Infective Endocarditis

Infective endocarditis can be a strange infection to meet on placement because the patient does not always look as though the problem is in the heart. One person may arrive acutely unwell with fever and breathlessness. Another may have spent several weeks feeling exhausted, losing weight and wondering why a fever keeps returning. Someone else may first come to attention because they have had a stroke.

Those presentations start to fit together once you picture where the infection is sitting. In infective endocarditis, microorganisms become established on the endocardial surface of the heart, most often on a valve. They do not simply sit on the surface as a thin layer of infection. They become caught within a growing mass of platelets and fibrin called a vegetation, and from there the infection can damage the valve, spread into nearby cardiac tissue or send infected material elsewhere in the circulation.

How does an infection take hold on a moving heart valve?

A healthy valve is surprisingly resistant to infection. Its endothelial surface is smooth and bacteria passing briefly through the bloodstream would not usually be expected to settle there. The situation changes when that surface is damaged or abnormal. Platelets and fibrin collect over the injured area as part of the body's normal response, creating a small thrombotic surface to which certain microorganisms can attach if they enter the bloodstream.

The bacteraemia may come from an obvious source such as an infected intravascular line, a skin or soft-tissue infection or injecting drug use. Microorganisms can also enter the blood from the mouth and other colonised surfaces. Brief episodes of bacteraemia happen more commonly than most of us realise and usually come to nothing because the organisms are cleared. Endocarditis develops when an organism is able to adhere, survive and multiply on the endocardial surface.

This helps explain why prosthetic valves, some forms of valve disease, previous infective endocarditis, certain congenital heart conditions and intracardiac devices increase risk. But a history of valve disease is not essential. Staphylococcus aureus is particularly important because it is sufficiently virulent to infect valves that were previously normal. Streptococci and enterococci are also common causes.

Once organisms have attached, further platelets and fibrin are deposited around them and the vegetation grows. This is a useful picture to keep in mind when thinking about treatment. The bacteria are not simply floating freely in the blood where an antibiotic can easily reach them. They are established within infected material attached to a valve, which is one reason treatment is prolonged and why identifying the organism matters so much.

The vegetation can cause trouble in three directions

First, it can damage the valve underneath it. Infection and inflammation can destroy leaflet tissue, cause perforation or interfere with the valve closing properly. Blood then leaks backwards through the damaged valve. If severe regurgitation develops quickly, the heart has not had time to adapt to the sudden change in volume and pressure. A patient who was admitted with an infection may therefore become acutely breathless, develop pulmonary oedema and deteriorate with heart failure.

Second, the infection can move beyond the valve. An abscess may form in the tissue around it. This becomes particularly significant around the aortic valve because the cardiac conduction system lies nearby. If a patient with endocarditis develops a new atrioventricular conduction abnormality, that is not something to file away as an unrelated ECG finding. It can be a clue that infection has extended into surrounding cardiac tissue.

Third, pieces of the vegetation can break away. Vegetations are friable, and they are sitting in blood that is moving past them with every heartbeat. When infected material detaches, it travels as a septic embolus.

Where it goes depends partly on which side of the heart is infected. Material leaving a left-sided vegetation enters the systemic circulation. It may reach the brain and cause a stroke, but the spleen, kidneys, limbs and other organs can also be affected. Suddenly the neurological observations, urine output, abdominal pain and peripheral circulation of a patient admitted with a heart infection no longer feel like separate issues.

With right-sided endocarditis, embolic material is carried towards the lungs instead. Septic pulmonary emboli can produce pleuritic pain, breathlessness and pulmonary lesions. Right-sided disease, particularly involving the tricuspid valve, is associated with injecting drug use and can also occur with intravascular or intracardiac devices.

There is another layer to the disease that does not come directly from pieces of vegetation travelling around the body. Persistent infection can drive immune-complex formation, and deposition of these complexes can contribute to glomerulonephritis. Renal impairment in endocarditis therefore deserves thought rather than a single explanation. Sepsis and haemodynamic compromise may reduce renal perfusion, an embolus may affect the kidney, immune-mediated glomerular injury may be present, and some of the medicines used during treatment can also affect renal function.

The classic peripheral signs students learn about, including splinter haemorrhages, Janeway lesions and Osler nodes, can occur through the vascular, embolic and immune effects of the disease. They are worth recognising, but their absence should never reassure you that endocarditis is not present. Many patients do not have the textbook collection of peripheral signs.

