except uncomplicated atrial

septal defect of secundum type), valvular aortic stenosis, prosthetic heart valve, previously documented

infective endocarditis and calcified mitral valve annulus (Circulation 1997; 96: 358-66).

How would you treat a patient suspected to have endocarditis?

Until the bacteriology results are available, with intravenous benzylpenicillin and gentamicin. In severely ill

patients intravenous cloxacillin would be added to this regimen (Circulation 1998; 98: 293648).


Mention a few prognostic factors.

· Heart failure.

· Non-streptococcal endocarditis, especially Staph. aureus, fungal endocarditis. · Infection of a prosthetic


· Elderly patients.

· Valve ring or myocardial abscess.

Mention a few conditions that can simulate clinical manifestations of infective endocarditis.

· Atrial myxoma.

· Non-bacterial endocarditis.

· Systemic lupus erythematosus (SLE).

· Sickle cell disease.

What do you know of prosthetic valve endocarditis (PVE)?

About 3% of patients will develop PVE by the end of the first year after valve replacement; thereafter, the

incidence is lower. PVE is classified into two groups:

· Early:occurring within 2 months of surgery. It develops as a result of intra-operative contamination of the

prosthetic valve or as a consequence of a post-operative nosocomial infection, such as sternotomy

infection, postoperative pneumonia, urinary tract infection or intravenous cathether-related insertion. The

clinical features may be masked by the ordinary events in the postoperative course or by another

infection. Cutaneous signs are not common.

· Late PVE: develops more than 2 months after valve surgery. It can occur after transient bacteraemia as

in minor skin or upper respiratory tract infections or following dental or urinary manipulations. The

non-cardiac manifestations resemble those of native valve infective endocarditis.

Although this classification is convenient, the high prevalence of Staph. epidermidis and diphtheroids

among patients suggests that this division is not absolute.

What are the complications of infective endocarditis?

· Congestive heart failure: may develop acutely or insidiously; it portends a grave prognosis.

· Conduction disturbances caused by abscesses in ventricular septum.

· Valve destruction: acute regurgitation, pulmonary oedema, heart failure.

· Embolism: occurs in 22-50% of cases, leading to infarction in any vascular bed including lungs,

coronary arteries, spleen, bowel, and extremities; renal: flank pain and haematuria.

· Local extension of infection: purulent pericarditis, aortic root abscess (may cause sinus Valsalva

fistula), myocardial abscess (conduction disturbance).

· Septic emboli to vasa vasorum: may lead to mycotic aneurysms anywhere in vas-cular tree; most

worrying in cerebral vessels, resulting in cerebral haemorrhage.

· Distal infection (metastatic): due to septic emboli, e.g. brain abscess, cerebritis.

· Candidal endocarditis: may be manifest by fungal endophthalmitis.

· Glomerulonephritis: the renal lesions of SBE are of two kinds, (a) a diffuse pro-liferative

glomerulonephritis and (b) focal embolic glomerulonephritis. This is associated with low complement

levels and immune complexes.

What are the indications for surgery?

· Positive blood cultures or relapse after several days of the best available antibiotic therapy indicate

the need for valve replacement.

· Drainage of myocardial or valve ring abscesses.

· Patients with aortic valve endocarditis who develop second- or third-degree heart block.

· Prosthetic valve replacement for non-streptococcal endocarditis, valve dysfunc-tion, valve

dehiscence or myocardial invasion.

· Development of a new aneurysm of the sinus of Valsalva.

· Fungal endocarditis.

What do you understand by the term 'marantic endocarditis'?

Marantic or Libman-Sacks endocarditis is seen in SLE and is a post-mortem diagnosis. It is rarely

clinically significant.

Sir William Osier (1849-1919) was successively Professor of Medicine in Montreal, Pennsylvania,

Baltimore and Oxford. He was reputed to be a brilliant clinician and educationalist.

M. Roth (1839-1914), Professor of Pathology in Basel, Switzerland.

E.G. Janeway (1841-1911) followed Austin Flint as Professor of Medicine at Bellevue Hospital, New York.

E. Libman(1872-1946), US physician.

B. Sacks (1873-1939), US physician who wrote on Hindu medicine.