Endocarditis refers to inflammation of the endocardium, the inner lining of the heart. It is most commonly caused by infection, usually bacterial. There are other causes which won’t be focused on much here. It is the valves of the heart which are most commonly affected.
The process starts with the development of a non-infective thrombus formation prior to the infective component. This formation occurs at locations in the heart where there is low pressure. This is usually at the valves because of the venturi effect (the energy is in the form of kinetic energy rather than potential energy due to the narrowing). This process can be acute or subacute in onset. As can therefore be well appreciate, there are a number of conditions that will promote this environment and so increase the risk of IE.
Risk factors include Structural:
Valvular heart disease
Structural congenital heart disease
Invasive procedures e.g. vascular, dental
However, some structural heart disease does not impart an increased risk:
Fully repaired VSD
Fully repaired PDA
Endothelialised closure devices
The valves that are most commonly involved, in descending order are:
There may be combined left sided disease. Right sided IE only makes up about 10% of cases.
The infection results in tissue destruction and the formation of vegetations. Whilst the problem is related to the heart, the location results in significant haematological exposure and so systemic effects.
The most common organisms are:
Coagulase negative Staph.
Group A, B, C, D, G
Haemophilus - parainfluenzae, paraphrophilus
There may also be a fungal pathogen (usually candida or aspergillus species).
Staph. Aureus is the most common cause overall and has a high mortality rate. It is particularly related to IVDU and prosthetic valves. Coagulase negative Staph. causes a subacute disease similar to Strep. viridans.
Strep. viridans is another common pathogen, usually causing a subacute picture. Many of the other strep. pathogens cause quite an acute and severe clinical picture. Group A, C, and G are associated with a high mortality.
The HACEK group are gram negatives with a slowly progressing picture but which are actually a fairly rare cause of IE.
There are a number of rarer organisms that may cause blood culture negative IE:
These require a high degree of suspicion and more focused microbiological investigation.
This can be highly variable and it is recognised that a high degree of suspicion is often needed to detect and diagnose it. The trajectory can be very acute, such as from a septic picture or rapid valvular compromise, through to a slower onset of more general systemic disturbance. In general, the effect of the disease can be broken down to:
Systemic features These are very common.
These may be the primary features in a less acute form of the disease. A severe septic shock picture may also occur.
Congestive cardiac failure
Other end organ infarction e.g. spleen
There are a number of clinical findings that can arise from IE that are worth knowing. However, it is important to bear in mind that these features are fairly rare. Soft tissue
Osler’s nodes - painful, purple/red nodules (oww! for Osler)
A good mnemonic for remembering the features is FROM JANE:
Nail bed haemorrhages
Part of these may be part of a general investigative process whilst others may be more specifically directed at confirming endocarditis as a diagnosis.
FBC - may show anaemia, raised WBC
ECG Changes may include:
T wave inversion
Blood cultures These are a key part of the diagnostic criteria. As such, a careful approach to culture should be taken:
Meticulous ANTT to avoid contamination
Before antibiotic administration when clinically able (i.e. stable enough)
Spaced in time - 3 sets with 6 hour gaps
In severely ill patients this can be reduced to 2 separate sets within an hour.
Serological testing may be needed in cases of culture negative IE.
Echo Transthoracic echo (TTE) is an important initial investigation and should be undertaken with 24h. It has a sensitivity of about 60%. Transoesophageal echo (TOE) is more sensitive (90-99%) and with a 90% specificity and so should be undertaken in the case of an inconclusive or negative TTE. In cases of high clinical suspicion but negative echo, a repeat exam should be undertaken after a week.
Echo findings of IE may include:
Oscillating intracardiac mass associated with a valve or supporting structure
Predisposition - predisposing heart condition or IVDU
Microbiologic evidence (not meeting major criteria)
Echo evidence (not meeting major criteria) - added in the modified Duke
These can be brought together to create a risk category:
1 major and 3 minor
1 major and 1 minor
An additional part of the Duke criteria is the pathological criteria. The presence of just one of these confirms the diagnosis:
Microorganisms in a vegetation
Histological examination of a lesion
Essentially this is usually based on a pathology investigation of samples taken at cardiac surgery, although the investigation of embolised material is also possible.
The components of management can be seen as:
Resuscitation (if needed)
Surgery (if indicated)
Antibiotics These remain the key part of IE treatment. Due to the nature of difficulty getting adequate antibiotic exposure to the bacteria (e.g. due to biofilm development) they are generally given IV and for a prolonged course. The antibiotic choice and duration will be guided by:
Nature of valve (native vs artificial)
Degree of systemic illness
Surgery A surgical opinion is recommended in all patients with an infected prosthetic valve, and they may need to advise in cases of native valve disease. Their main involvement will be in cases where there has been a degree of valvular/structural damage from the infection that surgical intervention is needed e.g. valve replacement. This is clearly challenging given problems of performing surgery at a sight of infection. Indications for surgery may include:
CVS failure relating to valvular compromise e.g. severe AR
Inadequate response to antimicrobial therapy
Prevention of embolism
Large vegetations with embolic phenomenon (left side of heart)
Very large vegetations
Valve destruction leading to heart failure occurs in about half of patients. This is a trigger for surgical intervention as untreated failure carries a significant mortality (80%).
Stroke can complicate between 20-40% of cases of left sided IE. It is a major contributor to morbidity and mortality. A vegetation larger than 10mm is a major risk factor.
Perioperative mortality for urgent/emergent surgical intervention is high (5-15%). In stable patients this approaches the normal risk for valve surgery.