Myocardial Abscess 

Updated: Nov 07, 2018
Author: Vibhuti N Singh, MD, MPH, FACC, FSCAI; Chief Editor: Mark R Wallace, MD, FACP, FIDSA 

Overview

Background

Myocardial abscess is a suppurative (pus-containing) infection of the myocardium, endocardium, native or prosthetic valves or perivalvular structures, or the cardiac conduction system. In this serious and life-threatening disease, early recognition and institution of appropriate medical and surgical therapy is necessary for patient survival.

In the past, most cases of myocardial abscess were discovered at autopsy. The very first report, published in 1933, was an autopsy report by Cossio and colleagues that involved the finding of a pneumococcal abscess in the region of infarcted myocardial tissue as a complication of bronchopneumonia.[1] Several more such cases were reported later, suggesting that myocardial abscess often occurs in the setting of septicemia and abscesses in other locations. Myocardial abscess can now be detected antemortem using various noninvasive diagnostic modalities.

Infective endocarditis (IE) has become the most common condition underlying myocardial abscesses. This article addresses the presenting features, diagnostic tests, therapeutic interventions, and follow-up strategies for myocardial abscess.

Pathophysiology

Endocarditis

The most common clinical setting for myocardial abscess is as a complication of endocarditis involving either native or prosthetic valves. In a review of 40 cases of infective endocarditis, Gonzalez Vilchez et al (1991) found that 67.5% (27 cases) involved native valves. The most common site was the aortic valve, followed in descending order by the ventricular septa, mitral valves, and papillary muscles. Approximately one third of cases involved the base of the aortic valve. Staphylococcus was the most prevalent species involved, isolated from one third of all cases. Prosthetic valve abscess comprised 34% of cases, and 50% of these were caused by staphylococcal infection.[2] An infected coronary artery stent may be a rare source of multiple myocardial abscesses.[3]

Bacteremia

In the past, the most common setting for myocardial abscess was generalized bacteremia, as described in older autopsy reports. Sanson and colleagues (1963) described 23 cases, 21 of which exhibited multiple abscesses in lungs, kidneys, brain, and myocardium. Myocardial abscesses were small in these patients, and the authors postulated that the patients died too early to develop larger abscesses.[4]

Site of myocardial infarction

Myocardial abscess may develop at the site of a myocardial infarction (MI) but usually develops in the setting of bacteremia. Cossio et al (1933) reported a myocardial abscess at the site of an acute MI.[1] In the case records of the Massachusetts General Hospital, Castleman and McNeely (1970) reported a secondary infection within an inferior wall MI in a patient with Bacteroides bacteremia following genitourinary surgery and placement of an infected indwelling catheter.[5]

In a review of 13 cases of myocardial abscess in acute MI, Weisz and Young (1977) found bronchopneumonia to be the probable source in 4 cases, gastrointestinal and renal sepsis in 2, and no definable source in the others. Organisms included Staphylococcus aureus, Clostridium perfringens, Bacteroides species, Escherichia coli, beta-hemolytic streptococci, and Streptococcus pneumoniae, in order of decreasing frequency.[6]

The propensity of cardiac muscle to develop myocardial abscess in the setting of acute MI and septicemia may be due to the presence of necrosis of the muscular fibers and surrounding inflammatory exudates, decreased or absent perfusion, and lack of cell-mediated immunity secondary to decreased blood flow. Such myocardium also appears to be at a greater risk of rupture than healthy myocardium (7-fold higher per Weisz and Young [1977][6] ), with a catastrophic outcome.

Other clinical settings

Other settings associated with myocardial abscesses that have been reported in the literature include the following:

  • Trauma

  • Deep penetrating wounds

  • Deep burns

  • Infected pseudoaneurysms

  • Suppurative pericarditis

  • Infected transplanted hearts

  • Extension from sternal abscess

  • HIV-associated myocarditis and suppuration

  • Parasitic infections

  • Infection of a left ventricular aneurysm or tumor

Microbiology

Usually, a single type of organism acts as the causal agent. However, not uncommonly, these abscesses have a polymicrobial etiology. Sanson and associates (1963) reported that more than 40% of cases involve more than one microbial agent, usually staphylococci or E coli.[4] Whether this reflected a polymicrobial etiology or a single-organism etiology with subsequent polymicrobial overgrowth is unclear. The increase in antibiotic use in general creates a setting in which polymicrobial involvement may become even more common, especially in patients with diabetes mellitus.

