3. Introduction
This is a condition in which patient’s endocardium is colonized by microbiological agents and they are
actively multiplying in the endocardium
Infective endocarditis is due to microbial infection of a heart valve (native or prosthetic), the lining of a
cardiac chamber or blood vessel, or a congenital anomaly (e.g. ventricular septal defect (VSD)).
It typically occurs at sites of pre-existing endocardial damage, although infection with particularly virulent
organisms (e.g. Staph. aureus) can cause endocarditis in a previously normal heart.
Areas of endocardial damage caused by a high-pressure jet of blood (e.g. VSD, mitral regurgitation, aortic
regurgitation) are particularly vulnerable.
When the infection is established, vegetations, composed of organisms, fibrin and platelets, grow and
may break away as emboli. Adjacent tissues are destroyed, abscesses may form and valve regurgitation
may develop through cusp perforation, distortion or rupture of chordae. Extracardiac manifestations, such
as vasculitis and skin lesions, are due to emboli or immune complex deposition.
4. Classification
Endocarditis can either be:
1. acute endocarditis
2. sub-acute endocarditis.
The clinical pattern is influenced by
1. The organism
2.Site of infection,
3. Prior antibiotic therapy
4.The presence of a valve or shunt prosthesis.
The sub-acute form may abruptly develop acute life-threatening complications, such as valve
disruption or emboli.
5. Microbiology
The viridans group of streptococci (from the upper respiratory tract or gums) and enterococci (from the
gut or urinary tract) may enter the blood stream and are common causes of subacute endocarditis.
While Staph. aureus is increasingly responsible for acute endocarditis, especially in IV drug-users. ● Staph.
epidermidis, a normal skin commensal, is the most common organism in post-operative endocarditis after
cardiac surgery.
● Other offending organisms include the Gram-negative HACEK group (Haemophilus spp., Actinobacillus
actinomycetemcomitans, Cardiobacterium hominis, Eikenella spp. and Kingella kingae).
● Coxiella burnetii (Q fever) and Brucella cause occasional cases in patients exposed to farm animals. ●
Yeasts and fungi may be responsible in immunocompromised patients.
6. Pathophysiology
Infection of the valves with bacteria (or rarely fungi) causes injury
to the valve and valvular regurgitation. The bacteria on the valve
can form a mass or vegetation. Parts of this can embolize. Immune
complexes form with the bacteria. Infection of the endothelium
causes
1. persistent bacteremia,
2. valvular disfigurement (with vegetations/regurgitation),
3. septic emboli and
4. immune complex phenomenon.
7. CLINICAL FEATURES
Infective endocarditis might present with:
Diagnostic triad: persistent fever, emboli, changing murmur
Roth's spots in fundi(rare, < 5%)
Splinter hemorrhages(10%)
Osler's nodes (5%)
Digital clubbing (10%, long-standing endocarditis)
Petechial rash (40–50%, may be transient)
Hematuria (60–70%)
Splenomegaly(30–40%, long-standing endocarditis)
Loss of pulses
9. Clinical features
1. Subacute endocarditis:
Should be suspected when a patient with congenital or valvular heart
disease develops a persistent fever, unusual tiredness, night sweats,
weight loss or new signs of valve dysfunction.
Other features include embolic stroke, petechial rash, splinter
haemorrhages and splenomegaly. Osler’s nodes (painful swellings at the
fingertips) are rare and finger clubbing is a late sign.
10. CLINICAL FEATURES
2. Acute endocarditis:
Usually presents as a severe febrile illness with prominent and
changing heart murmurs and petechiae.
Clinical stigmata of chronic endocarditis are usually absent but
embolic events (e.g. cerebral) are common, and cardiac or renal
failure may develop rapidly.
11. CLINICAL FEATURES
3.Post-operative endocarditis:
Should be considered in any patient who develops an
unexplained fever after heart valve surgery.
The pattern may resemble subacute or acute endocarditis,
depending on the virulence of the organism.
Morbidity and mortality are high and redo surgery is often
required
15. Investigations
Diagnosis: based on the modified Duke criteria.
Blood culture: the crucial investigation because it may identify the infection and guide antibiotic
therapy; 3–6 sets should be taken, using scrupulous aseptic technique, prior to commencing therapy.
Echocardiography: allows detection of vegetations and abscess formation, as well as assessment of
valve damage. Transoesophageal echo has a higher sensitivity than transthoracic echo for detecting
vegetations (90% vs 65%) and is particularly valuable for investigating patients with prosthetic heart
valves. Failure to detect vegetations does not exclude the diagnosis.
Normochromic, normocytic anemia and elevated WCC, ESR and CRP: common. CRP is superior to ESR
for monitoring progress. ● Microscopic hematuria: usually present. ● ECG: may show the development
of AV block (due to abscess formation). ● CXR: may show evidence of cardiac failure.
16. Management
Bed rest.
Any source of infection (e.g. dental abscess) should be removed as soon as possible.
Empirical antibiotic therapy is with flucloxacillin and gentamicin if the presentation is acute, or with
benzylpenicillin and gentamicin if it is subacute or indolent.
Subsequent antibiotic treatment is guided by culture results and is usually continued for at least 4
wks.
Indications for surgery (debridement of infected material, valve replacement) include heart failure,
abscess formation, failure of antibiotic therapy and large vegetations on left-sided heart valves
(high risk of systemic emboli)
17. Indications for cardiac surgery in infective endocarditis
Heart failure due to valve damage
Failure of antibiotic therapy(persistent/uncontrolled infection)
Large vegetations on left-sided heart valves with evidence or
‘high risk’ of systemic emboli
Abscess formation
Antimicrobial therapy must be started before surgery
18. Prevention
Patients with valvular or congenital heart disease should be made aware of the
risk of endocarditis and of the importance of maintaining good dental health.
Prophylaxis in case of dental procedures and tonsillectomy in patients at risk
(valvular defects, congenital heart disease, prosthetic valve). Give amoxicillin 2 g
(50 mg/kg for children) as a single dose, 1 hour before the procedure
Former advice for routine antibiotic prophylaxis to cover invasive or dental
procedures is not supported by evidence and prophylaxis is no longer
recommended.
19. References
Davidson’s Principles and Practice of Medicine 23rd
EDITION
Davidson’s Essentials of Medicine _ 2nd Edition _
J. Alastair Innes, Simon Maxwell