Blood cultures and echocardiography answer different questions

If endocarditis is suspected, blood cultures are trying to tell us what is growing. This is important because treatment for S. aureus is not interchangeable with treatment for a streptococcus, enterococcus or fungus. When the patient is clinically stable, blood cultures should be collected before antimicrobial treatment so that the chance of recovering the organism is not reduced. If the patient is critically unwell, cultures should be obtained promptly but should not create an unsafe delay in treatment.

Echocardiography is looking at a different part of the problem: what has the infection done to the heart? A transthoracic echocardiogram may show a vegetation, new regurgitation or another structural complication. Transoesophageal echocardiography brings the ultrasound probe much closer to the heart and can give better views when the transthoracic study is inconclusive, when prosthetic material is present or when there is concern about complications around the valve.

A negative first echocardiogram does not automatically rule out infective endocarditis when the clinical suspicion remains high. The diagnosis is assembled from the microbiology, cardiac imaging, clinical presentation, predisposing factors and evidence of complications. Current European Society of Cardiology guidance also incorporates other imaging, including cardiac computed tomography and nuclear imaging, in selected situations where echocardiography does not provide the whole answer.

Treatment is not simply 'give antibiotics and wait'

Antimicrobial treatment is prolonged and tailored to the organism, its susceptibility, whether the infected valve is native or prosthetic, and the patient's clinical circumstances. Renal function matters because both the illness and some antimicrobial regimens can affect the kidneys. Repeat blood cultures may be used to establish whether bacteraemia has cleared, while the patient's clinical course tells the team whether infection is actually coming under control.

Some valves cannot be rescued by antimicrobial treatment alone. Severe valve dysfunction causing heart failure, infection that remains uncontrolled, an abscess or other locally invasive disease, and particular situations with a high risk of further embolism can all lead to early discussion with cardiac surgeons. Modern endocarditis care is therefore multidisciplinary, involving cardiology, microbiology or infectious diseases, cardiac imaging and cardiac surgery as needed.

At the bedside, knowing what the vegetation can do makes the nursing assessment much more purposeful. New breathlessness, falling oxygen saturations and crackles may point towards worsening valve regurgitation and pulmonary oedema. New facial weakness, limb weakness, speech disturbance or confusion may represent cerebral embolism. New flank or abdominal pain, haematuria or worsening renal function may reflect complications beyond the heart. A new conduction abnormality may suggest extension around the valve. None of these changes should be dismissed simply because the patient is already receiving antibiotics.

There is also the less obvious work that is necessary during what can be a long admission. Intravenous access needs careful assessment, time-critical antimicrobials need to be administered correctly, blood results and renal function need to be followed, and the patient may be dealing with weeks of treatment while waiting to find out whether surgery will be necessary. Recovery can continue long after the bloodstream infection has cleared.

What about dental treatment and antibiotic prophylaxis?

The relationship between the mouth and infective endocarditis can make prophylaxis confusing. NICE does not recommend routine antibiotic prophylaxis against infective endocarditis for people undergoing dental procedures simply because they have a cardiac condition that places them at risk. That does not make oral health unimportant. Good dental and oral hygiene, prompt treatment of infection and individual advice for people at increased risk remain part of prevention and patient education.

There are differences between international recommendations on prophylaxis for selected very high-risk patients, which is one reason this should not be reduced to a rule remembered from a textbook. In UK practice, follow current national guidance alongside specialist and local advice for the individual patient.

If someone with suspected infective endocarditis is becoming systemically unwell, Bleepbook's Sepsis Six article looks more closely at recognising deterioration and escalating suspected sepsis.

References

Delgado, V. et al. (2023) 2023 ESC Guidelines for the management of endocarditis. European Society of Cardiology.

National Institute for Health and Care Excellence (NICE) (2008, updated 2016; surveillance reviewed 2024) Prophylaxis against infective endocarditis. CG64.

NHS Endocarditis.

Holland, T.L. et al. (2016) Infective endocarditis. Nature Reviews Disease Primers, 2, 16059.

Hubers, S.A., DeSimone, D.C., Gersh, B.J. and Anavekar, N.S. (2020) Infective endocarditis complicated by embolic events: pathogenesis and predictors. Clinical Cardiology, 43(10), pp. 1067–1075.

Rajani, R. and Klein, J.L. (2020) Infective endocarditis: a contemporary update. Clinical Medicine, 20(1), pp. 31–35.