Microorganisms

Microorganisms associated with myocardial abscess include the following:

  • S aureus

  • Haemophilus species

  • Enterococci

  • E coli

  • Beta-hemolytic streptococci

  • S pneumoniae

  • Bacteroides species

  • Parasitic organisms

  • Hydatid cysts, ie, from echinococci

  • Miscellaneous

Pathogenesis

Development of infective endocarditis and subsequent myocardial abscess involves interaction of multiple factors, as follows:

  • Vascular endothelium

  • Hemostatic mechanisms

  • Host immune system

  • Gross anatomic abnormalities in the heart

  • Surface properties of microorganisms

  • Extracardiac events that introduce bacteremia

Each of these components is in itself complex, affected by many factors, and not fully understood. The rarity of endocarditis despite the relatively high prevalence of transient asymptomatic and symptomatic bacteremia suggests that the intact endothelium is resistant to infection. If the endothelium on the valve surface is damaged, hemostasis is stimulated and the deposition of platelets and fibrin complex begins. This complex, called nonbacterial thrombotic endocarditis (NBTE), is more susceptible to bacterial colonization when bacteremia develops from an extracardiac source that allows the organisms access to the NBTE.

The intracardiac consequences of endocarditis range from trivial, characterized by an infected vegetation with no attendant tissue damage, to catastrophic, when infection is locally destructive or extends beyond the valve leaflet. Distortion or perforation of valve leaflets, rupture of chordae tendineae, and perforations or fistulas may result in progressive congestive heart failure (CHF). Infection, particularly that involving the aortic valve or prosthetic valves, may extend into paravalvular tissue and result in myocardial abscesses and persistent fever due to the infection's unresponsiveness to the antibiotic; disruption of the conduction system, with electrocardiographic conduction abnormalities; and clinically relevant arrhythmias or purulent pericarditis.

Epidemiology

Frequency

United States

Myocardial abscess rarely occurs in the United States.

International

Murdoch et al (2009) published a contemporary report on the presentation, etiology, and outcome of infective endocarditis in a large patient cohort from multiple locations worldwide. They analyzed a prospective cohort study of 2781 adults (median age 57.9 y) with definite infective endocarditis (72.1% of the native valve) who were admitted to 58 hospitals in 25 countries over a 5-year period. Seventy-seven percent of the patients presented early in the disease course (ie, within the first month), with few of the classic clinical hallmarks of infective endocarditis. Recent health care exposure was found in one quarter of the patients.

S aureus was the most common pathogen found (31.2% of patients). The mitral valve was found to be infected in 41.1% of cases and the aortic valve in 37.6%. The common complications included stroke (16.9%), embolization other than stroke (22.6%), heart failure (32.3%), and intracardiac abscess (14.4%). Surgical therapy was performed in 48.2% of the patients, and in-hospital mortality rates were high (17.7%).

Several factors portended a high fatality risk, including prosthetic valve involvement (odds ratio [OR], 1.47), increasing age (OR, 1.30), pulmonary edema (OR, 1.79), S aureus infection (OR, 1.54), coagulase-negative staphylococcal infection (OR, 1.50), mitral valve vegetation (OR, 1.34), and paravalvular complications (OR, 2.25). Streptococcus viridans infection (OR, 0.52) and surgery (OR, 0.61) were associated with a decreased fatality risk. In summary, in the early 21st century, infective endocarditis continues to be more often an acute disease, characterized by a high rate of S aureus infection and an unacceptably high mortality rate.[7]

The incidence of infective endocarditis remained relatively stable from 1950-1987, at approximately 4.2 cases per 100,000 patient-years.[8] During the early 1980s, the yearly incidence of infective endocarditis was 2 cases per 100,000 population in the United Kingdom and Wales and 1.9 cases per 100,000 population in the Netherlands. A higher incidence was noted from 1984-1990; 5.9 and 11.6 episodes per 100,000 population were reported from Sweden and metropolitan Philadelphia, respectively.[9]

Infections involving prosthetic valves, especially mechanical prostheses, in which the infection is entirely periannular, often extend into the adjacent myocardium, resulting in paravalvular abscess formation and partial dehiscence of the prosthetic valve with paravalvular regurgitation.

