Aureus or Escherichia Coli. Less Typically, Polymicrobial Abscesses Have Been Noted
Aureus or Escherichia Coli. Less Typically, Polymicrobial Abscesses Have Been Noted
Aureus or Escherichia Coli. Less Typically, Polymicrobial Abscesses Have Been Noted
prosthetic valve tissue. Similar to other abscesses, it develops either by dissemination from a
distant source such as bacteremia or sepsis or by direct extension of a pre-existing cardiac
infective focus. Infective endocarditis has long been identified as the main cause of the latter.
Although the incidence of cardiac abscesses continues to be investigated, it is presumably higher
than noted postmortem and is of great importance when deciding the prognosis and management
of patients. A single organism causes cardiac abscesses, usually Staphylococcus
aureus or Escherichia coli. Less typically, polymicrobial abscesses have been noted. [1],[2],[3]
Important complications of a cardiac abscess, whether alone or with valve tissue, are conduction
abnormalities on electrocardiogram (ECG). The incidence of perivalvular abscess among
patients with infective endocarditis is between 30% to 40%, with the aortic valve having a higher
predisposition than the mitral valve and annulus. Native aortic valve endocarditis, usually
located in a weak part of the annulus near the atrioventricular node (AV), clearly demonstrates
the anatomic predisposition and exemplifies why abscesses and heart block presents as frequent
sequelae.
Perivalvular abscesses are also more common with prosthetic valves. In this case, the annulus
instead of the leaflet is usually the primary site of infection. The degree of conduction disruption,
therefore, depends on the extent of the involvement of the conduction system and is more
commonly seen in perivalvular aortic abscesses. Additionally, the severe extension of
perivalvular infection can also result in extrinsic coronary compression, or disruption, leading to
an acute coronary syndrome. Thus far, only aortic valve involvement and current IV drug use
have been prospectively identified as independent risk factors for a perivalvular abscess. Any
patient with a cardiac abscess, regardless of all other factors, has an increased risk of
embolization, morbidity, and mortality.
Etiology
Cardiac abscesses are most commonly thought to occur primarily by the extent of a pre-existing
cardiac infection, as it is with the case of infective endocarditis (IE). Secondary causes of cardiac
abscess are believed to be due to bacteremia (persistent or transient) without a known cardiac
source, as well as susceptible heart tissue soon after myocardial infarction (MI), or prosthetic
valve disease, usually in the setting of bacteremia. Other less common predisposing factors may
be trauma, penetrating wounds, deep burns, infected transplanted hearts, infected sternal incision
site, pseudoaneurysm, HIV, or parasitic infections.
The following are organisms noted to be involved in cardiac abscess formation:
Staphylococcus aureus
Haemophilus species
Enterococci
Escherichia coli
Beta-hemolytic streptococci
Streptococcus pneumoniae
Bacteroides species
Parasitic organisms
Hydatid cysts
Miscellaneous
In the preantibiotic and earliest antibiotic era, streptococci were the most frequent cause of IE,
responsible for 80% of the cases.25,26 Their relative importance has diminished over the years due to
the regression of rheumatic heart disease, better oral and dental care, simpler chemoprophylaxis and
decreased incidence of streptococcal bacteremia.20 The largest group in percent term is viridans
streptococci, among which S sanguis I and II, S mutans, S mitior, S salivarius, and S milleri are the
most important species causing endocarditis (in order of frequency).
Pathophysiology
The number one predisposing factor for a cardiac abscess is current or prior infective
endocarditis. The most common sites involved are the aortic valve, followed by the ventricular
septa, mitral valves, and papillary muscles. S. aureus, the most commonly involved causative
agent, is present in up to one-third of all cases and has even higher incidence in patients with
prosthetic valves.
Secondly, bacteremia becomes of significant importance although abscesses due to bacteremia
alone tend not to be large enough to cause death and have been reported as an incidental
postmortem finding in most papers.
The site of prior MI has also been documented as a predisposing risk factor for the development
of a cardiac abscess in patients in whom bacteremia is of concern. Such a scenario is plausible in
a patient with known prior infection undergoing an acute coronary syndrome or acquiring the
infection soon following an MI. It is also suspected that the presence of necrosis of muscle fibers
post-MI, in addition to inflammatory state and decreased perfusion with lack of blood flow,
increases myocardium susceptibility to this complication.
Evaluation
Tests to consider include:
Blood and urine studies
Blood cultures
Echocardiography; transthoracic versus transesophageal (TEE), with TEE being more
sensitive and specific as well as recommended for the initial assessment of any patient
with a suspected perivalvular disease
Continuous electrocardiographic monitoring; new atrioventricular block has a positive
predictive value of 88% for abscess formation but low 45% sensitivity.
Always keep in mind that it is in the realm of possibility to obtain negative cultures and still have
a cardiac abscess. For example, a patient whose initial evaluation demonstrated bacteremia
with, initially, no physical signs of IE or cardiac conduction deficit may receive intravenous (IV)
antibiotics before a further workup, and therefore, cultures may not be reliable. Additionally, if
cultures are not drawn properly, the likelihood of positive results decreases significantly.
Treatment / Management
Intravenous antibiotics should be administered in a timely fashion once a patient is suspected of
IE or a cardiac abscess. Empiric broad-spectrum antibiotics until further characterization of
infective species should be monitored for at least 6 weeks of therapy in this patient
population. [9]
Surgery consult and the time of surgical intervention is of high importance when approaching a
patient with a cardiac abscess. There is increased morbidity and mortality in patients in whom
surgery is delayed. Thus early surgery is recommended. Surgery for these patients aims toward
the eradication of the infection and correction of hemodynamic abnormalities.
However, some patients with periannular extension of infection or myocardial abscess could
potentially be treated without surgical intervention. These patients include:
Patients with smaller (less than 1 cm) abscesses
Patients who do not have complications of heart block, an echocardiographic progression
of abscess during antibiotic therapy
Patients who do not have valvular dehiscence or insufficiency
It is recommended that patients who do not undergo surgery are monitored closely with serial
TEE repeated at 2, 4, and 8 weeks after completion of antibiotic therapy.
Complications
Heart block
Arrhythmias
Congestive heart failure
Stroke
Multiple organ failure
Acute respiratory distress syndrome
Death
Postoperative and Rehabilitation Care
These patients often require 6 to 8 weeks of parenteral antibiotic therapy. They also need
deep vein thrombosis (DVT) prophylaxis. Those with a prosthetic valve may require oral
anticoagulants.
Because the patients are critically ill, nutrition is essential.
To help prevent muscle atrophy and DVT, an exercise program is also recommended.
Pseudoaneurysms and fistulae are severe complications of IE and are frequently associated with
very severe valvular and perivalvular damage.213,231–233 The frequency of fistula formation in IE
has been reported to be 1.6%, with S. aureus being the most commonly associated organism
(46%).233
Despite high rates of surgery in this population (87%), hospital mortality remains high
(41%).213,233,234 Other complications due to major extension of infection are less frequent and may
include ventricular septal defect, third-degree atrio-ventricular block and acute coronary
syndrome.223,224,234
Perivalvular extension should be suspected in cases with persistent unexplained fever or new
atrio-ventricular block. Therefore an electrocardiogram should be performed frequently during
continuing treatment, particularly in aortic IE. TOE, MSCT and PET/CT103 are particularly useful
for the diagnosis of perivalvular complications, while the sensitivity of TTE is <50%225–228 (see
section 5). Indeed, perivalvular extension is frequently discovered on a systematic TOE.
However, small abscesses can be missed, even using TOE, particularly those in a mitral location
when there is co-existent annular calcification.