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Chapter: Medicine and surgery: Cardiovascular system

Infective endocarditis - Disorders of the endocardium

An infection of the endocardium (endothelial lining of the heart and valves).- Definition, Incidence, Aetiology, Pathophysiology, Clinical features, Complications, Investigations, Management, Prognosis.

Disorders of the endocardium

Infective endocarditis




An infection of the endocardium (endothelial lining of the heart and valves).



6 per 100,000 (1500 cases) per year in United Kingdom.




Although infective endocarditis may occur on normal endocardium, it is more common on a congenital or acquired cardiac abnormality. Patients most at risk include those with rheumatic valve disease, mitral valve prolapse, bicuspid aortic valve, coarctation, ventricular septal defect or persistent ductus arteriosus. Prosthetic valves may become infected either early (within 60 days of implantation) or late.


The clinical pattern is dependent on the infective organism:


Streptococcus viridans (α-haemolytic group of Strepto-coccus which includes Streptococcus milleri and Strep-tococcus mutans) causes 50% of cases. It is an upperrespiratory tract commensal.


·        Staphylococcus aureus and Staphylococcus epidermidis


·        (skin commensals) cause 25% of cases (in acute infective endocarditis, Staph. aureus is responsible for 50% of cases).


·        Enterococcus faecalis causes 10% of cases.


There are many other rarer bacterial causes and fungal causes include CandidaAspergillus and Histoplasma.


The disease is also dependent on the portal of entry, and risk factors include


·        Recent dental treatment (even descaling) or poor dental hygiene.


·        Infections such as pneumonia, urinary tract infection or any form of chronic sepsis including skin infection.


·        Carcinoma of the colon (Enterococcus endocarditis). Central lines and intravenous drug abuse (tricuspid valve particularly).


·        Post-surgery.




The clinical picture of infective endocarditis is a balance between the virulence of the organism, the susceptibility and immunity of the individual. The result is either an acute infection or a more insidious (subacute) course. The bacteria proliferate on the endocardium, causing the development of friable vegetations containing bacteria, fibrin and platelets. This may result in destruction of valve leaflets, perforation and hence disturbance of function. The disease process predisposes to the formation of thrombus with the potential for emboli. Cytokine generation causes fever. There is a vasculitis and the formation of immune complexes.


·        In acute endocarditis (particularly where Staph. aureus is the cause) the disease is rapid, progresses to cardiac failure and is often fatal.


·        The majority of cases are subacute in which bacterial multiplication is slower and the cardiac lesion may be less obvious; however, systemic manifestations become more significant.



Clinical features


A fever and a new or changing murmur is endocarditis until proven otherwise, although these signs are not universal.


Typical presentations:


Acute bacterial endocarditis presents with fever, new or changed heart murmurs, vasculitis and infective emboli. Severe acute heart failure may occur due to chordal rupture or acute valve destruction.


Subacute endocarditis presents with general symptoms such as fever, night sweats, weight loss, malaise and symptoms of cardiac failure or thromboem



General signs:


Malaise, pyrexia, anaemia and splenomegaly, which may be tender.


Clubbing of the nails is seen only in subacute forms as it takes months to develop.


Arthralgia may occur as a result of immune complex




Cardiac lesions:


New or changed murmurs are characteristic.


Cardiac failure occurs as a result of the haemodynamic disturbance due to the valve lesion(s), e.g. aortic or mitral regurgitation.


Skin lesions:


Osler’s nodes are tender nodules palpated at the tips of fingers and toes; they are embolic or vasculitic lesions causing pulp infarcts.

Splinter haemorrhages, linear dark streaks seen in the nail bed are due to vasculitis.


Janeway lesions are small, flat, erythematous lesions on soles and palms, particularly the thenar and hypothenar eminences, caused by vasculitis.


Petechiae may be embolic or vasculitic often seen on mucosa of pharynx and retinal haemorrhages may be seen (Roth’s spots are haemorrhages with a pale centre).





Blood cultures are positive in 90% when three sets of cultures are taken from differing sites.


Echocardiography is used to visualise vegetations and to assess the degree of valvular dysfunction. If the transthoracic echo is not diagnostic a transoesophageal echo is useful especially to show mitral valve disease, aortic root abscess and to visualise leaflet perforations.


Full blood count shows an anaemia with neutrophilia. There is a high ESR and CRP.


Microscopic haematuria results from the immune complexes. Urine cultures may be required to identify a urinary tract infection, and renal ultrasound may be indicated to demonstrate a renal abscess.


Chest X-ray may show heart failure or pulmonary infarction/abscess.


ECG may show a prolonged PR interval suggests aortic root abscess encroaching on the atrioventricular node.





Cardiac failure is the most serious potential complication particularly when treatment is delayed.


Virtually any organ system may be affected by mycotic emboli, which commonly develop into abscesses. For example cerebral, renal, splenic or mesenteric infarction and abscess formation in left-sided cardiac lesions, or pulmonary abscesses in right-sided cardiac lesions. Cerebral emboli may cause infarction or mycotic aneurysms resulting in convulsions, hemiplegia or other abnormal neurology. Emboli may even occur after treatment has been completed.


Nephrotic syndrome or renal failure due to the glomerulonephritis that occurs following immune complex deposition within the kidneys.




It is important to identify the organism responsible for the endocarditis; however, this should be balanced with the need to treat promptly. Once cultures are sent, intravenous antibiotics should be commenced based on the most likely pathogens if there is a high suspicion of bacterial endocarditis.


·        Blind treatment includes benzylpenicillin or flucloxacillin, and gentamicin for its synergistic effect, as these will cover the most common organisms Staphy-lococcus,Streptococcus and Enterococcus. Oral fusidic acid is added if Staphylococcus is suspected.


·        When the culture results are known endocarditis should be treated with the most appropriate antibiotics. It is best to have a multidisciplinary approach with early microbiological and surgical advice.


·        It is usually necessary to continue antibiotic treatment for 6 weeks, but this may be converted to oral therapy after 2 weeks if the organism is sensitive.


Indications for surgical intervention in infective endocarditis to repair or replace valves:


·        Sufficient valve damage to cause symptomatic heart failure.


·        Persistent infection refractory to treatment, or relapse following end of treatment.


·        Development of aortic root abscess (lengthening PR interval).


·        Fungal infection (large vegetations) rarely responds to medical treatment alone.


·        Multiple embolisation.


·        Prosthetic valves commonly require surgery together with medical therapy.


The timing of surgery is a balance between the desire to eradicate bacteria prior to the procedure and the need for early surgery due to the compromised haemodynamic state. After surgery a full course of drug treatment should be given to eradicate the organisms.


Prophylactic treatment: Abnormal or prosthetic heart valves, patent ductus or septal defects and patients with previous endocarditis are advised to have prophylactic oral or intravenous antibiotic cover for non-sterile pro-cedures. For example, amoxycillin for dental procedures, and amoxycillin and gentamicin for oropharyngeal, gastrointestinal or genitourinary procedures.




Despite advances in treatment, overall mortality is still 15% and as high as 40–60% in prosthetic valve endo carditis; this is due to changing patterns of the disease (elderly, drug addicts, prosthetic valves, antibiotic resistance).

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