Among 85 patients with endocarditis involving a mechanical prosthesis, annulus invasion and myocardial abscess were noted in 42% and 14% of patients, respectively.[10]

Ben Ismail et al (1987) found annulus infection and valve dehiscence in 38 of 41 (82%) infected mechanical valves examined at surgery or autopsy.[11]

Mortality/Morbidity

Myocardial abscess formation profoundly worsens the prognosis in patients with infective endocarditis.

The mortality rate associated with S aureus infective endocarditis is 42% overall. If treated with antibiotics only, the mortality rate is 75%, while a regimen that combines antibiotics and surgery reduces the mortality rate to 25%.

The presence of an intracardiac abscess or complications increases the mortality rate 13.7-fold.

Race

Myocardial abscess has no substantial racial predilection. However, the condition may be more prevalent in African Americans in urban settings.

Sex

The relative risk ranges from 3.5-8.2. Because mitral valve prolapse (MVP) is more common in women than in men, myocardial abscess is also more common in women than in men.

Among persons who abuse intravenous drugs, myocardial abscess is more prevalent in men (65%-80%).

In adults, MVP has emerged as a prominent predisposing structural abnormality that may account for 7%-30% of cases of nonvalvular endocarditis (NVE). However, myocardial abscess developing in such cases is exceedingly rare.

Age

Involvement of cardiac structures with endocarditis and myocardial abscess mainly depends on the incidence of various underlying structural heart conditions among different age groups.

The incidence of infective endocarditis among hospitalized children ranges from 1 case in 4500 to 1 case in 1280. In the Netherlands, incidences of 1.7 cases per 100,000 persons in boys and 1.2 cases per 100,000 persons in girls have been noted.[8] In neonates, the rate has been increasing because of contaminated intravenous lines and the increased use of right-sided heart catheters. Infective endocarditis usually involves the tricuspid valve and is caused primarily by S aureus. Congenital heart defects are predisposing conditions in toddlers and older children.

In adults, MVP is the most common structural heart abnormality associated with infectious endocarditis, found in as many as 7%-30% of patients with NVE, and the risk increases in patients older than 45 years.

Those who abuse intravenous drugs are increasingly susceptible (2%-5% per patient-year).

Prognosis

With early diagnosis and prompt surgical treatment, patients improve rapidly.

Without surgical intervention, the prognosis worsens very significantly.

Patient Education

Educate patients regarding their condition, and emphasize the importance of prophylaxis.

For excellent patient education resources, visit eMedicineHealth's Infections Center and Heart Health Center. Also, see eMedicineHealth's patient education articles Skin Abscess and Antibiotics.

 

Presentation

History

Physicians must maintain a high index of suspicion to diagnose patients who have myocardial abscess. Many of the clinical features of this condition reflect the symptoms and signs of the clinical setting that predisposes to development of the abscess.

Infective endocarditis is associated with the following:

  • Significant clinical deterioration, including worsening CHF and alteration of heart sounds and murmurs (eg, new-onset valvular regurgitation [100% of cases])[12]

  • Poor response to antibiotics, with persistent fever and other signs of infection despite adequate antibiotic coverage

  • Development of conduction defects or progression of heart block, such as bundle-branch block and atrioventricular block (45%)[2]

  • Sudden onset of complete heart block or Mobitz type II block (highly specific)

  • Type of valve involvement, eg, aortic valve endocarditis (40%-85% incidence)

  • Severe recurrent ventricular arrhythmias

  • Pericarditis (uncommon)

  • Infection of the prosthetic valves (bioprosthetic or mechanical)

  • Right-sided endocarditis in patients with congenital heart disease

The duration of symptoms is short.

The infecting organism is a Pneumococcus or Staphylococcus species.

Acute MI occurs in the setting of septicemia.

Sepsis may complicate a penetrating chest injury.

Myocardial abscess is more prevalent in the period following mechanical interventions or surgery and in patients with HIV/AIDS-related myocarditis.

Most cases of myocardial abscess occur in the setting of infective endocarditis. Symptoms and signs mainly reflect the presence of infective endocarditis. The clinical features persist or worsen upon development of a complicating myocardial abscess.

Myocardial abscess must be considered in patients who have longstanding persistent bacteremia and who do not respond to antibiotic therapy.

One must bear in mind certain constellations of symptoms that may raise the suggestion of myocardial abscess. For example, fever is the most common symptom, presenting in 80%-85% of patients. It is absent in some patients who are elderly; those who have CHF, severe debility, or chronic renal failure; and in patients with coagulase-negative staphylococcal infection and abscess. Another characteristic symptom is chills, which occurs in 42%-75% of cases.

Other signs and symptoms include the following:

  • Anorexia

  • Weight loss

  • Malaise

  • Dyspnea

  • Cough

  • Stroke

  • Headache

  • Nausea/vomiting

  • Myalgia

  • Arthralgia

  • Chest pain

  • Abdominal pain

  • Back pain

  • Confusion

  • Sweats

Physical

Physical examination findings commonly encountered in myocardial abscess are mainly due to the underlying infective endocarditis. These include the following:

  • Fever

  • Tachycardia

  • Murmur, especially changing or new murmur

  • Neurological abnormalities

  • Embolic event

  • Splenomegaly

  • Clubbing

  • Peripheral manifestations

  • Osler nodes

  • Splinter hemorrhages

  • Petechiae

  • Janeway lesions

  • Retinal lesions (Roth spots)

  • Widening pulse pressure, especially with involvement of the aortic valve and progression of aortic regurgitation

Causes

Causes of myocardial abscess associated with endocarditis may include the following:

  • Native valve endocarditis

  • Prosthetic valve endocarditis - Bioprosthesis, mechanical prosthesis

  • Myocardial (muscle) infection - Ventricular septal wall, left ventricular posterior wall

Causes of myocardial abscess associated with septicemia may include the following:

  • Bronchopneumonias

  • Genitourinary infections

  • Other infections

Miscellaneous causes of myocardial abscess may include the following:

  • Complications of acute MI

  • Trauma and deep penetrating wounds

  • Mechanical interventions - Catheterization, angioplasty, stent

  • Infection associated with left ventricular aneurysm

  • Infection associated with atrial myxoma (exceedingly rare)

  • Myocarditis and suppuration associated with HIV

  • Transplanted heart infection

  • Asymptomatic

  • Other

Complications

The following are potential complications of myocardial abscess:

  • Myocardial perforation

  • Significant clinical deterioration

  • Worsening CHF

  • Worsening heart sounds and murmurs

  • New-onset valvular regurgitation (100% of cases)[12]

  • Poor response to antibiotics

  • Development of conduction defects or progression of heart block, such as bundle-branch block and atrioventricular block (45%)[2]

  • Sudden onset of complete heart block or Mobitz type II block (highly specific)

  • Type of valve involvement, eg, aortic valve endocarditis (40%-85%)

  • Miscellaneous (severe recurrent ventricular arrhythmias, pericarditis [uncommon], infection of the prosthetic valves, right-sided endocarditis in patients with congenital heart disease)

 

DDx

 

Workup

Laboratory Studies

Routine blood tests

Complete blood cell count findings (ie, hematological parameters) commonly are abnormal.

Anemia with normochromic normocytic red cell indices is present. A low serum iron level is also observed. A low serum iron-binding capacity is observed in 70-90% of patients.

Anemia worsens with increased duration of illness.

In subacute endocarditis, the white blood cell count is usually normal. In contrast, a leukocytosis with increased segmented granulocytes is common in acute endocarditis and myocardial abscess.

Thrombocytopenia occurs only rarely.

Perform a metabolic chemistry panel.

Erythrocyte sedimentation rate

The erythrocyte sedimentation rate (ESR) is elevated (on average approximately 55 mm/h) in almost all patients with endocarditis and myocardial abscess; the exceptions are those with CHF, renal failure, or disseminated intravascular coagulation.

Although the results are nonspecific, the absence of an increased ESR, other than in the selected circumstances already mentioned, is evidence against a diagnosis of endocardial or myocardial infection or abscess.

Blood cultures

Blood cultures are the crucial laboratory tests for confirming the diagnosis of the underlying endocarditis.

Urinalysis

Urinalysis results are often abnormal, even when renal function remains normal.

Proteinuria and microscopic hematuria are noted in 50% of patients.

Urinalysis also plays a standard role in the evaluation of azotemia, which is frequently associated with myocardial abscess.

Other tests

Perform these as needed for the assessment of the primary source of bacteremia.

Imaging Studies

In the past, most cases of myocardial abscess were found during autopsy; however, detection of myocardial abscess can now be achieved antemortem using multiple noninvasive imaging modalities, including transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE), indium In 111 radionuclide scintigraphy, computed tomography (CT) scan, and magnetic resonance imaging (MRI).

Chest radiography

Perform chest radiography to look for associated pulmonary infection.

Chest radiographic findings help assess for CHF.

Transthoracic echocardiography

TTE helps evaluate patients in whom endocarditis or myocardial abscess is suggested clinically. Findings frequently allow the morphologic confirmation of infection and increasingly aid in making decisions regarding management.

One must perform an echocardiographic evaluation in all patients suspected of having an intracardiac or pericardial infection, including those with negative blood culture findings.

TTE has a sensitivity of 23% and specificity of 98.6%.

According to Ellis et al (1985), the following 5 criteria are 86% sensitive and 88% specific for myocardial abscess:[13]

  • Evidence of prosthetic valve rocking

  • Aneurysmal dilatation of the sinus of Valsalva

  • Posterior aortic root thickness greater than 10 mm

  • Perivalvular density in the septum of greater than 14 mm

  • The presence of "echo-free space" - Very specific but found relatively infrequently

Walker et al report a rare case of a myocardial abscess in valvular endocarditis that was difficult to assess with 2-dimensional TTE; however, real-time 3-dimensional contrast TTE allowed visualization of the full extent of the defect and its precise anatomical location, prior to successful surgical resection.[14]

Transesophageal echocardiography

Although many patients with NVE involving the aortic or mitral valve can be adequately assessed using TTE, TEE with color flow and continuous pulsed Doppler is the state-of-the-art technique. Doppler and color-flow Doppler or contrast 2-dimensional echocardiography helps optimally define fistulas and abscess pockets and extensions. See the image below.

Myocardial abscess. Color Doppler imaging showing Myocardial abscess. Color Doppler imaging showing flow into the aortic root abscess.

TEE has a sensitivity of 87% and specificity of 94.6%. Patients in whom an abscess is suggested but has not been detected using TEE should undergo MRI, including magnetic resonance angiography. See the images below.

Myocardial abscess. Transesophageal echocardiogram Myocardial abscess. Transesophageal echocardiogram exhibiting aortic valvular endocarditis and aortic root abscess.
Myocardial abscess. Aortic valvular ring abscess s Myocardial abscess. Aortic valvular ring abscess seen by transesophageal echocardiography.

Scintigraphy

Indium In 111 leukocyte scintigraphy is especially useful in prosthetic valve endocarditis, in which echocardiography shows too much scatter.

A few milliliters of venous blood is drawn and mixed with an anticoagulant solution. The white blood cells are separated and labeled with radioactive isotope111 In, centrifuged, resuspended in isotonic sodium chloride solution, and reinjected into the patient. Images are then obtained with a gamma-ray camera within 16-24 hours. The viable radioactive leukocytes potentially accumulate in the areas of inflammation or abscess. Obtain oblique views to avoid overshadowing by sternal accumulation.

The need for111 In scintigraphy is very low if TEE is used.

MRI

This is a good modality for helping delineate myocardial abscess. However, the portability and excellent resolution of echocardiography make it more practical than MRI.

CT scan

Only anecdotal reports of diagnosis are available. It is not very sensitive.

Intraoperative echocardiography

Although invasive, small abscesses can be detected in the operating room by means of intraoperative echocardiography, which may enable the operating surgeon to drain the abscess effectively.

Other Tests

Electrocardiography

New-onset and persistent electrocardiographic conduction abnormalities may be observed. Gradual PR prolongation may be observed, and it may suggest development of valve ring abscess.

Although not a sensitive indicator of perivalvular infection or abscess (28%), these findings are relatively specific (85-90%). See the image below.

Myocardial abscess. Complete heart block seen on a Myocardial abscess. Complete heart block seen on a 12-lead electrocardiogram in a patient with myocardial abscess involving the prosthetic aortic valve ring.

Tests of immune system stimulation

Tests results may show disease activity, but the tests are costly and not very efficient for diagnosis or monitoring response to therapy

These may include testing of circulating immune complexes, rheumatoid factor, quantitative immune globulin, cryoglobulins, and C-reactive protein.

Serologic tests

Serological test findings are used to evaluate cardiac sepsis in which blood culture findings are negative.

Tests to detect antibodies to ribitol teichoic acids from staphylococci may help distinguish uncomplicated S aureus bacteremia from that associated with cardiac involvement.

These tests have not been used in clinical applications because of their lack of adequate specificity or predictive value.

Procedures

Cardiac catheterization may add very little to the imaging studies and is not recommended unless coronary angiography is needed for patients undergoing valve surgery who also may have significant coronary artery disease.

Histologic Findings

Biopsy and histologic assessment is not a part of the diagnostic workup of myocardial abscess. However, surgically removed valves and autopsy findings from fatal cases reveal certain gross and microscopic features. See the images below.

Myocardial abscess (gross). Myocardial abscess (gross).
Myocardial abscess (opened). Myocardial abscess (opened).

The infection in native valves and mechanical prostheses that leads to development of myocardial abscess tends to extend beyond the valve ring into the annulus and periannular tissue and into the mitral-aortic intravalvular fibrosa, resulting in ring abscesses, septal abscesses, fistulous tracts, and dehiscence of the prosthesis with hemodynamically significant paravalvular regurgitation.

In autopsy experience with 74 patients, annular invasion was noted in 85%, myocardial abscess formation in 32%, valve obstruction by vegetation overgrowth in 19%, and erosion through the aortic annulus to cause pericarditis in 5%. In another series of 85 patients, the findings were annulus invasion in 42%, myocardial abscess in 14%, valve obstruction in 4%, and pericarditis in 2%. The intracardiac pathology of bioprosthetic valve infective endocarditis is more heterogeneous and includes invasive disease and leaflet destruction.

Myocardial abscess histology findings demonstrate damaged cardiac tissue with degraded collagen and polymorphonuclear predominance.

 

Treatment

Medical Care

Medical treatment includes the following:

  • Antibiotics

  • Agents for stabilization of hemodynamic status

Supportive treatment includes the following:

  • Fluid and electrolyte balance

  • Nutritional support

Surgical Care

Once the diagnosis of myocardial abscess is made, the treatment of choice is surgical in nature. Appropriate procedures include the following:

  • Open heart surgery

  • Valve replacement

  • Re-replacement of prosthetic valves

  • Abscess evacuation

Consultations

Myocardial abscess usually develops in patients who are generally very ill, with multiorgan system involvement and unremitting infective endocarditis. The expertise of several subspecialists is needed:

  • Cardiologist

  • Cardiovascular surgeon

  • Infectious disease specialist

  • Intensive care medicine and pulmonary medicine specialists

  • Nephrologist

  • Microbiologist/pathologist

Diet

Patients with myocardial abscess are often critically ill. Supplementation of nutritive food, either by the enteral or parenteral route, is very important.

Patients must be maintained without oral intake until a decision regarding surgical intervention has been made and surgery has been performed.

Postoperatively, gradual advancement in the diet is recommended.

Activity

Critically ill patients with myocardial abscess and infective endocarditis are usually bedridden, with minimal activity.

Frequently, such patients must receive prophylaxis to prevent development of deep venous thrombosis (DVT) and pulmonary embolization (PE).

Gradual increase in ambulation is recommended following surgical intervention.

Prevention

Prompt and effective treatment of infective endocarditis is required.

A high index of suspicion and early recognition of the changes that suggest development of myocardial abscess are necessary.

Regular prophylaxis for subacute bacterial endocarditis, with preoperative antibiotics according to the recommendations of the American Heart Association, is necessary.

Critically ill patients with myocardial abscess and infective endocarditis are usually bedridden, with minimal activity. Frequently, such patients must receive prophylaxis to prevent development of DVT and PE.

Further Outpatient Care

Further outpatient care may include the following:

  • Continuation of adjunctive therapy

  • Anticoagulation therapy, in case of metallic prosthetic valve replacement

  • Continuing antibiotic therapy

  • Diuretic use with CHF

  • Antiarrhythmic therapy for postoperative arrhythmias

  • Aggressive antibiotic prophylaxis prior to minor surgeries

Further Inpatient Care

Aggressive postoperative supportive therapy in patients with myocardial abscess includes the following:

  • Agents for stabilization of hemodynamics

  • Fluid and electrolyte balance

  • Nutrition (parenteral or enteral)

Continuation of antibiotic therapy may be necessary. Patients may still require a prolonged 6-week course of antibiotic therapy.

Inpatient & Outpatient Medications

These include the following:

  • Vancomycin

  • Gentamicin

  • Dopamine

  • Diuretics

  • Anticoagulants

Transfer

Patients with infective endocarditis usually exhibit rapid deterioration, and they may require transfer to a tertiary care facility for a diagnostic workup and open heart surgery. Such patients must be transported via an Advanced Cardiac Life Support ambulance staffed with well-trained and experienced paramedics.

 

Medication

Medication Summary

Even though the main mode of treatment is surgical, patients with myocardial abscess still require antibiotics and adjunct agents for stabilization of hemodynamic status (ie, pressors).

Antibiotics

Class Summary

These agents are used to treat susceptible organisms, especially Staphylococcus species, which are the most common organisms in myocardial abscesses.

Vancomycin (Lyphocin, Vancoled, Vancocin)

Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or have not responded to penicillins and cephalosporins or those who have infections with resistant staphylococci. For abdominal penetrating injuries, combine with an agent active against enteric flora and/or anaerobes. To avoid toxicity, current recommendation is to assay vancomycin trough levels after third dose drawn 0.5 h prior to next dosing. Use CrCl to adjust dose in patients diagnosed with renal impairment. Used in conjunction with gentamicin for prophylaxis in patients allergic to penicillin who are undergoing GI or GU procedures.

Gatifloxacin (Tequin)

Fluoroquinolone with antimicrobial activity based on ability to inhibit bacterial DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. Fluoroquinolones have broad activity against gram-positive and gram-negative aerobic organisms. Differences in chemical structure between quinolones have resulted in altered levels of activity against different bacteria. Altered chemistry in quinolones results in toxicity differences.

Gentamicin (Garamycin)

Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and one that covers anaerobes.

Not DOC. Consider if penicillins or other less-toxic drugs are contraindicated, when clinically indicated, and in mixed infections caused by susceptible staphylococci and gram-negative organisms.

Dosing regimens are numerous; adjust dose based on CrCl and changes in volume of distribution. May be given IV/IM.

Levofloxacin (Levaquin)

For pseudomonal infections and infections due to multidrug-resistant gram-negative organisms.

Vasopressors

Class Summary

These agents are used to raise blood pressure and improve tissue perfusion in patients with septic shock or hypotension.

Dopamine (Intropin)

Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect dependent on dose. Lower doses predominantly stimulate dopaminergic receptors, which, in turn, produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation produced by higher doses.

After initiating therapy, increase dose by 1-4 mcg/kg/min q10-30min until optimal response is obtained. More than 50% of patients are maintained satisfactorily on doses < 20 mcg/kg/min.

Anticoagulants

Class Summary

Antithrombin and anticoagulant agents may be needed for prevention of DVT. Anticoagulants are required for stroke prevention after replacement of cardiac valves with mechanical prostheses.

Heparin

Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis.

Warfarin (Coumadin)

Interferes with hepatic synthesis of vitamin K – dependent coagulation factors. Used for prophylaxis and treatment of DVT, PE, and thromboembolic disorders. Tailor dose to maintain INR in range of 2-3.